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Right and Left Ventricular Outflow Tract Tachycardias: Evidence for a Common Electrophysiologic Mechanism

babacon — Mon, 03 Nov 2014 07:58:52 GMT

Sei Iwai, MD, Daniel J. Cantillon, MD, Robert J. Kim, MD, Steven M. Markowitz, MD, Suneet Mittal, MD, Kenneth M. Stein, MD, Bindi K. Shah, MD, Ravi K. Yarlagadda, MD, Jim W. Cheung, MD, Vivian R. Tan, MD, Bruce B. Lerman,

Abstract

Introduction: "Idiopathic" ventricular arrhythmias most often arise from the right ventricular outflow tract (RVOT), although arrhythmias from the left ventricular outflow tract (LVOT) are also observed. While previous work has elucidated the mechanism and electropharmacologic profile of RVOT arrhythmias, it is unclear whether those from the LVOT share these properties. The purpose of this study was to characterize the electropharmacologic properties of RVOT and LVOT arrhythmias.

Methods and Results: One hundred twenty-two consecutive patients (61 male; 50.9 ± 15.2 years) with outflow tract arrhythmias comprise this series, 100 (82%) with an RVOT origin, and 22 (18%) with an LVOT origin. The index arrhythmia was similar: sustained ventricular tachycardia (VT) (RVOT = 28%, LVOT = 36%), nonsustained VT (RVOT=40%, LVOT=23%), and premature ventricular complexes (RVOT = 32%, LVOT = 41%) (P = 0.32). Cardiac magnetic resonance imaging and microvolt T-wave alternans results (normal/indeterminate) were also comparable. In addition, 41% with RVOT foci and 50% with LVOT foci were inducible for sustained VT (P = 0.48), and induction of VT was catecholamine dependent in a majority of patients in both groups (66% and 73%; RVOT and LVOT, respectively; P = 1.0). VT was sensitive to adenosine (88% and 78% in the RVOT and LVOT groups, respectively, P = 0.59) as well as blockade of the slow-inward calcium current (RVOT=70%, LVOT=80%; P = 1.00) in both groups.

Conclusions: Electrophysiologic and pharmacologic properties, including sensitivity to adenosine, are similar for RVOT and LVOT arrhythmias. Despite disparate sites of origin, these data suggest a common arrhythmogenic mechanism, consistent with cyclic AMP-mediated triggered activity. Based on these similarities, these arrhythmias should be considered as a single entity, and classified together as "outflow tract arrhythmias."

Introduction

The most common form of "idiopathic" ventricular tachycardia (VT) localizes to the right ventricular outflow tract (RVOT) and is referred to as RVOT tachycardia. Although less common, tachycardia arising from the left ventricular outflow tract (LVOT) is also observed. Up to 90% of outflow tract VT is thought to originate from the right ventricle, mainly from the RVOT but also from other regions of the right ventricle, including sites above the pulmonary valve.^[1]LVOT tachycardia can arise from endocardial sites, epicardial sites,^[2] the aorto-mitral continuity, as well as from foci accessible from the aortic sinuses of Valsalva.^[3,4]

RVOT tachycardia has been shown to have a unique arrhythmogenic substrate and electropharmacologic profile. In general, it is adrenergically mediated and sensitive to perturbations that lower intracellular calcium (e.g., adenosine and verapamil). These findings are consistent with VT due to cyclic adenosine monophosphate (cAMP)-mediated triggered activity dependent on delayed afterdepolarizations.^[5,6] It is unclear whether LVOT tachycardia shares a similar clinical phenotype, mechanism, and electrophysiologic properties, given its disparate location. To date, there has been no series comparing the clinical characteristics and electrophysiologic properties of LVOT and RVOT arrhythmias. Therefore, the purpose of this study was to fully characterize the electropharmacologic properties of these two entities in a large series of consecutive patients.

Methods

Study Population

We evaluated 122 consecutive patients with suspected outflow tract arrhythmias who presented to our laboratory for electrophysiologic evaluation, and underwent a complete electrophysiology study. Of note, 17 patients in our registry were excluded from this series due to incomplete electrophysiologic testing. For the purposes of this study, the LVOT includes foci in the aortic sinuses of Valsalva as well as the aortomitral continuity. Ectopy originating in nonoutflow tract sites (including epicardial foci) were excluded from this analysis. Reasons for referral included symptoms refractory to medical therapy, as well as suspected left ventricular dysfunction due to frequent ectopy. This analysis was approved by our institutional review board.

Noninvasive Evaluation

Patients underwent systematic evaluation of cardiac structure, function, and ectopy burden. When possible, this included cardiac magnetic resonance imaging (MRI) as well as 24-hour Holter monitoring and/or inpatient telemetry. The presence of coronary artery disease was assessed by stress testing and/or cardiac catheterization (defined as ≥70% stenosis of any major epicardial vessel). Left ventricular systolic function was quantified by echocardiography, radionuclide ventriculography, and/or ventricular cineangiography. Structural heart disease was defined as presence of coronary artery disease (defined above), left ventricular ejection fraction <40%, and/or moderate or severe valvular disease.

Electrophysiologic Testing

After giving informed written consent, patients underwent a standardized electrophysiologic testing protocol following an overnight fast. Patients were locally anesthetized with 0.25% bupivacaine and, if necessary, minimally sedated with intravenous midazolam and morphine or fentanyl. Quadripolar 6 F catheters were advanced to the high right atrium, His bundle position, and right ventricular apex and/or outflow tract. Bipolar intracardiac electrograms were filtered at 30–500 Hz. If further mapping and/or ablation in the left ventricle or sinuses of Valsalva was required, a retrograde aortic approach was used.

The stimulation protocol included burst atrial and ventricular pacing, and the introduction of single atrial and up to triple ventricular extrastimuli from up to two right ventricular sites. Stimuli were delivered as rectangular pulses of 2-msec duration at four times diastolic threshold. If necessary to facilitate induction of sustained tachycardia, programmed stimulation was repeated from at least one right ventricular site after isoproterenol or dobutamine (during a time period of national shortage of isoproterenol) was infused to decrease the sinus cycle length by approximately 20-30%.

When the systems were acquired, three-dimensional mapping was performed using one of two systems. The Biosense-CARTO electroanatomic mapping system (Biosense-Webster, Diamond Bar, CA, USA) was used in 86 patients, using previously described methods.^[7] The Endocardial Solutions noncontact mapping system (Endocardial Solutions, Inc., St. Paul, MN, USA) was employed in four patients, as previously described.^[8] All patients whose targeted ectopy had a left bundle inferior axis morphology initially had activation mapping performed in the right ventricle. If this failed to demonstrate an "early" (i.e., pre-QRS) site, mapping of the left ventricle via retrograde aortic approach was considered.

Evaluation of microvolt level T-wave alternans (TWA) was also performed, during atrial pacing at the time of the electrophysiologic study. TWA was not performed if the patient had incessant ectopy at baseline, or presented in an atrial arrhythmia. The current protocol (performed in 58 patients) involved recording at baseline and during right atrial pacing at 109 bpm for 5 minutes. TWA was analyzed using either the Cambridge Heart CH2000 or HearTwave system (Cambridge Heart, Inc., Bedford, MA, USA) according to standard criteria.^[9]

Pharmacologic Testing

Adenosine was given only when sustained VT (>30 seconds) was reproducibly induced during electrophysiologic testing. VT was considered adenosine sensitive if it terminated reproducibly within 20 seconds of administration of adenosine, in the absence of a premature ventricular complex (PVC). Adenosine (Adenocard; Astellas Pharma US, Inc., Deerfield, IL, USA) was administered as a rapid bolus through a central venous catheter, followed by a 10 mL flush of normal saline. The usual initial dose of adenosine was 6 mg, with the dose titrated incrementally by 6 mg until tachycardia terminated, suppressed, or ventriculo-atrial (VA) block occurred. Similarly, verapamil (5-20 mg i.v.) was also infused over 60 seconds when clinically appropriate/tolerated, to determine its effect on tachycardia.

Continuous variables were expressed as a mean standard deviation. Comparisons between groups were made using the independent samples t-test or Wilcoxon two-sample test where appropriate, according to normality of distribution. Categorical variables, expressed as numbers and percentages, were compared using Fisher's exact test or chi-square test, depending on the number of variables. All tests of significance were two-tailed, and P values of <0.05 were considered statistically significant.

Discussion

The principal finding in this study is that RVOT and LVOT tachycardias have similar electrophysiologic properties and underlying mechanism. The data in this study are unique, in that this is the largest single-center experience of outflow tract arrhythmias that utilizes a systematic approach to investigate the underlying arrhythmia mechanism. This included standardized electrophysiologic testing, pharmacologic perturbations, as well as TWA testing.

We found that both left and RVOT arrhythmias are inducible with programmed stimulation and are facilitated by catecholamine infusion. In addition, both forms of VT terminate in response to adenosine as well as verapamil. This pharmacologic profile distinguishes them from other forms of ventricular tachycardia,^[11] and suggests that arrhythmias from both of these sites appear to be caused by triggered activity due to cyclic adenosine monophosphate (cAMP)-mediated calcium-dependent delayed afterdepolarizations.^[6] Although there was a difference is cycle length of inducible sustained VT between the two groups, this cannot be easily explained. It is unlikely to have an underlying mechanistic etiology, and is possibly due to the small sample size of LVOT patients in combination with the slightly higher proportion of LVOT patients requiring catecholamine infusion to induce sustained VT.

HỘI CHỨNG KOUNIS

babacon — Sat, 06 Sep 2014 14:38:59 GMT

Abstract

Mối liên quan giữa biến cố mạch vành cấp tính và phản ứng dị ứng đã được công nhân trong nhiều năm. Trường hợp đầu tiên được báo cáo vào năm 1950, trong một phản ứng dị ứng với penicillin. Năm 1991, Kounis và Zavras mô tả hội chứng đau thắt ngực do dị ứng và dị ứng gây nhồi máu cơ tim, hiện nay được gọi là hội chứng Kounis. Có 2 loại được mô tả: loại I, xảy ra ở những bệnh nhân không có các tổn thương thực thể động mạch vành và được gây ra bởi sự co thắt động mạch vành, và loại II, xảy ra ở bệnh nhân có thương thực thể mạch vàkhi các sự kiện dị ứng gây ra xói mòn mảng bám hoặc làm vỡ các mãng xơ vữa. Hội chứng này đã được báo cáo gắn với một loạt các yếu tố tiếp xúc với môi trường, và tiếp xúc với thuốc. Trong bài này, chúng tôi thảo luận về các bệnh lý, các yếu tố gây dị ứng, các triệu chứng liên quan, và điều trị hội chứng Kounis.

