[The heart. 10. The pericardium, heart tumors and heart injuries].
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BACKGROUND: The aim of the present study is to clarify whether biased symptom perception towards heart symptoms may explain a reduced quality of life in patients with congenital heart disease (ConHD). The present study tested the hypothesis that the combination of ConHD and high trait anxiety increases the perception of heart symptoms during acute stress. METHODS: 25 patients and 24 healthy participants completed a stressful computer task. Participant's heart and non-heart symptoms were measured after stress and after relaxation. Heart rate, blood pressure, respiratory rate, and arterial partial pressure of CO2 were monitored continuously. RESULTS: In line with the prediction, a combination of high trait anxiety and ConHD resulted in an increased perception of specifically heart symptoms during stress. Moreover, the increased perception of heart symptoms could not be explained by acute heart dysfunction. CONCLUSIONS: Heart dysfunction is not the only cause of an increased perception of heart symptoms. A history of disease experience in combination with high trait anxiety may increase the perception of heart symptoms during stress and may eventually result in an increased risk of developing a reduced quality of life.
Electrophysiological remodeling of ion channels in heart failure causes action potential prolongation and plays a role in arrhythmia mechanism. The importance of down-regulation of potassium currents is well-known, but a role for Na current (I(Na)) in heart failure is less well established. We studied I(Na) in heart failure ventricular cells from a canine pacing model of heart failure and also from explanted failing human hearts. Peak I(Na) density was significantly decreased by 39% and 57% in the dog model and in human heart failure, respectively. The kinetics of peak I(Na) were not different in heart failure. Late I(Na) was measured 750 ms after the initial depolarization as the saxitoxin (STX)-sensitive current and also as the current remaining after contaminating currents were blocked. Late I(Na) as a percentage of the peak I(Na) was significantly increased in both conditions. In dogs, STX sensitive late I(Na) was 0.5 +/- 0.1% n = 16 cells from eight normal hearts and 3.4 +/- 1.4% n = 12 cells from seven failing hearts; in humans, it was 0.2 +/- 0.1% n = 4 cells from two normal hearts and 2.4 +/- 0.5% n = 10 cells from three human failing hearts (-40 mV). Quantitative measures of mRNA including RNase protection assays and real time quantitative PCR in the dog model showed no differences for different alpha subunit isoforms (NaV1.1, 1.3, 1.5) and for the beta1 and beta2 subunits. This suggests neither alpha subunit isoform switching nor altered beta subunit expression is a mechanism for increased late I(Na). We conclude that a peak I(Na) is decreased, and non-inactivating late I(Na) is increased in heart failure and this may contribute to action potential prolongation and the generation of arrhythmia.
Use of angiotensin-converting enzyme inhibitor in heart failure with left ventricular systolic dysfunction has revolutionized management of heart failure and resulted in several national heart failure guidelines. However, studies have documented underutilization of these life saving drugs. Subsequently, results of other randomized clinical trials revealed the beneficial effects of angiotensin receptor blockers, beta-blockers, and spironolactone in heart failure with systolic dysfunction, which prompted several other guidelines. However, all these guidelines were primarily restricted to systolic dysfunction. Heart failure is as much a geriatric syndrome as it is a cardiac. Most heart failure patients are older adults. About half of the heart failure in older adults is not associated with left ventricular systolic dysfunction. Two recent heart failure guidelines, from the European Society of Cardiology and the American College of Cardiology/American Heart Association, published respectively in September and December 2001 included recommendations for patients with preserved left ventricular systolic function and other special populations, including older adults and those at end of life. The purpose of this article is to review the relevance of these two guidelines to heart failure patients living in long-term care facilities. As our population is aging, more heart failure patients are expected to live in long-term care facilities. Appropriate evaluation and management of these patients are essential to improve quality of heart failure care in the coming decades.
AIMS: To characterise the frequency response of short-term heart rate variability to external periodic perturbations in healthy and ischemic heart disease subjects. METHODS: Eleven healthy men and 11 ischemic heart disease patients were enrolled in this study. The frequency response of heart rate variability was assessed during periodic eyes opening test and controlled breathing at frequencies ranging from 0.08 to 0.25 Hz using autoregressive spectral analysis. RESULTS: In subjects of both groups the mean heart rate and blood pressure were unchanged across experimental sessions. In healthy subjects eyes opening at rate of 8 and 6 times/min (0.12 and 0.10 Hz) evoked high-power peaks (P<0.05) at the same frequencies in the R-R power spectrum. The largest frequency response of heart rate variability was seen during eyes opening at 0.1 Hz (P<0.05). Ischemic heart disease patients failed to respond to periodic eyes opening with any changes in heart rate variability. During controlled breathing healthy subjects showed the highest heart rate variability frequency responses when breath frequency was 0.1 Hz (P<0.05). Comparatively, patients with ischemic heart disease had reduced frequency responses of heart rate variability at all breath rates and its magnitude did not depend on the perturbation frequency. CONCLUSIONS: Our results demonstrate that the frequency response of short-term heart rate variability to external periodic perturbations is dependent on the perturbation frequency and the presence disease processes in the cardiovascular system.
