Coronary angiographic, echocardiographic, and electrocardiographic studies on a patient with variant angina due to coronary artery spasm.

A 45-year-old Caucasian female patient with a clinical rehistory and ECG's conforming to the syndrome of variant angina as characterized by Prinzmetal is presented. ECG's recorded during spontaneous pain demonstrated ST-segment elevation and symmetrical peaking of the T-waves in the lateral precordial leads and short runs of ventricular tachycardia. Similar ECG changes were recorded during treadmill exercise- and hand-grip exercise-induced chest pain. An echocardiogram recorded during angina induced by hand-grip exercise demonstrated progressive flattening of septal motion. Multiple views of the coronary system by selective coronary cineangiography were normal with the patient at rest. Angina was then induced by hand-grip exercise and a repeat right anterior oblique view of the left coronary system revealed marked spasm of the left anterior descending artery proximal to the first septal perforator.     

Clinical transvenous cardioversion of recurrent life-threatening ventricular tachyarrhythmias: Low energy synchronized cardioversion of ventricular tachycardia and termination of ventricular fibrillation in patients using a catheter electrode

The purpose of this study was to test the efficacy, safety, and patient tolerance of transvenous cardioversion and defibrillation in patients who had recurrent ventricular tachyarrhythmias. In five of seven patients, a truncated exponential shock of 0.025 to 2.0 joules synchronized to the QRS complex terminated 47 episodes of recurrent sustained ventricular tachycardia (VT). Cardioversion threshold was ≤ 0.25 joule in three patients and 0.75 to 2.0 joules in two patients. Shocks of 0.75 joule and 2.0 joule failed to terminate VT in one patient each; higher energies were not tried because of hemodynamic decompensation. In one patient, a shock of 25 joules terminated ventricular fibrillation (VF) on three occasions, and in another patient a shock of 1.0 joule terminated atrial fibrillation on one occasion. Shocks ≤ 0.5 joule were well tolerated by the awake unsedated patient. One hundred forty of 141 synchronized shocks (including subthreshold shocks) produced no repetitive ventricular activity. In one seriously ill patient who had received multiple antiarrhythmic drugs and required balloon counterpulsation for hemodynamic support, on a single occasion each a synchronized transvenous shock and a synchronized conventional transthoracic shock produced ventricular flutter and ventricular fibrillation (VF), respectively. We conclude that synchronized transvenous cardioversion by a catheter electrode offers promise as a new therapeutic approach.     

Dissociation of the inotropic effect of digitalis from its effect on atrioventricular conduction.

The relation between sequential changes in left ventricular contractility and atrioventricular (A-V) nodal conduction and refractoriness was assessed in open chest dogs during intravenous administration of acetylstrophanthidin (5 mug/kg) at 5 minute intervals until toxic arrhythmias developed. At each time interval, high fidelity left ventricular pressure, its electronic derivative (dP/dt) and a His bundle electrogram were simultaneously recorded and the A-V nodal refractory period was measured by graded trains of stimuli. Animals were studied with an intact autonomic state (Group I), with pharmacologic blockade of both the beta adrenergic and parasympathetic system (Group II) and with parasympathetic blockade (Group III). Whereas contractility increased in response to small doses of digitalis, displaying a linear dose-response relation independent of autonomic tone, A-V nodal transmission indexes responded minimally to less than 50 percent of the toxic dose of digitalis, and the response was dependent upon autonomic tone. These results indicate a dissociation between the effects of digitalis on contractility and A-V transmission in that the major drug action on the ventricular contractile mechanism is a direct, linear one in contrast to the nonlinear response of A-V nodal transmission, which is predominantly mediated through the autonomic system. Clinically, these observations imply that the optimal dose and serum level of digitalis required to treat congestive heart failure may differ significantly from those required to treat supraventricular tachycardias, the therapeutic response of the latter being largely determined by the underlying autonomic tone.     

