Effect of coronary arterial bypass surgery on exercise-induced ventricular arrhythmias. Long-term follow-up of a prospective randomized study.

The effect of coronary arterial bypass surgery on exercise-induced ventricular arrhythmias and their relation to sudden death was examined in 102 patients with stable angina pectoris randomly assigned to medical and surgical therapy (54 and 48 patients, respectively). Symptom-limited treadmill tests were performed at entry and at 1 and 5 years. The surgical group demonstrated significant improvement in exercise performance at 1 year compared with the medical group, and at 5 years exercise-induced ischemia as evidenced by S-T depression and exertional angina remained substantially decreased in the surgical group with little change in the medical group. However, the frequency and severity of exercise-induced ventricular arrhythmias in each group remained unchanged at 1 and 5 years from those at entry. Similar results were obtained from an evaluation of ventricular arrhythmias in the electrocardiogram at rest. With the exception of exercise-induced ventricular tachycardia and fibrillation, no relation was found between ventricular arrhythmias and sudden death. Coronary bypass grafting does not decrease the frequency or severity of exercise-induced or resting ventricular arrhythmias. In patients with stable angina pectoris, with the exception of ventricular tachycardia and fibrillation, exercise-induced ventricular arrhythmias are poor predictors of sudden death. The data suggest that exercise-induced ventricular arrhythmias may not be related to ischemia but to other effects of exercise such as cardiac stimulation by catecholamines or other factors.

Sleep apnea syndrome in a patient with Shy-Drager syndrome.

A patient with autonomic insufficiency and extrapyramidal signs (Shy-Drager syndrome) and sleep apnea syndrome (SAS) underwent hemodynamic studies. In comparison to patients with SAS and intact autonomic reflexes, systemic hypertension was absent and marked sinus arrhythmia during sleep was blunted. Cyclical pulmonary hypertension associated with frequent apneic episodes during sleep persisted, reflecting a minor role of autonomic reflexes in the generation of this abnormality. Autopsy confirmed the Shy-Drager syndrome and multiple areas of degeneration were observed in areas of the CNS outside the medullary respiratory centers, suggesting their importance in the origin of the respiratory abnormalities in SAS.

Measurement of the human magnetic heart vector.

A unipositional lead system has been developed to record the human magnetic heart vector and to permit comparison with the electric heart vector recorded with a conventional Frank lead system. Recordings made in five normal subjects showed a remarkably consistent relation between the electric and magnetic heart vectors. However, the angle between electric heart vector R and T waves was markedly different from the magnetic heart vector R-T angle. In addition, recordings made in two patients with bundle branch block showed a different relation between the electric and magnetic heart vectors compared to normal subjects. These data support the hypothesis that magnetic measurements have a different sensitivity to some components of cardiac activation compared with body surface potential measurements.

Sleep-induced apnea syndrome. Prevalence of cardiac arrhythmias and their reversal after tracheostomy.

Cardiac arrhythmias during wakefulness and sleep in 15 patients with sleep-induced obstructive apnea, and the effect of atropine and tracheostomy on these arrhythmias were studied by continuous overnight Holter electrocardiographic, respiratory and electroencephalographic recordings. Sleep was characterized by marked sinus arrhythmia in 14, extreme sinus bradycardia ( less than 30 beats/minute) in six, asystole of 2.5 to 6.3 seconds in five, second degree atrioventricular (A-V) block in two, and ventricular arrhythmias--complex premature ventricular beats in 10 and ventricular tachycardia in two. Arrhythmias during wakefulness were limited to premature ventricular beats in six. Atropine administration was partially and tracheostomy highly effective in preventing the majority of these arrhythmias during sleep. Marked sinus arrhythmia during sleep is characteristic of the syndrome of obstructive sleep apnea and is frequently accompanied by potentially life-threatening tachy- and bradyarrhythmias. Possible mechanism of production of these arrhythmias, the mode of action of tracheostomy and atropine, and the probable role of similar arrhythmias in the sudden infant death syndrome are discussed.

Hemodynamics in sleep-induced apnea. Studies during wakefulness and sleep.

Twelve patients with predominantly obstructive type sleep apnea underwent cardiac catheterization, hemodynamic monitoring, and arterial blood gas analysis during wakefulness and sleep. Abnormalities during wakefulness included systemic hypertension in four of 12, exercise-induced mild pulmonary hypertension in five of 12, and alveolar hypoventilation in one. During sleep nine patients had cyclic elevations of arterial pressure with each apneic episode, exceeding 200 mm Hg systolic in three of 12. Pulmonary artery pressures increased in 10 of 12, exceeding 60 mm Hg systolic in five. Marked degrees of hypoxemia (arterial P02, less than 50 mm Hg in eight of 12) and moderate hypercapnia with respiratory acidosis were associated with these hemodynamic changes. Cyclic upper airway obstruction during sleep may result in hypercapnia, acidosis, and pronounced hypoxemia, which can lead to hemodynamic abnormalities during sleep. Sustained pulmonary hypertension and possibly systemic hypertension may follow. Tracheostomy is an effective therapy and is recommended to symptomatic patients who have predominantly obstructive apnea but no relievable anatomic cause of upper airway obstruction.