Role of circadian rhythmicity in the heart rate variability preceding non-sustained ventricular tachycardia

The difference in sympathovagal activity preceding non-sustained ventricular tachycardia (NSVT) was examined between patients with and without a circadian rhythm. Thirty-three patients' Holter monitoring data (41 NSVT episodes) were analyzed regarding the frequency domain measures (low-frequency component [LF: 0.04-0.15 Hz], high-frequency component [HF: 0.15-0.4 Hz], and the ratio of LF to HF [LF/HF]) for each 15-min average from 120 min before each episode of NSVT. The presence of a circadian rhythm was accepted when the rhythm adaptation was significant by cosinor analysis and the acrophase was located at night (22.00-06.00h) in HF (HF-positive group, n=17), and during the daytime (10.00-20.00h) in LF/HF (LF/HF-positive group, n=12). The negative groups were identified by the absence of a circadian rhythm (HF-negative group, n=16; LF/HF-negative group, n=21). The serial changes in the HF power before NSVT were significantly different between the HF-positive and -negative groups (p<0.05). The HF increased from 75-60 min before NSVT in the HF-positive group, whereas the HF decreased from 60-45 min in the HF-negative group. The serial changes in the LF/HF ratio were not significantly different between the LF/HF-positive and -negative groups. Thus, the circadian rhythmicity of vagal activity seems to have an important role in the genesis of NSVT.     

Effects of acute exposure to simulated altitude on heart rate variability during exercise

It has been shown that fluctuation of human heartbeat intervals [heart rate variability (HRV)] reflects variations in cardiac autonomic nervous system activity. The present study was designed to investigate whether the acute exposure to moderate levels of simulated altitude and the resultant hypoxia could modify HRV during exercise. Seven healthy men completed one resting measurement in the upright sitting position and two submaximal steady-state cycle ergometer exercises at intensities equivalent to 25 and 50% of their estimated maximal work rate. Experiments were conducted in random order at altitude equivalents of 500, 1,500, 2,500, and 3,500 m within 2 h of exposure to that altitude. Beat-to-beat HRV was measured continuously during the tests. HRV data were analyzed by "coarse-graining spectral analysis" (Y. Yamamoto and R.L. Hughson, Physica 68D: 250-264, 1993) to break down their total power (PT) into harmonic and nonharmonic (fractal) components. The harmonic component was further divided into low (0.0- to 0.15-Hz; PL)- and high (> 0.15-Hz; PH)-frequency components, and the indicators of relative sympathetic (SNS) and parasympathetic (PNS) nervous system activities were calculated by PL/PH and PH/PT, respectively. The fractal component was used to calculate the spectral exponent (beta) to evaluate the overall "irregularity" of HRV. The effects of exercise intensity (increase in heart rate, SNS indicator, and beta and decrease in PNS indicator) were significant (P < 0.05) at all altitude levels. The altitude effects (increase in heart rate and SNS indicator and decrease in PNS indicator) were found only during exercise at 3,500 m (P < 0.05). There was no significant effect of altitude on beta (P > 0.05). These data indicate that acute effects of altitude exposure on HRV were found 1) during exercise at moderate altitude (> 2,500 m) and 2) mainly for the harmonic components of HRV.     

Intoxicated behavioral disinhibition and the heart rate response to alcohol.

This study examined the association between the heart rate (HR) response to alcohol intoxication, which is thought to reflect sensitivity to alcohol-induced reward and alcohol-induced behavioral disinhibition. High- and low-HR responders to alcohol participated in a go/no-go task, under sober and intoxicated conditions. Errors of commission on this task have previously been related to behavioral disinhibition. High-HR responders made more intoxicated commission errors as compared with low-HR responders. High-HR responders also reported increased alcohol consumption, and controlling for the latter did not alter the significant association between high-HR responders and increased intoxicated errors of commission. These results are consistent with previous findings of an increased risk for addictive and disinhibited behavioral propensities in individuals with a high-HR response to alcohol intoxication. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Aggressiveness, family history of alcoholism, and the heart rate response to alcohol intoxication.

