eMedicine Specialties > Cardiology > Arrhythmias

Long QT Syndrome: Treatment & Medication

Author: Ali A Sovari, MD, Clinical and Research Fellow in Cardiovascular Medicine, Section of Cardiology, University of Illinois at Chicago
Coauthor(s): Abraham G Kocheril, MD, FACC, FACP, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago; Ramin Assadi, MD, Fellow, Department of Cardiology, Loma Linda University; Arnold S Baas, MD, FACC, FACP, Assistant Professor of Medicine, Division of Cardiology, University of California, Los Angeles School of Medicine; Attending Physician, UCLA Santa Monica Hospital and UCLA Westwood Hospital; Wojciech Zareba, MD, PhD, FACC, Associate Director of Heart Research, Associate Professor, Department of Medicine, Division of Cardiology, University of Rochester Medical Center; Spencer Rosero, MD, Assistant Professor, Department of Medicine, University of Rochester School of Medicine
Contributor Information and Disclosures

Updated: Jun 18, 2009

Treatment

Medical Care

All patients with long QT syndrome (LQTS) should avoid drugs that prolong the QT interval or reduce their serum potassium or magnesium levels. Potassium and magnesium deficiency should be corrected.

Although treating asymptomatic patients is somewhat controversial, a safe approach is to treat all patients with congenital LQTS because sudden cardiac death can be the first manifestation of LQTS.

  • Beta-blockers are drugs of choice for patients with LQTS. The protective effect of beta-blockers is related to their adrenergic blockade that diminishes the risk of cardiac arrhythmias. They may also reduce the QT interval in some patients.
    • Although for years the recommended dosage of beta-blockers was relatively large (eg, propranolol 3 mg/kg/d, or 210 mg/d in a 70-kg individual), recent data suggest that dosages lower than this have a protective effect similar to that of large dosages.
    • Beta-blockers are effective in preventing cardiac events in approximately 70% of patients, whereas cardiac events continue to occur despite beta-blocker therapy in the remaining 30%.
    • Propranolol and nadolol are the beta-blockers most frequently used, though atenolol and metoprolol are also prescribed in patients with LQTS. Different beta-blockers demonstrate similar effectiveness in preventing cardiac events in patients with LQTS.
  • The implantable cardioverter-defibrillator (ICD) was shown to be highly effective to prevent sudden cardiac death (SCD) in high-risk patients. In a study of 125 patients with LQTS with ICDs, there was 1.3% death in high-risk ICD patients, compared with 16% in non-ICD patients during mean 8-year follow-up (p=0.07).6 High-risk patients are defined as those with aborted cardiac arrest or recurrent cardiac events (eg, syncope or torsade de pointes) despite conventional therapy (ie, beta-blocker alone) and those with very prolonged QT interval (>500 ms).
    • An alternative is beta-blockade in combination with a pacemaker and/or stellectomy in some patients. Use of an ICD may be considered as primary therapy if the patient has a strong family history of SCD. However, since some studies showed that family history of SCD is not an independent risk factor7 , some experts do not recommend ICD therapy based on only a family history of SCD8 . Early ICD therapy should be considered in high-risk patients with Jervell and Lange-Nielsen syndrome, because the efficacy of beta-blockers was found to be more limited in these patients.9
    • The usefulness of implanted cardiac pacemakers is based on the premise that pacing eliminates arrhythmogenic bradycardia, decreases heart-rate irregularities (eliminating short-long-short sequences), and decreases repolarization heterogeneity, diminishing the risk of torsade de pointes ventricular tachycardia. Pacemakers are particularly helpful in patients with documented pause-bradycardia–induced torsade de pointes and in patients with LQT3.
    • However, recent data indicate that cardiac events continue to occur in high-risk patients with cardiac pacing. Because newer models of ICDs include a cardiac pacing function, cardiac pacing (without defibrillators) is unlikely to be used in patients with LQTS. Pacing alone may be used in low-risk patients with LQT3.
  • Left cervicothoracic stellectomy is another antiadrenergic therapeutic measure used in high-risk patients with LQTS, especially in those with recurrent cardiac events despite beta-blocker therapy.
    • Stellectomy decreases the risk of cardiac events in high-risk patients with LQTS, and it is more effective in patients with LQT1 than those with other types of LQTS.
    • Although this technique decreases the risk of cardiac events, it does not eliminate the risk. Therefore, ICD is superior therapy to cervicothoracic stellectomy.
    • Cervicothoracic stellectomy may be indicated in some high-risk patients and in patients who have several ICD discharges while being treated with beta-blockade and an ICD.
  • The triggering effect of exercise and tachycardia, and therefore the protective effect of beta-blockers, varies depending on the type of LQTS.
    • Exercise and tachycardia trigger LQT1 events. Therefore, patients with LQT1 should avoid strenuous exercise, and beta-blockers are expected to provide excellent help by preventing cardiac events. Syncope and sudden cardiac death during swimming or diving are strongly related to LQT1. Therefore, patients with LQT1 should avoid swimming with no supervision.
    • LQT2 is also exercise induced but to a lesser degree than LQT1.
    • Tachycardia and exercise do not trigger LQT3; events typically happen during sleep. Because tachycardia is not a trigger, the role of beta-blockers in preventing the cardiac events of LQT3 is debated. Mexiletine, a sodium channel blocker, may improve protection in this subgroup of the patients. Some experts suggest the use of a beta-blocker combined with mexiletine in patients with LQT3.
  • Gene-specific therapy is an area under investigation.
  • A summary of guidelines suggested by the American College of Cardiology, the American Heart Association, and the European Society of Cardiology, in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society for management of patients with LQTS include:10,11
    • No participation in competitive sports for patients with the diagnosis established by means of genetic testing only.
    • Beta-blockers should be given to patients who have QTc-interval prolongation (>460 ms in women and >440 ms in men) and is recommended (class IIa) for patients with a normal QTc interval.
    • ICD should be implanted for survivors of cardiac arrest and is recommended (class IIa) for patients with syncope while receiving beta-blockers. ICD therapy can be considered (class IIb) for primary prevention in patients with characteristics that suggest high risk; these include LQT2, LQT3, and QTc interval greater than 500 ms.

