Coffee consumption and myocardial infarction in women

The relation between coffee consumption and the risk of acute myocardial infarction was evaluated in a hospital-based case-control study conducted in northern Italy between 1983 and 1987. The study consisted of 262 women with acute myocardial infarction and 519 controls admitted to the hospital for acute, nondigestive tract disorders. Information was obtained on the average number of cups of coffee or decaffeinated coffee consumed per day before the onset of the disease which led to hospital admission and on the total duration in years of the habit. There was a positive association between heavy coffee drinking and risk of myocardial infarction (relative risk (RR) = 2.7 for consumption of four cups or more per day). After allowance for smoking and other relevant covariates, the relative risk was not elevated for consumption of up to three cups per day, but still above unity for consumption of four or more cups per day (RR = 1.7), and the multivariate trend in risk was still significant (X1(2) = 5.14, p = 0.02). The risk estimates were grossly elevated among hyperlipidemic women (multivariate RR = 7.6 for moderate and 17.9 for heavy coffee drinkers). As a result of small absolute numbers, these estimates were largely unstable and the interaction between coffee and hyperlipidemia was not statistically significant. Such estimates, nonetheless, are of potential interest in terms of etiologic correlates and implications for prevention.     

Coffee consumption and risk of myocardial infarction among older Swedish women

Numerous studies have examined the association between coffee consumption and risk of myocardial infarction (MI), but results have been inconsistent. Case-control studies generally suggest a harmful effect of coffee drinking, whereas cohort studies have mostly shown no association. Recent studies found that coffee may lower the risk of diabetes, a major coronary risk factor. The authors prospectively examined the effect of coffee consumption on MI risk in 32,650 older Swedish women, aged 40-74 years, participating in the Swedish Mammography Cohort; 459 cases of MI developed during 165,896 person-years of follow-up from 1997 to 2002. After adjustment for age, coronary heart disease risk factors, and dietary variables, the relative risk of MI associated with drinking >/=5 cups/week versus 0-4 cups/week was 0.68 (95% confidence interval (CI): 0.43, 1.07). The authors observed a nonsignificant trend toward lower risk with higher consumption levels. Compared with that for 0-4 cups/week, the relative risks of MI were 0.84 (95% CI: 0.51, 1.38) for 5-7 cups/week, 0.65 (95% CI: 0.41, 1.03) for 2-3 cups/day, 0.64 (95% CI: 0.39, 1.04) for 4-5 cups/day, and 0.65 (95% CI: 0.37, 1.12) for >/=6 cups/day (p-trend = 0.07). Contrary to previous case-control studies, the authors concluded that coffee consumption does not increase MI risk. Coffee consumption of >/=5 cups/week was nonsignificantly inversely associated with MI risk among older Swedish women.     

Coffee drinking and nonfatal myocardial infarction in men under 55 years of age

The relation of coffee consumption to the risk of nonfatal first myocardial infarction in men under 55 years of age was assessed in a hospital-based case-control study conducted from 1980 to 1983 in hospitals in Massachusetts, Rhode Island, Connecticut, and New York: 1,873 men with first nonfatal myocardial infarctions were compared with 1,161 controls admitted for conditions unrelated to coffee ingestion. After allowance for major risk factors for myocardial infarction, the relative risk estimate for recent consumption of caffeine-containing coffee increased with increasing level of daily intake, from 1.4 for one to two cups per day to 1.6 for three to four cups, 1.8 for five to nine cups, and 2.9 for greater than or equal to 10 cups, relative to consumption of no coffee (p less than 0.001 for trend). The association was apparent in each age group and in both smokers and nonsmokers. For those who drank decaffeinated coffee only, on the basis of small numbers, there was a suggestion of an increased risk among men who had consumed at least five cups daily for less than five years but not among those who had drunk this amount for at least five years; whether the apparent association among the shorter-term drinkers was due to previous consumption of caffeine-containing coffee could not be determined. The findings suggest that caffeine-containing coffee increases the risk of myocardial infarction and that men who drink at least five cups daily may increase their risk by about twofold or more.     

