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First-Degree Atrioventricular Block

  • Author: Jamshid Alaeddini, MD, FACC, FHRS; Chief Editor: Jeffrey N Rottman, MD  more...
 
Updated: Dec 30, 2015
 

Background

First-degree atrioventricular (AV) block, or first-degree heart block, is defined as prolongation of the PR interval on an electrocardiogram (ECG) to more than 200 msec.[1] The PR interval of the surface ECG is measured from the onset of atrial depolarization (P wave) to the beginning of ventricular depolarization (QRS complex). Normally, this interval should be between 120 and 200 msec in the adult population. First-degree AV block is considered “marked” when the PR interval exceeds 300 msec.[2]

Whereas conduction is slowed, there are no missed beats. In first-degree AV block, every atrial impulse is transmitted to the ventricles, resulting in a regular ventricular rate.

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Pathophysiology

The atrioventricular node (AVN) is the only normal electrical connection between the atria and the ventricles. It is an oval or elliptical structure, measuring 7-8 mm in its longest (anteroposterior) axis, 3 mm in its vertical axis, and 1 mm transversely. The AVN is located beneath the right atrial endocardium, dorsal to the septal leaflet of the tricuspid valve, and about 1 cm superior to the orifice of the coronary sinus.

The bundle of His originates from the anteroinferior pole of the AVN and travels through the central fibrous body to reach the dorsal edge of the membranous septum. It then divides into right and left bundle branches. The right bundle continues first intramyocardially, then subendocardially, toward the right ventricular apex. The left bundle continues distally along the membranous septum and then divides into anterior and posterior fascicles.

Blood supply to the AVN is provided by the AVN artery, a branch of the right coronary artery in 90% of individuals and of the left circumflex coronary artery in the remaining 10%. The His bundle has a dual blood supply from branches of anterior and posterior descending coronary arteries. Likewise, the bundle branches are supplied by both left and right coronary arteries.

The AVN has a rich autonomic innervation and is supplied by both sympathetic and parasympathetic nerve fibers. This autonomic innervation has a major role in the time required for the impulse to pass through the AVN.

The PR interval represents the time needed for an electrical impulse from the sinoatrial (SA) node to conduct through the atria, the AVN, the bundle of His, the bundle branches, and the Purkinje fibers. Thus, as shown in electrophysiologic studies, PR interval prolongation (ie, first-degree AV block) may be due to conduction delay within the right atrium, the AVN, the His-Purkinje system, or a combination of these.

Overall, dysfunction at the AVN is much more common than dysfunction at the His-Purkinje system. If the QRS complex is of normal width and morphology on the ECG, then the conduction delay is almost always at the level of the AVN. If, however, the QRS demonstrates a bundle-branch morphology, then the level of the conduction delay is often localized to the His-Purkinje system.

Occasionally, the conduction delay can be the result of an intra-atrial conduction defect. Some causes of atrial disease resulting in a prolonged PR interval include endocardial cushion defects and Ebstein anomaly.[3]

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Etiology

The following are the most common causes of first-degree AV block:

  • Intrinsic AVN disease
  • Enhanced vagal tone
  • Acute myocardial infarction (MI), particularly acute inferior wall MI
  • Myocarditis
  • Electrolyte disturbances (eg, hypokalemia, hypomagnesemia)
  • Drugs (especially those drugs that increase the refractory time of the AVN, thereby slowing conduction)

A number of specific disorders and events have been implicated (see below).

Athletic training

Well-trained athletes can demonstrate first-degree (and occasionally higher degree) AV block owing to an increase in vagal tone.

Coronary artery disease

Coronary artery disease is a factor. First-degree AV block occurs in fewer than 15% of patients with acute MI admitted to coronary care units. His bundle electrocardiographic studies have shown that, in most of these patients, the AVN is the site of conduction block.

AV block is more common in the setting of inferior MI. In the Thrombolysis in Myocardial Infarction (TIMI) II study, high-degree (second- or third-degree) AV block occurred in 6.3% of patients at the time of presentation and in 5.7% in the first 24 hours after thrombolytic therapy.[4]

Patients with AV block at the time of presentation had a higher in-hospital mortality than patients without AV block; however, the 2 groups had similar mortalities during the following year.[4] Patients who developed AV block after thrombolytic therapy had higher mortalities both in hospital and during the following year than patients without AV block. The right coronary artery was more often the site of infarction in patients with heart block than in those without heart block.

Patients with AV block are believed to have larger infarct size. However, the prevalence of multivessel disease is not higher in patients with AV block.

