eMedicine Specialties > Radiology > Cardiac

Cardiomyopathy, Dilated

Author: Haroon R Afridi, MBBS,, Interventional Radiologist, RCI Iowa Plc, Cedar Rapids, Iowa
Coauthor(s): George Hartnell, MB, Professor of Radiology, Tufts University School of Medicine, Director of Cardiovascular and Interventional Radiology, Department of Radiology, Baystate Medical Center
Contributor Information and Disclosures

Updated: Feb 22, 2010

Introduction

Background

The World Health Organization (WHO) defines dilated cardiomyopathy as a condition in which the ventricular chambers exhibit increased diastolic and systolic volume and a low (<40%) ejection fraction.1,2 In the WHO/International Society and Federation of Cardiology classification, dilated cardiomyopathy in its primary (eg, idiopathic or familial) and secondary forms is the most common cause of the clinical syndrome of chronic heart failure.

Apical 2-dimensional echocardiogram with color Do...

Apical 2-dimensional echocardiogram with color Doppler display (systolic image) in a patient with dilated cardiomyopathy shows a jet of mitral regurgitation (MR) into a large left atrium (LA) (Doppler encoded blue). Note the dilatation of the left ventricle (LV) compared with the right ventricle.

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Apical 2-dimensional echocardiogram with color Do...

Apical 2-dimensional echocardiogram with color Doppler display (systolic image) in a patient with dilated cardiomyopathy shows a jet of mitral regurgitation (MR) into a large left atrium (LA) (Doppler encoded blue). Note the dilatation of the left ventricle (LV) compared with the right ventricle.


The prevalence of heart failure is approximately 1-1.5% in the adult population of Western countries. Dilated cardiomyopathy is associated with a large number of systemic or cardiac diseases, including specific heart muscle diseases (eg, ischemic cardiomyopathy, diabetic cardiomyopathy, alcoholic cardiomyopathy).

Dilated cardiomyopathy comprises approximately 90% of all cardiomyopathies; approximately 25% of all cases of dilated cardiomyopathy are of unknown etiology.3 Despite improved treatment, the mortality rate for dilated cardiomyopathy remains high, with a median period of survival of 1.7 years for men and 3.2 years for women. The natural history of the condition is progressive, and its cost, disability, and morbidity are among the highest of any disease.4,5,6

For excellent patient education resources, visit eMedicine's Heart Center, Immune System Center, and Blood and Lymphatic System Center. Also, see eMedicine's patient education articles Atrial Fibrillation, Lupus (Systemic Lupus Erythematosus), Alcoholism, Sickle Cell Crisis, and Growth Failure in Children.

Recent studies

Andreini et al investigated the efficacy of using 64-slice multidetector computed tomography (MDCT) angiography for coronary artery evaluation in patients with dilated cardiomyopathy of unknown etiology. In an examination of 130 patients with this condition, the authors determined that MDCT scan findings for the number of patients with normal or diseased coronary arteries (88 patients and 42 patients, respectively) matched those derived from invasive coronary angiography. In the detection of stenosis greater than 50%, MDCT scanning displayed a sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of 98.1%, 99.9%, 98.7%, 99.8%, and 99.7%, respectively. For stenosis of greater than 70%, figures for these same measures were 99.5%, 98.6%, 94.1%, 99.9%, and 99.4%, respectively. The authors concluded that, in patients with dilated cardiomyopathy of unknown etiology, MDCT scanning is ideal for the anatomic evaluation of coronary circulation.7

In a study of 64 patients, 33 with and 31 without dilated cardiomyopathy and severe systolic left ventricular dysfunction, Burianova et al investigated the efficacy of contrast-enhanced echocardiography (CEE) in the evaluation of left ventricular function. The authors found that CEE significantly underestimated left ventricular end-diastolic and end-systolic volumes and that it overestimated left ventricular ejection fractions. They also determined that intraobserver and interobserver reproducibility were better in MDCT scanning than in CEE, particularly in patients with no left ventricular dilation or severe systolic dysfunction.8

Pathophysiology

Decreased contractility is the hallmark of failing human hearts. In idiopathic dilated cardiomyopathy, this most likely is caused by myocardial cell loss or by changes in the gene expression of proteins responsible for the regulation of muscle contraction.9,10 This process occurs at 2 levels. That is, the heart's intrinsic mechanisms for sustaining a reasonable ejection fraction begin to fail (eg, contractile proteins and excitation-contraction coupling mechanisms, cell remodeling, bioenergetics), with the problem compounded by the effects of endogenous bioactive chemicals (eg, hormones, neurotransmitters, cytokines).

