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Meditation allows you to clear your mind, relax, and experience emotions in a non-threatening way, which is why it is the perfect gift for someone in recovery. It is still an ideal one year of sobriety gift, as recovery requires a lifetime effort. Addiction takes a mental and physical hold on an individual, and meditation is a tool for taking back control of your life.

• Many different styles are available, so find one that fits your loved one.
• Life in sobriety opens doors for new hobbies, and trying new things is great for well-being.
• If it’s a resort that advertises a poolside bar, or a hotel that boasts about its rooftop bar, maybe opt for something else.
• Do this and you could be giving them the best possible sober gift.

They can turn to it as a reminder of the memories in recovery and the beautiful things they have in their life. Help your loved one document and reflect on their journey with a Recovery Journal. This guided journal includes space for daily gratitude, reflections on progress, and thoughts on challenges faced. As mentioned before, there is no short supply of sobriety-related items like keychains, mugs, and clothing.

Addictions

Find the one that best suits the person you are purchasing it for. There are a number of options for personalized milestones and sobriety date medallions available online. Alternatively, pay for a cleaning service to free up more time for your loved one to enjoy sober life. Buy them some new fitness equipment in line with their interests.

• Many of them know what you are going through personally and can answer any of your questions.
• A custom engraved sobriety necklace is a unique and appropriate gift to commemorate a sobriety anniversary or 1-year sober gift to give someone you care about.
• Whether it is a garden kit, a cooking kit, or something else, there are a number of online tools to help keep your loved one occupied.
• The gift could be skydiving, snowboarding or skiing, rollercoaster passes, rock climbing, cave diving, etc.

There are a number of DIY kits online that you can get for your loved one. Not only will these keep your loved one occupied they will also sobriety gifts learn a new skill and may discover a new hobby. You can even cater it to interests your loved one has as there are many options.

Sobriety Gift Ideas for Her

Lastly, a heartfelt letter expressing your admiration, support, and encouragement can be a simple yet powerful gift to acknowledge their sobriety milestone and celebrate them being on the right path. Giving gifts for sobriety is a common way to honor a friend or family member who has worked hard on their journey to recovery and substance abuse treatment. If you’ve supported a friend or family member through their journey to recovery from addiction, you are probably excited to celebrate their sobriety. While you know your loved one best, it’s better to have a list of sobriety gifts you may choose from. Finding the right gift for a sober friend or family member can be challenging.

This fact has been assessed with echocardiographic monitoring in women consuming high doses of ethanol both in the subclinical period of disease [46] as well as in the clinical period when congestive heart failure appears [95]. At the experimental level, some gender differences also are evident in functional proteomic analysis, with sex-dependent differences in structural and energy-producing myocardial proteins in a rat model of alcoholic cardiomyopathy [96]. The biological reason for this gender difference is based on different ethanol absorption rates, distribution pattern, and metabolism in women compared to men [52]. Therefore, efforts to prevent ACM development in women should be specifically addressed [97]. During pregnancy, ethanol consumption should be clearly discouraged because of the possibility of fetal alcohol syndrome or the development of other congenital heart diseases [97].

Laboratory Studies

Proteins that were increased were signal transduction proteins such as tyrosine kinase (~2.1 fold increase) and mitogen-activated protein kinase phosphatase (~17.5 fold increase) (45). The postulated mechanism includes mitochondria damage, oxidative stress injury, apoptosis, modification of actin and myosin structure, and alteration of calcium homeostasis. Studies have shown an increase in reactive oxygen species (ROS) level in myocytes following https://ecosoberhouse.com/ alcohol consumption and thus causes oxidation of lipids, proteins, and DNA leading to cardiac dysfunction. These changes are related to both direct alcohol toxicity on cardiac cells and the indirect toxicity of major alcohol metabolites such as acetaldehyde. The signs and symptoms of alcoholic cardiomyopathy (ACM) can vary depending on the severity of the condition.[6] In the early stages, people with ACM may not experience any symptoms.

