Alcoholic cardiomyopathy can it be reversed

A short duration of symptoms of heart failure and abstinence from alcohol are the two factors associated with favourable outcomes 4. Improvement in left ventricular function has been observed as early as six months after abstinence from alcohol, and complete recovery can be achieved in 18 months 5 , 6. In an echocardiographic study of 13 patients with alcohol-induced cardiomyopathy, five demonstrated the normalization of left ventricular function after total abstinence for six months 6.

In our patient, acute myocardial injury and cardiomyopathy improved significantly with abstinence from alcohol. Compared with previously reported cases 5 , 6 of recovery of left ventricular function with abstinence from alcohol, the present report shows the prompt recovery within one month of a patient with acute alcohol intoxication and cardiomyopathy who attained completely normal left ventricular function.

The diagnosis of alcohol-induced cardiomyopathy in our patient relied on the absence of known causes of dilated cardiomyopathy, the identification of excessive alcohol consumption and the improvement of cardiac function after the abstention from alcohol ingestion. Specifically, there was no evidence of a preceding viral infection or presence of another toxin. The distinction between alcohol-induced cardiomyopathy and dilated cardiomyopathy due to other causes eg, idiopathic or viral may be difficult.

Patients with dilated cardiomyopathy are apt to have history of some ethanol consumption, and the histological changes of both diseases are nonspecific. Teragaki et al 6 studied the clinical and histological findings of patients with cardiomyopathy and significant alcohol consumption compared with patients with cardiomyopathy and no alcohol intake. Histologically, myocyte fibrosis and nuclear changes were found to be less significant, while the potential for clinical reversibility of left ventricular dysfunction was greater in patients whose alcohol abuse was associated with cardiomyopathy.

The exact mechanism of alcoholic cardiomyopathy is unknown. Electron microscopic studies 7 , 8 of biopsies from patients with alcohol-induced cardiomyopathy have shown evidence of damage to the myofibres, including separation of filaments and loss of striation. In animal studies, loss of contractile proteins and defects in myocardial protein synthesis may partly explain the altered contractility.

Various studies have shown that alcohol exerts a negative inotropic effect on the myocardium. It is possible that changes in calcium hemostasis may contribute toward this phenomenon, because this divalent cation plays an integral part in transmembrane ion movement and muscle contraction 9.

Some have also suggested that lipid peroxidation may play a role in the pathogenesis of alcoholic cardiomyopathy In conditions of acute alcohol toxicity, ethanol has been shown to increase circulating catecholamine, which may play a role in myocardial damage.

Thiamine deficiency beriberi is a nutritional factor that may be associated with heart muscle diseases, particularly in alcoholics. However, it is now widely accepted that thiamine deficiency is a contributory factor in only a small proportion of alcohol abusers.

Other agents, such as cobalt previously used as a foaming agent in beer can cause cardiotoxicity in heavy drinkers. In general, nutritional deficiencies have been dismissed in the pathogenesis of alcohol-induced cardiomyopathy 9.

Excess acute alcohol intoxication causes troponin release. Earlier studies by Puszkin and Rubin 10 were the first to suggest that alcohol had effects on the regulatory proteins, troponins or tropomyosins. They found that high concentrations of alcohol mmol to mmol administered acutely inhibited calcium binding to troponin-tropomyosin protein complexes in vitro.

Also, acute alcohol administration in a rat model significantly raised plasma cardiac troponin T level after 2.

In our patient, the elevated troponin T is suggestive of acute myocardial damage. However, the falling level of troponin T in hospital suggested that the myocardial damage had occurred before admission. In the absence of other causes, this was likely due to alcohol toxicity. The association between alcohol-induced cardiomyopathy and myocarditis is controversial.

In one six-patient study 12 focusing on alcoholic cardiomyopathy, the surprising histological findings on endomyocardial biopsy of two patients was found to be myocarditis with lymphocytic infiltration in association with myocyte degeneration or focal necrosis. However, no other biopsy study of patients with presumed alcohol-induced cardiomyopathy has found this.

It is likely that those two patients were incorrectly labelled with alcohol-induced cardiomyopathy. In the absence of myocardial biopsy, the diagnosis of myocarditis is always questionable. In our patient, myocardial biopsy was contemplated, but given the rapid recovery of ventricular function, its diagnostic limitations and the absence of its clinical implications, the risk of this procedure outweighed its benefits, and thus, it was not performed.

However, given the characteristic rise and fall of cardiac enzyme levels, this supports the diagnosis of acute alcohol-induced myocardial damage.

