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A 62-year-old white patient presents with markedly ischemic electrocardiogram, notable for Tombstone sign.

We present an electrocardiogram that may be passed on as showing a simple right bundle branch block, but for the vigilant interpreter, a posterior infarction could be easily gleaned from the presence of a tall initial R wave in V1-V2.

A 64-year-old man with known coronary disease presented to the hospital with sinus bradycardia, chest pain, and normal cardiac enzymes. During an exercise stress test he developed ventricular fibrillation that spontaneously resolved.

A 37-year-old man without a significant medical history had an out-of-hospital sudden cardiac arrest. A bystander started cardiopulmonary resuscitation, and emergency medical services arrived promptly, confirmed ventricular fibrillation, and restored sinus rhythm. An emergent coronary arteriogram was normal. Transthoracic echocardiography revealed a severely reduced left ventricular ejection fraction and suggested left ventricular noncompaction. The patient’s heart failure with reduced ejection fraction was treated with carvedilol, lisinopril, and spironolactone, and after he was weaned from the ventilator he received an implantable cardioverter-defibrillator. The patient’s identical twin was treated in the same fashion for a sudden cardiac arrest. Although many experts think that left ventricular noncompaction cardiomyopathy is a distinct nosological entity, others think that it is simply a dilated cardiomyopathy with unusually prominent left ventricular trabeculae.

A man with an acute anterolateral myocardial infarct had electrocardiographic features suggesting triple vessel coronary arterial disease and infarct-related regional pericarditis.

A 27-year-old man presents with successfully resuscitated ventricular fibrillation. Structural and electrical causes of ventricular fibrillation in the young are presented along with a diagnostic strategy. Electrocardiographic features of malignant early repolarization are discussed.

In a 75-year-old woman with left-sided chest pain and an abnormal electrocardiogram the etiology is not cardiac.

A 58-year-old man with his first episode of chest pain had an acute anterior myocardial infarct. After balloon angioplasty and stenting of a completely occluded left anterior descending coronary artery, the anterolateral ST-T changes had largely resolved.

A 66-year-old man presented with a moderate-sized ventricular septal defect and severe pulmonary hypertension that was responsive to vasodilator therapy. His electrocardiogram demonstrated biatrial enlargement and biventricular hypertrophy. Presentation at this age is unusual for this type of shunt.

A man whose congenital ventricular septal defect (VSD) was closed operatively in childhood apparently remained in sinus rhythm into his mid-30s. Like most VSD closures, his almost certainly was per...

Several findings on an exercise electrocardiogram predicted left main and/or 3-vessel coronary arterial disease, which was confirmed by coronary arteriography, and the 56-year-old man underwent a multivessel coronary arterial bypass operation the following day.

In a man with a wide-QRS complex tachycardia, a history of an inferior left ventricular scar, atrioventricular dissociation during the tachycardia, and a QRS morphology inconsistent with right or left bundle branch block exclude a diagnosis of supraventricular tachycardia with aberrant ventricular conduction due to bundle branch block or ventricular preexcitation and establish a diagnosis of ventricular tachycardia.

A 37-year-old man came to the emergency department because of several days of intermittent chest pain. An electrocardiogram (ECG) showed sinus rhythm, left atrial and left ventricular enlargement, and an early repolarization pattern. A second ECG recorded 10 minutes later was strikingly different, with ST-segment elevation and large upright T waves in the anterior precordial leads, interpreted as evidence of an ST-segment elevation myocardial infarction, and the cardiac catheterization team was activated. Closer inspection of the ECG, however, disclosed that the changes were because of intermittent ventricular pre-excitation of the Wolff-Parkinson-White type, and no electrocardiographic, echocardiographic, or serum markers of myocardial infarction were found.

Most patients with double-chambered right ventricles are diagnosed in childhood, but some escape definitive diagnosis until adulthood, as was the case in the patient described here.

In a woman with chest pain

Severe hypokalemia in the absence of other electrolyte abnormalities, the result of diarrhea, caused striking electrocardiographic changes, generalized weakness, flaccid paralysis of the lower extremities, and biochemical evidence of mild skeletal and cardiac rhabdomyolysis in a 33-year-old man. Repletion of potassium reversed all abnormalities in 24 hours.

Physical examination, electrocardiograms, and an echo-Doppler study document multiple consequences of a right coronary arterial occlusion.

The electrocardiogram shown in Figure 1 was read by the computer as arm-lead reversal. The computer reading went on to say that no further analysis would be attempted. This clearly is a programming mistake because the precordial leads make the diagnosis. Figure 1. Electrocardiogram recorded with the leads in the usual locations. See text for explication. Although we would estimate that 95% of electrocardiograms with negative P, QRS, and T waves in lead I are due to arm-lead reversal, a small number are due to situs inversus totalis with mirror-image dextrocardia. In this condition, the left-sided precordial leads show progressive diminution in the size of the complexes from leads V1 to V6 as the leads are placed ever farther away from the right-sided heart (Figure 1). In contrast, the left-sided precordial leads are unaffected by simple arm-lead reversal. Another diagnostic point is that the QRS morphology is similar in leads I and V6 in mirror-image dextrocardia, whereas it is quite different in those leads in simple arm-lead reversal (1). Situs inversus totalis with mirror-image dextrocardia is perhaps the most common of the congenital cardiac malpositions and is only infrequently associated with hemodynamically significant congenital cardiac malformations. In contrast, situs solitus with congenital dextrocardia, sometimes called isolated dextrocardia or dextroversion, is usually associated with significant malformations, as is situs inversus with isolated levocardia (2). This patient, a 52-year-old man, came to the hospital because of intermittent leg claudication with walking. He had no other cardiovascular symptoms. When the limb leads were reversed and the precordial leads were recorded on the right side of the chest (Figure 2), his electrocardiogram was normal except for voltage criteria for left ventricular hypertrophy, probably due to systemic arterial hypertension (3). Figure 2. Electrocardiogram recorded with the limb leads reversed and the precordial leads on the right side of the chest. See text for explication.

