Dilated

CLEVELAND CL IN IC JOURNAL OF MEDICINE VOLUME 69 • NUMBER 6 JUNE 2002 481

REAT THE UNDERLYING DISEASE. We hearthis all the time. But many cases of heart

failure are due to idiopathic dilated cardiomy-opathy, which by definition has no knowncause.

The challenge is to identify and treat theknown and treatable causes of dilated car-diomyopathy early enough to improve symp-toms and survival. In this article, we reviewcurrent classification schemes, theories ofpathogenesis, and the current range of diag-nostic and therapeutic options.

■ BACKGROUND

Dilated cardiomyopathy is much more com-mon than the other major forms of cardiomy-opathy (hypertrophic, restrictive, and arrhyth-mogenic right ventricular cardiomyopathy). Itis a heterogeneous disease characterized byventricular and sometimes atrial dilatation,with normal or reduced wall thickness, even-tually leading to varying degrees of impairedsystolic function. The clinical picture at thetime of diagnosis can vary widely from patientto patient; some have no symptoms, whereasothers have progressive refractory heart failure.

Incidence and impactDilated cardiomyopathy has an incidence ofmore than 36.5 cases per 100,000 persons,1and it accounts for nearly 50,000 hospitaliza-tions and 10,000 deaths each year in theUnited States.2 The incidence has increasedover the past 5 to 10 years, perhaps due both tothe development of noninvasive diagnostictools and to improved physician awareness.

SIVA B. MOHAN, MDDepartment of Internal Medicine,Atlanta Medical Center

MIRIAM PARKER, MDDepartment of Internal Medicine,Atlanta Medical Center

Idiopathic dilated cardiomyopathy:A common but mystifying causeof heart failure

REVIEW

■ ABSTRACT

While researchers try to elucidate the origins of idiopathicdilated cardiomyopathy, clinicians continue to face thechallenges of identifying and treating the causes of thiscondition to improve symptoms and survival. We reviewclassification schemes for dilated cardiomyopathy and thecurrent range of diagnostic and therapeutic options andtreatment goals.

■ KEY POINTS

Idiopathic dilated cardiomyopathy may result from acombination of factors, among them genetic predisposition,chronic viral myocarditis, and immune system dysfunction.

The clinical presentation of idiopathic dilatedcardiomyopathy varies from patient to patient, but mostpatients present later, ie, at some point in the spectrum ofheart failure.

Numerous studies show that angiotensin-convertingenzyme inhibitors improve symptoms and decreasemorbidity and mortality from heart failure, and that long-term beta-blocker treatment improves symptoms andlowers hospitalization and death rates.

T

MOHAMMAD WEHBI, MDDepartment of Internal Medicine,Atlanta Medical Center

PAUL DOUGLASS, MDDepartment of Cardiology,Atlanta Medical Center

on November 30, 2013. For personal use only. All other uses require permission.www.ccjm.orgDownloaded from

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482 CLEVELAND CL IN IC JOURNAL OF MEDICINE VOLUME 69 • NUMBER 6 JUNE 2002

Dilated cardiomyopathy represents amajor health burden. As a result, muchresearch is underway to find better diagnostictechniques and treatments that can decreasemorbidity and death. For now, dilated car-diomyopathy remains the primary indicationfor heart transplantation in the United States.

WHO classification nomenclatureThe World Health Organization/InternationalSociety and Federation of Cardiology TaskForce report3 classifies dilated cardiomyopathyas primary (idiopathic or familial) or secondary(most commonly ischemic, hypertensive,valvular, alcohol-related, or viral or autoim-mune in origin). According to this scheme,types of cardiomyopathy secondary to specificdisease processes are “specific” cardiomy-opathies. For example, dilated cardiomyopathydue to coronary artery disease is known asischemic cardiomyopathy. The report alsodefined dilated types of cardiomyopathy as acardiac muscle disorder with impaired ventric-ular function (ejection fraction < 40%) andincreased end-diastolic and systolic volumes.3We will discuss specific diagnostic criteria later.