Dilated cardiomyopathy is usually characterized by ventricular dilatation, initially usually of the left ventricle (LV), with myocyte hypertrophy and diminished systolic function.11 Remodeling occurs with normal or reduced wall thickness, although total cardiac mass is increased.

Consequences of failing systolic function include a reduction in ejection fraction, reduced stroke volume (unless valvular regurgitation is present), and increased chamber size. To maintain cardiac output, diastolic ventricular filling is increased, with an increase in end-diastolic pressure. Wall stress increases as the ventricle dilates, thus increasing the amount of cardiac work required to maintain output. As the ventricle dilates, atrioventricular valve regurgitation develops because of stretching of the valve rings.

Etiology

Dilated cardiomyopathy can be classified broadly into the following 2 types:

  • Idiopathic
  • Known etiology - Ischemic, valvular, infectious, toxic, or genetic causes

Current theories postulate that molecular mechanisms resulting from altered gene expression are the cause of idiopathic cardiomyopathy. These can be categorized broadly into 3 general categories: single gene defects, polymorphic variation in modifier genes, and maladaptive regulated expression of nondefective genes.12

Specific cardiomyopathies can be caused by direct toxicity; overwork resulting from high cardiac output, as in thyrotoxicosis, pregnancy, and severe anemia; or overwork resulting from increased strain, as in hypertension, valvular regurgitation, or stenosis. The range of causes in adults is different from that in children, although some overlap exists.

Causes of dilated and specific cardiomyopathies can be summarized as follows:
  • Dilated
    • Idiopathic
    • Familial/genetic (autosomal dominant, X-linked)
    • Viral
    • Immune-related
    • Associated with the intake of alcohol and other toxins (eg, anthracyclines, antiretroviral agents [eg, zidovudine, didanosine, zalcitabine], cocaine, lithium, phenothiazines)
  • Specific heart muscle diseases
    • Myocardial ischemia
    • Valvular heart disease
    • Chronic systemic hypertension
    • Inflammatory
    • Infections caused by viruses (infection with coxsackievirus, cytomegalovirus, or human immunodeficiency virus [HIV]), mycobacteria, or parasites (Chagas disease, toxoplasmosis, trichinosis)
    • Tachycardia induced
  • Metabolic diseases
    • Nutritional deficiencies (such as a deficiency of thiamine or protein)
    • Endocrine disorders (eg, diabetes mellitus hypothyroidism, thyrotoxicosis, acromegaly, Cushing disease, pheochromocytoma)
    • Electrolyte disturbances (eg, hypocalcemia, hypophosphatemia)
  • Systemic disorders (eg, systemic lupus erythematosus, hemochromatosis, amyloidosis, sarcoidosis)
  • Peripartum state
  • Arrhythmogenic right ventricular dysplasia or cardiomyopathy
  • Neuromuscular dystrophies (eg, Duchenne muscular dystrophy, Friedreich ataxia, myotonic dystrophy, X-linked cardioskeletal myopathy)
  • Hematologic disorders (eg, chronic anemia, as in sickle cell disease or thalassemia)

Causes of dilated and specific cardiomyopathy in children can be summarized as follows:

  • Congenital
    • Progressive muscular dystrophy
    • Noonan syndrome
  • Idiopathic
    • Endomyocardial fibrosis
    • Dilated cardiomyopathy
  • Infection
    • Bacterial (Staphylococcus species)
    • Viral (coxsackievirus B)
  • Autoimmune
  • Metabolic disorders
  • Ischemia
  • Anomalous coronary artery
  • Kawasaki disease (also termed mucocutaneous lymph node syndrome)
  • Toxic (steroids, cytotoxic drugs, drug hypersensitivity, heavy metals)

Frequency

United States

The reported incidence of dilated cardiomyopathy varies annually from approximately 5 cases to 8 cases per 100,000 population. However, the frequency is likely underestimated owing to underreporting or underdetection of asymptomatic patients, which may occur in as many as 50-60% of cases. The age-adjusted prevalence in the United States averages 36 cases per 100,000 population.13,14,15

International

In Western countries, 1-1.5% of the adult population has dilated cardiomyopathy.

