Alcohol and Acute Myocardial Infarction

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1 The Journal of International Medical Research 2007; 35: Alcohol and Acute Myocardial Infarction I BIYIK 1 AND O ERGENE 2 1 Department of Cardiology, Uşak State Hospital, Uşak, Turkey; 2 Department of Cardiology, Atatürk Education and Training Hospital, Izmir, Turkey A number of studies from different countries and several large-scale metaanalyses have reported reduced coronary heart disease rates among those regularly consuming mild to moderate amounts of alcohol compared with those abstaining from alcohol. In contrast, various studies have also reported that heavy alcohol consumption promotes the progression of atherosclerosis and that binge drinking might trigger embolic stroke and acute myocardial infarction. We discuss the association between alcohol consumption and acute myocardial infarction on the basis of evidence from literature published recently. Alcohol consumption has both favourable and unfavourable effects on metabolism, lipid profile, blood coagulation and fibrinolysis, blood pressure and vascular tone depending on the amount of alcohol consumed and the way that it is drunk (i.e. drinking habits). We conclude that it is extremely important to warn people of the risks associated with binge drinking and to encourage them to remain within the recommended safe limits for alcohol consumption. KEY WORDS: ALCOHOL; ACUTE MYOCARDIAL INFARCTION; BINGE DRINKING; COAGULATION; FIBRINOLYSIS Introduction There have been suggestions that mild regular alcohol consumption is associated with a reduced risk of coronary heart disease. 1 Many studies have shown that regular light to moderate alcohol intake protects against ischaemic heart disease. 2,3 Several studies have also indicated that moderate alcohol intake protects against ischaemic stroke of atherothrombotic origin and peripheral arterial disease. 4,5 Furthermore, some epidemiological studies have suggested that moderate alcohol consumption is associated with a decreased risk of the development of coronary artery disease, angina pectoris and acute myocardial infarction (AMI). 6,7 In contrast, other studies have reported that heavy alcohol consumption promotes the progression of atherosclerosis in the carotid arteries and that binge drinking might trigger an embolic stroke and AMI In this review we discuss the association between alcohol consumption and AMI. The amount of alcohol consumed, the duration of drinking, and drinking habits may all play a substantial role in the development of AMI. 46

2 Drinking habits In contrast to mild and moderate alcohol consumption, heavy drinking has been shown to increase mortality from all causes, including cardiovascular events. 11 A pattern of drinking known as binge drinking was demonstrated in two studies from Finland and Austria to be strongly associated with fatal myocardial infarctions (MI). 9,12 In a Finnish study, Kauhanen et al. 9 reported that the risk of death from fatal MI was more than six times greater in men who consumed six or more beers per session than in those who drank less than three beers. The results of McElduff and Dobson 12 revealed an odds risk ratio of 2.62 for a major coronary event in men who consumed nine or more drinks daily for 1 or 2 days per week compared with men who consumed the same amount of alcohol spread over the entire week. Blood coagulation Coagulation and fibrinolysis are important determinants of AMI. A significant reduction in fibrinolysis has been shown after heavy alcohol ingestion. 13 Van de Wiel et al. 13 showed an increased level of plasminogen activator inhibitor-1 (PAI-1) antigen and PAI-1 activity and a decreased tissue plasminogen activator (t-pa) activity after heavy alcohol intake. A large alcohol intake in the evening might cause acute inhibition of fibrinolysis that persists to the next morning. 13 Such inhibition may play a critical role in the pathogenesis of MI that occurs after binge drinking. In healthy subjects, the circadian rhythm of fibrinolysis shows enhanced activity in the evening and its lowest activity in the morning. 13 After binge drinking a large quantity of alcohol, ongoing inhibition of fibrinolysis might be superimposed on the physiological morning dip, thus prolonging this unfavourable state. 13 Data obtained from this study revealed that the threshold for significant inhibition of fibrinolysis was between two and four glasses of wine, which is the equivalent to g of alcohol. 13 Consumption of two glasses of wine did not interfere with the normal circadian rhythm of fibrinolysis. 13 In the case of very high alcohol consumption (eight glasses of wine in an evening) inhibition of fibrinolysis might persist until the next morning. 13 This effect has also been shown for both beer and spirits, 14 suggesting that it is the ethanol component of alcoholic beverages that might be the cause of this effect on fibrinolysis. The inhibition of fibrinolysis after repeated doses of large amounts of alcohol contributes to the development and progression of atherosclerosis and increased risk of AMI. What are the mechanisms of this effect? Impaired fibrinolysis facilitates the formation of fibrin deposits on an injured or dysfunctional intima and causes fibrin incorporation into the intima, leading to plaque growth. Increased PAI-1 binds more fibrin components and protects them against t-pa-mediated endogenous thrombolysis. 15 Reduced t-pa activity also facilitates coronary thrombosis and occlusion. Alcohol consumption may lead to an increase in clotting factor VII, which may trigger activation of the extrinsic pathway of coagulation and fibrin formation. 16 Platelet functions The role of platelet aggregation and adhesion in the pathogenesis of coronary occlusion within the context of AMI is well known. It has been reported that resistance to thrombolysis is associated with plateletrich coronary thrombi. 17 Inhibition of platelet function is of critical importance in the treatment of AMI. Serebruany et al. 18 showed a relationship between moderate 47

