J. A. Salerno

Left atrial isolation associated with mitral valve operations

Surgical isolation of the left atrium was performed for the treatment of chronic atrial fibrillation secondary to valvular disease in 100 patients who underwent mitral valve operations. From May 1989 to September 1991, 62 patients underwent mitral valve operations (group I); 19, mitral valve operations and DeVega tricuspid annuloplasty (group II); 15, mitral and aortic operations (group III); and 4, mitral and aortic operations and DeVega tricuspid annuloplasty (group IV). Left atrial isolation was performed, prolonging the usual left paraseptal atriotomy toward the left fibrous trigone anteriorly and the posteromedial commissure posteriorly. The incision was conducted a few millimeters apart from the mitral valve annulus, and cryolesions were placed at the edges to ensure complete electrophysiological isolation of the left atrium. Operative mortality accounted for 3 patients (3%). In 79 patients (81.4%) sinus rhythm recovered and persisted until discharge from the hospital. No differences were found between the groups (group I, 80.7%; group II, 68.5%; group III, 86.7%; group IV, 75%; p = not significant). Three late deaths (3.1%) were registered. Long-term results show persistence of sinus rhythm in 71% of group I, 61.2% of group II, 85.8% of group III, and 100% of group IV. The unique risk factor for late recurrence of atrial fibrillation was found to be preoperative atrial fibrillation longer than 6 months. Due to the satisfactory success rate in recovering sinus rhythm, we suggest performing left atrial isolation in patients with chronic atrial fibrillation undergoing valvular operations.

Treatment of angina at rest with nifedipine: A short-term controlled study

The effectiveness of nifedipine in treating angina pectoris at rest was evaluated in 14 patients with frequent ischemic episodes associated with S-T segment elevation or depression. The trial consisted of (1) a 48 hour control period; (2) a placebo period and a period of treatment with nifedipine of 48 hours each; and (3) a second placebo period and a second period of treatment with nifedipine of 24 hours each. The efficacy of treatment was evaluated by continuous electrocardiographic recording to detect painless ischemic episodes. During coronary angiography coronary spasm was demonstrated in five patients. The ergonovine maleate test was positive in seven of eight patients. No statistically significant difference was found in the mean daily number of ischemic episodes between the control period and the first placebo period, or between the control and the second placebo periods. Nifedipine produced a highly significant reduction in the mean daily number of episodes compared with the response to placebo during the first as well as the second period. Nifedipine is effective in angina at rest caused by coronary arterial spasm. The prevention of ischemia may be related to the ability of nifedipine to decrease calcium-dependent coronary muscle tone and to prevent coronary spasm.

Ventricular tachyarrhythmias in prinzmetal's variant angina: Clinical significance and relation to the degree and time course of S-T segment elevation

Fifty-six patients with active Prinzmetals variant angina were studied to determine the incidence and clinical significance of ventricular tachyarrhythmias and the correlation between arrhythmias and degree and time course of S-T segment changes during the ischemic attacks. Twenty-nine patients (Group I) had no ventricular arrhythmias in any of the 1,083 recorded episodes, while 27 patients (Group II) developed arrhythmias in 18% of the attacks. No significant differences in clinical, electrocardiographic, angiographic, or hemodynamic findings could be found between the 2 groups. In 23 of the 27 Group II patients, ventricular arrhythmias developed during maximal S-T segment elevation (occlusion arrhythmias), while in 10 they occurred during resolution of S-T segment changes (reperfusion arrhythmias); 6 of the latter patients also had occlusion arrhythmias. Eight of the 23 patients with occlusion arrhythmias and 6 of the 10 with reperfusion arrhythmias had ventricular fibrillation or ventricular tachycardia. Maximal S-T segment elevation was significantly greater (p less than 0.001) in patients with occlusion arrhythmias than in those without arrhythmias. The episodes with reperfusion arrhythmias were significantly longer (p less than 0.001) and showed a significantly greater S-T segment elevation (p less than 0.001) than those without arrhythmias in Group I patients. This study shows that significant ventricular tachyarrhythmias develop during ischemic attacks in about 50% of patients with active variant angina; clinical and angiographic features are not useful in distinguishing patients with arrhythmias from the others. Our findings suggest that in variant angina ventricular arrhythmias may be due to the effects of both coronary artery occlusion and reperfusion; both types of arrhythmias are correlated with the severity of ischemia, as measured by the degree of S-T segment elevation. Reperfusion arrhythmias also appear to be correlated with the duration of ischemia.

Hyperventilation and ergonovine tests in Prinzmetal's variant angina pectoris in men.