Some sons of male alcoholics (SOMAS) are characterized by an increased heart rate (HR) response to alcohol intoxication, which is thought to reflect increased sensitivity to alcohol-induced reward. Such a response has also been related to increased physical aggression. However, the confounding effect of aggression in SOMAS may be obscuring the interpretation of these findings. The HR response to alcohol was therefore assessed in 4 groups: high/low aggressive SOMAS and high/low aggressive non-SOMAS. Results indicate that aggressive SOMAS had the highest intoxicated HR response and that they reported the most alcohol consumption. This suggests that in some cases the high comorbidity between alcohol misuse and aggression is related to an increased sensitivity to alcohol-induced reward. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Nonreentrant supraventricular tachycardia due to double ventricular response via dual atrioventricular nodal pathways

In twenty eight patients with iron deficiency the efficacy of iron-acetil-transferrin treatment (2-3 mg/kg/die) has been evaluated from the changes of the following variables: RBC and reticulocyte count, Hb concentration, MCV, MCH, serum ferritin, serum iron, TIBC, and ZnPP. These variables were assessed before and after three months of treatment in all patients, and after three months from the end of the treatment in thirteen patients. At the end of the treatment there was a significant increase of RBC count, Hb concentration, MCV, MCH, serum ferritin, serum iron, and TIBC, a significant decrease of ZnPP, while reticulocyte count remained essentially unchanged. After three months from the end of the treatment only serum ferritin and ZnPP underwent an additional significant increase and decrease, respectively. In twenty-six patients serum ferritin values returned to normal. The changes of RBC and reticulocyte count, Hb concentration, MCV, serum iron, and TIBC were larger the lower the initial values, suggesting that the efficacy of the treatment is greater the more serious the iron deficiency.     

Distinction between arrhythmic and nonarrhythmic death after acute myocardial infarction based on heart rate variability, signal-averaged electrocardiogram, ventricular arrhythmias and left ventricular ejection fraction

OBJECTIVES: We investigated whether heart rate variability, the signal-averaged electrocardiogram (ECG), ventricular arrhythmias and left ventricular ejection fraction predict the mechanism of cardiac death after myocardial infarction. BACKGROUND: Postinfarction risk stratification studies have almost exclusively focused on predicting the risk of arrhythmic death. The factors that identify and distinguish persons at risk for arrhythmic and nonarrhythmic death are poorly known. METHODS: Heart rate variability, the signal-averaged ECG, ventricular arrhythmias and left ventricular ejection fraction were assessed in 575 survivors of acute myocardial infarction. The patients were followed up for 2 years; arrhythmic and nonarrhythmic cardiac deaths were used as clinical end points. During the follow-up period, 47 cardiac deaths occurred, 29 (62%) arrhythmic and 18 (38%) nonarrhythmic. RESULTS: All risk factors were associated with cardiac mortality in univariate analysis. With the exception of left ventricular ejection fraction, they were also predictors of arrhythmic death. Depressed heart rate variability (p < 0.001), ventricular ectopic beats (p < 0.001) and low ejection fraction (p < 0.001) were related to nonarrhythmic death. In multivariate analysis, depressed heart rate variability (p < 0.001) and runs of ventricular tachycardia (p < 0.05) predicted arrhythmic death. Nonarrhythmic death was associated with depressed heart rate variability (p < 0.001), ventricular ectopic beats (p < 0.001) and low ejection fraction (p < 0.01). By selecting patients with depressed heart rate variability, long filtered QRS duration or ventricular arrhythmias and excluding patients with the lowest ejection fraction, we identified a group in which 75% of deaths were arrhythmic. Similarly, by selecting patients with a low ejection fraction and excluding patients with the lowest heart rate variability, we identified a group in which 75% of deaths were nonarrhythmic. CONCLUSIONS: Arrhythmic death was associated predominantly with depressed heart rate variability and ventricular tachycardia runs, and nonarrhythmic death with low ejection fraction, ventricular ectopic beats and depressed heart rate variability. A combination of risk factors identified patient groups in which a majority of deaths were either arrhythmic or nonarrhythmic.     