Coffee use prior to myocardial infarction restudied: heavier intake may increase the risk

Because of conflicting evidence about the relation of coffee use to coronary artery disease, the authors conducted a new cohort study of hospitalizations among 101,774 white persons and black persons admitted to Kaiser Permanente hospitals in northern California in 1978-1986. In analyses controlled for eight covariates, use of coffee was associated with higher risk of myocardial infarction (p = 0.0002). Compared with nondrinkers of coffee, the following relative risks (RRs) were found: at 1-3 cups/day, RR = 1.14 (95% confidence interval (CI) 0.91-1.42); at 4-6 cups/day, RR = 1.42 (CI 1.10-1.84), p = 0.007; and at greater than 6 cups/day, RR = 1.41 (CI 1.00-1.99), p = 0.05. The relation remained significant when also controlled for blood cholesterol, blood glucose, blood pressure, and adiposity, singly or combined. Tea use was unrelated to myocardial infarction; neither coffee nor tea was related to other coronary diagnoses. Although causality remains unestablished and uncertainty remains, the authors conclude that 1) these data suggest a weak independent relation of coffee use to acute myocardial infarction, not mediated by an effect on blood cholesterol; and 2) persons at risk of myocardial infarction should consider limitation of coffee intake to less than 4 cups/day.     

microRNAs与心肌梗死

microRNAs(miRNAs)是一类内源性的非编码单链小分子RNA,约22个核苷酸。miRNAs通过调控其靶基因的表达,参与细胞发育、增殖、分化、凋亡等一系列重要的生理学途径。近些年的研究发现,miRNAs在心肌梗死的发生、发展过程中起着关键的作用。现就miRNAs在心肌梗死发生、发展过程中的作用机制进行阐述。     

Silent myocardial infarction

INTRODUCTION: By autopsies of patients expired from different diseases not rarely chronic myocardial infarction is found, that was known before neither to patient nor to medical attendant (silent myocardial infarction) and is interpreted as incidental finding. AIM: Study of frequency, role in expectation of life, diagnosis and prognosis of silent myocardial infarction in relation to localisation. METHODS: Retrospective study and statistical analysis of 1568 autopsies performed during 10 years. RESULTS: Acute or chronic myocardial infarction was found in 470 cases (30%), acute infarction in 177 cases (37%), 90% of which was diagnosed in vivo and patients died of infarction and its direct complications. In 293 cases (63%) chronic myocardial infarction was found, 109 cases (37%) were known and 184 cases (63%) were silent myocardial necrosis, the ratio of female/male patients was nearly the same (90/94 persons). 97 patients (32%) with chronic myocardial infarction died of cardiac cause - mostly in cardiac failure -, 196 (68%) of extracardiac cause, most of them of stroke, predominantly the patients with inferior infarction. CONCLUSION: Considering the silent causes, the myocardial infarction is more frequent and has better prognosis, than it is known from epidemiological data without autopsies, because 42% of these patients dies of extracardiac diseases, and the continuity of life is not shorter, than by patients without myocardial infarction. Knowledge of silent infarction gives possibility to estimate the physical charge of patients, their treatment and to prevent recurrence.     

C-reactive protein and myocardial infarction

C-reactive protein (CRP) has been shown to predict cardiovascular disease. Whether predictions differ across risk factor strata and for short and long-term follow-up has not been clearly examined. The purpose of this report is to assess the relation between CRP and the development of myocardial infarction (MI) over a 20-year period in men in the Honolulu Heart Program. Subjects were aged 48 to 70 years and free of prevalent disease at the time when CRP levels were measured and follow-up began. Using a case-control design, 369 cases of MI were compared with 1,348 control subjects. After risk factor adjustment, the odds of an MI rose with increasing levels of CRP as early as 5 years into follow-up (P = 0.009). Associations appeared to persist beyond this time, but after 15 years, effects became modest. Adverse effects of an elevated CRP level were observed in middle-aged men (< or =55 years), in men without hypertension or diabetes, and in those who were nonsmokers (P < 0.05). Although positive effects were also observed in those who were hypertensive and smoking at the time of CRP measurement, findings suggest that in clinically healthy men, atherosclerosis could have origins more closely linked with inflammation than with other processes.     

