eMedicine Specialties > Cardiology > Arrhythmias
Sinus Node Dysfunction
Updated: Aug 31, 2009
Introduction
Background
Sinus node dysfunction (SND) first appeared in the literature as a clinical entity in 1968 under the name of sick sinus syndrome.1 Today SND refers to abnormalities in sinus node impulse formation and propagation, and includes sinus bradycardia, sinus pause/arrest, chronotropic incompetence, and sinoatrial exit block.2 SND is frequently associated with conduction system disease in the heart and various supraventricular tachyarrhythmias, such as atrial fibrillation and atrial flutter. When associated with supraventricular tachyarrhythmias, SND is often termed tachy-brady syndrome.2
Although SND may occur at any age, it is primarily a disease of the elderly and, presumably, related to the senescence of the sinus node, which is often accompanied with the senescence of the atrium and the conduction system in the heart. When SND occurs earlier in life, it is often secondary to other cardiac disease processes.3 The natural history of SND may be highly variable, although it tends to be progressive in nature. The only effective treatment for patients with chronic symptomatic SND is pacemaker therapy. Asymptomatic patients do not require therapy.
Pathophysiology
SND involves abnormalities in sinus node impulse formation and propagation, which are often accompanied with similar abnormalities in the atrium and the conduction system in the heart. Together, these abnormalities may result in inappropriately slow ventricular rates and long pauses at rest or during various stresses. When SND is mild, patients are usually asymptomatic. As SND becomes more severe, patients may develop symptoms due to organ hypoperfusion and pulse irregularity. Among these symptoms are fatigue, dizziness, confusion, fall, syncope, angina, heart failure symptoms and palpitations.
Frequency
United States
The exact incidence of sinus node dysfunction is unknown. The syndrome occurs in approximately one in 600 cardiac patients older than 65 years.4
International
Due to its relationship with advanced age, SND is more prevalent in countries where citizens have a longer life expectancy.
Mortality/Morbidity
Symptoms of sinus node dysfunction almost invariably progress over time. The most dramatic symptom in patients with SND is syncope. About 50% of patients with SND develop tachy-brady syndrome over a lifetime8 ; such patients have higher risk of stroke and death. The survival of patients with SND appears to depend primarily on the severity of underlying cardiac disease and is not significantly changed by pacemaker therapy.5,6,7 However, incidence of sudden death owing directly to SND is extremely low.5
Race
No racial preponderance exists.
Sex
Men and women are affected in equal numbers.
Age
Sinus node dysfunction may occur at any age but is primarily a disease of the elderly, with the average age being about 68 years-old9 . SND in young patients is often related to underlying heart diseases.
Clinical
History
With mild SND, patients are usually asymptomatic. As SND progresses, patients often develop symptoms due to pulse irregularity and organ hypoperfusion. The severity of organ hypoperfusion symptoms depends on the severity of SND and on the functional reserve state of an organ.
- Cerebral symptoms - Irritability, labile mood swings, forgetfulness, dizziness, slurred speech, blanking periods, falls, and syncope
- Cardiac symptoms - Palpitations, angina, congestive heart failure symptoms, and sudden cardiac death (rare)
- Other symptoms
- Vague gastrointestinal symptoms and oligurea
- Tachy-brady syndrome may include palpitations due to tachycardia and stroke/transient ischemia attack (TIA) symptoms
Physical
- Inappropriately slow heart rate.
- Carotid sinus massage: may reveal sinus pause of more than 3 seconds ± hypotension in patients with carotid sinus hypersensitivity.
Causes
Although the exact etiology is usually not identified, most cases are believed to be attributable to a combination of various intrinsic and extrinsic factors. The most common intrinsic causes are cardiac age-related sinus node changes and coronary artery disease. The most common extrinsic causes are medications and autonomic hyperactivity.
Intrinsic SND
- Age-related changes: the most common cause of SND is the replacement of sinus node tissue with fibrotic tissue. These fibrotic changes also occur in the atrium and the conduction system of the heart, and are believed to contribute to the association among SND, tachy-brady syndrome, conductive system disease and an inappropriately slow escape rhythm. Recently, age-related down-regulation of calcium channel expression in the sinus node has also been suggested as a potential cause of SND.10
- Coronary artery disease: coronary artery disease is believed to be a common contributory cause of SND, probably through atherosclerotic changes in the sinus node artery.
