Respiratory symptoms and long-term risk of death from cardiovascular disease, cancer and other causes in Swedish men. (1/2144)

BACKGROUND: Depressed respiratory function and respiratory symptoms are associated with impaired survival. The present study was undertaken to assess the relation between respiratory symptoms and mortality from cardiovascular causes, cancer and all causes in a large population of middle-aged men. METHODS: Prospective population study of 6442 men aged 51-59 at baseline, free of clinical angina pectoris and prior myocardial infarction. RESULTS: During 16 years there were 1804 deaths (786 from cardiovascular disease, 608 from cancer, 103 from pulmonary disease and 307 from any other cause). Men with effort-related breathlessness had increased risk of dying from all of the examined diseases. After adjustment for age, smoking habit and other risk factors, the relative risk (RR) associated with breathlessness of dying from coronary disease was 1.43 (95% CI : 1.16-1.77), from stroke 1.77 (95% CI: 1.07-2.93), from any cardiovascular disease 1.48 (95% CI : 1.24-1.76), cancer 1.36 (95% CI : 1.11-1.67) and from any cause 1.62 (95% CI: 1.44-1.81). An independent effect of breathlessness on cardiovascular death, cancer death and mortality from all causes was found in life-time non-smokers, and also if men with chest pain not considered to be angina were excluded. An independent effect was also found if all deaths during the first half of the follow-up were excluded. Men with cough and phlegm, without breathlessness, also had an elevated risk of dying from cardiovascular disease and cancer, but after adjustment for smoking and other risk factors this was no longer significant. However, a slightly elevated independent risk of dying from any cause was found (RR = 1.18 [95% CI: 1.02-1.36]). CONCLUSION: A positive response to a simple question about effort related breathlessness predicted subsequent mortality from several causes during a follow-up period of 16 years, independently of smoking and other risk factors.  (+info)

Molecular heterogeneity in very-long-chain acyl-CoA dehydrogenase deficiency causing pediatric cardiomyopathy and sudden death. (2/2144)

BACKGROUND: Genetic defects are being increasingly recognized in the etiology of primary cardiomyopathy (CM). Very-long-chain acyl-CoA dehydrogenase (VLCAD) catalyzes the first step in the beta-oxidation spiral of fatty acid metabolism, the crucial pathway for cardiac energy production. METHODS AND RESULTS: We studied 37 patients with CM, nonketotic hypoglycemia and hepatic dysfunction, skeletal myopathy, or sudden death in infancy with hepatic steatosis, features suggestive of fatty acid oxidation disorders. Single-stranded conformational variance was used to screen genomic DNA. DNA sequencing and mutational analysis revealed 21 different mutations on the VLCAD gene in 18 patients. Of the mutations, 80% were associated with CM. Severe CM in infancy was recognized in most patients (67%) at presentation. Hepatic dysfunction was common (33%). RNA blot analysis and VLCAD enzyme assays showed a severe reduction in VLCAD mRNA in patients with frame-shift or splice-site mutations and absent or severe reduction in enzyme activity in all. CONCLUSIONS: Infantile CM is the most common clinical phenotype of VLCAD deficiency. Mutations in the human VLCAD gene are heterogeneous. Although mortality at presentation is high, both the metabolic disorder and cardiomyopathy are reversible.  (+info)

Sudden death in hypertrophic cardiomyopathy: potential importance of altered autonomic control of vasculature. (3/2144)

Current evidence suggests that alterations in the autonomic function and abnormal vascular control play a significant role either as independent triggers themselves or as modifiers of ischaemia and tolerance to to arrhythmias. A combination of several factors--that is, arrhythmia, hypotension, altered autonomic function including vascular control, and ischaemia are therefore likely to act as triggers for sudden death. The relative contribution of each of these factors needs further detailed study.  (+info)

Effect of angiotensin converting enzyme inhibition on sudden cardiac death in patients following acute myocardial infarction. A meta-analysis of randomized clinical trials. (4/2144)

Estimate the effect of angiotensin converting enzyme (ACE) inhibitors on the risk of sudden cardiac death (SCD) following myocardial infarction (MI). BACKGROUND: Trials in post-MI patients have shown that ACE inhibitor therapy reduces mortality. However, the effect on SCD as a mechanism has not been clarified. METHODS: Trials of ACE inhibitor therapy following MI reported between January, 1978 and August, 1997 were identified. Studies were included if they met the following criteria: 1) randomized comparison of ACE inhibitor to placebo within 14 days of MI; 2) study duration/blinded follow-up of > or =6 weeks; 3) the number of deaths and modes of death were reported or could be obtained from the investigators. RESULTS: We identified 374 candidate articles, of which 15 met the inclusion criteria. The 15 trials included 15,104 patients, 2,356 of whom died. Most (87%) fatalities were cardiovascular and 900 were SCDs. A significant reduction in SCD risk or a trend towards this was observed in all of the larger (N > 500) trials. Overall, ACE inhibitor therapy resulted in significant reductions in risk of death (random effects odds ratio [OR] = 0.83; 95% confidence interval [CI] 0.71-0.97), cardiovascular death (OR = 0.82; 95% CI 0.69-0.97) and SCD (OR = 0.80; 95% CI 0.70-0.92). CONCLUSIONS: This analysis is consistent with prior reports showing that ACE inhibitors decrease the risk of death following a recent MI by reducing cardiovascular mortality. Moreover, this analysis suggests that a reduction in SCD risk with ACE inhibitors is an important component of this survival benefit.  (+info)

Detection of abnormal high-frequency components in the QRS complex by the wavelet transform in patients with idiopathic dilated cardiomyopathy. (5/2144)