急性心肌梗死的溶栓治疗

自从 1 979年心肌梗死溶栓治疗获得成功以来 ,各地相继开展了急性心肌梗死的溶栓治疗研究 ,不但挽救了数以百万计人口的生命 ,同时也积累了大量的临床经验。在我国溶栓治疗已日益完善 ,成为治疗急性心肌梗死的一项有效措施。1　常用溶栓药物的分类及现状1 .1　非纤维蛋白特异性溶栓剂　在激活血栓处的纤溶酶原的同时 ,也激活全身血液系统中的纤溶酶原。1 1 1　尿激酶 (UK)　可以直接激活纤溶酶原成纤溶酶 ,无抗原性 ,不产生过敏 ,近期内可重复使用 ,是当前国内应用最广的溶栓剂。一般 70kg体重者 ,用量约 1 5 0万U ,30min内输注 ,梗死…     

Cerebral infarction and myocardial infarction due to cisplatin-containing chemotherapy

A 33-year-old man was treated for a testicular non-seminoma carcinoma with three different chemotherapeutic agents: bleomycin, etoposide en cisplatin (BEP). During the second course of BEP he experienced two cerebral infarctions and a myocardial infarction at almost the same time. A CT-scan of the brain revealed a subcortical infarction in the left hemisphere. Angiography of the head and neck arteries revealed an almost completely thrombotic left carotid artery. ECG recordings showed signs of transmural ischaemia of the heart and an echocardiogram demonstrated irreversible myocardial damage. The time interval between the chemotherapy and the complications suggests a cisplatin-related cause (such adverse effects are unknown with bleomycin or etoposide). Cisplatin toxicity can give rise to serious vascular complications for which several factors appear to be responsible, such as an increased thrombogenicity and vascular spasm due to hypomagnesaemia.     

急性心肌梗死患者的护理

急性心肌梗死是指因冠状动脉供血急剧减少或中断,而使相应心肌严重而持久缺血所致心肌坏死。临床上表现为胸痛、急性循环功能障碍以及心电图反映心观急性损伤、缺血和坏死的一系列特征性演变,此病发病突然、病死率高。笔者所在科2008年1月至2008年12月收治急性心肌梗死患者48例,现将护理介绍如下。     

Cocaine-associated myocardial infarction.

Myocardial ischaemia and infarction has become a well-recognized sequelae of cocaine use. The possibility of recent cocaine use should be assessed in patients with potential myocardial ischaemia because the treatment of patients with myocardial ischaemia related to cocaine differs from that of patients with myocardial ischaemia unrelated to cocaine. Patients with cocaine-associated myocardial ischaemia should receive initial treatment with benzodiazepines to decrease central adrenergic stimulation. Aspirin should be used to reduce thrombus formation, and nitroglycerin to reverse coronary vasoconstriction. Patients with continued ischaemia can be treated with either low doses of phentolamine, or verapamil. If ischaemia continues after treatment with these agents mechanical reperfusion or thrombolytic therapy should be considered depending upon the clinical circumstances. Patients with myocardial ischaemia secondary to cocaine should not receive treatment with beta adrenergic antagonists as these agents enhance coronary vasoconstriction thereby worsening ischaemia.     

Thrombolysis for myocardial infarction

Treating myocardial infarction by dissolving occlusive thrombi in coronary arteries is an attractive idea. Although some thrombolytic agents have been available for many years their use in this role has only recently been critically examined. The place of thrombolysis in the management of myocardial infarction has yet to be determined.     

Height and mortality after myocardial infarction

A case-control analysis was conducted to determine the relationship between height and mortality among patients enrolled in the already completed Beta Blocker Heart Attack Trial (BHAT). In a basic model including height (continuous) and relevant covariates the relative risk (RR) per 4-inch reduction in height (approximately 1 standard deviation) was 1.18 (95% confidence interval, 0.92 to 1.51). When sex was considered, the effect of short stature on mortality was found to be restricted to male subjects. The male RR per 4-inch reduction in height was 1.26 (0.96 to 1.63) whereas for women it was 0.89 (0.49 to 1.59). In males not randomized to propranolol (untreated) the effect was further modified with a RR per 4-inch reduction in height of 1.41 (1.00 to 1.99). It is hypothesized that short stature could be a marker for factors operating as far back as childhood that predispose males to mortality from coronary heart disease in later life.This study was supported by research grants HL39641 and MR00096 from the National Institutes of Health. Funds for a pilot study were provided by the Henry L. Goldberg Foundation. We wish to express our gratitude to Bert Holland for computer assistance.