- Familial sick sinus syndromes and SND in children: Several molecular defects in human hearts (defects in the sodium channel, calcium channel and hyperpolarization-activated cyclic nucleotide-gated cation (HCN) channel, ankyrin-B and connexin 40) have been associated with familial sick sinus syndromes.3 SND is seen in children with congenital and acquired heart disease, particularly after corrective surgery. The cause of SND in these children is likely related to the underlying structural heart disease and surgical trauma to the sinus node and/or sinus node artery.
- Tachy-brady syndrome: tachycardia-mediated remodeling of the sinus node is present in patients with atrial fibrillation/flutter and it may contribute to SND in these patients. In patients with tachy-brady syndrome, atrial fibrillation ablation can reverse sinus node dysfunction as evidenced by a reduction in sinus node recovery time, increase in mean and maximal heart rates and lack of symptoms related to sinus bradycardia or pause.11
- Other structural heart diseases are uncommon causes of SND. These include, but are not limited to various cardiomyopathies, myocarditis, pericarditis, infiltrative heart diseases (amyloidosis, hemochromatosis, neoplasm), collagen vascular diseases (systemic lupus, scleroderma), neuromuscular diseases (myotonic dystrophy, Friedreich ataxia).
Extrinsic SND
- Medications: Beta-blockers, calcium channel blockers, digoxin, and various anti-arrhythmic drugs suppress sinus node function.
- Autonomic dysfunction: SND can be secondary to autonomic nervous system dysfunction in patients with neurocardiogenic syncope, and carotid sinus hypersensitivity. Conditions associated with marked hypervagotonia, as in well-trained athletes, can also result in SND. Recent evidence, however, suggests that there may be some intrinsic factor as well in well-trained athletes who develop SND.12 .
- Endocrine-metabolic diseases (hypothyroidism and hypothermia) and electrolyte imbalances (hypokalemia and hypocalcemia) can contribute to SND.
Differential Diagnoses
Atrial Fibrillation
Atrial Flutter
Atrioventricular Block
Other Problems to Be Considered
Premature ventricular beats in bigeminy may cause apparent slow pulse rate in physical examination.
Workup
Laboratory Studies
Because hypothyroidism and electrolyte imbalances can contribute to SND, thyroid function test and serum electrolyte test (Na+, K+ and Ca2+) can be useful.
Imaging Studies
- No specific imaging studies are required in the initial workup of SND.
- An echocardiogram should be considered because it can document the presence of underlying valvular or ischemic heart disease.
Other Tests
Electrocardiograph recording studies
The electrocardiograph recording is the most important method for the diagnosis of SND. Depending on the level of clinical suspicion, the frequency of symptoms and symptom relationship to exertion, the following methods are often used in combination to establish the diagnosis. Because SND symptoms are often intermittent, long term monitoring with an event recorder or implantable loop recorder can be very useful.
- ECG - 12-lead ECG recording
- Holter - 24-48 hours continuous 3-lead ECG recording
- Event recorder study - Symptom-triggered 1-lead ECG recording during a 2-3 month period
- Implantable loop recorder study - Predefined parameters that trigger single-lead electrocardiograph recordings for up to 3 years duration (These parameters may include bradycardia, tachycardia, pauses, and symptoms.)
- Exercise testing - ECG recordings during exercise to evaluate maximal heart rate at peak exercise
The ECG criteria for SND diagnosis include the following:
- Inappropriate sinus bradycardia: The arbitrary cutoff for a low sinus rate in a person at rest but awake is usually defined as <55-60 bpm. However, a study in 500 healthy subjects suggests the low afternoon sinus rate for men and women should be around 46 and 51 bpm respectively.13 Asymptomatic isolated sinus bradycardia is not an indication for pacemaker therapy.
