Abstract 2908: Heart-rate Dependent Regulation Of Intrinsic Contractility And Hemodynamics In Patients With Diastolic Heart Failure
Background: In systolic heart failure, the positive force-frequency relatinship is blunted, and this contributes to exertional dyspnea in these patients. However, there is little information on heart-rate dependent regulation of contractility and hemodynamics in patients with diastolic heart failure (i.e., heart failure with normal ejection fraction, HFNEF). We tested intrinsic contractility and hemodynamic consequences of increasing heart rates in patients with HFNEF.
Methods: 11 patients (9 female; age 66 ± 3 years, no coronary artery disease) fulfilling recent criteria for HFNEF as proposed by the Working Group on Heart Failure of the ESC were invasively evaluated. Pressure-volume-loops were obtained by conductance catheter technique (CD Leycom, Leiden, Netherlands) at baseline and during atrial pacing to 80, 100, and 120 beats/min (bpm). At each heart rate, preload reduction was performed by transient vena cava inferior occlusion.
Results (see Table⇓): At an average baseline heart rate of 64±3 bpm, stroke volume, cardiac output and measures of intrinsic contractility (maximum rate of systolic left ventricular pressure rise (dp/dt); endsystolic elastance (Ees) as a relatively preload-independent measure of left ventricular contractility) were normal, but left ventricular end-diastolic pressure (LVEDP) was increased. With increasing heart rates, contactility parameters continuously increased suggesting a preserved force-frequency relationship. In contrast, stroke volume declined at higher heart rates, probably related to impaired diastolic filling. In consequence, cardiac output was maximum at 100 bpm and even declined with further increases in heart rate.
Conclusion: Patients with HFNEF show a preserved force-frequency relation, but a pronounced reduction in stroke volume at higher pacing rates. These unique hemodynamic properties in diastolic heart failure are distinctive from systolic heart failure.