QT interval prolongation and increased plasma catecholamine levels in patients with mitral valve prolapse

The heart rate corrected QT interval (QTc) and plasma catecholamine (CA) and norepinephrine (NE) levels were measured in 15 symptomatic patients with idiopathic mitral valve prolapse (MVP) and in 19 control subjects. MVP patients showed longer mean QTc and were divided into two groups: group A normal QTc (greater than 440 msec) and group B prolonged QTc (less than 440 msec). In supine resting conditions CA levels were as follows: group A 0.420 +/- 0.035 ng/ml and group B 0.619 +/- 0.104 ng/ml (p less than 0.05); both were greater than control values (0.348 +/- 0.017 ng/ml, p less than 0.005). NE levels were as follows: group A 0.350 +/- 0.031 ng/ml and group B 0.376 +/- 0.052 ng/ml (NS); both were greater than control values (0.242 +/- 0.025 ng/ml, (p less than 0.05). When a standing position was assumed, CA and NE levels increased significantly in all groups but this was most marked in group B as compared to control levels (CA: 1.039 +/- 0.123 ng/ml versus 0.625 +/- 0.037 ng/ml; NE: 0.737 +/- 0.076 ng/ml versus 0.504 +/- 0.031 ng/ml) (p less than 0.001 and p less than 0.05, respectively). Thus the longest QTc was observed in patients with MVP who had the highest levels of CA and NE, in both supine and standing positions. These data may account, in part, for the occurrence of severe ventricular arrhythmias in some patients with MVP and may offer a rationale for adrenergic blockade in that subset of patients with MVP and markedly prolonged QTc.     

Orthostatic hypotension: A commonly unrecognized cause of symptoms in mitral valve prolapse

To test the hypothesis that orthostatic hypotension could represent an alternative mechanism contributing to the symptoms of mitral valve prolapse, the systolic and diastolic arterial blood pressures were measured in the supine and standing positions in 86 patients with the diagnosis confirmed by echocardiography. Orthostatic hypotension was demonstrated in 12 patients. Ten of them presented with a history of recurrent lightheadedness, dizziness or syncope and constitute 59 percent of the total number of patients with such symptoms in this series. Although nine of these 10 patients reported transient lightheadedness or dizziness during periods of ambulatory electrocardiographic recording, in only one were the symptoms chronologically related to cardiac arrhythmias. On the other hand, eight of them described lightheadedness and two experienced near-syncope during the postural test in association with the orthostatic drop in blood pressure. Improvement in symptoms and correction of the orthostatic hypotension were demonstrated in seven patients after beta-adrenergic blockade with propranolol. Before therapy, the mean systolic blood pressure dropped from 114 ± 3 mm Hg in the supine position to 78 ± 1 mm Hg upon standing (p < 0.001). In repeated postural tests performed after four weeks of treatment, the systolic blood pressure changed from 120 ± 3 mm Hg supine to 115 ± 1 mm Hg upon standing (p > 0.01).We conclude that orthostatic hypotension is a commonly unrecognized mechanism responsible for some of the symptoms of mitral valve prolapse, particularly in patients affected by recurrent lightheadedness, dizziness or syncope.     

Maximal revascularization (reperfusion) in intact conscious dogs after 2 to 5 hours of coronary occlusion.

Acute infarction was produced in intact conscious dogs by inflating a previously implanted balloon cuff around the left anterior descending coronary artery was occluded in 26 control dogs and reperfused by deflating the balloon cuff after 2 hours of occlusion in 19 dogs (group II) and after 5 hours in 11 dogs (group III). Serial studies were performed and repeated after 48 hours and 7 days. All three groups revealed hemodynamic and metabolic deterioration with coronary occlusion and infarct production. Immediately after reperfusion, arrhythmias developed in groups II and III and persistent ventricular tachycardia was present 2 to 3 hours after reperfusion in 74 percent of animals in group II and 82 percent of those in group III compared with 6 percent and 13 percent incidence rates at corresponding times in control dogs. Q waves developed in 83 percent of animals in group II and 100 percent of those in group III but in only 12 and 27 percent of control animals at corresponding times. Hemodynamic deterioration was accelerated in the postreperfusion period in both groups II and III. Angiographic assessment revealed improvement in 42 percent of dogs in group II, but in none of those in group III after reperfusion. Myocardial oxygen extraction diminished to subnormal levels after reperfusion, indicating either reactive hyperemia or shunting effect. Mortality was not significantly influenced by reperfusion. Infarct size was more than 15 percent of ventricular mass in 92 percent of control dogs and in 100 percent of dogs in group III, but in only 50 percent of those in group II. The data indicate that reperfusion in conscious dogs representing early, noninvasive maximal revascularization under ideal circumstances fails to prevent deterioration or death; instead it hastens the development of arrhythmias and myocardial injury. Reperfusion, although deleterious in the first hours, can reduce infarct size if performed after 2 hours, but not after 5 hours, of occlusion.     

