• Steven J Lavine and Jeremy A Lavine.
• University of Florida--Jacksonville, Jacksonville, Florida 32209, USA. steven.lvine@jax.ufl.edu <steven.lvine@jax.ufl.edu>
• J Am Soc Echocardiogr. 2006 Nov 1; 19 (11): 1350-8.

BackgroundDecompensated heart failure with preserved left ventricular (LV) ejection fraction (EF) is often accompanied by hypertensive episodes. We hypothesized that acute increase in arterial pressure results in elevated early and late diastolic LV pressures as a result of further impaired LV relaxation.MethodsTo test this hypothesis, we used a chronic canine model of LV systolic dysfunction with preserved LV function (LVDPEF) (EF > 50%) and elevated LV end-diastolic pressure using coronary microsphere embolization. At baseline and with LVDPEF, each dog was paced 10 beats above their baseline heart rate and high-fidelity LV pressures, echocardiographic LV volumes, and transmitral Doppler were obtained before and after methoxamine pressure loading.ResultsWith normal LV function, LV pressures at peak negative dP/dt (+18 mm Hg, P < .05) and at LV pressure minimum (+3.6 mm Hg, P < .01) increased. Both tau (P < .05) and LV end-diastolic pressure increased (5 +/- 3 vs 13 +/- 4 mm Hg, P < .01). EF was unchanged, although LV end-diastolic volume increased (P < .01). Pressure loading with LVDPEF resulted in a timing delay (P < .05) and a greater increase in LV pressures at peak negative dP/dt (+45 mm Hg) and LV minimal pressure (+7.5 mm Hg) as compared with normal LV function (P < .01). LV end-diastolic pressure increased (9 +/- 2-23 +/- 5 mm Hg, P < .001), diastolic filling period shortened (288 +/- 51-204 +/- 54 milliseconds, P < .01), and tau increased (P < .001). EF declined from 54 +/- 9% to 43 +/- 9% (P < .05) and LV size increased (P < .01).ConclusionsPressure loading with normal LV function and with LVDPEF results in increased LV diastolic pressures, which are further exaggerated with LVDPEF as a result of prolonged relaxation and shortened diastolic filling.

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