Braunwald lưu ý rằng đau thắt ngực vasospastic có thể được gây ra bởi các phản ứng dị ứng, với các trung gian như histamin và leukotrienes tác động lên cơ trơn mạch máu vành. [8,9] do đó, đau thắt ngực dị ứng và dị ứng nhồi máu cơ tim đã trở thành công nhận là hội chứng Kounis. [6,7]

Hội chứng Kounis (KS), hoặc sự đồng thuận của biến cố mạch vành cấp tính với các phản ứng dị ứng hoặc quá mẫn, đã ngày càng được báo cáo trong y văn. Tần suất thực sự của KS là không rõ. Tuy nhiên, trong một nghiên cứu nọc độc của côn trùng thách thức chẩn đoán Brown và cộng sự báo cáo rằng 9,5% tình nguyện khỏe mạnh phát triển đau ngực bất thường trên điện tâm đồ phù hợp với thiếu máu cục bộ cơ tim cấp tính. [10]

Classification and Clinical Presentation

Loại I là sự xuất hiện của đau ngực trong một phản ứng dị ứng cấp tính ở bệnh nhân không có tổn thương thực thể động mạch vành. Một sự kiện dị ứng cấp tính gây ra co thắt động mạch vành, dẫn đến đau ngực và thay đổi trên điện thiếu máu cục bộ, và men tim, hoặc có thể là bình thường hoặc phản ánh sự tiến triển đến một nhồi máu cơ tim cấp tính. [6,11] Những trường hợp này có bình thường tưới máu cơ tim quét, bình thường chụp mạch vành, và thử nghiệm ergonovine tích cực. [11] Lời giải thích cho loại rối loạn chức năng nội mô sẽ là đau thắt ngực hoặc vi mạch máu. [12]

Type II là sự xuất hiện của đau ngực ở bệnh nhân có bằng chứng chụp angiographic của bệnh động mạch vành trong một phản ứng dị ứng cấp tính. [6,11] loại này bao gồm những bệnh nhân có bệnh từ trước, phản ứng dị ứng cấp tính có thể gây ra xói mòn mảng bám hoặc vỡ biểu hiện như một nhồi máu cơ tim cấp tính. [1,6,12]

Biểu hiện lâm sàng của KS bao gồm một hỗn hợp của các triệu chứng và dấu hiệu của một phản ứng dị ứng và hội chứng mạch vành cấp tính, đau ngực, khó thở, vừa thấy muốn ngất, buồn nôn, nôn mửa, ngất, ngứa, nổi mề đay, toát mồ hôi, xanh xao, đánh trống ngực, hạ huyết áp, nhịp tim chậm, vv . [13]

Mặc dù hội chứng này đã được báo cáo chủ yếu ở người lớn, Biteker và các cộng sự vừa công bố một đánh giá thú vị của trẻ em với KS [14] lứa tuổi của bệnh nhân giữa chín và mười ba tuổi. Hai trong số họ đã phát triển một phản ứng dị ứng với amoxicillin / clavulanic acid, một sau một nọc ong, và một sau một nọc ong. Tất cả bốn trẻ em phát triển đau ngực liên quan đến độ cao đoạn ST và men t im dương tính. Mức tryptase huyết thanh đã được nâng lên trong tất cả các trẻ em, và cụ thể immunoglobulin E (IgE) đã được nâng lên ở một trong hai bệnh nhân tiếp xúc với amoxicillin / clavulanic. Các bệnh nhân được điều trị thành công với thuốc kháng histamin đường uống, prednisolone và ổn định tế bào mast.

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PHÂN BIỆT NHỊP NHANH THẤT TỪ BUỒNG TỐNG THẤT PHẢI VÀ TRÁI TRÊN ECG (RVOT/LVOT VT)

babacon — Thu, 03 Jul 2014 06:31:02 GMT

DR. Babacon

Usually focal in nature.

May be an indicator of early stages of ARVD.

Activation is high to low as shown in the inferior leads.

Transition of the precordial leads helps to determine RVOT vs LVOT origins.

Chart for different locations

A Look at RVOT VT

The following images were collected from one procedure. The images selected provide some valuable insight to RVOT arrhythmias. To the right of each image is an explanation of what the image displays and what role the information displayed plays in the overall procedure. Note that the first image is a standard surface 12 lead recording. When ectopy presents itself at the start of any procedure, it is important to record a 12 lead. Many times it is difficult to reproduce focal arrhythmias in the lab once a patient is supine or sedated. If you have a 12 lead recording based upon the lead placement within the lab, then you can always resort to pacemapping if the rhythm is not induceable once the procedure starts.

	To determine if the origin of an ventricular ectopic lies within the RVOT look at the inferior leads and the initial R wave in the precordial leads. . All three of the inferior leads use a positive recording electrode located below the heart. A ventricular ectopic originating in either outflow track will have a positive deflection in these leads. The second step is to determine right or left breakout. This is done using the precordial leads, V1-V6. The key to differentiating RVOT from LVOT lies in where the first R wave is visualized in these leads. If an R wave can be seen in V1 or V2, it suggests that the point of breakout lies within the LVOT. If the R wave does not present itself until V3, then a breakout within the right ventricular output is indicated.
	This is an alternate view of the 12 lead with all the leads shown in a vertivle display. This view is often used during EP studies. On either of the 12 lead recordings used, the positive deflection in the inferior leads and the transition in the precordial leads should be noted. These indicators help confirm RVOT breakout.
	A single run of VT is displayed using a faster sweep speed. This allows us to read the cycle length measured by the EP recording system easier. Most RVOT PVC's and VT's are focal in nature and are thus, a result of an abnormality of automaticity. (For more info, see the section of Focal Tach's.) Note the cycle length changes during this run of VT. The initial rate is 380ms. This decreases to 400ms, then to 420ms, 450ms and finally to 550ms where the run terminates. Whenever you see a tachycardia that displays variable rate of this type, you can be pretty certain you are dealing with a focal tach.
	It is also worth noting what happens to the arterial pressure during tachycardia. While many patients may tolerate RVOT VT without a significant pressure drop, it is also possible that patients experience a hemodynamically signifficant decrease in pressure.
	As the case progresses, the ablation catheter is moved closer to the area where the origin is believed to be based upon the surface ECG. In essence, this is an early form of intracardiac mapping. By comparing timing on the onset of the surface QRS, it is easy to see that the RF distal catheter starts later than the onset of surface. We know that the catheter is not yet in position for ablation. If this were a good target for ablation, the onset of the RF signal should preceed the onset of surface QRS by around 30ms.
	Another interesting event on the preceeding recording is a catheter induced PVC that is referred to as a "bump". When the RF catheter is being positioned and inadvertantly "bumps" the wall, it often causes an ectopic that is different from the recorded morphology. In the displayed leads, the morphology of the third beat is notably different that the other recorded beats. It also occurs significantly earlier and "out of sync" with the other beats in this run. An analysis of the timing between the onset of signal at the RF catheter and the onset of surface ECG show that the intracardiac signal initiates much ealier than the onset of surface for this beat only! This is a good indication of an ectopic caused by moving the RF catheter.
	One of the conventional mapping tools used in determining the origin of focal ectopics is a pacing maneuver referred to as pace mapping. This technique is performed by pacing from the RF catheter when it is believed to be at, or close to, the suspected location of breakout for the beat of interest. (For more information on pace mapping, see the page on Pacing Maneuvers.) Pace mapping is performed by splitting the review screen into two windows. The first window is a recording of the surface 12 lead of the clinical VT. The second window shows a 12 lead of the paced morphology. Each lead of the two recordings is reviewed to determine if a 12 of 12 match is obtained. In this case, there is substantial difference between the two displays. We are not at the ideal location to target ablation energy.
	By moving the ablation catheter around and pacemapping at a number of different locations, a good 12 of 12 match is located. This degree of correlation between the paced recording on the right and the original morphology on the left indicates a prime target for successful ablation.

A Look to the Left.... (LVOT)

Now that we know how to identify RVOT origins of PVC's / VT, let us compare this to the morphology of ectopics that originate from the Left Ventricular Outflow Track.

All outflow track PVC's will have strong positive deflections in leads II, III and aVF. To distinguish if the origin is right or left, look to the precordial leads V1 - V3.

The LVOT lies posterior to the RVOT. To reach the positive electrodes of the first three precordial leads, the electrical wavefront must travel a greater distance from the LVOT than it would if it originated from the RVOT. This extra distance causes an R wave to appear in V1 or V2. The more pronounced the R wave in these leads, the more posterior the origin lies.

This image shows the complete endocardial surface of the heart. The blue right ventricle is the most anterior structure in the heart. The outflow track connects the main chamber of the right ventricle to the Pulmonary Artery (PA).

The left ventricle is shown in red and lies posterior to the right ventricle. The LVOT is tucked in behind the RVOT. Thus, the wave front of depolarization from beats originating in the LVOT must travel further to reach leads V1 and V2. This is what causes the positvie deflection in these leads..

Here is an alternate look at the right and left ventricular outflow tracks. In this image, the right atrium is no longer visible allowing the viewer unobstructed look of the relationship of the RVOT and LVOT.

Note how the RVOT is anterior to the LVOT. When performing an outflow track case where there is any indication of LVOT possabile origin such as small R waves in V1 or V2, consider using unipolar EGM's to map the AO valve annulus. This is especially true when the earliest activation is found in the posterior septal aspect of the RVOT.

This image is useful in helping to visualize how much further an electrical wave front (orange arrow) would have to travel to reach the anterior location of the early precordial leads.

Coronary Heart Disease and Pregnancy (bệnh mạch vành ở phụ nữ có thai)

babacon — Sat, 08 Mar 2014 03:42:10 GMT

Abstract

The prevalence of coronary artery disease in female patients is increasing due to changing lifestyle patterns including cigarette smoking, diabetes and stress. Since women are delaying childbearing until older age, acute coronary syndrome will more frequently occur during pregnancy. Although rare, acute coronary syndrome during pregnancy often has devastating consequences. It is associated with increased maternal and neonatal mortality and morbidity compared with the nonpregnant situation. Furthermore, it constitutes an important problem for the patient and the treating physician, because the selection of diagnostic and therapeutic approaches is greatly influenced not only by maternal, but also by fetal safety.

Introduction

Coronary heart disease is a major health problem. Although rare in pregnant women, during pregnancy acute coronary syndrome (ACS) is estimated to occur three- to four-times more often compared with the nonpregnant women in this age group.^[1] The incidence of ACS during pregnancy is estimated at 1 per 10,000 pregnancies ( Table 1 ).^[1,2] Actual incidence ratios may even be higher. Chest discomfort is not primarily attributed to heart problems in, otherwise healthy, pregnant women. Myocardial ischemia during pregnancy can mimic complaints typical for pregnancy. Therefore, the diagnosis of ACS is often missed during pregnancy.

The changes in the cardiac, hemodynamic, hemostatic and hormonal situation during pregnancy and in the puerperium form a broad spectrum of causes of ACS, and contribute to the increased mortality rate among pregnant women with ACS. This review will summarize the available information about pregnancy-related coronary heart disease.

