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AUTHOR AND EDITOR INFORMATION
Section 1 of 11  
Author: Robert E Shaddy, MD, Professor of Pediatrics, University of Pennsylvania School of Medicine; Division Chief of Pediatric Cardiology, Children's Hospital of Philadelphia
Robert E Shaddy is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Medical Association, International Society for Heart and Lung Transplantation, Phi Beta Kappa, Society for Pediatric Research, and Western Society for Pediatric Research
Editors: Jeffrey Towbin, MD, Associate Chair of Pediatric/Cardiology, Departments of Pediatrics, Molecular and Human Genetics, Cardiovascular, Professor, Baylor College of Medicine and Texas Children's Hospital; Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc; Ameeta Martin, MD, Associate Professor, Department of Pediatrics, Section of Pediatric Cardiology, University of Nebraska College of Medicine; Gilbert Herzberg, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Steven Neish, MD, SM, Director of Pediatric Cardiology Fellowship Program, Department of Pediatrics, Baylor College of Medicine
Author and Editor Disclosure
Synonyms and related keywords:
restrictive cardiomyopathy, RCM, restriction of diastolic filling, dyspnea, right ventricular failure, idiopathic RCM, familial RCM, myocardial RCM, endomyocardial RCM, hypertrophic cardiomyopathy, diabetic cardiomyopathy with a restrictive component, amyloidosis, sarcoidosis, Gaucher disease, Gaucher's disease, Hurler disease, Hurler's disease, glycogen storage disease, amyloidosis, endomyocardial fibrosis, endocardial fibroelastosis, paroxysmal nocturnal dyspnea, orthopnea, peripheral edema, ascites, congestive heart failure, tachypnea, sarcoidosis, carcinoid syndrome
Background
Restrictive cardiomyopathy (RCM) is a rare disorder in children that is characterized by abnormal diastolic filling or compliance with normal or decreased diastolic volume of the ventricular chamber. The heart is structurally normal, although histologic abnormalities are often present, depending on the etiology of the RCM. Systolic ventricular function is usually preserved. RCM may manifest as a solitary abnormality, although restrictive filling patterns of the left ventricle can be seen in patients with dilated or hypertrophic cardiomyopathy. Because this disease is so rare, its pathogenesis, natural history, and treatment are not well defined. Treatment is constantly changing as more data accumulate. Some investigators have divided RCM into the following subtypes: (1) pure restrictive form, (2) hypertrophic-restrictive form, and (3) mildly dilated restrictive form.
Pathophysiology
The pathophysiology is diverse. RCM can be associated with rare diseases, such as amyloidosis, hemosiderosis, hypereosinophilia, and endocardial fibroelastosis; it can also result from radiation therapy. However, these may be considered separate diseases because the etiology is known.
In true idiopathic RCM, pathologic specimens have shown myocyte hypertrophy, myofibrillar disarray, and increased interstitial connective tissue. Endomyocardial biopsy findings are usually abnormal, although findings may not be diagnostic for any one disease. Findings include myocyte hypertrophy, interstitial fibrosis, and myocytolysis. The physiological consequences of RCM are more uniform than those of its diverse etiologies. Physiology is typically characterized by an abrupt premature cessation of ventricular filling in early diastole, causing a dip-plateau pattern on ventricular pressure tracing. Therefore, ventricular filling is limited to early diastole. This ultimately results in decreased compliance of the ventricle with development of left atrial dilation. Typical hemodynamic characteristics include normal systolic function and equalization of increased ventricular end-diastolic pressures. Morphologic findings include atrial enlargement without increased ventricular wall thickness or ventricular cavity dilation, the absence of eosinophilic infiltration, and the absence of pericardial disease. The natural history varies and at least partially depends on the etiology of the RCM, if any is identified. Because the number of patients that have subclinical RCM is unknown, the natural history can be determined only when symptoms develop. Once symptoms develop, the morbidity and mortality are high (see Morbidity/Mortality).
Frequency
United States
Although exact incidence is unknown, RCM is the least common cardiomyopathy and represents approximately 5% of pediatric cardiomyopathies.
International
Reports from Europe and Asia suggest similar international infrequency.
Mortality/Morbidity
- Mortality rates in children with idiopathic RCM are high, particularly in the absence of heart transplantation.
- Rates have been reported to be as high as 63% within 3 years of diagnosis and 75% within 6 years of diagnosis.
- Actuarial survival range is 44-50% at 1-2 years after presentation. This decreases to 29-37% at 3-4 years after presentation.
Race
No racial predilection is known.
Sex
Some studies suggest that idiopathic RCM may be slightly more common in girls than in boys.1
Age
Idiopathic RCM has been described in children of all ages.
