Nicardipine and propranolol in the treatment of essential hypertension.

Two hundred thirty-four patients with supine diastolic blood pressure of between 95 and 114 mm Hg were enrolled into a double-blind, randomized, parallel, multicenter trial. The patients were randomized to either nicardipine 30 mg tid, propranolol 40 mg tid, or nicardipine 30 mg tid and propranolol 40 mg tid for six weeks. Two hundred six patients yielded data for analyses. Of the 28 not included, seven had missing data, whereas the remaining 21 were excluded because they either failed to meet inclusion criteria or were noncompliant at endpoint. Both nicardipine and propranolol as monotherapies and in combination achieved statistically significant, (P less than .01), supine diastolic blood pressure reduction relative to baseline. The combination of nicardipine and propranolol showed a greater reduction in supine diastolic and systolic measurements than either of the monotherapies. Nicardipine produced greater blood pressure reductions one hour after dosing, whereas the propranolol treatment tended to produce slightly greater blood pressure decreases eight hours after dose. The combination always resulted in the greatest blood pressure reduction, independent of time after dose. Adverse experiences were reported by 26% of patients in the nicardipine-treated group, most often transient vasodilatory effects, by 17% of the propranolol-treated patients, and by 18% of the combination-treated group. This study demonstrated at the doses studied that nicardipine alone produced equivalent blood pressure reductions to those obtained by propranolol alone, but that the combination of these two drugs produced greater reductions in blood pressures than either of the monotherapies.

Noninvasive myocardial imaging with potassium-43 and rubidium-81 in patients with left bundle branch block.

Noninvasive myocardial imaging with potassium-43 and rubidium-81 has been used successfully to identify areas of infarction and exercise-induced ischemia as regions of decreased radioactivity. The image defects observed are believed to be due to a decreased radionuclide uptake in regions of myocardial scar or to heterogeneous myocardial accumulation of tracer as a result of regional ischemia. Of 27 patients with left bundle branch block studied with noninvasive imaging at rest and during exercise, 25 manifested at rest reduced radioactivity in the region of the interventricular septum. This pattern is similar to that seen in patients with anteroseptal myocardial infarction. Sixteen of the 27 patients underwent diagnostic coronary arteriography and left ventriculography. Only five of these patients had evidence of either previous infarction or significant obstructive coronary artery disease as assessed with clinical or angiographic criteria, or both. Although the image defect was routinely demonstrated at rest in patients with left bundle branch block, this defect was generally normalized or less distinct with exercise in patients with no anatomic heart disease. In contrast, a larger, more distinct or new image defect with exercise correctly identified the presence of significant obstructive coronary artery disease in patients with left bundle branch block. In the clinical application of noninvasive myocardial imaging, these image defects observed at rest can lead to the false pasitive radionuclide interpretation of anteroseptal myocardial infarction.

Clinical correlates of coronary cineangiography in young males with myocardial infarction.

Thirty-eight men who suffered acute transmural myocardial infarction before age 40, and after recovery were New York Heart Association functional Class I or II, were studied by noninvasive means and by coronary angiography in order to determine whether these nonivasive studies could predict the presence of significant coronary artery disease remote from that felt to be responsible for the previous myocardial infarction. Patients were divided into two groups on the basis of the absence (Group I) or presence (Group II) of obstructive disease in a major coronary artery supplying myocardium remote from the prior myocardial infarction. There were 21 patients in Group I and 17 patients in Group II. They did not differ with respect to age, abnormalities of lipid or glucose metabolism, family history, history of hypertension or cigarette use, presence of obesity, or infarct localization. Ten of 17 patients in Group II had angina pectoris; only 3/21 patients in Group I had angina pectoris (p less than 0.01). All 12 patients tested in Group II had a positive maximal exercise tolerance test; only 1/17 patients tested in Group I was similarly positive (p less than 0.001). The absence of angina pectoris and the presence of a negative maximal exercise tolerance test is strong evidence against the pressure of significant CAD remote from that responsible for the prior myocardial infarction.

Transient ST-segment elevation with postmyocardial infarction angina: prognostic significance.

Fifty-seven patients with acute myocardial infarction were observed for early postmyocardial infarction angina and associated transient ST-segment changes. Nine patients had postinfarction angina with transient ST-segment elevation (group 1), seventeen patients had postinfarction angina with ST-segment depression or no ST-segment changes (Group 2), and 31 patients had no postinfarction angina (Group 3). The patients in Group 1 had a statistically significant increased incidence of early reinfarction and death, when compared with the other two groups, singly or combined. There was no significant difference in the incidence of reinfarction and death when Group 2 is compared with Group 3. Patients with transient ST-segment elevation associated with early postmyocardial infarction angina may be an appropriate group in whom to consider newer, more aggressive modes of postinfarction management.