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Restrictive Cardiomyopathy Medication

  • Author: Alan Vainrib, MD; Chief Editor: Henry H Ooi, MD, MRCPI  more...
Updated: Dec 18, 2014

Medication Summary

Treatment of restrictive cardiomyopathy (RCM) is symptomatic. Treatment goals include decreasing systemic and pulmonary congestion, lowering ventricular filling pressure, augmenting systolic pump function, and reducing the risk for embolism.[14]



Class Summary

Diuretics are used to reduce pulmonary and systemic congestion. Symptomatic treatment may improve symptoms of venous congestion through elimination of retained fluid and preload reduction. Initiate therapy with a low dosage because relatively high levels of ventricular filling pressure must be maintained for adequate diastolic filling.

Hydrochlorothiazide (Microzide)


Hydrochlorothiazide inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium and water as well as potassium and hydrogen ions.

Furosemide (Lasix)


Furosemide increases excretion of water by interfering with the chloride-binding cotransport system, which in turn inhibits sodium and chloride reabsorption in the ascending loop of Henle and the distal renal tubule. The dose must be individualized to the patient. Depending on response, administer furosemide at increments of 20-40 mg no sooner than 6-8 hours after the previous dose until the desired diuresis occurs. When treating infants, titrate with 1-mg/kg/dose increments until a satisfactory effect is achieved.



Class Summary

Nitrates are used to reduce preload in diastolic dysfunction.

Nitroglycerin PO


Nitroglycerin causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production. The result is a decrease in blood pressure. This agent is available as lingual pump spray, sublingual tablets, oral tablets, patches, and ointments.


Beta-Blockers, Alpha Activity

Class Summary

May improve symptoms by increasing left ventricular filling time, improving ventricular relaxation, and decreasing compensatory sympathetic stimulation.

Carvedilol (Coreg, Coreg CR)


Nonselective beta- and alpha-adrenergic blocker. Also has antioxidant properties. Does not appear to have intrinsic sympathomimetic activity. May reduce cardiac output and decrease peripheral vascular resistance.


Calcium Channel Blockers

Class Summary

May improve symptoms by increasing left ventricular filling time, improving ventricular relaxation, and decreasing compensatory sympathetic stimulation.

Verapamil (Calan, Isoptin)


Nondihydropyridine calcium-channel blocker that inhibits extracellular calcium ion influx across membranes of myocardial cells and vascular smooth muscle cells, resulting in inhibition of cardiac and vascular smooth muscle contraction and thereby dilating main coronary and systemic arteries.

Diltiazem (Cardizem, Cardizem CD, Dilacor Tiazac)


Nondihydropyridine calcium-channel blocker that inhibits extracellular calcium ion influx across membranes of myocardial cells and vascular smooth muscle cells, resulting in inhibition of cardiac and vascular smooth muscle contraction and thereby dilating main coronary and systemic arteries.



Class Summary

Vasodilators are used to reduce ventricular filling pressure. Avoid excessive decrease in preload and diastolic filling.



Hydralazine decreases systemic resistance through direct vasodilation of arterioles.

Isosorbide dinitrate/hydralazine (BiDil)


A fixed-dose combination of isosorbide dinitrate (20 mg/tab), a vasodilator with effects on both arteries and veins, and hydralazine (37.5 mg/tab), a predominantly arterial vasodilator, is indicated for heart failure in blacks, in part on the basis of results from the African American Heart Failure Trial.

Two previous trials in the general population of patients with severe heart failure found no benefit but suggested benefit in patients who are black. In comparison with placebo, this combination showed a 43% reduction in mortality, a 39% decrease in hospitalization rate, and a decrease in symptoms from heart failure among blacks.


Anticoagulants, Cardiovascular

Class Summary

Anticoagulants are used to prevent embolism from ventricular thrombus.

Warfarin (Coumadin)


Warfarin interferes with hepatic synthesis of vitamin K–dependent coagulation factors. It is used for prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders.



Heparin augments the activity of antithrombin III and prevents conversion of fibrinogen to fibrin. It does not actively lyse but is able to inhibit further thrombogenesis. Heparin prevents reaccumulation of clot after spontaneous fibrinolysis.


Inotropic Agents

Class Summary

Cardiac glycosides are used to treat atrial fibrillation and systolic dysfunction in RCM. Digitalis and other positive inotropic agents generally are not indicated unless systolic pump function and contractility are impaired. Digitalis must be used with caution in patients with amyloid cardiomyopathy; such patients may be digoxin sensitive (arrhythmogenic) because of amyloid fibril binding of digoxin.

