[2-(2-dimethylaminoethyl)-5-(4-methoxyphenyl)-3-oxo-6-thia-2- azabicyclo[5.4.0]undeca-7,9,11-trien-4-yl]ethanoate

Diltiazem HCl抑制鈣離子流入房室結及末梢血管、冠狀動脈等血管平滑肌細胞，而具擴張血管及延長房室結傳導時間的作用，因對高血壓、不整脈、狹心症有效果。

Absorption
IV
T max is 2 to 3 h.

Extended release (ER)
T max is 10 to 14 h.

Immediate release (IR)
T max is 2 to 4 h.

Distribution
Vd approximately 305 L. 70% to 80% protein bound (approximately 40% to α l -acid glycoprotein and approximately 30% to albumin). Excreted in breast milk.

Metabolism
Metabolized in the liver (including via CYP-450) to several metabolites; desacetyl diltiazem is 25% to 50% as potent as diltiazem. Undergoes first-pass metabolism after oral administration.

Elimination
The t ½ is approximately 3.4 h (IV), 4 to 9 h (ER), and 3 to 4.5 h (IR). 2% to 4% excreted unchanged in urine (oral). Systemic Cl approximately 65 L/h (IV).

Peak
2 to 5 min (IV).

Special Populations
Hepatic Function Impairment
Bioavailability is increased, and t ½ is prolonged.

Anesthetics
Depression of cardiac contractility, conductivity, and automaticity as well as vascular dilation associated with anesthetics may be potentiated.

Benzodiazepines (eg, midazolam, triazolam), carbamazepine, cyclosporine, digitalis, encainide, lovastatin
Plasma levels of these agents may be elevated by diltiazem, increasing the pharmacologic and toxic effects.

Beta-blockers
May have additive negative inotropic and chronotropic effects.

Cimetidine, ranitidine
Diltiazem levels may be increased.

Other antihypertensive agents
May have additive effects.

Rifampin
Coadministration lowered diltiazem plasma concentrations to undetectable levels.