A 50-year-old man with a murmur since birth developed systemic arterial hypertension as an adult. He came to the hospital because of dyspnea. He had a pulmonic valve ejection click and a murmur of pulmonic stenosis. His echocardiogram showed biventricular hypertrophy, a flat ventricular septum, a D-shaped left ventricle, systolic doming of the pulmonic valve, and Doppler evidence of a 70 mm Hg peak systolic pressure gradient across the pulmonic valve and a peak right ventricular systolic pressure of 100 mm Hg. His electrocardiograms showed no evidence of the right ventricular and right atrial enlargement so evident on echocardiogram, presumably because it was obscured by the marked changes of left ventricular hypertrophy. Three years later, when he was admitted for sepsis and worsening heart failure with anasarca, the voltage changes of left ventricular hypertrophy had virtually disappeared, likely due to the large amount of fluid between the heart and the electrodes.

A 55-year-old man with syncopal episodes was found to have sinus bradycardia at a rate of 37 beats/min, an episode of nonsustained ventricular tachycardia, and left ventricular noncompaction cardiomyopathy. After placement of a dual-chamber cardioverter defibrillator 4 years ago, he has had no further syncopal episodes, and there have been no defibrillator shocks.

An 18-year-old man came to the hospital because of 1 day of chest pain typical of pericarditis. He had had an upper respiratory infection 10 days earlier. His electrocardiograms indicated evolving pericarditis. His echocardiogram showed mild, diffuse left ventricular hypokinesia, and his troponin I level peaked at 47.5 ng/ml. Thus, he had myopericarditis.

(2017). Atrial Fibrillation 50 Years After Acute Rheumatic Fever as the First Manifestation of Rheumatic Mitral Stenosis. Baylor University Medical Center Proceedings: Vol. 30, No. 2, pp. 232-233.

A woman with systemic lupus erythematosus and a regular supraventricular tachycardia continues to have electrocardiographic abnormalities after the spontaneous return of normal sinus rhythm.

A 72-year-old woman with a history of systemic arterial hypertension presented to the emergency department with chest pain, and an electrocardiogram showed acute anterior myocardial infarction with striking ST-segment elevation, upright T waves, and large Q waves in leads V1 to V4 (Figure). Furthermore, the ST-segment elevation > 0.25 mV in lead V1, the ST depression ≥ 0.1 mV in lead III, and the ST elevation ≥ 0.1 mV in lead aVL indicated that the left anterior descending coronary artery was occluded proximal to both the first major septal perforating branch and the first diagonal branch (1–4). Figure. Electrocardiogram recorded on the patient's arrival in the emergency department. See text for explication. Also, note that there was sinus rhythm at a rate of 106 beats/min with the next to last QRS complex being a fusion of a premature ventricular complex ... Anterior infarcts from such proximal left anterior descending occlusions tend to be quite large and are often associated with cardiogenic shock (2, 4, 5), which this woman manifested soon after her arrival in the emergency department. An echocardiogram showed a left ventricular ejection fraction of approximately 40% with akinesis of the apex and distal two-thirds of the ventricular septum. The right ventricle was considerably dilated. Through a defect in the distal ventricular septum, blood shunted from left to right during systole with reversal of flow during diastole, suggesting an elevated right ventricular diastolic pressure. Laboratory studies of the patient's blood confirmed myocardial damage and indicated chronic kidney disease and acute metabolic acidosis (Table). Table. Laboratory results from blood drawn on admission The patient had a run of ventricular tachycardia while in the emergency department. Once stable, she was transported to the cardiac catheterization laboratory; an intra-aortic balloon was placed via the left femoral artery, and 1:1 counterpulsation was begun. Coronary arteriography, performed via the right femoral artery, showed proximal total occlusion of the left anterior descending coronary artery, diffuse disease of the left circumflex coronary artery with a totally occluded first obtuse marginal branch and 90% narrowing of the third obtuse marginal branch, and diffuse disease of the right coronary artery with a long 80% to 90% narrowing in its mid segment. Despite repeated inflations of first a 2.5 × 20 mm balloon and then a 2.0 × 25 mm balloon in the proximal and distal portions of the left anterior descending artery, there was no flow. Hypotension, bradycardia, and acidosis (arterial blood pH = 6.9; reference = 7.4) were temporarily combated with atropine, epinephrine, and sodium bicarbonate, and the patient was sent to the intensive care unit with an intravenous dopamine infusion and 1:1 intra-aortic balloon counterpulsation. She died several hours later. Ventricular septal rupture formerly occurred in 1% to 3% of patients with acute myocardial infarction and did so within the first week in more than 75% of them (6). Subsequently, among patients treated with fibrinolysis, the incidence of ventricular septal rupture was only 0.2%, and the median time from the onset of the infarct was 1 day (7). Approximately one-half of ventricular septal ruptures are in the setting of an anterior infarct, and one-half occur in patients with inferior infarcts (8, 9). At least two-thirds of patients with myocardial infarction and ventricular septal rupture die, and many of these, like our patient, are older and have cardiogenic shock; early operation by superb surgeons seems to improve the chances of survival (10). The large upright fused ST segments and T waves seen in the figure have been referred to as “tombstoning,” probably because of the appearance of tombstones and because they are signs of more extensive myocardial damage and of a poor prognosis (11). Sclarovsky believes that this pattern of deep anterior Q waves with persistently elevated ST segments and tall T waves indicates lack of reperfusion of the myocardium due to a severely damaged microcirculation (12).