• Moreover, there is a decrease in the left ventricular mass index and ejection fraction, falling below the normal range.
• Although physicians are aware of this disease, several pitfalls in the diagnosis, natural history, prognosis and treatment are still present.
• Elevated systemic blood pressure may reflect excessive intake of alcohol, but not AC per se.
• G., in medieval times, when people took advantage of the vasodilating properties of alcohol to treat angina pectoris or heart failure.
• In addition, ethanol has a widespread diffusion because of the potential for distribution though biological membranes, achieving targets not only in the membrane receptors and channels but also in endocellular particles and at the same nuclear compartment [29,99,100].
• By following this methodology, we aim to contribute to the existing body of knowledge on ACM, providing a reliable and up-to-date understanding of its pathogenesis, clinical features, diagnostic approaches, treatment options, and potential preventive strategies.
• In addition, ethanol is an immunosuppressive drug that is pro-inflammatory and pro-oncogenic [14,15,16,17].

6. Cardiac Hypertrophy and Remodeling in ACM

Investigating the mechanisms, consequences, and potential treatment options for ACM remains a very important area of research. In this section, we briefly discuss the patterns of drinking, specifically binge, as well as genetic variants in certain proteins/enzymes and variability in nutrition or dietary nutrients that may influence the occurrence of ACM. In addition, also reviewed are potential ethnic or sex difference influences. Some people only have a mild form of the condition they can control after making a few lifestyle changes. There’s increasing evidence that prolonged, strenuous exercise makes the symptoms of ACM worse. It’s important that people with or at risk of ACM discuss this in detail with their heart specialist (cardiologist).

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In the second study, Gavazzi led a multicentre study in which, from 1986 to 1995, 79 patients with ACM and 259 patients with DCM were recruited[10]. Transplant-free survival after 7 years was worse among patients with ACM than among those with DCM (41% vs 53%). Among patients who continued drinking heavily, transplant-free survival was significantly worse than in non-drinkers (27% vs 45%). Moreover, ranolazine prevents ethanol-induced atrial arrhythmias both in vitro and in vivo by blocking the late sodium current, which is activated by CaMKII.112 Its effect on preventing the decrease of LVEF in AC is currently unknown. Alcohol-induced cardiomyopathy treatment includes a combination of lifestyle modifications, pharmacological treatment, management of arrhythmia, and supportive care.

Quantity of Alcohol Intake in Cardiac Disease

In fact, mitochondrial structural changes have been described in chronic alcohol consumers, with swollen megamitochondria and the distortion of inner cristae [107,108]. Functionally high ethanol produces disruptions in the alcoholic cardiomyopathy symptoms myocyte oxidative pattern and decreases in Complex I, II, and IV of the mitochondrial respiratory chain [100,109,110]. As a reflection of this metabolic derangement, cytoplasmic lipid droplets and glycogen deposits appear.

• These investigators found that cardiac microsomal CYP2E1 activity was increased and corresponded to decreased superoxide dismutase and glutathione peroxidase activities and increased malondialdehyde levels in dogs that received alcohol (22%) in their water once per day for 6 months (30).
• The primary treatment for ACM involves complete abstinence from alcohol or other drugs.
• In a subsequent study using electron microscopy, the authors found histological features that could be superimposed onto those found in hearts that had suffered hypoxia, anoxia or ischemia[43].
• Atrial fibrillation and supraventricular tachyarrhythmias are common findings in 15–20 % of patients [111], whereas ventricular tachycardias are rare [112].
• Alcohol-induced cardiomyopathy remains a relevant health problem, for which the mainstay of treatment is alcohol abstinence.
• The signs and symptoms of alcoholic cardiomyopathy (ACM) can vary depending on the severity of the condition.[6] In the early stages, people with ACM may not experience any symptoms.

As a point of reference, consuming 80 grams of alcohol daily for at least 5 years can significantly increase the risk of ACM. If you’ve been diagnosed with an inherited type of cardiomyopathy, you may be advised to have a genetic test to identify the faulty gene (mutation) that caused this. If you have severe hypertrophic cardiomyopathy, you’ll need to see your doctor regularly so your condition can be monitored. These heart changes can cause dizziness, chest pain, shortness of breath and temporary loss of consciousness. To date, none of the ACM studies have proposed a treatment for ACM other than that recommended for DCM in current HF guidelines.

