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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.

A 57-year-old man with diabetes mellitus, systemic arterial hypertension, and end-stage kidney disease came to the hospital because his arteriovenous fistula used for hemodialysis had clotted. His blood hemoglobin level was 12.8 g/dL (reference, 13.5-17.5); and serum chemistry levels were creatinine 6.7 mg/dL (0.7-1.3), sodium 132 mEq/L (136-146), potassium 4.0 mEq/L (3.5-5.1), chloride 94 mEq/L (98-106), carbon dioxide 24 mEQ/L (23-29), calcium 9.1 mg/dL (8.4-10.2), and phosphorus 9.1 mg/dL (2.7-4.5). An electrocardiogram was recorded (Figure 1).

A 27-year-old man was admitted to the coronary care unit because of chest pain and an electrocardiogram (ECG) read by the computer as an inferior infarct and left ventricular hypertrophy (Figure).

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.

A family brought their 61-year-old mother to the emergency department because for 4 days she had been confused, incoherent, and somnolent. She also had dysphagia, dysarthria, diplopia, and had fallen out of bed. She had been in the hospital 3 weeks earlier for atrial fibrillation and an exacerbation of congestive heart failure. She also carried a diagnosis of chronic obstructive pulmonary disease and used an albuterol inhaler. She was obese (BMI of 45); and had adult-onset diabetes mellitus. She had a 43 pack-year history of cigarette smoking but had recently quit. Soon after arriving in the emergency department, she had an ECG (Figure);.

Police found a confused 93-year-old woman wandering the streets and brought her to the hospital where an electrocardiogram (ECG) was recorded.

A 61-year-old man came from out of state to attend a football game. He felt well during the game, but when he stood up to leave, he became dizzy and dyspneic. The symptoms lasted 15 to 20 minutes, and when the paramedics arrived, they diagnosed an idioventricular rhythm and brought the patient to the emergency department where a 12-lead electrocardiogram (ECG) was recorded (Figure 1).

In a woman with chest pain

A 49-year-old man visiting New Orleans from Chile comes to the hospital complaining of exertional dyspnea for 2 months with the more recent onset of ankle edema. He is a slender man with a blood pressure of 91/60 mmHg, crackles at both lung bases, and markedly distended neck veins. His cardiac rhythm is irregular. A soft murmur of mitral regurgitation and a soft S-3 are heard at the left ventricular apex. All four pedal pulses are easily palpable. Epigastric tenderness is noted on palpation; although the patient has a history of peptic ulcer disease, the tenderness is probably due to an enlarged left lobe of his liver, the result of hepatic congestion from his heart failure. A chest radiograph shows generalized cardiomegaly with an especially large left ventricle. Pulmonary congestion and small bilateral pleural effusions also are noted. The Figure shows the electrocardiogram recorded on admission.

A 31-year-old man had an hour of pain across the upper portion of his chest anteriorly, and it radiated down the inner aspects of both arms. The pain came while he was walking and gradually disappeared as he sat quietly. Six Rolaid tablets did not seem to alter the pain. The pain was unaccompanied by dyspnea, sweating, nausea or vomiting. The night before the patient had had similar pain relieved by Rolaids and belching. After the second episode of pain, he went to the emergency department of a local hospital where an ECG was recorded.

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.

A furuncle on the leg of a 23-year-old woman led to methicillin-resistant staphylococcus aureus sepsis and adult respiratory distress syndrome (ARDS) requiring tracheal intubation in the intensive care unit (ICU). Initially her electrocardiograms (ECGs) showed sinus tachycardia, but otherwise were unchanged from prior ECGs. A week into her ICU stay a different rhythm occurred.

An obese 49-year-old man with a history of systemic arterial hypertension, diabetes mellitus, dyslipidemia, three myocardial infarcts, an ischemic cardiomyopathy, a four-vessel coronary artery bypass operation 7 years earlier, and implantation of a cardioverter-defibrillator 2 years earlier comes to the hospital with palpitations and dyspnea. An ECG is recorded.