In patients with acute chest pain and left bundle branch block, repolarization changes often are helpful in confirming acute myocardial infarction. 1e6 Diagnosing old myocardial infarction in the presence of left bundle branch block is a tougher assignment. In this regard, the presence of Q waves in leads usually devoid of them in patients with left bundle branch block has received considerable attention. For example, in the presence of left bundle branch block, pathologic Q waves in the left lateral leads (I, aVL, V5, and V6) or a Q in lead V6 with a prominent R wave in lead V1 are insensitive but specific markers of an infarct, not in the lateral portion of the left ventricle but in its ante

The clinical and electrocardiographic features of anomalous left coronary artery from the pulmonary trunk, ALCAPA, a frequently fatal congenital cardiac malformation, are described in an 8 1/2-month-old female.

The most striking feature of this electrocardiogram (ECG) is a markedly wide QRS complex with an S wave that merges with a peaked T wave without an isoelectric ST segment (Figure 1). This is best seen in leads I and V4 to V6. No definite P waves are seen, although a long PR interval and fusion of Ps with the preceding T waves cannot be excluded in leads II and V2. This is the ECG of severe hyperkalemia; it belongs to a 35-year-old man with renal failure and a serum potassium level of 8.7 mEq/L. As the serum potassium level rises above the upper limit of normal (5.0 mEq/L), the first electrocardiographic change noted usually is a peaked symmetrical T wave with a narrow base. With ever higher levels of serum potassium, conduction slows resulting in a wide, low Pwave, a long PR interval, and a wide QRS complex with slurring of the S wave into a rapidly ascending limb of the T wave. Eventually P waves disappear, and the QRS comes to resemble a sine wave. Death may result from asystole or ventricular fibrillation. Although the ECG of hyperkalemia may resemble right or left bundle branch block or myocardial infarction, it is usually the absence of typical features of those conditions in someone with the electrocardiographic features described previously and a reason for hyperkalemia that alert the physician to the correct diagnosis. The commonest cause of hyperkalemia is renal failure, and the patient’s ECGmay also reflect hypocalcemia or left ventricular hypertrophy before the ECG is severely distorted as in this case.

Glenn P. Kelley, M.D.,∗ Ghassan A. Dalati, M.D.,∗ Frederick R. Helmcke, M.D.,∗ Neeraj Jain, M.D.,∗ Mohammed Al-Bataineh, M.D.,∗ D. Luke Glancy, M.D.,∗ and Edmund Kenneth Kerut, M.D.∗,†,‡ ∗Section of Cardiology, Department of Medicine, Louisiana State University Health Sciences Center, New Orleans, Louisiana †Heart Clinic of Louisiana, Marrero, Louisiana ‡Departments of Physiology and Pharmacology, Louisiana State University Health Sciences Center, New Orleans, Louisiana