One interesting aspect of the present case is that although the patient had been a heavy user of alcohol for many years, there had been no previous evidence of cardiomyopathy. It was only after the recent significant increase in alcohol intake that the myocardial dysfunction became apparent. Both atrial fibrillation and ventricular tachycardia are forms of arrhythmias in common with alcohol abuse. Alcohol-Related Strokes — A more serious concern is the risk of strokes with alcohol abuse.

Binge drinking and chronic alcohol consumption for months or even a few short years can increase the risk of ischemic strokes and hemorrhagic strokes. Alcohol-induced strokes can occur in otherwise healthy patients and without existing coronary artery disease. Alcoholic Hypertension — Binge drinkers and chronic drinkers know all too well the fact that heavy alcohol use raises blood pressure — sometimes raising it to dangerous levels. Alcohol causes your arteries and veins to stiffen, instead of flexing to the beat of the heart.

Worsening the problem, continued alcohol abuse can cause the blood vessels to constrict within the already shrinking arteries and veins. Hypertension is an early sign of the increased risk of stroke and heart disease. Alcoholic Cardiomyopathy is the most serious concerns of the effects of alcohol on the heart. Alcoholic cardiomyopathy is a progressive disease, meaning that it worsens over time — especially with continued alcohol use.

It is good to note first that just because you have one or more of these symptoms, it does not mean that you immediately have heart failure. Moderate drinking can reduce the incidence and mortality of coronary artery disease, heart failure, diabetes, ischemic and hemorrhagic stroke.

More than this amount can lead to alcoholic cardiomyopathy, which is defined as alcohol toxicity to the heart muscle itself by ethanol and its metabolites. Chronic heavy alcohol abuse will also increase blood pressure and cause a downregulation of the immune system that could lead to increased susceptibility to infections, which in turn could add to the development of heart failure.

Myocardial tissue analysis resembles idiopathic cardiomyopathy or chronic myocarditis. In the diagnostic work-up of alcoholic cardiomyopathy, the confirmation of alcohol abuse by carbohydrate deficient transferrin CDT and increased liver enzymes, and the involvement of the heart by markers of heart failure e.

Treatment of alcoholic cardiomyopathy consists of alcohol abstinence and heart failure medication. Histologisch ist die alkoholische nicht von der idiopathischen Kardiomyopathie und einer chronischen Myokarditis zu unterscheiden. According to the definition of the World Health Organization WHO , alcoholism is subgrouped in two categories: alcohol abuse and alcohol dependence [ 1 ]. This corresponds roughly with the concept of the American Psychiatric Association [ 2 , 3 ].

Alcohol abuse describes the psychological dependence on ethanol for adequate functioning together with occasional heavy consumption, while alcohol dependence is defined as an increased alcohol tolerance together with physical symptoms upon withdrawal. The highest prevalence is detected in the third to fifth decade of life, and alcoholism is seen in all races, ethnic groups, and socioeconomic strata. Germany with a total population of 81 million inhabitants is a permissive society with respect to the drinking of alcohol.

Alcohol consumption is part of the local culture. About 40 million individuals drink alcohol. The per capita alcohol consumption of 9. More than 1. For an additional 1. In a world-wide setting, alcohol use disorders show similarities in developed countries, where alcohol is cheap and readily available [ 8 ]. The many complications of alcohol use and abuse are both mental and physical—in particular, gastrointestinal [ 9 ], neurological [ 10 , 11 ], and cardiological [ 12 , 13 ].

The relationship of alcohol with heart disease or dementia is complicated by the fact that moderate alcohol consumption was shown not only to be detrimental but to a certain degree also protective against cardiovascular disease [ 14 ] or to cognitive function in predementia.

We reviewed the effects of ethanol on the cardiovascular system in [ 15 ], including aspects of inflammation [ 16 ], rhythm disturbances [ 17 ], and hypertension [ 18 ]. In we updated the data on the ambivalent relationship between alcohol and the heart [ 19 ] and in added new evidence on a larger cohort of patients with different forms of cardiomyopathy and increased alcohol intake from the German competence network on heart failure [ 20 ].

This review revisits our past and deals with our current thinking on the epidemiology, pathophysiology, clinical characteristics, and treatments available for alcoholic cardiomyopathy.