Hemodynamic changes

To ensure an adequate supply of nutrients and oxygen to the developing fetus, several hemodynamic changes take place during pregnancy. Blood volume increases by 1100-1600 ml, a raise of 30-50%.^[3] At the same time red cell mass increases to a lesser extent than plasma volume, resulting in physiological anemia and decreased blood viscosity. The blood volume expands rapidly until the 34th week, after which there is only a modest rise. Cardiac output increases by 30-50%. First, preload increases owing to the rise in blood volume. Second, gestational hormones, circulating prostaglandins in combination with the low vascular resistance of the placenta and uterus, decrease the peripheral vascular resistance and blood pressure, therefore, reducing the cardiac afterload and increasing the vascular compliance.^[4] In addition, there is an increase in heart rate of 10 to 20 beats per minute (Figures 1 & 2).^[5,6

Finally, an extra effort of the cardiac function is demanded during and immediately after delivery. Uterine contractions during labor result in increased cardiac output.^[7] After delivery, cardiac preload increases as a result of decompression of the inferior caval vein and return of uterine blood into the circulation (autotransfusion). Intravascular volume is further increased by reabsorption of extracellular fluids into the circulation. After a rapid decline in the first 2 weeks, hemodynamic adaptations will slowly resolve in 3 to 6 months after delivery.^[8]

Hemostatic changes

Changes take place in all aspects of hemostasis in order to maintain placental function during pregnancy and to prevent excessive bleeding at delivery. There is an increase in the coagulation factors V, VII, VIII, IX, X and XII and von Willebrand factor increases.^[9] Resistance to activated protein C increases in the second and third trimester.^[10] Protein S decreases throughout the entire pregnancy. Plasma activator inhibitors increase during pregnancy. At the time of delivery coagulability is further enhanced through the release of tissue plasminogen-activator inhibitors from the placenta and myometrium. The plasma concentrations of the plasminogen-activator system return to normal 6 weeks after pregnancy.^[11]

Etiology of coronary heart disease in pregnancy

The prevalence of coronary artery disease is increasing as a result of changing lifestyle patterns, including cigarette smoking, diabetes and stress. As women are delaying childbearing until older age, the occurrence of an acute myocardial infarction during pregnancy is more frequently encountered. Age appears to be one of the major determinants of pregnancy-related myocardial infarction. At the age of 40 years and older, the incidence of myocardial infarction is three per 10,000 deliveries.^[1]

Increased cardiac workload and greater myocardial oxygen demand during pregnancy puts the heart in a situation where myocardial ischemia may have a more severe course. Before the current practise of percutaneous coronary intervention (PCI), the estimated mortality among pregnant women with ACS was 20%.^[12] Currently, with the application of PCI, maternal mortality rate has dropped to 5%.^[1]

Although the common cause of coronary heart disease is atherosclerosis, a spectrum of causes is found during pregnancy.^[12] Coronary atherosclerosis (with or without a thrombus) was found in 43% and a thrombus, without signs of atherosclerosis, was present in 21% of the patients who underwent coronary angiography for ACS during pregnancy. Coronary dissection was found in 16%, while normal coronary arteries were reported in 29% of patients. Coronary atherosclerosis was the primary cause of infarction in the antepartum group, while in the post-partum period dissection was the primary cause of ACS.

Symptoms of coronary heart disease in pregnancy

ACSs or progression of previous angina may at times be difficult to differentiate from signs and symptoms typically reported during normal pregnancy. Common complaints during normal pregnancy include fatiguability, decreased exercise tolerance and chest pain at rest due to oesophageal reflux. Indicators of heart disease include severe or progressive dyspnea, syncope with exertion and chest pain related to effort or emotion ( Table 2 ).^[13]

Therapeutic modalities

Treatment of ACSs is not based on randomized trials, but on limited data taken from case reports, observational studies and clinical individual experience.

Treatment of acute myocardial infarction

In the acute phase, the treatment options for ACS are thrombolysis, PCI or coronary artery bypass grafting (CABG). During pregnancy, decision-making not only depends on best maternal results, but is also influenced by fetal safety. However, if there is no other alternative therapeutic modality, the safety of the mother prevails over the possible negative influence of the therapy on fetal outcome.

Thrombolysis

A common cause of ACS is a thromboembolic process, therefore, thrombolytic therapy is useful in the general population. However, in pregnancy a substantial part of ACS is caused by nonthromboembolic processes (e.g., dissection). It is important to perform a diagnostic catheterization before giving thombolytic therapy.

There is little experience with thrombolytic therapy for ACS during pregnancy. Streptokinase and recombinant tissue-plasminogen activator do not cross the placenta in animals, but it is unknown whether they cross the human placenta. Most experience with thrombolytic therapy during pregnancy is from patients with pulmonary embolisms, deep venous thrombosis and prosthetic valve thrombosis. The complications observed included maternal hemorrhage (2.5%), uterine hemorrhages with emergency cesarean section (2%), preterm delivery (6%), fetal loss (2%), abruptio placenta (2.5%) and spontaneous abortion (1.5%).^[12,14] No teratogenic effects were mentioned in the few available reports.

Percutaneous coronary intervention

In the general population, PCI is the first-line therapy for ACS. However, PCI in pregnancy implies exposure of the fetus to higher radiation levels compared with a diagnostic angiogram alone. High doses of radiation place the fetus at risk of spontaneous abortion, organ deformation, mental retardation and childhood cancer.

The amount of fetal exposure to radiation during chest radiography in PCI results in a mean exposure of 0.02 mSv and a maximum of 0.1 mSv in difficult PCI procedures (National Council of Radiation Protection and Measurements 1998) ( Table 3 ). Radiation that scattered from the directly irradiated area reaches the fetus; this is only a small fraction of the radiation delivered to the thorax.^[15] Shielding the abdomen and pelvis will not intercept the scattered irradiation. Catheterization through the radial artery will keep fetal-radiation exposure to a minimum.

PCI in pregnancy can be considered relatively safe, taking into account the minimal radiation exposure. However, before completion of major organogenesis (before 15 weeks after menses) radiation exposure must, whenever possible, be avoided. Doses in excess of 50–100 mSv increase the incidence of fetal malformation ( Table 4 ).

With regards to the spectrum of causes of myocardial infarction in pregnancy, catheterization appears to be the first step, and in most cases, PCI will be the therapy of choice during pregnancy. Not only can thromboembolic processes be treated, but also other causes, such as coronary artery dissection, can be detected and treated immediately. Considering the use of stenting during PCI implies the use of platelet-aggregation inhibitors in the post-PCI period. In particular, the increasing use of drug-eluting stents necessitates the use of clopidogrel in the post-PCI period. No information is available about the effects of clopidogel on the fetus, although, animal experiments do not demonstrate a teratogenic effect. There are no studies in pregnant women, therefore, clopidogrel should only be used in pregnancy if clearly needed.

Coronary artery-bypass grafting

Cardiac surgery can be performed during pregnancy. Maternal mortality equals mortality in nonpregnant cardiac surgery, but fetal mortality risk is still high with an incidence of 20%.^[16] Most of the experience of cardiac surgery during pregnancy is obtained from valve surgery. The best results are obtained by performing surgery in the second trimester since surgery may cause abortion and fetal malformations in the first and preterm labor in the third trimester.^[16] Cardiopulmonary bypass adversely affects placental perfusion as a result of nonpulsatile blood flow and hypotension and, therefore, disrupts organogenesis and influences fetal outcome. One study found a tendency towards increased fetal mortality with increased cardiopulmonary-bypass time. Fetal mortality was also related to a longer anoxic time.^[16]Cardiopulmonary bypass in pregnancy must be performed at high flow, high pressure, in normothermia and with the shortest possible extracorporeal circulation time.

Drug therapy

Following the acute phase of myocardial infarction, several drugs can reduce the risk of recurrence of myocardial infarction, reduce the progression of atherosclerosis and prevent anginal symptoms.

Drug therapy for coronary artery disease consists of antithrombotic drugs, antianginal drugs, drugs reducing the progression of atherosclerosis and drugs used to improve myocardial remodeling after an acute myocardial infarction (Table 5 ).

The use of low-dose aspirin (<150 mg/day) is considered safe during pregnancy.^[17-19] Higher doses are associated with premature closure of the ductus arteriosus, fetal congenital abnormalities and fetal and maternal hemorrhage. There is no information available about clopidogrel during pregnancy. Treatment with (low molecular weight) heparins is safe during pregnancy. It does not cross the placenta and it can be administered up to 12 h before delivery. Coumadins can be teratogenic when used in pregnancy. Coumadins cause teratogenic effects in 6% of babyies when given in the period between the 6th and 9th week of pregnancy.^[20] There is probably a dose–effect relation. Furthermore, coumadins increase the risk of miscarriage when used in the second and third trimester. Due to an increased risk of hemorrhage, acenocoumarol should be stopped and replaced by (low molecular weight) heparins several weeks before delivery.^[21]Fenprocoumon is more teratogenic than acenocoumarol and, therefore, should not be used.

Angina pectoris is treated by decreasing the oxygen demand, decreasing cardiac workload and improving coronary perfusion. By slowing down the heart rate, oxygen demand decreases. In general, β-blockers are relatively safe. However, severe bradycardia should be avoided in order to prevent uteroplacental hypoperfusion. The use of β-blockers is associated with a mildly lower birth weight and this can theoretically cause post-partum fetal bradycardia.

Nitrates and calcium antagonists are used to induce vasodilatation. The preload increases while afterload decreases. This results in a decreased cardiac workload. Coronary perfusion is improved through coronary vasodilatation. High-dose nitrates may cause maternal hypotension and subsequent fetal hypoperfusion. No other adverse effects of nitrates during pregnancy have been reported. The calcium antagonist, diltiazem, has teratogenic effects (skeletal abnormalities) in animals. There is no information about its use in human pregnancy, therefore, it should not be used.^[22] Nifedipine is frequently used during pregnancy for the treatment of hypertension, preeclampsia and tocolysis. It appears to be safe.^[23]

Improving the lipid-profile reduces atherosclerotic progression. Hydroxymethylglutarylco-enzyme A (HMG-CoA)-reductase inhibitors (statins) are the first-line therapy for dyslipidemias in the general population. However, statins are contraindicated in pregnancy as a result of possible teratogenic effects. Evidence of fetal abnormalities (mainly skeletal defects) has been observed in animal studies.^[24] All statins are labeled as US FDA category X. There is only limited data available regarding the efficacy of ezitimibe (even in the general population).

Angiotensin converting enzyme (ACE)-inhibitors improve myocardial remodeling after an acute myocardial infarction. ACE-inhibitors are teratogenic in pregnancy, even during the first trimester and, therefore, should not be given.^[25] Reported complications include neonatal lung hypoplasia, intra-uterine growth restriction, persisting ductus arteriosus and skull hypoplasia. Few data are available regarding angiotensin (AT)-II-receptor antagonists in pregnancy, but their actions, similar to that of ACE-inhibitors, also makes them contraindicated.^[26]

Previous myocardial infarction

Besides patients with an ACS presenting during pregnancy, patients with previous coronary disease may also wish to have children. Impairment of left ventricular function is one of the main determinants of poor maternal and fetal outcome. Pregnancy should be discouraged if the left ventricular ejection fraction is below 40%.^[27]

It is important to provide general advice to patients with heart disease and to their close relatives before conception. Before taking any medication during pregnancy and during lactation, the safety and tolerability for the fetus and infant, the physiological maternal changes and the risk:benefit ratio must all be considered. In patients who are already taking cardiovascular medications, the discontinuation or the switch to a ‘safer' drug should be discussed and tried before conception. ACE-inhibitors and/or AT-II should be stopped and echocardiographic and exercise evaluation can be performed 3 months later to assess changes in the cardiac condition before deciding on pregnancy advice.

