title: Postextrasystolic potentiation of systolic gradient in valvular aortic stenosis: clinical usefulness and analysis of hemodynamic factors.
abstract: To analyze the behavior of aortic valve gradient (AVG) after ventricular extrasystole (VE), we studied 36 pure valvular aortic stenoses (AS) free of coronary artery disease and obstructive hypertrophic cardiomyopathy, in whom basal (B) (74 +/- 32 mm Hg) and catheter-induced post-VE (110 +/- 50 mm Hg) AVG were obtained. In all 26 cases with valve area less than 0.70 cm2, the post-VE AVG was greater than or equal to 70 mm Hg. In 19 cases AVG after two or more consecutive VE were also obtained. Maximal post-VE AVG was obtained after multiple VE (19 cases) and/or after one VE causing a post-VE pause equal or longer than 1.7 basal cardiac cycles (post-VE RR greater than or equal to 1.7 B RR) (9 cases). Basal and postsingle VE AVG, up to a post-VE RR greater than or equal to 1.7 B RR, were a linear function of previous RR (r greater than or equal to 0.90), regression line slope increasing with AS severity (P = .05). Inotropic state measured by PEP/LVET only increased after multiple VE, P less than .01. AVG after multiple VE was independent of post-VE RR. Thus, 1) post-VE potentiation of AVG may be seen with fixed valvular AS without obstructive cardiomyopathy; 2) post-VE AVG is a function of compensatory pause after single VE and of increased inotropism after multiple VE; 3) analysis of maximal post-VE AVG generated as described is reliable and useful for assessing AS severity (post-VE AVG greater than or equal to 70 mm Hg meaning an aortic valve area less than 0.70 cm2) and may supplement valve area calculations.
mesh_terms: D001021:Aortic Valve / Q000503:physiopathology; D001024:Aortic Valve Stenosis / Q000503:physiopathology*; D006328:Cardiac Catheterization; D005117:Cardiac Complexes, Premature / Q000503:physiopathology*; D002312:Cardiomyopathy, Hypertrophic / Q000503:physiopathology; D006352:Heart Ventricles / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D009200:Myocardial Contraction; D013599:Systole