History
- Reasons for referral
- Abnormal chest radiography findings during a respiratory illness
- Abnormal physical findings (see Physical)
- Syncope
- Positive family history
- Respiratory symptoms
- Dyspnea with exertion or at rest
- Paroxysmal nocturnal dyspnea
- Orthopnea
- Peripheral edema
- Ascites
- General fatigue and weakness
- Typical history of congestive heart failure
Physical
- Findings usually reflect the degree of congestion from the diastolic dysfunction of the affected ventricle and the resultant degree of decreased cardiac output. In patients who are only mildly affected, physical examination findings may be normal. However, patients with significant left ventricular restrictive cardiomyopathy (RCM) have pulmonary venous congestion with tachypnea. Older patients in this category occasionally present with crackles.
- Murmurs and gallop rhythms are common. Evidence of right-sided congestion (manifested as hepatomegaly and/or jugular venous distention) is usually present, either because of right-sided RCM or as a secondary congestion from left-sided RCM. Sometimes, the jugular venous pulse fails to fall during inspiration and may actually rise (Kussmaul sign).
- In more severe forms, patients can present with peripheral edema or ascites and frank congestive heart failure.
- Arrhythmias may occur in RCM, including atrial fibrillation, flutter, and ventricular tachycardia.
Causes
- The etiology is unknown in most pediatric cases, hence the title idiopathic RCM.
- RCM can be divided into myocardial or endomyocardial types.
- Noninfiltrative myocardial types include the following:
- Idiopathic
- Familial
- Hypertrophic cardiomyopathy
- Diabetic cardiomyopathy with a restrictive component
- Infiltrative myocardial diseases include the following:
- Amyloidosis
- Sarcoidosis
- Rare congenital diseases such as Gaucher disease, Hurler disease, and glycogen storage diseases
- Outside the tropics, the most common cause of RCM is amyloidosis. However, in tropical areas of the world, endomyocardial fibrosis is endemic.
- Common causes of other forms of endomyocardial RCM include the following:
- Hypereosinophilic syndromes
- Carcinoid heart disease
- Metastatic cancers
- Pseudoxanthoma elasticum
- Certain drugs
- Common causes of secondary RCM include the following:
- Radiation
- Anthracycline toxicity
- Most RCMs (including idiopathic) are not inherited. However, some inherited infiltrative disorders can cause RCM. These include Fabry disease (X-linked recessive), Gaucher disease (autosomal recessive), glycogen storage diseases, and autosomal recessive hemochromatosis.
- Risk factors for RCM are unknown.
- Associated syndromes and noncardiac conditions include scleroderma, amyloidosis, sarcoidosis, Gaucher disease, Hurler disease, glycogen storage diseases, hypereosinophilic syndrome, and carcinoid syndrome.
- Significant progress has been made in defining the genetic causes of RCM. These causes include mutations in the following genes: troponin I, troponin T, lamin A/C, RSK2, and desmin.2, 3, 4, 5, 6
Pericarditis, Constrictive
Other Problems to be Considered
The main differential diagnosis is constrictive pericarditis. Differentiation can be difficult, particularly in children who have received anthracycline drugs and thoracic radiation as cancer therapy. Cardiac catheterization and Doppler echocardiography are generally able to distinguish between the conditions, although both are characterized by abnormal diastolic ventricular filling and elevated ventricular end-diastolic pressures.
For example, ventricular end-diastolic pressures in restrictive cardiomyopathy are generally discordant, with left ventricular end-diastolic pressure higher than right ventricular end-diastolic pressure. In addition, echocardiographic evidence of minimal respiratory variation in Doppler ventricular inflow signals is observed in patients with restrictive cardiomyopathy (RCM) compared with the significant respiratory variation that is observed in patients with constrictive pericarditis.
Lab Studies
- Laboratory studies generally do not contribute to the diagnosis.
Imaging Studies
- Chest radiography
- In children, heart size is usually enlarged, often with evidence of right or left atrial enlargement.
- Pulmonary venous congestion is often evident.
- Echocardiography
- Echocardiography is often diagnostic for restrictive cardiomyopathy (RCM). Results usually include marked atrial enlargement with normal left ventricular end-diastolic dimensions. Ventricular hypertrophy and atrioventricular valve dysfunction are often present.
- Atrial thrombi and pulmonary vein atrial flow reversal duration that exceeds mitral a wave duration have also been described.
- Echocardiography is very useful in distinguishing RCM from constrictive pericarditis. Patients with constrictive pericarditis show marked respiratory variation in left ventricular isovolumic relaxation time and in early mitral and tricuspid flow velocities. Prolongation of the ratio of systole to diastole is observed in pediatric RCM, although this abnormality is also found in children with dilated cardiomyopathy.