Echocardiographic and haemodynamic studies in alcoholics

Up to 42 percent of people who keep drinking alcohol after being diagnosed with alcoholic cardiomyopathy will likely die within three years.4 However, the disease may be reversible if you stop drinking alcohol. Alcoholic cardiomyopathy treatment may include medications, surgery, or a combination. In some cases, alcoholic cardiomyopathy is caused by a genetic mutation that makes your body process alcohol much slower than others.5 You can become intoxicated or damage your body with fewer drinks.

Moreover, there is a decrease in the left ventricular mass index and ejection fraction, falling below the normal range. Diastolic dysfunction, characterized by impaired left ventricular relaxation and reduced diastolic filling capacity, serves as an early indicator of ACM. Ventricular dilatation is the first echocardiographic change seen in alcohol use disorder patients, coming before diastolic dysfunction and hypertrophy.

Quebec‘s beer drinker disease

Also, current common cardiac therapies such as ICD and CRT devices were not used because of the period when the study was conducted. After a follow-up period of 47 mo, a significantly higher survival rate was observed among patients with DCM compared to patients with ACM. In this study, the only independent predictor of cardiac death was alcohol abstinence. The first study, which specifically focused on the amount of alcohol necessary to cause ACM, was conducted by Koide et al[20] in 1975. The authors examined the prevalence of cardiomegaly by means of chest x-rays and related it to alcohol consumption among a consecutive series of Japanese males of working age.

Findings from this study suggested that the presence of a moderate to high amount of dietary fat increased the production of free radicals over low-fat ethanol- containing diets. Interestingly, the amount of fat deemed high (35% of calories) is similar to the amount consumed by most Americans. Ballester specifically analysed the effects of alcohol withdrawal on the myocardium using antimyosin antibodies labelled with Indium-111[72]. This radiotracer has been acknowledged as an indicator of irreversible myocardial damage. Of the 56 patients included in the study, 28 were former drinkers and 28 continued consuming alcohol during the study.

Histologic Findings

• For tens of years, the literature has documented many clinical cases or small series of patients who have undergone a full recovery of ejection fraction and a good clinical evolution after a period of complete alcoholic abstinence.
• If your heart is severely damaged, your doctor may recommend an implantable defibrillator or pacemaker to help your heart work.
• The main symptoms are chest pain and breathlessness, similar to those of a heart attack.
• Therefore, efforts for the prevention, early detection, and specific treatment in this relevant disease should be established [45].

This activity describes the pathophysiology of ACM, its causes, presentation and the role of the interprofessional team in its management.ACM is characterized by increased left ventricular mass, dilatation of the left ventricle, and heart alcoholic cardiomyopathy symptoms failure (both systolic and diastolic). This activity examines when this condition should be considered on differential diagnosis. This activity highlights the role of the interprofessional team in caring for patients with this condition.

• In this section, we briefly discuss the patterns of drinking, specifically binge, as well as genetic variants in certain proteins/enzymes and variability in nutrition or dietary nutrients that may influence the occurrence of ACM.
• Your doctor might prescribe ACE inhibitors and beta-blockers to help lower your blood pressure.
• New strategies are addressed to decrease myocyte hypertrophy and interstitial fibrosis and try to improve myocyte regeneration, minimizing ethanol-related cardiac damage.
• Studies have shown an increase in reactive oxygen species (ROS) level in myocytes following alcohol consumption and thus causes oxidation of lipids, proteins, and DNA leading to cardiac dysfunction.
• In that study, zinc supplementation suppressed some of the ethanol-induced changes in both the metallothionein knock-out mouse model and wild-type; however, ethanol-induced mitochondrial swelling and disorganization remained in both mouse groups.

Coronary artery disease and atherosclerosis

There may be more than one cellular event happening and similar to other chronic health conditions, mechanisms maybe synergistic and inter-related. For tens of years, the literature has documented many clinical cases or small series of patients who have undergone a full recovery of ejection fraction and a good clinical evolution after a period of complete alcoholic abstinence. New therapeutic strategies for AC are being developed with the support of animal models. As the pathogenesis of AC is complex, specific treatments focus on different targets. These include damaging factors such as acetaldehyde or ROS, cardiac fibrosis, or apoptosis. Unfortunately, it is well known that abstinence is difficult to achieve, and it is important to stress that alternative treatments are needed, including therapies to help with alcohol withdrawal, heart failure drugs, and other promising therapeutic approaches that focus on pathogenesis.

