Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The injury-vasospasm hypothesis of IHD was discussed in relation to coronary artery autoregulation and the anoxic-feedback mechanism. Observations in the recent literature, not usually attributed to spasm, were examined in light of this phenomenon. This includes reperfusion models of experimental AMI, the association of AMI with myocarditis, and findings in AMI and SCD as necrotic microlesions, prodromata, and epicardial arterial plaque rupture and hemorrhage. The disparity between the severity of coronary disease and the occurrence of the various types of IHD suggest that atherosclerosis itself does not precipitate attacks of chest pain. It was emphasized that plaque rupture due to spasm might help induce CAT. With exercise, the possible importance of the autoregulatory system was explored in the prevention and induction of AMI and SCD, and the improvement of AP. The role of spasm in IHD should be defined.
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PMID:The injury-vasospasm hypothesis of ischemic heart disease, revisited. 33 91

The purpose of this study is to investigate the long-term prognosis of ventricular tachycardia (VT) mainly with respect to sudden death (SCD) in patients with ischemic heart disease (IHD), idiopathic cardiomyopathy (ICM), miscellaneous heart disease (MHD) and idiopathic ventricular tachycardia (IVT). The study included 117 patients with VT (80 male, 37 female). The number of patients with IHD, ICM, MHD and IVT were 40, 18, 26 and 33, respectively. Follow-up was conducted by means of a mailed standardized questionnaire. The mean follow-up period was 46.8 +/- 32.0 months (range from 6 to 125 months). In 24 out of the 117 patients the cause of death was SCD, in 9 there was no sudden cardiac death and in 5 no cardiac death. The other 76 were surviving. The number of SCD in IHD, ICM, MHD and IVT was 14/40 (35%), 4/17 (24%), 6/25 (24%) and zero (0%), respectively. The number of having had syncope in IHD, ICM, MHD and IVT was 19/40 (48%), 7/18 (39%), 6/26 (23%) and 6/33 (18%), respectively. Out of the 19 IHD patients with syncope, 15 had had ventricular fibrillation (VF). As for IVT with syncope, only one of the 6 had VF, which was induced by a disopyramide injection. In IVT, the patients with syncope had a significantly higher VT rate than those without syncope (p less than 0.01). There were no significant differences in the electrocardiographical high risk parameters for SCD, the age, follow-up periods, the presence or absence of VF and ejection fraction between the SCD and the surviving groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term prognostic assessment of ventricular tachycardia with respect to sudden death in patients with and without overt heart disease. 263 26

Ischemic heart disease as a basic disease with accompanying findings and exogenous factors comes to a typical triad of SCD. There is a critical midlife situation due to O2-shortage. Dispositional and situational conditions come to be important, especially in cases in which morphological substrates are absent. The complex incident takes place on three levels (organism, heart, and myocardium). Several dying types may occur. Clinical accuracy and morphological diagnosis are of limited value for the relatively fatal importance of each of the single findings.
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PMID:[Acute cardiac death in chronic-ischemic heart disease (CIHD)]. 268 3

The circadian variation of major cardiovascular disorders, that is, TMI, AMI, SCD, and stroke, reflects an increased vulnerability to myocardial and cerebral ischemia and myocardial dysfunction in the early hours of the morning after awakening and rising. A comprehensive approach to treatment in patients with ischemic heart disease must take into consideration the chronobiology of the cardiovascular system and its relevance to the underlying disease process that affects the cardiovascular system.
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PMID:Circadian influence on coronary events. 341 71