Stability of AV conduction in sick sinus node syndrome patients with implanted atrial pacemakers

Single-chamber atrial pacing is effective in the management of sinus node dysfunction, subject to the uncertainty of long-term atrioventricular conduction. Despite the accepted observation that many patients with sinus node dysfunction also have atrioventricular conduction disease, data do not exist on the development of atrioventricular block in those patients with permanent single-chamber atrial pacing. Of 70 patients who received single-chamber atrial pacing from 1967 to 1982 (mean duration of pacing was 33 months), only two patients of 58 (3.4%) of those with sinus node dysfunction developed atrioventricular (AV) block—after 14 months in one patient and after 23 months of successful atrial pacing in the other. None of the 12 patients paced for tachyarrhythmia management developed AV block. Of the 70 patients, 37 had assessment of AV conduction by incremental atrial pacing at the time of implant and 20 patients underwent atrial pacing on the basis of surface ECG and clinical judgment. Electrophysiologic studies were conducted only in those patients being paced for control of supraventricular arrhythmias. Only 5 of the 70 patients required conversion to ventricular pacing for technical difficulties; three of these conversions occurred in the early 1970's before the advent of atrial tined or J leads; one was for irreparable lead fracture and only one occurred in a patient with a newer design atrial lead. In conclusion, progression to AV block in patients with permanent atrial pacing is uncommon; formal electrophysiologic studies are necessary mainly in patients with supraventricular arrhythmias; and in the majority of patients, AV conduction can be assessed at the time of implant. Continued improvement in atrial leads should make atrial pacing even more successful.     

Effects of intravenously administered propranolol on wall motion abnormalities

Although propranolol is frequently utilized as therapy for angina pectoris in patients with previous myocardial infarction, its effects on wall motion abnormalities in such patients have not been adequately defined. Accordingly, using external wall motion video tracking, we studied 18 patients with previous myocardial infarction and wall motion disorders and 5 normal subjects before and after administration of propranolol, 5 mg intravenously. Systolic time intervals, heart rate and left heart size (measured by the distance between the mid-line and left heart border in an X-ray film triggered at end-diastole after a standard inspiration) were also measured before and after administration of propranolol. In each instance propranolol produced a reduction in the amplitude and velocity of wall motion in areas of normal movement, hypokinesis and paradox, resulting in decreased outward bulging. In the normal subjects, the amplitude and velocity of wall motion also decreased. In the patients with previous myocardial infarction, propranolol increased the ratio of the preejection period to the left ventricular ejection time from a mean of 0.377 ± 0.03 (standard error of the mean) to 0.409 ± 0.03 (P <0.001); decreased heart rate by an average of 7.5 beats/min (P <0.001); and increased the distance from the mid-line to the left heart border from 94.3 ± 2.6 to 97.3 ± 2.6 mm (P <0.001). Similar changes occurred in the 5 normal subjects. We conclude that doses of propranolol sufficient to increase the ratio of the preejection period to left ventricular ejection time, decrease heart rate and increase heart size do not exaggerate preexisting paradoxical wall motion or accentuate latent areas of paradox in patients with previous myocardial infarction.     

Bacterial endocarditis with ruptured sinus of valsalva and aorticocardiac fistula

A case is presented of bacterial endocarditis with a ruptured sinus of Valsalva and formation of an aorticocardiac fistula from the right coronary sinus into the right atrium and right ventricle. The pathologic, clinical and surgical aspects of bacterial endocarditis complicated by a ruptured sinus of Valsalva and an aorticocardiac fistula are analyzed. This complication of bacterial endocarditis is still uncommon, but alertness to its diagnosis makes possible early and successful surgical treatment.     

Atherosclerotic ulcerative disease and associated aneurysms of the coronary arteries.

Abnormal cardiac muscle function has been reported in experimental diabetes mellitus from this laboratory. To examine left ventricular performance in diabetic patients without clinical evidence of myocardial ischemia or other cardiovascular disease, a noninvasive measurement of the systolic time intervals was carried out. Simultaneous recordings of the electrocardiogram, heart sounds, and carotid pulse were made in 25 diabetic subjects, 20 to 56 years of age, and compared with 37 normal subjects. The diabetic subjects had a shorter left ventricular ejection time, longer pre-ejection period, and a higher ratio of pre-ejection period/left ventricular ejection time (P < 0.001). The isovolumic time was prolonged (P < 0.001), while heart rate and arterial pressure were within normal limits. Abnormal function was independent of apparent duration and treatment by diet alone, insulin, or hypoglycemic agents. On the basis of available morphologic data in human and canine diabetes, an alteration of the myocardial interstitium may be the basis for this preclinical abnormality in diabetic patients.