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Prognosis of acute myocardial infarction complicated by complete heart block (the Worcester Heart Attack Study).

As part of a community-based study of patients hospitalized with acute myocardial infarction (AMI) in the Worcester, Massachusetts, metropolitan area, changes over time in the incidence rates of complete heart block (CHB) complicating AMI, and the prognostic impact of CHB on the in-hospital and long-term survival of these patients were examined. In all, 4,762 patients with validated AMI hospitalized at 16 hospitals in the Worcester metropolitan area during 1975, 1978, 1981, 1984, 1986 and 1988 constituted the study sample. The incidence rates of CHB complicating AMI remained relatively stable at 5.8% over the 13-year (1975 to 1988) period studied. The incidence rates of CHB were approximately twice as high in patients with inferior/posterior wall AMI (7.7%) as in those with anterior wall AMI (3.9%). Use of a multivariate regression analysis to control for factors affecting the incidence rates of CHB revealed that patients were at highest risk for developing CHB during the latter 2 study years (1986 and 1988). Patients with AMI developing CHB had higher in-hospital case fatality rates than did those without CHB overall, as well as during each of the 6 periods studied. The in-hospital survival associated with CHB did not improve over time. After use of a multivariate regression analysis to control for additional prognostic factors, the independent effect of CHB on in-hospital prognosis remained (adjusted risk of dying = 2.10; 95% confidence intervals = 1.37, 3.21). Patients with inferior wall AMI complicated by CHB were at significantly increased risk of dying during hospitalization compared with those without CHB (adjusted risk of dying = 2.71; 95% confidence intervals = 1.60, 4.59).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Does vitamin E decrease heart attack risk? summary and implications with respect to dietary recommendations.

The hypothesis that oxidative stress has a role in atherosclerosis rests on a large body of experimental work carried out in animal models of heart disease. The situation is more complex in humans, in that the results from vitamin E supplementation trials have been conflicting. Nonetheless, there is emerging information that alpha-tocopherol may play a critical role in maintaining the function of key cellular components in the atherosclerotic process through its ability to inhibit the activity of protein kinase C, a key player in many signal transduction pathways. alpha-Tocopherol modulates pathways of platelet aggregation, endothelial cell nitric oxide production, monocyte/macrophage superoxide production and smooth muscle cell proliferation. Regulation of adhesion molecule expression and inflammatory cell cytokine production by alpha-tocopherol has also been reported. More studies are required to relate alpha-tocopherol intakes to optimal tissue responses in humans.

Animals↗

Identifying men at high risk of heart attacks: strategy for use in general practice.

A strategy was devised for identifying men at high risk of acute myocardial infarction or sudden ischaemic death. A risk score was devised using cigarette smoking, mean blood pressure, recall of ischaemic heart disease or diabetes mellitus diagnosed by a doctor, history of parental death from "heart trouble," and the presence of angina reported on a questionnaire. The top fifth of the score distribution identified 53% of ischaemic heart disease cases--that is, men who subsequently experienced major ischaemic heart disease over the next five years. The addition of serum total cholesterol concentration and electrocardiographic evidence only slightly improved prediction (to 59%) and would have considerably increased the cost and effort of screening. Using this risk score on an opportunistic basis could be particularly valuable in general practice. Management of this high risk group is regarded as appropriate medical care and is complementary to the population approach to preventing ischaemic heart disease. Such a strategy for reducing the incidence of and mortality from ischaemic heart disease in men at high risk would also increase professional and public awareness of the need for preventive action.

Adult↗

Molecular mechanism of emotional stress-induced and catecholamine-induced heart attack.

Emotional or physical stress triggers 'tako-tsubo' cardiomyopathy or 'transient left ventricular apical ballooning', but the pathogenesis is unclear. In response to the immobilization stress of rats, a useful model of emotional stress, rapid activation of p44/p42 mitogen-activated protein kinase was observed in the heart, followed by a transient upregulation of immediate early genes in the smooth muscle cells of coronary arteries, the endothelial cells and the myocardium. Heat shock protein 70 was induced in the aortic and coronary arterial smooth muscle cells and in the myocardium. Natriuretic peptide genes were also upregulated in the myocardium. Sequential gene expression can be considered as an adaptive response to emotional stress. Blocking of both alpha-adrenoceptors and beta-adrenoceptors eliminated the upregulation of immediate early genes induced by stress, while alpha-agonists and beta-agonists upregulated immediate early genes in the perfused heart. Activation of alpha-adrenoceptors and beta-adrenoceptors is the primary trigger of emotional stress-induced molecular changes in the heart.

Animals↗