1. In the isolated perfused rat heart, the contractile activity and the oxygen uptake were varied by altering the aortic perfusion pressure, or by the atrial perfusion technique (;working heart'). 2. The maximum increase in the contractile activity brought about an eightfold increase in the oxygen uptake. The rate of glycolytic flux rose, while tissue contents of hexose monophosphates, citrate, ATP and creatine phosphate decreased, and contents of ADP and AMP rose. 3. The changes in tissue contents of adenine nucleotides during increased heart work were time-dependent. The ATP content fell temporarily (30s and 2min) after the start of left-atrial perfusion; at 5 and 10min values were normal; and at 30 and 60min values were decreased. ADP and AMP values were increased in the first 15min, but were at control values 30 or 60min after the onset of increased heart work. 4. During increased heart work changes in the tissue contents of adenine nucleotide and of citrate appeared to play a role in altered regulation of glycolysis at the level of phosphofructokinase activity. 5. In recirculation experiments increased heart work for 30min was associated with increased entry of [(14)C]glucose (11.1mm) and glycogen into glycolysis and a comparable increase in formation of products of glycolysis (lactate, pyruvate and (14)CO(2)). There was no major accumulation of intermediates. Glycogen was not a major fuel for respiration. 6. Increased glycolytic flux in Langendorff perfused and working hearts was obtained by the addition of insulin to the perfusion medium. The concomitant increases in the tissue values of hexose phosphates and of citrate contrasted with the decreased values of hexose monophosphates and of citrate during increased glycolytic flux obtained by increased heart work. 7. Decreased glycolytic flux in Langendorff perfused hearts was obtained by using acute alloxan-diabetic and chronic streptozotocin-diabetic rats; in the latter condition there were decreased tissue contents of hexose phosphates and of citrate. There were similar findings when working hearts from streptozotocin-diabetic rats with insulin added to the medium were compared with normal hearts. 8. The effects of insulin addition or of the chronic diabetic state could be explained in terms of an action of insulin on glucose transport. Increased heart work also acted at this site, but in addition there was evidence for altered regulation of glycolysis mediated by changes in tissue contents of adenine nucleotides or of citrate.
AIM: To evaluate the clinical and prognostic value of the heart rate variability index in patients with congestive heart failure. METHODS: Sixty-four patients with chronic congestive heart failure and sinus rhythm underwent clinical assessment, 24-h ambulatory electrocardiography and echocardiography. Patients were followed for 6 to 30 months. Cardiac death or heart transplantation constituted the primary end-point of the study. RESULTS: The heart rate variability index was related to left ventricular ejection fraction (r=0.29, P=0.02) and New York Heart Association class (P=0.01). Patients with a restrictive left ventricular filling pattern had a lower heart rate variability index compared to patients with a non-restrictive pattern (26+/-11 vs 33+/-9 units, P=0.01). Patients who died (n=11) or underwent heart transplantation (n=4) had a lower heart rate variability index compared to survivors (21+/-10 vs 33+/-9 units, P<0.0001). In multivariate survival analysis, a reduced heart rate variability index was related to survival independent of parameters of left ventricular function. CONCLUSION: The heart rate variability index provides independent information on clinical status and prognosis in patients with chronic congestive heart failure.
The heartbeat counting task is used widely to assess the ability to perceive cardiac sensations. However, performance on this task may be determined by processes other than sensitivity to cardiac stimuli. Beliefs about the effects of postural and exercise challenges on heart rate were assessed by questionnaire prior to performing the heartbeat counting task, and then actual heart rate was manipulated during the counting task by changes in posture and exercise. On average, counted heart rates were closer to beliefs about heart rate than to actual heart rate. Hierarchical multiple regression analyses indicated that (a) believed heart rates predicted counted heart rates while controlling for actual heart rates and (b) actual heart rates also predicted counted heart rate while controlling for heart rate beliefs. These data suggest that the rate of heartbeat counting is influenced by beliefs about heart rate and by the processing of cardiac sensations.