• Ethanol-induced disruption of ribosomal protein synthesis also contributes to non-contractile protein depletion [104].
• Post-mortem biopsies from the hearts of human alcoholics revealed that the myocardial mitochondria is enlarged and damaged [1-9].
• Blood flow from the heart may be reduced or restricted (called obstructive hypertrophic cardiomyopathy).
• The latest two papers to be published, unlike previous papers, reported worse outcomes for ACM patients compared to DCM patients.
• In 2001 we updated the data on the ambivalent relationship between alcohol and the heart [19] and in 2008 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].
• In ACM, it is relevant to consider the treatment of the other alcohol-induced systemic damage, such as liver cirrhosis, malnutrition, and vitamin and electrolyte disturbances [2,11,52].

The Effects of Ethanol on the Heart: Alcoholic Cardiomyopathy

Therefore, because of its multiple actions, acetaldehyde may influence ACM pathogenesis in addition to ethanol effect itself [20,76,77]. The first clinical recognition of ACM was performed by Hippocrates in Greece during the 4th century B.C. However, its modern clinical report was delayed until the 19th century, where specific ACM cases were clinically described in Germany and England [1].

The findings were analysed taking into account the amount and chronicity of intake and they were compared with the same parameters measured in a control group of non-drinkers. Apoptosis may be induced by ethanol through mitochondrial membrane permeabilization and the release of pro-apoptotic factors (cytochrome c) from the mitochondrial inter-membrane space to the cytosol. Chronic ethanol exposure, in combination with https://ecosoberhouse.com/ other stress signals, provides a trigger for cardiac apoptosis through activation of the mitochondrial permeability transition pore by physiological calcium oscillations [111]. Prior studies have investigated the impact of ethanol on changes in the activity and levels of oxidative enzymes. Catalase activity is significantly increased in postmortem heart samples acquired from people who have been diagnosed with ACM.

Demakis et al[70] in 1974 divided a cohort of 57 ACM patients according to the evolution of their symptoms during follow-up. The sub-group of patients in whom symptoms improved was made up of a larger proportion of non-drinkers (73%), compared to 25% in the group who did not improve, or 17% in the group whose condition worsened. However, a possible confusion factor was identified because the group with clinical improvement also exhibited a shorter evolution of the symptoms and the disease. The suspicion that there may be an individual susceptibility to this disease is underscored by the finding that only a small group of alcoholics develop ACM, and that a proportional relationship between myocardial damage and alcohol intake has not been proven.

Individuals with certain mitochondrial deoxyribonucleic acid (DNA) mutations and angiotensin-converting enzyme (ACE) genotypes (DD genotype) may be particularly susceptible to the damaging effects of alcohol. Pharmacologic therapy should include goal-directed heart failure therapy as used in idiopathic dilated cardiomyopathy with reduced ejection fraction. This includes a combination of beta-blockers, an angiotensin-converting enzyme inhibitor, diuretics, aldosterone receptor antagonist and angiotensin blocker-neprilysin inhibitor (if LVEF is less than or equal to 40%). The use of carvedilol, trimetazidine with other conventional heart failure drugs have been proven to be beneficial in some studies. Alcoholic cardiomyopathy (ACM) is a type of heart disease that can result from chronic alcohol consumption.

3. Ethanol-induced Heart Fibrosis

Mortality in ACM is related to the progression of heart failure and malignant arrhythmias [58,65]. In long-term follow-up studies, a mortality rate of 10% of patients/year has been observed in the group of patients with persistent high-dose ethanol consumption [19,52]. Incidence of alcoholic cardiomyopathy ranges from 1-2% of all heavy alcohol users. It is estimated, approximately 21-36% of all non-ischemic cardiomyopathies are attributed to alcohol. The prevalance of alcoholic cardiomyopathy in addiction units is estimated around %.

