OBJECTIVES: We sought to compare left ventricular (LV) systolic stiffness and contractility in normal subjects, hypertensive patients without heart failure, and patients with heart failure and preserved ejection fraction (HFpEF) and to determine whether LV systolic stiffness or myocardial contractility is associated with the rate of mortality in patients with HFpEF. BACKGROUND: Arterial load is increased in patients with hypertension and is matched by increased end-systolic LV stiffness (ventricular-arterial coupling). Increased end-systolic LV stiffness may be mediated by enhanced myocardial contractility or processes that increase passive myocardial stiffness. METHODS: Healthy control patients (n = 617), hypertensive patients (no heart failure, n = 719), and patients with HFpEF (n = 244, 96% hypertensive) underwent echo-Doppler characterization of arterial (Ea) and LV end-systolic (Ees) stiffness (elastance), ventricular-arterial coupling (Ea/Ees ratio), and chamber-level and myocardial contractility (stress-corrected midwall shortening). RESULTS: We found that Ea and Ees were similarly increased in hypertensive patients with or without HFpEF compared with control patients, but ventricular-arterial coupling was similar across groups. In hypertensive patients, increased Ees was associated with enhanced chamber-level and myocardial contractility, whereas in patients with HFpEF, chamber and myocardial contractility were depressed compared with both hypertensive and control patients. Group differences persisted after adjusting for geometry. In patients with HFpEF, impaired myocardial contractility (but not Ees) was associated with increased age-adjusted mortality. CONCLUSIONS: Although arterial load is increased and matched by increased LV systolic stiffness in hypertensive patients with or without HFpEF, the mechanisms of systolic LV stiffening differ substantially. These data suggest that myocardial contractility increases to match arterial load in asymptomatic hypertensive heart disease, but that progression to HFpEF may be mediated by processes that simultaneously impair myocardial contractility and increase passive myocardial stiffness.
OBJECTIVES: We sought to compare left ventricular (LV) systolic stiffness and contractility in normal subjects, hypertensivepatients without heart failure, and patients with heart failure and preserved ejection fraction (HFpEF) and to determine whether LV systolic stiffness or myocardial contractility is associated with the rate of mortality in patients with HFpEF. BACKGROUND: Arterial load is increased in patients with hypertension and is matched by increased end-systolic LV stiffness (ventricular-arterial coupling). Increased end-systolic LV stiffness may be mediated by enhanced myocardial contractility or processes that increase passive myocardial stiffness. METHODS: Healthy control patients (n = 617), hypertensivepatients (no heart failure, n = 719), and patients with HFpEF (n = 244, 96% hypertensive) underwent echo-Doppler characterization of arterial (Ea) and LV end-systolic (Ees) stiffness (elastance), ventricular-arterial coupling (Ea/Ees ratio), and chamber-level and myocardial contractility (stress-corrected midwall shortening). RESULTS: We found that Ea and Ees were similarly increased in hypertensivepatients with or without HFpEF compared with control patients, but ventricular-arterial coupling was similar across groups. In hypertensivepatients, increased Ees was associated with enhanced chamber-level and myocardial contractility, whereas in patients with HFpEF, chamber and myocardial contractility were depressed compared with both hypertensive and control patients. Group differences persisted after adjusting for geometry. In patients with HFpEF, impaired myocardial contractility (but not Ees) was associated with increased age-adjusted mortality. CONCLUSIONS: Although arterial load is increased and matched by increased LV systolic stiffness in hypertensivepatients with or without HFpEF, the mechanisms of systolic LV stiffening differ substantially. These data suggest that myocardial contractility increases to match arterial load in asymptomatic hypertensive heart disease, but that progression to HFpEF may be mediated by processes that simultaneously impair myocardial contractility and increase passive myocardial stiffness.
Authors: Marc Klapholz; Matthew Maurer; April M Lowe; Frank Messineo; Jay S Meisner; Judith Mitchell; Jill Kalman; Robert A Phillips; Richard Steingart; Edward J Brown; Robert Berkowitz; Robert Moskowitz; Anita Soni; Donna Mancini; Rachel Bijou; Khashayar Sehhat; Nikita Varshneya; Marrick Kukin; Stuart D Katz; Lynn A Sleeper; Thierry H Le Jemtel Journal: J Am Coll Cardiol Date: 2004-04-21 Impact factor: 24.094
Authors: Margaret M Redfield; Steven J Jacobsen; John C Burnett; Douglas W Mahoney; Kent R Bailey; Richard J Rodeheffer Journal: JAMA Date: 2003-01-08 Impact factor: 56.272
Authors: Leroy L Cooper; Katja E Odening; Min-Sig Hwang; Leonard Chaves; Lorraine Schofield; Chantel A Taylor; Anthony S Gemignani; Gary F Mitchell; John R Forder; Bum-Rak Choi; Gideon Koren Journal: Am J Physiol Heart Circ Physiol Date: 2012-02-03 Impact factor: 4.733
Authors: Barry A Borlaug; Horng Chen; Grace Lin; Margaret M Redfield; Gregory D Lewis; Marc J Semigran; Steven E McNulty; Martin LeWinter; Anita Deswal; Kenneth B Margulies Journal: Circ Heart Fail Date: 2015-07 Impact factor: 8.790
Authors: Giovanni Cioffi; Giorgio Faganello; Stefania De Feo; Nicola Berlinghieri; Luigi Tarantini; Andrea Di Lenarda; Bruno Pinamonti; Riccardo Candido; Pompilio Faggiano Journal: Exp Clin Cardiol Date: 2013