cardiomyopathies israel freeman, md associate professor of clinical medicine

Cardiomyopathies

Israel Freeman, MD

Associate Professor of Clinical Medicine

Cardiomyopathies

• The cardiomyopathies are a diverse group of disease

that are not related to the usual causes of hear disease.

• Cardiomyopathies are classified according to

hemodynamicc characteristics and etiology.

CardiomyopathiesWHO Classification

• Unknown cause(primary)– Dilated

– Hypertrophic

– Restrictive

– unclassified

• Specific heart muscle disease (secondary)– Infective

– Metabolic

– Systemic disease

– Heredofamilial

– Sensitivity

– Toxic

Br Heart J 1980; 44:672-673

CardiomyopathiesFunctional Classification

• Dilatated (congestive, DCM, IDC)– ventricular enlargement and syst dysfunction

• Hypertrophic (IHSS, HCM, HOCM)– inappropriate myocardial hypertrophy

in the absence of HTN or aortic stenosis

• Restrictive (infiltrative)– abnormal filling and diastolic function

Hemodynamic

Cardiac output Normal Normal to Normal or

Stroke volume Normal or ↑ Normal or

Normal or

Ventricular fillingpressure

↑ ↑ Normal or ↑ ↑ ↑ Usually ↑

Chamber size ↑ ↑ Normal or Normal or ↑ Typically

Ejection fraction

↑ ↑ Normal to Normal to

Diastolic compliance Normal or

Other findingsMay have associated functional mitral or tricuspid regurgitation

Obstruction may develop between interventricular septum and septal leaflet of mitral valveMitral regurgitation may be present

Characteristic ventricular pressure tracings that resemble those recorded in constrictive pericarditis, with early diastolic dip- and-plateau configuration

May be seen as a feature of the hypereosinophilic syndromesSome investigators consider it a form of restrictive cardiomyopathy

Dilated Hypertrophic RestrictiveObliterative

(Restrictive-Obliterative)

Morphologic

Biventricular dilatation

Marked hypertrophy of left ventricle and occasionally of right ventricle; usually but not always, disproportionate hypertrophy of septum

Reduced ventricular compliance; usually caused by infiltration of myocardium (e.g., by amyloid, hemosiderin, or glycogen deposits)

Thickened endocardium or mural thrombi, or both, act as space-occupying lesions

Morphologic and Hemodynamic Characteristics of the Cardiomyopathies

Etiologic Classification of Cardiomyopathies

Cardiomyopathies of Unknown Etiology

Idiopathic dilated cardiomyopathy Peripartum cardiomyopathy* Hypertrophic cardiomyopathy Endomyocardial fibrosis Subendocardial fibroelastosis Eosinophilic endomyocardial disease (also called

Löffler endocarditis or fibroplastic endocarditis) Right ventricular dysplasia Idiopathic restrictive cardiomyopathy

Secondary Cardiomyopathies

• When a cardiomyopathy has a definite etiology

(e.g. sarcoidosis or scleroderma) – signs of that

process are usually evident.

• On rare occasions, cardiac involvement may

precede other systemic manifestations.

Dilated (Congestive) Cardiomyopathies

• Idiopathic • Known etiology– Pregnancy

– Alcohol

– Toxic effects of drugs

– Tachycardia induced

– Sleep apnea?


Cardiomyopathies of Known Etiology

InfectiousViral and rickettsial myocarditis (e.g., human immunodeficiency virus, coxsackievirus B,* cytomegalovirus*)Septic (bacterial endocarditis*)SyphilisParasitic disease (e.g., Chagas disease, trichinosis,

toxoplasmosis)*Bacterial toxins (e.g., diphtheria toxin) or hypersensitivity (rheumatic fever)

Etiologic Classification of Cardiomyopathies Cardiomyopathies of Known Etiology

Toxic Alcohol* Cobalt* Carbon tetrachloride Carbon monoxide* Thioridazine drugs Anticancer agents (e.g. daunorubicin doxorubicin, cyclophosphamide) Antimonials Cocaine* Antiretroviral agents (e.g., zidovudine,* dideoxyinosine*) Interferon alfa



Systemic Diseases

Neuromuscular syndromes: muscular dystrophies (e.g., progressive muscular dystrophy, myotonic dystrophy), Friedreich ataxia Collagen vascular disease Sarcoidosis* Endocrine diseases* (e.g., thyrotoxicosis, myxedema,pheochromocytoma, acromegaly)

* Is potentially reversible



Infiltrative†

Amyloidosis Hemochromatosis Glycogen storage disease Fabry disease Hurler syndrome Primary or metastatic tumors (e.g., lymphoma, melanoma) † Usually causes a restrictive hemodynamic picture



Nutritional

Beriberi* Selenium deficiency* Kwashiorkor * Is potentially reversible



Ischemic *

* Is potentially reversible !!!