Risk Factors of Alcoholic Cardiomyopathy

There’s usually no cure for cardiomyopathy, but the treatments can be effective at controlling symptoms and preventing complications. Some types of cardiomyopathy have specific treatments and early diagnosis is very important. It results in reduced blood flow from the heart and can lead to symptoms of heart failure, such as breathlessness, tiredness and ankle swelling, as well as heart rhythm problems. Cardiomyopathy is a general term for diseases of the heart muscle, where the walls of the heart chambers have become stretched, thickened or stiff.

For some people, a combination of factors could also lead to a weakened heart. Without an adequate supply of blood and oxygen, the body’s organs and tissues can no longer function properly. The source was identified to be the filter of choice for wine and beer, i.e., diatomaceous earth [36]. The German word for it is Kieselguhr, a beige powder made up of the skeletons of diatoms.

At clinical level, the course of ACM is similar to idiopathic dilated CMP [54]. The subject with excessive alcohol consumption, after more than 10 years of high ethanol consumption, usually develops subclinical heart functional changes before symptom appearance or signs of heart failure [55,56]. These may be detected with echosonography in around one-third of high-dose chronic consumers with preliminary evidence of subclinical left-ventricle (LV) diastolic dysfunction before progression to subclinical LV systolic dysfunction [57]. Symptomatic management in people with secondary heart failure to address any related consequences is also vital in managing ACM.

• The walls of the main heart chambers become stiff and rigid and cannot relax properly after contracting.
• The preponderance of data suggests that drinking one to two drinks in men and one drink in women will benefit the cardiovascular system over time.
• For instance, a single drink of beer is typically considered as a 12-ounce (355 ml) serving of regular beer, usually containing around 5% alcohol by volume (ABV).

Acknowledgements

• The cardiovascular system is, after the liver and gastrointestinal system, the second most affected system by global ethanol toxicity [1,33,34].
• They found that there is about 14% loss of myocardial cells in the left ventricle of those rats.
• According to recent data, a genetic form of DCM could be present in up to 50% of idiopathic DCM cases, and other specific forms of DCM such as peripartum cardiomyopathy have been shown to have a genetic basis in a significant number of cases[68].
• Others have found an increased level of fatty acid ethyl esters in the alcoholic heart, which can attach to the mitochondria and disrupt mitochondria respiratory function (32).

Physical examination findings in alcoholic cardiomyopathy (AC) are not unique compared with findings in dilated cardiomyopathy from other causes. Elevated systemic blood pressure may reflect excessive intake of alcohol, but not AC per se. Some studies have suggested that a genetic vulnerability exists to the myocardial effects of alcohol consumption.

Enhancing Healthcare Team Outcomes

Alcohol can have a toxic effect on many of your organs, such as the liver and heart. Alcoholic cardiomyopathy is diagnosed when the heart muscle and surrounding blood vessels stop functioning correctly. Men between 35 and 50 have a higher risk of developing alcohol-induced cardiomyopathy. Elevations in troponin can signify heart damage or an increase in cardiac output that results in demand ischemia. This is where the heart has an increased need for oxygen that exceeds the body’s ability to supply it.

Broken heart syndrome

This can cause various symptoms, including shortness of breath, fluid retention, and fainting. For instance, healthcare professionals can carry out a stress test or heart catheterization to rule out coronary artery disease (CAD), which is another cause of cardiomyopathy. Cardiac MRI may be helpful in the differential diagnosis to hypertrophic cardiomyopathy, storage diseases, and inflammatory cardiomyopathy. For a comprehensive overview see Table 1 (combined data from [6, 8, 24, 28]).

1. The Natural Course of ACM

We then proceeded with screening and selection based on the titles and abstracts of the initial search results. Two independent reviewers assessed each article for relevance and eligibility https://ecosoberhouse.com/ for full-text review. Once the 15 articles were selected (see Appendix Table 1 for the list of included articles), we extracted and organized relevant information from them.

Another nutritional factor classically involved in the pathophysiology of AC was cobalt excess. The ‘Quebec beer drinkers’ cardiomyopathy’ was related to cobalt supplementation to beer that was made in the past. It was described as a form of DCM with severe pericardial effusion, low cardiac output, and purplish skin coloration.

