eMedicine Specialties > Cardiology > Myocardial Disease and Cardiomyopathies

Cardiomyopathy, Alcoholic: Treatment & Medication

Author: Eric D Popjes, MD, Assistant Professor, Department of Medicine, Division of Cardiology, Penn State Milton S Hershey Medical Center
Coauthor(s): Frank E Silvestry, MD, Director, PENN Cardiac Care at Radnor; Assistant Professor, Department of Medicine, Division of Cardiovascular Disease, University of Pennsylvania Health System
Contributor Information and Disclosures

Updated: Mar 13, 2008

Treatment

Medical Care

  • The mainstay of therapy for alcoholic cardiomyopathy (AC) is to treat the underlying cause, ie, complete and perpetual abstinence from all alcohol consumption. The efficacy of abstinence has been shown in those with early disease (eg, prior to the onset of severe myocardial fibrosis) and in those with more advanced disease (see Prognosis).
  • Medical therapy for AC is identical to conventional therapy for other forms of heart failure. This includes treatment with an ACE inhibitor, digoxin for those with symptomatic LV dysfunction, and the symptomatic use of diuretics. Newer therapies such as beta-blockers in stable patients without decompensated heart failure are also used.
  • Electrolyte abnormalities, including hypokalemia, hypomagnesemia, and hypophosphatemia, should be corrected promptly because of the risk of arrhythmia and sudden death.
  • Although anticoagulation may be of benefit to patients with profound LV dysfunction and atrial fibrillation, the risks must be weighed heavily in this patient population.
  • Thiamine (200 mg once daily), multivitamins, vitamin B-12, folate, and mineral supplementation are beneficial for patients with AC because of the significant prevalence of concomitant nutritional or electrolyte deficiencies in these patients. Animal studies have suggested a benefit from vitamins B-1 and B-12, speculated to be due to protective effects against apoptosis and protein damage.
  • A summary of the treatment for AC is as follows:
    • Abstaining from alcohol
    • Vasodilators - ACE inhibitors, angiotensin receptor blockers (the work of Cheng and colleagues in 2006 suggested that ARBs may prevent the development of AC9 ), nitrates, hydralazine
    • Digoxin
    • Diuretics
    • Beta-blockers
    • Anticoagulation (possibly)
    • Intravenous inotropic agents
    • Cardiac transplantation

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Angiotensin-converting enzyme (ACE) inhibitors

Recommended for patients with systolic heart failure. Slow the progression of heart failure and improve survival rates.


Ramipril (Altace)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Adult

2.5 mg PO bid initially; titrate up to 5 mg bid or 10 mg qd, when possible

Pediatric

Not established

NSAIDs may reduce hypotensive effects of ramipril; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases ramipril levels; probenecid may increase ramipril levels; the hypotensive effects of ACE inhibitors may be enhanced when given concurrently with diuretics

Documented hypersensitivity; history of angioedema

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

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal impairment, valvular stenosis, or severe congestive heart failure


Lisinopril (Prinivil, Zestril)

Prevents conversion of angiotensin I to angiotensin II (a potent vasoconstrictor), resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Adult

10 mg/d PO qd or divided bid; increase by 5-10 mg/d at 1- to 2-wk intervals; not to exceed 80 mg/d

Pediatric

Not established

NSAIDs may reduce hypotensive effects of lisinopril; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases lisinopril levels; probenecid may increase lisinopril levels; the hypotensive effects of ACE inhibitors may be enhanced when given concurrently with diuretics

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

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal impairment, valvular stenosis, or severe congestive heart failure


Benazepril (Lotensin)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Adult

20-40 mg/d PO qd or divided bid; make dose adjustments prn

Pediatric

Not established

May increase digoxin, lithium, and allopurinol levels; probenecid may increase levels; coadministration with diuretics increases hypotensive effects; NSAIDs decrease effects

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

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal impairment, valvular stenosis, or severe CHF


Captopril (Capoten)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Adult

6.25-12.5 mg PO tid; not to exceed 150 mg tid

Pediatric

Not established

NSAIDs may reduce hypotensive effects; may increase digoxin, lithium, and allopurinol levels; rifampin decreases levels; probenecid may increase levels; hypotensive effects may be enhanced when given concurrently with diuretics

