Dilated cardiomyopathy

Titles

All titles Clinical Sense Prognosis: Your Diagnosis Explain Medicine QBank Prepper

Library

Core specialties Subspecialties Organ systems Cutting edge innovations

Library

Core specialties Subspecialties Organ systems Cutting edge innovations

About Clinical Odyssey

Why trust us Pricing Subscribe For organizations

Editorial

Authors Peer reviewers

Medical Joyworks, LLC

About Jobs Contact

Read Discuss

Hi there!

You’re looking at a short reference article from Explain Medicine (one of four distinct learning formats available in Clinical Odyssey). Try it out, and have fun improving your clinical skills.

Medicine

Last updated on:
August 14^th, 2020

Medicine

Last updated on:
August 14^th, 2020

Hi there!

You’re looking at a short reference article from Explain Medicine (one of four distinct learning formats available in Clinical Odyssey). Try it out, and have fun improving your clinical skills.

Clinicals - History

Fact	Explanation
Symptoms of heart failure	These are encountered in 80% of patients. Heart failure is a consequence of the progressive left ventricular (LV) dilation and systolic dysfunction encountered in dilated cardiomyopathy (DCM).
Palpitations	This is due to supraventricular or ventricular tachyarrhythmias. DCM predisposes to arrhythmias due to the disruption of the conduction system of the heart caused by progressive dilation, and progressive interstitial fibrosis contributing to an arrhythmic substrate. In individuals with DCM caused by inflammatory or infiltrative disease, the resulting injury to the myocardium may also be a contributing factor.
Constitutional symptoms	These are prominent in advanced cases, and include anorexia, nausea, abdominal discomfort, and cachexia. They are a consequence of chronic heart failure.
Sudden cardiac death	Sudden cardiac death may occur following ventricular arrhythmias such as monomorphic or polymorphic ventricular tachycardia, or ventricular fibrillation. The pathophysiology underlying the occurrence of arrhythmias is discussed under "palpitations".
Positive family history	Familial transmission occurs in 20% to 35% of cases. Autosomal dominant inheritance is the most common form of transmission. However, autosomal recessive, x-linked, and mitochondrial inheritance may also occur.
Chronic alcohol abuse	Chronic alcohol abuse accounts for 21% to 36% of cases in high-income countries. In this context, the alcohol intake must have been >80-100 g/day for >10 years. Alcohol appears to exert a direct toxic effect on the myocardium, while also depressing cardiac contractility and activating the neurohormonal system. All of these factors contribute to the development of DCM.
Recreational drug use	Cocaine and methamphetamine abuse is an important cause of DCM in younger adults. These drugs are potent sympathomimetic agents. They appear to cause cardiac toxicity via myocardial ischemia due to increased oxygen consumption, prothrombotic effects, coronary vasospasm, and accelerated coronary atherosclerosis.
Pregnancy	DCM may occur in the last month of pregnancy or within the first five (5) months of delivery, without any discernible cause. This is termed "peripartum cardiomyopathy". The underlying pathophysiology is still unclear.
Chemotherapy	DCM is an important complication of anthracycline (e.g. doxorubicin, daunorubicin, etc.) therapy. This may occur during the therapy, or any time afterwards. The causes of anthracycline-induced cardiotoxicity appear to include oxidative stress, changes in mitochondrial membrane permeability, and suppression of respiratory chain activity.
HIV Infection	Human immunodeficiency virus (HIV) infection can also give rise to DCM, and should be considered in individuals whose DCM has no clear cause. The underlying pathogenic mechanisms include: direct myocyte toxicity, activation of indirect pathways that induce myocardial inflammation and damage, and cardiac autoimmunity. Micronutrient deficiency is common in HIV-infected persons due to gut malabsorption, diarrhea, and wasting syndrome. The resulting free radical formation may cause further myocardial injury. Therapy with the reverse-transcriptase inhibitor zidovudine (AZT) may cause myocardial damage. AZT may potentially contribute to the above, or independently cause DCM.
Autoimmune disease	Certain autoimmune conditions are known to cause DCM. These include: systemic lupus erythematosus, connective tissue diseases (such as scleroderma and dermatomyositis), and vasculitides (e.g., eosinophilic granulomatosis with polyangiitis, polyarteritis nodosa, and Kawasaki disease). The underlying mechanisms of these conditions include immune-mediated cardiac injury and thrombotic or inflammatory microvascular coronary disease.
Chagas disease	In endemic regions, Chagas disease (caused by infection with the protozoan parasite Trypanosoma cruzi) is an important etiology of DCM. The pathogenesis is incompletely understood but may involve several mechanisms, including: parasite-dependent myocardial damage, immune-mediated myocardial injury, and microvascular and neurogenic disturbances.

