Smoking, catecholamines, and the ischemic myocardium.
Catecholamine stimulation increases the heart rate and the force of cardiac contraction. Cardiac output then increases, with a decrease occurring in total peripheral resistance due to smooth muscle dilation in the vascular beds of the muscle and heart, though there is constriction of the skin and viscera; this leads to a net decrease in total peripheral resistance. Consequently, systolic pressure rises and diastolic pressure falls. The net effect is to increase myocardial oxygen demand. Smoking stimulates catecholamine secretion and may therefore be expected to have detrimental effects in patients with angina. In a double-blind study of ten patients with stable angina pectoris treated with nifedipine, propranolol, and atenolol, smoking was found to have direct and adverse effects on the heart and to interfere with the efficacy of all three antianginal drugs, but with that of nifedipine the most. Differences between the two beta blockers may be related, at least in part, to the known different metabolic pathways of these drugs.
Fox
K M
KM
National Heart Hospital, London.
D000787:Angina Pectoris / Q000188:drug therapy; D001262:Atenolol / Q000493:pharmacokinetics; D002395:Catecholamines / Q000097:blood / Q000378:metabolism*; D003327:Coronary Disease / Q000503:physiopathology*; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D008297:Male; D009543:Nifedipine / Q000493:pharmacokinetics; D011433:Propranolol / Q000493:pharmacokinetics; D012907:Smoking / Q000009:adverse effects* / Q000503:physiopathology
D002395:Catecholamines; D001262:Atenolol; D011433:Propranolol; D009543:Nifedipine