Idiopathic Dilated Cardiomyopathy

Congestive (Dilated) Cardiomyopathy - Definition

• a disease of unknown etiology that principally affects the myocardium

• LV dilatation and systolic dysfunction

• pathology– increased heart size and weight– ventricular dilatation, normal wall thickness– heart dysfunction out of portion to fibrosis

Secondary Congestive (Dilated) Cardiomyopathy

• Infectious and Autoimmune processes (Myocarditis)

– Coxsackie virus B e.t.

– Autoimmune processes

• Acute Myocarditis vs. Congestive Cardiomyopathy

– Fever with CHF

– Pericarditis

– Elevated CPK – MB , TnT ( less than 30% of myocarditos)

Dilated (Congestive) Cardiomyopathy

• A familial form may be present in 10 – 30%

• Characterized by diminished myocardial

contractility

– Reflected in reduction of systolic function. ( EF , LV

EDP , SV , C.O )

– RV dysplasia characterized by RV failure and VT

Dilated (Congestive)Cardiomyopathy Clinical Manifestations

• Highest incidence in middle age– blacks 2x more frequent than whites– men 3x more frequent than women

• symptoms may be gradual in onset• acute presentation

– misdiagnosed as viral URI in young adults– uncommon to find specific myocardial disease

on endomyocardial biopsy

Dilated (Congestive) Cardiomyopathy• Clinical Features

– Dyspnea and fatigue– Palpitation, occasionally syncope– Systemic and pulmonary emboli (+4 % / year)– Chest pain ( 1/3 of patients)-atypical

• Physical Finding– Reflects the variable severity of CHF

• Diagnostic Studies– CXR, EKG, Echocardiogram (segmental vs global asynergy)– MRI (Dysplastic RV Cardiomyopathy)– Gallium 67 ( sarcoidosis, myocarditis)

• Cardiac Catheterization

Posteroanterior CXR of a 52 y.o man with idiopathic dilated cardiomyopathy exhibit diffuse cardiomegaly. The LA can be seen as a faint double density.

Lateral view of the same patient

Echocardiogram: Severe Dilated Cardiomyopathy

Apical four-chamber echocardiographic view of a patient with severe dilated cardiomyopathy. All four cardiac chambers are markedly enlarged. The left ventricular ejection fraction was 22%, and the left ventricular end-diastolic

diameter was 74 mm.

Dilated (Congestive) Cardiomyopathy

• Endomyocardial Biopsy

– Low diagnostic yield

– Uncertainty regarding role of immunosuppressive therapy

– Led most investigators to abandon it routine use

Endomyocardial Biopsy: Myocarditis

A 19y.o. man; presented with DCM and VPCs. The findings of focal lymphocytic infiltrates, interstitial edema, and myocyte degeneration are typical of myocarditis. The patient responded to prednisone.

Biopsy: End-Stage Dilated Cardiomyopathy

An 80 y.o. man with end-stage CM. There is marked hypertrophy of myocytes, interstitial and focal fibrosis,and no evidence of interstitial inflammation. Immunosuppressive therapy was not indicated.

Dilated Cardiomyopathy (DCM)Course and Prognosis

• The most common complication of DCM is progressive CHF – the cause of death in 50 – 75%

• Sudden death (SD) by arrhythmia is common especially in patients with complex ventricular ectopy and severe LV dysfunction.

• Systemic / pulmonary embolism is found at autopsy in 50% of patients with DCM – emboli can cause catastrophic complications but rarely death.

• Prognosis varies considerably from fulminent cases that result in death within a few weeks, or conversely some patients do remarkably well for years. Most death within 5 years.

• Spontaneous improvement in LV function occurs in 20 – 40%, most frequently within 6 months.

• A peak 02 uptake less than 14 ml/kg /min predicts 1 year survival of 70%.