A 21-year-old woman was transferred from another hospital in her 23rd week of pregnancy. She had had an audible precordial murmur the day of her birth and had had pneumonia three times in the first few years of life. Otherwise, she was asymptomatic during childhood and adolescence. Aside from being small (4′11″ tall and 85 lbs before becoming pregnant), she had developed normally. When she was transferred, she was asymptomatic and on no medication. Pertinent physical findings were a regular pulse at 96 beats/min; a blood pressure of 116/60 mm Hg; normal neck veins; brisk, full, symmetrical arterial pulses in the arms and legs with no radial-femoral delay; a loud and palpable second heart sound along the upper and mid left sternal border; and a small apical impulse just outside the left mid-clavicular line. A harsh, grade 4/6, systolic ejection murmur, heard over the entire chest and back and in the neck, was loudest at the cardiac base and of equal intensity on the right and left sides. A decrescendo diastolic murmur was maximal in the third left intercostal space. There was no gallop, ejection click, cyanosis, or clubbing. The admission electrocardiogram showed normal sinus rhythm, left axis deviation of the QRS complex, and no septal Q waves in leads I, aVL, V5, or Vw, but Q waves were present in leads II, III, aVF, and V1 (Figure ​(Figure11). The history, physical examination, chest radiograph (Figure ​(Figure22), and electrocardiogram provided some, albeit incomplete, insight into the patient's congenital cardiac malformations and the consequent pathophysiology. A systolic murmur heard the day of birth suggested right or left ventricular outflow obstruction; it would have taken several days for pulmonary vascular resistance to fall sufficiently for the murmur of a ventricular septal defect to be heard. The patient's brisk pulses excluded aortic stenosis, so the outflow tract obstruction had to be right ventricular. Frequent bouts of pneumonia in infancy suggested a sizable left-to-right shunt, a supposition supported by the large pulmonary arteries and pulmonary plethora noted on chest radiograph (Figure ​(Figure2).2). The absence of septal Q waves in leads I, aVL, V5, and V6 and their presence in leads V1, II, III, and aVF suggested ventricular inversion, an integral feature of congenitally corrected transposition of the great arteries, a diagnosis also brought to mind by the chest radiograph (Figure ​(Figure2)2) (1). The anterior position of the aortic valve in that condition would have produced the loud and palpable second heart sound. Figure 1 Admission electrocardiogram. See text for explication. Figure 2 Admission posterior-anterior chest radiograph. The proximal right and left pulmonary arteries are at the same level. A hump is seen on the left cardiac border, and the ascending aorta is seen on the left side of the cardiac base rather than the right. ... In congenitally corrected transposition of the great arteries, there are discordant atrioventricular and ventriculo-arterial connections. The right atrium receives blood from the two vena cavas and sends it across a mitral valve into a morphologic left ventricle that pumps it across a pulmonic valve, which is in fibrous continuity with the mitral valve, and into the pulmonary artery. Pulmonary venous blood travels through the left atrium and across a tricuspid valve into a morphologic right ventricle that pumps the blood across the infundibulum and the aortic valve into the aorta. Thus, ventriculoarterial discordance “corrects” the atrioventricular discordance, and the path of the blood through the heart is normal if there are no other malformations (2). Such patients have lived into their 70s (3). Whether the morphologic right ventricle, i.e., the systemic ventricle, in a patient with isolated congenitally corrected transposition of the great arteries functions as long and as well as a morphologic left ventricle does in a normal person has been affirmed by some experts (4) and denied by others (5). The vast majority of patients with congenitally corrected transposition of the great arteries, however, have associated cardiac malformations. Three of these occur frequently enough to be considered part of the anomaly: ventricular septal defect in approximately two thirds of patients (2); left ventricular (pulmonary ventricular) outflow tract obstruction, which can be valvular and/or subvalvular, in one half (1); and anatomic abnormalities of the tricuspid (systemic atrioventricular) valve in 90%, many of which are not clinically significant and the most common of which is Ebstein's anomaly (2). Other malformations seen in patients with congenitally corrected transposition of the great arteries include atrial septal defect; subaortic obstruction, which is often associated with coarctation of the aorta; aortic valve atresia with hypoplasia of the morphologic right ventricle; and pulmonary atresia with hypoplasia of the morphologic left ventricle. Because of malalignment of the atrial septum with the inlet ventricular septum, the atrioventricular conduction system is abnormal (2), and up to 75% of patients with congenitally corrected transposition of the great arteries eventually have atrioventricular block ranging from first degree to third degree (1). Wolff-Parkinson-White type ventricular preexcitation may occur, as it does in other persons with Ebstein's anomaly of the tricuspid valve, and some, but not all, supraventricular arrhythmias in congenitally corrected transposition of the great arteries are associated with a left-sided accessory pathway (1). Because the morphologic left ventricle and the left bundle branch lie to the right of the morphologic right ventricle in congenitally corrected transposition of the great arteries, initial septal depolarization is from right to left and often inferosuperiorly as well, as seen in Figure ​Figure11. As is often the case, especially with congenital heart disease, the echocardiogram and Doppler examination added important diagnostic information to that obtained by history, physical, chest radiograph, and electrocardiogram. In this patient, echo-Doppler confirmed congenitally corrected transposition of the great arteries, a nonrestrictive ventricular septal defect, and pulmonic valvular and subvalvular stenosis with a 75 mm Hg peak systolic pressure gradient between the pulmonary ventricle (morphologic left ventricle) and the pulmonary artery. Because her systemic arterial systolic pressure at the time was 105 mm Hg and the ventricular septal defect was nonrestrictive, her pulmonary arterial systolic pressure was approximately 30 mm Hg. The echo-Doppler also revealed a restrictive patent ductus arteriosus, which explained the full, brisk pulses and the decrescendo diastolic murmur. The systolic component of the continuous murmur of the patent ductus was obscured by the louder murmur of pulmonic stenosis. Both ventricles had normal systolic function, and both atrioventricular valves were completely competent. The patient stayed on the obstetrical service throughout the remainder of her pregnancy. She entered active labor at 34 weeks of gestation and under epidural anesthesia delivered a 2425 g daughter with Apgar scores of 8 and 9. Bilateral tubal ligation was then performed. Mother and daughter were doing well at discharge on postoperative day 4. Two questions remain. First, why, with such a complex congenital cardiac malformation, was this woman asymptomatic after the first years of life and able to have a successful pregnancy? It was because the severe malformations were balanced in such a way that the circulatory system was quite adequate. Pulmonic stenosis prevented early severe heart failure or subsequent Eisenmenger reaction from the nonrestrictive ventricular septal defect. At the same time, there was sufficient blood flow through the pulmonic valve and the restrictive ductus to prevent cyanosis and allow normal activity and a successful pregnancy. Thus far she has avoided two common accompaniments of congenitally corrected transposition of the great arteries, i.e., tricuspid (systemic atrioventricular) valvular regurgitation and atrioventricular block. Second, should the patient undergo operative repair? An article from the Mayo Clinic points out that most persons with congenitally corrected transposition of the great arteries eventually undergo cardiac surgery and that for many, the operation comes too late for optimal results (6). Those statements are difficult to refute. On the other hand, in this patient, so-called complete repair would require extensive complicated surgery, which is difficult to recommend to an asymptomatic patient. In addition, few institutions have a Gordon Danielson, one of the paper's authors and one of the foremost congenital cardiac surgeons of his or any other day. Most importantly, the patient prefers not to undergo an operation as long as she feels well.

