Risks of noncardiac surgery in the cardiac patient.

Patients with ischemic heart disease undergoing surgery under general anesthesia have a substantially increased associated risk of myocardial infarction and cardiac death. Preoperative risk assessment, anticipation of intraoperative problems, and postoperative management are important in improving prognosis. Elective surgery generally poses a lower risk than emergency surgery.

Anticipation of bypass surgery: can it induce silent myocardial ischemia?

Psychological stress has been demonstrated to induce myocardial ischemia. To determine whether stressful events before a coronary artery bypass grafting procedure precipitate myocardial ischemia, silent or symptomatic, and whether this can have an effect on the prognosis, 26 patients were evaluated before a bypass operation with continuous Holter monitor recording. Specific events monitored were signing surgical consent, receiving preoperative medications, shaving and preparing, and transfer to the operating room. A positive Holter result was defined as an ST segment depression of 1 mm or more lasting one minute or longer. Six patients (23%) were found to have one or more episodes of substantial ST segment depression, with a total of ten episodes lasting 208 minutes recorded. All episodes were silent and not associated with an increase in mean heart rate. The majority of episodes occurred randomly, although three episodes did occur between 5 and 6 AM at the time of transport to the operating room. This appeared to be related more to the circadian rhythm than to the stress of transport. No perioperative or postoperative myocardial infarctions occurred, and all patients were alive at 30 days. In conclusion, silent myocardial ischemia present in the immediate preoperative period does not appear to be related to specific preoperative events. Frequency of early morning ischemia may warrant changes in the medication schedule to provide additional protection during these hours.

Influence of oral verapamil on glucoregulatory hormones in man.

We evaluated the effect of treatment with placebo or verapamil (320 mg/day) for 2 weeks on glucose-induced insulin secretion and hypoglycemia-stimulated counterregulatory hormone secretion in hypertensive patients. Verapamil treatment was associated with a significant reduction in diastolic blood pressure (P = 0.02 vs. placebo). During a hyperglycemic clamp (plasma glucose raised 125 mg/dl above basal level) maintained for 90 min, plasma insulin increased 4- to 5-fold (early) and then to values 8- to 10-fold above baseline (late). These increments were identical during placebo or verapamil treatment. The rates of glucose metabolized during each study also were similar, suggesting that no significant change in insulin action occurred during drug treatment. When plasma glucose was allowed to decline precipitously from hyperglycemic levels (220 mg/dl) to nadirs ranging from 42-77 mg/dl, plasma concentrations of glucagon, cortisol, epinephrine, and norepinephrine all increased; however, no consistent differences in the counter-regulatory hormone responses could be attributed to verapamil therapy. We conclude that physiologically effective drug concentrations of verapamil capable of influencing blood pressure do not have a significant effect on secretion of glucoregulatory hormones in man.