Catheter ablation of incessant ventricular tachycardia: acute and long-term results

SUBJECTS: Seventeen patients with incessant ventricular tachycardia refractory to anti-arrhythmic therapy underwent catheter ablation between 1987 and 1993. Fifteen patients had coronary heart disease and two had dilated cardiomyopathy. The mean age of the patients was 65 +/- 8 and the mean left ventricular ejection fraction was 31 +/- 9%. METHODS: Ablation sites were selected on the basis of endocardial activation mapping, concealed entrainment or bundle branch mapping. Catheter ablation was performed with direct current in nine patients and with radiofrequency energy in eight patients. Incessant ventricular tachycardia was terminated by catheter ablation in all 17 patients. RESULTS: One patient died after the ablation procedure due to pericardial tamponade. During electrophysiological testing 5-14 days later, 7 of 16 patients (44%) had inducible sustained or non-sustained ventricular tachycardia. Five of them underwent implantation of an automatic cardioverter/defibrillator, and three of these experienced discharges of the device during a mean follow-up of 30 +/- 12 months. another patient underwent implantation of a cardioverter/defibrillator after spontaneous recurrence of ventricular tachycardia. Out of the nine patients without inducible ventricular tachycardia, one died as a result of sudden cardiac death, and another had spontaneous ventricular tachycardia. Thus, ventricular tachycardia recurred clinically in 6 of 16 patients (38%), in whom ventricular tachycardia with the same morphology as that of the ablated ventricular tachycardia could be determined only in one patient. CONCLUSION: Catheter ablation is the method of choice for the emergency treatment of patients with incessant ventricular tachycardia. Due to the high risk of recurrence, additional anti-arrhythmic management, such as the implantation of a cardioverter/defibrillator, has to be considered.     

Fatality due to intravenous diltiazem for acute ventricular rate control

Progressive, sustained bradycardia resulting in asystole and subsequent death is reported in a 70-year-old woman with hyperkalemia and suspected digoxin toxicity following a 0.25 mg/kg intravenous diltiazem dose for treatment of atrial fibrillation with a rapid ventricular response. The possible pharmacodynamic and pharmacokinetic interactions between diltiazem, digoxin, and an elevated plasma potassium concentration are discussed and related to the outcome of the case. The routine practice of concomitant administration of diltiazem for rapid ventricular rate control and digoxin for long-term control may be dangerous in a subset of patients.     

Blood parameter and heart rate response to training in Andalusian horses

The psychopathology and associated disabilities experienced by persons with schizophrenia have only partially responded to conventional pharmacological and psychosocial treatment approaches. Biobehavioral treatment and rehabilitation employs behavioral assessment, social learning principles, skills training, and a focus on the recovery process to amplify the effects of pharmacotherapy. Utilizing the Medline database, we review a selection of English-language studies published from 1970 to 1994 that support the effectiveness of each of the components of biobehavioral therapy, such as case management, psychopharmacology with behavioral assessment, psychoeducation, family involvement, and social skills training. An integrated biobehavioral therapy directed toward early detection and treatment of schizophrenic symptoms, collaboration between consumers and caregivers in managing treatment, family and social skills training, and teaching coping skills and self-help techniques has been documented to improve the course and outcome of schizophrenia, as measured by symptom recurrence, social functioning, and quality of life. A case vignette is presented to illustrate the successful integration of biobehavioral therapies into a treatment system that focuses on consumers' attempts to become increasingly responsible for recovering from illness.     

Coincident loss of consciousness and ventricular tachycardia during +GZ stress

The environment of the advanced fighter aircraft represents a unique combination of stressful factors. Each of the individual stresses is hazardous, with the summation of these factors possibly resulting in an additional risk for sudden in-flight incapacitation. Advanced fighter aircraft are capabble of producing both rapid onset and high sustained +GZ forces which, on occasion, can exceed the tolerance limits of the pilot. The +GZ forces encountered during aerial combat maneuvering are physiologically stressful and have a profound effect on the regulatory mechanisms of the body. The influence of these stresses, including +GZ stress, on the autonomic nervous system is complex. The overall normal regulation of the cardiovascular system depends on a balance between both branches of the autonomic nervous system. An imbalance between sympathetic and parasympathetic tone can result in cardiac dysrhythmias and symptoms not conducive to safe and effective flight. An episode of ventricular tachycardia, coincident with an episode of loss of consciousness, was observed in an apparently healthy aircrewman during +GZ stress on the USAF School of Aerospace Medicine human centrifuge. The implications of autonomic imbalance in the production of similar potentially hazardous dysrhythmias and symptoms in the multistress environment deserve more in-depth investigation.     