■ PATHOGENESIS: NEW HYPOTHESES

TABLE 1 outlines the known causes of dilatedcardiomyopathy. However, in most cases, thecause is not known—hence the label “idio-pathic.”4 Some experts have postulated thatthese cases are attributable to a single cause;however, idiopathic dilated cardiomyopathy isnow thought to be multifactorial, with severalnew hypotheses.5

Genetic predispositionOver the past few years, much attention hasbeen given to finding a genetic cause for idio-pathic dilated cardiomyopathy, as some 20% ofcases of idiopathic dilated cardiomyopathy arefound to have a familial link6 and are termedfamilial dilated cardiomyopathy. Moreover, inpractice, this percentage most likely representsan underestimation, as our diagnostic toolslack the sensitivity needed to demonstrate agenetic linkage. Given the absence of accept-ed diagnostic criteria, some investigatorsbelieve that a much larger percentage of casesare familial than was initially suspected.7

IDIOPATHIC DILATED CARDIOMYOPATHY MOHAN AND COLLEAGUES

Known causes of dilatedcardiomyopathyElectrolyte abnormalities

HypocalcemiaHypophosphatemiaUremia

Endocrine abnormalitiesCushing diseaseDiabetes mellitusGrowth hormone abnormalitiesHypothyroidism/hyperthyroidismPheochromocytoma

Hypertension (long-standing)

Infectious causesBacterial (brucellosis, diphtheria, psittacosis,

typhoid fever)FungalMycobacterialParasitic (Chagas disease, schistosomiasis,

toxoplasmosis)RickettsialViral (coxsackie A and B viruses,

cytomegalovirus, Epstein-Barr virus, humanimmunodeficiency virus, varicella virus)

Infiltrative diseasesAmyloidosisHemochromatosisSarcoidosis

Ischemia

Neuromuscular diseasesDuchenne muscular dystrophyFriedreich ataxiaMyotonic dystrophy

Nutritional abnormalitiesCarnitineSeleniumThiamine

Rheumatologic diseasesGiant cell arteritisSclerodermaSystemic lupus erythematosus

Tachyarrhythmias

ToxinsAmphetaminesAntiretroviral agentsCarbon monoxideChemotherapeutic agents, radiationChloroquine, phenothiazinesCobalt, lead, mercuryCocaineEthanol

Valvular heart disease

T A B L E 1

Dilatedcardiomyopathyis the mainindicationfor hearttransplantation




Most of these cases are now known toexhibit an autosomal-dominant pattern oftransmission. While autosomal-recessive, X-linked, and mitochondrial patterns have beenstudied, these are quite rare. Several genemutations have been isolated that are specificfor each mode of transmission. Most of theisolated genes code for contractile or structur-al proteins within the myocyte, leading tocompromised myocyte structural integrity orimpaired inotropic activity or both.8 Othergenes have been found to interrupt cardiacenergy metabolism via alteration of transcrip-tion factors, leading to obvious deleteriouseffects on overall myocyte function.8

Typically, penetrance is variable, and theclinical progression of the disease seems to beage-dependent, with a much higher incidenceat older ages.9 This indicates that early diag-nosis may alter the clinical course in familialdilated cardiomyopathy.

Chronic viral myocarditisCoxsackie A and B viruses or echoviruses cancause acute myocarditis, so experts havehypothesized that idiopathic dilated car-diomyopathy results from a chronic viralmyocarditis with progressive myocyte damageand, eventually, death. Studies10–12 haveshown increased viral particles within the car-diac myocyte via endomyocardial biopsy andviral serology in the setting of idiopathic dilat-ed cardiomyopathy. But these studies werequite small, with a wide range of viral involve-ment (10%–50%). Ongoing trials, which arenearing completion, may provide further datato support this hypothesis.

Immune system dysfunctionBoth humoral and cell-mediated immuneresponses have been implicated in idiopathicdilated cardiomyopathy. Some investigatorshave proposed an autoimmune process, whileothers point out that impaired immune func-tion may play a large role. HLA associations(HLA-B27, HLA-A2, HLA-DR4, and HLA-DQ4) have been identified,13 but further evi-dence is required to show a causal relationship.Some have argued either that heightenedimmune responses may occur in response to achronic infectious process such as viralmyocarditis, or that impaired immune response

may lead to increased susceptibility to chronicviral myocarditis. Likely, immune and infec-tious processes concurrently play a role in thedevelopment of idiopathic dilated cardiomy-opathy.

■ CLINICAL FEATURES

The clinical presentation of idiopathic dilatedcardiomyopathy varies from patient topatient, but most patients are in overt heartfailure by the time they present. Patients oftenpresent with symptoms relating to left ven-tricular or biventricular failure. Initially, gen-eralized fatigue, weight loss, loss of appetite,and other vague, nonspecific symptoms maypredominate. Patients who present in thelater stages of heart failure tend to have pro-gressive shortness of breath on exertion,peripheral edema, orthopnea, and paroxysmalnocturnal dyspnea as the most common signsand symptoms. Less frequently, idiopathicdilated cardiomyopathy may present with syn-cope, chest pain, thromboembolism, dys-rhythmias, and, rarely, sudden death. Theseare seen most often in patients who are diag-nosed late in the disease course.

