The effects of intracoronary
nifedipine on coronary bloodflow, its regional distribution, myocardial oxygen consumption and
lactate metabolism during pacing-induced angina were evaluated in 15 subjects. These responses were directly compared to 10 subjects who received an alcohol-based control
solvent. Myocardial bloodflow was measured by thermodilution, with changes in regional coronary flow assessed using a dual radiolabelled (technetium-99m and indium-111) intracoronary
microsphere technique and single photon emission tomography. Neither intracoronary
nifedipine (100 micrograms) or the control
solvent produced changes in systemic arterial pressure (
nifedipine -2 mmHg and control +2 mmHg, both not significant). Intracoronary
nifedipine markedly increased left ventricular end diastolic pressure (pre-
nifedipine 13.0 mmHg versus post
nifedipine 20.1, P less than 0.05), while increasing total coronary sinus bloodflow (pre-
nifedipine 134 mL/min versus post
nifedipine 189, P less than 0.05): Regional coronary bloodflow increased in all myocardial segments, regardless of the severity of
coronary stenosis (64 to 132% baseline, all P less than 0.05). In addition, intracoronary
nifedipine increased myocardial oxygen consumption (pre-
nifedipine 12.3 mL/min versus post
nifedipine 15.7, P less than 0.05), with a trend towards improved
lactate extraction (pre-
nifedipine 0.24 mg/mL versus post
nifedipine 0.12, not significant). Although decreased ventricular afterload (left ventricular systolic wall stress) may contribute to
nifedipine's antianginal properties, a primary increase in regional coronary bloodflow also appears to be an important factor in the alleviation of
myocardial ischemia.