These studies were performed in experimental conditions in which there may be multiple mitochondrial deficits and therefore need to be interpreted with caution. More research is required using more contemporary measures of mitochondrial function as well as determining changes in mitochondrial DNA. Despite the key clinical importance of alcohol as a cause of DCM, relatively few studies have investigated the effects of alcohol on the heart and the clinical characteristics of DCM caused by excessive alcohol consumption (known as alcoholic cardiomyopathy). Symptoms of ACM are not specific and overlap with other forms of heart failure [30,41,58]. They appear when ventricle dilatation, hypertrophy, and dysfunction are established.

• There’s also a risk of heart valve problems, an irregular heartbeat and blood clots.
• In 1819 the Irish physician Dr. Samuel Black, who had a special interest in angina pectoris described what is probably the first commentary pertinent to the ”French Paradox“ [91].
• As the syndrome could be attributed to the toxicity of this trace element, the additive was prohibited thereafter.
• If you have severe hypertrophic cardiomyopathy, you’ll need to see your doctor regularly so your condition can be monitored.

Coronary artery disease and atherosclerosis

This review will provide an updated view of this condition, including its epidemiology, pathogenesis, diagnosis, and treatment (Graphical Abstract). Electrocardiographic findings are frequently abnormal, and these findings may be the only indication of heart disease in asymptomatic patients. A 12-month observational study of 20 patients with AC noted smaller cavity diameters, better clinical evaluation findings, and fewer hospitalizations in the 10 patients who abstained from alcohol use. Many changes can be observed including premature atrial or ventricular contractions, supraventricular tachycardias, atrioventricular blocks,  bundle branch blocks, QT prolongation, non-specific ST and T wave changes and abnormal Q waves. If the disease is caught early, stopping alcohol use completely and taking certain medications can help restore the heart’s function.

The preponderance of data suggests that drinking one to two drinks in men and one drink in women will benefit the cardiovascular system over time. Moderate drinking below that threshold might even reduce the incidence of coronary artery disease, diabetes, and heart failure. Although the severity of histological alterations on endomyocardial biopsy correlates with the alcoholic cardiomyopathy symptoms degree of heart failure in one of our studies, biopsy is not in common use for prognostic purposes [117]. Even the recovery after abstinence of alcohol is hard to predict based on morphometric evaluation of endomyocardial biopsies [118]. Interestingly, many decades ago ACM was thought to arise due to nutritional deficiency, specifically thiamine (vitamin B12).

Mathews and Kino found a small, but significant increase in left ventricular mass in individuals consuming at least 12 oz of whisky during 6 years and 60 g of ethanol per day, respectively[22,40]. More recently, Lazarevic found a modest increase in end-systolic and diastolic left ventricular volumes and a subsequent thickening of the posterior wall in a cohort of alcoholics consuming at least 80 g during 5 years[23]; however, no differences in systolic function were observed. Finally, only Urbano-Márquez et al[24] found a clear decrease in the ejection fraction, in a cohort of 52 alcoholics, which was directly proportional to the accumulated alcohol intake throughout the patients’ lives. The quantity of alcohol consumed daily and the duration of alcohol misuse are linked to the development of ACM, although the precise thresholds for causing cardiac dysfunction remain unknown.

• Data suggests patients with successful quitting of alcohol have improved overall outcomes with a reduced number of inpatient admissions and improvement in diameter size on echocardiogram.
• Patients who consume more than two drinks per day have a 1.5- to 2-fold increase in hypertension compared with persons who do not drink alcohol, and this effect is most prominent when the daily intake of alcohol exceeds five drinks.
• One of the few papers analysing genetic susceptibility in ACM was published by Fernández-Solà et al[64] in 2002.
• For comparison, the mean annual beer consumption in Bavaria is nowadays estimated to be 145 l and in the rest of Germany around 100 l beer per person and year [24].
• Clinical Review BoardAll Healthwise education is reviewed by a team that includes physicians, nurses, advanced practitioners, registered dieticians, and other healthcare professionals.

Who is At Risk of Alcoholic Cardiomyopathy?