Hyperventilation and ergonovine tests were carried out in a group of 30 patients with variant angina to assess the sensitivity of the 2 tests and to correlate the response with spontaneous disease activity. Hyperventilation produced a positive response in 83% (25 of 30) and ergonovine in 93% (28 of 30) of the patients. After hyperventilation 22 of 25 showed ST-segment elevation, 2 ST depression and 1 T-wave pseudonormalization; after ergonovine ST-segment elevation developed in 23 patients, ST depression in 4 and T-wave pseudonormalization in 1. In all cases the electrocardiographic changes occurred in the same leads as during the spontaneous attacks. The incidence of chest pain and ventricular arrhythmias was similar during both tests; spontaneous remission of ischemia, however, was more frequent (48 vs 14%) after hyperventilation than after ergonovine. Acute ischemia developed at a mean of 218 +/- 112 seconds after the end of hyperventilation in 19 of 25 positive tests; at that time double product was not significantly different from basal values. The sensitivity of hyperventilation was similar (95 vs 100%) to ergonovine in the patients with greater than or equal to 1 daily attack, while in those with less than 1 daily attack the sensitivity of hyperventilation decreased to 55% compared to 77% with ergonovine. Thus, in variant angina the sensitivity of both tests correlates with disease activity. Hyperventilation is a safe provocative test with a sensitivity similar to ergonovine in patients with active disease; however, in patients with sporadic attacks hyperventilation has a lower sensitivity than ergonovine and therefore a limited diagnostic value.

Effects of nifedipine on coronary hemodynamic findings during exercise in patients with stable exertional angina.

To investigate the mechanism by which nifedipine improves exercise tolerance in patients with coronary artery disease, we studied 14 patients with stable exertional angina and left anterior descending artery disease by measuring great cardiac vein flow (GCVF) and calculating anterior regional coronary resistance (ARCR) during exercise before and after sublingual administration of 20 mg of nifedipine. After nifedipine seven patients (group I) had no increase in exercise capacity and showed a similar magnitude of ST segment depression at peak exercise, while another seven patients (group II) had prolonged exercise duration (p less than .001) with less ST segment depression at peak exercise (p less than .01). Such effects were achieved despite a significant increase in double product, an indirect index of myocardial oxygen consumption. In group I patients no significant change was induced by nifedipine in GCVF or in ARCR either at rest or at peak exercise. In contrast, in group II patients nifedipine significantly increased GCVF at rest (p less than .05) and at peak exercise (p less than .001). Moreover, resting ARCR was decreased (p less than .01) and remained significantly lower at peak exercise (p less than .01) compared with the prenifedipine values. These data show that nifedipine may increase GCVF and decrease ARCR at rest and at peak exercise in patients with left anterior descending artery disease. Such increase in myocardial oxygen supply seems the most likely mechanism by which nifedipine may improve exercise capacity in patients with stable exertional angina.

Significance of exercise-induced ST-segment elevation in patients without myocardial infarction.

SUMMARY Sixteen patients with exercise-induced ST-segment elevation and without a history of myocardial infarction or left ventricular aneurysm were studied. Fourteen complained of angina at rest, which was associated with ST-segment elevation in the same leads where it was recorded during exercise, and two patients had only exertional angina. Exercise-induced ST-segment elevation was generally reproducible in subsequent exercise tests performed in different hours of the day, but exercise tests repeated a mean of 15 months later did not induce this electrocardiographic abnormality. All patients had a marked susceptibility to coronary spasm, as shown by the response to the ergonovine test (12 positive tests in 12 patients) and by the occurrence of spontaneous spasm during coronary arteriography in two patients. In addition, coronary arteriography, performed in seven patients at the time of exercise-induced ST-segment elevation, revealed spasm of a major coronary vessel in all. In two patients we documented that exercise-induced ST-segment elevation was accompanied by a decreased coronary blood flow and increased coronary vascular resistance. We conclude that exercise-induced ST-segment elevation in patients without a history of myocardial infarction or left ventricular aneurysm is caused by coronary spasm of a major coronary vessel.

Dipyridamole Test in Angina Pectoris: Diagnostic Value and Pathophysiological Implications

The value of the dipyridamole test (0.75 mg/kg i.v.) in the diagnosis of angina pectoris was studied in 54 patients with angina pectoris (35 with angina on effort associated or not associated with rest angina and 19 with angina only at rest) and in 12 control subjects. The test induced electrocardiographic signs of ischemia (positive test) in 74% of patients with angina on effort, while it was negative in all cases with angina only at rest and in control subjects. All anginal patients with normal coronary arteries or less than 50% stenosis had a negative test; a positive response was observed in 36, 79 and 60% of cases with one-, two-or three-vessel disease, respectively. Hemodynamic changes with a marked arteriolar vasodilatation were observed both in the negative and in the positive tests. In the positive tests no significant change of double product, blood pressure and left ventricular end-diastolic pressure occurred before ischemia appeared. The results of the study show that dipyridamole as a diagnostic test in angina pectoris has a high specificity but a lower sensitivity than exercise test. The hemodynamic and eletrocardiographic findings in the positive tests suggest that dipyridamole-induced ischemia is due to a flow maldistribution with selective subendocardial ischemia secondary to the coronary arteriolar dilatation caused by the drug.

