Resting global and regional left ventricular contractility in patients with heart failure and normal ejection fraction: insights from speckle-tracking echocardiography. Issue 4 (30th December 2010) - Yip, Gabriel Wai-Kwok
Abstract : Obejctive: To compare left ventricular (LV) systolic performance and contractility in patients with heart failure and normal ejection fraction (HFNEF), compared with patients with heart failure and reduced ejection fraction (HFREF) and healthy subjects using newer echocardiographic techniques. Design: A case–control trial. Setting: University teaching hospital (tertiary referral centre). Patients: Sixty healthy control subjects (53±10 years), 112 patients with HFNEF (74±12 years) and 175 patients with HFREF (67±13 years). Interventions: All underwent standard two-dimensional, Doppler and speckle-tracking echocardiography. Main outcome measures: Effective arterial (Ea) and LV end-systolic elastance (Ees), stress-corrected mid-wall shortening, preload recruitable stroke work, two-dimensional strain and torsion. Comparisons were adjusted for age, gender and body size. Results: Besides diastolic dysfunction, patients with HFNEF had impaired load-independent ventricular contractility with a progressive decrease of the corrected Ees from controls (2.9±0.8 mm Hg/g) to HFNEF (2.2±0.9 mm Hg/g) followed by HFREF (0.8±0.3 mm Hg/g; all p<0.001). Ventricular-arterial coupling ratio was preserved in the HFNEF subgroup (normal 0.48±0.09 vs 0.65±0.16; p=NS) at the expense of both increased LV systolic stiffness and Ea. In addition, there was progressive decrease of global 2D circumferential, radial and longitudinal strain as well as torsion from normal, HFNEF to HFREF groups, even after adjustment for LV end-systolic wall stress or end-diastolic volume (all p<0.01). About 50% of patients with HFNEF had ≥1 global strain or torsion parameter depressed below normal after correction for LV end-systolic wall stress, with >85% falling below their corresponding stress-corrected mean. Conclusions: Impaired myocardial contractility is evident in many patients with HFNEF and this may contribute towards pathophysiology of HFNEF more than previously thought.