Marine n-3 PUFA have potential antiatherogenic, antithrombotic, and antiinflammatory properties. However, recent research have addressed the antiarrhythmic effect of these fatty acids as a major explanation for their beneficial role in IHD and such an effect may explain the reduction in the incidence of SCD observed among fish eaters. SCD remains a serious problem in the Western Countries and although prevention of SCD is one of the main targets in modern cardiology the incidence of SCD has not declined during the past decades. Therefore, there is a need for other approaches to reduce the incidence of SCD. Thus, the aims of this study were 1) to study the impact of n-3 PUFA on 24-hour HRV, a recognized predictor of arrhythmic events and SCD in high-risk patients and in healthy subjects, and 2) to review the current knowledge about n-3 PUFA and the risk of SCD in humans and the proposed actions of n-3 PUFA responsible for an antiarhythmic effect. Subjects eating a modest amount of marine n-3 PUFA have an approximately 50% reduction in the risk of SCD compared to subjects not eating fish and in one study there was a close negative association between the risk of SCD and the cellular level of n-3 PUFA. Two large intervention studies support a beneficial effect of n-3 PUFA on the risk of SCD. In the DART study from 1989 a significant 29% reduction was found among post-MI men advised to eat fatty fish twice a week compared to those not advised so. This reduction could not be explained by an antiatherosclerotic or an antithrombotic effect of n-3 PUFA and an antiarrhythmic effect was considered operative. Ten years later the GISSI Prevenzione trial showed a 45% reduction in SCD among post-MI patients given one fish oil capsule daily (equal to 0.85 g of n-3 PUFA). The mechanisms behind the protection against SCD from marine n-3 PUFA have mainly been addressed in animal and in-vitro studies in which n-3 PUFA have shown profound antiarrhythmic effects. Based on the emerging hard end point data on the effect of n-3 PUFA on SCD in humans it is of importance to investigate if n-3 PUFA have actions in humans comparable to data from non-human studies. A surrogate for the risk of developing ventricular arrhythmias and SCD in humans is 24-hour HRV. Thus, in patients with IHD the risk of malignant ventricular arrhythmias and SCD is increased with decreased HRV. On the opposite, pharmacological interventions resulting in an improved patient survival have been associated with an increased HRV. In our studies we found positive associations between the cellular levels of marine n-3 PUFA and HRV in post-MI patients and in patients referred for coronary angiography suspected of IHD. Also, in these patients cellular levels of marine n-3 PUFA were independently correlated with HRV. When post-MI patients were given 5.2 g of marine n-3 PUFA daily for 12 weeks their HRV significantly increased. These findings may help explain why marine n-3 PUFA offer protection against SCD in patients with IHD. Patients with CRF and patients with DM comprise patient populations with an increased risk of SCD and an attenuated HRV. In these two groups of patients we found a close positive association between the cellular level of marine n-3 PUFA and HRV suggesting a beneficial effect of marine n-3 PUFA on HRV. Further research with dietary intervention with n-3 PUFA to CRF and DM patients should clarify if this effect can be translated into a reduction of coronary events. A decreased HRV may predict a poor outcome among healthy subjects due to an increased risk of SCD. We found a close positive association between cellular levels of marine n-3 PUFA and HRV in healthy men but not in healthy women. Dietary intervention with either 2.0 g or 6.6 g of marine n-3 PUFA daily for 12 weeks revealed a dose-dependent increase in HRV among men with a low base-line HRV. The results may help explain why dietary marine n-3 PUFA may reduce the risk of SCD in healthy men. It is a novel observation that n-3 PUFA have a beneficial impact on HRV in humans. The results from non-human studies showing effects of n-3 PUFA on sodium channels, calcium-channels and adrenergic receptors may, if applicable to humans, explain this effect of n-3 PUFA on HRV. However, n-3 PUFA may also cause a central modulation of HRV and, n-3 PUFA may thus modulate HRV both at the level of the brain and in the heart. In conclusion, the data suggest that marine n-3 PUFA have a beneficial impact on HRV in patients at high risk of SCD and in healthy men. Furthermore, our data may indicate that the protective effect of n-3 PUFA on SCD found among post-MI patients and healthy subjects is caused by a modulation of autonomic control with increased vagal tone. Therefore, given the safety and low cost of implementing a modest amount of marine n-3 PUFA in the diet, an adequate dietary fish intake may have a significant role to play in the primary and secondary prevention of out-of-hospital SCD.
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PMID:n-3 fatty acids and the risk of sudden cardiac death. Emphasis on heart rate variability. 1469 51

