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Intravenous nicardipine, 5 mg, was administered in two comparable groups of eight patients with chronic coronary artery disease but no clinical signs of heart failure. One group had received no previous treatment and served as a control group, and the other had received long-term treatment with large oral doses of propranolol. Blood concentrations of nicardipine were higher, and the area under the plasma concentration curve was greater in the group previously treated by propranolol. The total clearance of nicardipine was decreased in patients taking propranolol, without a change in the half-life of the drug. Typical hemodynamic responses, namely, a decrease in aortic pressure and in arterial resistances, were greater and more lasting in patients previously treated orally by propranolol. Filling pressure remained stable in both groups. The nicardipine infusion did not induce signs of dromotropic or inotropic negative effects in either group. The greater and more lasting hemodynamic effects of nicardipine in the group previously treated orally by propranolol do not seem to be related to an overall hemodynamic action of propranolol, but are probably due to higher nicardipine plasma levels, and may be caused by a decrease in hepatic blood flow induced by propranolol, with a consequent decrease in nicardipine clearance and by a smaller nicardipine volume of distribution in the propranolol group.

Intravenous nicardipine, 5 mg, was infused over 5 minutes in 2 comparable groups of 8 patients with chronic coronary artery disease but no clinical signs of heart failure. Eight patients had received no previous treatment and served as a control group; 8 other patients had received long-term treatment with large doses of propranolol. The hemodynamic responses to nifedipine were similar in the 2 groups, but was greater in patients taking propranolol. At 10 minutes, systemic vascular resistance decreased by 47% in patients taking propranolol and by 39% in the control group; mean aortic pressures decreased by 25% and 10%; heart rate increased by 23% and 19%; and cardiac index increased by 45% in both groups. At 20 minutes, left ventricular end-systolic volume index decreased by 20% in patients taking propranolol and 15% in the control patients; angiographic stroke index increased by 19% and 8%; left ventricular ejection fraction increased by 22% and 11%; and mean circumferential fiber velocity increased by 46% and 32%. Intravenous nicardipine infusion (5 mg) did not induce negative inotropic effects in patients with chronic coronary heart disease, and no evidence of congestive heart failure was seen, even in patients receiving large doses of propranolol. Nicardipine counteracted the potential deleterious effects of propranolol; increased peripheral vascular resistance and left ventricular stroke work and decreased cardiac output.

Coronary arteriography is the only examination by which the diagnosis of single coronary artery may be made in vivo by demonstrating the presence of an entire coronary system arising from a common trunk. The discovery may be made under two distinct sets of circumstances: 1 degree Coronary ischaemia in a young subject. Arteriography confirms the diagnosis and the customary 2 degrees Coronary ischaemia in an older individual. Arteriography shows atherosclerotic lesions in a single coronary artery. The severity of the condition is related to the proximal character of the stenoses. The most logical therapeutic approach is aorto-coronary bypass if the quality of the distal network as seen at arteriography makes it possible.

In the search for any deleterious hemodynamic effects of the acute administration of intravenous diltiazem (0.25 mg/kg), in patients on beta blockers, studies were performed in two comparable groups of eight patients with chronic coronary heart disease without clinical signs of heart failure. In the first group, with no previous treatment, the only significant variations observed were a decrease in systemic vascular resistance (p less than 0.01) and an increase in cardiac index (p less than 0.01), which were noted only at 5 minutes. In the second group, receiving long-term oral doses of 120 to 240 mg/day of propranolol, at 5 minutes, despite a slight decrease in peak positive first derivative of left ventricular pressure (p less than 0.05), cardiac index and systolic index increased (p less than 0.05 and p less than 0.01) with decreases in systemic vascular resistance (p less than 0.01) and mean blood pressure (p less than 0.05); at 15 minutes, systemic vascular resistance was still decreased (p less than 0.05) and cardiac index and systolic index were still increased (p less than 0.05). In conclusion, intravenous administration of diltiazem (0.25 mg/kg) to patients with chronic coronary heart disease and no evidence of congestive heart failure, who were receiving propranolol, was safe and prevented, in these patients, the potential deleterious effects of beta blockers, that is, increased peripheral vascular resistance and decreased cardiac output.