Valve replacement, a possible factor in myocardial deterioration
Acar, J.; Brunet, F.; Slama, M.; Luxereau, P.; Vahanian, A.; Enriquez-Sarano, M.
Archives des Maladies du Coeur et des Vaisseaux 77(10): 1120-1125
1984
ISSN/ISBN: 0003-9683 PMID: 6439148 Document Number: 225359
Cardiopulmonary bypass (CPB) may be a cause of myocardial damage in a small number of patients undergoing valve replacement (4 out of 1576 valve replacements). The responsibility of CPB can only be presumed when: the degree of myocardial dysfunction after surgery can be quantified; other causes of myocardial dysfunction are excluded; the type of valvular disease is taken into consideration. Variations in load after correction of certain lesions (mitral regurgitation) makes changes of LV systolic function difficult to interpret. The 1st case concerned a 23 yr old patient operated for aortic regurgitation (Bjork prosthesis) under local and general hypothermia and followed-up for 1 yr after surgery. Ventricular extrasystoles and left bundle branch block were observed during surgery and radiological and echocardiographic LV dilatation persisted with deterioration of echographic, isotopic, hemodynamic and angiographic parameters of LV function; ejection fraction fell from 62% before surgery to 35% with diffuse hypokinesia and persistant LV dilatation (191 vs. 188 ml). In the absence of prosthetic valve dysfunction, associated valve lesions or coronary artery disease, LV deterioration was attributed to CPB and inadequate myocardial protection. In 2 other cases (60 and 62 yr) correction of aortic stenosis (Starr 1260) with coronary perfusion was followed by cardiac failure with left bundle branch block, deterioration of LV function, and death after 3 yr in 1 case and precarious survival at 10 yr in the other. In a 4th case (mixed mitral valve disease corrected by a Starr prosthesis under aortic clamping), the variation of cardiac load before and after surgery made changes in LV function difficult to interpret. The conditions during surgery (normothermia with intermittent clamping of the aorta and induced ventricular fibrillation) and the autopsy findings (death after 30 mo; myocardial infarct without coronary atheroma and diffuse myocardial fibrosis) suggest that myocardial anoxia was the probable cause. Improved myocardial protection would prevent these iatrogenic complications. The fact that none of these patients benefited from modern methods of cardioplegia associated with hypothermia is discussed.