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J M Burroughs

Publications and source records attributed to J M Burroughs.

3 recordsLinked to original sources
PubMed1996

Asymptomatic bradyarrhythmias as a marker for sleep apnea: appropriate recognition and treatment may reduce the need for pacemaker therapy.

Sleep apnea is associated with many adverse cardiovascular sequelae, including hypertension, nocturnal angina, decreased cardiac output, and bradyarrhythmias. The purpose of this study was to determine if patients referred for pacemaker therapy with asymptomatic bradyarrhythmias have underlying sleep apnea as the etiology of their bradyarrhythmias. This study included eight patients (7 males, 1 female) referred to a cardiac electrophysiology practice for pacemaker therapy. Patients included had asymptomatic bradyarrhythmias that consisted of severe sinus bradycardia, second-degree atrioventricular block, and complete heart block. In 7 of 8 patients, the bradyarrhythmias occurred at night or during the day while asleep. No patients were conditioned athletes. Symptoms often associated with bradyarrhythmias, such as lightheadedness and syncope, were not present. However, seven patients had at least one symptom suggestive of sleep apnea, such as excessive daytime fatigue, snoring, cessation of breathing during sleep (apnea), or frequent night-time awakenings. Overnight polysomnography studies were obtained on patients who had one or more symptoms suggestive of sleep apnea. In this study 7 of 8 patients (88%) referred for pacemaker therapy with asymptomatic bradyarrhythmias were documented by polysomnography to have sleep apnea. When treated with either sleep position modification, nasal continuous positive airway pressure (nasal CPAP), or tracheostomy, all seven patients had improvement in sleep apnea symptoms and remained asymptomatic from their bradyarrhythmias without pacemaker therapy over an average follow-up period of 22 months. One patient without symptoms suggestive of sleep apnea declined pacemaker therapy and remained asymptomatic. From these results, we concluded that asymptomatic transient bradyarrhythmias may suggest a diagnosis of sleep apnea. The evaluation of a patient referred for pacemaker therapy with asymptomatic bradyarrhythmias should include questions related to sleep apnea symptoms. Establishing the diagnosis of sleep apnea may reduce the need for pacemaker therapy and permit appropriate treatment of the underlying cause of these bradyarrhythmias.

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PubMed1993

The effects of the ATP-dependent potassium channel antagonist, glyburide, on coronary blood flow and susceptibility to ventricular fibrillation in unanesthetized dogs.

Extracellular potassium rapidly increases during myocardial ischemia and has been implicated in the development of ventricular fibrillation (VF). Recent evidence suggests that ischemically induced potassium efflux results from the opening of ATP-dependent potassium channels. If extracellular potassium accumulation contributes to VF, one would predict that drugs that block the ATP-dependent potassium channels should protect against these arrhythmias. Therefore, VF was induced in 15 mongrel dogs with healed myocardial infarctions by a 2-min coronary occlusion during exercise. This exercise (Ex) plus ischemia test consistently induced VF during each control (vehicle) presentation. However, glyburide, a sulfonylurea drug that selectively blocks the ATP-dependent potassium channel, prevented VF in 13 of 15 animals tested (p < 0.001, chi 2). Glyburide (G) elicited significant reductions in left ventricular dP/dtmax (Ex: control, 5,031 +/- 386.4; G, 3,286 +/- 116.6 mm Hg/s) and mean coronary blood flow (Ex: control, 49.6 +/- 8.7; G, 31.3 +/- 5.5 ml/min) both before and during exercise. The heart rate responses to exercise and coronary occlusion were also reduced. Since heart rate reductions could contribute to the cardioprotection, the exercise plus ischemia test was repeated with the heart rate held constant by ventricular pacing. Glyburide still protected four of five animals under these conditions. These data indicate that glyburide, a drug that blocks the ATP-dependent potassium channels, can prevent VF independently of changes in the heart rate. The data further suggest that these channels may contribute to the coronary vasodilation elicited by an increase in metabolic demand during exercise.

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