Potential sequelaeA small percentage of patients develop pul-monary or systemic emboli, usually in thelater stages of disease, but earlier if the treat-ment regimen is not optimal. Cardiac dys-rhythmias such as ventricular tachycardia andsupraventricular tachycardia are not uncom-mon. Approximately 25% to 35% of patientshave intermittent nonsustained ventriculartachycardia, while fewer have supraventricu-lar tachycardia (usually atrial fibrillation).Thus, syncope and sudden death are usually afunction of the severity of dysrhythmia.

■ DIAGNOSIS

The diagnosis of idiopathic dilated cardiomy-opathy involves first excluding known causes ofdilated cardiomyopathy, which may or may notbe reversible. Although most cases of dilatedcardiomyopathy are irreversible, ruling outreversible causes is essential, as this will affectthe diagnostic approach and treatment scheme.TABLE 2 outlines specific inclusion and exclusion


Most patientsare already inheart failurewhen theypresent





criteria for idiopathic dilated cardiomyopathybased on a report by Mestroni et al.14

Detailed history and physical examinationAs with any disease, a detailed and directedhistory and physical examination are critical.The clinician should conduct the history so asto identify clues of known causes of dilatedcardiomyopathy. For example, always ask thepatient about alcohol use, cocaine use, past ill-nesses (including infections involving theheart, history of arrhythmias), past medica-tions taken, travel (for possible infectiousexposure), pregnancies, and occupations (torule out exposure to specific toxins). A thor-ough family history is also paramount becauseof the reasonably high incidence of familialdilated cardiomyopathy, as discussed above.

Laboratory testingRoutine laboratory testing should include testsfor known causes of dilated cardiomyopathy,such as fasting blood sugar (diabetes mellitus),thyroid studies (hypothyroidism or hyperthy-roidism), iron studies (hemochromatosis andiron overload), a comprehensive metabolic

panel, liver function tests, creatine kinase, anderythrocyte sedimentation rate (TABLE 1).

In patients strongly suspected of havingfamilial dilated cardiomyopathy, genetic test-ing may be prudent. The diagnosis of familialdilated cardiomyopathy is usually made if idio-pathic dilated cardiomyopathy is found in twoor more members of the same family, or ifthere is a history of a first-degree relative withsudden death of unknown cause before age35.14

Chest radiographyRadiographs usually show cardiomegaly withor without pulmonary vascular congestion,depending on the degree of heart failure.

ElectrocardiographyElectrocardiograms are usually normal inpatients who have dilated cardiomyopathy butare asymptomatic. However, electrocardio-grams in symptomatic patients often showconduction defects, atrial dysrhythmias, andventricular hypertrophy. The test is worth per-forming in any patient suspected of havingdilated cardiomyopathy, because evidence ofischemia, hypertrophy, or conduction systemdisease helps direct further testing to rule outknown causes of these changes.

EchocardiographyEchocardiography is useful in any patient sus-pected of having any form of dilated car-diomyopathy: it is quick, noninvasive, and rel-atively inexpensive and aptly visualizes mostof the anatomy of the heart. It helps rule outknown causes of dilated cardiomyopathy, suchas valvular heart disease, in which four-cham-ber dilatation is seen with an impaired leftventricular ejection fraction (< 40%).

Exercise testing, coronary angiographyExercise testing should be included as part ofthe workup to assess for coronary artery dis-ease. It may also help in evaluating functionalcapabilities in patients with previously diag-nosed idiopathic dilated cardiomyopathy.

Coronary angiography may also berequired to definitively exclude ischemic heartdisease as a cause of dilated cardiomyopathy.Idiopathic dilated cardiomyopathy remains apossible diagnosis even if none of the major


Diagnostic criteriafor idiopathic dilated cardiomyopathy

Inclusion criteriaEjection fraction of the left ventricle < 45% and/or fractionalshortening < 25% (> 2 SD below the mean), as ascertained byechocardiography, radionuclide scanning, or angiography

Left-ventricular end-diastolic diameter > 117% of the predictedvalue corrected for age and body surface area, whichcorresponds to 2 SD above the predicted normal limit +5%

Exclusion criteriaSystemic hypertension (> 160/100 mm Hg)Coronary artery disease (> 50% in one or more major branches)Chronic excess alcohol (> 40 g/day in women, > 80 g/day in men

for more than 5 years after 6-month abstinenceSystemic disease known to cause dilated cardiomyopathyPericardial diseasesCongenital heart diseaseCor pulmonaleRapid, sustained supraventricular tachycardia

T A B L E 2

Always askabout alcoholand cocaineuse




vessels is occluded by more than 50%, as thedegree of dilatation may be out of proportionto the extent of ischemia. Newer tests such asdobutamine echocardiography and radionu-clide imaging may help distinguish ischemiccardiomyopathy from idiopathic dilated car-diomyopathy.