Heart failure

One of the complications of myocardial infarction is deterioration of left ventricular function with subsequent heart failure. Treatment of heart failure consists primarily of diuretics. Furosemide has been proven safe during pregnancy, however, it should be used with caution to prevent hypovolemia and subsequent reduction in uteroplacental flow. ACE-inhibitors and/or AT-II antagonists are contraindicated. Hydralazine is safe and can be useful in the treatment of heart failure in pregnancy. β-blockers are indicated to optimize diastolic filling once the patient is in a stable situation.

Advice during pregnancy should include salt and fluid restriction and limitation of physical activity up to complete bed rest in the case of manifest heart failure. Self-weighing should be encouraged, and in the case of sudden unexpected weight gain (although pregnant), contacting the physician is recommended.

Arrythmias

Acute and previous myocardial infarctions might cause potential life-threatening arrythmias. Particular attention should be given to the recognition of ventricular arrythmias during pregnancy and during, and after, delivery. Pregnancy might increase the incidence of arrythmias due to increased mechanical stretch of the myocardium. Conservative therapy is recommended for benign, well-tolerated arrhythmias, but, if the systolic function of the heart becomes impaired or life-threatening arrhythmias occur, treatment is important and should not be withdrawn. Most of the antiarrythmic drugs can be prescribed safely in pregnancy. All antiarrhythmic drugs cross the placental barrier and their potentially toxic effect on the fetus should be taken in consideration, particularly during the initial weeks of pregnancy.

Delivery

During delivery, cardiac workload increases to maximum. In the case of recent infarction this can theoretically lead to myocardial rupture. Therefore, in order to allow adequate healing, delivery should be postponed, if possible, for at least 2–3 weeks after myocardial infarction. The mode of delivery should be determined by obstetric reasons and the clinical status of the mother. No convincing data proclaiming either vaginal delivery or cesearean section have been reported. However, cesearean section leads to more blood loss at delivery, therefore, vaginal delivery is preferable in patients with heart disease. Cardiac effort during delivery can further be reduced by administering epidural anesthesia for pain relief and shortening the second stage of labour.

Puerperium

In the puerperium patients with coronary heart disease are still at risk for new events. Delivery causes a volume overload due to autotransfusion. Patients at risk have a higher chance of developing heart failure or arrythmias and, therefore, clinical observation for at least 3 days after delivery is recommended.

Conclusion

ACS is rare in pregnancy, however, because of older maternal age and changing lifestyle patterns (e.g., smoking and diabetes) it will be encountered more frequently. Acute myocardial infarction in pregnancy is estimated to occur in one per 10,000 pregnancies and is associated with high maternal and neonatal mortality and morbidity. Atherosclerosis is one of the causes of myocardial infarction during pregnancy, but other causes, such as dissection and thrombus, are found relatively frequent. A possible explanation could be found in the combined changes of the hemodynamic, hemostatic and hormonal system during pregnancy. Thrombolytic therapy can be given, but not without a definite diagnosis of the etiology. Serious side effects of thrombolytic therapy have been reported. Radiation exposure of the fetus during cardiac catherization is acceptable, especially after the 15th week of pregnancy. The widespread use of PCI has led to a drastic reduction in maternal death.^[1,12] Therefore, PCI is the first-choice treatment during pregnancy when indicated. Cardiac surgery during pregnancy is associated with high fetal mortality. We recommend that pregnant women with ACS should be treated in tertiary centers with interventional possibilities.

References

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Ladner HE, Danielsen B, Gilbert WM: Acute myocardial infarction in pregnancy and the puerperium: a population-based study. Obstet. Gynecol. 105 (3),480-484 (2005).
Whittaker PG, Macphail S, Lind T: Serial hematologic changes and pregnancy outcome. Obstet. Gynecol. 88 (1), 33-39 (1996).
Spaanderman ME, Willekes C, Hoeks AP, Ekhart TH, Peeters LL: The effect of pregnancy on the compliance of large arteries and veins in healthy parous control subjects and women with a history of preeclampsia. Am. J. Obstet. Gynecol. 183 (5), 1278-1286 (2000).
Mabie WC, DiSessa TG, Crocker LG, Sibai BM, Arheart KL: A longitudinal study of cardiac output in normal human pregnancy. Am. J. Obstet. Gynecol. 170 (3), 849-856 (1994).
Robson SC, Hunter S, Boys RJ, Dunlop W: Serial study of factors influencing changes in cardiac output during human pregnancy. Am. J. Physiol. 256 (4 Pt 2), H1060-H1065 (1989).
•• Important study describing the normal hemodynamic changes in pregnancy.
Robson SC, Dunlop W, Boys RJ, Hunter S: Cardiac output during labour. Br. Med. J. (Clin. Res. Ed.) 295 (6607), 1169-1172 (1987).
Robson SC, Hunter S, Moore M, Dunlop W: Haemodynamic changes during the puerperium: a Doppler and M-mode echocardiographic study. Br. J. Obstet. Gynaecol. 94 (11), 1028-1039 (1987).
Brenner B: Haemostatic changes in pregnancy. Thromb. Res. 114 (5-6), 409-414 (2004).
Walker MC, Garner PR, Keely EJ, Rock GA, Reis MD: Changes in activated protein C resistance during normal pregnancy. Am. J. Obstet. Gynecol. 177 (1), 162-169 (1997).
Coolman M, de Groot CJ, Steegers EA et al.: Concentrations of plasminogen activators and their inhibitors in blood preconceptionally, during and after pregnancy. Eur. J. Obstet. Gynecol. Reprod. Biol. 128 (1-2), 22-28 (2006).
Roth A, Elkayam U: Acute myocardial infarction associated with pregnancy. Ann. Intern. Med. 125 (9), 751-762 (1996).
• Good review article that summarized the causes of acute coronary syndrome during pregnancy.
Presbitero P, Somerville J, Stone S et al.: Pregnancy in cyanotic congenital heart disease. Outcome of mother and fetus. Circulation 89 (6), 2673-2676 (1994).
Leonhardt G, Gaul C, Nietsch HH, Buerke M, Schleussner E: Thrombolytic therapy in pregnancy. J. Thromb. Thrombolysis 21 (3), 271-276 (2006).
Hirshfeld JW Jr, Balter S, Brinker JA et al.: ACCF/AHA/HRS/SCAI clinical competence statement on physician knowledge to optimize patient safety and image quality in fluoroscopically guided invasive cardiovascular procedures: a report of the American College of Cardiology Foundation/American Heart Association/American College of Physicians Task Force on Clinical Competence and Training. Circulation 111 (4), 511-532 (2005).
Arnoni RT, Arnoni AS, Bonini RC et al.: Risk factors associated with cardiac surgery during pregnancy. Ann. Thorac. Surg. 76 (5), 1605-1608 (2003).
CLASP: a randomized trial of low-dose aspirin for the prevention and treatment of pre-eclampsia among 9364 pregnant women. CLASP (Collaborative low-dose aspirin study in pregnancy) collaborative group. Lancet 343 (8898), 619-629 (1994).
Knight M, Duley L, Henderson-Smart D, King J: Antiplatelet agents for preventing and treating pre-eclampsia.Cochrane Database Syst. Rev. (3), CD000492 (2007) (Withdrawn).
Roberts JM, Catov JM: Aspirin for pre-eclampsia: compelling data on benefit and risk. Lancet 369 (9575), 1765-1766 (2007).
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Roos-Hesselink JW, Meijboom FJ, Leebeek FWG, de Groot CJM: Zwangerschap en mechanische kunstklep: dilemma's bij de keuze van antitrombotische profylaxe. Nederlands Tijdschrift voor Geneeskunde 151 (7), 389-394 (2007).
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Cooper WO, Hernandez-Diaz S, Arbogast PG et al.: Major congenital malformations after first-trimester exposure to ACE inhibitors. N. Engl. J. Med. 354 (23), 2443-2451 (2006).
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• Identified four predictors for maternal cardiac complications during pregnancy in women with heart disease.
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Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronary artery disease? (P3)

babacon — Sun, 22 Sep 2013 16:59:47 GMT

A total of 23 patients that underwent CA (40%) had no ECG confounders (ECG is "otherwise unremarkable”). LMCA disease was found in only 3 of them (13%), LMEQ in 2 (9%) and three vessel disease in 5 (22%). The prevalence of three vessel disease, LMCA or LMEQ was 43%, not different from that of the whole group. A total of 16 patients (70%) underwent revascularization with 30% undergoing PCI and 43% CABG.

Most of the patients that underwent CA had positive T waves (53 patients). Among the 4 patients with negative T waves, one had three vessel disease, one LMCA and two nonsignificant coronary artery disease (Table 4).

Among the 57 patients that underwent CA, 25 (44%) had dynamic ECG changes and in 17 patients (30%) the pattern of diffuse ST segment depression with ST elevation in aVR was a chronic pattern. Previous ECG was unavailable in 15 patients (26%). There was no difference in the prevalence of LMCA (p=0.11), LMEQ (p=0.50) or LMCA/LMEQ/three vessel disease (p=0.41) among the groups. However, LMCA or LMEQ (p=0.18) tended to occur more often in the group with dynamic ECG changes (Table 5). Patients who had dynamic ECG changes underwent more often revascularization than patients with stable or unknown ECG pattern (p=0.09), with more patients in with dynamic ECG changes needed CABG (p=0.134).

Discussion

The LMCA supplies blood to a majority of the anterolateral and septal aspects of the left ventricle as it branches into the LAD and left circumflex arteries. A decrease in blood flow after LMCA narrowing affects a significant region of the heart, producing electrical disturbances visible by ECG due to myocardial ischemia/injury. Isolated ST segment elevation in lead aVR as well as diffuse ST segment depression with/without ST segment elevation in aVR has been described previously as patterns consistent with either LMCA or triple vessel stenosis.^{1, 7 and 8}

Isolated ST elevation in aVR and V₁

Gorgels et al were the first to report that ST elevation in lead aVR, together with ST depression in leads I, II and V4–V6 were predictive of LMCA or three vessel disease, especially when the total magnitude of ST changes exceeded 12 mm.⁹ Yamaji et al. reported that ST elevation in lead aVR (> 0.05 mV) that was greater than ST elevation in lead V₁ "distinguished” LMCA obstruction from LAD and right coronary artery obstruction with 81% and 88% sensitivity, 80% and 92% specificity and 81% and 90% accuracy, respectively.> 0.15 mV ST elevation in lead aVR predicted mortality with 75% sensitivity, 75% specificity and 75% accuracy in patients with ACS.¹⁰ The positive end of lead aVR points toward the patient's right shoulder, so if the LMCA is obstructed, the septal branches of the LAD would also be affected. It is believed that LMCA obstruction leads to ischemia/injury of the basal septum with a resultant right superior pointing injury vector causing ST segment elevation in lead aVR.¹⁰ Since lead aVR faces into the left ventricular cavity, the same electrical vector that causes ST segment depression in leads V₅ and V₆ (that are oriented towards the left ventricular apex) will be recorded by lead aVR as ST segment elevation.¹¹ These reciprocal changes may be seen in situations where the left ventricular end diastolic pressure is elevated. Gorgels et al. suggested that ischemia of the basal interventricular septum should cause ST elevation in leads aVR and V_1.¹² Thus, both proximal LAD obstruction and LMCA occlusion should cause ST segment elevation in leads aVR and V₁.¹²Kosuge et al. reported that ST elevation in aVR has a sensitivity of 78%, specificity of 86%, positive predictive value (PPV) of 57%, negative predictive value (NPV) of 95% and predictive accuracy of 84% for predicting LMCA or 3VD in a retrospective study of 310 patients with NSTE-ACS.⁴

