Abstract 15248: Tachycardia-Induced Incomplete Relaxation and Left Ventricular Volume Loss in Concentric Hypertrophy
Background: Concentric LV hypertrophy (LVH) is a precursor to heart failure with normal ejection fraction. We have shown that when isolated human LV myocardium from patients with LVH is electrically stimulated at rates typical for tachycardia, incomplete relaxation (IR) develops. This is due to reduced sarcolemmal calcium extrusion reserve. IR should translate clinically into a more pronounced reduction in LV end-diastolic volume (LVEDV) during tachycardia in patients with LVH.
Methods: LV parameters including dimensions and volumetric measurements were obtained at increasing heart rates during dobutamine stress echocardiography in 48 patients, with LVH (n=26) and without LVH (n=22). None of the patients had evidence of myocardial ischemia during dobutamine stress.
Results: With an increase in heart rate of 50 bpm patients with LVH had a more pronounced decrease in LVEDV than those without LVH (non-LVH: -16±13 mL, LVH: -26±18 mL, p=0.02). We also found that the loss in LVEDV paralleled the degree of LVH. The associated decrease in stroke volume in patients with a moderate degree of LVH (septal wall: 14±1 mm) led to an inability to significantly increase cardiac output with tachycardia (baseline: 3.78±1.28 l/min, peak: 3.74±0.99 l/min, p=0.94). In stark contrast, patients without LVH nearly doubled their cardiac output (baseline: 2.34±0.65 l/min, peak: 4.40±2.56 l/min, p<0.01).
Conclusion: Patients with LVH display pronounced LV diastolic volume loss during dobutamine stress compared with non-LVH controls, consistent with tachycardia-induced incomplete relaxation. This volume loss prevents the normal increase in cardiac output with tachycardia. Thus, tachycardia-induced incomplete relaxation may play an important role in symptom development in patients with concentric hypertrophic remodeling.
- © 2011 by American Heart Association, Inc.