Open AccessComparison of myocardial flow, hemodynamic changes, and lactate metabolism during isoproterenol stress in patients with coronary heart disease and severe aortic stenosis
Author(s) -
Thormann J.,
Schlepper M.
Publication year - 1979
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960020609
Subject(s) - medicine , cardiology , ejection fraction , ventricle , coronary sinus , coronary artery disease , hemodynamics , valvular heart disease , stenosis , coronary circulation , ischemia , cardiac index , ventricular pressure , blood flow , cardiac output , heart failure
The evidence of subendocardial ischemia was studied during isoproterenol stress in seven patients with aortic valve disease before (group A) and approximately 6 months after Björk‐Shiley valvular replacement (group B), in seven patients with coronary artery disease (group C), and in seven patients without heart disease (group D). Ejection fraction, thermodilution coronary sinus flow, and lactate metabolism were determined at rest and during isoproterenol stress. Potential subendocardial blood supply was estimated from a diastolic pressure‐time index (DPTI), calculated from aortic and left ventricular pressure curves, and oxygen demand, estimated from the tension‐time index (TTI). The ratio of DPTI/TTI was used to estimate the supply‐demand relationship. Impaired left ventricular myocardial function was apparent by a lack of increase of the ejection fraction during stress in groups A and C as compared to controls. After aortic valvular replacement (group B) during stress, an adequate increase of the ejection fraction, a normal stress response of the O 2 supply‐demand ratio, and a lactate extraction rather than production (all p>0.05) were found. During isoproterenol infusion (at equal heart rates and normal coronary sinus flow) a significant lactate production and decreased O 2 supply‐demand ratio in group A and C patients were induced, but not in group B and D patients. The more massive lactate production in group A as opposed to group C reflected subendocardial ischemia of the hypertrophic left ventricle as compared to the more regional and nonuniform distribution of ischemic areas in coronary artery disease. The results of this study suggest that ischemia and cardiac failure can be induced by isoproterenol stress in coronary artery disease as well as in hypertrophic myocardium caused by aortic stenosis. Aortic valvular replacement repaired the ischemic response found in aortic valve disease 6 months prior to surgery. Stress‐induced lactate production rather than coronary sinus flow changes allow discrimination between ischemic and nonischemic myocardium. A critical DPTI/TTI ratio (≤0.4) indicates ischemia in hypertrophic myocardium caused by aortic valve disease, but this concept does not apply to ischemia caused by coronary artery disease.