- Mid-diastolic reversal of flow across mitral and tricuspid valves is also more common in RCM. Unfortunately, Doppler echocardiographic findings still show overlap between RCM and constrictive pericarditis.
- Echocardiography may demonstrate a thickened pericardium in patients with constrictive pericarditis.
- CT scanning and MRI: These may be useful for assessing pericardial thickness in patients when constrictive pericarditis is in the differential diagnosis.
Other Tests
- Electrocardiography
- Electrocardiography usually reveals evidence of atrial enlargement and ST-T wave changes.
- Infiltrative diseases can have low voltage changes.
- An arrhythmia may be present, including atrial fibrillation.
- Familial RCM is associated with atrioventricular block.
- Because of risk of sudden deterioration and death, some investigators recommend serial electrocardiography and Holter monitoring to observe for evidence of ischemia and arrhythmia.
Procedures
- Cardiac catheterization
- This is generally indicated to assess hemodynamics.
- Pulmonary artery pressures are usually elevated. Right and left ventricular end-diastolic pressures are elevated, and left ventricular end-diastolic pressure is usually significantly higher (>5 mm Hg) than right ventricular end-diastolic pressure.
- Endomyocardial biopsy: This may reveal a specific cause but appears to be much more helpful in adults than in children. Thus, indications must be individualized.
Histologic Findings
Findings from biopsy or autopsy are usually abnormal but are not necessarily diagnostic. Varying degrees of myocyte hypertrophy, interstitial fibrosis, myocytolysis, and endocardial sclerosis have been found. In those patients (usually adults) with an infiltrative cause, such as amyloidosis, biopsy findings may be diagnostic.
Medical Care
- Therapy for idiopathic restrictive cardiomyopathy (RCM) is limited to symptomatic treatment and is often ineffective in improving outcome.
- Diuretics reduce pulmonary or systemic venous congestion; however, some patients may require high ventricular filling pressures to maintain cardiac output and may actually feel worse after diuresis.
- Digoxin has not been shown to be beneficial with normal systolic function and should be used with caution.
- Anticoagulation should be considered because of significant risk of thromboembolic complications.
- Previous pediatric studies have suggested that angiotensin-converting enzyme inhibitors may acutely reduce systemic blood pressure without increasing cardiac output; therefore, they should probably be avoided.
Surgical Care
Surgical options are limited to heart transplantation. - Children with RCM should be considered early for heart transplantation, particularly if they are symptomatic or have evidence of pulmonary hypertension. Children with RCM are at higher risk for development of pulmonary hypertension than children with dilated or hypertrophic cardiomyopathy and need to be closely monitored for progression of pulmonary hypertension.
- Patients with significantly elevated but reversible pulmonary hypertension should be considered early for heart transplantation. However, those with normal or only mildly elevated pulmonary vascular resistance may remain stable for years and may not require urgent listing for heart transplantation. In patients with systemic infiltrative processes such as sarcoidosis, transplantation may not be a viable option because recurrence is a major concern.
- Standard techniques for heart transplantation are used in children with RCM, although they may require careful monitoring and treatment of pulmonary hypertension postoperatively.7 Sildenafil may be beneficial in helping to manage postoperative pulmonary hypertension in these patients, even in those who require heterotopic heart transplantation.8
- Results of heart transplantation in children with RCM are generally quite good but depend on the degree of pulmonary hypertension and resultant postoperative complications.
- Children who have undergone heart transplantation for RCM are treated with the usual immunosuppressive protocols. In those with pretransplant evidence of pulmonary hypertension, special attention must be paid to monitoring and treating this complication. Some patients may require such treatments as high levels of inspired oxygen or hyperventilation. Pulmonary vasodilators, such as prostaglandin E1 (PGE1), prostacyclin, sodium nitroprusside, enoximone, alkalinization, and nitric oxide, have all been used with some success in this situation. In extreme cases, mechanical circulatory assistance (eg, extracorporeal membrane oxygenation [ECMO]) may be necessary.
Diet
A normal diet is recommended.
Activity
The degree of hemodynamic abnormality and the risk of sudden death are significant, and patients should be restricted from competitive athletics, although this is not well documented.
