In patients with severe, nonischemic dilated cardiomyopathy who were treated with ACE inhibitors and beta-blockers, the implantation of a cardioverter-defibrillator significantly reduced the risk of sudden death from arrhythmia and was associated with a nonsignificant reduction in the risk of death from any cause.

T-wave alternans is a strong independent predictor of spontaneous ventricular arrhythmias or death. It performed as well as programmed stimulation and better than SAECG in risk stratifying patients for life-threatening arrhythmias.

Myocardial propagation may contribute to fatal arrhythmias in patients with idiopathic dilated cardiomyopathy (IDC). We examined this property in 15 patients with IDC undergoing cardiac transplantation and in 14 control subjects. An 8 X 8 array with electrodes 2 mm apart was used to determine the electrical activation sequence over a small region of the left ventricular surface. Tissue from the area beneath the electrode array was examined in the patients with IDC. The patients with IDC could be divided into three groups. Group I (n = 7) had activation patterns and estimates of longitudinal (OL = 0.84±0.09 m/s) and transverse (OT = 0.23±0.05 m/s) conduction velocities that were no different from controls (OL = 0.80±0.08 m/s, OT = 0.23±0.03 m/s). Group II (n = 4) had fractionated electrograms and disturbed transverse conduction with normal longitudinal activation, features characteristic of nonuniform anisotropic properties. Two of the control patients also had this pattern. Group III (n = 4) had fractionated potentials and severely disturbed transverse and longitudinal propagation. The amount of myocardial fibrosis correlated with the severity of abnormal propagation. We conclude that (a) severe contractile dysfunction is not necessarily accompanied by changes in propagation, and (b) nonuniform anisotropic propagation is present in a large proportion of patients with IDC and could underlie ventricular arrhythmias in this disorder. (J.

Heart rate rose, whereas LFP, LFPn and LFP/HFP fell before the onset of VT. This pattern of changes could be explained by a rise in sympathetic activity and saturation of the HRV signal resulting in dissociation of the average and rhythmical effects of sympathetic activity. These findings suggest that alterations in autonomic activity contributed to arrhythmogenesis in this group of patients.

Much is known about the effects of high environmental temperature (HT) on egg production, but very little is understood about the mechanisms that underlie them. Two experiments were conducted to examine the effects of acute heat stress on circulating estradiol, on calcium uptake by gut tissue, on bone resorption, and on the dynamic relationship between estradiol and calcium in the hen during one ovulatory cycle. In one study, hens were moved individually and randomly into a hot [HT: temperature (T) = 35 C, relative humidity (RH) = 50%; n = 18] or a control, thermoneutral (TN: T = 23 C, RH = 50%; n = 18) environment immediately after a mid-sequence oviposition and brachial vein cannulation. Blood samples (2 mL) were collected every 3 h for 21 h for ionized calcium (Ca2+) and pH determinations and from which aliquots were frozen for 17 beta-estradiol (E2), total calcium (TCa), and inorganic P analysis. Excreta and urine were assayed for TCa and hydroxyproline (OHPr), respectively. A second study was conducted to determine the effects of HT (T = 35, H = 50%, 12 h) vs TN (T = 23 C, RH = 50%, 12 h) on the ability of duodenal cells to take up calcium (CaT). Blood pH and calcium responded to HT as expected (pH increased, Ca2+ decreased, and TCa decreased) and the cyclic pattern of Ca2+ in blood was abolished. The ratio of Ca2+:TCa decreased sharply at approximately the onset of shell calcification in control hens, but in HT hens there was no clear change in the ratio of any point in the cycle. The pattern of E2 typical of hens under normal conditions was significantly depressed in plasma of HT hens. Calcium uptake by duodenal epithelial cells of HT hens was lower than in TN hens. There was a clear inverse correlation between blood Ca2+ and urine OHPr in TN hens (r2 = -73, P = 0.0021) but not in HT hens (r2 = -27, P = 0.32). In addition to alterations in acid-base balance and the status of Ca2+, diminished ability of duodenal cells to transport calcium may be a critical factor in the detrimental effects of heat stress on egg production (numbers), eggshell characteristics, and skeletal integrity often documented in the laying hen.

A noninvasive method based on high-resolution measurements and bandpass filtering of spontaneous skin temperature oscillations (approximately 4.0 x 10(-2) degrees C) in the low-frequency range (0.01-0.04 Hz) was investigated in normal human subjects. We hypothesized that the oscillations (temperature variability) originate from vasomotor activity of small arteries and arterioles in subcutaneous tissues. To test this hypothesis, continuous blood pressure waveforms were obtained with the use of an external piezoelectric sensor. The peak-to-peak envelope of the pressure signal (pressure variability) was used as an indicator of vasomotor activity. The variabilities of temperature and pressure were compared using cross-spectral and coherence analysis. The correlation between the peak frequency of the signals was 0.92, and the coherence was greater than 0.9. The signals demonstrated similar changes in spectral energy and peak frequency in response to mental stress. Reproducibility of the temperature variability in individual subjects was verified by repeating measurements 1-12 wk later. The differences in peak frequency were small (0.0155 +/- 0.001 Hz), and in each subject the signals exhibited similar patterns in response to stress. Correlation between spectral characteristics of the signals suggests that temperature variability can be attributed to changes in blood flow resulting from oscillations in vasomotor smooth muscle tone.

A major expansion in utilization of implantable cardioverter-defibrillators (ICDs) is anticipated based on the results of randomized clinical trials (RCT) that demonstrate increased survival in a sizable population of patients with reduced left ventricular function. However, if RCT accurately reflect clinical practice, then a substantial proportion of patients will die suddenly despite ICD implantation. ICD-unresponsive sudden cardiac death (SCD) has been recognized since the initial ICD experience. Yet, despite 25 years of technical advances, the frequency of ICD-unresponsive SCD has not declined. Pooled analysis of RCT indicates a crude rate of ICD-unresponsive SCD of 5%. This may not cause alarm in an average practice, but it comprises about 30% of cardiac deaths. Meta-analyses of RCT show that ICD therapy is associated with a relative risk reduction of SCD of approximately 60%, far less than the greater than 90% efficacy that many expect. The suboptimal performance of ICD therapy accounts for the failure of some RCT to achieve statistically significant effects on survival. The number of patients with ICD-unresponsive SCD is highly correlated with the number of cardiac deaths among control patients as well as ICD recipients. Otherwise, no definite patterns have emerged that clearly distinguish this mode of demise from other modes of cardiac death. Retrospective post-hoc analyses have not revealed distinguishing characteristics of patients with ICD-unresponsive SCD with respect to clinical variables, pre-terminal symptoms or to the setting of the terminal event. Despite advanced storage capabilities of implanted devices, almost no information has become available from RCT regarding the terminal rhythm or the response of the ICD. These observations have implications for clinical management and research. Candidates for ICD implantation based on RCT should be accurately informed about the residual risk of SCD. Investigators seeking to identify populations likely to benefit from ICD therapy based on SCD incidence should recognize that a significant fraction may not respond to ICD therapy. Reducing the incidence of ICD-unresponsive SCD would substantially improve survival and cost-effectiveness related to ICD therapy. Close cooperation between clinicians, investigators and representatives of industry and government is urgently needed to develop strategies to identify patients prone to ICD-unresponsive SCD, to determine its mechanisms and to develop methods of prevention and treatment.

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