Diffuse ST depression

Nikus et al. describe that the ECG pattern of widespread ST-segment depression and inverted T waves, maximally in leads V_4–5 is associated with LMCA disease, LMEQ coronary artery disease, or severe there vessel disease.¹³ In 50 patients with NSTE-ACS this pattern had a sensitivity of 100%, specificity of 57%, PPV of 24% and NPV of 100% for severe 3VD. While a sensitivity of 91%, specificity of 79%, PPV of 76% and NPV of 92% were reported for LMCA or LMEQ coronary artery disease. This pattern had a sensitivity of 93%, specificity of 100%, PPV of 100% and NPV of 92% for severe 3VD, LMCA or LMEQ coronary artery disease.¹³ In another study, Nikus and Sclarovsky describe "transient ST depression with negative T waves seen maximally in leads V₄ and V₅” as a pattern associated with significant LMCA/3VD. The pattern had a PPV of 100% and an NPV of 92% in a prospective study of 25 patients. ST elevation in aVR was explained as reciprocal changes to the ST depression in leads V₄ and V₅, which are electrically opposite to aVR.¹³Taglieri et al. describe the predictive value of isolated diffuse ST depression compared to ST depression plus ST elevation in lead aVR in identifying LMCA disease and in-hospital as well as one-year cardiovascular mortality in patients with NSTE-ACS. They concluded that only diffuse ST depression plus ST elevation in lead aVR was useful in identifying LMCA disease and mortality. Multivariable analysis showed an odds ratio (4.72; 95% CI 2.31 to 9.64; p < 0.001) for this combined pattern to predict LMCA obstruction.¹⁴ The same analysis was completed for prediction of mortality, providing a hazard ratio (1.52; 95% CI 1.44 to 3.64; p < 0.001), favoring the combined pattern over isolated diffuse ST deviation as well.¹⁴ Hanna and Glancy describe that during an episode of ischemic chest pain, a pattern of diffuse ST depression in eight or more leads combined with ST elevation in aVR and V₁ has a 75% predictive accuracy for LMCA or 3-VD.¹⁵

However, as abovementioned, diffuse ST depression may not even be the most common ECG pattern seen in patients presenting with LMCA obstruction. Atie et al reported that only 60% of the patients with NSTE-ACS due to LMCA obstruction had ST elevation in lead aVR and 67% had maximal ST depression in lead V₄.¹⁶ The average number of leads with ST-T changes was only 6.4, suggesting that in many patients there were less than 6 leads with ST depression.¹⁶ More recently, Taglieri et al reported that only 24 out of 57 patients (42%) with NSTE-ACS due to LMCA stenosis had ST elevation in lead aVR with ST depression in other leads.¹⁴ ST elevation, predominantly in the precordial leads is probably the most frequent ECG presentation in patients with complete occlusion of the LMCA, followed by right bundle branch block.^{5, 6,7 and 17}

The current recommendations by the AHA/ACCF/HRS for "resting ECGs that reveal ST-segment depression greater than 0.1mV in 8 or more body surface leads coupled with ST-segment elevation in aVR and/or V1 but are otherwise unremarkable” are that the automated interpretation should suggest "ischemia due to multivessel or left main coronary artery obstruction”.¹ Although in the text it is written that "It has been reported that in patients with angina at rest, ST-segment depression in 8 or more body surface ECG leads, combined with ST elevation in aVR and V₁, is associated with a 75% predictive accuracy of 3-vessel or left main stenosis”,¹ the recommendations do not mentioned symptoms during ECG recording. Obviously, currently we cannot add symptoms or risk factors to the computerized automated interpretation. Thus, the current recommendations suggest that the ECG should be interpreted independent of the clinical presentation.

Nikus et al. on behalf of an International Society of Holter and Non-Invasive Electrocardiology (ISHNE) working group recommended that the AHA/ACCF/HRS recommendation is supported by prior studies, "but needed minor modifications: 1.) The presence of left ventricular hypertrophy, left bundle branch block with QRS > 130 msec and/or tachycardia (rate > 100/min) invalidates these criteria. 2.) The number of required leads with ST depression should be reduced from 8 to 7. 3.) The threshold for ST depression in the V leads should be adjusted for age and gender. 4.) The threshold for ST elevation in aVR should be specified as 0.05 mV”.⁸ Nikus et al recommended that urgent CA should be considered if the patient is hemodynamically unstable or ischemic symptoms persist, but there are not enough data to recommend urgent CA based on the ECG findings alone.^5 and 8

The current study questions the accuracy of interpreting the ECG pattern of diffuse ST segment depression with ST elevation in aVR as a sign of diffuse three vessel disease or LMCA/LMEQ disease, using the above mentioned recommendations. Here we collected consecutive patients with ECGs showing diffuse ST depression and ST elevation in lead aVR. LMCA or LMEQ disease was found in only 23% of the patients that underwent CA. Thus, the positive predictive value of the ECG pattern for LMCA/LMEQ was significantly lower in our cohort than that reported in previous studies.¹³ In contrast to the previous studies, most of our patients were not diagnosed with ACS. Interestingly, the prevalence of LMCA/LMEQ was not higher among patients with presentation compatible with ACS as compared to all the 57 patients that underwent CA. It should be remembered that in about 30% of the patients with acute myocardial infarction, presentation can be atypical, especially in the elderly, diabetic patients and women.^2 and 18 Shortness of breath, hypotension, epigastric pain and arrhythmia, all can be manifestation of ACS are common in patients with cardiomyopathies, hypertensive heart disease and significant valvular disease that cause diffuse ST depression with ST elevation in aVR. Moreover, the prevalence of LMCA/LMEQ was not significantly higher among patients with dynamic ECG changes as compared to those with chronic pattern of diffuse ST depression and ST elevation in aVR. It should be remembered that the amount of ST depression in patients with repolarization abnormalities (LVH, cardiomyopathies, intraventricular conduction delay, etc) is dependent on the heart rate and the degree of QRS prolongation and therefore, may show dynamic changes. In the present study, presence of symptoms suggestive of ACS or dynamic ECG changes did not improve the association between the ECG pattern and the presence of LMCA, LMEQ or three vessel disease.

An important component of the recommendations is that the ECG should be "otherwise unremarkable”.¹There is no specification what is actually considered "unremarkable”. It is clear that repolarization changes secondary to LVH or left bundle branch block may cause diffuse ST depression with ST elevation in lead aVR. We did not include patients with left bundle branch block or QRS duration of > 130 msec in our cohort. Interestingly, after exclusion of the 14 patients with ECG signs of LVH, the prevalence of LMCA, LMEQ and/or three vessel disease did not significantly changed compared to the whole cohort. Even when we included only patients without ECG confounders, the percentage of patients with LMCA, LMEQ and/or three-vessel disease did not increase. Obviously, diffuse coronary artery disease may result in pathological Q waves, QRS widening and QRS axis changes. Moreover, hypertension, a major risk factor for coronary artery disease, may results in LVH. As these changes are considered "abnormal”, excluding high-risk patients with such abnormalities decreases the clinical applicability of the ECG sign by excluding a large number of high-risk patients.

Nikus et al emphasized the importance of the T wave polarity in leads V4-V5 in predicting LMCA/LMEQ disease. Patients with negative T waves had higher prevalence of LMCA/LMEQ and poorer outcome than patients with positive T waves.^13 and 19 Hence, the position manuscript by Nikus et al suggests that "sudden occlusion of the LMCA may present as widespread ST depression and inverted T waves with ST elevation in lead aVR.”⁵ We used strict criteria for the definition of T wave polarity. Investigators are using different definitions for the polarity of the T waves.²⁰ For example, Nikus et al considered the T wave to be positive or negative if it was 1 mm or more above or below the isoelectric line, measured more than 120 ms after the J point.¹³ As ST depression may affect the initial part of the T wave and during ischemia QRS may prolonged, we defined negative T wave based on the terminal part of the T wave. Interestingly, most of our patients had positive T waves per this definition. Moreover, two out of the four patients with negative T waves did not have significant coronary artery disease. Indeed, diffuse horizontal, and especially upsloping ST depression with prominent tall positive T waves may signify different coronary anatomy (regional subendocardial ischemia)²¹; however, small positive terminal T waves may carry the same significance as negative T waves. Further studies are needed to clarify this issue, especially to see if the definition used by Nikus et al.¹³ has better prediction.

Although the prevalence of LMCA, LMEQ or diffuse three-vessel disease was relatively high in our patients, it is clear that not all patients with such ECG pattern had LMCA/LMEQ disease. When combined with the right clinical scenario, this ECG pattern is associated with high prevalence of LMCA/LMEQ disease. It is plausible that in patients presenting with typical symptoms, this ECG pattern is more predictive for LMCA/LMEQ, especially if their baseline ECG is completely normal.^5 and 8 Gorgels et al have shown that during chest pain the number of leads with ST depression and the amount of ST deviation in the ECG correlate with the number of diseased coronary arteries.⁹ The authors mentioned that the absolute shift of ST deviation from the baseline ECG, obtained when the patient did not have symptoms, is important as ST abnormalities could be present at the baseline ECG even if the patient is free of ischemia.⁹ In particular, they suggested that ST depression in leads I, II and V4–V6 and ST elevation in lead aVR are predictive of LMCA or three vessel disease.⁹ However, if the abovementioned recommendations are adopted, urgent activation of the catheterization laboratory for patients with atypical presentation (shortness of breath, epigastric pain, hypotension, etc.) solely based on ECGs showing diffuse ST depression with ST elevation in lead aVR in order not to misdiagnose acute myocardial infarction due to LMCA/LMEQ/three-vessel disease, will probably lead to high rate of false activation. Similar high rates of false activation of the catheterization laboratory have been shown for patients with atypical symptoms presenting with presumably new left bundle branch block.^{22, 23 and 24}

We cannot exclude the possibility that small vessel disease or supply/demand imbalance leads to diffuse subendocardial ischemia in some of our patients. It has previously been reported that other medical conditions, such as hypothermia²⁵ and various neurological disorders²⁶ may present with such transient ECG pattern. Thus, the term "circumferential subendocardial ischemia” as suggested by Samuel Sclarovsky or "circumferential subendocardial stress” may be better than "ischemia due to multivessel or left main coronary artery obstruction”.¹

Study limitations

This is a retrospective review of patients based on ECGs that were identified during routine reading at the St. Luke's Episcopal Hospital ECG laboratory. Just over half of our patients presented with chest pain and/or shortness of breath. All ECGs met the pattern of diffuse ST depression with elevation in aVR, which is the pattern described by the current AHA/ACCF/HRS guidelines. We did not limit ourselves to patients presenting with clinical scenario that may be compatible with ACS, as we tested the accuracy of the ECG pattern for predicting LMCA or LMEQ-induced ischemia. Larger prospective studies are needed to confirm our results and assess the predictive value of this particular ECG pattern for LMCA/LMEQ disease in patients with and without typical clinical presentations. An alternative approach to compare the incidence of such ECG pattern among patients with ACS with or without LMCA/LMEQ/3VD has been reported (27). However, it is obvious that not all patients with such coronary anatomy have diffuse ischemia due to LMCA or LMEQ lesions. They may have culprit lesions leading to ACS in more distal locations. In many patients with NSTE-ACS, ischemia is intermittent and may not be detected by sporadic ECG recordings. In others, such pattern may be related to etiologies other than acute diffuse subendocardial ischemia.

