CARDIZEM inhibits the influx of calcium (Ca²⁺) ions during membrane depolarization of cardiac and vascular smooth muscle. The therapeutic benefits of CARDIZEM in supraventricular tachycardias are related to its ability to slow AV nodal conduction time and prolong AV nodal refractoriness. CARDIZEM exhibits frequency (use) dependent effects on AV nodal conduction such that it may selectively reduce the heart rate during tachycardias involving the AV node with little or no effect on normal AV nodal conduction at normal heart rates.

CARDIZEM slows the ventricular rate in patients with a rapid ventricular response during atrial fibrillation or atrial flutter. CARDIZEM converts paroxysmal supraventricular tachycardia (PSVT) to normal sinus rhythm by interrupting the reentry circuit in AV nodal reentrant tachycardias and reciprocating tachycardias, eg, Wolff-Parkinson-White syndrome (WPW).

CARDIZEM prolongs the sinus cycle length. It has no effect on the sinus node recovery time or on the sinoatrial conduction time in patients without SA nodal dysfunction. CARDIZEM has no significant electrophysiologic effects on tissues in the heart that are fast sodium channel dependent, eg, His-Purkinje tissue, atrial and ventricular muscle, and extranodal accessory pathways.

Like other calcium channel antagonists, because of its effect on vascular smooth muscle, CARDIZEM decreases total peripheral resistance resulting in a decrease in both systolic and diastolic blood pressure.

In patients with cardiovascular disease, CARDIZEM Injectable (diltiazem hydrochloride injection) administered intravenously in single bolus doses, followed in some cases by a continuous infusion, reduced blood pressure, systemic vascular resistance, the rate-pressure product, and coronary vascular resistance and increased coronary blood flow. In a limited number of studies of patients with compromised myocardium (severe congestive heart failure, acute myocardial infarction, hypertrophic cardiomyopathy), administration of intravenous diltiazem produced no significant effect on contractility, left ventricular end diastolic pressure, or pulmonary capillary wedge pressure. The mean ejection fraction and cardiac output/index remained unchanged or increased. Maximal hemodynamic effects usually occurred within 2 to 5 minutes of an injection. However, in rare instances, worsening of congestive heart failure has been reported in patients with preexisting impaired ventricular function.

The prolongation of PR interval correlated significantly with plasma diltiazem concentration in normal volunteers using the Sigmoidal E_max model. Changes in heart rate, systolic blood pressure, and diastolic blood pressure did not correlate with diltiazem plasma concentrations in normal volunteers. Reduction in mean arterial pressure correlated linearly with diltiazem plasma concentration in a group of hypertensive patients.

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