3 alcohol consumption and decreased platelet activity in patients presenting with AMI. In their study, the platelets morphological (flow cytometry), physiological (aggregometry) and release functions (estimated using enzyme-linked immunosorbent assay) were lower in patients consuming moderate levels of alcohol. In contrast, Numminen et al. 19 suggested that a relatively large intake of alcohol transiently increases thromboxane-mediated platelet activation. Furthermore, acute ingestion of a large quantity of alcohol causes tachycardia and increases blood flow. 19 Although these effects are transient and dose-dependent, they might lead to platelet activation because of increased shear. Drinking time and beverage type Some recent reports have suggested that moderate wine drinking was associated with a reduced risk of cardiovascular disease complications in middle-aged male survivors of a recent AMI. 20 In a meta-analysis conducted on more than subjects, an inverse association was shown between wine drinking and vascular diseases. 21 However, drinking habits might also play a very important role in such an association. In an Italian study, Augustin et al. 22 reported that regular alcohol intake during meals was inversely related to the risk of AMI, whereas alcohol intake during and outside mealtimes or only outside mealtimes was not related to the risk. In this study, there was no difference among types of alcoholic beverage consumed. These results might be related to the metabolic effects of alcohol consumption. Alcohol induces an increase in the highdensity lipoprotein cholesterol level, reductions in low-density lipoprotein and lipoprotein (a) levels and a decrease in insulin resistance. 13,23 Alcohol has hypoglycaemic and hypoinsulinaemic effects when ingested with foods; wine has been shown to reduce the glycaemic response to high-glycaemic-index foods by approximately 35%. 22 High levels of glucose and insulin are known risk factors for coronary artery disease, and regular consumption of moderate amounts of alcohol has been associated with a reduced risk of diabetes, reduced fasting insulin, improved glucose levels and improved insulin sensitivity The amount of alcohol consumed is important in providing these favourable responses. Alcohol intake outside of meals results in faster absorption of ethanol, which might cause a detrimental increase in blood pressure. 26 In contrast, consumption of 250 ml of red wine with a meal at noon may reduce blood pressure in centrally obese hypertensive patients; 27 and binge drinking leads to the loss of the protective effect induced by regular moderate alcohol intake and may pose an increased risk of AMI and cardiovascular death. 28 Acute ethanol intoxication and AMI? Coronary vasospasm induced by acute ethanol intoxication, a prothrombotic state and endothelial damage may be some of the mechanisms responsible for causing AMI. Although we do not know the mechanism by which alcohol causes coronary vasospasm, this effect may last for approximately 9 h after binge drinking a large amount of alcohol when plasma alcohol levels have already returned to baseline. It has also been reported that a reduction in plasma prostaglandin F 1α and cyclic guanosine monophosphate levels resulting from acute alcohol intoxication may contribute to this effect

4 TABLE 1: Effects of alcohol consumption on clinical outcomes, atherosclerosis progression and blood coagulation parameters Binge drinking large Regular light-to-moderate amounts of alcohol alcohol consumption Morbidity and mortality Increase Decrease Major coronary event Increase Decrease Atherosclerosis progression Increase Decrease Fibrinolysis Decrease Increase Platelet activity Increase Decrease Vascular tone Increase Decrease In some societies alcohol consumption has become an important part of the social aspect of many sporting activities, and it is common among sports participants and athletes to consume alcohol soon after competing and/or training. 30 After physical exercise, consumption of a large amount of alcohol may trigger an AMI even in very young patients with normal coronary arteries. 31 El-Sayed et al. 32 have suggested that alcohol intake after heavy physical exercise, which is a known trigger of AMI, may further perturb blood haemostasis in favour of thrombosis and constitute an additional coronary thrombotic risk. Conclusions Although light-to-moderate alcohol consumption has some protective and possibly favourable effects, a U-shaped association appears to exist between the degree of alcohol intake and the risk of AMI. Thus, heavy alcohol consumption may be associated with increased cardiac morbidity and mortality rates (Table 1). 12,18,33 Since alcohol consumption and concomitant smoking are very common in the general population, informing people about the effect that binge drinking a large amount of alcohol and smoking has on triggering AMI may help to decrease the incidence of this life-threatening acute coronary event. Although more data are needed to support the acute detrimental effects of alcohol intake on triggering AMI, it appears to be vitally important to encourage people to remain within the safe limits of alcohol consumption. These limits are g of alcohol for men and g of alcohol for women per day, as recommended by the Second Joint Task Force of European and other Societies on Coronary Prevention. 34 However, making any recommendation on alcohol consumption is very difficult and considerable caution must be exercised in relation to acceptable limits of alcohol consumption. 33,35 Conflicts of interest No conflicts of interest were declared in relation to this article. Received for publication 23 May 2006 Accepted subject to revision 26 May 2006 Revised accepted 2 October 2006 Copyright 2007 Cambridge Medical Publications 49

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The effects of different alcoholic drinks on lipids, insulin and haemostatic and inflammatory markers in older men

2003 Schattauer GmbH, Stuttgart Blood Coagulation, Fibrinolysis and Cellular Haemostasis The effects of different alcoholic drinks on lipids, insulin and haemostatic and inflammatory markers in older men