Prolongation of the QT interval induced by probucol: demonstration of a method for determining QT interval change induced by a drug

Sudden death has occurred in monkeys fed large doses of probucol, a cholesterol-lowering drug, given in combination with an atherogenic diet. These monkeys develop prolonged QT intervals and high serum levels of probucol. We investigated the effect of probucol on QT interval and the incidence of ventricular ectopy during a double-blind placebo-controlled study in 16 patients with less than 600 premature ventricular complexes (PVCs) per day and a corrected QT interval of less than 0.44 second. Seven patients received probucol and nine patients received placebo. Three 24-hour continuous ECG recordings were obtained prior to entry into the study and three additional recordings were obtained after 6 months of drug or placebo therapy. A 15-second ECG tracing was sampled from the continuous ECG recording every 30 minutes and, for the group, 15,000 QT intervals were measured permitting construction of QT versus R-R regression lines for each patient before and during therapy. Comparison of the regression lines revealed that the measured QT interval prolonged 20 +/- 18 msec during the awake state and 24 +/- 20 msec during sleep (mean + standard deviation) at matched heart rates in the seven patients receiving probucol (p less than 0.01). Using Bazett's formula to correct for rate, corrected QT interval prolonged 22 +/- 23 msec in the awake state and 20 +/- 18 msec in the asleep state (p less than 0.01). In probucol treated patients QT interval prolongation was directly related to increasing probucol plasma levels (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Echocardiographic manifestations of valvular vegetations

Eight patients with autopsy or surgically proved valvular vegetations were examined using echocardiography. Five of these patients had lesions on the aortic valve and three had lesions on the mitral valve. The echocardiographic finding in these patients was a non-uniform thickening of valve leaflets which exhibited unrestricted motion. Often the abnormal echoes which produced the thickened valve had a shaggy appearance. In all eight patients the location of the echocardiographic abnormality correlated with the anatomic findings at surgery or autopsy. In one patient the diagnosis of bacterial endocarditis was first suspected following the echocardiographic examination and only subsequently was a heart murmur heard. These findings indicate that echocardiography may play a useful role in elucidating the pathological anatomy of the bacterial endocarditis with vegetation; however, the length of time from the onset of clinical illness to echocardiographic diagnosis remains unknown.     

Prevalence and reproducibility of exercise-induced ventricular arrhythmias during maximal exercise testing in normal men.

The occurrence of ventricular arrhythmias at rest or during ordinary daily activities has been implicated as a risk factor for future coronary-related events and sudden death. However, the clerical significance of exercise-induced ventricular arrhythmias remains uncertain. To assess the prevalence and reproducibility of such arrhythmias, two serial maximal treadmill exercise tests were performed in a study population of 543 male Indian State policemen at an average interval of 2.9 years. Four hundred sixty-two subjects were clinically free of evidence of cardiovascular disease, and 81 had evidence of definite or suspected cardiovascular disease. The prevalence of exercise-induced ventricular arrhythmias during the first test was 30% in men aged 25 to 34 years, 32% in those aged 35 to 44 years and 36% in those aged 45 to 54 years. The prevalence rate in these age groups with repeat testing was 36, 38 and 42%, respectively. These differences were not statistically significant. The group with definite or suspected cardiovascular disease had a greater prevalence of exercise-induced ventricular arrhythmias than normal subjects during both tests but the prevalence rate with repeat testing remained constant. The occurrence of exercise-induced ventricular arrhythmias was reproducible in individual subjects during the second test in 55% of 25 to 34 year olds, 58% of 35 to 44 year olds and 62% of 45 to 54 year olds. Thus, individual reproducibility in two consecutive tests was only slightly greater than reproducibility by chance alone. The group with known or suspected cardiovascular disease demonstrated a trend toward greater reproducibility with repeat testing. Exercise-induced ventricular arrhythmias were not reproducible by type or complexity. The marked variability of exercise-induced ventricular arrhythmias during repeat maximal exercise testing in a clinically normal population appears to negate the usefulness of this finding during a single test as a marker of future cardiovascular disease. Nevertheless, subjects whose arrhythmias were reproducible may form a group destined to manifest clinical cardiovascular disease in long-term follow-up studies.     

Studies with aprindine

Aprindine is a very effective antiarrhythmic agent with a narrow therapeutic-toxic ratio. It has been used successfully in treating patients who have both supraventricular and ventricular tachyarrhythmias. Aprindine slows conduction in all cardiac fibers and suppresses digitalis-induced after-depolarizations. Voltage-clamp studies indicate that aprindine, in higher doses, suppresses the slow inward current in frog atria. In the dog subjected to coronary artery occlusion, aprindine may be arrhythmogenic, antiarrhythmic, or have no effect on the development of arrhythmias, depending on the temporal relationship between time of administration and time of occlusion.     

Percutaneous balloon atrial septostomy in infants with transposition of the great arteries.