Documented hypersensitivity; renal impairment

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

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal impairment, valvular stenosis, or severe CHF


Enalapril (Vasotec)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Adult

2.5-5 mg/d PO (increase prn)
Dosing range: 10-40 mg/d PO in 1-2 divided doses
Alternatively, 1.25 mg/dose IV over 5 min q6h

Pediatric

Not established

NSAIDs may reduce hypotensive effects; may increase digoxin, lithium, and allopurinol levels; rifampin decreases levels; probenecid may increase levels; hypotensive effects may be enhanced when given concurrently with diuretics

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

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal impairment, valvular stenosis, or severe CHF

Angiotensin II receptor antagonists

Interfere with the binding of formed angiotensin II to its endogenous receptor.


Candesartan (Atacand)

Blocks vasoconstriction and aldosterone-secreting effects of angiotensin II. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors, does not affect response to bradykinin, and is less likely to be associated with cough and angioedema. Use in patients unable to tolerate ACE inhibitors.

Angiotensin II receptor blockers reduce blood pressure and proteinuria, protecting renal function, and delaying onset of end-stage renal disease.

Adult

8-16 mg/d PO initially; not to exceed 32 mg/d

Pediatric

Not established

May increase digoxin, lithium, and allopurinol levels; probenecid may increase candesartan levels; coadministration with diuretics, increase hypotensive effects; NSAIDs may reduce hypotensive effects of candesartan; may increase risk of hyperkalemia if taken concurrently with potassium supplements or other potassium-sparing diuretics

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

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal impairment (serum creatinine >3.5), valvular stenosis, or severe congestive heart failure; watch for serum potassium


Valsartan (Diovan)

For patients unable to tolerate ACE inhibitors. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors. Do not affect response to bradykinin and are less likely to be associated with cough and angioedema.

Adult

40-320 mg PO qd or in divided doses

Pediatric

Not established

May increase digoxin, lithium, and allopurinol levels; probenecid may increase valsartan levels; coadministration with diuretics increase hypotensive effects; NSAIDs may reduce hypotensive effects of valsartan; may increase risk of hyperkalemia if taken concurrently with potassium supplements or other potassium-sparing diuretics

Documented hypersensitivity; severe hepatic insufficiency; biliary cirrhosis or obstruction; primary hyperaldosterism; bilateral renal artery stenosis

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

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in hyperkalemia, suspected bilateral renal artery stenosis (RAS), or solitary kidney with unilateral RAS

Cardiac glycosides

Decrease AV nodal conduction primarily by increasing vagal tone. Used primarily in the setting of AF and atrial flutter with CHF.


Digoxin (Lanoxicaps, Lanoxin)

Used in patients with symptomatic LV dysfunction. Has direct inotropic effects in addition to indirect effects on the cardiovascular system. 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.

Adult

0.125-0.375 mg PO qd

Pediatric

<5 years: Not established
5-10 years: 20-35 mcg/kg PO
>10 years: 10-15 mcg/kg PO
Maintenance dose: Use 25-35% of PO loading dose

IV calcium may produce arrhythmias in digitalized patients; medications that may increase levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, oral amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil
Medications that may decrease serum levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, oral colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, and procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid

Documented hypersensitivity; beriberi heart disease, idiopathic hypertrophic subaortic stenosis, constrictive pericarditis, and carotid sinus syndrome

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

Precautions

Hypokalemia may reduce positive inotropic effect; hypercalcemia predisposes patient to digitalis toxicity, and hypocalcemia can make digoxin ineffective until serum calcium levels are normal; magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity; patients diagnosed with incomplete AV block may progress to complete block when treated with digoxin; exercise caution in hypothyroidism, hypoxia, and acute myocarditis; adjust dose in renal impairment; highly toxic (overdoses can be fatal)

Beta-adrenergic blockers

For use in stable patients without decompensated heart failure and patients with symptoms despite treatment with an ACE inhibitor and diuretic. May improve heart function, probably by blocking effects of sympathetic nervous system.


Metoprolol (Lopressor, Toprol XL)

Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions.