Digoxin (Lanoxin)


Digoxin is a cardiac glycoside with direct inotropic effects in addition to indirect effects on the cardiovascular system. It acts directly on cardiac muscle, increasing myocardial systolic contractions. Indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.

Contributor Information and Disclosures

Alan Vainrib, MD Fellow, Department of Cardiology, Stony Brook University Medical Center

Disclosure: Nothing to disclose.


Asa William (Peter) Viccellio, MD Professor, Vice-Chair, Department of Emergency Medicine, State University of New York at Stony Brook

Asa William (Peter) Viccellio, MD is a member of the following medical societies: Medical Society of the State of New York, National Association of EMS Physicians, New York Academy of Medicine, New York Academy of Sciences, New York County Medical Society, American Association for the Advancement of Science, American College of Emergency Physicians, American Medical Association

Disclosure: Nothing to disclose.

Vivek J Goswami, MD Director of Nuclear Cardiology, Austin Heart; Clinical Assistant Professor, Texas A&M Health Science Center College of Medicine

Vivek J Goswami, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Heart Association, American Medical Association, Illinois State Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

A Antoine Kazzi, MD Deputy Chief of Staff, American University of Beirut Medical Center; Associate Professor, Department of Emergency Medicine, American University of Beirut, Lebanon

A Antoine Kazzi, MD is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Henry H Ooi, MD, MRCPI Director, Advanced Heart Failure and Cardiac Transplant Program, Nashville Veterans Affairs Medical Center; Assistant Professor of Medicine, Vanderbilt University School of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Gary Edward Sander, MD, PhD, FACC, FAHA, FACP, FASH Professor of Medicine, Director of CME Programs, Team Leader, Root Cause Analysis, Tulane University Heart and Vascular Institute; Director of In-Patient Cardiology, Tulane Service, University Hospital; Visiting Physician, Medical Center of Louisiana at New Orleans; Faculty, Pennington Biomedical Research Institute, Louisiana State University; Professor, Tulane University School of Medicine

Gary Edward Sander, MD, PhD, FACC, FAHA, FACP, FASH is a member of the following medical societies: Alpha Omega Alpha, American Chemical Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Society for Pharmacology and Experimental Therapeutics, American Society of Hypertension, American Thoracic Society, Heart Failure Society of America, National Lipid Association, Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.


The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Sarath Reddy, MD, Alan Forker, MD, Gunateet Goswami, MD, Nafisa Kuwajerwala, MD, Paul J Kaloudis, MD, and Andrew Wackett, MD, to the development and writing of the source articles.

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Table 1. Clinical Features of Constrictive Pericarditis and Restrictive Cardiomyopathy
Clinical Features Constrictive Pericarditis Restrictive Cardiomyopathy
History Prior history of pericarditis or condition that causes pericardial disease History of systemic disease (eg, amyloidosis, hemochromatosis)
General examination Peripheral stigmata of systemic disease
Systemic examination - Heart sounds Pericardial knock, high-frequency sound Presence of loud diastolic filling sound S3, Low-frequency sound
Murmurs No murmurs Murmurs of mitral and tricuspid insufficiency
Prior chest radiograph Pericardial calcification Normal results of prior chest radiograph
Table 2. Investigation of Constrictive Cardiomyopathy and Restrictive Cardiomyopathy
Investigation Constrictive Cardiomyopathy Restrictive Cardiomyopathy
Chest radiograph Pericardial calcification Atrial dilatation causing increased cardiothoracic ratio, normal ventricular size
CT scan/MRI Pericardial thickening No pericardial thickening
Echocardiography Normal-sized ventricles and atria; pericardial thickening, pericardial effusion may be observed Nondilated, normally contracting, nonhypertrophied ventricles and marked dilatation of both atria; speckled texture of myocardium in cases of amyloid infiltration of the heart
Doppler flow velocities on echocardiography Respiratory changes (ie, decreased peak transmitral diastolic flow) during inspiration Equalization of the right- and left-sided filling pressures No respiratory changes Greater elevation in the left-sided filling pressures
Catheterization hemodynamics:


2) RVEDP:RVSP ratio

3) RVEDP/LVEDP equalization


1) = 50 mm Hg

2) = 0.33

3) = 5 mm Hg difference


1) = 50 mm Hg

2) = 0.33

3) = 5 mm Hg difference

Cardiac biopsy Normal myocardium Often diagnostic, showing abnormal myocardium
CT = computed tomography; LVEDP = left ventricular end-diastolic pressure; MRI = magnetic resonance imaging; RVEDP = right ventricular end-diastolic pressure; RVSP = right ventricular systolic pressure.
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