Alcohol and Heart

DR. MAHENDRA

CARDIOLOGY,JIPMER

Cardiomyopathy

• sarcoplasmic reticulam and swollen mitochondria, along with fragmented cristae and glycogen-filled vacuoles.

• sustained exposure to ethanol, myofibrillar degeneration and replacement fibrosis appear.

• acute or chronic consumption may adversely influence myofibrillar protein synthesis.

• Microscopically, increased accumulation of collagen in the extracellular matrix, as well as increased intermolecular cross-links.

• left ventricular diastolic and/or systolic dysfunction.

• Diastolic dysfunction, by interstitial fibrosis, is often demonstrable in heavy consumers of ethanol even in the absence of symptoms or obvious signs.

• half of asymptomatic chronic alcoholics have echocardiographicevidence of left ventricular hypertrophy

• 30% of asymptomatic chronic alcoholics have echocardiographicevidence of left ventricular systolic dysfunction.

• The likelihood of ethanol-induced dilated cardiomyopathy is

directly correlate to ethanol that is consumed in a lifetime.

• it develops have consumed more than 80 g of ethanol per day for at least 5 years.

• Women are more susceptible.

• light to moderate ethanol consumption (5 to 25 g/day) have a lower incidence of congestive heart failure than do those who do not drink at all.

• In patients with left ventricular dysfunction, light to moderate ethanol ingestion does not exacerbate heart failure.

• Pt with ischemic cardiomyopathy, light to moderate ethanol consumption reduces mortality.

• Treatment of ethanol-induced cardiomyopathy is complete abstinence or reduction .

• Although most of this improvement occurs in the first 6 months of abstinence, it often continues for as long as 2 years of observation.

• Systemic Arterial Hypertension• causal importance in up to 11% of men with hypertension

• more than two drinks daily are 1.5 to 2 times more likely to have hypertension than nondrinkers.

• This effect is dose related and most prominent when daily ethanol intake exceeds five drinks (i.e., 30 g of ethanol).

• ethanol consumption increases plasma levels of catecholamines, renin, cortisol, and aldosterone, each of which may cause systemic arterial vasoconstriction.

abstinence often normalizes systemic arterial pressure.

• Ethanol and Lipid Metabolism• inhibits the oxidation of free fatty acids by the liver, which

stimulates hepatic triglyceride synthesis and the secretion of very low-density lipoprotein cholesterol and causing hypertriglyceridemia.

• increase in total cholesterol and low-density lipoprotein (LDL) cholesterol.

• Regular ethanol consumption increases the serum concentration of high-density lipoprotein (HDL) cholesterol.

• Coronary Artery Disease

The French have a reduced incidence of coronary artery disease when

compared with people of other countries despite high smoking rates and a diet high in fat (the so-called French paradox).

Although this diminished incidence was initially attributed to the resveratrol and antioxidant and haemostatic properties of red wine, similar findings were subsequently reported with other drinks. cardioprotection is strongest with the consumption of wine.

moderate drinkers have 30% to 70% less likely than nondrinkers or heavy consumers to manifest coronary artery disease .

• The mechanisms is

• (1) an increase in the serum concentrations of HDL cholesterol, apolipoprotein A-I, and adiponectin;

• (2) inhibition of platelet aggregation;

• (3) decreased serum fibrinogen concentration;

• (4) increased antioxidant activity (from the phenolic compounds and flavonoids contained in red wine);

• (5) anti-inflammatory effects (with lower concentrations of white blood cells and C-reactive protein);

• (6) improved fibrinolysis (resulting from increased concentrations of endogenous tissue plasminogen activator and a concomitant decrease in endogenous plasminogen activator inhibitor activity);

• (7) improved insulin sensitivity

• cardio protective effect is greater for middle-aged and elderly individuals than for young adults.

• In survivors of MI, moderate ethanol consumption reduce subsequent mortality.

• an acute MI pt, those with light or moderate alcohol use have a better prognosis than do heavy drinkers or abstainers,

• even though recent ingestion does not reduce infarct size or appearance of arrhythmia or HF.

• Arrhythmias

The most common is atrial fibrillation

Causal importance in about a third of subjects with new-onset atrialfibrillation;

• Most episodes occur after binge drinking, usually on weekends or holidays— “holiday heart.”

• Acute ethanol ingestion induces diuresis, which is accompanied by the concomitant urinary loss of sodium, potassium, and magnesium.

• The presence of myocardial interstitial fibrosis, ventricular hypertrophy, cardiomyopathy, or autonomic dysfunction may also enhance the likelihood of dysrhythmias.

• concomitant factors may predispose to arrhythmias, including cigarette smoking, electrolyte disturbances, metabolic abnormalities, hypertension, and sleep apnea.

• EP studies in humans without cardiac disease has shown that ethanol enhances vulnerability to the induction of atrial flutter and fibrillation

• Treatment is abstinence.

Prolongation of the QT interval, decreased heart rate variability, diminished vagal modulation, and reduced baroreflex sensitivity have been noted.

• Sudden Death• the decrease in cardiovascular mortality is largely from a reduction in

the incidence of sudden death

• heavy ethanol consumption (i.e., six or more drinks per day) or binge drinking was associated with an increased risk for sudden death independent of the presence of coronary artery disease.

• The incidence of ethanol-induced sudden death increases with age and the amount of ethanol that is ingested.

Of the more than 21,000 men in the Physicians Health Study,those who consumed two to four or five to six drinks per week had a significantly reduced risk for sudden death (relative risks, 0.40 and 0.21, respectively) when compared with those who rarely or never drank