Although in many cases no cause is apparent,<unk>  is probably the result of damage to the myocardium produced by a variety of toxic, metabolic, or infectious agents. In many cases the cause remains unclear. It may be due to fibrous change of the myocardium from a previous myocardial infarction. Or, it may be the late sequelae of acute viral myocarditis, such as with Coxsackie B virus and other enteroviruses possibly mediated through an immunologic mechanism. Other causes include: * Chagas disease, due to Trypanosoma cruzi. This is the most common infectious cause of<unk>  in Latin America * Pregnancy:<unk>  occurs late in gestation or several weeks to months postpartum as a peripartum<unk> . It is reversible in half of cases. * Alcohol use disorder (alcoholic<unk>  * Non-alcoholic toxic insults include administration of certain chemotherapeutic agents, in particular doxorubicin (Adriamycin), and cobalt. * Thyroid disease * Inflammatory diseases such as sarcoidosis and connective tissue diseases * Tachycardia-induced<unk>  * Muscular dystrophy * Tuberculosis: 1 to 2% of TB cases. * Autoimmune mechanisms * Thiamine deficiency Recent studies have shown that those subjects with an extremely high occurrence (several thousands a day) of premature ventricular contractions (extrasystole) can develop<unk> . In these cases, if the extrasystole are reduced or removed (for example, via ablation therapy) the<unk>  usually regresses. Genetics Genetic associations with<unk>  Type OMIM Gene Locus CMD1A LMNA 1q21 CMD1B unknown (TMOD1 candidate) 9q13 CMD1C LDB3 10q22-q23 CMD1D TNNT2 1q32 CMD1E SCN5A 3p CMD1F 6q23 CMD1G TTN 2q31 CMD1H 2q14-q22 CMD1I DES CMD1K 6q12-q16 CMD1L SGCD 5q33 CMD1M CSRP3 11p15.1 CMD1N TCAP 17q12 CMD1O ABCC9 12p12.1 CMD1P PLN 6q22.1 CMD1Q 7q22.3-q31.1 CMD1R ACTC 15q14 CMD1S MYH7 14q12 CMD1T TMPO 12q22 CMD1U PSEN1 14q24.3 CMD1V PSEN2 1q31-q42 CMD1W VCL 10q22-q23 CMD1X FCMD 9q31 CMD1Y TPM1 15q22.1 CMD1Z TNNC1 3p21.3-p14.3 CMD1AA ACTN2 1q42-q43 CMD2A TNNI3 19q13.4 CMD3A TAZ Xq28 CMD3B DMD Xp21.2 ALPK3 15q25.3 About 25–35% of affected individuals have familial forms of the disease, with most mutations affecting genes encoding cytoskeletal proteins, while some affect other proteins involved in contraction. The disease is genetically heterogeneous, but the most common form of its transmission is an autosomal dominant pattern. Autosomal recessive (as found, for example, in Alström syndrome), X-linked (as in Duchenne muscular dystrophy), and mitochondrial inheritance of the disease is also found. Some relatives of those affected by<unk>  have preclinical, asymptomatic heart-muscle changes. Other cytoskeletal proteins involved in<unk>  include α-cardiac actin, desmin, and the nuclear lamins A and C. Mitochondrial deletions and mutations presumably cause<unk>  by altering myocardial ATP generation. Kayvanpour et al. performed 2016 a meta-analysis with the largest dataset available on genotype-phenotype associations in<unk>  and mutations in lamin (LMNA), phospholamban (PLN), RNA Binding Motif Protein 20 (RBM20), Cardiac Myosin Binding Protein C (MYBPC3), Myosin Heavy Chain 7 (MYH7), Cardiac Troponin T 2 (TNNT2), and Cardiac Troponin I (TNNI3). They also reviewed recent studies investigating genotype-phenotype associations in<unk>  patients with titin (TTN) mutations. LMNA and PLN mutation carriers showed a high prevalence of cardiac transplantation and ventricular arrhythmia. Dysrhythmias and sudden cardiac death (SCD) was shown to occur even before the manifestation of<unk>  and heart failure symptoms in LMNA mutation carriers.
Dilated cardiomyopathy
Pulmonary embolism
Amyloid cardiomyopathy
Coronary artery disease
Alcoholic cardiomyopathy
Cardiomyopathy
Ischemic cardiomyopathy
Valvular heart disease