- Sinus pause or arrest
- Sinus pause or arrest is defined as absence of sinus P waves on the ECG for more than 2 seconds due to a lack of sinus nodal pacemaker activity. The duration of the pauses should have no arithmetical relationship to the baseline sinus rate (ie, the P-P interval should not be an interval of the pause), otherwise the diagnosis of sinoatrial exit block should be considered.
- A sinus pause of 2 seconds is not unusual in a healthy person.14 However, a sinus pause of more than 3 seconds is very uncommon except under certain conditions, such as sleep apnea, hypervagotonia state, or seizure activity.14
- Sinoatrial exit block (SA exit block)
- First-degree SA exit block reflects a conduction delay between the sinus node and atrium that cannot be recognized on regular ECG recordings.
- Second-degree SA exit block reflects intermittent conduction block between the sinus node and atrium. It has 2 classic types and likely some atypical types. Only the classic types can be recognized on regular ECG recordings.
- Type I (Wenckebach type) is manifested as group beating, which is progressive shortening of the P-P intervals, and then a pause that is less than twice the shortest P-P interval.
- Type II is manifested as a pause that is a multiple of the baseline sinus P-P interval.
- Third-degree SA exit block reflects complete conduction block from sinus node to atrium. It cannot be definitely distinguished from sinus arrest on regular ECG recordings.
- Chronotropic incompetence: Chronotropic incompetence is defined as failure to achieve 70-80% of maximal predicted heart rate (maximal predicted heart rate = 220-age) at peak exercise. The clinical value of this definition, however, has not been well validated.15 The peak exercise heart rate can be influenced by multiple factors.
Pharmacological stimulation tests
Due to its moderate sensitivity and specificity for SND diagnosis, intrinsic heart rate and atropine stimulation tests are occasionally used as accessory tests in selected patients (such as patients with suspected hypervagotonia). The value of isoproterenol, propranolol, and adenosine stimulation tests in SND diagnosis is more controversial.
- Intrinsic heart rate (IHR): Atropine (0.04 mg/kg) and propranolol (0.2 mg/kg) have been used to pharmacologically denervate the sinus node, which is then followed 5-20 minutes later by an evaluation of its IHR. The IHR in a healthy person is approximately equal to 117.2 – [0.53 x Age].16 Intrinsic SND is presumed to be present if the sinus rate after medications is below calculated IHR. Patients with mild SND may have a normal or exacerbated response. This test is probably helpful in patients with sinus bradycardia due to suspected hypervagotonia17 , in whom the IHR is expected to be normal.
- Atropine test: Atropine alone (up to 0.04 mg/kg) may provide as much information as the combination of atropine (0.04 mg/kg) and propranolol (0.2 mg/kg).18 Atropine (1-3 mg) is the most commonly used agent to assess the parasympathetic tone. A normal response is an increase in sinus rate above 90 bpm or an increase of more than 25% above the baseline sinus rate.15 Patients with symptomatic sinus node dysfunction usually demonstrate a decrease in IHR. However, patients with only mild SND may have a normal or exacerbated response to atropine.
Electrophysiological study (EPS)
Due to its moderate sensitivity and specificity for SND diagnosis, EPS is only occasionally used when other tests yield ambiguous results.
Corrected sinus node recovery time (CSNRT): CSNRT is the most commonly used method in EPS for diagnosing SND.
At a site close to the sinus node, sinus rhythm is overdrive paced at different rates for one minute. The overdrive pacing rate starts at a rate just above basal sinus rate, and increases by 10-20 bpm with each successive overdrive pacing cycle until the overdrive pacing rate reaches 200 bpm. At each overdrive pacing cycle, the sinus node recovery time is measured as the time from the last paced atrial beat to the first post-paced spontaneous sinus beat. The corrected sinus node recovery time at each overdrive pacing cycle is calculated as follows:
For normal sinus nodes, the maximal corrected sinus node recovery time should be less than 450 ms.18 In the THEOPACE study, patients with syncope and CSNRT ≥800 ms treated with permanent pacemaker had a 25% reduction of syncope over 4 years as compared with patients treated with theophylline or no therapy.19Corrected sinus node recovery time = Sinus node recovery time – Basal sinus cycle length before the overdrive pacing
Sinus node conduction time (SNCT) is another EPS parameter used in evaluating sinus node function.18 It is used less frequently than CSNRT.