Survival in Symptomatic Idiopathic Dilated Cardiomyopathy

Survival symptomatic IDC in seven reported series. Study A, 1986-89 (basis for selection unspecified); study B, 1975-84 (population based); study C, 1973-87 (referral based); study D, 1962-82 (referral based); study E, 1960-73 (referral based); study F, 1972-82 (referral based); study G, 1965-86 (autopsy series). (N

number of patients)

Dilates Cardiomyopathy Medical Treatment

• Limit activity based on functional status

• salt restriction of a 2-g Na+ (5g NaCl) diet

• fluid restriction for significant low Na+

• initiate medical therapy– ACE inhibitors, diuretics– digoxin, carvedilol– hydralazine / nitrate combination

Dilates Cardiomyopathy Medical Treatment

• Principally standard CHF therapy

• Anticoagulation therapy is controversial some arthritis recommend

with marked right sided failure and/or BF < 30

• Antiarrhythmics: arrhythmias are common Empirical suppression in

symptomatic patient is contraindicated (CAST) due to proarrhythmic

effect. In symptomatic patients – amiodarone (GESICA 26% reduced

mortality vs. STAT – CHF)

• Defibriallation: SAEKG and EP are not reliable in assessing prognosis

or guide antiarrhythimic therapy in patients with DCM. ICD is

indicated in patients with sustained V.T. In NSVT the MADIT trail

demonstrated an advantage for ICD those were IHD (inducible )

patient, MADIT doesn’t apply. Trial results pending.

Hypertrophic Cardiomyopathy


• The hallmark of the disease is unexplained myocardial hypertrophy

• In the obstructive form: ASH, SAM. MR

• Obstruction may be fixed or labile

• Hyper-contractile LV (EF 80 – 90%) with reduced ESV.

• Reduced LV compliance (if patient in CHF – diastolic)

• Factor that provoke or increase/decrease obstruction:

– Change in contractile stale

– Change chamber – size (preload and after load)

Coronal Section in Hypertrophic Cardiomyopathy

The thickening of the IVS is disproportionately greater than that of the LV wall behind the posterior mitral leaflet. The LV chamber is small and elongated.

Myofibrillar Pattern in HCM vs. HTN

Different myofibrillar patterns in tissue taken from the septum of a patient with HCM (left) and from the hypertrophied LV of a patient with HTN (right). Note the chaotic

arrangement of the cells of septal myocardium taken from the HCM. In contrast, note the orderly parallel arrangement of myofibrils in ventricular myocardium in the HTN patient.

Hemodynamic

Cardiac output Normal Normal to Normal or

Stroke volume Normal or ↑ Normal or

Normal or

Ventricular fillingpressure

↑ ↑ Normal or ↑ ↑ ↑ Usually ↑

Chamber size ↑ ↑ Normal or Normal or ↑ Typically

Ejection fraction

↑ ↑ Normal to Normal to

Diastolic compliance Normal or

Other findingsMay have associated functional mitral or tricuspid regurgitation

Obstruction may develop between interventricular septum and septal leaflet of mitral valveMitral regurgitation may be present

Characteristic ventricular pressure tracings that resemble those recorded in constrictive pericarditis, with early diastolic dip- and-plateau configuration

May be seen as a feature of the hypereosinophilic syndromesSome investigators consider it a form of restrictive cardiomyopathy

Dilated Hypertrophic RestrictiveObliterative

(Restrictive-Obliterative)

Morphologic

Biventricular dilatation

Marked hypertrophy of left ventricle and occasionally of right ventricle; usually but not always, disproportionate hypertrophy of septum

Reduced ventricular compliance; usually caused by infiltration of myocardium (e.g., by amyloid, hemosiderin, or glycogen deposits)

Thickened endocardium or mural thrombi, or both, act as space-occupying lesions

Morphologic and Hemodynamic Characteristics of the Cardiomyopathies

Pathophysiology

• Systole– dynamic outflow tract gradient

• Diastole– impaired diastolic filling, filling pressure

• Myocardial ischemia muscle mass, filling pressure, O2 demand vasodilator reserve, capillary density– abnormal intramural coronary arteries– systolic compression of arteries

Hypertrophic Cardiomyopath

Hypertrophic Cardiomyopath*

• Obstructive (fixed, Rabile)

• Non Obstructive– Concentric

– Mid ventricular

– Apical

* The vast majority of cases of hypertrophic cardiomyopathy result from specific defects in the genes regulating the formation of cardiac muscle This defect is either sporadic or hereditary in 50% of cases (autosomal dominant).