Conclusion

The Texas Heart Institute at St Luke Episcopal Hospital is a tertiary center for heart disease, treating numerous patients with complex heart diseases, cardiomyopathies and heart failure. In our patient population, the pattern of diffuse ST depression in > 7 leads with ST elevation in aVR was associated with acute coronary syndromes in only in 28% of the patients.

Although coronary artery disease is prevalent among the patients that were selected to undergo CA, only 23% of the patients had LMCA/LMEQ disease. We cannot exclude that this pattern represents "circumferential subendocardial ischemia” due to "small vessel disease”, vasospasm or altered supply/demand ratio. Yet, the AHA/ACCF/HRS recommendation for interpreting this ECG pattern as representing "ischemia due to multivessel or left main coronary artery obstruction,” implying that these patients should be referred for urgent coronary angiography based on the ECG pattern alone may not be supported by our findings and the term "circumferential subendocardial ischemia” is probably more accurate.

Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronary artery disease? (P2)

babacon — Sun, 22 Sep 2013 16:57:58 GMT

Methods

We collected 142 electrocardiograms (ECGs) with dates ranging from March 2, 2008 to April, 13 2011 from the ones sent for routine reading at the St. Luke's Episcopal Hospital ECG laboratory and read by one investigator (YB). ECGs showing diffuse ST segment depression in > 7 leads with ST-segment elevation in aVR were collected. Patients with left bundle branch block, QRS duration of > 130 msec, ventricular rhythm or ventricular paced rhythm were excluded. The polarity of the T waves in the leads with maximal ST depression was defined as positive if the terminal part of the T wave was > 0.1 mV above the isoelectric line, or negative.

Demographic data, date of ECG, the indication for the ECG, presence of elevated cardiac markers, diagnosis of cardiac conditions (non-ST elevation acute coronary syndrome [NSTE-ACS], non-ischemic dilated cardiomyopathy [NIDCM], ischemic cardiomyopathy, hypertrophic obstructive cardiomyopathy and hypertensive heart disease, and significant valvular disease), performance of coronary angiography (if so, number of diseased vessels [> 70% diameter stenosis] and presence of left main stenosis > 50%), performance of revascularization (percutaneous intervention [PCI] or CABG) following the ECG and the existence of previous ECG (> 24 hours) with the same pattern or without this pattern were obtained from the patients' medical records. Angiographic data were broken up into LMCA, LMEQ disease or three-vessel disease (3VD), two-vessel disease (2VD), one-vessel disease (1VD) or no significant coronary artery narrowing. If the patients were post-CABG and the grafts to the left anterior descending (LAD) and/or obtuse marginals were patent we did not list them as LMCA or LMEQ disease. The ECG patterns were classified as chronic (present for at least 24 hours prior to selected ECG), dynamic (more significant changes or new pattern) or no prior ECG obtained.

Results

Out of the 142 patients that were chosen for our study, 9 (6.3%) had insufficient data. Of the remaining 133 patients, 57 (43%) underwent coronary angiography (CA) (Table 1).

Demographic and clinical characteristics of the patients are shown in Table 1. The prevalence of men was higher among patients undergoing CA than among those who did not undergo CA; however, there was no difference in mean age or race. The chief indication for the ECG was chest pain in more than half of the patients that underwent CA compared to only 20% in the group without CA. There were no differences between the groups in the percentage of patients having ECG for shortness of breath, palpitations or arrhythmia, syncope, heart failure or abdominal pain. ACS was clinically suspected in 83% of the patients who underwent CA and in only 50% of the patients who did not undergo CA. The pattern of diffuse ST depression with ST elevation in lead aVR was chronic in 30% and 26% of the patients who underwent or did not undergo CA, respectively. Dynamic changes were noted in 44% and 53%, respectively (Table 1). A quarter of the patients in each group had ECG criteria for LVH. There were no significant difference in the prevalence of intraventricular conduction delay [incomplete right bundle branch block (incRBBB), complete right bundle branch block (RBBB), nonspecific intraventricular conduction delay (IVCD) or incomplete left bundle branch block (incLBBB)] among groups. Interestingly, the majority of the patients (93%) in the CA group had positive T waves, whereas only 60% of the patients who did not undergo CA had positive T waves (Table 1).

At discharge, ACS was diagnosed in 34 patients (60%) who underwent CA and in only 3 (4%) patients who did not undergo CA (p<0.00001).

Medical diagnoses that were associated with the ECG pattern are listed in Table 2. As mentioned above, only 37 (28%) patients were diagnosed with NSTE-ACS. Almost half of the patients had hypertensive heart disease.

Among the 57 patients that underwent CA, 24 (42%) had a history of diabetes mellitus, 46 (81%) had hypertension, 39 (68%) had known coronary artery disease and 21 (37%) had known cardiomyopathy. Twenty-two patients (39%) had prior CABG and 19 (33%) had a history of prior PCI. A total of 38 (67%) of the patients that underwent CA presented with either chest pain or shortness of breath; 22 (58%) of these patients were diagnosed with NSTE-ACS; 4 (9.1%) developed ST elevation myocardial infarction later on during their hospitalization. Angiographic results of the patients that underwent CA are listed in Table 3. Of note, 15 (26%) of these patients had normal coronary arteries or no significant coronary artery disease, while only 10 (18%) had LMCA narrowing, 3 (5%) patients had LMEQ disease, and 10 (18%) had 3VD. Thus, three vessel disease, LMCA or LMEQ was present in only 23 patients (40%). Significant left anterior descending narrowing (> 70% luminal diameter stenosis) was detected in 22 patients (39%), significant left circumflex artery narrowing in 19 patients (33%), significant right coronary artery narrowing in 24 patients (42%). One patient with prior CABG had > 70% luminal narrowing of the left internal mammary artery and 6 had significant narrowing of saphenous vein grafts. A total of 29 patients (51%) needed revascularization, with 14 (25%) undergoing PCI and 16 (28%) undergoing CABG, while the other half were either treated medically or underwent a different procedure, such as septal ablation for hypertrophic obstructive cardiomyopathy.

CA results of the 35 patients that did not have prior CABG are also listed in Table 3. A total of 12 (34%) of these patients had normal coronary arteries or no significant coronary artery disease, while only 7 (20%) had LMCA narrowing, 3 (9%) had LMEQ disease, and 5 (14%) had 3VD. Thus, 15 patients (43%) had three vessel disease, LMCA or LMEQ, without a significant difference from the whole group. Sixteen patients (46%) needed revascularization (6 patients (17%) underwent PCI and 10 (29%) CABG), while the rest (54%) were treated either medically or underwent a different procedure.

In 34 patients who underwent CA (60%), the initial presentation was suspicious of ACS. The prevalence of LMCA, LMEQ or three vessel disease was comparable to that of the whole group (Table 3). As expected, more patients presented with ACS underwent revascularization (74%), with 41% undergoing PCI and 35% CABG.

Among the patients that underwent CA, 43 patients (75%) did not have ECG criteria for LVH. There were no significant differences in the prevalence of LMCA, LMEQ or three vessel disease between patients without LVH criteria and the whole group (Table 3). Among the patients without LVH, 22 (51%) underwent revascularization with 26% undergoing PCI and 28% CABG.

Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronary artery disease? (P1)

babacon — Sun, 22 Sep 2013 16:35:15 GMT

Robert J. Knotts, MD^a,

James M. Wilson, MD^a^,^b,

Edward Kim, MD^a,

Henry D. Huang, MD^a,

Yochai Birnbaum, MD^a^,^b^,

Abstract

Background and Purpose

We assess whether the electrocardiographic (ECG) pattern of ST depression in > 7 body surface leads combined with ST elevation in aVR and V₁ is predictive of left main coronary artery (LMCA) stenosis or left main equivalent (LMEQ) disease.

Methods

We collected 133 patients showing this particular ECG pattern. Patients with left bundle branch block, ventricular rhythm or ventricular paced rhythm were excluded.

Results

Only 28% of the patients had non-ST elevation acute coronary syndrome (NSTE-ACS). ECGs were classified as chronic, dynamic or no prior in 28%, 48% and 24%, respectively. A total of 57 patients (44%) underwent coronary angiography (CA). No significant coronary artery disease was found in 26%. LMCA/LMEQ disease was found in only 23% of these patients. The positive predictive value of the ECG pattern was not improved after exclusion of patients with intraventricular conduction abnormalities and left ventricular hypertrophy or in patients with dynamic ECG changes.

Conclusions

This ECG pattern is not always caused by LMCA/LMEQ disease; therefore, the term "suspect circumferential subendocardial ischemia” may be preferred. Other medical conditions may also be associated with a similar ECG pattern.