A previously healthy 39-year-old male cigarette smoker came to the emergency department because of the new onset of retrosternal chest pressure. The electrocardiogram recorded on admission showed sinus rhythm at a rate of 64 beats per minute, nondiagnostic Q waves in the inferior leads (II, III, and aVF), and inferior ST-segment elevation of 0.5 mm (0.05 mV) when compared to the PR segment or the TP segment. The inferior ST segments were normally concave upward, and there was no reciprocal ST depression in lead I or lead aVL (Figure 1) (1).

Study objectives: Prior studies have proposed several ECG criteria for identifying the culprit artery in patients with acute inferior myocardial infarction (MI). We applied each criterion to our patients to assess its utility. In doing so, we discovered a previously unreported, but highly useful, criterion utilizing lead aVR. Study design: Retrospective review. Patients: Thirty consecutive patients with symptoms of acute MI, ST-segment elevation in the inferior ECG leads, an appropriate rise and fall of creatine kinase and troponin I levels, and coronary arteriography within 7 days of the onset of symptoms. Measurements: The ECG recorded within 24 h of the onset of symptoms that had the most prominent ST-segment changes was analyzed. In the 12 standard leads and in lead V4R, ST-segment elevation or depression was measured 0.06 s after the J point. Results: Four previously described criteria were useful in identifying the right coronary artery (RCA) or the left circumflex coronary artery (LCX) as the culprit: ST-segment elevation in lead I, ST-segment more or less elevated in lead II than in lead III, ST-segment elevation > 0.5 mm in lead V4R, and various combinations of ST-segment elevation or depression in leads V1 and V2 .A new criterion was found to be at least as useful as any previously described: the presence and amount of ST-segment depression in lead aVR. Conclusions: At least five different ST-segment criteria help to identify the RCA or the LCX as the culprit artery in patients with acute inferior MI. One of these, the amount of ST-segment depression in lead aVR, has not been reported previously and needs validation in a larger study. (CHEST 2002; 122:134 –139)

Wolff-Parkinson-White-type ventricular preexcitation was recognized for the first time in a 67-year-old man four days after aortic valve replacement. The preexcitation was intermittent.

A 72-year-old diabetic, hypertensive man presents with waxing and waning episodes of sharp chest pain that started 9 hours earlier. The current episode of pain has been ongoing for the past 3 hours. On physical examination, the pain appears to be reproducible with palpation, and the patient does not demonstrate any distress or diaphoresis. The first troponin I level is 0.03 ng/ml. The presenting electrocardiogram (Figure 1) shows sinus rhythm; one aberrantly conducted premature atrial complex; left anterior fascicular block; left ventricular hypertrophy by Cornell criteria; and subtle ST-T signs of inferior, lateral, and posterior injury. The ST-segment depression in leads V1 through V3 implies posterior ST-segment elevation of infarction. Although the ST segment is only slightly elevated in the inferior leads and in leads V5 and V6 (w0.05 mV), it has a convex morphology with a wide, hyperacute T wave, particularly evident on the aberrant complex. This morphology suggests an injury pattern, even if the ST-segment elevation is subtle. Moreover, reciprocal ST-segment depression and T-wave inversion are seen in lead aVL, further confirming that the inferior ST-T changes represent an injury pattern. Once it has been determined that ST-elevation injury is present, the next step is to identify the culprit artery. A left circumflex coronary arterial occlusion is associated with ST

A50-year-oldmanpresentedtotheemergencydepartment withchestpainandhisinitialelectrocardiogramshowedsinus tachycardia at a rate of 139 beats/min and left bundle branch block (Figure 1). Because of persistent chest pain and ST-segment elevation of 0.7 mV in lead V2, he underwent coronary arteriography, which demonstrated subtotal occlusion of the left anterior descending coronary artery and highgrade narrowing of its diagonal branch and of the left circumflex and right coronary arteries. A left ventriculogram revealed an ejection fraction of 15%. Urgent multivessel coronary artery bypass grafting was then performed. The electrocardiographic diagnosis of myocardial infarction in patients with right bundle branch block, which deforms the terminal portion of the QRS complex, usually is only minimally more difficult than in patients without a conduction defect. In contrast, left bundle branch block, which deforms the initial portion of the QRS, makes the diagnosis of myocardial infarction considerably more difficult. Seventy years ago, the preeminent electrocardiographer Wilson et al 1 wrote, “In the presence of left bundle branch block it is seldom possible to make a diagnosis of myocardial infarction on the basis of electrocardiographic findings alone.” Patients with acute myocardial infarction and left bundle branch block have a higher mortality rate than infarct patients with normal conduction, regardless of whether theleft bundle branch block preceded the infarct or resulted from it. 2,3 Prompt diagnosis of the infarct and reperfusion improve prognosis and are essential. Although the diagnosis of old myocardial infarction in the presence of left bundle branch block is nearly as difficult now as in Wilson’s day, we have made progress with acute myocardial infarction. Analysis of patients in the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries-1 trial who had left bundle branch block and acute chest pain has yielded 3 electrocardiographic criteria with independent value in the diagnosis of infarction. 4 In order of decreasing predictive accuracy, these were ST-segment elevation 0.1mVandconcordantwiththeQRScomplex;ST-segment depression 0.1 mV in lead V1 ,V 2 ,o r V3; and ST-segment elevation 0.5 mV and discordant with the QRS complex (Figure 1). Comparison of the electrocardiogram with previoustracingsandserialelectrocardiographicchangeshavealso been found to be useful in diagnosing acute myocardial infarction in patients with left bundle branch block. 5 A variety of imaging techniques and cardiac markers may improve diagnostic accuracy 6 but may also cost valuable time. The history has always been vital as it was in Wilson’s time. In our patient, the history was essential in making a prompt diagnosis and facilitating early revascularization.