65% 35%

10%

Survival Curves in Hypertrophic Cardiomyopathy

The surviv al of patients with hypertrophic cardiomyopathy caused by different mutations: cardiac troponin T mutations (introns 15 G1 A, Ile79Asn, Glu160,

and Arg92Gln) is similar to that in persons with a malignant -myosin heavy-chain mutation (Arg403Gln) but significantly shorter than that observed in persons with a benign myosin mutation (Val606Met).

Factors That Influence the Degree of Obstruction in Hypertrophic Cardiomyopathy*

Factors That Increase Obstruction Factors That Decrease Obstruction

Mechanism Physiologic or Pharmacologic Factor Mechanism Physiologic or Pharmacologic Factor

Increase in contractility

Digitalis glycosidesBeta-adrenergic stimulation (e.g., isoproterenol, epinephrine)TachycardiaPremature beats

Decrease in contractility

Beta-adrenergic blockade (e.g., propranolol)Heavy sedation and general anesthesiaCalcium channel blockers, disopyramide, and other drugs that depress myocardial function

Reduction in preload

Valsalva maneuver†

Decrease in intravascular volume (e.g., from hemorrhage, diuresis, GI losses)Standing†

Nitroglycerin and related drugs†

Vasodilator drugsTachycardia

Increase in preload

Intravascular volume expansionSquatting†

BradycardiaBeta-adrenergic blockade

Reduction in afterload

HypovolemiaNitroglycerin and related drugs†

Vasodilator drugs

Increase in afterload

Intravascular volume expansionSquatting†

Alpha-adrenergic stimulation (e.g., phenylephrine, mephentermine)Handgrip exercise†

*In general, anything that increases obstruction will increase the intensity of the associated murmurs, whereas factors that reduce obstruction will diminish murmur intensity.

†May assist in diagnosis at the bedside.

Hypertrophic Cardiomyopathic Diagnosis

• Symptoms

– Angina (recumbent position)

– Syncope (after exercise, arrhythmia)

– Palpitations (A.F, VT)

– CHF (atrail contraction, AF with fast response)

– Systemic embolism

– S.D. (even in asymptomatics) lethal arrhythmia more

likely in young

• Physical examination

• EKG, Echocardiography, Cardiac Cath

Changes of Murmer in Obstructive Hypertrophic Cardiomyopathy

Variations in the quality of the murmur associated with HOCM are observed before (a), during (b), and after (c) the Valsalva maneuver. Before the Valsalva maneuver, a soft systolic murmur is recorded at the apex. The arterial pulse contour is normal. During the Valsalva maneuver, there is a dramatic increase in the intensity of the murmur. After Valsalva release, the murmur becomes softer, but the carotid pulse exhibits the classic spike-and-dome configuration characteristic of obstructive hypertrophic cardiomyopathy.

Change in Gradient and Murmur Contractility Preload Afterload valsalva (strain) -- standing --postextrasystole -- isoproterenol digitalis --amyl nitrite nitroglycerine exercise tachycardia --hypovolemia

Hypertrophic Cardiomyopathic

Change in Gradient and Murmur

Contractility Preload Afterloadvalsalva (overshoot) -- squatting --- passive leg elevation __--phenylephrine -- beta-blocker -- -- general anesthesia -- --isometric grip --

Hypertrophic Cardiomyopathic

Hypertrophic Cardiomyopathy HCM vs Aortic Stenosis

HCM Fixed Obstruction

carotid pulsespike and dome parvus et tardus

murmur radiate to carotids valsalva, standing squatting, handgrip passive leg elevation

systolic thrill 4th left interspace 2nd right interspacesystolic click absent present

ECG in Obstructive Hypertrophic Cardiomyopathy

Abnormal Q waves suggestive of an old anterior myocardial infarct are observed in leads V3 through V6 in an ECG recorded in a 45-year-old woman with obstructive hypertrophic cardiomyopathy.

Hypertrophic Cardiomyopathy -Echocardiography

Pressure Tracings: Obstructive Hypertrophic Cardiomyopathy

Classic left ventricular and radial arterial pressure tracings are recorded simultaneously in a patient with Obstructive HCM. An initial rapid upstroke is observed in both recordings. As obstruction develops, a notch (arrow) appears in the left ventricular tracing, accompanied by a fall in the arterial pressure. Slower ejection follows, producing a second rise in the arterial tracing. The events are observed slightly later in the radial artery than in the left ventricle because some delay occurs in the transmission of the impulse to the artery.