Procedures
Pacemaker implant
Treatment
Medical Care
The only effective medical care in patients with SND is to correct extrinsic causes.
Surgical Care
Pacemaker therapy is the only effective surgical care for patients with chronic symptomatic SND.
Because the incidence of sudden death in patients with SND is extremely low and pacemaker therapy does not appear to affect survival, the major goal of pacemaker therapy in patients with SND is to relieve symptoms.
Pacemaker indications
According to the American College of Cardiology guidelines in 20082 , pacemaker therapy has the following:
- Class I indication for patients with documented symptomatic sinus bradycardia, sinus pause, and chronotropic incompetence. This includes patients who have iatrogenic SND secondary to essential medications for which no acceptable alternatives exist.
- Class IIa indication for patients with SND and a sinus rate <40 bpm when a clear association between symptoms (ie, symptoms consistent with bradycardia) and bradycardia has not been documented.
- Class IIa indication for patients with syncope of unexplained origin when clinically significant abnormalities of sinus node are discovered or provoked in electrophysiological studies.
- Class IIb indication for patients with minimal symptoms and chronic heart rate less than 40 bpm while awake.
Pacemaker therapy is contraindicated (class III indication) for patients with asymptomatic SND or symptomatic bradycardia due to medications that are not essential.
- Single versus dual chamber pacemaker: In patients with SND, the annual incidence of complete heart block is about 0.6 %.20 In the United States, a dual-chamber pacemaker is preferred in practice because it anticipates the possible subsequent development of conducting system dysfunction. A single-chamber atrial pacemaker with AAI mode, however, is acceptable therapy in patients with SND and normal AV conduction/intraventricular conduction as the overall incidence of complete heart block in very low. In patients with SND and known AV conduction abnormality (including bundle branch block and bifascicular block), dual-chamber pacemaker should be used due to the high risk of AV block (about 36% in a 5-year follow-up study).21
- Pacemaker programming features: AAI and dual chamber pacing are better than VVI pacing mode.22,23 If a dual chamber pacemaker is used, it is very important to use various programming algorithms to promote intrinsic AV conduction, thus reducing right ventricular pacing. Chronic right ventricular pacing has been shown to be associated with an increased incidence of atrial fibrillation, stroke, heart failure, and probably death.22,23,24
- Mode switch is an important feature to monitor atrial flutter and fibrillation events. Because over time more than 50% of patients with SND may develop tachy-brady syndrome8 , it is very important to identify these patients through pacemaker monitoring and anticoagulate them to reduce their risk of stroke.
- Pacemakers with a "rate drop" response program may benefit some patients with neurocardiogenic syncope. Rate response to activity program is generally used in patients with SND and chronotropic incompetence. The clinical benefits of this program are still controversial.25
Consultations
Cardiac electrophysiology consult.
Diet
No specific dietary recommendations exist.
Activity
Patients with symptomatic SND and not on pacemaker therapy should titrate their level of activity to minimize symptoms.
Medication
Currently no medications are routinely used to treat symptomatic SND.
Follow-up
Further Inpatient Care
Admit patients for testing and pacemaker placement when indicated.
Further Outpatient Care
Asymptomatic patients with SND should be observed for symptoms.
In patients with a pacemaker, the following should be performed on routine pacemaker interrogations:
- Monitor leads and battery status.
- Ensure adequate heart rate support at rest, during daily activities, and exercise.
- Monitor for pacemaker malfunction, such as pacemaker-mediated tachycardia.
- Ensure minimal right ventricular pacing.
- Monitor for atrial fibrillation and atrial flutter events.
Transfer
Transfer patients for complicated dysarrhythmias and pacemaker implant.
Deterrence/Prevention
Treat heart diseases related to SND and extrinsic causes to delay and prevent SND.