Mortality/Morbidity

Dilated cardiomyopathy accounts for 10,000 deaths annually in the United States.13,14,15 Mortality rates are highest in older persons, men, and blacks (Framingham Heart Study, National Heart, Lung and Blood Institute).

  • The median survival of patients with dilated cardiomyopathy is 1.7 years for men and 3.2 years for women.
  • The natural history is progressive, and the cost, disability, and morbidity of the condition are among the highest of any disease.4,5,6
  • Mortality rates are reduced by use of angiotensin-converting enzyme (ACE) inhibitors and by treatment of some of the specific causes (eg, ischemia, hemochromatosis, sarcoidosis).

Race

Compared with whites, African Americans have an almost 3-fold greater risk of developing dilated cardiomyopathy. This increased risk is not explained by differences in hypertension, cigarette smoking, alcohol use, or socioeconomic factors. Moreover, African Americans have approximately a 1.5- to 2-fold higher risk of dying from dilated cardiomyopathy than age-matched whites. Although the reasons for these differences are not entirely understood, several potential explanations include differences in the number of risk factors for heart failure, as well as differences in the etiology of heart failure, in the response to medical treatment, and in the access to medical care.

Sex

There are no available statistics regarding the incidence of dilated cardiomyopathy in males versus females. However, in general, heart failure is more common in men. The overall effect of gender on the prognosis of heart failure is not yet clear, largely because many of the early clinical heart failure trials consisted predominantly of male patients.

  • The treatment arm of the Studies on Left Ventricular Dysfunction (SOLVD), in which only 15% of the patients were women, reported no sex-related difference in survival in either the placebo group or the enalapril group.16 Findings from the SOLVD registry, in which approximately 20% of the patients were female, suggested that women had a significantly higher annual risk of heart failure – related mortality and higher rates of hospitalization than did age-matched male patients.17
  • In the Italian Multicenter Cardiomyopathy Registry, women with idiopathic dilated cardiomyopathy tended to present with more advanced heart failure.18

Age

Age distribution depends on the age distribution of any underlying disease. However, advancing age is reported as an independent risk factor for mortality in several studies.19,20

Presentation

Dyspnea secondary to volume overload is usually the predominant presentation, although features of low cardiac output may predominate. Other presentations range from atrial or ventricular arrhythmias to angina with healthy coronary arteries to sudden cardiac death. Dyspnea may be accompanied by orthopnea, hypotension, fatigue, malabsorption, peripheral edema, ascites, and anorexia. Thromboembolism is common.

A family history may provide major clues regarding etiology and prognosis. A substantial number of patients with left ventricular systolic dysfunction (as shown on echocardiography, indicating early dilated cardiomyopathy) may be asymptomatic.21

Preferred Examination

Evaluation of dilated cardiomyopathy is directed toward identifying causes, some of which may be treatable, and toward assessing cardiac function and detecting complications.

Nonimaging investigations include a complete blood count determination, urinalysis, electrolyte analysis, serum albumin measurement, and analysis of thyroid-stimulating hormone levels. Additional specific laboratory studies may be performed if a certain type of dilated cardiomyopathy is suggested. For example, iron studies may be ordered in cases of hemochromatosis, and specific antibody assays may be useful in systemic lupus erythematosus and sarcoidosis. Almost all patients with congestive heart failure resulting from dilated cardiomyopathy have electrocardiogram (ECG) abnormalities.

Currently available radiologic investigations are as varied in technique and sophistication as they are in cost. Studies vary from the noninvasive to the invasive and from the dynamic to the static. Radiologic tests are used to help make a diagnosis, to assess the degree of cardiac dysfunction, to identify a cause (though this is unusual), and to guide therapy.

It is difficult to make an accurate clinical identification of heart failure resulting from poor ventricular function, but it is important to do so because of the need to relieve symptoms. A substantial number of patients with heart failure have normal ECG results.22 In other patients with apparent heart failure, echocardiography provides extra information on the nature of the cardiac disease that affects management.23 In addition, providing appropriate treatment is important in patients affected more severely (ejection fraction <35-40%), in whom treatment can significantly reduce the mortality rate.16

The initial chest radiograph should usually be followed by echocardiography. These studies may be the only investigations required, and this approach is by far the most common method for diagnosing dilated cardiomyopathy. Subsequent evaluation of cardiac function may be performed by using cine computed tomography (CT) scanning (in rare cases), nuclear scintigraphy, or magnetic resonance imaging (MRI).