Adult

25 mg PO qd; may increase dose prn

Pediatric

Not established

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effects; toxicity may increase with coadministration of sparfloxacin, phenothiazines, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; may increase toxicity of digoxin, flecainide, clonidine, epinephrine, nifedipine, prazosin, verapamil, and lidocaine

Documented hypersensitivity; uncompensated CHF, bradycardia, asthma, cardiogenic shock, and AV conduction abnormalities

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

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Beta-adrenergic blockade may reduce signs and symptoms of acute hypoglycemia and may decrease clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; monitor patient closely and withdraw drug slowly; during IV administration, carefully monitor blood pressure, heart rate, and ECG


Carvedilol (Coreg and Coreg CR)

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

Adult

3.125 mg PO bid for 2 wk initially; then increase to 6.25 mg PO bid for 2 wk; double dose q2wk as tolerated, not to exceed 25 mg bid if <85 kg or 50 mg bid if >85 kg
Note: Dose of digitalis, diuretics, or ACE inhibitors must be stabilized prior to initiation

Pediatric

<18 years: Not established
>18 years: Administer as in adults

Rifampin, barbiturates, cholestyramine, colestipol, NSAIDs, salicylates, and penicillins may decrease effects; may increase effects of antidiabetic agents, digoxin, and calcium channel blockers; concurrent administration with clonidine may increase blood pressure and decrease heart rate; may decrease effect of sulfonylureas; cimetidine, fluoxetine, paroxetine, and propafenone may increase levels

Documented hypersensitivity; hypotension; bradycardia; AV/SA node disease; cardiogenic shock; overt cardiac failure

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

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in CHF being treated with digitalis, diuretics, or ACE inhibitors (AV conduction may be slowed); discontinue if liver impairment occurs; caution in peripheral vascular disease, hyperthyroidism, and diabetes mellitus


Bisoprolol (Zebeta)

Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions.

Adult

5 mg PO qd; may increase to 10 mg and then to 20 mg qd prn

Pediatric

Not established

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effects; toxicity may increase with coadministration of sparfloxacin, phenothiazines, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; may increase toxicity of digoxin, flecainide, clonidine, epinephrine, nifedipine, prazosin, verapamil, and lidocaine

Documented hypersensitivity; uncompensated CHF, bradycardia, asthma, cardiogenic shock, and AV conduction abnormalities

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

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Beta-adrenergic blockade may reduce signs and symptoms of acute hypoglycemia and may decrease clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; monitor patient closely and withdraw drug slowly; during IV administration, carefully monitor blood pressure, heart rate, and ECG

Diuretics

May improve symptoms of venous congestion through elimination of retained fluid and preload reduction.


Furosemide (Lasix)

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule.
Dose must be individualized to patient. Depending on response, administer at increments of 20-40 mg, no sooner than 6-8 h after previous dose, until desired diuresis occurs. When treating infants, titrate with increments of 1 mg/kg/dose until a satisfactory effect is achieved. Diuretics have major clinical uses in managing disorders involving abnormal fluid retention (edema) or in treating hypertension, in which their diuretic action causes decreased blood volume. Medical management of AC targeted toward heart failure.

Adult

20-80 mg/d PO/IV/IM; titrate up to 600 mg/d for severe edematous states

Pediatric

1-2 mg/kg/dose PO; not to exceed 6 mg/kg/dose; do not administer >q6h
1 mg/kg IV/IM slowly under close supervision; not to exceed 6 mg/kg

Metformin decreases concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently; increased plasma lithium levels and toxicity are possible when taken concurrently

Documented hypersensitivity; hepatic coma, anuria, and state of severe electrolyte depletion

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

Precautions

Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter


Hydrochlorothiazide (Esidrix, HydroDIURIL, Microzide)

Inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium and water and potassium and hydrogen ions. Treatment may improve symptoms of venous congestion through elimination of retained fluid and preload reduction.

Adult

25-100 mg PO qd or in divided doses; may administer qod

Pediatric

Not established

May decrease effects of anticoagulants, antigout agents, and sulfonylureas; may increase toxicity of allopurinol, anesthetics, antineoplastics, calcium salts, loop diuretics, lithium, diazoxide, digitalis, amphotericin B, and nondepolarizing muscle relaxants

Documented hypersensitivity; anuria or renal decompensation

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal disease, hepatic disease, gout, diabetes mellitus, and erythematosus


Spironolactone (Aldactone)

Potassium-sparing diuretic that nonselectively antagonizes aldosterone receptors.

