Author: James Anderson

Alcohols Effects on the Cardiovascular System PMC

A greater decrease in heart rate in ethanol treated rats compared with control rats during β-adrenoreceptor blockade with propranolol indicates that the ethanol treated rats had an increased sympathetic activity. An increase in sympathetic activity is consistent with impairment of the baroreceptors that, when activated, inhibit the sympathetic nervous system[45,47]. It is important to note that, unlike other studies with more discrete alcohol consumption categories, alcohol use was nonspecifically defined in INTERHEART as the consumption of at least 1 alcoholic beverage within the previous 12 months (Leong et al. 2014). Interestingly, the strength of this association was not consistent across different geographic regions. Alcohol use was protective against CHD for subjects in most countries, except for people of South Asian ethnicity living in South Asia (India, Bangladesh, Nepal, Pakistan, and Sri Lanka).

1. Recently, Guzzo-Merello and colleagues (2015) reported that, among 282 patients with a dilated cardiomyopathy phenotype, 33 percent had ACM.
2. Cheng et al[65] have shown that angiotensin II type 1 receptor blockade prevents alcoholic cardiomyopathy in dogs.
3. Despite the progress in standardizing measurement of alcohol, studies still vary in how they define the different levels of drinking, such as low-risk or moderate and heavy drinking.
4. A recent study shows the least mortality at 100 g/week or less of alcohol, with a dose-dependent relationship between alcohol and stroke, IHD, fatal hypertensive disease, heart failure, and fatal aortic aneurysm.
5. Some research noted that endothelial function is impaired in abstinent individuals with a long-term history of alcohol abuse or alcoholism(Di Gennaro et al. 2007, 2012; Maiorano et al. 1999).

Subjects who drank wine more often, however, were less likely to have symptoms of depression and more likely to have a better perception of health status. They also had lower levels of circulating inflammatory markers, such as C-terminal proendothelin-1 and pentraxin-3 (Cosmi et al. 2015). Results from another meta-analysis of 12 cohort studies found a similar dose–response relationship between alcohol consumption and HTN for males.

It is possible that alcohol ingestion raises the blood pressure by decreasing the vasodilators such as NO in the vascular endothelium either due to inhibition of endothelial nitric oxide synthase (eNOS) or inflammatory/oxidative injury to the endothelium. Earlier studies have also shown that chronic ethanol consumption either interferes with NO production or release of NO from endothelial cells[80,85-87]. The diminished NO bioavailability may either be related to reaction with superoxide anion to form peroxynitrite radicals[88] or oxidative inactivation/uncoupling of eNOS by ethanol-induced free radicals[80,89,90]. The production of NO in the endothelium is critically dependent on the function of eNOS which is regulated by vascular endothelial growth factor[91,92]. Alcohol inhibits the enzyme that converts arginine into NO[93] as well as eNOS protein expression[80]. In the endothelium, depletion of NO production or NO reaction with superoxide anion to form toxic peroxynitrite radical which causes endothelial injury, impairment and hypertension in alcohol treated rats[20-22,62,80,94].

Other risks of alcohol use

When blood pressure decreases, these receptors help minimize how much the blood vessels stretch to increase blood pressure. Similarly, when blood pressure increases, these receptors increase the stretching of the blood vessel walls in order to decrease blood pressure. The current paper, which appears in the journal Nutrients, aimed to review all current studies dealing with the association between alcohol and blood pressure.

Data from animal models and human beings with a history of long-term drinking suggest that oxidative stress may be an early and initiating mechanism. Many cellular events, such as intrinsic myocyte dysfunction, characterized by changes in calcium homeostasis and regulation and decreased myofilament sensitivity, can come about due to oxidative stress. Some investigators have suggested that drinking wine may offer more protection against CV disease because it contains polyphenols, such as resveratrol and flavonoids, which are micronutrients with antioxidant activity (Tangney and Rasmussen 2013). However, among studies designed to examine the influence of beverage type, no differences have been found in CV disease outcomes or biologic markers, such as HDL-c (Mukamal et al. 2003a; Volcik et al. 2008).

Data from isolated papillary and heart muscle cell (myocyte) experiments demonstrate that acute physiologic intoxicating doses of alcohol (80 mg% to 250 mg%) can have a negative inotropic effect (Danziger et al. 1991; Guarnieri and Lakatta 1990). Hypertension leads to an increased risk of other health problems, including stroke, heart attack, and heart disease. One area of interest is how the consumption of alcohol impacts blood pressure.