Drug Category: Diuretic agents
These agents promote excretion of water and electrolytes by the kidneys. Treatment with diuretics may improve symptoms of venous congestion. However, these agents should be used with caution, because some patients require high venous filling pressures to maintain adequate cardiac output.
| Drug Name | Furosemide (Lasix) |
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| Description | Loop diuretic that blocks the sodium-potassium-chloride transporter and works primarily on thick ascending limb of the loop of Henle. Also inhibits sodium and chloride absorption from the proximal and distal tubules. |
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| Adult Dose | 10-80 mg/dose PO/IV/IM qd or prn |
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| Pediatric Dose | 0.5-2 mg/kg/dose PO/IV/IM qd or prn |
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| Contraindications | Documented hypersensitivity; hypokalemia; renal failure; hepatic failure with impending encephalopathy; severe uncorrected electrolyte abnormalities |
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| Interactions | NSAIDs diminish response because they increase solute reabsorption; NSAIDs can cause hyperkalemia; probenecid can diminish proximal tubular secretion of loop diuretics; ACE inhibitors enhance hypotension; sotalol enhances hypotension and risk of cardiac arrhythmia; increases nephrotoxicity of cephalosporins; ototoxicity may be increased with concomitant administration of aminoglycosides |
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| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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| Precautions | Use with caution in hepatic disease; potential adverse effects include ototoxicity, electrolyte disturbances (hypokalemia, hypocalcemia, alkalosis), hyperuricemia, dehydration, and nephrocalcinosis; administer PO dose with food or milk to decrease stomach upset |
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| Drug Name | Chlorothiazide (Diuril) |
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| Description | Thiazide diuretics block the electroneutral sodium-chloride transporter. |
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| Adult Dose | 25-100 mg/kg/d PO qd or divided bid; typically 0.5-2 g/d |
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| Pediatric Dose | Neonates: 20-40 mg/kg/d PO divided bid
Children: 20 mg/kg/d PO divided bid |
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| Contraindications | Documented hypersensitivity; dehydration; anuria |
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| Interactions | NSAIDs diminish response to thiazide diuretics because they increase solute reabsorption; NSAIDs can also cause hyperkalemia; may decrease the effectiveness of anticoagulants, antigout agents, and sulfonylureas; amphotericin B and anticholinergics may increase the toxicity |
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| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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| Precautions | May cause electrolyte imbalances and hyperuricemia; safety of IV use in children has not been established; not to administer IM/SC |
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| Drug Name | Metolazone (Zaroxolyn) |
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| Description | Quinazoline diuretic with properties similar to thiazide diuretics. Inhibits sodium resorption at cortical diluting site and proximal convoluted tubule. |
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| Adult Dose | 5-20 mg PO qd |
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| Pediatric Dose | 0.2-0.4 mg/kg/d PO qd or divided bid |
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| Contraindications | Documented hypersensitivity; anuria; hepatic coma |
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| Interactions | Concurrent administration with loop diuretics can result in unusually large or prolonged diuresis; increases the toxicity of digoxin and lithium |
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| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
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| Precautions | Can cause electrolyte imbalance, GI disturbance, hyperglycemia, marrow suppression, chills, hyperuricemia, chest pain, hepatitis, and rash |
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| Drug Name | Spironolactone (Aldactone) |
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| Description | An aldosterone antagonist that spares potassium. Competes with aldosterone for receptor sites in distal renal tubules, increasing water excretion while retaining potassium and hydrogen ions. |
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| Adult Dose | 25-200 mg/d PO divided bid/tid/qid |
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| Pediatric Dose | 1-3 mg/kg/d PO divided bid/tid/qid |
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| Contraindications | Documented hypersensitivity; acute renal failure; hyperkalemia; anuria; Addison disease |
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| Interactions | May potentiate ganglionic blocking agents and other antihypertensives; ACE inhibitors, cyclosporin, and potassium supplements increase risk of hyperkalemia; may increase the risk of digoxin toxicity |
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| Pregnancy | D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
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| Precautions | May cause hyperkalemia, GI distress, rash, and gynecomastia; concomitant use with indomethacin or ACE inhibitors may cause hyperkalemia |
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Complications
- Complications include worsening congestive heart failure, arrhythmia (including sudden death), and thromboembolic complications.
- If restrictive cardiomyopathy (RCM) results in advanced congestive heart failure, end-organ damage may result from low cardiac output.
- Pulmonary hypertension is more prevalent in this type of cardiomyopathy than in dilated or hypertrophic cardiomyopathy. Patients must be closely monitored.
- Incidence of thromboembolic complications is high enough that many investigators have recommended anticoagulation with warfarin or aspirin as a preventative measure.
Prognosis
- Prognosis can be very poor in children.
- Patients are at risk for various acute and chronic complications that require close monitoring.
- Those who ultimately require and undergo heart transplantation before development of severe pulmonary hypertension have a reasonably good prognosis similar to other types of cardiomyopathy.
Patient Education
- A healthy lifestyle is recommended.
Special Concerns
- Pregnancy is not recommended.
| Media file 1:
Echocardiographic 4-chamber view of a child with restrictive cardiomyopathy demonstrating characteristic marked enlargement of right atrium (RA) and left atrium (LA), which are larger than left ventricle (LV). |
 |  View Full Size Image | |
Media type: Echo
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Cardiomyopathy, Restrictive excerpt Article Last Updated: Jan 2, 2008
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