MRI also is rarely used to diagnose or investigate dilated cardiomyopathy, because the information obtained during echocardiography is often adequate. Although MRI has a valuable role in the diagnosis of specific causes of dilated cardiomyopathy (eg, myocarditis, sarcoidosis, hemochromatosis), the expertise required to evaluate these conditions is not widely available.

Limitations of Techniques

Chest radiography is good for assessing the effects of cardiac dysfunction on pulmonary perfusion and the development of pulmonary edema. Radiographs seldom help in identifying the etiology of the dysfunction.

Echocardiography is an excellent method for assessing cardiac function, determining the presence of valve lesions, detecting complications such as thrombus or pericardial effusion, and assessing response to treatment. Echocardiography may be limited in 10-20% of patients by restricted acoustic access and is dependent on operator experience.

Cine CT scanning and CT angiography scanning require radiation and intravenous contrast enhancement; therefore, these techniques are seldom used.

Nuclear scintigraphy is a repeatable technique that often is used when serial examination of cardiac function is required. It is not as valuable as echocardiography, since it provides little anatomic information.

MRI and magnetic resonance angiography (MRA) are the most accurate methods for assessing cardiac anatomy or function. MRI/MRA is used when echocardiography is inadequate, but this study is often not used because of its relatively high cost and limited availability, as well as contraindications if ferromagnetic metallic foreign bodies are present in the patient.

Differential Diagnoses

Aortic Stenosis
Cardiomyopathy, Restrictive
Congestive Heart Failure

Other Problems to Be Considered

Multiple valvular disease of the heart
Ischemic heart disease
Myocarditis

More on Cardiomyopathy, Dilated

Overview: Cardiomyopathy, Dilated
Imaging: Cardiomyopathy, Dilated
Follow-up: Cardiomyopathy, Dilated
Multimedia: Cardiomyopathy, Dilated
References
Further Reading
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References

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Keywords

dilated cardiomyopathy, cardiomyopathy, congestive heart failure, hypertrophic cardiomyopathy, ischemic cardiomyopathy, idiopathic dilated cardiomyopathy, cardiomyopathy causes, congestive cardiomyopathy, diabetic cardiomyopathy, alcoholic cardiomyopathy, postpartum cardiomyopathy

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Contributor Information and Disclosures

Author

Haroon R Afridi, MBBS,, Interventional Radiologist, RCI Iowa Plc, Cedar Rapids, Iowa
Haroon R Afridi, MBBS, is a member of the following medical societies: American College of Radiology, British Society of Interventional Radiology, Cardiovascular and Interventional Radiological Society of Europe, Radiological Society of North America, Royal College of Radiologists, and Society of Cardiovascular and Interventional Radiology
Disclosure: Nothing to disclose.

Coauthor(s)

George Hartnell, MB, Professor of Radiology, Tufts University School of Medicine, Director of Cardiovascular and Interventional Radiology, Department of Radiology, Baystate Medical Center
George Hartnell, MB is a member of the following medical societies: American College of Cardiology, American College of Radiology, American Heart Association, Association of University Radiologists, British Institute of Radiology, British Medical Association, Massachusetts Medical Society, Radiological Society of North America, Royal College of Physicians, Royal College of Radiologists, and Society of Cardiovascular and Interventional Radiology
Disclosure: Nothing to disclose.

Medical Editor

Justin D Pearlman, MD, PhD, ME, MA, Director of Advanced Cardiovascular Imaging, Professor of Medicine, Professor of Radiology, Adjunct Professor, Thayer Bioengineering and Computer Science, Dartmouth-Hitchcock Medical Center
Justin D Pearlman, MD, PhD, ME, MA is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, International Society for Magnetic Resonance in Medicine, and Radiological Society of North America
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Resolution Imaging Medical Corporation
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

Eugene C Lin, MD, Consulting Radiologist, Virginia Mason Medical Center; Clinical Assistant Professor of Radiology, University of Washington School of Medicine
Eugene C Lin, MD is a member of the following medical societies: American College of Nuclear Medicine, American College of Radiology, Radiological Society of North America, and Society of Nuclear Medicine
Disclosure: Nothing to disclose.

 
 
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