Sympathetic nervous system in alcohol-induced hypertension

The associations between drinking and CV diseases such as hypertension, coronary heart disease, stroke, peripheral arterial disease, and cardiomyopathy have been studied extensively and are outlined in this review. Although many behavioral, genetic, and biologic variants influence the interconnection between alcohol use and CV disease, dose and pattern of alcohol consumption seem to modulate this most. Low-to-moderate alcohol use may mitigate certain mechanisms such as risk and hemostatic factors affecting atherosclerosis and inflammation, pathophysiologic processes integral to most CV disease. Both the negative and positive effects of alcohol use on particular CV conditions are presented here.

Alcohol ingestion in dogs caused sustained RAS activation with progressive increases in plasma levels of Angiotensin II, renin activity, left ventricular ACE enzyme activity, and left ventricular myocyte Ang II AT1 receptor expression[65]. Imbalance of specific endogenous vasoconstrictor such as angiotensin II, endothelin-1 and nor-epinephrine and vasodilator nitric oxide (NO) may also play an important role in alcohol-induced hypertension. Alcohol stimulates the release of endothelin 1 and 2 from vascular endothelium in a dose dependent manner[81]. Alcohol also increases the angiotensin II levels in the blood and vessels[62,63].

Increased intracellular calcium and vascular reactivity in alcohol-induced hypertension

A 2018 study showed that no amount of alcohol is considered safe, because its risks lead to a loss of healthy life. Studies have shown a link between alcohol and hypertension, or high blood pressure. Hypertension occurs when the pressure of blood against the artery walls becomes higher than normal. There is evidence that reducing alcohol intake can help lower blood pressure in those suffering from hypertension and even prevent its development. Alcohol consumption increases the amount of calcium that binds to the blood vessels. This increases the sensitivity of the blood vessels to compounds that constrict them.

Alcohol increases the risk of several other short- and long-term health issues. Alcohol prevents the body’s baroreceptors from detecting a need to stretch the blood vessels and increase their diameter, causing an increase in blood pressure. Cortisol increases the release of catecholamines, which are chemicals in the body that help regulate many processes and help keep the body functioning as it should. It has also become clear over time that no amount of alcohol is considered safe for consumption, regardless of the type of alcohol.

In most investigations, this means consuming more than 5 standard drinks on a single occasion for men and more than 4 standard drinks for women. NIAAA defines binge drinking as a pattern of drinking alcohol that brings the blood alcohol concentration to 0.08 percent or above. A typical adult consuming the defined number of standard drinks for binge drinking would reach a blood alcohol concentration of 0.08 in about 2 hours (NIAAA 2015b). Studies have shown that a reduction in alcohol intake is effective in lowering the blood pressure both in hypertensives and normotensives and may help to prevent the development of hypertension[12,41,95,96]. Heavy drinkers who cut back to moderate drinking can lower their systolic blood pressure by 2 to 4 mm of mercury (mm Hg) and their diastolic blood pressure by 1 to 2 mmHg.

One common risk factor for CV disease is the composition of the lipids found in the blood, and the effects of alcohol consumption on lipid profiles have been extensively studied. Many researchers have found that alcohol intake increases HDL cholesterol (HDL-c) levels, HDL (“good cholesterol”) particle concentration, apolipoprotein A-I, and HDL-c subfractions (Gardner et al. 2000; Muth et al. 2010; Vu et al. 2016). High triglyceride levels in the blood stream have been linked to atherosclerosis and, by extension, increased risk of CHD and stroke. However, in a recently conducted Mendelian randomization study, Vu and colleagues (2016) reported that low-to-moderate alcohol consumption reduced triglyceride and LDL-c and increased HDL-c, in particular the HDL2-c subfraction.

Physical conditioning attenuates the chronic ethanol-induced hypertension by augmenting the NO bioavailability and reducing the oxidative stress response in rats[19,79,108]. Altered platelet responses (e.g., increased platelet activation/aggregation) leads to blood-clot formation (or thrombosis) in certain CV conditions. Anticlotting therapies are therefore the cornerstone of managing acute coronary syndromes.

If you have high blood pressure, it’s important to discuss any risk factors with your healthcare provider, including alcohol consumption. This article explains the connection between alcohol and hypertension, explores the effects of different types of alcohol, and discusses safe alcohol consumption. Cortisol, plasma renin activity (causing vasoconstriction and sodium and water retention), and impaired endothelial function (inhibiting vasodilatory responses and promoting oxidative stress) have also been reported in heavy drinkers. Finally, in studies of people from certain Eastern European countries, investigators have failed to find a cardioprotective effect with any level of ethanol consumption (Britton and McKee 2000).