Complications
- Sudden cardiac death (rare)
- Syncope
- Fall
- Thromboembolic events including stroke (especially in patients with tachy-brady syndrome)
- Congestive heart failure
- Arrhythmias
Prognosis
The incidence of sudden cardiac death in patients with SND is very low.5 The mortality in patients with SND is primarily determined by underlying heart diseases. The patients with tachy-brady syndrome have a worse prognosis than patients with isolated SND. Pacemaker therapy does not appear to affect survival in patients with SND5,6,7 and is, therefore, used primarily for alleviation of symptoms.
Patient Education
- Educate patients to recognize symptoms of SND.
- Educate patients on pacemakers.
- Family members should learn cardiopulmonary resuscitation (CPR).
Miscellaneous
Medicolegal Pitfalls
- Failure to diagnose symptomatic SND
- Inappropriate pacemaker therapy
References
Ferrer MI. The sick sinus syndrome in atrial disease. JAMA. Oct 14 1968;206(3):645-6. [Medline].
[Guideline] Epstein AE, DiMarco JP, Ellenbogen KA, Estes NA 3rd, Freedman RA, Gettes LS, et al. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices) developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons. J Am Coll Cardiol. May 27 2008;51(21):e1-62. [Medline].
Dobrzynski H, Boyett MR, Anderson RH. New insights into pacemaker activity: promoting understanding of sick sinus syndrome. Circulation. Apr 10 2007;115(14):1921-32. [Medline].
Rodriguez RD, Schocken DD. Update on sick sinus syndrome, a cardiac disorder of aging. Geriatrics. Jan 1990;45(1):26-30, 33-6. [Medline].
Menozzi C, Brignole M, Alboni P, Boni L, Paparella N, Gaggioli G, et al. The natural course of untreated sick sinus syndrome and identification of the variables predictive of unfavorable outcome. Am J Cardiol. Nov 15 1998;82(10):1205-9. [Medline].
Simon AB, Janz N. Symptomatic bradyarrhythmias in the adult: natural history following ventricular pacemaker implantation. Pacing Clin Electrophysiol. May 1982;5(3):372-83. [Medline].
Alt E, Völker R, Wirtzfeld A, Ulm K. Survival and follow-up after pacemaker implantation: a comparison of patients with sick sinus syndrome, complete heart block, and atrial fibrillation. Pacing Clin Electrophysiol. Nov 1985;8(6):849-55. [Medline].
Lamas GA, Lee KL, Sweeney MO, Silverman R, Leon A, Yee R, et al. Ventricular pacing or dual-chamber pacing for sinus-node dysfunction. N Engl J Med. Jun 13 2002;346(24):1854-62. [Medline].
Adán V, Crown LA. Diagnosis and treatment of sick sinus syndrome. Am Fam Physician. Apr 15 2003;67(8):1725-32. [Medline].
Jones SA, Boyett MR, Lancaster MK. Declining into failure: the age-dependent loss of the L-type calcium channel within the sinoatrial node. Circulation. Mar 13 2007;115(10):1183-90. [Medline].
Hocini M, Sanders P, Deisenhofer I, Jaïs P, Hsu LF, Scavée C, et al. Reverse remodeling of sinus node function after catheter ablation of atrial fibrillation in patients with prolonged sinus pauses. Circulation. Sep 9 2003;108(10):1172-5. [Medline].
Stein R, Medeiros CM, Rosito GA, Zimerman LI, Ribeiro JP. Intrinsic sinus and atrioventricular node electrophysiologic adaptations in endurance athletes. J Am Coll Cardiol. Mar 20 2002;39(6):1033-8. [Medline].
Spodick DH. Normal sinus heart rate: sinus tachycardia and sinus bradycardia redefined. Am Heart J. Oct 1992;124(4):1119-21. [Medline].
Hilgard J, Ezri MD, Denes P. Significance of ventricular pauses of three seconds or more detected on twenty-four-hour Holter recordings. Am J Cardiol. Apr 1 1985;55(8):1005-8. [Medline].
Katritsis D, Camm AJ. Chronotropic incompetence: a proposal for definition and diagnosis. Br Heart J. Nov 1993;70(5):400-2. [Medline].