This review assembles and selects pertinent literature on the ambivalent relationship of ethanol and the cardiovascular system, including guidelines, meta-analyses, Cochrane reviews, original contributions, and data from the Marburg Cardiomyopathy registry. Drinks as measures of alcohol are often given in ounces oz , whereby 1 oz equals Distilled spirits: 1.

For more than years, alcoholic beverages have been consumed in multiple societies through the centuries and cultures. The name alcohol is much younger than the many beverages containing it. Pulverized antimony was used as eye shadow by Egyptian women and named al-Kol. In the 16th century Paracelsus Theophrastus Bombastus from Hohenheim used this term for distilled liquor and called it alcohol [ 15 ].

The beneficial cardiovascular effects of alcohol have been appreciated, e. So Hildegard von Bingen — , one of the most prominent mysticians of her time, recommended her heart wine as a universal remedy.

One liter of wine was cooked for 4 min with 10 fresh parsley stems, 1 spoon of vinegar, and g honey and then filtered [ 11 ]. This recipe is still in use today. As early as , Wood incriminated alcohol as a cause of heart failure. In , Friedrich reported idiopathic hypertrophy as associated with alcoholism. In , Walshe described myocardial cirrhosis in alcoholics, which includes a spectrum of hepatic derangements that occur in the setting of right-sided heart failure.

Conversely cirrhosis fibrosis was found both in heart and liver. High cardiac output in patients with liver cirrhosis may have contributed to this cardiomyopathy in a vicious circle.

Myofibers show partly hypertrophy and atrophy. Fibrosis is present as reparative interstitial and perivascular fibrosis. With kind permission from H. Frenzel and B. Schwartzkopff [ 22 ]. In Munich, the annual consumption of beer reached l per capita and year in the last quarter of the 19th century. In , the pathologist and veterinarian Otto von Bollinger Fig. For comparison, the mean annual beer consumption in Bavaria is nowadays estimated to be l and in the rest of Germany around l beer per person and year [ 24 ].

In , Maguire reported on 2 patients with severe alcohol consumption who benefitted from abstinence. He suggested that alcohol was poisoning the heart. In , Graham Steell, well known for the Graham Steell murmur due to pulmonary regurgitation in pulmonary hypertension or in mitral stenosis, reported 25 cases in whom he recognized alcoholism as one of the causes of muscle failure of the heart. In his review article, Bridgen was the first to introduce the term alcoholic cardiomyopathy [ 27 ].

Thus, the concept of beriberi heart disease dominated thinking about alcohol and the heart for decades and caused many to doubt that alcohol was actually cardiotoxic [ 28 ]. But vitamin B1 thiamine deficiency is accompanied by an elevated cardiac output and diminished peripheral vascular resistance [ 29 , 30 ].

In contrast, alcoholic cardiomyopathy is characterized by a low cardiac output, associated with systemic vasoconstriction [ 4 ]. However, the high output state can lead to cardiac dilation, thus, representing a characteristic subentity of cardiomyopathy different from low output dilated cardiomyopathy. Therefore, thiamine deficiency per se is just a historical nutritional anomaly in the history of alcoholic cardiomyopathy. In , the Manchester arsenic-in-beer epidemic was a serious food poisoning outbreak affecting several thousand people across the North-West and Midlands of England, with many cases proving fatal.

The arsenic had come from the glucose for which sulphuric acid was used in the sugar production process of a company in Leeds. Brewers had been using this sugar, thus, unknowingly poisoning the beer and as a result their customers for many years even prior to the epidemic [ 33 ]. Arsenic poising caused a multisystem disease in over cases with more than 70 deaths [ 34 ]. The syndrome included the usual signs and symptoms of arsenic poisoning, with skin, nervous system, and gastrointestinal manifestations.

Unusual in arsenic poisoning, but especially prominent in this epidemic, were the cardiovascular findings. This outbreak had been the first known trace metal cardiotoxic syndrome.

In , the issue of arsenic in beer and wine was again prominent, when Mehmet Coelhan, a researcher at the Weihenstephan research center at the Technical University of Munich, reported at a meeting of the American Chemical Society that many of the nearly beers tested in Germany had trace amounts of arsenic. The source was identified to be the filter of choice for wine and beer, i.

The German word for it is Kieselguhr, a beige powder made up of the skeletons of diatoms. The trace amounts of arsenic have not been comparable to the arsenic-in-beer endemic in Manchester but may still reach up to times the amount admitted for arsenic in drinking water in the European Union and the US.

In the mids, another unexpected heart failure epidemic among chronic, heavy beer drinkers occurred in two cities in the USA, in Quebec, Canada, and in Belgium. It was characterized by congestive heart failure, pericardial effusion, and an elevated hemoglobin concentration.

