Angina pectoris during cardiac catheterization was associated with impaired augmentation in systolic ejection rate, subnormal increases in cardiac output, and myocardial excess lactate production.
Observational (n=16)
What are the hemodynamic and metabolic changes during an anginal attack in patients undergoing cardiac catheterization?
Angina pectoris is associated with impaired left ventricular systolic ejection rate, subnormal cardiac output increases, and myocardial lactate production, reflecting inadequate myocardial oxygen supply.
Sixteen patients developed angina pectoris during cardiac catheterization. During an anginal attack, left ventricular end-diastolic pressure did not uniformly rise. When it did occur, it seemed to be more closely related to acute left ventricular hypertension. During a stress-induced anginal attack, the rise, if any, in systolic ejection rate of the left ventricle, was markedly decreased below that achieved in normal subjects or in subjects with coronary artery disease without angina. The impaired augmentation in systolic ejection rate was associated with subnormal increases in cardiac output as well as in stroke volume during the anginal state. Average heart rate and systolic ejection period were no different from the nonanginal patients. Myocardial excess lactate was found in the vast majority of cases during an anginal episode, and actual myocardial lactate production was seen in one half of the patients during angina. The abnormalities in left ventricular function may be related to abnormalities in oxygen supply to the myocardium.
Cohen et al. (Mon,) conducted a observational in Angina pectoris (n=16). Angina pectoris vs. Normal subjects or subjects with coronary artery disease without angina was evaluated on Hemodynamic and metabolic changes (systolic ejection rate, cardiac output, stroke volume, myocardial lactate). Angina pectoris during cardiac catheterization was associated with impaired augmentation in systolic ejection rate, subnormal increases in cardiac output, and myocardial excess lactate production.
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