The individual amount of alcohol consumed acutely or chronically decides on harm or benefit to a person's health. Available data suggest that one to two drinks in men and one drink in women will benefit the cardiovascular system over time, one drink being 17.6 ml 100 % alcohol. 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. Historical examples of interest are the Munich beer heart and the Tubingen wine heart. Associated with chronic alcohol abuse but having different etiologies are beriberi heart disease (vitamin B1 deficiency) and cardiac cirrhosis as hyperdynamic cardiomyopathies, arsenic poising in the Manchester beer epidemic, and cobalt intoxication in Quebec beer drinker's disease. 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.g., NT-proBNP) and of necrosis (e.g., troponins or CKMb) is mandatory. Treatment of alcoholic cardiomyopathy consists of alcohol abstinence and heart failure medication.

/pdf/alcoholic-cardiomyopathy-the-result-of-dosage-and-individual-41it83zrdx.pdf

Alcoholic cardiomyopathy : The result of dosage and individual predisposition.

ardiomyopathies are diseasesof the heart muscle that renderthe heart unable to properlypump enough blood to the body. In thedilated form of cardiomyopathy(called dilated cardiomyopathy orDCM), the heart is enlarged (Figure 1).As the heart enlarges, it becomes lesseffective in pumping blood, whichthen leads to symptoms of heart failureand irregular heart rhythms (arrhyth-mias). It is estimated that approxi-mately 1 out of every 2500 persons hasDCM, although the disease is probablyeven more common. DCM affects bothmen and women and can affect bothadults and children. As with othertypes of cardiomyopathies, DCM is achronic disease without a known cure.However, the treatments currentlyavailable can significantly improve itscourse.

https://heart.bmj.com/content/heartjnl/72/6_Suppl/S35.full.pdf

Familial dilated cardiomyopathy

A Comprehensive Review on Breast Cancer Detection, Classification and Segmentation Using Deep Learning

https://www.internationaljournalofcardiology.com/article/S0167-5273(97)00332-X/pdf

Monocyte activation in congestive heart failure due to coronary artery disease and idiopathic dilated cardiomyopathy

Viral infection of the heart is relatively common, usually asymptomatic and has a spontaneous and complete resolution. It can, however, in rare cases, lead to substantial cardiac damage, development of viral cardiomyopathy and congestive heart failure. Viral cardiomyopathy is defined as viral persistence in a dilated heart. It may be accompanied by myocardial inflammation and then termed inflammatory viral cardiomyopathy (or viral myocarditis with cardiomegaly). If no inflammation is observed in the biopsy of a dilated heart (<14 lymphocytes and macrophages/mm ) the term viral cardiomyopathy or viral persistence in dilated cardiomyopathy should be applied. The diagnosis of myocarditis and viral cardiomyopathy can be made only by endomyocardial biopsy, implementing the WHO/WHF criteria, and PCR techniques for identification of viral genome. The most frequent cardiotropic viruses detected by endomyocardial biopsy are Parvo B19, enteroviruses, adenoviruses, cytomegalovirus, and less frequently Epstein-Barr virus, and influenza virus.

Human viral cardiomyopathy.

MRI can accurately diagnose breast cancer during lactation

Value of immunohistological and immunoserological monitoring in cardiac transplantation

Dilated cardiomyopathy (DCM) according to the definition of the WHO/ISCF task force as “heart disease of unknown cause” [47] is a feasible working definition for the clinician. On hemodynamic grounds it defines DCM as systolic pump failure, which — as we know better today — may also have features of a diastolic compliance disturbance and severe dysrhythmias. For the cardiologist interested in pathogenetic mechanisms of this form of heart failure and its etiology, it is, however, not a satisfying explanation. Instead, it more likely describes our lack of knowledge than a disease entity. Recent evidence has pointed to viral etiology and the persistence of the enteroviral genome in a proportion of patients. Similary, also the presence of cytomegalovirus DNA in active myocarditis could be ascertained (own unpublished results) in about 15% of patients. In addition, the investigation of immunologic regulator [1, 10, 11, 27, 28, 39, 54, 57], humoral [3, 5, 15, 19, 22–38, 40–47, 49–51, 55, 56], and cellular effector mechanisms in humans [2, 8, 9, 12, 13, 20, 27, 28, 34, 35, 41, 43, 55, 56] has broadened both our understanding of the primary etiology and secondary immunopathogenesis in DCM.

Humoral and Cell-Mediated Immunity: Pathogenetic Mechanisms in Dilated Cardiomyopathy

INTRODUCTION
A pacemaker may affect the utility of a mammogram in several ways. The aim of this study is to summarize our institution's experience with mammograms among patients with a cardiac pacemaker, focusing on the diagnostic workup among patients with a newly diagnosed ipsilateral breast cancer.


METHODS
A retrospective search of all mammography reports between January 2011 and April 2021 was conducted for identifying cases of patients with a pacemaker. Demographic and clinical characteristics as well as mammography-derived quality parameters and findings were categorized and statistically compared.


RESULTS
The incidence of pacemaker concurrence in mammographic examination, although apparently slightly under-documented, accounted for 0.33% of cases. Population mean age was 71.7 years, and most patients (79%) had a left-sided pacemaker. The pacemaker was much more likely to be projected on the medio-lateral-oblique (96%) than on the cranio-caudal view (10%), on the axilla rather than the breast, and on the retro-pectoral rather than the pre-pectoral region (P < 0.001 for all). Compression force decreased by up to 23.0% (P < 0.001) and breast thickness increased by up to 9.5% (P < 0.001) for the ipsilateral vs. the contralateral side. Among 11 patients with newly diagnosed ipsilateral breast cancer, the pacemaker partially projected on the tumour region in two cases, and significantly obscured the tumour in another two.


CONCLUSION
Although rare, the coexistence of a pacemaker in patients undergoing mammography is associated with reduced image quality due to suboptimal breast visualization and reduced compression, and as a result, this may eventually lead to decreased diagnostic efficacy.

Pacemaker in patients undergoing mammography: A limitation for breast cancer diagnosis?

The etiology and pathogenesis of myocarditis, postmyocarditic heart muscle disease, and dilated cardiomyopathy (DC) are still matters of controversy and have remained partly unresolved. Not only enterovirus [1, 11], but also cytomegalovirus [36, 40], herpes virus (unpublished), and rickettsia [14] or borrelia induced [12] infection and persistence as evidenced by in situ hybridization, slot blot, conventional light or electron microscopy have been made responsible for the early and/or for the late alterations in cardiac ultrastructure and hemodynamic performance in acute myocardial inflammation and its sequelae. As derived from animal experiments of murine myocarditis [7–9, 37] and in man cellular [14, 17, 19–22, 27, 32, 35] and humoral autoreactive processes [4–7, 13–35, 39, 41, 42, 45, 46] have been demonstrated to be operative in inflammatory and dilated heart muscle diseases. We were the first to demonstrate cross-reactive, complement-dependent cardiocytolytic anti-sarcolemmal (AsAs) and anti-myolemmal antibodies (AMLAs) in coxsackievirus B myocarditis [23, 35] and recently demonstrated that certain sarcolemmal membrane epitopes cross-react, for example, the 110-, 48-, 35-, 31-, and 28-kDa proteins cross-react with enteroviral proteins [23] in western blot experiments. Apart from the crossreactive, cardio- and virus-specific antibodies were also described.

Are Anti-cardiac Antibodies in Dilated Cardiomyopathy “Natural” Antibodies?

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