eMedicine Specialties > Cardiology > Arrhythmias

Lown-Ganong-Levine Syndrome: Treatment & Medication

Author: Daniel M Beyerbach, MD, PhD,, Consulting Staff, Florida Electrophysiology Associates; Affiliate Clinical Assistant Professor of Biomedical Science, Florida Atlantic University, Regional Campus of University of Miami Miller School of Medicine
Coauthor(s): Christopher Cadman, MD, Director of Arrhythmia Service, Assistant Professor, Department of Internal Medicine, Division of Cardiology, University of New Mexico
Contributor Information and Disclosures

Updated: Sep 4, 2009

Treatment

Medical Care

Because LGL is an outdated diagnosis, no specific therapy is indicated. In the acute setting of tachycardia, the goals of medical care include identifying the cause of tachycardia and, in symptomatic cases, controlling the ventricular rate. Treatment should be based on the cause of tachycardia. As with any tachycardia, hospitalization is warranted in cases of hemodynamic instability.

In the outpatient setting, empiric therapies for recurrent PSVT may be instituted. These therapies may include beta-blockers, calcium channel blockers, and digoxin. A full discussion of these therapies lies outside the scope of this article (see Paroxysmal Supraventricular Tachycardia).

Surgical Care

Rare patients for whom the criteria of LGL are met may have no inducibility of tachyarrhythmias by EP study. Rarely, medical therapy fails in these patients, who continue to have recurrent, intolerable symptoms. In such extreme cases, pacemaker implantation, followed by
radiofrequency (RF) ablation of the AV node or bundle of His may be considered.

Consultations

An immediate cardiology consultation is warranted if the patient has presyncope, syncope, hypotension with tachycardia, angina, or other evidence of instability at the time of evaluation.

  • Conditions appropriate for consideration of RF catheter ablation and referral to an electrophysiologist include the following:
    • Failure of pharmacologic therapy to control symptoms
    • Recurrence of any signs of hemodynamic instability or of intolerable symptoms under medical management
    • Patient's desire to avoid daily medication
    • Intolerable adverse effects of medication

Diet

No dietary restrictions are required.

Activity

Patients who have experienced an episode of syncope should be counseled to not drive or operate vehicles of public transport for 6 months from the time of the most recent episode of syncope, or until the cause of syncope has been identified and adequately treated.

Medication

No medication therapy is specific to LGL. The goals of therapy are to identify the cause of tachycardia and to treat this cause appropriately.

Beta-blockers

Inhibit chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation and slow AV nodal conduction.


Metoprolol (Lopressor, Toprol XL)

Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. During IV administration, carefully monitor BP, heart rate, and ECG.

Adult

50 mg/d PO qd or divided bid/tid initially and increase at 1-wk intervals prn to total of 200 mg/d if necessary

Pediatric

1-5 mg/kg/24h PO divided bid

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

Documented hypersensitivity; uncompensated CHF; 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 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 the drug slowly; during IV administration, carefully monitor blood pressure, heart rate, and ECG


Atenolol (Tenormin)

Selectively blocks beta1-receptors with little or no effect on beta2 types.

Adult

50 mg PO qd; increase to 100 mg/d if necessary

Pediatric

1-2 mg/kg/dose PO qd

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

Documented hypersensitivity; CHF; pulmonary edema; cardiogenic shock; AV conduction abnormalities; heart block (without pacemaker)

Pregnancy

C - Safety for use during pregnancy has not been established.

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, carefully monitor BP, heart rate, and ECG

Calcium channel blockers (nondihydropyridine)

In specialized conducting and automatic cells in the heart, calcium is involved in the generation of the action potential. Calcium channel blockers inhibit movement of calcium ions across the cell membrane, depressing both impulse formation (automaticity) and conduction velocity.


Verapamil (Calan, Covera, Isoptin)

Can diminish PVCs associated with perfusion therapy and decrease risk of ventricular fibrillation and ventricular tachycardia. By interrupting reentry at AV node, can restore normal sinus rhythm in patients with PSVT.

Adult

80-120 mg PO tid or 120-360 mg SR formulation; alternatively, 5-10 mg IV followed by second dose 15-30 min later if PSVT does not respond satisfactorily to initial dose

Pediatric

Not established

May increase carbamazepine, digoxin, and cyclosporine levels; amiodarone can cause bradycardia and decrease in cardiac output; beta-blockers may increase cardiac depression; cimetidine may increase levels; may increase theophylline levels

Documented hypersensitivity; severe CHF; sick sinus syndrome; second- or third-degree AV block; hypotension (<90 mm Hg systolic)

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Hepatocellular injury may occur; transient elevations of transaminases with and without concomitant elevations in alkaline phosphatase and bilirubin have occurred (elevations have been transient and may disappear with continued treatment); monitor liver functions periodically


Diltiazem (Cardizem)

During depolarization, inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.

Adult

30-90 mg PO tid, or 120-300 mg PO qd of CD formulation

Pediatric

Not established

May increase carbamazepine, digoxin, cyclosporine, and theophylline levels; amiodarone may cause bradycardia and decrease in cardiac output; beta-blockers may increase cardiac depression; cimetidine may increase levels

Documented hypersensitivity; severe CHF; sick sinus syndrome; second- or third-degree AV block; hypotension (<90 mm Hg systolic)

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in impaired renal or hepatic function; may increase LFT levels, and hepatic injury may occur

Cardiac glycosides

Decrease AV nodal conduction, primarily by increasing vagal tone.


Digoxin (Lanoxin)

Cardiac glycoside with direct inotropic effects in addition to indirect effects on 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 loading dose PO
>10 years: 10-15 mcg/kg loading dose PO
Maintenance dose: 25-35% of PO loading dose administered qd

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 may increase levels
Aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, oral colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid may decrease levels

Documented hypersensitivity; beriberi heart disease; idiopathic hypertrophic subaortic stenosis; constrictive pericarditis; 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; IV calcium may produce arrhythmias in digitalized patients; 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 with incomplete AV block may progress to complete block when treated with digoxin; use caution in hypothyroidism, hypoxia, and acute myocarditis

More on Lown-Ganong-Levine Syndrome

Overview: Lown-Ganong-Levine Syndrome
Differential Diagnoses & Workup: Lown-Ganong-Levine Syndrome
Treatment & Medication: Lown-Ganong-Levine Syndrome
Follow-up: Lown-Ganong-Levine Syndrome
Multimedia: Lown-Ganong-Levine Syndrome
References

References

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Further Reading

Keywords

Lown-Gangong-Levine syndrome, LGL syndrome, Clerc-Levy-Critesco syndrome, enhanced atrioventricular nodal conduction, accelerated atrioventricular nodal conduction, short PR/normal QRS syndrome, short PR/narrow QRS syndrome, accessory pathway, WPW syndrome, Wolff-Parkinson-White syndrome

Contributor Information and Disclosures

Author

Daniel M Beyerbach, MD, PhD,, Consulting Staff, Florida Electrophysiology Associates; Affiliate Clinical Assistant Professor of Biomedical Science, Florida Atlantic University, Regional Campus of University of Miami Miller School of Medicine
Daniel M Beyerbach, MD, PhD, is a member of the following medical societies: American College of Cardiology
Disclosure: Nothing to disclose.

Coauthor(s)

Christopher Cadman, MD, Director of Arrhythmia Service, Assistant Professor, Department of Internal Medicine, Division of Cardiology, University of New Mexico
Christopher Cadman, MD is a member of the following medical societies: American College of Cardiology and Phi Beta Kappa
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

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

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.

 
 
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