A 61-year-old man with no significant medical history suddenly developed dyspnea at rest, quickly followed by collapse. Emergency medical services found the patient in severe respiratory distress (first electrocardiogram [ECG]), and soon after, he became pulseless despite preserved sinus rhythm on the monitor, that is, pulseless electrical activity (PEA). Cardiopulmonary resuscitation (CPR), including intravenous epinephrine, reestablished a pulse (Figure 1). A second ECG was recorded on his arrival to the emergency department. The patient had multiple subsequent episodes of PEA, with return of his pulse soon after CPR each time. He had marked jugular venous distension (Figure 2). The first ECG shows sinus tachycardia, 126 beats/min, and right-axis deviation of the QRS. ST-segment elevation, seen in leads V1eV3 and aVR, is particularly prominent in leads V1eV2 (3 mm), with Q waves in those 2 leads. The differential diagnosis includes both anterior wall myocardial infarction and isolated right ventricular injury from acute pulmonary emboli (PE). The latter diagnosis is suggested by right-axis deviation, ST elevation in aVR, and the ST-segment elevation being more prominent in lead V1 than in lead V3, the opposite of what is characteristically seen in anterior myocardial infarction. The second ECG shows atrial flutter with a rate of 236 flutter waves per minute, 2:1 atrioventricular conduction, complete right bundle branch block (RBBB), and rightaxis deviation. The anterior ST-segment elevation and the lead V2 Q wave have resolved. Acute RBBB is commonly seen with occlusion of the left anterior descending coronary artery proximal to the first major

A 58-year-old man, who had used cocaine and other illicit drugs in the past, had mild, intermittent exertional chest discomfort for 2 weeks followed by severe, prolonged chest pain, which began while he was dancing and was unrelieved by rest. An electrocardiogram recorded on arrival at the emergency department (Figure 1) showed acute inferoposterior myocardial infarction with some features of right coronary arterial occlusion, i.e., ST elevation lead III > lead II and ST depression in lead I, and some features of left circumflex occlusion, i.e., ST depression in leads V1, V2, and aVR (1). Right-sided chest leads showed no significant ST elevation. The cardiac rhythm was marked sinus arrhythmia that did not meet criteria for type I or type II sinoatrial block. The P-R intervals were at the upper limit of normal (0.18 to 0.22 seconds). Over the next several hours, there was minimal sinus arrhythmia. The PR interval varied from 0.42 to 0.18 seconds, and there was further evolution of the changes of inferoposterior myocardial infarction. Figure 1. Electrocardiogram at the time of presentation to the hospital. See text for explication. Twelve hours after the first electrocardiogram, the tracing changed dramatically (Figure 2). Marked sinus arrhythmia was completely dissociated from a regular accelerated idioventricular rhythm, so-called block-acceleration dissociation, i.e., the presence of some degree of atrioventricular block with the atrioventricular dissociation probably being accentuated by the accelerated idioventricular rate (2). Accelerated idioventricular rhythm is common in acute myocardial infarction and, unlike ventricular tachycardia, does not worsen prognosis (3). Figure 2. Electrocardiogram 12 hours after arrival at the hospital. See text for explication. Although the electrocardiogram has features of both right and left circumflex coronary arterial occlusion, two facts suggest the right as the culprit. First, the right is the culprit four times as often as the left circumflex in patients with acute inferior myocardial infarction (1). Second, the artery to the atrioventricular node arises from the right coronary 90% of the time, and any degree of new atrioventricular block suggests the right as the culprit; a caveat here is that inferior myocardial infarction, especially early in its course, often is accompanied by an increase in vagal tone that could be responsible, at least in part, for the atrioventricular block, as well as the marked sinus arrhythmia. Coronary arteriography revealed total occlusion of the right coronary in its mid portion and 90% narrowing of the left circumflex beyond a large first obtuse marginal branch. A bare metal stent was placed in the right coronary artery, and the patient had an uneventful postprocedural course with no further arrhythmia.

