Calcium channel blockers in myocardial infarction.

Calcium channel blockers are currently approved for use in patients with arrhythmias, stable and unstable angina pectoris, and systemic hypertension. The hemodynamic and electrophysiologic properties of these agents suggest that their use would be appropriate in both the immediate and the long-term management of patients who suffered a myocardial infarction. Some experimental evidence accumulated from animal models supports the ability of these drugs to reduce both myocardial infarct size and the incidence of ventricular arrhythmias. The clinical trials with these drugs, however, have yielded disappointing results. Some data suggest a role of diltiazem therapy in reducing the incidence of transmural wall infarction and angina in those patients sustaining non-Q-wave myocardial infarctions. In the setting of Q-wave infarction, calcium channel blockers seem to be less effective than beta-blockade both for acute and long-term management. Finally, calcium channel blockers appear to be contraindicated in patients who have suffered a myocardial infarction and who have concomitant left ventricular dysfunction.

Beta-adrenergic blockade and calcium channel blockade in myocardial infarction.

Because of their hemodynamic and antiarrhythmic actions, beta-adrenergic blockers and calcium-entry blockers have been suggested for use in patients with myocardial infarction (MI) for reducing infarct size, preventing ventricular ectopy, and for prolonging life in survivors of acute MI. Experimental studies have suggested their usefulness in these areas. Clinical studies have demonstrated a role for beta-blockers in the hyperacute phase of MI, and in longterm treatment of infarct survivors. Calcium channel blockers appear to have somewhat less utility in patients with Q wave MIs, but may have an important role in therapy of the non-Q wave infarct.

Effects of calcium entry blockade on hypertension-induced left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) is a structural adaptation of the heart and is a response to increased hemodynamic and metabolic demands, which are most commonly caused by systemic hypertension. LVH induced by hypertension is associated with reduced myocardial compliance, structural alterations, and changes in coronary perfusion. Calcium entry blockers have caused LVH regression both in experimental studies and in clinical trials. Although their efficacy as antihypertensive agents is primarily due to their vasodilating properties, the mechanisms by which calcium entry blockers accomplish LVH regression are complex and include various hemodynamic and neurohumoral factors. Calcium entry blockade has decreased LVH with no apparent deterioration of left ventricular function. Because LVH is a major risk factor for sudden cardiac death and other cardiac morbidities, it is possible that the regression of LVH can improve the prognosis in hypertensive patients.

Elevated creatine kinase and malignancy.

Increased serum levels of CK isoenzymes variously signal heart, brain, or skeletal muscle damage. They may also be markers for advanced tumors with poor prognosis.