Differential heart rate dynamics in transient left ventricular apical and midventricular ballooning.

BACKGROUND: The aim of the present study was to assess potential differences in cardiac autonomic nervous modulation in patients with transient left ventricular apical ballooning syndrome (AB) and the midventricular variant (MB) of this syndrome. OBJECTIVE: We hypothesized that differences in regional distribution of cardiac autonomic innervation in AB and MB may induce alterations in autonomic modulation, and we tested this assumption by using a combination of traditional and novel nonlinear parameters of heart rate variability (HRV). METHODS: In a prospective single-center study, 49 consecutive patients with transient left ventricular dysfunction syndrome underwent Holter electrocardiographic recording on the third day after admission. A total of 27 recordings of patients with AB and 10 recordings of patients with MB were valid for analysis of HRV, nonlinear dynamic measures of HRV, detrended fluctuation analysis (DFA), and phase-rectified signal averaging (PRSA). RESULTS: There were no significant differences in baseline clinical characteristics between AB and MB patients. Patients with MB showed significantly lower values for mean RR interval (835 ± 104 ms vs. 908 ± 118 ms; P < .05), 1/f power law slope (-1.28 ± 0.2 vs. -1.13 ± 0.2; P < .01), and deceleration capacity (DC) (4.6 ± 1.4 ms vs. 6.0 ± 1.4 ms; P < .01), and significantly higher values for low-frequency (LF) spectral component (5.3 ± 0.5 ln ms(2)/Hz vs. 4.8 ± 0.5 ln ms(2)/Hz), LF/high-frequency (HF) (1.7 ± 0.9 ms vs. 1.3 ± 0.6 ms; P < .05), and DFA α1 (1.09 ± 0.1 vs. 0.99 ± 0.1; P < .01) than patients with AB. There were no significant correlations between parameters of HRV, DFA, 1/f power law slope, and PRSA. CONCLUSION: There are significant differences in heart rate dynamics between AB and MB syndromes. Patients with MB show stronger fractal correlations of heart rate dynamics. Thus, inhomogeneous efferent bilateral sympathetic coactivation and differences in reflex autonomic regulation may be underlying pathophysiological mechanisms for AB and MB syndromes.

Gender effects on novel time domain parameters of ventricular repolarization inhomogeneity.

INTRODUCTION: Parameters of ventricular repolarization variability are increasingly being used in an attempt to understand better and predict the occurrence of ventricular tachycardia. Nevertheless, some of the measures used have thus far not been analyzed regarding gender differences in a large group of healthy subjects. Furthermore, new parameters might give further insight. METHODS AND RESULTS: We investigated 139 healthy volunteers (mean age 41.6 +/- 15.3 years, range 20-77, median 40.0 years, 76 women) without evidence of organic cardiac disease. Mean RR interval and established time domain parameters of heart rate variability (rMSSD; SDNN) were measured for each subject. Beat-to-beat QT interval and time-domain QT interval variability were analyzed. Characteristics of the QT interval and QT interval variability were determined as hourly mean values. The standard deviation of all QT intervals/hour (SDQT) and the standard deviation of all QTc intervals/hour (SDQTc) were used to measure QT interval variability. Four novel ratios of repolarization inhomogeneity (VRI: SDQT/SDNN; VR II: SDQT/rMSSD; VR III: SDQTc/SDNN; VR IV: SDQTc/rMSSD) were introduced. Female subjects exhibited significantly higher values in all four ratios of variability. CONCLUSION: The obvious gender differences in repolarization inhomogeneity found in this study might be valuable in better understanding differences between men and women in the genesis of ventricular tachycardia.

Direct adipotropic actions of atorvastatin: differentiation state-dependent induction of apoptosis, modulation of endocrine function, and inhibition of glucose uptake.

Statins exert anti-inflammatory, anti-atherogenic actions. The mechanisms responsible for these effects remain only partially elucidated. Diabetes and obesity are characterized by low-grade inflammation. Metabolic and endocrine adipocyte dysfunction is known to play a crucial role in the development of these disorders and the related cardiovascular complications. Thus, direct modulation of adipocyte function may represent a mechanism of pleiotropic statin actions. We investigated effects of atorvastatin on apoptosis, differentiation, endocrine, and metabolic functions in murine white and brown adipocyte lines. Direct exposure of differentiating preadipocytes to atorvastatin strongly reduced lipid accumulation and diminished protein expression of the differentiation marker CCAAT/enhancer binding protein-beta (CEBP-beta). In fully differentiated adipocytes, however, lipid accumulation remained unchanged after chronic atorvastatin treatment. Furthermore, cell viability was reduced in response to atorvastatin treatment in proliferating and differentiating preadipocytes, but not in differentiated cells. Moreover, atorvastatin induced apoptosis and inhibited protein kinase B (AKT) phosphorylation in proliferating and differentiating preadipocytes, but not in differentiated adipocytes. On the endocrine level, direct atorvastatin treatment of differentiated white adipocytes enhanced expression of the pro-inflammatory adipokine interleukin-6 (IL-6), and downregulated expression of the insulin-mimetic and anti-inflammatory adipokines visfatin and adiponectin. Finally, these direct adipotropic endocrine effects of atorvastatin were paralleled by the acute inhibition of insulin-induced glucose uptake in differentiated white adipocytes, while protein expression of the thermogenic uncoupling protein-1 (UCP-1) in brown adipocytes remained unchanged. Taken together, our data for the first time demonstrate direct differentiation state-dependent effects of atorvastatin including apoptosis, modulation of pro-inflammatory and glucostatic adipokine expression, and insulin resistance in adipose cells. These differential interactions may explain variable clinical observations.