The explanation proved to be the addition of small amounts of cobalt chloride. Cobalt was used as a foam stabilizer by certain breweries in Canada and in the USA. In McDermott et al. Human pathology was first described by Bonefant et al. Animal models investigated ultrastructure [ 41 ] and treatment e. Removal of the cobalt additive ended the epidemic in all locations.

Cobalt poisoning and alcohol together acted synergistically in these patients. As the syndrome could be attributed to the toxicity of this trace element, the additive was prohibited thereafter. Not alcohol but cobalt itself recently caused severe heart failure in a year-old man, who was referred to the university hospital in Marburg to rule out coronary artery disease as the cause of his heart failure.

He had become almost deaf and blind, with fever of unknown cause, hypothyroidism, and enlarged lymph nodes. Both his hips had been replaced, the left side by a CoCrMo Protasul metal prosthesis. Remembering a similar case in an episode of the TV series Dr. House , the team of J.

One should note, however, that cobalt is needed in minute amounts of 0. The heart and liver interact in several different ways. Acute or chronic right heart failure leads to elevation of liver enzymes most likely due to liver congestion, whereas cirrhosis due to cardiac disease is infrequent. Chronic liver disease such as cirrhosis may in turn affect the heart and the whole cardiovascular system, leading to a syndrome named cirrhotic cardiomyopathy CCM.

Thus, CCM has been introduced as an new entity separate of the cirrhosis etiology. Increased cardiac output due to hyperdynamic circulation, left ventricular dysfunction systolic and diastolic , and certain electrophysiological abnormal findings are pathophysiological features of the disease. In pathophysiological terms, heart failure in liver cirrhosis belongs to the hyperdynamic cardiomyopathies. As early as in , Lian [ 45 ] reported in middle-aged French servicemen during the first world war that heavy drinking could lead to hypertension.

It took almost 60 years before further attention was paid to the complex interaction between the heart and the peripheral vasculature in various cross-sectional and prospective epidemiologic studies, which have empirically confirmed this early report.

One is aware today that alcohol may cause an acute but transient vasodilation, which may lead to an initial fall in blood pressure probably mediated by the atrial natriuretic peptide ANP [ 46 ].

But also short- and long-term pressor effects mediated by the renin—aldosterone system and plasma vasopressin have been described [ 47 , 48 ].

The long-term hypertensive effect of alcohol has been confirmed in many studies [ 49 — 52 ]. Remarkably, alcohol also interacts with brain stem receptors and exerts thereby central hypertensive effects [ 18 ]. There seems to be independence from adiposity, salt intake, education, smoking, beverage type wine, liquor, or beer , and several other potential confounders. Clinical observation confirmed that several days to weeks of drinking show higher and weeks of abstinence lower pressures.

Alcohol intake may also interfere with the drug and dietary treatment of hypertension. This altogether supports a causal relationship between alcohol consumption and a hypertensive state.

The landmark report of Urbano-Marquez et al. Further evidence came from data on acute alcohol effects [ 54 ] and from clinical observation [ 55 — 57 ]. After consumption of large quantities of alcohol over years the clinical picture of heavy alcohol drinkers could be indistinguishable from other forms of dilated or familial cardiomyopathy.

Alcohol is still suspected to be the major cause or contributory factor of secondary nonischemic dilated cardiomyopathy being involved in up to one third of all cases of dilated cardiomyopathy [ 59 — 61 ].

In alcoholic cardiomyopathy, dilation and impaired contraction of the left or both ventricles is observed [ 4 ]. Thus, the diagnosis of alcoholic cardiomyopathy is still based on the coincidence of heavy alcohol consumption and a global myocardial dysfunction, which cannot be explained by any other underlying myocardial disease [ 64 ]. However, the prevalence of alcoholic cardiomyopathy may be underestimated, as autopsy findings reveal pathologic changes of the heart in individuals with no clinical symptoms [ 65 ], when analyzing in large cross-sectional studies.

Further evidence suggests that not only ethanol but also the first metabolite acetaldehyde may directly interfere with cardiac and skeletal muscle homeostasis [ 53 , 66 ].

In vitro studies have further elucidated the direct effect of ethanol on electromechanical coupling, indicating a decrease in myofilament—calcium sensitivity during alcohol consumption, changes in the transmembrane action potential, the amplitude of the cytosolic calcium transients, and the shortening of the action potential duration [ 67 — 71 ].