However, no differences were found in these parameters between the sub-group of individuals who had been drinking for 5 to 14 years and the sub-group of individuals who had a drinking history of over 15 years. Kino et al[22] found increased ventricular thickness when consumption exceeded 75 mL/d (60 g) of ethanol, and the increase was higher among those subjects who consumed over 125 mL/d (100 g), without specifying the duration of consumption. In another study on this topic, Lazarević et al[23] divided a cohort of alcoholic cardiomyopathy symptoms 89 asymptomatic individuals whose consumption exceeded 80 g/d (8 standard units) into 3 groups according to the duration of their alcohol abuse. Subjects with a shorter period of alcohol abuse, from 5 to 10 years, had a significant increase in left ventricular diameter and volume compared to the control group. However, a systolic impairment was not found as the years of alcoholic abuse continued. New strategies to improve the natural course of ACM have been proposed as promising agents in this field [112,147].

Derangements in Fatty Acid Metabolism and Transport

This mechanism is also important for cell and organism survival during stress and nutrient deprivation. Under the latter conditions, autophagy via degradation of macromolecular intracellular constituents becomes important in generating and recycling carbons https://ecosoberhouse.com/ and amino acids. However, there is evidence that there is enhanced autophagy in certain cardiac pathological conditions such as heart failure, cardiomyopathy, and cardiac hypertrophy, conditions in which there are increased levels of angiotensin II (69).

Pathological Aspects of ACM

In fact, the particular effects that ethanol produces in a specific organ depend on several factors [18,19]. One is the physical characteristics of ethanol itself, with a low molecular size, high distribution capacity, and high tissue reactivity. In addition, there is a relevant role on each organ, particularly on defense and adaptive mechanisms, with a clear induction of anti-oxidant, metabolic, and anti-inflammatory protective responses as a result of ethanol aggression [18,25,26]. This multi-factorial effect is attributed to genetic factors [27] and ethnic [28] variability. The final damage is an equilibrium between the intensity of damaging effects and the possibility of defense, plasticity, regeneration, and adaptation for every specific organ [29,30,31]. Thus, alcohol-dilated cardiomyopathy (ACM) is the result of dosage and individual predisposition [32].

Mitochondria play an essential role in cellular metabolism, and disruption of their function can have profound effects on the entire cell. The myocyte mitochondria in the hearts of persons exposed to alcohol are clearly abnormal in structure, and many believe that this may be an important factor in the development of AC. To identify the causative agent of AC, investigators administered ethanol to rats pretreated with inhibitors of ethanol metabolism. Use of ethanol alone or ethanol with an alcohol dehydrogenase inhibitor resulted in a 25% decrease in protein synthesis.

5. The effects of Moderate Consumption of Ethanol and Binge-drinking

• There are no specific targeted histological or immunological biomarkers for the diagnosis of alcohol-induced cardiomyopathy.
• However, if alcoholic cardiomyopathy is caught early and the damage isn’t severe, the condition can be treated.
• In the setting of acute alcohol use or intoxication, this is called holiday heart syndrome, because the incidence is increased following weekends and during holiday seasons.
• Due to its significant toxicity, studies have avoided its direct instillation, as it produces indiscriminate cell damage even at low doses.
• Finally, we analyzed and presented the synthesized literature, along with relevant findings and conclusions from the included studies, in a coherent manner.

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. Unfortunately Lazarević et al[23], as in most of these studies, systematically excluded patients with a history of heart disease or with HF symptoms. It is therefore possible that most of these studies may have also consistently omitted most alcohol abusers in whom alcohol had already caused significant ventricular dysfunction. Cardiac remodeling is a global process that myocardium establishes as a result of different aggressions [31,132]. Heart myocytes are relatively resistant to the toxic effect of ethanol, developing a functional and structural compensatory mechanism able to minimize or repair the ethanol-induced myocyte damage [20,31,39].

• During pregnancy, ethanol consumption should be clearly discouraged because of the possibility of fetal alcohol syndrome or the development of other congenital heart diseases [97].
• Furthermore, alcohol consumption has also been classified in the literature by ranges of consumption as mild, moderate, and heavy drinking.11 In this regard, these categories have the following consumption thresholds that also differ according to sex.
• It may be caused by a surge of hormones, particularly adrenaline, during a period of stress.
• The key to diagnosis is a personal history of chronic heavy alcohol use and the absence of other etiologies.
• Acetaldehyde is a potent oxidant and, as such, increases oxidative stress, leading to the formation of oxygen radicals, with subsequent endothelial and tissue dysfunction.