Adult

12.5-50 mg PO qd or in divided doses

Pediatric

Not established

May potentiate hyperkalemia caused by ACE inhibitors, receptor blockers, and other drugs that may raise serum potassium levels; may increase levels of digoxin; effectiveness may be diminished by NSAIDS

Documented hypersensitivity; severe renal insufficiency; hyperkalemia

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

Precautions

Liver dysfunction and impaired renal function


Eplerenone (Inspra)

Selectively blocks aldosterone at the mineralocorticoid receptors in epithelial tissues (eg, kidney) and nonepithelial tissues (eg, heart, blood vessels, brain); thus, decreases blood pressure and sodium reabsorption. Can be used in patients who are intolerant of spironolactone due to side effects of gynecomastia or menstrual irregularities.

Adult

25-50 mg PO qd

Pediatric

Not established

CYP450 3A4 substrate; potent CYP3A4 inhibitors (eg, ketoconazole) increase serum levels about 5-fold; less potent CYP3A4 inhibitors (eg, erythromycin, saquinavir, verapamil, fluconazole) increase serum levels about 2-fold; grapefruit juice increases serum levels about 25%; coadministration with potassium supplements, salt substitutes, or drugs known to increase serum potassium (eg, amiloride, spironolactone, triamterene, ACE inhibitors, angiotensin II inhibitors) increases risk of hyperkalemia

Documented hypersensitivity; renal (creatinine clearance <30) and liver impairment; preexisting hyperkalemia

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May cause hyperkalemia, headache, and dizziness; caution with hepatic insufficiency

Electrolyte supplements

Help correct electrolyte abnormalities, including hypokalemia, hypomagnesemia, and hypophosphatemia.


Phosphate salts (Neutra-Phos-K)

IV preparations are available as sodium or potassium phosphate (K2 PO4). Response to IV serum phosphorus supplementation is highly variable and is associated with hyperphosphatemia and hypocalcemia. Infusion rate and initial dosage based on severity of hypophosphatemia and presence of symptoms.

Adult

8 mmol q6h IV (32 mmol/d) initially
Aggressive IV replacement: 15 mmol over 6 h

Pediatric

0.25-0.5 mmol/kg IV over 4-6 h; repeat if symptomatic hypophosphatemia persists

Magnesium- and aluminum-containing antacids or sucralfate can act as phosphate binders and decrease serum phosphate levels; potassium-sparing diuretics, ACE inhibitors, and salt substitutes may increase serum levels

Do not administer if patient diagnosed with hyperphosphatemia, hypocalcemia, hypomagnesemia, hyperkalemia, or renal failure

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

Precautions

Caution in patients with renal insufficiency or metabolic alkalosis; admixture of phosphate and calcium in IV fluids can result in calcium phosphate precipitation


Magnesium sulfate

Nutritional supplement in hyperalimentation; cofactor in enzyme systems involved in neurochemical transmission and muscular excitability. In adults, 60-180 mEq of potassium, 10-30 mEq of magnesium, and 10-40 mmol of phosphate per day may be necessary for optimum metabolic response.

Adult

1 g IV/IM q6h for 4 doses up to 8-12 g/d in severe hypomagnesemia
Alternatively, 3 g PO q6h for 4 doses prn

Pediatric

25-50 mg/kg/dose IV/IM q4-6h for 3-4 doses

Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade seen with aminoglycosides and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, and succinylcholine; may increase CNS effects and toxicity of CNS depressants and betamethasone and cardiotoxicity of ritodrine

Documented hypersensitivity; heart block, Addison disease, myocardial damage, or severe hepatitis

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Magnesium may alter cardiac conduction, leading to heart block in digitalized patients; monitor respiratory rate, deep tendon reflex, and renal function when electrolyte is administered parenterally; caution when administering magnesium dose because may produce significant hypotension or asystole; in overdose, calcium gluconate, 10-20 mL IV of 10% solution, can be given as antidote for clinically significant hypermagnesemia


Potassium chloride (Cena-K, Kaochlor, K-Dur, Klor-Con)

Essential for transmission of nerve impulses, contraction of cardiac muscle, maintenance of intracellular tonicity, skeletal and smooth muscles, and maintenance of normal renal function. Gradual depletion occurs via renal excretion, through GI loss, or because of low intake.
Depletion usually results from diuretic therapy, primary or secondary hyperaldosteronism, diabetic ketoacidosis, severe diarrhea, if associated with vomiting, or inadequate replacement during prolonged parenteral nutrition.
Potassium depletion sufficient to cause 1 mEq/L drop in serum potassium requires a loss of approximately 100-200 mEq from total body store.