Initial experience with PBAS in early management of neonate with TGA is described. Standard percutaneous techniques were used and modified by a series of dilations designed to introduce a septostomy catheter into the femoral vein. Thirty infants with TGA were catheterized, and PBAS was accomplished in 25. The mean aortic oxygen saturation rose from 55 to 72 per cent. Twenty-four infants were clinically palliated for at least 3 months; however, five required pre-elective surgery thought due to inadequate atrial mixing. No severe complications followed PBAS. Twenty-three patients underwent follow-up catheterization, in 17 through the vein used for PBAS. When compared to patients with TGA who had cutdown insertion of balloon septostomy catheters, the group treated by PBAS was similar in patient material, and successful septostomy. Those ballooned percutaneously had fewer complications and required slightly less time for the procedure. We feel that PBAS is a relatively easy and safe palliative procedure when performed in an infant with TGA. It should be considered by all those performing percutaneous diagnostic catheterization in infants and children.     

Anterior left ventricular wall echoes in coronary artery disease. Linear scanning with a single element transducer

The feasibility and usefulness of obtaining anterior left ventricular wall echoes were studied using a linear cardiac scan with a single element tranducer and M mode recordings. One hundred four patients were examined: 50 with acute myocardial infarction and 54 who underwent left ventricular angiography and coronary cineangiography for evaluation of chest pain. Of the 54 patients with cardiac catheterization studies, 11 had no evidence of cardiac disease, 42 had 50 percent or greater obstruction in one or more of the three major coronary arteries and one had aortic insufficiency. Anterior left ventricular wall echo motion toward the transducer or absence of motion during ejection was called abnormal, and motion away from the transducer during ejection was interpreted as normal. Abnormal motion was seen in four of four patients with an isolated lesion of the anterior descending coronary artery, in one of three with an isolated lesion of the right coronary artery and in neither of two with an isolated lesion of the left circumflex artery. Of the 20 patients with obstructive coronary artery disease by arteriography and abnormal left ventricular wall echo motion, 18 had obstruction of the left anterior descending artery with or without other disease. Correlation of the anterior left ventricular echograms with the left ventricular angiograms was poor, with agreement in only 66 percent (33 of 50) of cases. Twenty-five of 26 patients with acute infarction and abnormal anterior left ventricular wall echo motion had electrocardiographic changes indicative of anterior or lateral wall infarction, or both. Twenty-five of 34 patients with electrocardiographic changes indicative of anterior wall infarction had an abnormal anterior wall motion echo. This study shows that obtaining the anterior left ventricular wall echo is feasible and useful in patients with coronary artery disease since abnormal anterior left ventricular wall motion is closely associated with anterior wall ischemia or infarction in these patients.     

Echocardiographic differentiation of infundibular from valvular pulmonary stenosis.

Echocardiographic tracings of the pulmonary valve were examined in 24 normal subjects, 16 patients with valvular pulmonary stenosis and 3 patients with infundibular pulmonary stenosis. In normal subjects, atrial contraction produced a slight posterior opening motion of the pulmonary valve leaflet (a wave). This presystolic opening motion (a wave) varied with respiration, and maximal a wave depth recorded during quiet inspiration (Amax) averaged 3.7 plus or minus 1.2 (standard error of the mean) mm (range 2 to 7 mm). In the 10 cases with moderate or severe valvular pulmonary stenosis, increased force of right atrial contraction and elevated right ventricular end-diastolic pressure resulted in an increased posterior or opening motion of the pulmonary valve leaflet, and Amax averaged 9.6 plus or minus 2.0 mm (range 8 to 13 mm, P less than 0.001 versus normal). When both anterior and posterior leaflets were recorded, presystolic opening or doming of the valve was observed. In six cases of mild valvular pulmonary stenosis, Amax averaged 4 plus or minus 2.5 mm (not significant). In patients with infundibular pulmonary stenosis, marked chaotic systolic fluttering of the valve leaflet, which lies in the turbulent stream of blood distal to the obstruction, was recorded. This finding was never seen with valvular pulmonary stenosis. In two cases of mild infundibular pulmonary stenosis, the amplitude of presystolic opening motion was within the normal range of 3 and 7 mm. In one case of severe infundibular pulmonary stenosis, no presystolic opening motion was recorded, thus suggesting that the small pressure changes produced by atrial systole failed to reach the valve leaflets. Echocardiography, therefore, should be of use in differentiating valvular from infundibular pulmonary stenosis.