Haemodynamic effects of encainide, flecainide, lorcainide and tocainide

The haemodynamic effects of encainide, flecainide, lorcainide and tocainide in man are reviewed. Most of the investigations discussed are acute intervention studies after intravenous administration of the drugs. With all four drugs, haemodynamic changes, when present, were moderate. In most studies a decrease in left ventricular maximal dp/dt is demonstrated, suggesting a negative inotropic action. Left ventricular filling pressures are unchanged or slightly increased. A small decrease in cardiac performance, as determined by measurements of cardiac output and left ventricular ejection fraction, is usually observed, while systemic vascular resistance is increased or remains unchanged. Haemodynamic deterioration and/or hypotensive reactions after intravenous administration of any of the above drugs are uncommon in patients

Acute coronary hemodynamic effects of equihypotensive doses of nisoldipine and diltiazem

The hemodynamic effects of nisoldipine and diltiazem were investigated in two groups of patients undergoing investigation for suspected coronary artery disease. Emphasis was placed on the coronary hemodynamic changes. Approximately equihypotensive doses of these two calcium channel blockers, nisoldipine (6 micrograms/kg) and diltiazem (500 micrograms/kg) were given intravenously. Although both drugs decreased peak systolic pressure by 28% and 24%, respectively, heart rate increased with nisoldipine (68 +/- 9 to 82 +/- 12 bpm) and remained unchanged with diltiazem (70 +/- 9 to 67 +/- 10 bpm). Nisoldipine increased mean coronary sinus blood flow from 146 +/- 40 to 176 +/- 35 ml/min and great cardiac vein flow from 87 +/- 20 to 109 +/- 24 ml/min, producing a significant reduction in the calculated global (from 0.79 +/- 0.2 to 0.43 +/- 0.12 mmHg min/ml) and regional (from 1.43 +/- 0.2 to 0.70 +/- 0.13 mmHg min/ml) coronary vascular resistances. There were no significant flow changes when corrected for heart rate. Global and regional myocardial oxygen consumptions were not significantly altered. Diltiazem had no significant effects on heart rate or global and regional blood flows, although the vascular resistances decreased by 32% and 35%, respectively. Diltiazem reduced global and regional arterio-coronary sinus oxygen differences, resulting in significant decreases in global (from 14.9 +/- 4.7 to 12.1 +/- 2.3 ml/min) and regional (from 5.6 +/- 0.9 to 5.2 +/- 1.2 ml/min) myocardial oxygen consumptions. The major difference between the drugs was in heart rate, despite the similar reductions in aortic pressure. The lack of a positive chronotropic response after diltiazem may explain the reduction in myocardial oxygen consumption

Effect of long-term oral nifedipine therapy on left ventricular regional wall function at rest and during supine bicycle exercise

15 patients, 1 to 3 year after coronary bypass surgery, underwent symptom limited supine bicycle exercise tests without nifedipine and after acute and chronic (3 months) administration of the drug. Haemodynamic variables were monitored as was epicardial marker motion, using biplane cineradiography during exercise, the markers having been implanted at the time of surgery. We found significant (P less than 0.001) reductions in end-diastolic and end-systolic regional dimensions at maximal exercise after oral nifedipine, associated with a significant reduction in exertional angina, which persisted during long-term treatment. No adverse effects of the drug were observed

Effects of short-term intravenous administration of diltiazem on left ventricular function and coronary hemodynamics in patients with coronary artery disease

The hemodynamic effects of diltiazem were investigated in 15 patients with suspected coronary artery disease undergoing routine cardiac catheterization. Diltiazem was given in a high dose of 500 micrograms/kg over a period of 5 min and measurements made before and after drug administration during spontaneous heart rate and during matched atrial pacing. Spontaneous heart rate did not change (-5%; NS). Left ventricular (LV) systolic pressure decreased 24% (p less than 10(-6)) and LV end-diastolic pressure (LVEDP) did not change (-5%; NS). During coronary blood flow measurement, mean aortic pressure decreased 30% (p less than 10(-6)) as global (coronary sinus) and regional (great cardiac vein) coronary vascular resistance diminished with no change in coronary blood flow. Myocardial oxygen consumption decreased 19% (p less than 0.02). During matched pacing, although no change occurred in calculated systolic isovolumic indexes of contractility, end-systolic pressure-volume index decreased 15% (p less than 0.05). The time constant of isovolumic relaxation assessed by a biexponential model decreased. No net change occurred in either global or regional wall motion. In summary, high-dose diltiazem was administered safely to patients with coronary artery disease. It is concluded that, at this dose, diltiazem acted as a peripheral and coronary vasodilator. Hemodynamic changes consistent with a direct negative inotropic and chronotropic effect of the drug were observed. Myocardial oxygen consumption decreased with no change in coronary blood flow