Keyword

Diffuse ST depression;
Left main stenosis;
Lead aVR

Introduction

Diffuse ST segment depression in the inferior and anterolateral leads that is associated with ST segment elevation in leads aVR and V₁ (Fig. 1, Fig. 2, Fig. 3 and Fig. 4) is thought to represent circumferential subendocardial ischemia, suggesting an injury vector directed toward the ventricular chamber. When accompanied by angina at rest, this ECG is believed to have a 75% predictive accuracy of left main coronary artery (LMCA) occlusion or three-vessel coronary artery disease.¹ The current recommendation by the American Heart Association/American College of Cardiology Foundation/Heart Rhythm Society (AHA/ACCF/HRS) for "resting ECGs that reveal ST-segment depression greater than 0.1 mV in 8 or more body surface leads coupled with ST-segment elevation in aVR and/or V₁ but are otherwise unremarkable,” is that the automated interpretation should suggest "ischemia due to multivessel or LMCA obstruction”.¹ In this document, presence of typical symptoms is not mentioned and the guidelines are read as a "stand alone” recommendation for ECG interpretation either at bed side or off line. Moreover, there is no specification as to what is an ECG that is "otherwise unremarkable”. For example, does the presence of Q waves or QRS axis deviation considered "remarkable”? Furthermore, it is unclear whether in patients with diffuse ST depression with ST elevation in aVR as a chronic stable pattern, the same association with LMCA exist. These recommendations were endorsed by the recently published 2012 European Society of Cardiology Guidelines for the management of ST elevation acute myocardial infarction.² Dual antiplatelet therapy is recommended by the guidelines for all patients presenting with acute coronary syndromes (ACS), regardless of whether they are to receive percutaneous coronary intervention (PCI) or medical treatment alone.³ Oral P2Y₁₂receptor inhibitors, such as clopidogrel, prasugrel and ticagrelor, improve clinical outcomes in patients with ACS, but are associated with an increased risk of operative bleeding when administered within five days of coronary artery bypass graft (CABG) surgery. Since most of the patients with LMCA disease or left main equivalent (LMEQ, proximal narrowing in both the left anterior descending and left circumflex arteries) will likely need CABG surgery, some authors have recommended withholding P2Y₁₂ receptor inhibitors in patients presenting with such ECG pattern until the treatment plan has been established.⁴ Thus, early identification of patients with ACS due to LMCA or LMEQ disease is of extreme importance. However, in our experience, the same ECG pattern of diffuse ST segment depression with ST elevation in lead aVR may be seen in patients with cardiomyopathies as well as left ventricular hypertrophy with repolarization changes and in numerous other medical conditions that may or may not be associated with circumferential subendocardial ischemia. Diffuse ST depression with ST elevation in aVR is not even the most common ECG pattern seen in patients presenting with LMCA obstruction.^{5, 6 and 7} This study assesses the diagnostic accuracy of the criteria defined by the 2009 AHA/ACCF/HRS recommendations as written.¹ The main objectives of this study were to assess 1) the prevalence of acute ischemia caused by LMCA or LMEQ disease among patients having the ECG pattern of diffuse ST depression along with ST elevation in lead aVR; 2) what other medical conditions are associated with such an ECG pattern; and 3) whether ECG confounders, such as left ventricular hypertrophy (LVH) or various forms of intraventricular conduction delay affect the accuracy of predicting LMCA/LMEQ by this particular ECG pattern. In the present study, we used a common situation in which the cardiologist is analyzing ECGs from various areas of a tertiary hospital (in patients, intensive care units, as well as outpatient clinics) without complete access to patients' clinical data.

: Fig. 1. ECG of an 87-year-old man showing sinus rhythm with right bundle branch block and left anterior fascicular block. Patient was known to have severe aortic stenosis. Patient presented with chest pain and was diagnosed as having a non-ST elevation myocardial infarction. There is ST depression with negative T waves in the inferior leads and leads V3–V6 and ST elevation in leads aVR and V1. Subsequent coronary angiography revealed 70% diameter stenosis of his left main coronary artery, 50% stenosis in the distal left anterior descending artery and 50% distal right coronary artery stenosis. Patient underwent aortic valve replacement and coronary artery bypass grafting with left internal mammary artery graft to the left anterior descending artery and a saphenous vein graft to the obtuse marginal branch.; Figure options

: Fig. 2. ECG of a 31-year-old woman with known non-ischemic cardiomyopathy (non-compaction) and recurrent ventricular tachycardia for which a defibrillator was implanted. The ECG shows sinus rhythm with left ventricular hypertrophy. There is ST depression with negative T waves in leads I, II, III, aVF and V4-V6. There is ST elevation in lead aVR, V1 and V2. This pattern was present in several previous ECGs in the preceding 4 months. Coronary angiography did not reveal any significant coronary artery disease. Echocardiogram showed left ventricular ejection fraction of 38% with global hypokinesis.; Figure options

: Fig. 3. ECG of a 67-year-old man with a history of coronary artery disease (two myocardial infarction in the past), severe aortic stenosis, and symptomatic peripheral artery disease who came with progressive symptoms of effort induced angina. ECG shows sinus tachycardia, ST depression in leads I, II, III, aVF, V3–V6 with positive T waves. There is ST elevation in leads aVR and V1. These changes were not present in a previous ECG done several months earlier. Cardiac markers were negative. Coronary angiography revealed significant LMCA and right coronary artery stenosis. The patient underwent CABG and aortic valve replacement.; Figure options

: Fig. 4. ECG of a 55-year-old man with known coronary artery disease and pulmonary hypertension secondary to scleroderma was admitted due to non STE-myocardial infarction. During hospitalization he developed chest pain and ECG shows sinus rhythm with right axis deviation with ST depression and negative T waves in leads I, II, III, aVF, V3–V6. There was also ST elevation in lead aVR. The ST deviation was not present on his admission ECG. Urgent coronary angiography revealed 70% proximal stenosis in his left anterior descending artery. No other lesions were identified. The patient underwent PCI with stenting.; Figure options

Methods

NHỊP NHANH KỊCH PHÁT TRÊN THẤT

babacon — Fri, 13 Sep 2013 08:53:02 GMT

NHỊP NHANH TRÊN THẤT

DR: Osama ban Obama

Nhịp nhanh xoang (Sinus Tachycardia)

H/c nhịp nhanh tư thế đứng (Postural Orthostatic Tachycardia Syndrome)

Nhịp nhanh nhĩ (Atrial Tachycardia)

Nhịp nhanh bộ nối (Junctional Tachycardia)

Nhịp nhanh vào lại nút nhĩ thất (AV Nodal Reentrant Tachycardia)

Nhịp nhanh vào lại nhĩ thất (AV Reentrant Tachycardia)

Rung nhĩ (Atrial Fibrillation) Cuồng nhĩ (Atrial Flutter)

XEM ĐẦY ĐỦ BÀI VIẾT Ở ĐÂY

https://docs.google.com/file/d/0BxzRAFseuHeDSVVHcE1lZkc1NU0/edit?usp=sharing

Dilated cardiomyopathy (bệnh cơ tim giãn)

babacon — Thu, 12 Sep 2013 18:12:59 GMT

Dilated cardiomyopathy or DCM is a condition in which the heart becomes weakened and enlarged and cannot pump blood efficiently. The decreased heart function can affect the lungs, liver, and other body systems.