Consultations

  • A cardiologist and a cardiac electrophysiologist are typically consulted when patients with long QT syndrome (LQTS) are evaluated.
  • In families of patients with genotypically confirmed LQTS, genetic counseling of patients and family members should be considered.

Activity

Physical activity, swimming, and stress-related emotions frequently trigger cardiac events in patients with long QT syndrome (LQTS). Therefore, discourage patients from participating in competitive sports. This recommendation is most important for patients with LQT1 or LQT2. See also the Medical Care section.

Medication

No treatment addresses the cause of long QT syndrome (LQTS). Antiadrenergic therapeutic measures (eg, use of beta-blockers, left cervicothoracic stellectomy) and device therapy (eg, use of pacemakers, ICDs) aim to decrease the risk and lethality of cardiac events.

Beta-adrenergic blocking agents

Antiadrenergic therapy effectively protects most patients with LQTS. Beta-blockers, especially propranolol, are the drugs most frequently used in patients with LQTS. Inform patients and their family members that beta-blockers should be continued indefinitely and not stopped. Interruption in beta-blocker therapy may increase the risk of cardiac events.


Propranolol (Inderal)

Decreases effect of sympathetic stimulation on heart. Decreases conduction through atrioventricular (AV) node and has negative chronotropic and inotropic effects. Consult cardiologist because dosing varies and is individualized in patients with LQTS. Patients with asthma should use cardioselective beta-blockers. Patients with LQTS who cannot take beta-blockers may require ICDs as first-line therapy.

Adult

2-3 mg/kg/d PO

Pediatric

Administer as in adults

Coadministration with aluminum salts, barbiturates, nonsteroidal anti-inflammatory drugs (NSAIDs), penicillins, calcium salts, cholestyramine, and rifampin may decrease effects; cimetidine, loop diuretics, and monoamine oxidase inhibitors (MAOIs) may increase toxicity; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase; cardiotoxicity may increase when administered concurrently with calcium channel blockers, quinidine, flecainide, and digoxin (all affect conduction)

Documented hypersensitivity; uncompensated congestive heart failure, bradycardia, cardiogenic shock, 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

Precautions

Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor closely; should be taken by pregnant women with LQTS during pregnancy and postpartum period, when risk of cardiac events increases


Nadolol (Corgard)

Frequently prescribed because of long-term effect. Decreases effect of sympathetic stimulation on heart. Decreases conduction through AV node and has negative chronotropic and inotropic effects. Consult cardiologist because dosing varies and is individualized in patients with LQTS. Patients with asthma should use cardioselective beta-blockers. Patients with LQTS who cannot take beta-blockers may require ICDs as first-line therapy.