Sinus rhythm; an atrial premature complex; sagging ST-segments, low T-waves, and prominent U-waves suggesting hypokalemia. The ST-T and U-wave changes described above are characteristic of hypokalemia. When the serum potassium level is between 3.0 and 3.5 mEq/L, one or more of the findings may be present. All three are common when the serum potassium level is below 2.5 mEq/L. At the lowest serum potassium levels the T-wave becomes a notch on the upstroke of a giant U-wave, as occurs here in the ECG of this woman with a serum potassium of 1.7 mEq/L.1,2 This configuration is occasionally mistaken for the ST-segment depression and long QT interval of myocardial ischemia.3 Atrial premature complexes are common with hypokalemia, and atrial fibrillation may occur. This patient's potassium was repleted, and the following day her ECG was essentially normal (Figure 2) and virtually unchanged from an ECG recorded two years earlier.

There is a sinus P wave in front of each QRS, and the rate is 122 beats/min. The QRS voltage is large and meets many criteria for left ventricular hypertrophy: RI13 mm (1.3 mV); RaVF19 mm; SaVR14 mm; SV124 mm; SV230 mm; RV626 mm; RV6RV5; SV1 + RV5 or RV635 mm; SV2 + RV5 or RV645 mm; RaVL + SV320 mm in a woman.1 In addition, there are two non-voltage criteria for LVH: QRS duration = 0.11 s and typical repolarization changes: J-point depression with a downsloping ST segment into an inverted T wave and a more rapid upslope back to the baseline. The prolonged QRS duration and repolarization changes are also typical of incomplete left bundle branch block (ILBBB). LVH is present in most patients with complete LBBB,2,3 and probably in most with ILBBB. The patient underwent aortic valvotomy at age 5 to relieve congenital stenosis. Although different valvular morphologies can result in aortic stenosis, when hemodynamically significant stenosis is present in infancy or early childhood the valve is usually unicuspid/unicommissural. Aortic valvotomy can greatly reduce the left ventricular outflow obstruction in such patients, but the majority eventually need reoperation. This usually means aortic valve replacement. This woman now has severe aortic stenosis and regurgitation with not only left but also right ventricular failure, which is a late development with pure aortic valve disease. She needs aortic valve replacement. Unfortunately having one severe disease does not preclude another, and her operative course will be complicated by multiple sclerosis which she developed some 12 years ago.

Multifocal atrial tachycardia; right bundle branch block. The rhythm is totally irregular at a rate of 103 beats/min and originally was read as atrial fibrillation. Close examination, however, reveals a P wave before each QRS and ≥ 3 different P- wave morphologies with no dominant morphology. These are the criteria for multifocal atrial tachycardia MAT, also known as chaotic atrial rhythm,1 chaotic atrial tachycardia,2 and chaotic atrial mechanism.3 The wide QRS complexes ≥ 0.12 s with broad S waves in leads I, aVL, and the lateral precordial leads and broad R or R´ waves in leads aVR and V1 indicate right bundle branch block. MAT is frequently seen in patients with acute pulmonary or other non-cardiac disease and tends to resolve when the underlying disease is brought under control. Patients with MAT also tend to have bouts of other arrhythmias,2 and 3 months earlier this.

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

Sinus bradycardia (48 beats/min), long P-R interval (0.29 s), long QT interval (0.53 s with QTc of 0.47 s), and prominent J waves suggest hypothermia; non-specific ST abnormality.

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.

(2017). Listen to the Patient! Baylor University Medical Center Proceedings: Vol. 30, No. 4, pp. 439-440.

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).

A 20-year-old Hispanic woman presented to the emergency department complaining of six months of progressive dyspnea on exertion associated with intermittent palpitations. Her only past medical history was a stillbirth at 32 weeks gestation about two years ago. Her vital signs in the emergency department were a heart rate of 120 beats/minute, a blood pressure of 145/86 mmHg, and an arterial oxygen saturation of 98 percent with her breathing air. Significant laboratory values included a blood hemoglobin of 14.5 gm/dL, a hematocrit of 49 percent, a brain naturetic peptide (BNP) level of 177 pg/mL, a D-dimer level of 330 ng/ml, a prothrombin time of 12.85 s with an INR of 1.2, and a partial thromboplastin time of 45.7s. Urine pregnancy test was positive, and serum beta-human chorionic gonadotropin level was 81 MIU/mL consistent with a fetus of 3-4 weeks gestational age. An electrocardiogram was recorded.

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).