Abstract

Hypertension (HT) may lead to LV systolic impairment through chronic pressure overload. LV hypertrophy and systolic dysfunction occur late. An impaired contractile reserve (CR) may be an early manifestation of LV dysfunction in hypertensive patients. We examined CR and its correlates in hypertensive patients and compared that with normotensive controls. Methods: 129 prospectively recruited patients (68 men, aged 58.6 ± 9.5 years) underwent dobutamine echocardiography. Patients with diabetes, coronary disease, or significant valvular disease were excluded. 72 patients (56%) had treated HT. LV global longitudinal strain (GLS) was measured at rest and at low dose dobutamine. Absolute CR was calculated as the difference in GLS between low dose and resting values. Relative CR is the ratio of absolute CR to resting GLS. Results: There was no difference in LV ejection fraction between hypertensive patients and controls (64.5 ± 6.1% vs 64.5 ± 6.6% at rest, 72.1 ± 6.6% vs 71.2 ± 6.9% at low dose dobutamine; both p = NS). LVGLS in hypertensive patients was significantly impaired at rest (-16.8 ± 2.2% vs -19.5 ± 1.5%; both p < 0.001) and at low dose dobutamine (-17.9 ± 2.7% vs -22.7 ± 2.6%; both p < 0.001). More importantly, both the absolute and relative CR were significantly lower in hypertensive patients (-1.12% vs -3.17%; 7.24% vs 16.4% respectively, both p < 0.001). CR was not correlated with LV mass, prevailing blood pressure, septal e’ velocities, E/e’ ratio. Conclusions: Compared with controls, hypertensive patients not only had impaired LV GLS at rest, but also an impaired ability to augment contractility with inotropic stimulation, i.e. CR. This impaired CR is independent of LV mass, diastolic function or filling pressures.

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