Adult

20-160 mg/d PO

Pediatric

Administer as in adults

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, calcium channel blockers, quinidine, flecainide, and oral contraceptives; may increase toxicity of digoxin, flecainide, clonidine, epinephrine, nifedipine, prazosin, verapamil, and lidocaine

Documented hypersensitivity; uncompensated congestive heart failure, bradycardia, asthma, cardiogenic shock, 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

Precautions

Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor closely; should be taken by pregnant women with LQTS during pregnancy and postpartum period, when risk of cardiac events increases


Metoprolol (Lopressor)

Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. During IV administration, carefully monitor BP, heart rate, and ECG. Consult cardiologist because dosing varies and is individualized in patients with LQTS. Patients with LQTS who cannot take beta-blockers may require ICDs as first-line therapy.

Adult

25-200 mg PO bid

Pediatric

Administer as in adults

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly decreasing pharmacologic effects; toxicity may increase with coadministration of sparfloxacin, phenothiazines, astemizole (recalled from US market), calcium channel blockers, quinidine, flecainide, and contraceptives; may increase toxicity of digoxin, flecainide, clonidine, epinephrine, nifedipine, prazosin, verapamil, and lidocaine

Documented hypersensitivity; uncompensated congestive heart failure, bradycardia, asthma, cardiogenic shock, 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 BP, heart rate, and ECG


Atenolol (Tenormin)

Selectively blocks beta1-receptors with little or no affect on beta2 types. Consult cardiologist because dosing varies and is individualized in patients with LQTS. Patients with LQTS who cannot take beta-blockers may require ICDs as first-line therapy.

Adult

25-200 mg/d PO

Pediatric

Administer as in adults

Coadministration with aluminum salts, barbiturates, calcium salts, cholestyramine, NSAIDs, penicillins, and rifampin may decrease effects; haloperidol, hydralazine, loop diuretics, and MAOIs may increase toxicity

Documented hypersensitivity; congestive heart failure, pulmonary edema, cardiogenic shock, AV conduction abnormalities, heart block (without a pacemaker)

Pregnancy

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

Precautions

Beta-adrenergic blockade may reduce symptoms of acute hypoglycemia and mask signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism and cause thyroid storm; monitor patients closely and withdraw drug slowly; during IV administration, carefully monitor BP, heart rate, and ECG

More on Long QT Syndrome

Overview: Long QT Syndrome
Differential Diagnoses & Workup: Long QT Syndrome
Treatment & Medication: Long QT Syndrome
Follow-up: Long QT Syndrome
Multimedia: Long QT Syndrome
References
[ CLOSE WINDOW ]

References

  1. Border WL, Benson DW. Sudden infant death syndrome and long QT syndrome: the zealots versus the naysayers. Heart Rhythm. Feb 2007;4(2):167-9. [Medline].

  2. Medeiros A, Kaku T, Tester DJ, et al. Sodium channel B4 subunit mutation causes congenital long QTsyndrome. Heart Rhythm. 2006;3:S34.

  3. Wu G, Ai T, Kim JJ, et al. Alpha-1-Syntrophin Mutation and the Long QT Syndrome: a disease of sodium channel disruption. Circulation. May 28, 2008;Online, ahead of print.

  4. [Best Evidence] Hinterseer M, Beckmann BM, Thomsen MB, Pfeufer A, Dalla Pozza R, Loeff M, et al. Relation of increased short-term variability of QT interval to congenital long-QT syndrome. Am J Cardiol. May 1 2009;103(9):1244-8. [Medline].

  5. Schwartz PJ, Moss AJ, Vincent GM. Diagnostic criteria for the long QT syndrome: an update. Circulation. 1993;88:782-4. [Medline].

  6. Zareba W, Moss AJ, Daubert JP, Hall WJ, Robinson JL, Andrews M. Implantable cardioverter defibrillator in high-risk long QT syndrome patients. J Cardiovasc Electrophysiol. Apr 2003;14(4):337-41. [Medline].

