Ara G. Tilkian

CYCLICAL VARIATION OF THE HEART RATE IN SLEEP APNOEA SYNDROME: Mechanisms, and Usefulness of 24 h Electrocardiography as a Screening Technique

400 sleep-apnoeic patients with an intact autonomic nervous system underwent twenty-four-hour electrocardiography with simultaneous polygraphy recording at night. At onset of sleep apnoea all showed progressive bradycardia, followed by abrupt tachycardia on resumption of breathing. The electrocardiographic pattern, which is identifiable by computer analysis, can be used as a screening tool for sleep apnoea; it was not seen in controls without sleep apnoea syndrome. A subgroup of patients with sleep apnoea and impairment of autonomic nervous control of the heart (heart transplants, autonomic neuropathy, Shy-Drager syndrome) did not show the cyclical heart rate pattern. In obstructive sleep apnoeic patients with normal autonomic nervous function, atropine sulphate blocked the pattern by eliminating the bradycardia component, while 100% oxygen, even at high rates of administration, caused only moderate blunting of the heart rate variation. The electrocardiographic changes observed in sleep apnoea syndrome are therefore mediated by the autonomic nervous system; hypoxia is not the only factor involved.

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.

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.

Surgical management of airway obstructions during sleep

Anatomical or physiological airway obstructions during sleep, of which the patient is unaware, cause daytime sleepiness at first, then signs of decreasing mental function, and eventually in some individuals, pulmonary and systemic hypertension. A few of these patients had been recognized before, the Pickwickian syndrome and in children with cardiac problems and large tonsils. The majority, however, present as sleep disorders. This paper describes our surgical experience with improving the airways of 19 children and adults with daytime somnolence.

The effect of coronary bypass surgery on exercise-induced ventricular arrhythmias

Ninety-one patients with angiographically proved coronary artery disease and stable angina were randomly assigned into surgical and medical therapy. Graded exercise tests were performed on entry into the study and repeated in 1 year. Ventricular arrhythmias during exercise and 8 minutes of recovery were studied. Arrhythmias were graded on a scale of 0 to 7 by their presumed severity. On entry, both groups were similar in the severity of coronary disease, exercise capacity, and frequency and severity of exercise-induced ventricular arrhythmias. At 1 year, the frequency and severity of arrhythmias remained unchanged in both groups, whereas the surgically treated patients showed a marked improvement in their exercise capacity (p less than 0.005). The medically treated patients had a slight deterioration in their work capacity which, however, did not achieve statistical significance (p = 0.08). Twelve patients died suddenly. In seven medically treated patients who died suddenly, the frequency and severity of ventricular arrythmias on exercise were not different from those of the rest of the medical patients. In the five surgically treated patients who died suddenly, one had multiform premature ventricular beats, a second developed ventricular fibrillation (2 years before dying suddenly), and a third had no arrhythmias during exercise. Two died before the 1 year evaluation. Successful coronary surgery improves exercise capacity without decreasing associated ventricular arrhythmias. Exercise-induced ventricular arrhythmias, with the exception of ventricular fibrillation, may not be closely associated with the risk of sudden death.

Effect of lithium on cardiovascular performance: Report on extended ambulatory monitoring and exercise testing before and during lithium therapy☆

To assess the effect of long-term lithium therapy on cardiac arrhythmias and cardiovascular performance, extended ambulatory electrocardiographic monitoring was performed in 12 patients, and rest and exercise electrocardiograms in 10 of 12, before and during lithium therapy. Lithium increased the frequency of premature ventricular contractions in three patients, decreased it in one, and produced no change in eight. Three of four patients with atrial arrhythmias showed improvement during lithium therapy. Exercise performance was unchanged. Although 7 of the 12 patients manifested T wave flattening in the resting electrocardiogram, none had S-T segment displacement at rest or on treadmill exercise. Before lithium therapy, arrhythmias on exercise included premature atrial contractions in four patients, ventricular arrhythmias in four (premature ventricular contractions in four, with couplets in two and with ventricular tachycardia in one). During lithium therapy, exercise did not provoke premature atrial contractions or ventricular tachycardia in any of the patients, but three patients had premature ventricular contractions (with couplets in one case). We conclude that lithium at therapeutic levels may precipitate or aggravate ventricular arrhythmias. When administered to patients with heart disease, factors that interfere with renal clearance of lithium (heart failure, salt restriction, long-term diuretic therapy) must be recognized and doses must be adjusted accordingly. Careful follow-up and electrocardiographic monitoring are advisable if lithium is to be used in the presence of ventricular arrhythmias. Cardiovascular performance as assessed by treadmill exercise testing was not affected by long-term lithium therapy.

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.