Nifedipine, a calcium channel blocking agent, has been shown safe and effective in the treatment of various cardiac disorders. In Prinzmetal's variant angina, nifedipine relieves the acute spasm of a large coronary artery, and thereby reverses the sudden decrease in myocardial oxygen supply. In chronic stable angina, the efficacy of nifedipine stems from an interplay of direct and reflex effects. A decrease in systemic vascular resistance, and thus, myocardial oxygen demand, is considered the most important effect. Although this is partially offset by baroreceptor-mediated reflex increases in blood pressure and heart rate, the net effect is a decrease in myocardial oxygen consumption. The importance of nifedipine-induced increases in coronary blood flow in relieving stable angina remains controversial. Numerous clinical trials in patients with chronic angina have demonstrated that nifedipine increases exercise tolerance by lowering the heart rate-blood pressure product (an approximation of myocardial oxygen consumption). The maximal double product during exercise, however, does not increase, suggesting that the drug does not importantly improve myocardial oxygen supply. Nifedipine may also be of value in the therapy of unstable angina, acute myocardial infarction, and hypertension, as well as in the protection of the myocardium at risk during open heart surgery. However, definite recommendations on the use of the drug for these indications must await results of ongoing randomized studies. The effects of nifedipine are dose-related. Larger doses have been shown more effective than smaller doses, as long as an appropriate blood pressure is maintained. The side effects of nifedipine are mild and related to its vasodilating action.

Angina Pectoris↗

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The role of propranolol in the treatment of acute myocardial infarction.

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Acute Disease↗

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TNK-tissue plasminogen activator compared with front-loaded alteplase in acute myocardial infarction: results of the TIMI 10B trial. Thrombolysis in Myocardial Infarction (TIMI) 10B Investigators.

BACKGROUND: Bolus thrombolytic therapy is a simplified means of administering thrombolysis that facilitates rapid time to treatment. TNK-tissue plasminogen activator (TNK-tPA) is a highly fibrin-specific single-bolus thrombolytic agent. METHODS AND RESULTS: In TIMI 10B, 886 patients with acute ST-elevation myocardial infarction presenting within 12 hours were randomized to receive either a single bolus of 30 or 50 mg TNK-tPA or front-loaded tPA and underwent immediate coronary angiography. The 50-mg dose was discontinued early because of increased intracranial hemorrhage and was replaced by a 40-mg dose, and heparin doses were decreased. TNK-tPA 40 mg and tPA produced similar rates of TIMI grade 3 flow at 90 minutes (62.8% versus 62.7%, respectively, P=NS); the rate for the 30-mg dose was significantly lower (54.3%, P=0.035) and was 65. 8% for the 50-mg dose (P=NS). A prespecified analysis of weight-based TNK-tPA dosing using median TIMI frame count demonstrated a dose response (P=0.001). Similar dose responses were observed for serious bleeding and intracranial hemorrhage, but significantly lower rates were observed for both TNK-tPA and tPA after the heparin doses were lowered and titration of the heparin was started at 6 hours. CONCLUSIONS: TNK-tPA, given as a single 40-mg bolus, achieved rates of TIMI grade 3 flow similar to those of the 90-minute bolus and infusion of tPA. Weight-adjusting TNK-tPA appears to be important in achieving optimal reperfusion; reduced heparin dosing appears to improve safety for both agents. Together with the safety results from the parallel Assessment of the Safety of a New Thrombolytic: TNK-tPA (ASSENT I) trial, an appropriate dose of this single-bolus thrombolytic agent has been identified for phase III testing.

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