Follow-up catheterization of patients with myocardial infarction during coronary artery bypass surgery.

Of 197 consecutive patients having aortocoronary bypass grafts over a 30 month period, 38 (19 per cent) had ECG evidence of myocardial infarction. The infarctions occurred more commonly in patients receiving multiple grafts. The infarctions were usually in areas supplied by grafted vessels. The infarctions occurred most often in the inferior wall, even when multiple vessels were grafted. Eleven patients with intraoperative infarction have had repeat postoperative coronary arteriograms. Seven had all grafts patent; three of these patients had hypokinesis of the infarcted wall. Four of the 11 patients had one or more occluded grafts; three of these patients had an area of hypokinesis. We conclude that intraoperative myocardial infarction is a common problem in aortocoronary bypass surgery and is not necessarily caused by graft occlusion.     

Effect of digitalis on skeletal muscle in man

Although an inotropic effect of digitalis on skeletal muscle has been demonstrated in animals, it has not been shown in man. Digitalis, in previous studies, has failed to improve voluntary exercise performance. In this investigation the strength of nerve-stimulated involuntary thumb adduction was measured before, during and after infusion of ouabain into the brachial artery. With this experimental design, the many uncontrolled factors that govern ordinary exercise tolerance were avoided. Large doses of ouabain (0.5 mg) produced significant augmentation of peak strength of thumb adduction whereas smaller doses (75 μg) more likely to reach the thumb during systemic digitalization produced only suggestive increases in peak contraction strength. In patients previously digitalized for heart failure, the large doses of ouabain did not significantly change contractility. The findings suggest that skeletal muscle is less sensitive than cardiac muscle to ouabain, and that systemic digitalization has a minor effect on skeletal muscle. When the differences between skeletal and cardiac muscle in excitation-contraction coupling are considered, the reduced effect of ouabain on skeletal muscle contraction is compatible with a cell membrane locus of action in both tissues.     

Angiotensin blockade: its clinical significance.

An understanding of the possible role of excessive angiotensin II activity in the pathogenesis of hypertension in every patient is therapeutically desirable, but it is frustrated by the lack of complete reliability of peripheral plasma measurements of renin activity. Observation of a clear-cut, supranormal decrease in blood pressure during the intravenous infusion of the angiotensin II antagonist, saralasin, has provided a far more reliable indication of the presence of an angiotensinogenic component in the hypertension. There is convincing evidence, however, that the presence of sodium-overload may prevent a decrease in blood pressure during saralasin infusion in persons known to have angiotensinogenic hypertension and that saralasin may cause a slight decrease in the blood pressure of normal subjects after natriuresis. For these reasons, it is important to study hypotensive responses to saralasin under standardized conditions after the administration of a potent diuretic and to compare the observations with those made on normal subjects under identical circumstances. This angiotensin antagonist may be used in the therapy of malignant or advanced hypertension and as an aid to therapeutic decisions in hypertensive patients who have known renal diseases, are taking oral contraceptives or have had severe trauma to the area of the kidneys. Side effects of saralasin are limited to excessive falls in blood pressure levels, mainly when vasodilators or ganglioplegic drugs are being taken at the time of the saralasin infusion, and excessive rises in blood pressure levels, especially in hypertensive subjects with "low renin" activity during high rates of saralasin infusion or after intravenous injections of large boluses. This safe and reliable drug is a valuable tool in the investigation and therapy of hypertension.     

A prospective randomized study to determine the efficacy of steroids in treatment of croup.

We evaluated the use of dexamethasone in the management of acute laryngotracheobronchitis (croup). Thirty patients, ranging in age from eight to 60 months, were evaluated in a prospective, double-blind study. Patients received dexamethasone, 0.3 mg/kg at the time of admission and a similar dose 2 hours later, and were compared with a placebo group receiving saline. Sixteen patients received dexamethasone and 14 patients received the placebo. Severity of each group was scored by a standardized system. Patients receiving dexamethasone had a mean admission score of 8.46 points; patients receiving placebo, 8.14. Twenty-four hours after admission the patients in the treatment group had a mean score of 1.19 as contrasted with a score of 5.58 for the placebo group (P less than 0.01). We concluded that dexamethasone when administered in adequate dosage by an intramuscular route hastens the recovery of infants and children with acute uncomplicated croup.     

Systemic and pulmonary hemodynamic effects of saralasin infusion in hypertension: Predictability of plasma renin status from hemodynamic changes

Hemodynamic measurements were obtained before and after 30 minutes of saralasin infusion in 26 fasting adults with hypertension (25 men and 1 woman). Nine showed a depressor response with a decrease in mean intraarterial pressure greater than 20 mm Hg. Ten were nonresponders and seven had an agonistic response with an increase in mean arterial pressure of greater than 10 mm Hg. Heart rate, pulmonary arterial and wedge pressures and pulmonary vascular resistance were nearly identical in the three groups and remained unchanged. Cardiac index decreased from a mean of 2.76 ± 0.14 (standard error of the mean) to 2.48 ± 0.1 liters/min per m² in the nonresponders (P < 0.02) but remained unchanged in the groups with a depressor or an agonistic response. The mean systemic vascular resistance decreased from 2,406 ± 303 to 1,839 ± 265 dynes sec/cm⁵ in the group with a depressor response (P < 0.001) and increased in nonresponders (< 0.02) and those with an agonistic response (P < 0.01). However, regardless of the response of mean arterial pressure, systemic vascular resistance decreased only in the 10 patients with a plasma renin activity greater than 5 ng/ml per hour (8 from the depressor response group and 1 each from the nonresponse and agonistic response groups).

It is concluded that (1) classification based solely on the response of arterial pressure to saralasin ignores important hemodynamic changes; (2) the response of cardiac index—no change in the patients with a depressor response and a reduction in nonresponders—suggests that endogenous angiotension II supports cardiac output in these groups; (3) a decrease in systemic vascular resistance is better than a decrease in mean arterial pressure as a predictor of the status of the plasma renin activity; and (4) lack of change in pulmonary vascular resistance suggests that endogenous angiotension II plays an insignificant role in maintaining the resistance of the pulmonary vasculature.     

Death from cerebral hypoperfusion during nitroprusside treatment of acute angiotensin-dependent hypertension

A 37-year-old woman, while being treated with nitroprusside for acute hypertension due to an intramural renal artery hemorrhage, became blind on the fourth hospital day, comatose on the fifth, and brain dead on the seventh. Postmortem examination of her brain revealed border-zone infarcts in the parietal-occipital regions and cerebrellum of the sort associated with cerebral hypoperfusion due to hypotension. Yet her blood pressure had been lowered judiciously to a mean pressure in the vicinity of 110 to 120 mm Hg, and episodes of hypotension had been avoided. As possible explanations for this unusual complication, the roles of acute hyperangiotensinemia and nitroprusside administration are discussed.