ABSTRACT
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.
Subject(s)
Elasticity Imaging Techniques/methods , Heart Rate , Heart Ventricles/physiopathology , Image Interpretation, Computer-Assisted/methods , Magnetic Resonance Imaging/methods , Ventricular Dysfunction, Left/physiopathology , Dilatation, Pathologic/physiopathology , Elastic Modulus , Female , Humans , Male , Middle Aged , Stress, MechanicalABSTRACT
BACKGROUND: Decreased heart rate variability (HRV) has been shown to reflect disturbances of the autonomic nervous system that is related to increased cardiovascular mortality. Most studies investigated HRV in patients with systolic left ventricular dysfunction due to remote myocardial infarction or dilated cardiomyopathy. To date, only few data are available on HRV in patients with predominant diastolic dysfunction in the presence of cardiac hypertrophy of different etiologies. METHODS: Time domain analysis of HRV was performed from digital 24-hour Holter electrocardiogram recordings in 86 patients with sinus rhythm and cardiac hypertrophy, which was due to aortic valve stenosis in 33 patients, hypertrophic cardiomyopathy in 29 patients, and hypertensive heart disease in 24 patients. Heart rate variability analysis was compared with 91 healthy controls. RESULTS: The SD of all normal-to-normal R-R intervals (SDNN) was reduced in patients with aortic valve stenosis, hypertrophic cardiomyopathy, and hypertensive heart disease when compared with controls (SDNN 119 +/- 42 vs 154 +/- 36 milliseconds, P < .001). The extent of cardiac hypertrophy indexed by echocardiography based left ventricular mass calculation and increased patient age were independent predictors for depression of SDNN. CONCLUSIONS: Cardiac hypertrophy of various etiologies is related to decreased HRV on 24-hour Holter electrocardiogram. Both the patient age and the extent of left ventricular hypertrophy are independently associated with depression of HRV. These findings are independent of the cause of cardiac hypertrophy. The significance of these findings remains to be determined by future studies.