The present study investigated the immunohistochemical distributions and mRNA expressions of myocardial hypoxia-inducible factor (HIF)-1 alpha and its downstream factors, erythropoietin (Epo) and vascular endothelial growth factor (VEGF), in cardiac deaths. Medico-legal autopsy cases (n=114, within 48-h postmortem) of cardiac deaths (n=58) and control cases (n=56) were examined. Immunohistochemical positivities of HIF-1 alpha, Epo and VEGF were patchily observed in cardiomyocytes in the acute ischemic lesions of myocardial infarction (n=37), showing a relationship to morphological cardiomyocyte damage: the staining was intense in the regions with early ischemic changes and weak in the necrotic regions. Immunopositivities were sporadically detected in cardiomyocytes in some cases of sudden cardiac death without infarction (SCD, n=13). In chronic congestive heart disease (CHD, n=8), weak positivities were diffusely observed in the cardiomyocytes. However, there were no such findings in cases of mechanical asphyxiation (n=16) or drowning (n=18). HIF-1 alpha, Epo and VEGF mRNA expressions, as measured by real-time reverse transcription-polymerase chain reaction (RT-PCR), showed localized elevations related to acute myocardial infarction (AMI) lesions, whereas such findings were mild in recurrent myocardial infarction (RMI) and SCD cases. CHD showed significant elevations of these mRNAs irrespective of the sampling site. The mRNA expressions were significantly lower in cases of drowning. These findings suggest that focal immunopositivities and increased mRNAs of these factors are indicative of short and substantial duration of myocardial ischemia, respectively. The combined analyses may not only be useful for investigating the site, phase and severity of acute myocardial ischemia and the severity of chronic ischemic stress, but also contribute to differentiating cardiac deaths from asphyxiation and drowning or interpreting the possible contribution of cardiac disease in traumatic death.
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PMID:Forensic pathological investigation of myocardial hypoxia-inducible factor-1 alpha, erythropoietin and vascular endothelial growth factor in cardiac death. 1769 91

Although few doubts remain that physical exercise should be widely promoted for maintenance of health and fitness, the risk of adverse events such as sudden death (especially due to cardiac causes, i.e., sudden cardiac death [SCD]) during exercise remains tangible. The overall risk of sudden death in athletes is relatively low (i.e., usually comprised between 0.1 and 38/100,000 person-years), and globally comparable to that of the general population. However, up to 20% of all sudden death cases are still recorded while exercising. The most frequent underlying disorders encountered in SCD are hypertrophic cardiomyopathy and coronary artery disease (CAD), representing three quarters of all conditions. The risk related to CAD increases with aging (>35 years old), while that attributable to cardiomyopathies or fatal arrhythmias is especially frequent among young people (<35 years old). Taken together, these findings would lead to the conclusion that physical exercise may be seen as an acute trigger of myocardial ischemia or arrhythmias in some predisposed individuals. Nonetheless, the prevalence of coronary atherosclerosis seems to be higher in athletes than in sedentary subjects with comparable risk profile. On the contrary, coronary plaques in physically active subjects appear more stable, thereby attenuating the risk of rupture and subsequent myocardial ischemia. These findings, along with evidence of a considerable increase of peak coronary blood flow during exercise, make it very likely that an imbalance between oxygen demand and supply may be the most frequent cause of myocardial ischemia in athletes suffering SCD and/or cardiac arrest. Therefore, all subjects who wish to practice moderate- to high-intensity exercise are recommended to undergo preparticipation screening and annual follow-up.
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PMID:Sudden Cardiac and Noncardiac Death in Sports: Epidemiology, Causes, Pathogenesis, and Prevention. 2986 76