Viral serologic testingThe role of viral serologic testing in idiopath-ic dilated cardiomyopathy remains controver-sial. It may be helpful in patients with chron-ic immunosuppression (ie, human immunode-ficiency virus, cancer). While it is useful inpatients with suspected acute viral myocardi-tis, at this time viral serologic testing is notroutinely recommended in patients with sus-pected dilated cardiomyopathy, because theresults of serologic testing do not influencethe treatment.

Endomyocardial biopsyEndomyocardial biopsy should not be per-formed on all patients with suspected idio-pathic dilated cardiomyopathy.15 Instead, itshould be reserved for patients with suspectedinfiltrative disease of the myocardium, such ashemochromatosis or amyloidosis. It may alsobe considered in patients with fulminantheart failure to exclude giant cell myocarditis,which requires early and aggressive treatment.As our understanding of the pathogenesis ofdilated cardiomyopathy improves and ourtreatment options expand, endomyocardialbiopsy will undoubtedly be used more.

Skeletal muscle biopsySkeletal muscle biopsy may be performed inrare cases in which a primary muscle disorder(ie, Duchenne muscular dystrophy) is sus-pected.

■ TREATMENT

The treatment of idiopathic dilated cardiomy-opathy is similar to that of other types of low-output heart failure with systolic impairment.Lifestyle modification is important, with thor-ough patient education about proper diet andexercise and the need to avoid all cardiotox-ins (eg, alcohol). ACE inhibitors, beta-block-ers, diuretics, digoxin, anti-arrhythmics, and

anticoagulation are all used to some extent inthe medical management of all types of heartfailure, including idiopathic dilated cardiomy-opathy. We discuss below the significance ofseveral of these medications in the treatmentof low-output heart failure secondary to idio-pathic dilated cardiomyopathy.

Angiotensin-converting enzyme inhibitorsBy suppressing the activation of the renin-aldosterone-angiotensin system, therebydecreasing both preload and afterload, and bypreventing, slowing, or perhaps even reversingremodeling, angiotensin-converting enzyme(ACE) inhibitors are paramount in the treat-ment of idiopathic dilated cardiomyopathy.More than 30 large placebo-controlled clinicaltrials have shown that ACE inhibitorsimprove symptoms and significantly decreasemorbidity and mortality in heart failure,including heart failure due to idiopathic dilat-ed cardiomyopathy. At present, enalapril, cap-topril, lisinopril, quinapril, ramipril, and fos-inopril are all approved for the treatment oflow-output heart failure due to any cause.

Beta-blockersBeta-blockers have recently become standardtreatment for chronic compensated heart fail-ure, complementing the use of ACE inhibitors.By dampening the adrenergic neurohormonalrelease, beta-blockers have also been shown innumerous studies to decrease cardiovascularmorbidity and mortality in heart failure. Thecaveat is that is that beta-blockers may in factbe of more benefit to those with cardiomyopa-thy due to ischemia.16,17

Some investigators have observed thatmost patients with idiopathic dilated car-diomyopathy derive some benefit from beta-blocker treatment, while a small percentagemay demonstrate disease regression or evennormalization of the myocardium. As evi-denced by some 20 large, placebo-controlled,randomized trials including the US carvediloltrials, the Cardiac Insufficiency BisoprololStudy (CIBIS I and II), and MetoprololCR/XL Randomized Intervention Trial inCongestive Heart Failure (MERIT-HF), long-term treatment with beta-blockers improvessymptoms and lowers hospitalization anddeath rates. At present, carvedilol and meto-


More than 30large studiesshow that ACEinhibitorsreducemorbidity andmortality inheart failure





prolol are the only two beta-blockers approvedfor the treatment of chronic compensatedheart failure.

