Key result
Exercise testing in elderly female hypertensives demonstrated that poor stroke volume reserve (<15%, n=10) is caused by simultaneous failure of LV preload and arterial vasodilatory reserves.
Why the study?
Does arterial function determine the stroke volume response to exercise in elderly female hypertensive patients?
Observational (n=21)
Does arterial function determine the stroke volume response to exercise in elderly female hypertensive patients?
Poor stroke volume reserve during exercise in elderly female hypertensives is driven by simultaneous failure of LV preload and arterial vasodilatory reserves, contributing to HFpEF risk.
May implicate dual preload and arterial reserve failure in exercise intolerance among elderly hypertensive women; hypothesis-generating for HFpEF mechanisms.
Elderly female hypertensives with arterial stiffening constitute a majority of patients with heart failure with preserved ejection fraction (HFpEF), a condition characterized by inability to increase cardiac stroke volume (SV) with physical exercise. As SV is determined by the interaction between the left ventricle (LV) and its load, we wished to study the role of arterial hemodynamics for exertional SV reserve in patients at high risk of HFpEF. Twenty-one elderly (67 ± 9 yr) female hypertensive patients were studied at rest and during supine bicycle stress using echocardiography including pulsed-wave Doppler to record flow in the LV outflow tract and arterial tonometry for central arterial pressure waveforms. Arterial compliance was estimated based on an exponential relationship between pressure and volume. The ratio of aortic pressure-to-flow in early systole was used to derive characteristic impedance, which was subsequently subtracted from total resistance (mean arterial pressure/cardiac output) to yield systemic vascular resistance (SVR). It was found that patients with depressed SV reserve (NoRes; reserve <15%; n = 10) showed decreased arterial compliance during exercise, while patients with SV reserve ≥15% (Res; n = 11) showed increased compliance. Exercise produced parallel increases in LV end-diastolic volume and arterial volume in Res patients while NoRes patients exhibited a lesser decrease in SVR and a drop in effective arterial volume. Poor SV reserve in elderly female hypertensives is due to simultaneous failure of LV preload and arterial vasodilatory reserves. Abnormal arterial function contributes to a high risk of HFpEF in these patients.
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Sahlén et al. (2011) conducted an observational in Hypertension (n=21). Supine bicycle stress vs. Rest was evaluated on Stroke volume reserve and arterial compliance. Exercise testing in elderly female hypertensives demonstrated that poor stroke volume reserve (<15%, n=10) is caused by simultaneous failure of LV preload and arterial vasodilatory reserves.
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