1 Causes:
Bệnh cơ tim giãn là bệnh chưa rõ bệnh nguyên gây ra hậu quả làm mất dần chức năng co bóp của cơ tim. Chẩn đoán xác định khi không tìm thấy các nguyên nhân thông thường như bệnh động mạch vành, bệnh tim bẩm sinh, bệnh van tim, tăng huyết áp hoặc bệnh màng ngoài tim. Trong một vài trường hợp bệnh cơ tim giãn thấy có các yếu tố thuận lợi trên lâm sàng như nghiện rượu, thai sản hoặc tiền sử gia đình có mắc bệnh cơ tim. Tuy nhiên người ta cha tìm ra một nguyên nhân có mối liên quan chắc chắn nào dẫn đến bệnh cơ tim giãn. Giới khoa học vẫn đang tiếp tục nghiên cứu các mối liên quan đến bệnh cơ tim giãn của hệ thống tạo keo, tự miễn, thần kinh cơ, các quá trình viêm, hay chuyển hóa nhằm góp phần lý giải bệnh sinh phức tạp của bệnh này.
- 1.1 Genetics:
- Khoảng 25-35% bệnh nhân có các tính chất gia đình, với hầu hết các đột biến ảnh hưởng đến gen mã hóa protein cytoskeleta.
2 Signs and symptoms:
2.1. Triệu chứng cơ năng
a. Tất cả các lứa tuổi đều có thể gặp bệnh cơ tim giãn, tuy nhiên lứa tuổi gặp nhất là tuổi trung niên. Các dấu hiệu thường diễn ra rất từ từ và bệnh nhân thường có một giai đoạn dài từ vài tháng đến vài năm hoàn toàn không có triệu chứng. Một vài trường hợp bệnh khởi phát đột ngột như ở các bệnh nhân sau một thời kỳ tăng nhu cầu hoạt động của tim như sau phẫu thuật hay nhiễm trùng.
b. Dần dần sau đó bệnh nhân thường có các biểu hiện của suy tim trái như khó thở khi gắng sức, khó thở khi nằm và khó thở về đêm. (suy tim trái xuất hiên trước)
c. Giai đoạn nặng lên của bệnh sẽ thấy các dấu hiệu của suy tim phải như phù ngoại biên, nôn, căng tức bụng do gan to, đi tiểu đêm và cổ chướng. Các dấu hiệu khác có thể gặp là biểu hiện của hội chứng cung lượng tim thấp như mệt mỏi và suy nhược cơ thể. Đau ngực cũng có thể gặp mặc dù hệ thống động mạch vành hoàn toàn bình thường. Các dấu hiệu ngất và xỉu thường có nguồn gốc do rối loạn nhịp hoặc do dùng thuốc gây hạ huyết áp tư thế đứng.
2.2. Triệu chứng thực thể
a. Khám lâm sàng thường không có dấu hiệu đặc hiệu và thường chỉ liên quan đến mức độ suy tim của bệnh nhân. Huyết áp bệnh nhân thường bình thường nhưng nếu tình trạng rối loạn chức năng thất trái tiến triển có thể dẫn đến hạ huyết áp, mạch nhỏ và yếu.
b. Khám tim thường thấy nhịp tim nhanh, đôi khi có tiếng ngựa phi. Thường nghe thấy tiếng thổi tâm thu của hở van hai lá và ba lá do giãn các buồng tim. Ngoài ra còn thấy các dấu hiệu buồng tim giãn với mỏm tim xuống thấp và sang trái (giãn thất trái) hay giãn về phía mũi ức của thất phải.
c. Khám phổi trong trường hợp ứ trệ tuần hoàn nhiều có thể thấy xuất hiện các ran ẩm, bệnh nhân khó thở kiểu nhanh nông, thở khò khè và thờng có tràn dịch màng phổi phối hợp.
d. Khám bụng nhằm phát hiện các dấu hiệu của suy tim phải với gan to. Trong các trường hợp nặng có thể dẫn đến xơ gan tim với bụng cổ chướng trên lâm sàng. Phản hồi gan tĩnh mạch cổ dương tính, nhưng đa phần các bệnh nhân có tĩnh mạch phổi nổi tự nhiên.
e. Khám ngoại biên phát hiện phù chi dưới sau đó có thể dẫn đến phù toàn thân. Hay gặp dấu hiệu giảm tưới máu ngoại biên với chi lạnh, tái hay tím. Đây chính là những bằng chứng thể hiện mức độ cung lượng tim giảm ở các bệnh nhân bệnh cơ tim giãn không rõ nguyên nhân.
3 Pathophysiology
- 3.1. Cơ chế sinh bệnh hàng đầu của bệnh cơ tim giãn là giảm khả năng co bóp của tế bào cơ tim. Hậu quả là làm giảm phân số tống máu và tăng thể tích cuối tâm trương thất trái, như tất cả các nguyên nhân khác dẫn đến hậu quả cuối cùng là suy tim. Tuy nhiên do quá trình này diễn ra từ từ làm bệnh nhân thích ứng tốt, vì vậy có rất nhiều trường hợp tuy chức năng tâm thu thất trái đã giảm nhiều nhưng bệnh nhân vẫn có rất ít triệu chứng lâm sàng.
  3.2. Thay đổi đáng kể nhất được nhận thấy trong bệnh cơ tim giãn không rõ nguyên nhân là phức hợp thụ thể adrenergic G protein adenylate của cơ tim. Trong các bệnh nhân suy tim nặng thấy có giảm 60 đến 70% thụ thể bêta 1 adrenergic và tăng thụ thể bêta 1 mRNA.(http://http://vi.wikipedia.org/wiki/Adenylat_cyclaza)
4 Diagnosis:
Không có một xét nghiệm nào được coi là tiêu chuẩn vàng để chẩn đoán xác định bệnh cơ tim giãn. Việc chẩn đoán cần phải kết hợp giữa lâm sàng và các xét nghiệm cận lâm sàng.
4.1. Điện tâm đồ (ĐTĐ): Không có dấu hiệu ĐTĐ điển hình cho bệnh cơ tim giãn. Chúng ta có thể thấy dấu hiệu nhịp xoang nhanh nhưng cũng có thể gặp các rối loạn nhịp nhĩ và thất phức tạp. Rối loạn dẫn truyền trong thất hay gặp mà điển hình là bloc nhánh, đoạn ST và sóng T cũng rất hay biến đổi. Một vài bệnh nhân lại có sóng r nhỏ và Q sâu ở các chuyển đạo trước tim làm ta dễ nhầm lẫn với các trường hợp nhồi máu cơ tim cũ. Dấu hiệu dày thất trái và trục trái cũng hay gặp.
4.2. Chụp tim phổi: Bóng tim to, với chỉ số tim ngực lớn. Phù phổi là dấu hiệu có thể thấy trên phim do tăng áp ở hệ tĩnh mạch phổi. Tĩnh mạch chủ trên và tĩnh mạch đơn (azygos) giãn do tăng áp hệ tĩnh mạch chủ. Có thể gặp tràn dịch màng phổi.
4.3. Siêu âm tim: Là phương pháp hữu hiệu nhất để chẩn đoán và theo dõi tiến triển của bệnh cơ tim giãn cũng như loại trừ các nguyên nhân có thể dẫn đến giãn các buồng tim như bệnh tim bẩm sinh, bệnh van tim, bệnh mạch vành...
a. Siêu âm hai chiều: cho thấy các buồng tim giãn ở nhát cắt 4 buồng tim từ mỏm và cạnh ức trái.Độ dày của vách liên thất và thất trái vẫn trong giới hạn bình thường, nhưng biên độ di động của toàn bộ các vách tim thuộc thất trái đều giảm. Có thể thấy dịch màng ngoài tim trong một số các trường hợp. Siêu âm tim cũng giúp đánh giá chính xác phân số tống máu của thất trái.
b. Siêu âm Doppler: giúp đánh giá dòng hở van hai lá, ba lá và ớc tính áp lực động mạch phổi.
4.4. Thông tim và chụp buồng tim:
a. Hình ảnh chụp buồng thất trái thấy thất trái giãn và giảm vận động toàn bộ.
b. Về mặt huyết động, thấy có suy thất trái hay suy cả hai thất với tăng áp lực cuối tâm trơng của thất trái trong khi áp lực tâm thu lại giảm nhiều.
c. Hệ thống động mạch vành bình thường hay hẹp không đáng kể (hẹp dưới 50%).
4.5. Sinh thiết cơ tim: Để xác định những nguyên nhân dẫn đến suy tim dễ nhầm với bệnh cơ tim giãn không rõ nguyên nhân như viêm cơ tim, sarcoidose, hemosiderosis...
5 Treatment:
Nhằm mục đích ổn định tình trạng suy tim. Việc điều trị bao gồm chế độ ăn hạn chế muối và nước, giảm hoạt động của tim bằng giảm tiền gánh, hậu gánh và nhịp tim, tăng sức co bóp của cơ tim.
5.1. Thuốc lợi tiểu khi cho phải căn cứ vào chức năng thận và thể tích dịch trong cơ thể. Chỉ định tốt trong trường hợp tăng áp ĐMP, ứ trệ tại phổi và ngoại biên rõ ràng. Quá liều lợi tiểu sẽ làm rối loạn điện giải và urê máu từ đó làm giảm cung lượng tim. Lợi tiểu được lựa chọn là các loại lợi tiểu quai như Furosemid, Torsemid hay Bumetanide. Còn Thiazid thường không được khuyên dùng do hiệu quả kém.
5.2. Thuốc giãn mạch làm giảm gánh cho tim như ức chế men chuyển dạng Angiotensin, Nitrat và Hydralazin trong đó ức chế men chuyển dạng Angiotensin là thuốc nên được lựa chọn hàng đầu. Cần chú ý tác dụng hạ huyết áp tư thế của thuốc giãn mạch.
5.3. Digitalis là thuốc được lựa chọn trong các trường hợp rung nhĩ có tần số thất cao. Hơn nữa các nghiên cứu còn chỉ ra rằng nó có tác dụng cải thiện phân số tống máu, cải thiện khả năng gắng sức của bệnh nhân và triệu chứng lâm sàng ngay cả đối với các bệnh nhân có nhịp xoang. Tuy nhiên trong nghiên cứu mới đây (nghiên cứu DIG) Digoxin không làm thay đổi tỷ lệ tử vong ở các bệnh nhân suy tim khi so sánh với giả dược. Do đó ở các trường hợp nhịp xoang chỉ nên dùng Digitalis khi bệnh nhân có tim to, rối loạn chức năng thất trái nhiều và không đáp ứng với điều trị lợi tiểu cũng như thuốc ức chế men chuyển dạng Angiotensin.
5.4. Thuốc kháng vitamin K cần được sử dụng khi bệnh nhân có huyết khối trong buồng tim, có rung nhĩ hay đã có tiền sử tắc mạch, chức năng tâm thu thất trái EF<30% và đường kính thất trái tâm trương trên siêu âm tim >75mm.
5.5. Điều trị rối loạn nhịp trong bệnh cơ tim giãn thường gặp nhiều khó khăn. Trong số các loại thuốc chống loạn nhịp thì Amiodaron là thuốc dường như có hiệu quả và ít tác dụng phụ nhất. Tại các nước phát triển việc sử dụng máy phá rung tự động cho kết quả tương đối khả quan đối với các rối loạn nhịp phức tạp.
5.6. Thuốc chẹn bêta giao cảm. Hiện tại duy nhất chỉ có Carvedilol là thuốc được chấp nhận dùng để điều trị suy tim tại Hoa Kỳ. Tuy nhiên, các nghiên cứu mới đây cũng chỉ ra rằng các thuốc khác như Bisoprolol hay Metoprolol cũng có hiệu quả làm giảm tỷ lệ tử vong ở các bệnh nhân suy tim. Liều khởi đầu cần rất thấp và hết sức thận trọng khi nâng liều điều trị.

Keyword:

âm thổi tống máu : ejection murmur

(http://www.youtube.com/watch?v=ApomG3ci3Eg&list=PL4AAC8BD1E1618162)

âm thổi phụt ngược: regurgitant murmur

âm thổi phụt ngược hình chủ nhật: pansistolic

âm thổi phụt ngược toàn tâm thu: holosystolique

hở 2 lá : mitral regurgitation

(Mitral Regurgitation Murmur)

Animated Aortic Regurgitation Murmur

http://youtu.be/HtDzHWNYKQM

Dilated CardioMyopathy, DCM, Echocardiography
http://youtu.be/DOhZk3-3mNM

Tài liệu tham khảo
1. Braunwald E, ed. Heart disease: a textbook of cardiovascular medicine, 5th ed. Philadelphia: WB Saunders, 1997:1077-1104.
2. Fauci AS, ed. Harrison's principles of internal medicine, 14th ed. New York: McGraw-Hill, 1998:785-791.
3. Topol EJ, ed. Textbook of cardiovascular medicine. Philadelphia: Lippincott-Raven Publishers, 1998:607-637.

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AN APPROACH TO RESPIRATORY FALIURE

babacon — Sat, 25 Aug 2012 09:59:06 GMT

                                                                                                                        WARREN ISAKOW, MD

        Respiratory failure is a common reason for intensive care unit admisson and is the final pathway for a number of disease of differing pathophysiology. an mechanism-based approach enables the clinician to identify the most likely cause for the respiratory failure and to treat appropriately. In general, patients with respiratory failure may be classified into groups, depending on the component of the respiratory system that is involved.
        Hypercapnic respiratory failure is a consequence of ventilatory failure and is recognized by an elevated PaCO2 above normal (>45mmHg at sea level). This denotes failure of the respiratory pump an can occur with normal lungs.
        Hypoxemic respiratory failure is a consequence of gas exchange failure and is recognized by hypoxemia ( PaO2 < 60mmHg ) with or without widening of the alveolararterial O2 gradient.

HYPERCAPNIC RESPIRATORY FAILURE

        The hallmark of hypercapnic respiratory failure is an elevated PaCO2 above 45mmHg.

                  PaCO2 = K x [VcO2/(1-Vd/Vt)x VA]
                 where PaCO2 = the partial pressure of carbon dioxide in the blood,
                          K = constant,
                          VcO2 = carbon dioxide production,
                          Vd/Vt = dead-space ratio of each tidal volume breath,
                          VA = minute ventilation.
       Analysis of the previous equation shows that hypercapnia can occur from three processes.: (a) an increase in CO2 production, (b) a decrease in minute ventilation, and (c) an increase in dead-space ventilation. Understanding of the "respiratory pump" enables the clinician to systematically consider the cause of hypercapnic respiratory failure in different patients, as depicted in Algorithm 7.1.

33gia

Right and Left Ventricular Outflow Tract Tachycardias: Evidence for a Common Electrophysiologic Mechanism

Abstract

Introduction

Methods

Study Population

Noninvasive Evaluation

Electrophysiologic Testing

Pharmacologic Testing

Discussion

HỘI CHỨNG KOUNIS

Abstract

Classification and Clinical Presentation

References

PHÂN BIỆT NHỊP NHANH THẤT TỪ BUỒNG TỐNG THẤT PHẢI VÀ TRÁI TRÊN ECG (RVOT/LVOT VT)

A Look at RVOT VT

A Look to the Left.... (LVOT)

Coronary Heart Disease and Pregnancy (bệnh mạch vành ở phụ nữ có thai)

Abstract

Introduction

Hemodynamic changes

Hemostatic changes

Etiology of coronary heart disease in pregnancy

Symptoms of coronary heart disease in pregnancy

Therapeutic modalities

Treatment of acute myocardial infarction

Thrombolysis

Percutaneous coronary intervention

Coronary artery-bypass grafting

Drug therapy

Previous myocardial infarction

Heart failure

Arrythmias

Delivery

Puerperium

Conclusion

References

Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronary artery disease? (P3)

Isolated ST elevation in aVR and V1

Diffuse ST depression

Study limitations

Conclusion

Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronary artery disease? (P2)

Methods

Results

Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronary artery disease? (P1)

Abstract

Background and Purpose

Methods

Results

Conclusions

Keyword

Introduction

Methods

NHỊP NHANH KỊCH PHÁT TRÊN THẤT

Dilated cardiomyopathy (bệnh cơ tim giãn)

Dilated CardioMyopathy, DCM, Echocardiography http://youtu.be/DOhZk3-3mNM

AN APPROACH TO RESPIRATORY FALIURE

Isolated ST elevation in aVR and V₁

Dilated CardioMyopathy, DCM, Echocardiography
http://youtu.be/DOhZk3-3mNM