HOCM-Brockenbrough Phenomenon

Simultaneous LV and radial arterial pressure tracings in a patient with HOCM show the Brockenbrough phenomenon in response to a VPB. The gradient across the LVOT is about 80 mm Hg. After the VPB, there is a compensatory pause. In the beat that follows the compensatory pause, the radial pulse pressure narrows, and the arterial pressure falls despite an increase in the left ventricular systolic pressure.

Clinical Manifestation

• Asymptomatic, echocardiographic finding

• Symptomatic– dyspnea in 90%– angina pectoris in 75%– fatigue, pre-syncope, syncope

risk of SCD in children and adolescents– palpitation, PND, CHF, dizziness less frequent


Hypertrophic Cardiomyopathy Course and Prognosis

• Course and prognosis exceedingly variable– Most patient do very well– Some experience progression of symptoms

• S.D.– More common in children and young adults (younger than 25

years) with the familial form of the disease– May result from arrhythmia even without significant LVH or

LVOT obstruction– May result from development of LVOT obstruction with

exercise– Hyperthrophy progresses, some patient with no obstruction

will develop it later in life (progression is faster in the younger)

Hypertrophic CardiomyopathyTreatment of symptomatic patients

– Beta blockers and calcium channel blockers• Provide relief of angina, dyspnea syncope and improve exercise capacity • Diuretics• Digitalis glycosides (AF?)

– Prophylactic measures (secondary)• Endocarditis• S.D. – Markers of increased risk: young age

– massive hypertrophy,m VT, NSVT, VF– h/o syncope and family h/o of S.D. – Troponin T gene mutations

Treatment of asymptomatic patients – Primary prophylaxis • Beta Blockers• If strong family history of S.D – amioclorone / ILD• Prohibition from engagement in competitive sports

Hypertrophic – Cardiomypathy Surgical Treatment

• Cardiac Pacing

• Septostomy

• Chemical septal ablation

Chemical Septal Ablation in Hypertrophic Cardiomyopathy

Results of chemical septal ablation in a 77-year old woman with HOCM. Simultaneous left ventricular and radial artery pressure recordings (a) show a gradient of approximately 140 mm Hg across the LVOT. Moments after injection of alcohol into the interventricular septum (b), the gradient is abolished. (LV-left ventricle; RAD-radial artery)

Risk Factors for SCD

• Young age (<30 years)• “Malignant” family history of sudden death• Gene mutations prone to SCD (ex. Arg403Gln)• Aborted sudden cardiac death• Sustained VT or SVT• Recurrent syncope in the young• Nonsustained VT (Holter Monitoring)• Brady arrhythmias (occult conduction disease)

Br Heart J 1994; 72:S13


Hypertrophic Cardiomyopathy Recommendations for Athletic Activity

• Avoid most competitive sports (whether or not symptoms and/or outflow gradient are present)

• Low-risk older patients (>30 yrs) may participate in athletic activity if all of the following are absent

Hypertrophic Cardiomyopathy Recommendations for Athletic Activity

• Low-risk older patients (>30 yrs) may participate in athletic activity if all of the following are absent– ventricular tachycardia on Holter monitoring

– family history of sudden death due to HCM

– history of syncope or episode of impaired consciousness

– severe hemdynamic abnormalities, gradient 50 mmHg

– exercise induced hypotension

– moderate or sever mitral regurgitation

– enlarged left atrium (50 mm)

– paroxysmal atrial fibrillation

– abnormal myocardial perfusion

Hypertrophic Cardiomyopathy –Key Points

•Medical therapy with -blockers is first-line management of hypertrophic cardiomyopathy; verapamil is an alternative.

•Patients with syncope, a family history of sudden death, or documented ventricular tachycardia are at highest risk of sudden death and should be promptly referred for evaluation by an electrophysiologist.

•For patients with hypertrophic cardiomyopathy refractory to medical therapy, surgical septal myectomy or percutaneous ethanol septal ablation can be considered. Pacing therapy has limited efficacy.

•Participation in all but low-intensity competitive sports is contraindicated for patients with hypertrophic cardiomyopathy.

