Hemodynamic and metabolic responses to pacing in patients with chest pain and normal coronary arteriograms.
Hemodynamic and metabolic responses to pacing from either the coronary sinus or right atrium were evaluated in 41 patients with chest pain and normal coronary arteriograms. A group of patients (group II) with angina, lactate production, or significant ST segment depression had a significantly higher mean pulmonary capillary pressure on peak pacing or angina than did a group of patients considered to have a normal pacing response (group I). In 6 of 9 group II patients, the left ventricular end-diastolic pressure either rose abnormally with pacing or was greater than 14 mm Hg immediately after pacing and resembled that of a group of patients with coronary artery disease; Patients with a prolapsing mitral valve (group III) also had a significantly higher pulmonary capillary pressure on peak pacing as compared to those of group I, although abnormal left ventricular pressure responses occurred in only 2 of 9 of these patients. The stroke index was significantly lower in group III on peak pacing while group II was no different from group I. Lactate production occurred in 6 of 9 group II patients. However, only 1 of 6 patients with a prolapsing mitral valve who were studied for lactate production was found to produce lactate, suggesting a different mechanism for their pain.
D000328:Adult; D000368:Aged; D000787:Angina Pectoris / Q000378:metabolism / Q000503:physiopathology*; D001794:Blood Pressure; D002302:Cardiac Output; D017023:Coronary Angiography; D004562:Electrocardiography; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005260:Female; D006321:Heart / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D007773:Lactates / Q000096:biosynthesis; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism; D010138:Pacemaker, Artificial; D011312:Pressure
D005230:Fatty Acids, Nonesterified; D007773:Lactates