  7. Goldenberg I, Moss AJ, Peterson DR, McNitt S, Zareba W, Andrews ML, et al. Risk factors for aborted cardiac arrest and sudden cardiac death in children with the congenital long-QT syndrome. Circulation. Apr 29 2008;117(17):2184-91. [Medline].

  8. Goldenberg I, Moss AJ. Long QT syndrome. J Am Coll Cardiol. Jun 17 2008;51(24):2291-300. [Medline].

  9. Goldenberg I, Moss AJ, Zareba W, McNitt S, Robinson JL, Qi M, et al. Clinical course and risk stratification of patients affected with the Jervell and Lange-Nielsen syndrome. J Cardiovasc Electrophysiol. Nov 2006;17(11):1161-8. [Medline].

  10. Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Circulation. Sep 5 2006;114(10):e385-484. [Medline].

  11. Roden DM. Long QT Syndrome. N Engl J Med. Jan 2008;358(2):169-76. [Medline].

  12. Ackerman MJ. Genotype-phenotype relationships in congenital long QT syndrome. J Electrocardiol. Oct 2005;38(4 Suppl):64-8. [Medline].

  13. Ali RH, Zareba W, Moss AJ, et al. Clinical and genetic variables associated with acute arousal and nonarousal-related cardiac events among subjects with long QT syndrome. Am J Cardiol. Feb 15 2000;85(4):457-61. [Medline].

  14. Antzelevitch C. Arrhythmogenic mechanisms of QT prolonging drugs: is QT prolongation really the problem?. J Electrocardiol. 2004;37 Suppl:15-24. [Medline].

  15. Antzelevitch C, Oliva A. Amplification of spatial dispersion of repolarization underlies sudden cardiac death associated with catecholaminergic polymorphic VT, long QT, short QT and Brugada syndromes. J Intern Med. Jan 2006;259(1):48-58. [Medline].

  16. Chiang CE, Roden DM. The long QT syndromes: genetic basis and clinical implications. J Am Coll Cardiol. Jul 2000;36(1):1-12. [Medline].

  17. Ching CK, Tan EC. Congenital long QT syndromes: clinical features, molecular genetics and genetic testing. Expert Rev Mol Diagn. May 2006;6(3):365-74. [Medline].

  18. Gowda RM, Khan IA, Wilbur SL, Vasavada BC, Sacchi TJ. Torsade de pointes: the clinical considerations. Int J Cardiol. Jul 2004;96(1):1-6. [Medline].

  19. Kao LW, Furbee RB. Drug-induced q-T prolongation. Med Clin North Am. Nov 2005;89(6):1125-44, x. [Medline].

  20. Lankipalli RS, Zhu T, Guo D, Yan GX. Mechanisms underlying arrhythmogenesis in long QT syndrome. J Electrocardiol. Oct 2005;38(4 Suppl):69-73. [Medline].

  21. Modell SM, Lehmann MH. The long QT syndrome family of cardiac ion channelopathies: a HuGE review. Genet Med. Mar 2006;8(3):143-55. [Medline].

  22. Moss AJ, Robinson J. Clinical features of the idiopathic long QT syndrome. Circulation. Jan 1992;85(1 Suppl):I140-4. [Medline].

  23. Moss AJ, Schwartz PJ, Crampton RS, et al. The long QT syndrome. Prospective longitudinal study of 328 families. Circulation. Sep 1991;84(3):1136-44. [Medline].

  24. Moss AJ, Zareba W, Benhorin J, et al. ECG T-wave patterns in genetically distinct forms of the hereditary long QT syndrome. Circulation. Nov 15 1995;92(10):2929-34. [Medline].

  25. Moss AJ, Zareba W, Hall WJ, et al. Effectiveness and limitations of beta-blocker therapy in congenital long-QT syndrome. Circulation. Feb 15 2000;101(6):616-23. [Medline].

  26. Napolitano C, Bloise R, Priori SG. Long QT syndrome and short QT syndrome: how to make correct diagnosis and what about eligibility for sports activity. J Cardiovasc Med (Hagerstown). Apr 2006;7(4):250-6. [Medline].

  27. Rashba EJ, Zareba W, Moss AJ, et al. Influence of pregnancy on the risk for cardiac events in patients with hereditary long QT syndrome. LQTS Investigators. Circulation. Feb 10 1998;97(5):451-6. [Medline].

  28. Roden DM. Acquired long QT syndromes and the risk of proarrhythmia. J Cardiovasc Electrophysiol. Aug 2000;11(8):938-40. [Medline].