Transient Left Posterior Hemiblock Report of Four Cases Induced by Exercise Test

Four cases with transient electrocardiographic features which have been attributed to left posterior hemiblock (LPH) are reported. These features were induced by the exercise test in patients with severe coronary artery disease. In all of them the following exercise-induced changes were noted: (1) A shift of the main QRS forces inferiorly and to the right (between +90° and +120°). (2) A definite shift of the initial 0.02 QRS vectors superiorly and to the left, causing a small Q wave to appear in leads II, III, and aVF and/or to disappear from leads I and aVL. (3) A SIQIII pattern. (4) A leftward displacement of the precordial transition zone. (5) An increase of QRS duration in about 0.02 sec. Gradual disappearance of the exercise-induced axis shift was observed in all four cases and these findings were compatible with multiple degrees of “incomplete’ LPH. The occurrence of transient LPH patterns was related to the development of acute, transient injury in the posteroinferior wall of the left ventricle in the presence of segmental or widespread coronary artery disease and chronic posteroinferior damage. Before the exercise test, two patients had electrocardiographic patterns suggesting old myocardial infarction and the other two had repolarization changes related to inferior myocardial ischemia according to the angiographic findings.

Ventricular septal rupture after myocardial infarction: Diagnosis by two-dimensional and pulsed doppler echocardiography

Rupture of the ventricular septum in the acute phase of myocardial infarction (MI) requires prompt recognition for correct management. The 2-dimensional and pulsed Doppler echocardiographic findings are reported from 11 patients with ventricular septal (VS) rupture. VS rupture was confirmed by cardiac catheterization in 9 patients, surgery in 4 patients and necropsy examination in 3 patients. Two-dimensional echocardiography (echo) directly visualized the rupture in 7 patients and assessed the size and location of an associated aneurysm in 10. In all patients, M-mode pulsed Doppler echo allowed detection of the left-to-right shunting due to VS rupture, but failed to indicate the rupture site. M-mode pulsed Doppler echo was reliable for detecting VS rupture after MI. Conversely, 2-dimensional echo was less effective in the direct visualization of the rupture, but provided anatomic and functional information that was useful in medical and surgical management. Thus, the techniques are complementary and should be used in combination for the assessment of VS rupture in acute MI.

Which strategy is "best" after myocardial infarction? The Beta-blocker Strategy plus Implantable Cardioverter Defibrillator Trial: rationale and study design.

The Beta-blocker Strategy plus Implantable Cardioverter Defibrillator (BEST-ICD) Trial is a multicenter prospective randomized trial that started in June 1998, in 95 centers in Italy and Germany. The trial will test the hypothesis whether, in high-risk post myocardial infarction (MI) patients already treated with beta blockers, electrophysiologic study (EPS)-guided therapy (including the prophylactic implantation of implantable cardioverter defibrillator [ICD] in inducible patients) will improve survival compared with conventional therapy. Patients eligible for the study are survivors of recent MI (> or = 5 and < or = 21 days), aged < or = 80 years, with left ventricular ejection fraction < or = 35% and > or = 1 of the following additional risk factors: (1) ventricular premature beats > or = 10/hour; (2) decreased heart rate variability (standard deviation of unusual RR intervals < 70 msec); and (3) presence of ventricular late potentials. Furthermore, all enrolled patients must be able to tolerate at least 25 mg of metoprolol per day. These patients constitute about 9% of all patients with recent MI and are expected to have a 2-year all-cause mortality > 25% of which 50% is anticipated to be from sudden death. The main criteria of exclusion from the study are (1) a history of sustained ventricular arrhythmia; (2) documentation of nonsustained ventricular tachycardia during the screening phase; and (3) the need for myocardial revascularization and contraindications or intolerance to beta-blocker therapy. Eligible patients will be randomized to 2 different therapeutic strategies: conventional strategy or EPS/ICD strategy. Patients allocated to the EPS/ICD strategy will undergo further risk stratification, and electrophysiologically inducible patients (approximately 35%) will receive prophylactic ICDs, in addition to the conventional therapy, whereas noninducible patients will be only conventionally treated. The primary endpoint of the study will be death from all causes. By hypothesizing a 30% reduction in the 2-year mortality (from 20% to 14%) in the EPS/ICD group compared with conventionally treated patients, 1,200 patients will have to be included. A triangular, 2-sided sequential design with preset boundaries, for a 5% significance level and 90% power to detect a reduction in 2-year mortality from 20% to 14%, will be used to permit early termination of the trial if the strategy is found to be efficacious, no difference, or inefficacious.