The cardiac surgery performed from 1991 to 1994 in a unit dedicated specifically for grown-up congenital heart (GUCH) patients was reviewed to determine the frequency of various procedures, incidence of first and reoperations, early mortality, and its determinants. The 295 patients, aged 16 to 77 years (31 +/- 13), had 307 operations. First operations (n = 128, 42%) were most commonly for closure of atrial septal defect (n = 40), aortic valve replacement (n = 31) or repair of aortic coarctation (n = 14). Reoperations were more frequent (n = 179, 58%) and divided among first corrective repair (n = 49), reoperation after corrective repair (n = 115), and further palliation (n = 15). First corrective surgery was mainly for aortic valve disease (n = 17), Fallot (n = 7), and lesions needing a Fontan procedure (n = 5). Reoperations after corrective repair were needed for aortic valve disease (n = 43), right-sided conduit (n = 30), or recoarctation (n = 11). Early mortality was influenced by presence of central cyanosis (9 of 49, 18% in cyanotic patients; 12 of 258, 5% in acyanotic; p 2 = 13%; p = 0.003), and increasing age of patients. Cyanotic patients had more serious postoperative complications: pleural and pericardial effusions, severe bleeding, renal insufficiency, and sepsis, and their hospital stay was longer compared with acyanotic patients (20 +/- 17 vs 11 +/- 8 days; p

A 53-year-old woman first had a heart murmur noted at age 3. She was symptom free until age 47 but since then has had repeated episodes of cardiac failure. On this occasion she noted increasing shortness of breath, bilateral leg edema up to her knees, and a 10-lb weight gain over a week's time. Increasing her furosemide from 20 to 40 mg daily did not relieve her symptoms. On physical examination, this small, slender woman had a blood pressure of 140/84 mm Hg, bilateral expiratory wheezes, and crackles at both lung bases. Neck veins were elevated to 15 cm above the angle of Louis, and there was 1–2+/4+ edema up to her knees. A 2+/4+ right ventricular lift was felt at the left sternal edge. A hyperdynamic 4+/4+ left ventricular impulse was felt and a third heart sound was heard in the anterior axillary line. A 4+/6+ continuous murmur peaked at the second heart sound and was best heard in the second left intercostal space. There are many causes of continuous murmurs. When the intensity of the murmur peaks at the second heart sound and the murmur is loudest in the second left intercostal space or just below the medial portion of the left clavicle, the cause is almost always a patent ductus arteriosus. When the murmur is maximal elsewhere, the cause usually is not a ductus. An electrocardiogram (Figure) recorded at half standard, i.e., 1 mV = 5 mm, showed sinus rhythm with atrial premature complexes, biatrial enlargement, left axis deviation of the QRS complex (−35°), and left ventricular hypertrophy with repolarization abnormality, including a long QT interval (405 ms with a QTc of 473 ms). Although left ventricular hypertrophy with repolarization abnormality, i.e., a wide angle between the QRS and the ST-T vectors, is classically seen with pressure overload of the left ventricle, such as occurs with systemic hypertension or aortic stenosis, this repolarization change may occur whenever left ventricular hypertrophy is severe, no matter the cause (1). Figure. Electrocardiogram recorded in a 53-year-old woman with a continuous murmur and congestive heart failure. See text for explication. The chest radiograph demonstrated a huge cardiac silhouette, prominent pulmonary vasculature, bilateral pulmonary edema, and scoliosis of the spine, which is more common in patients with congenital heart disease than in the general population. In the past, patients with patent ductus arteriosus occasionally have lived to be far older than our patient (2), but for 75 years now closure of the arterial duct, first by surgical ligation (3) and more recently by catheter-delivered closure devices (4), has been available as a highly effective and relatively low-risk cure for the malformation. Consequently most arterial ducts are now closed in infancy or early childhood. Our patient, however, has always refused any invasive treatment. In her, the duct is large enough to allow a moderately large left-to-right shunt that over time has produced severe left atrial and left ventricular enlargement. Although her left ventricular ejection fraction 18 months ago was 50% as judged by echocardiogram, the left ventricle clearly is failing and the resulting pulmonary arterial hypertension has caused right ventricular and right atrial enlargement. This has been accentuated by chronic obstructive pulmonary disease caused by her smoking 1½ packs of cigarettes per day for 25 years and manifested by a forced expiratory volume in 1 second of 35% and wheezing even when she is not in overt cardiac failure, and by a hemoglobin of 17 g/dL and a hematocrit of 53% on the current admission. The patient responded to medical treatment for congestive heart failure but was lost to follow-up after discharge.

In 1982, Goldberger described an electrocardiographic triad (SV1 or SV2 + RV5 or RV6 ≥ 3.5 mV, total QRS amplitude in each of the limb leads ≤ 0.8 mV, and R/S ratio1 in lead V4) that was 70% sensitive and90% specific for detecting severe left ventricular (LV) dysfunction. To confirm his sensitivity results, in 51 consecutive patients (36 men) aged 28 to 84 years (mean 56) with LV ejection fractions ≤ 20%, the electrocardiographic triad was sought in the electrocardiogram (ECG) recorded closest in time to the echocardiographic study. All 51 patients had systemic arterial hypertension. Evidence of ischemia was present in 7 and absent in 38, and in 6 patients, ischemic status was unknown. In 49 patients, New York Heart Association functional class was available: class II in 8, class III in 32, and class IV in 9. LV ejection fractions ranged from 4% to 20% (mean 14%), and LV internal end-diastolic diameters ranged from 5.7 to 8.6 cm (mean 6.6). Left atrial anteroposterior diameters ranged from 2.9 to 6.1 cm (mean 4.7) and were ≥ 4.0 cm in 47 of the 51 patients. The right ventricular cavity was enlarged in 22 patients. SV1 or SV2 + RV5 or RV6 was ≥ 3.5 mV in 29 of the 51 ECGs; total QRS amplitude was ≤ 0.8 mV in each of leads I, II, and III in 10; and the R/S ratio was1 in lead V4 in 37. Only 1 of the 51 ECGs met all 3 criteria. In contrast to Goldberger's finding of the triad to be 70% sensitive for severe LV dysfunction, in this study, the triad was found to be only 2% sensitive. The difference is likely due to his patients' having idiopathic dilated cardiomyopathy, whereas those in this study had hypertensive cardiomyopathy with or without ischemia. Also, in this study, 1 specific ECG was used for each patient, whereas Goldberger reviewed all of the patients' ECGs looking for the triad. In conclusion, Goldberger's triad is a sensitive or insensitive marker for severe LV dysfunction depending on the patient population and the number of ECGs reviewed.