Adult

Serum levels >2.5 mEq/L: 10 mEq IV over 1 h and prn based on frequently obtained lab values; not to exceed 200 mEq/24h
Serum levels <2.5 mEq/L: 40 mEq IV over 1 h and prn based on frequently obtained lab values; not to exceed 400 mEq/24h

Pediatric

Initially, administer 1 mEq/kg IV over 1-2 h and prn based on frequently obtained lab values

Concurrent use with ACE inhibitors may result in elevated serum potassium concentrations; potassium-sparing diuretics and potassium-containing salt substitutes can produce severe hyperkalemia; in patients taking digoxin, hypokalemia may result in digoxin toxicity; caution if discontinuing potassium administration in patients maintained on digoxin

Hyperkalemia, renal failure, conditions in which potassium retention is present, oliguria or azotemia, crush syndrome, severe hemolytic reactions, anuria, and adrenocortical insufficiency

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Do not infuse rapidly; high plasma concentrations may cause death due to cardiac depression, arrhythmias, or arrest; plasma levels do not necessarily reflect tissue levels; monitor replacement therapy whenever possible by performing continuous or serial ECG; when a concentration >40 mEq/L is infused, local pain and phlebitis may also follow

More on Cardiomyopathy, Alcoholic

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Follow-up: Cardiomyopathy, Alcoholic
References

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Further Reading

Keywords

alcoholism, alcohol consumption, alcohol abuse, ethanol consumption, ethanol abuse, ethanol toxicity, alcohol toxicity, cardiovascular disease, CVD, cardiac enlargement, cardiac failure, heart failure, alcoholic cardiomyopathy, AC, arrhythmia, atrial fibrillation, atrial flutter, supraventricular arrhythmia, premature ventricular contractions, sudden death, hypertension, stroke, dilated cardiomyopathy, DC, acute ethanol-induced injury, beriberi heart disease, thiamine deficiency, acetaldehyde, myocarditis

Contributor Information and Disclosures

Author

Eric D Popjes, MD, Assistant Professor, Department of Medicine, Division of Cardiology, Penn State Milton S Hershey Medical Center
Eric D Popjes, MD is a member of the following medical societies: American College of Cardiology, Heart Failure Society of America, and International Society for Heart and Lung Transplantation
Disclosure: Nothing to disclose.

Coauthor(s)

Frank E Silvestry, MD, Director, PENN Cardiac Care at Radnor; Assistant Professor, Department of Medicine, Division of Cardiovascular Disease, University of Pennsylvania Health System
Frank E Silvestry, MD is a member of the following medical societies: American College of Cardiology, American Medical Association, and American Society of Echocardiography
Disclosure: Nothing to disclose.

Medical Editor

Gary E Sander, MD, PhD, Professor, Department of Internal Medicine, Division of Cardiology, Tulane University Health Sciences Center
Gary E Sander, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Heart Association, American Society of Hypertension, Heart Failure Society of America, Louisiana State Medical Society, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Frank M Sheridan, MD, Cardiology, Providence Everett Medical Center
Frank M Sheridan, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Patrice Delafontaine, MD, FACC, FAHA, FACP, FESC, Sidney W and Marilyn S Lassen Professor of Cardiovascular Medicine, Chief, Section of Cardiology, Director, Cardiovascular Center of Excellence, Tulane University; Professor of Physiology, Chair, Department of Medicine, Tulane University School of Medicine
Patrice Delafontaine, MD, FACC, FAHA, FACP, FESC is a member of the following medical societies: Alpha Omega Alpha, American Association for the Advancement of Science, American College of Cardiology, American College of Physicians, American Diabetes Association, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Medical Association, American Society for Clinical Investigation, Association of American Physicians, Association of Professors of Cardiology, Association of Professors of Medicine, Endocrine Society, European Society of Cardiology, Louisiana State Medical Society, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

 
 
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