Altered ventricular and myocyte response to angiotensin II in pacing-induced heart failure

Alterations in the cardiac response to angiotensin II (Ang II) may contribute to the functional impairment in tachycardia-induced heart failure (congestive heart failure [CHF]). Accordingly, we studied the response to Ang II in eight conscious instrumented dogs before and after inducing CHF. Left ventricular (LV) performance was assessed by measuring LV pressure and LV volume. Isolated myocyte function was evaluated using computer-assessed videomicroscopy. In conscious animals before CHF, Ang II produced a load-dependent slowing of the time constant of LV relaxation (tau) and did not depress intact LV contractile function. After CHF, although Ang II produced a similar increase in LV systolic pressure, the increases in LV diastolic pressure and time constant tau were much greater, and contractile performance was depressed. These changes persisted when the elevation of end-systolic pressure was prevented by nitroprusside. Similar changes were also present after autonomic blockade. In isolated myocytes, before CHF, Ang II (10(-6) mol/L) produced a slight positive inotropic effect. In contrast, after CHF, Ang II produced a negative inotropic effect and slowed the rate of relengthening. The effects in the intact LV and myocytes were reversed by an Ang II AT1 receptor blocker (losartan). We conclude that pacing-induced CHF alters the LV and myocyte response to Ang II, so that Ang II produces direct depressions in intact LV contraction, relaxation, and filling and exacerbates myocyte contractile dysfunction. These effects are mediated through the activation of AT1 receptors.     

Determinants of inducible ventricular tachycardia in patients with clinical ventricular tachyarrhythmia and no apparent structural heart disease

Thirty-seven patients with symptomatic ventricular tachyarrhythmia and no apparent structural heart disease were evaluated with multiple cardiovascular tests to establish the relationship between the results of programmed electric stimulation and other clinical and arrhythmia variables. Of 37 patients, 12 (32%) had inducible sustained ventricular tachycardia. Factors associated with the results of programmed electric stimulation included a history of ventricular tachycardia > or = 30 seconds requiring intervention for termination and global right heart abnormality documented by echocardiography. During treatment for a mean follow-up of 50 months, 29 patients did well, 6 patients had recurrences of major arrhythmia symptoms, 1 was lost to follow-up and 1 had a noncardiac death. Those patients with an adverse outcome were more likely to have inducible ventricular tachycardia. Thus certain clinical and echocardiographic data are associated with the results of programmed electric stimulation, which in turn have important prognostic value in this group of patients. Sustained ventricular tachycardia is unlikely to be induced in patients with no evidence of structural heart disease and clinical nonsustained ventricular tachycardia.     

Termination of ventricular tachycardia in the human heart. Insights from three-dimensional mapping of nonsustained and sustained ventricular tachycardias

BACKGROUND: To define the electrophysiological basis for the termination of ventricular tachycardia (VT), three-dimensional cardiac mapping and analysis of the terminal beats of nonsustained VT and beats of sustained VT were performed in six patients with healed myocardial infarcts. METHODS AND RESULTS: Termination of VT was due to activation from multiple initiation sites that were discordant from those responsible for the maintenance of sustained VT in 45% of cases, to repetitive activation from single sites that were discordant from those responsible for the maintenance of sustained VT in 24% of cases, or to activation from sites concordant with the sites of repetitive activation during sustained VT in 31% of cases. Sustained VT was characterized by occasional shifting of initiation sites, even after the tachycardia entered the stable monomorphic phase. Mapping was of sufficient density to define the mechanisms for 21 terminating beats of VT. In 5 cases, termination was due to intramural reentry, which initiated with the total activation time of the preceding beat of 204 +/- 11 milliseconds (ms) but terminated primarily because of a decrease in total activation time (144 +/- 23 ms, P = .03) that was associated with the development of intramural conduction block or with significant changes in the activation sequence along the reentrant circuit. In 16 cases, terminal beats were initiated by a focal mechanism on the basis of the absence of intervening electrical activity from the termination of the preceding beat to the initiation of the terminating beat (172 +/- 9 ms). Focal activation was associated with less conduction delay of the preceding beat (115 +/- 6 ms) than terminating reentrant beats (P < .001) and usually terminated suddenly without oscillations in cycle length or total activation time. CONCLUSIONS: Termination of VT is associated with alterations in initiation sites that are most often discordant from those maintaining sustained VT and is due to either reentrant or focal mechanisms.