A 49-year-old man complained of worsening headaches after using crack cocaine a week earlier. He had a slow heart rate (32 beats per minute) and high blood pressure (174/90 mm Hg), and an electrocardiogram recorded on admission showed sinus bradycardia with junctional escape complexes (Figure).

A 51-year-old security officer had an electrocardiogram recorded because of a strong family history of coronary arterial disease (Figure ​(Figure11). His medical history was significant for a gunshot wound to the left side of his chest in the line of duty 25 years earlier. Figure 1 Electrocardiogram. See text for explication. The electrocardiogram shows sinus rhythm and prominent R waves in leads V1 to V3 and otherwise is normal. The Table lists many of the causes of tall R waves in the right precordial leads and confirming clues to their diagnoses (1). Table Causes and diagnosis of tall R waves in lead V1∗ In this patient, the chest radiograph makes the diagnosis (Figure ​(Figure22). Eventration of the left hemidiaphragm, the result of left phrenic nerve damage from the gunshot, allows upward displacement of the gut that pushes the heart far enough to the right that leads V1 to V3 lie over the left ventricle and record complexes resembling those usually recorded from the left precordial leads. A similar appearance may occur when atelectasis of the right lung causes a rightward displacement of the heart (2). Figure 2 Anteroposterior chest radiograph showing eventration of the left hemidiaphragm. Much of the gut is at the level of the heart and pushes it toward the right side of the chest.

The simultaneously recorded lead II and lead V1 electrocardiographic rhythm strips show a narrow QRS followed by a wide QRS and then by a pause (Figure ​(Figure11). The cycle then recurs repeatedly. Superficially, this sequence suggests sinus rhythm with ventricular premature complexes occurring in a bigeminal pattern. Closer observation, however, reveals P waves in front of the wide QRSs as well as in front of the narrow ones. This raises the possibility of atrial bigeminy with the atrial premature complexes being conducted to the ventricles with aberration of the left-bundle-branch-block type. Even closer inspection shows that each cycle contains a third P wave, which is best seen as a negative deflection at the end of each second T wave in lead V1. In lead II this third P wave appears as minimal widening, occasionally with a slight notch on the downslope, of the second T wave. Furthermore, the P-P intervals are regular. Thus, the rhythm is sinus tachycardia (rate = 118 beats/min), and second-degree atrioventricular block is present with a conduction ratio of 3:2. Figure 1 Initial electrocardiogram. See text for explication. Two questions remain. First, is this type I or type II atrioventricular block? Because the P-R intervals of all conducted P waves appear to be the same, this is type II block. Second, why is the first QRS of each cycle narrow while the second QRS is wide ? There is rate-related left bundle branch block; the interval preceding the first QRS is long, allowing normal intraventricular conduction, but the interval preceding the second QRS is shorter than the refractory period of the left bundle branch. An electrocardiogram recorded a day later further clarifies the rhythm (Figure ​(Figure22). The sinus rate has slowed to 98 beats per minute, and more P waves are conducted. The slower rate allows separation of the P waves from the preceding T waves. All QRSs except the one following the pause show left bundle branch block that is clearly rate related. In each group of beats, the first P-R interval is approximately 0.02 seconds shorter than all of the subsequent P-R intervals, which are identical at 0.16 seconds as measured in lead II. Pick and Langendorf have pointed out that the constancy of the P-R intervals after the first one is what establishes the diagnosis of type II atrioventricular block (1). The first P-R of each cycle may be shorter because the first QRS is actually a junctional escape beat. In addition, when the QRS morphology changes as in this case, the second QRS may have a longer initial isoelectric period, making the P-R interval appear slightly longer. Figure 2 Electrocardiogram recorded the following day. See text. Bigeminal rhythms are common and have many causes (2). High on the list is 3:2 atrioventricular block, in this case type II block. This and the even more common rate-related bundle branch block are the salient features of this electrocardiogram.

A 58-year-old woman with a past medical history significant for tobacco use presented with shortness of breath. Physical examination revealed a 30 mm Hg difference in upper-extremity blood pressures (right arm greater than left), elevated jugular venous pressure, and leg edema. A two-dimensional echocardiogram revealed an ejection fraction of 20%. During angiography a heavily calcified lesion was noted in the aortic arch, across which a significant gradient was measured. Computed tomographic scanning identified a focal calcified area in the aortic arch and diffuse atherosclerosis elsewhere. Acquired thromboatheromatous coarctation of the aorta is an uncommon entity found in patients who smoke and are hypertensive. It is almost always seen in conjunction with severe peripheral vascular disease, which this patient had. She was started on heart failure therapy and referred for surgical repair.