Robert A. Chahine

Anomalous coronary arteries: angiographic findings in 80 patients

Among 13010 adults who underwent coronary arteriography, 80 (0.61%) patients had a total of 83 anomalous coronary arteries. Thirty-three (41%) of the patients were of Hispanic origin, while out of the entire population studied 30% were Hispanic. The right coronary artery was the most common anomalous vessel. It was identified in 50 (62%) patients, arising in 35 from the left aortic sinus, in 14 from the posterior sinus, and in 1 from the left coronary artery. An anomalous circumflex artery was recognized in 22 (27%) patients. Nine (11%) patients presented an anomalous left anterior descending artery, 1 patient an anomalous left main coronary artery, and another an anomalous septal perforator artery. Twenty-three (29%) patients had concomitant congenital heart abnormalities, most commonly. bicuspid aortic valve and mitral valve prolapse. In each of 5 patients with complex congenital heart disease the course of the anomalous vessel could have interfered with a surgical procedure. In 4 cases anomalous coronary arteries were associated with either anomalous systemic venous circulation or anomalous cardiac veins. In 5 (6%) patients only, the anomalous coronary artery was solely responsible for a clinical event. Coronary atherosclerosis of the anomalous arteries was found in 28% of the patients, while the overall incidence of the disease in this series was 65%. Thus, anomalous coronary arteries are associated with a high incidence of congenital heart diseases, but do not appear to be associated with an increased risk for development of coronary atherosclerosis. The angiographic recognition of these vessels is important in patients who undergo coronary angioplasty or cardiac surgery. Variations in the frequency of congenital coronary anomalies as reported herein may be attributed to a genetic background.

ST segment tracking for rapid determination of patency of the infarct-related artery in acute myocardial infarction

OBJECTIVES This study was designed to test the hypothesis that monitoring the ST segment on a single electrocardiographic (ECG) lead reflecting activity in the infarct zone provides sensitive and specific recognition of reperfusion within 60 min of initiation of therapy in acute myocardial infarction. BACKGROUND Infarct-related arteries that fail to recanalize early may benefit from immediate rescue angioplasty. Hence, detection of reperfusion has important practical clinical implications. METHODS Of 41 patients with acute myocardial infarction who had ambulatory ECG (Holter) monitors placed, 38 had adequate ST segment monitoring for 3 h; 35 of the 38 were treated with thrombolytic agents and 3 with primary angioplasty. All patients underwent early coronary angiography and were classified into two groups: Group P (22 patients) had angiographic patency (Thrombolysis in Myocardial Infarction [TIMI] grade 2 or 3 flow), the Group O (16 patients) had persistent occlusion (TIMI grade 0 or 1 flow) of the infarct-related vessel at 60 min from initiation of therapy. The initial ST segment level was defined as the first ST segment level recorded; the peak ST segment level was defined as the highest ST segment level measured during the 1st 60 min. To assess the optimal ST segment recovery criteria for reperfusion, the presence or absence of a > or = 75%, > or = 50% and > or = 25% decrement from initial and peak ST segment levels, sampled and analyzed at 2.5-, 5-, 10-, 15-and 20-min intervals, was correlated with patency of the infarct-related artery at 60 min. RESULTS ST segment recovery of > or = 50% reduction from peak ST segment levels with sampling rates at < or = 10-min intervals provided the optimal criterion for recognizing coronary artery patency at 60 min (sensitivity 96%, 95% confidence interval [CI] 77% to 99%; specificity 94%, 95% CI 69% to 99%, p < 0.0001). The subgroup of 13 patients in Group P with TIMI grade 3 reperfusion flow all met this criterion (sensitivity 100%, 95% CI 75% to 100%). The use of the initial ST segment level as the baseline for determining the presence of a > or = 50% reduction in ST segment levels within 60 min was less sensitive. Prediction of coronary reperfusion within 60 min of therapy on the basis of a > or = 75% decrement from peak ST segment levels was less sensitive, and the use of a > or = 25% decrement was less specific. CONCLUSIONS ST segment monitoring of a single lead reflecting the infarct zone provides a reliable method for assessing reperfusion within 60 min of acute myocardial infarction. Optimal criteria for ECG reperfusion include a > or = 50% decrease from peak ST segment levels, with ST segment measurements recorded continuously or at least every 10 min.