Isolated cardiomyocytes of alcohol-fed rats did not maintain ATP levels upon energy demand due to an inadequate increase in mitochondrial ATP-synthase activity, which led altogether to further myocyte loss [ 72 , 73 ]. Ultrastructural disarray of the contractile apparatus [ 74 ] is associated with a depressed myofibrillar and sarcoplasmic protein synthesis in cardiac muscle after ethanol exposure [ 75 — 77 ].

This reduces contractile cardiac filaments with subsequent negative inotropic effects on heart contractility [ 78 , 79 ]. An apoptotic effect of ethanol on cardiac muscle has also been described, which could be counteracted by insulin-like growth factor IGF -I [ 80 ] and confirmed in later studies [ 81 , 82 ].

In a study in rats that were fed with two different doses of alcohol 5 mM [low alcohol], mM [high alcohol] or in pair-fed nonalcohol controls for 4—5 months , caspase-3 activity as putative marker of apoptosis was decreased in the low alcohol diet, which went along with increased or normal contractility, whereas high doses of ethanol showed increased caspase activity, wall thinning, and a reduction of shortening velocity [ 83 ].

Of note, rats are a relatively alcohol resistant species. Alcohol abuse coinciding with myocarditis was reported in by McKenzie [ 26 ]. Perivascular increase of leukocytes and fibrosis, myocytes in variable sizes with some myocytolysis.

Indirect immunofluorescent test. This may have to do with the susceptibility for infections due to a suppressed immune system in a compromised human host and also in experimental animal [ 85 ].

Ethanol can alter lymphocyte functions, inhibit neutrophil chemotaxis, and suppress the production of cytokines, which are involved in regulating acute inflammatory responses to infectious challenges [ 86 — 88 ]. Furthermore, autoimmunity and circulating autoantibodies seem to be associated in some patients with chronic alcohol consumption [ 16 , 20 , 84 ].

The beneficial heart wine as universal remedy in medieval ages by Hildegard von Bingen [ 11 ] found its later correlates in many observations at the beginning of modern medicine when coronary artery disease CAD and its risk factors and symptoms received more attention. This observation led to the erroneous belief that alcohol is an immediate coronary vasodilator. Alcohol is not a direct coronary vasodilator [ 90 ]. Symptomatic relief of angina could be through the anesthetic effect of ethanol or through peripheral vasodilation, which could transiently reduce oxygen demand of the heart.

In the Irish physician Dr. This refers to the finding in the last century that moderate alcohol consumption could be the reason for the relatively low cardiovascular disease incidence in wine-drinking regions [ 92 ]. Renaud and de Lorgeril [ 93 ] suggested that the inhibition of platelet reactivity by wine may be one explanation for protection from CAD in France. However, there was further evidence on this and other dietary mechanisms with the observation that France and Finland have similar intakes of cholesterol and saturated fat, but consumption of vegetables and vegetable oil containing monounsaturated and polyunsaturated fatty acids is greater in France than in Finland.

This inverse relation on mortality resembles in most population based studies a U- or J-shaped curve: Total abstinence has a slightly increased mortality when compared to low or moderate alcohol consumption. It is present in individuals with and without overt CAD, with diabetes, and with hypertension and has been underlined by a large number of studies [ 94 , 95 ]. The cardioprotective effect of alcohol can be attributed to the increase in total high-density lipoproteins HDL , and especially by an increase in subfractions HDL2 and HDL3, whereas established cardiovascular risk factors like low-density lipoproteins LDL or lipoprotein a are thought to be moderately decreased [ 96 ].

Moderate alcohol intake also exerts beneficial effects on the blood coagulation system. It leads to an increase of endogenous plasminogen activators [ 97 ], or a decrease in fibrinogen concentrations [ 98 ]. In the Caerphilly prospective heart disease study, platelet aggregation induced by adenosine diphosphate was also inhibited in subjects who drank alcohol [ 99 ]. Assessing differences between various forms of alcoholic beverages it should be noted that resveratrol leads in vitro to platelet inhibition in a dose-dependent manner [ ] and has shown effects on all-cause mortality in a community-based study [ ].

Polyphenols of red barrique wines and flavonoids have been shown to inhibit endothelin-1 synthase [ ] and PDGF-induced vasoproliferation thus also contributing to cardiovascular protection [ ]. As a net effect, negative inotropism may result and contribute to heart failure. Acute effects of alcohol can result in rhythm disturbances.