Why the study?
Is increased left ventricular wall stress associated with depressed heart rate variability in patients with LV dilatation or dysfunction?
Is increased left ventricular wall stress associated with depressed heart rate variability in patients with LV dilatation or dysfunction?
Left ventricular end-diastolic wall stress, measured by cardiac magnetic resonance, is independently associated with depressed heart rate variability in patients with LV dysfunction.
LVED wall stress may link load to reduced HRV in LV dysfunction; leaves open whether targeting wall stress improves autonomic function.
BACKGROUND: Heart failure is characterized by neurohumoral dysfunction that can be assessed by measurement of heart rate variability (HRV). Depression of HRV is related to several hemodynamic parameters. We hypothesized that an increased left ventricular (LV) wall stress is related to a depressed HRV in patients with LV dilatation or dysfunction. METHODS: Cardiac function and mass were measured in 31 patients with LV dilatation or dysfunction and 21 controls using cardiac magnetic resonance (CMR) imaging. LV wall stress was calculated using a CMR-based thick-walled sphere model. Standard deviation of normal-to-normal (NN) intervals (SDNN) and average NN intervals over 5 minutes (SDANN-i) were calculated. RESULTS: LV end-diastolic (ED) and end-systolic (ES) wall stress were significantly increased in patients with SDNN < 75 ms (P < 0.05). SDNN and SDANN-i were decreased (P = 0.001, P < 0.001) in patients with LVED wall stress >8 kPa and LVES wall stress >30 kPa (P < 0.05). To examine potential effects of LVEF, LVED and LVES volume, and wall stress on HRV, a multiple linear regression analysis was performed, which revealed LVED wall stress as the only independent parameter influencing SDNN (P = 0.039). LV ejection fraction, LV mass, and volumes were not significantly related to HRV. CONCLUSIONS: LV wall stress was independently related with depression of HRV. Therefore, LV wall stress might be prognostically important and a therapeutic target in heart failure.
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Alter et al. (2009) studied this question.
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