Effect of nifedipine on exercise-induced left ventricular dysfunction and myocardial hypoperfusion in stable angina

To assess the effects of nifedipine on left ventricular function and regional myocardial perfusion, exercise radionuclide ventriculography was performed in 15 men (median age 59 years) and exercise thallium-201 scintigraphy was done in 11 of them, before and 90 minutes after the oral administration of 20 mg of nifedipine. All patients had stable angina and angiographically proved coronary artery disease without evidence of spasm. Exercise tolerance after administration of nifedipine increased from 343 +/- 42 seconds to 471 +/- 50 seconds (p less than 0.01), whereas the peak exercise double product remained essentially unchanged (difference not significant). Ejection fraction improved significantly at rest (from 49 +/- 3.6% to 52 +/- 3.3%, p less than 0.05) and at peak exercise (42 +/0 3.3% to 47 +/- 3.7%, p less than 0.05). Nifedipine also resulted in an improved segmental wall motion score (4.3 +/- 2.3 to 3.0 +/- 2.3, p less than 0.05; 0 = normal and 4 = worst degree of dysfunction). The ejection fraction increased by more than 5% in one third of the patients at rest, and in more than half of the patients at peak exercise. Improved exercise myocardial perfusion occurred in 5 of 11 patients (45%) and in 7 of 28 segments (25%) with reversible hypoperfusion. Thus, nifedipine produces significant improvement in global and regional left ventricular function in patients with coronary artery disease and stable angina. This may be accounted for, at least in part, by improvement in myocardial perfusion.

Design of a multicenter randomized trial for the stroke prevention in atrial fibrillation study

Individuals with nonvalvular atrial fibrillation are at increased risk of stroke. The Stroke Prevention in Atrial Fibrillation Study is a 15-center randomized clinical trial examining the risks and benefits of low-intensity warfarin (prothrombin time of 1.3-1.8 times control) and aspirin (325 mg/day) in patients with constant or intermittent atrial fibrillation. Candidates for anticoagulation (group I) are randomized to receive warfarin in an open-label fashion, aspirin, or placebo; the last two treatments are given in a double-blind fashion. Warfarin-ineligible patients (group II) are randomized to receive aspirin or placebo in a double-blind fashion. Primary end points are ischemic stroke and systemic embolism. Secondary end points are death, transient ischemic attack, myocardial infarction, and unstable angina pectoris. Analysis is based on the intention-to-treat principle. The anticipated rate of primary end points in patients receiving placebo is 6%/yr. The sample size of 1,644 patients is based on a projected reduction in the rate of primary end points of 50% by warfarin and of 33% by aspirin (beta = 0.2, alpha = 0.05). Patient entry commenced in June 1987 and will continue for 3 years, with an additional year of follow-up. High-risk subsamples identified by clinical and echocardiographic criteria are sought prospectively.

Interpretation of the exercise-induced ST-segment elevation

E lectrocardiographic ST-segment elevation during exercise testing has been recognized since the early days of the Master 2-step tes@-; it was thought at the time that it represented another manifestation of severe myocardial ischemia. Subsequent studies further characterized the exercise-induced ST-segment elevation as reflecting a more severe or unstable form of ischemic heart disease? Prinzmetal’s variant angina,4 or marked abnormality of left ventricular f&ction or left ventricular aneurysm, or both.5 The prevalence of this tinding has varied depending on the population being evaluated, the criteria used to define ST elevation, and the number of leads monitored.5-13 The average reported incidence is approximately 5% in a general population undergoing stress testing predominantly for ischemic heart disease, and ranges between 0.5 and 52.0% in selected populations.12~13 Clinical correlations: Since the early 1970s the focus regarding exercise-induced ST-segment elevation has vacillated between the abnormality of left ventricular function and specific types of myocardial ischemia.3-25 In this issue, Gallik et al26 focus once more on the severity of ischemia secondary to fixed proximal coronary artery disease. They also stress the reversibility of the exercise-induced electrocardiographic tindings after correction of the underlying problem by an interventional procedure (percutaneous transluminal coronary angioplasty or coronary artery bypass surgery) or optimization of medical therapy. The most common characteristic that separates patients in whom the exercise-induced ST-segment elevation reflects severe reversible ischemia from those with marked abnormality of left ventricular function appears to be the absence of past history or electrocardiographic pattern of transmural myocardial infarction.5-*5 Gaflik et al appropriately stress that their patient selection was based on the absence of previous myocardial infarction. However, they do not focus sufficiently in their discussion on the relative rarity of the type of patients they describe in relation to the overall prevalence of exercise-induced STsegment elevation. The ST-segment elevation secondary to markedly abnormal left ventricular function or aneurysm usually accounts for most patients with such tindings when unselected stress tests are reviewed.5,6,gJ3 The data of Gallik et al do not contradict this percep-

Efficacy and safety of amlodipine in vasospastic angina: An interim report of a multicenter, placebo-controlled trial

Amlodipine demonstrated significant antianginal and antiischemic effects and was well tolerated, with a low incidence of serious side effects. The double product remained unchanged during exercise testing, suggesting that the antiischemic effects of amlodipine occur without a decrease in myocardial oxygen consumption. There was a reduction in angina1 episodes and nitroglycerin consumption during singleblind and double-blind active treatment but not during double-blind placebo therapy. Total exercise time, time to 1 mm ST segment depression, time to onset of angina, and maximal ST segment depression were improved by active compared with placebo therapy. In conclusion, amlodipine is well-tolerated and efficacious antiischemic and antianginal therapy for patients with chronic stable angina pectoris. In once-daily doses of 10 mg, amlodipine significantly reduces the number of angina1 attacks and consumption of sublingual nitroglycerin tablets. Amlodipine also improves exercise test variables as long as 24 hours after dosage.