Antiarrhythmics,implantable cardiac defibrillatorAs discussed earlier, many patients with idio-pathic dilated cardiomyopathy experiencesome type of dysrhythmia, such as supraven-tricular tachycardia or nonsustained ventricu-lar tachycardia. As maintaining sinus rhythmis essential to maximize cardiac output andreduce the occurrence of emboli, treatment ofsupraventricular tachycardia in these patients

does not differ from that in any other clinicalsetting. Nonsustained ventricular tachycardia,a very common entity in these patients, usual-ly requires no treatment, whereas sympto-matic sustained ventricular tachycardia mayrequire placement of an implantable cardiacdefibrillator. Several trials are underway todetermine if implantable defibrillators are use-ful in idiopathic dilated cardiomyopathy.

AnticoagulantsCurrently, the role of anticoagulants in idio-pathic dilated cardiomyopathy is not welldefined. However, if the patient has a historyof thromboembolism or persistent or paroxys-mal atrial fibrillation, or has severe chamberdilatation, the clinician may consider initiat-ing anticoagulant therapy, typically warfarin.

If all else fails, cardiac transplantationWhen all other treatment options proveunsuccessful and the patient is deemed tohave terminal-stage heart failure, heart trans-plantation may be considered. Idiopathicdilated cardiomyopathy remains the primaryindication for heart transplantation in theUnited States. Success rates are high and con-tinue to improve. Prognosis after transplanta-tion has also improved dramatically, as sur-vival rates at 5 years and 10 years are now 74%and 55%, respectively.18 Cardiac transplanta-tion seems to be of more benefit in patientswith idiopathic dilated cardiomyopathy thanin patients with dilated cardiomyopathy dueto a known cause. Unfortunately, the scarcityof donor hearts currently limits the use of thistreatment option.

■ PROGNOSIS

Clinical survival studies show varying results,some of which may not be applicable at thistime with the advent of newer treatments.Before ACE inhibition was commonplace, themean survival rate at 5 years was approxi-mately 50%.19 At this time, some investiga-tors suggest that the mean survival rate at 5years is closer to 80%.20 Such improved sur-vival is thought to be due to improved physi-cian awareness of the condition, moreadvanced diagnostic and monitoring tech-niques, and improved medical and surgical


Predictors of poor prognosisin idiopathic dilated cardiomyopathy

Biochemical featuresElevated levels of angiotensin IIElevated levels of atrial natriuretic factorElevated levels of epinephrine (adrenaline)Elevated levels of norepinephrine (noradrenaline)

Clinical featuresHistory of syncopeMale sexNew York Heart Association class IVOlder agePersistent third heart sound, gallop rhythmSigns of right heart failure

Electrocardiographic featuresAtrial fibrillationFirst-degree or second-degree atrioventricular blockLeft bundle branch blockVentricular tachycardia

Exercise test featuresPeak oxygen consumption < 12 mL/kg/minute

Hemodynamic featuresCardiac indexHigh right atrial pressureLow mean arterial pressurePulmonary capillary wedge pressure >20 mm Hg

Ventriculographic featuresDecreased ventricular mass-volume ratioGlobal diffuse wall motion abnormalityLow left ventricular ejection fractionLarge left ventricular end-diastolic dimensionRight ventricular dilatationSpherical left ventricular geometry

T A B L E 3




treatments.During the clinical course of idiopathic

dilated cardiomyopathy, a number of clinicaland diagnostic measures may be monitored topredict prognosis (TABLE 3). The most impor-tant and best predictors are the New YorkHeart Association heart failure functionalclass, the left ventricular ejection fraction,and the peak oxygen consumption.

■ FUTURE CONSIDERATIONS

As our understanding of the pathogenesis ofidiopathic dilated cardiomyopathy evolves,many of the currently proposed etiologic path-ways may be elucidated and new ones discov-

ered, and future treatments may be tailored toparticular pathways. For example, severalstudies are currently examining the potentialrole of immunosuppressive drugs in the treat-ment of idiopathic dilated cardiomyopathy,with some encouraging preliminary results.21

As the prevalence of heart failure steadilyrises, the fact that more than half of all dilat-ed cardiomyopathy cases are still labeled idio-pathic is disturbing and frustrating to manyclinicians. We hope that the intensiveresearch efforts now underway provide a bet-ter understanding of and better treatmentoptions for idiopathic dilated cardiomyopathyin the future.


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17. MERIT-HF Investigators. Effect of metoprolol CR/XL inchronic heart failure: metoprolol CR/XL randomised inter-vention trial in congestive heart failure (MERIT-HF).Lancet 1999; 353:2001–2007.

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ADDRESS: Siva Mohan, MD, Atlanta Medical Center,Department of Internal Medicine/GME, 303 Parkway Drive NE,Box 423, Atlanta, GA 30312.

Too many casesof dilatedcardiomyopathyare still labeled‘idiopathic’

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