Symptoms of heart failure

These are encountered in 80% of patients. Heart failure is a consequence of the progressive left ventricular (LV) dilation and systolic dysfunction encountered in dilated cardiomyopathy (DCM).

Palpitations

This is due to supraventricular or ventricular tachyarrhythmias. DCM predisposes to arrhythmias due to the disruption of the conduction system of the heart caused by progressive dilation, and progressive interstitial fibrosis contributing to an arrhythmic substrate. In individuals with DCM caused by inflammatory or infiltrative disease, the resulting injury to the myocardium may also be a contributing factor.

Constitutional symptoms

These are prominent in advanced cases, and include anorexia, nausea, abdominal discomfort, and cachexia. They are a consequence of chronic heart failure.

Sudden cardiac death

Sudden cardiac death may occur following ventricular arrhythmias such as monomorphic or polymorphic ventricular tachycardia, or ventricular fibrillation. The pathophysiology underlying the occurrence of arrhythmias is discussed under "palpitations".

Positive family history

Familial transmission occurs in 20% to 35% of cases. Autosomal dominant inheritance is the most common form of transmission. However, autosomal recessive, x-linked, and mitochondrial inheritance may also occur.

Chronic alcohol abuse

Chronic alcohol abuse accounts for 21% to 36% of cases in high-income countries. In this context, the alcohol intake must have been >80-100 g/day for >10 years. Alcohol appears to exert a direct toxic effect on the myocardium, while also depressing cardiac contractility and activating the neurohormonal system. All of these factors contribute to the development of DCM.

Recreational drug use

Cocaine and methamphetamine abuse is an important cause of DCM in younger adults. These drugs are potent sympathomimetic agents. They appear to cause cardiac toxicity via myocardial ischemia due to increased oxygen consumption, prothrombotic effects, coronary vasospasm, and accelerated coronary atherosclerosis.

Pregnancy

DCM may occur in the last month of pregnancy or within the first five (5) months of delivery, without any discernible cause. This is termed "peripartum cardiomyopathy". The underlying pathophysiology is still unclear.

Chemotherapy

DCM is an important complication of anthracycline (e.g. doxorubicin, daunorubicin, etc.) therapy. This may occur during the therapy, or any time afterwards. The causes of anthracycline-induced cardiotoxicity appear to include oxidative stress, changes in mitochondrial membrane permeability, and suppression of respiratory chain activity.

HIV Infection

Human immunodeficiency virus (HIV) infection can also give rise to DCM, and should be considered in individuals whose DCM has no clear cause. The underlying pathogenic mechanisms include: direct myocyte toxicity, activation of indirect pathways that induce myocardial inflammation and damage, and cardiac autoimmunity.

Micronutrient deficiency is common in HIV-infected persons due to gut malabsorption, diarrhea, and wasting syndrome. The resulting free radical formation may cause further myocardial injury. Therapy with the reverse-transcriptase inhibitor zidovudine (AZT) may cause myocardial damage. AZT may potentially contribute to the above, or independently cause DCM.

Autoimmune disease

Certain autoimmune conditions are known to cause DCM. These include: systemic lupus erythematosus, connective tissue diseases (such as scleroderma and dermatomyositis), and vasculitides (e.g., eosinophilic granulomatosis with polyangiitis, polyarteritis nodosa, and Kawasaki disease). The underlying mechanisms of these conditions include immune-mediated cardiac injury and thrombotic or inflammatory microvascular coronary disease.

Chagas disease

In endemic regions, Chagas disease (caused by infection with the protozoan parasite Trypanosoma cruzi) is an important etiology of DCM. The pathogenesis is incompletely understood but may involve several mechanisms, including: parasite-dependent myocardial damage, immune-mediated myocardial injury, and microvascular and neurogenic disturbances.

Want to continue reading?

Subscribe to Clinical Odyssey today.

Enjoy unlimited access to 700+ learning modules.
Safely improve your skills, anytime and anywhere.
Get answers to your follow-up questions from practicing physicians.

Learn more ➜