  29. Roden DM. Long QT syndrome: reduced repolarization reserve and the genetic link. J Intern Med. Jan 2006;259(1):59-69. [Medline].

  30. Schwartz PJ. The congenital long QT syndromes from genotype to phenotype: clinical implications. J Intern Med. Jan 2006;259(1):39-47. [Medline].

  31. Schwartz PJ, Locati EH, Moss AJ, et al. Left cardiac sympathetic denervation in the therapy of congenital long QT syndrome. A worldwide report. Circulation. Aug 1991;84(2):503-11. [Medline].

  32. Schwartz PJ, Priori SG, Spazzolini C, et al. Genotype-phenotype correlation in the long-QT syndrome: gene-specific triggers for life-threatening arrhythmias. Circulation. Jan 2 2001;103(1):89-95. [Medline].

  33. Vincent GM, Timothy KW, Leppert M, Keating M. The spectrum of symptoms and QT intervals in carriers of the gene for the long-QT syndrome. N Engl J Med. Sep 17 1992;327(12):846-52. [Medline].

  34. Zareba W, Moss AJ, le Cessie S, et al. Risk of cardiac events in family members of patients with long QT syndrome. J Am Coll Cardiol. Dec 1995;26(7):1685-91. [Medline].

  35. Zareba W, Moss AJ, Schwartz PJ, et al. Influence of genotype on the clinical course of the long-QT syndrome. International Long-QT Syndrome Registry Research Group. N Engl J Med. Oct 1 1998;339(14):960-5. [Medline].

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

long QT syndrome, LQTS, congenital long QT syndrome, Romano-Ward syndrome, Jervell and Lange-Nielsen syndrome, JLN syndrome, ventricular tachyarrhythmias, syncope, cardiac arrest, sudden death, Anderson syndrome, Timothy syndrome

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Ali A Sovari, MD, Clinical and Research Fellow in Cardiovascular Medicine, Section of Cardiology, University of Illinois at Chicago
Ali A Sovari, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, and American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Abraham G Kocheril, MD, FACC, FACP, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago
Abraham G Kocheril, MD, FACC, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, Cardiac Electrophysiology Society, Central Society for Clinical Research, Heart Failure Society of America, and Illinois State Medical Society
Disclosure: Nothing to disclose.

Ramin Assadi, MD, Fellow, Department of Cardiology, Loma Linda University
Ramin Assadi, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, and American Medical Association
Disclosure: Nothing to disclose.

Arnold S Baas, MD, FACC, FACP, Assistant Professor of Medicine, Division of Cardiology, University of California, Los Angeles School of Medicine; Attending Physician, UCLA Santa Monica Hospital and UCLA Westwood Hospital
Arnold S Baas, MD, FACC, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, and American Society of Echocardiography
Disclosure: Pfizer Honoraria Speaking and teaching

Wojciech Zareba, MD, PhD, FACC, Associate Director of Heart Research, Associate Professor, Department of Medicine, Division of Cardiology, University of Rochester Medical Center
Wojciech Zareba, MD, PhD, FACC is a member of the following medical societies: American College of Cardiology, American Heart Association, European Society of Cardiology, International Society for Holter and Noninvasive Electrocardiology, International Society of Electrocardiology, and Polish Society of Cardiology
Disclosure: Nothing to disclose.

Spencer Rosero, MD, Assistant Professor, Department of Medicine, University of Rochester School of Medicine
Spencer Rosero, MD is a member of the following medical societies: American College of Cardiology
Disclosure: Nothing to disclose.

Medical Editor

Justin D Pearlman, MD, PhD, ME, MA, Director of Advanced Cardiovascular Imaging, Professor of Medicine, Professor of Radiology, Adjunct Professor, Thayer Bioengineering and Computer Science, Dartmouth-Hitchcock Medical Center
Justin D Pearlman, MD, PhD, ME, MA is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, International Society for Magnetic Resonance in Medicine, and Radiological Society of North America
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Brian Olshansky, MD, Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine
Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences
Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Reliant Grant/research funds Other; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

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

Jeffrey N Rottman, MD, Professor of Medicine and Pharmacology, Director, Clinical Cardiac Electrophysiology Fellowship Program, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center
Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association and North American Society of Pacing and Electrophysiology (NASPE)
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.