Other Causes of Hypertrophy

• Clinical mimics

– glycogen storage, infants of diabetic mothers, amyloid

• Genetic

– Noonan’s, Friedreich’s ataxia, Familial restrictive cardiomyopathy with disarray

• Exaggerated physiologic response

– Afro-Caribbean hypertension, old age hypertrophy, athlete’s heart

Hypertrophic Cardiomyopathy HCM vs Athlete’s Heart

HCM Athlete+ Unusual pattern of LVH -+ LV cavity <45 mm -- LV cavity >55 mm ++ LA enlargement -+ Bizarre ECG paterns -+ Abnormal LV filling -+ Female gender -- thickness with deconditioning ++ Family history of HCM -

Circulation 1995; 91:1596

Hypertensive HCM of the Elderly Characteristics

– modest concentric LV hypertrophy (<12 mm)– small LV cavity size– associated hypertension– ventricular morphology greatly distorted with

reduced outflow tract– sigmoid septum and “grandma SAM”

Restrictive Cardiomyopathy

Restrictive Cardiomyopathies

• Hallmark: abnormal diastolic function

• rigid ventricular wall with impaired ventricular filling

• bear some functional resemblance to constrictive pericarditis

• importance lies in its differentiation from operable constrictive pericarditis


• Usually results from diseases that infiltrate the

myocardium

– Amyloidosis

– Hemochromatosis

– Glycogen storage diseases

• Many cases of restrictive cardiomyopathies are

idiopathic

Restrictive Cardiomyopathies Ethiology

• Idiopathic• Myocardial

1. Noninfiltrative– Idiopathic– Scleroderma

2. Infiltrative– Amyloid– Sarcoid– Gaucher disease– Hurler disease

3. Storage Disease– Hemochromatosis– Fabry disease– Glycogen storage

• Endomyocardial– endomyocardial fibrosis– Hyperesinophilic synd– Carcinoid– metastatic malignancies– radiation, anthracycline


• Etiology– Usually a product of infiltrative disease such as:

Aermytoidosis, Hemochromatosis Glycogen stroge disease.– Idiopathic – not uncommon.

• Pathophysiology– Rigid myocardium impeding ventricular LVEDP increased,

systolic performance is often reduced

• Diagnosis– CHF often predominant right sided failure (Kussmaul sign)– Differential diagnosis – constrictive Pericarditis.

• Unequal diastolic pressures, more ventricular independence in constriction, pulmonary HTN more in restriction .

Clinical Manifestations

• Symptoms of right and left heart failure

• Jugular Venous Pulse – prominent x and y descents

• Echo-Doppler– abnormal mitral inflow pattern– prominent E wave (rapid diastolic filling)– reduced deceleration time ( LA pressure)

Restrictive Cardiomyopathies

Restrictive Cardiomyopathy- Pressure Tracing

Shown is a right atrial pressure tracing in a patient with restrictive cardiomyopathy secondary to amyloidosis; some functional tricuspid regurgitation is present. The cardiac rhythm is atrial fibrillation. Large systolic (V) waves appear, followed by a typical early diastolic dip-and-plateau configuration.

Constrictive - Restrictive Pattern“Square-Root Sign” or “Dip-and-Plateau”

Constrictive Pericarditis

• Fibrous scarring, adhesion and calcification of the pericardium

(shell around the heart)

• Similar to tamponade in restricting diastolic filling of the

heart. Kussmaul sign v.s. paradoxical pulse.

• Difficult diagnosis: Venous congestion, fatigue, effusions with

normal LV function, normal pulmonary pressure and a small

cardiac silhouette no pulmonary congestion.

• CT / MRI: pericardial thickening

• Echo / Doppler: Flow respiratory variation

• Treatment: Conservative / Surgical

Restriction vs Constriction

History provide can important clues• Constrictive pericarditis

– history of TB, trauma, pericarditis, sollagen vascular disorders

• Restrictive cardiomyopathy– amyloidosis, hemochromatosis

• Mixed– mediastinal radiation, cardiac surgery

Restrictive Cardiomyopathies Treatment

• No satisfactory medical therapy

• Drug therapy must be used with caution– diuretics for extremely high filling prssures– vasodilators may decrease filling pressure– ? Calcium channel blockers to improve

diastolic compliance– digitalis and other inotropic agents are not

indicated

Restrioctive Cardiomyopathy Key Points

. Restrictive cardiomyopathy often manifests as an insidious onset of exercise intolerance and right-sided heart failure similar to constrictive pericarditis

cardiomyopathies israel freeman, md associate professor of clinical medicine

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