Attenuation of coronary vascular resistance by selective alpha1,-adrenergic blockade in patients with coronary artery disease

Alpha-adrenergic-mediated coronary vasoconstriction during stress such as cold pressor testing may contribute to myocardial ischemia by increasing coronary vascular resistance in patients with severe coronary artery disease. Nonselective alpha-receptor blockade with phen-tolamine abolishes both the peripheral and coronary vasoconstriction during cold pressor testing, but causes reflex tachycardia and increased inotropy. To determine the role of selective alpha1-receptor blockade, the changes in coronary vascular resistance during cold pressor testing were measured in 18 patients with coronary artery disease before and after intravenous administration of 100 mg of trimazosin. Cold pressor testing was performed at a constant paced subanginal heart rate of 95 ± 5 beats/min (± 1SD). Before trimazosin, cold pressor testing increased mean arterial pressure by 9 ± 4% (102 ± 14 to 111 ± 14 mm Hg, p < 0.001) with no change in coronary sinus blood flow, but significantly increased coronary vascular resistance by 15 ± 19% (1.02 ± 0.46 to 1.15 ± 0.57 units, p < 0.05). Five minutes after trimazosin, cold pressor testing increased mean arterial pressure by 6 ± 5% (p < 0.001) with a marked attenuation of the increase in coronary vascular resistance (6 ± 11%, p = NS), which was significantly less than before trimazosin (p < 0.02). Trimazosin did not increase plasma norepinephrine concentration at rest, suggesting that in the dosage used trimazosin caused selective alpha1-receptor blockade.These data suggest that although the hypertensive response to cold pressor testing is somewhat blunted by selective alpha1,-adrenoceptor blockade, the reflex coronary vasoconstriction during adrenergic stimulation in some patients with coronary artery disease can be significantly attenuated. Use of agents that block alpha2-adrenoceptors has been clinically unsatisfactory because of the adverse myocardial effects of increased norepinephrine release. Selective alpha1-receptor blockade may have an additional advantage over nonselective alpha-adrenergic blockade in that the release of norepinephrine is also attenuated, thus potentially producing less augmentation of heart rate and myocardial oxygen demand

ACC/AHA/ASNC Guidelines for the Clinical Use of Cardiac Radionuclide Imaging—Executive Summary: A Report of the American College of Cardiology/American HeartAssociation Task Force on Practice Guidelines (ACC/AHA/ASNC Committee to Revise the 1995 Guidelines for the Clinical Use of Cardiac Radionuclide Imaging)

The American College of Cardiology (ACC)/American Heart Association (AHA) Task Force on Practice Guidelines regularly reviews existing guidelines to determine when an update or full revision is needed. Guidelines for the Clinical Use of Cardiac Radionuclide Imaging were originally published in 1986 and updated in 1995. Important new developments have continued to occur since 1995, particularly in the areas of acute and chronic ischemic syndromes and heart failure. The Task Force therefore believed the topic should be revisited de novo and invited the American Society for Nuclear Cardiology (ASNC) to cosponsor the undertaking, which represents a joint effort of the 3 organizations

Comparison of the effects of nitroprusside and nifedipine on diastolic properties in patients with hypertrophic cardiomyopathy: Altered left ventricular loading or improved muscle inactivation?

The calcium channel blocking agent, nifedipine, has been shown to improve indexes of left ventricular relaxation, diastolic filling and compliance in patients with hypertrophic cardiomyopathy. The mechanism of action of nifedipine on diastolic properties in patients with hypertrophic cardiomyopathy is unclear and could result from an improvement in myocardial inactivation or from systemic vasodilation and left ventricular unloading. To distinguish between these mechanisms, the effects of nifedipine and the vasodilator nitroprusside on left ventricular diastolic properties were compared in 10 patients with nonobstructive hypertrophic cardiomyopathy using simultaneous micromanometer left ventricular pressure and echocardiographic measurements.Left ventricular peak systolic pressure was comparable during nitroprusside infusion (132 ± 38 mm Hg) and after nifedipine (132 ± 32 mm Hg). During nitroprusside infusion, the decrease in left ventricular enddiastolic pressure (22 ± 11 to 17 ± 11 mm Hg, p < 0.05) was associated with a decrease in left ventricular end-diastolic dimension. In contrast, the decrease in left ventricular end-diastolic pressure after nifedipine (22 ± 11 to 18 ± 10 mm Hg, p < 0.05) was associated with no reduction of left ventricular eand-diastolic dimensions, suggesting an increase in left ventricular distensibility. Compared with nitroprusside, nifedipine was associated with less prolongation of the left ventricular isovolumic relaxation time and less depression of the peak left ventricular posterior wall thinning rate and peak left ventricular internal dimension filling rate.These data suggest that the effects of the calcium channel blocker, nifedipine, on diastolic mechanics in hypertrophic cardiomyopathy result not only from systemic vasodilation but also from improved cardiac muscle inactivation