Jose AD, Collison D. The normal range and determinants of the intrinsic heart rate in man. Cardiovasc Res. Apr 1970;4(2):160-7. [Medline].
Jordan JL, Yamaguchi I, Mandel WJ. Studies on the mechanism of sinus node dysfunction in the sick sinus syndrome. Circulation. Feb 1978;57(2):217-23. [Medline].
Josephson, ME. Clinical Cardiac Electrophysiology. 3rd edition. 2002.
Alboni P, Menozzi C, Brignole M, Paparella N, Gaggioli G, Lolli G, et al. Effects of permanent pacemaker and oral theophylline in sick sinus syndrome the THEOPACE study: a randomized controlled trial. Circulation. Jul 1 1997;96(1):260-6. [Medline].
Rosenqvist M, Obel IW. Atrial pacing and the risk for AV block: is there a time for change in attitude?. Pacing Clin Electrophysiol. Jan 1989;12(1 Pt 1):97-101. [Medline].
Brandt J, Anderson H, Fåhraeus T, Schüller H. Natural history of sinus node disease treated with atrial pacing in 213 patients: implications for selection of stimulation mode. J Am Coll Cardiol. Sep 1992;20(3):633-9. [Medline].
Andersen HR, Thuesen L, Bagger JP, Vesterlund T, Thomsen PE. Prospective randomised trial of atrial versus ventricular pacing in sick-sinus syndrome. Lancet. Dec 3 1994;344(8936):1523-8. [Medline].
Lamas GA, Lee KL, Sweeney MO, Silverman R, Leon A, Yee R. Ventricular pacing or dual-chamber pacing for sinus-node dysfunction. N Engl J Med. Jun 13 2002;346(24):1854-62. [Medline].
Sweeney MO, Bank AJ, Nsah E, Koullick M, Zeng QC, Hettrick D, et al. Minimizing ventricular pacing to reduce atrial fibrillation in sinus-node disease. N Engl J Med. Sep 6 2007;357(10):1000-8. [Medline].
Lamas GA, Knight JD, Sweeney MO, Mianulli M, Jorapur V, Khalighi K, et al. Impact of rate-modulated pacing on quality of life and exercise capacity--evidence from the Advanced Elements of Pacing Randomized Controlled Trial (ADEPT). Heart Rhythm. Sep 2007;4(9):1125-32. [Medline].
Keywords
sick sinus syndrome, sinus node dysfunction, SND, sinoatrial disease, sinoatrial dysfunction, sluggish sinus syndrome, sinus nodal dysfunction, Valsalva maneuver, carotid sinus massage, idiopathic degenerative disease, coronary artery disease, autonomic hyperactivity, intrinsic sinus nodal dysfunction, infiltrative diseases, cardiomyopathy, hypertension, collagen vascular diseases, congenital heart disease, heart transplant, musculoskeletal disorders, myocarditis, pericarditis, beta-blockers, nondihydropyridine calcium channel blockers, cardiac glycosides, sympatholytic antihypertensives, membrane-active antiarrhythmics, autonomic dysfunction, vasovagal syncope, carotid sinus syndrome, extrinsic sinus nodal dysfunction, electrolyte imbalance, hypothyroidism, hyperthyroidism, hypothermia, sepsis
Contributor Information and Disclosures
Author
Yingbo Yang, MD, PhD, Clinical Assistant Professor of Cardiovascular Medicine, Division of Cardiology, Lawrence J Ellison Ambulatory Care Center, University of California, Davis, Medical Center
Yingbo Yang, MD, PhD is a member of the following medical societies: American College of Cardiology and Heart Rhythm Society
Disclosure: Nothing to disclose.
Coauthor(s)
Yasir Batres, MD, Fellow, Division of Cardiology, University of California, Davis, Medical Center
Yasir Batres, 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
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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
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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
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Chief Editor
Michael E Zevitz, MD, Assistant Professor of Medicine, Finch University of the Health Sciences, The Chicago Medical School; Consulting Staff, Private Practice
Michael E Zevitz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Medical Association, and Michigan State Medical Society
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