Dilated cardiomyopathy (DCM) is a condition in which the heart becomes enlarged and cannot pump blood effectively.

[9] In those with heart failure, treatment may include medications in the ACE inhibitor, beta blocker, and diuretic families.

[9] Dilated cardiomyopathy develops insidiously, and may not initially cause symptoms significant enough to impact on quality of life.

[12] Although in many cases no cause is apparent, dilated cardiomyopathy is probably the result of damage to the myocardium produced by a variety of toxic, metabolic, or infectious agents.

Or, it may be the late sequelae of acute viral myocarditis, such as with Coxsackie B virus and other enteroviruses[14] possibly mediated through an immunologic mechanism.

[16] Other causes include: Recent studies have shown that those subjects with an extremely high occurrence (several thousands a day) of premature ventricular contractions (extrasystole) can develop dilated cardiomyopathy.

[14] Nuclear coding variations for mitochondrial complex II have also shown pathogenicity for dilated cardiomyopathy, designated 1GG for SDHA.

They also reviewed recent studies investigating genotype-phenotype associations in DCM 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 DCM and heart failure symptoms in LMNA mutation carriers.

[25] The progression of heart failure is associated with left ventricular remodeling, which manifests as gradual increases in left ventricular end-diastolic and end-systolic volumes, wall thinning, and a change in chamber geometry to a more spherical, less elongated shape.

The concept of cardiac remodeling was initially developed to describe changes that occur in the days and months following myocardial infarction.

Eventually, however, these mechanisms become detrimental, intravascular volume becomes too great, and progressive dilatation leads to heart failure symptoms.

[citation needed] Cardiac dilatation is a transversely isotropic, irreversible process resulting from excess strains on the myocardium.

[citation needed] As the ventricles enlarge, both the mitral and tricuspid valves may lose their ability to come together properly.

When left bundle-branch block (LBBB) is accompanied by right axis deviation (RAD), the rare combination is considered to be highly suggestive of dilated or congestive cardiomyopathy.

[29][30] Echocardiogram shows left ventricular dilatation with normal or thinned walls and reduced ejection fraction.

[28] Genetic testing can be important, since one study has shown that gene mutations in the TTN gene (which codes for a protein called titin) are responsible for "approximately 25% of familial cases of idiopathic dilated cardiomyopathy and 18% of sporadic cases.

"[31] The results of the genetic testing can help the doctors and patients understand the underlying cause of the dilated cardiomyopathy.

Standard therapy may include salt restriction, ACE inhibitors, diuretics, and beta blockers.

[36] Artificial pacemakers may be used in patients with intraventricular conduction delay, and implantable cardioverter-defibrillators in those at risk of arrhythmia.

These forms of treatment have been shown to prevent sudden cardiac death, improve symptoms, and reduce hospitalization in patients with systolic heart failure.

[37] In addition, an implantable cardioverter-defibrillator should be considered as a therapeutic option for the primary prevention of sudden cardiac death in patients with a confirmed LMNA mutation responsible for dilated cardiomyopathy disease phenotype and clinical risk factors.

[39] https://www.ikard.pl/SVA/ Archived 2021-11-16 at the Wayback Machine In patients with advanced disease who are refractory to medical therapy, heart transplantation may be considered.

[citation needed] Dilated cardiomyopathy is a heritable disease in some dog breeds, including the Boxer, Dobermann, Great Dane, Irish Wolfhound, and St Bernard.

[citation needed] An acquired variation of dilated cardiomyopathy describing a link between certain diets was discovered in 2019 by researchers at University of California, Davis School of Veterinary Medicine who published a report on the development of dilated cardiomyopathy in dog breeds lacking the genetic predisposition, particularly in Golden Retrievers.

The incidence is high enough that several strains of Golden Hamster have been developed to serve as animal models in clinical testing for human forms of the disease.