Sinus Node Dysfunction Clinical Presentation

  • Author: Yingbo Yang, MD, PhD; Chief Editor: Jeffrey N Rottman, MD   more...
 
Updated: Apr 6, 2011
 

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 oliguria
    • Patients with tachy-brady syndrome may have symptoms of stroke or transient ischemia attack (TIA).
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Physical

  • Inappropriately slow heart rate.
  • Carotid sinus massage may reveal sinus pause of more than 3 seconds and/or hypotension symptoms in patients with carotid sinus hypersensitivity.
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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: Age-related changes are believed to be the most common cause of SND and are related to fibrosis in sinus node. 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, the pacemaker activity in sinus node was found to be related to voltage and calcium clocks.[10] Age-related down-regulation of calcium channel expression in the sinus node has been suggested as a potential cause of SND with aging.[11]
  • 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 and young adults: Several molecular defects in human hearts (defects in the sodium channel, calcium channel, 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.[12] The mechanism of SND in tachy-brady syndrome may involve the abnormal function of voltage and calcium clocks in the sinus node.[13, 14]
  • 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.[15]
  • Endocrine-metabolic diseases (hypothyroidism and hypothermia) and electrolyte imbalances (hypokalemia and hypocalcemia) can contribute to SND.
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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.

Specialty Editor Board

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.

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

Disclosure: Medscape Salary Employment

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; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

Amer Suleman, MD  Private Practice

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, 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.

Acknowledgments

We thank Dr. Adrian W Messerli, MD and professor Alan D Forker, MD for their important contributions to this article as the authors of its previous edition.

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