Prediction of cardiac death in patients with a very low ejection fraction after myocardial infarction: A Cardiac Arrhythmia Suppression Trial (CAST) study

The Cardiac Arrhythmia Suppression Trial (CAST) database was analyzed with a Cox proportional hazards regression model to predict the mortality of patients with very poor left ventricular systolic function (ejection fraction < or = .20). Predictors of total death or cardiac arrest were (relative risk), QRS duration (1.10/10 msec increase), coronary artery bypass grafting (0.38), basal heart rate (1.26/10 min-1 increase), diastolic blood pressure (0.79/10 mm Hg increase), diabetes mellitus (1.59), EF (0.94/1 U increase), and ease of suppression (the ability to suppress ambient ventricular ectopy on the lowest dose of the first randomly chosen CAST drug) (0.64). Predictors of arrhythmic death or arrhythmic cardiac arrest included thrombolysis (0.44), coronary artery bypass grafting (0.38), diuretic use (1.71), heart rate (1.21/10 min-1 increase), calcium channel blocker use (1.69), and QRS duration (1.10/10 msec increase). Thus easily measurable clinical and laboratory variables help predict prognosis in this clinically important subgroup. The pathophysiologic basis for and the clinical implications of the ease of ventricular arrhythmia suppression correlating with prognosis requires further study.

Cardiac arrhythmias associated with prophylactic pacing during coronary angiography

Data from 518 consecutive cardiac catheterizations were analyzed to test the value of prophylactic pacemaker insertion during coronary angiography and to compare the incidence of arrhythmic complications in patients with and without pacemakers. In patients without pacing (n = 273), 1 episode of ventricular fibrillation occurred, which responded promptly to defibrillation. Sinus bradycardia (fewer than 30 beats/min for 10 seconds) was recorded in 74 patients (27%) and required treatment in 30 (11%). No patient required or would have benefited from pacemaker placement. Of the 245 patients with prophylactic pacemakers, there was an increased incidence of all ventricular (9 vs 1; p less than 0.013) and supraventricular (5 vs 0; p less than 0.046) arrhythmias. Pacemaker-associated induction of ventricular fibrillation occurred in 2 patients and was clearly related to electrical stimulation during a normally non-vulnerable period of the cardiac cycle. In conclusion, routine prophylactic pacemaker insertion during coronary angiography is not warranted in patients with normal sinus rhythm and normal atrioventricular conduction. More information is needed to determine if pacing is needed in patients with conduction system disease.

Unusual hemodynamics in Löffler's endomyocarditis.

Abstract A necropsy-proved case of Lofflers endomyocarditis in which unusual hemodynamic measurements were recorded at a terminal stage is presented. The right ventricle, as a result of extensive fibrosis, functioned as a mere conduit, and atrial contraction provided the propelling force in the right side of the heart. A right atrial thrombus that partially obstructed the tricuspid valve was also found at postmortem study and probably contributed to the unusual hemodynamic findings. Cardiac catheterization studies in more patients with Lofflers endomyocarditis at various stages of the illness may increase understanding of the course of this obscure disease.

Two-dimensional echocardiographic appearance of pseudo-dehiscence of Hancock aortic prosthesis

1. Dessertenne F: La tachycardie ventriculaire a deux foyers opposis variables. Arch Ma1 Coeur 59:263, 1966. 2. Dessertenne F, Gourgon R, Coumel P, Fabiato A: Tachycardie ventriculaire et torsades de pointes. Ann Cardiol Angeiol 20:243, 1971. 3. Krikler DM, Curry PVL: Torsades de pointes, an atypical ventricular tachycardia. Br Heart J 38:117, 1976. 4. Horowitz L, Greenspan AM, Spielmann SR, Josephson ME: Torsade de pointes: Electrophysiologic studies in patients without transient pharmacologic or metabolic abnormalities. Circulation 63:1120, 1981. 5. Smith WM, Gallagher JJ: Les torsades de pointes. Ann Intern Med 931578, 1980. 6. Griffin J, Most AS: Torsade de pointes complicating acute myocardial infarction. AM HEART J 107:169, 1984. 7. Bashour T, Jokhadar M, Cheng TO: Effective management of the long QT syndrome with amiodarone. Chest 79:704, 1981.