In order to investigate whether increased fine, fractionated signals within the QRS complex can detect arrhythmogenic substrates and how these fine signals link with ventricular mechanical dysfunction, wavelet analysis was performed on averaged QRS complexes obtained from the left precordial lead in 26 patients with idiopatic dilated cardiomyopathy (IDCM) and in 12 normal subjects. The number of local maxima and the duration of the wavelet transform were significantly greater in patients with IDCM than in normal subjects; the number at 100 Hz was 8.8+/-3.1 vs 6.0+/-1.1 (p<0.01), and the duration at 100Hz was 93+/-15 vs 75+/-7ms (p<0.01). Both of these indices were greater in the patients with than in those without late potentials, repetitive ventricular premature beats or cardiac death. In addition, significant inverse curvilinear relationships were observed between the left ventricular ejection fraction and both the number of local maxima and the duration of the wavelet transform. In conclusion, fine fragmented signals in the QRS complex detected by wavelet analysis would be an important marker for potentially arrhythmogenic substrates and seemed to progress in parallel with left ventricular mechanical dysfunction in IDCM.  (+info)

Sudden death in the general population in Okinawa: incidence and causes of death. (6/2144)

Sudden unexpected death is generally considered to be caused by acute myocardial infarction and/or arrhythmia. To document the incidence and causes of sudden death in Japan, where the incidence of myocardial infarction is low, the present study examined death certificates, hospital records, the forensic medical records, and the police records of residents of the southern part of Okinawa island who died at the age of 20-74 years during a 3-year period from January 1, 1992 to December 31, 1994. Sudden death was defined as death within 24 h from the onset of unexpected symptoms. The study documented 126 (87 men and 39 women) sudden deaths. The crude incidence rate was 0.37/1,000 person per year (0.51 in men and 0.23 in women). According to the death certificates, 78 cases died of heart diseases. However, the cause of death could be determined by examination of all available records in only 64 cases: myocardial infarction in 10, non-ischemic heart diseases in 13, and stroke in 23 cases. Even when the analysis was limited to the cases who died within 1 h from the onset of symptoms, heart disease was the cause of death in only 22% of the cases while the cause of death could not be determined in 53% of the cases. Only 13% of those diagnosed as heart diseases on the death certificate were verified. The agreement rate between the diagnosis reached by the re-evaluation of the records and that on the death certificate was 82% for stroke and 33% for other diseases. In Okinawa, Japan, the frequencies of heart disease and stroke as the cause of sudden death may be similar. Except for stroke, the diagnosis appearing on the death certificate has substantial inaccuracy.  (+info)

Mechanisms of death in the CABG Patch trial: a randomized trial of implantable cardiac defibrillator prophylaxis in patients at high risk of death after coronary artery bypass graft surgery. (7/2144)

BACKGROUND: The CABG Patch trial compared prophylactic implantable cardiac-defibrillator (ICD) implantation with no antiarrhythmic therapy in coronary bypass surgery patients who had a left ventricular ejection fraction <0.36 and an abnormal signal-averaged ECG. There were 102 deaths among the 446 ICD group patients and 96 deaths among the 454 control group patients, a hazard ratio of 1.07 (P=0.63). The mechanisms of death were classified, and hypotheses were tested about the effects of ICD therapy on arrhythmic and nonarrhythmic cardiac deaths in the CABG Patch Trial and the Multicenter Automatic Defibrillator Implantation Trial (MADIT). METHODS AND RESULTS: The 198 deaths in the trial were reviewed by an independent Events Committee and classified by the method of Hinkle and Thaler. Only 54 deaths (27%) occurred out of hospital; 145 deaths (73%) were witnessed. Seventy-nine (82%) of the 96 deaths in the control group and 76 (75%) of the 102 deaths in the ICD group were due to cardiac causes. Cumulative arrhythmic mortality at 42 months was 6.9% in the control group and 4.0% in the ICD group (P=0. 057). Cumulative nonarrhythmic cardiac mortality at 42 months was 12. 4% in the control group and 13.0% in the ICD group (P=0.275). Death due to pump failure was significantly associated with death >1 hour from the onset of symptoms, dyspnea within 7 days of death, and overt heart failure within 7 days of death. CONCLUSIONS: In the CABG Patch Trial, ICD therapy reduced arrhythmic death 45% without significant effect on nonarrhythmic deaths. Because 71% of the deaths were nonarrhythmic, total mortality was not significantly reduced.  (+info)

Drug-induced heart failure. (8/2144)

Heart failure is a clinical syndrome that is predominantly caused by cardiovascular disorders such as coronary heart disease and hypertension. However, several classes of drugs may induce heart failure in patients without concurrent cardiovascular disease or may precipitate the occurrence of heart failure in patients with preexisting left ventricular impairment. We reviewed the literature on drug-induced heart failure, using the MEDLINE database and lateral references. Successively, we discuss the potential role in the occurrence of heart failure of cytostatics, immunomodulating drugs, antidepressants, calcium channel blocking agents, nonsteroidal anti-inflammatory drugs, antiarrhythmics, beta-adrenoceptor blocking agents, anesthetics and some miscellaneous agents. Drug-induced heart failure may play a role in only a minority of the patients presenting with heart failure. Nevertheless, drug-induced heart failure should be regarded as a potentially preventable cause of heart failure, although sometimes other priorities do not offer therapeutic alternatives (e.g., anthracycline-induced cardiomyopathy). The awareness of clinicians of potential adverse effects on cardiac performance by several classes of drugs, particularly in patients with preexisting ventricular dysfunction, may contribute to timely diagnosis and prevention of drug-induced heart failure.  (+info)