Contractility and Ventricular Systolic Stiffening in Hypertensive Heart DiseaseInsights Into the Pathogenesis of Heart Failure With Preserved Ejection Fraction
Barry A. Borlaug, MD,
Carolyn S.P. Lam, MBBS,
Véronique L. Roger, MD, MPH,
Richard J. Rodeheffer, MD and
Margaret M. Redfield, MD*
Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic Rochester, Minnesota
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Figure 1 VA Coupling and Contractility
(A) The relationship between Ees and Ea was similar among each group (dashed lines show 95% prediction bands). (B to D) Load-independent chamber contractility (PRSW and sc-eFS) and myocardial contractility (sc-mFS) were increased in hypertensive patients without HF and decreased in patients with HFpEF compared with hypertensive and control patients. Data are mean ± SD. *p < 0.05 versus control;  p < 0.05 versus hypertension. Ea = effective arterial elastance; Ees = end-systolic elastance; eFS = endocardial fractional shortening; HFpEF = heart failure with preserved ejection fraction; mFS = midwall fractional shortening; PRSW = pre-load recruitable stroke work; sc = stress-corrected; VA = ventricular-arterial.
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Figure 2 Myocardial Contractility
(A) The relationship between midwall myofiber shortening (mFS) and end-systolic wall stress (log cESS) showing mean regression (solid line) and 95% confidence limits (dotted line) in control patients (CON; black line) with data points and regression line for hypertensive patients (HTN; blue line) shifted upward, indicating enhanced myocardial contractility in hypertension. (B to C) In patients with HFpEF (red lines), the data points and regression line are shifted down as compared with both control (black line) and hypertensive (blue line) patients, indicating depressed contractility. (D) Cumulative distribution plot for sc-mFS show that compared with healthy control patients (CON; black line), myocardial contractility is depressed in HFpEF (red line) and enhanced in hypertensive patients without HF (HTN; blue line). Abbreviations as in Figure 1.
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Figure 3 Geometry and Its Effect on End-Systolic Elastance and Contractility Indexes
(A) The distributions of LV geometry differed among control, hypertensive, and HFpEF patients. Even within the healthy control group, Ees varied according to geometry pattern (B), as did PRSW, sc-eFS, and sc-mFS (C). See text for discussion. Data are mean ± standard error. LV = left ventricular; other abbreviations as in Figures 1 and 2.
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Figure 4 VA Coupling and Contractility According to Group and Geometry
(A) Ees was elevated in HFpEF (red) and hypertensive patients (blue) compared with control patients (black) for each pattern of geometry. In contrast, PRSW (B), sc-eFS (C), and sc-mFS (D) were each consistently depressed in HFpEF and increased in hypertensive patients compared with control patients. See text for discussion. Data are mean ± standard error. *Geometry p < 0.0001; group p < 0.0001. CH = concentric hypertrophy; CR = concentric remodeling; EH = eccentric hypertrophy; other abbreviations as in Figure 1.
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Figure 5 Kaplan-Meier Plot of Survival in Patients With HFpEF
Stress-corrected midwall myofiber shortening (sc-mFS) below the median value is associated with reduced survival in patients with HFpEF. Abbreviations as in Figure 1.
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