Idiopathic degenerative diseases of conduction system

Lev disease is due to progressive degenerative fibrosis and calcification of the neighboring cardiac structures, or “sclerosis of the left side of cardiac skeleton” (including the mitral annulus, central fibrous body, membranous septum, base of the aorta, and crest of the ventricular septum). Lev disease has an onset about the fourth decade and is believed to be secondary to wear and tear on these structures caused by the pull of the left ventricular musculature. It affects the proximal bundle branches and is manifested by bradycardia and varying degrees of AV block.

Lenègre disease is an idiopathic, fibrotic degenerative disease restricted to the His-Purkinje system. It is caused by fibrocalcareous changes in the mitral annulus, membranous septum, aortic valve, and crest of the ventricular septum. These degenerative and sclerotic changes are not attributed to inflammatory or ischemic involvement of adjacent myocardium. Lenègre disease involves the middle and distal portions of both bundle branches and affects a younger population than Lev disease does.

Drugs

Drugs that most commonly cause first-degree AV block include the following:

  • Class Ia antiarrhythmics (eg, quinidine, procainamide, disopyramide)
  • Class Ic antiarrhythmics (eg, flecainide, encainide, propafenone)
  • Class II antiarrhythmics (beta-blockers)
  • Class III antiarrhythmics (eg, amiodarone, sotalol, dofetilide, ibutilide)
  • Class IV antiarrhythmics (calcium channel blockers)
  • Digoxin or other cardiac glycosides
  • Magnesium

Although first-degree AV block is not an absolute contraindication for administration of drugs such as calcium channel blockers, beta-blockers, digoxin, and amiodarone, extreme caution should be exercised in the use of these medications in patients with first-degree AV block. Exposure to these drugs increases the risk of developing higher-degree AV block.

Mitral or aortic valve annulus calcification

The main penetrating bundle of His is located near the base of the anterior leaflet of the mitral valve and the noncoronary cusp of the aortic valve. Heavy calcium deposits in patients with aortic or mitral annular calcification is associated with increased risk of AV block.

Infectious disease

Infective endocarditis, diphtheria, rheumatic fever, Chagas disease, Lyme disease, and tuberculosis all may be associated with first-degree AV block. Extension of the infection to the adjacent myocardium in native or prosthetic valve infective endocarditis (ie, ring abscess) can cause AV block. Acute myocarditis caused by diphtheria, rheumatic fever, or Chagas disease can result in AV block.

Collagen vascular disease

Rheumatoid arthritis, systemic lupus erythematosus (SLE), and scleroderma all may be associated with first-degree AV block. Rheumatoid nodules may occur in the central fibrous body and result in AV block. Fibrosis of the AVN or the adjacent myocardium in patients with SLE or scleroderma can cause first-degree AV block.

Doppler echocardiographic signs of first-degree AV block have been demonstrated in about 33% of fetuses of pregnant women who are anti-SSA/Ro 52-kd positive.[5] In most of these fetuses, the blocks resolved spontaneously. However, progression to a more severe degree of block was seen in 2 of the fetuses. Serial Doppler echocardiographic measurement of AV-time intervals can be used for surveillance of these high-risk pregnancies.

Iatrogenesis

First-degree AV block occurs in about 10% of patients who undergo adenosine stress testing and is usually hemodynamically insignificant. Patients with baseline first-degree AV block more often develop higher degrees of AV block during adenosine stress testing. These episodes, however, are generally well tolerated and do not require specific treatment or discontinuance of the adenosine infusion.[6]

Marked first-degree AV block may occur after catheter ablation of the fast AVN pathway with resultant conduction of the impulse via the slow pathway. This may result in symptoms similar to those of the pacemaker syndrome.

First-degree AV block (reversible or permanent) has been reported in about 2% of patients who undergo closure of an atrial septal defect using the Amplatzer septal occluder.[7] First-degree AV block can occur following cardiac surgery. Transient first-degree AV block may result from right heart catheterization.

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Epidemiology

In the United States, the prevalence of first-degree AV block among young adults ranges from 0.65% to 1.6%. Higher prevalence (8.7%) is reported in studies of trained athletes. The prevalence of first-degree AV block increases with advancing age; first-degree AV block is reported in 5% of men older than 60 years.[8] The overall prevalence is 1.13 cases per 1000 lives.

In a study of 2,123 patients aged 20-99 years, first-degree AV block was more prevalent among African-American patients than among Caucasian patients in all age groups except for those in the 8th decade of life.[8] In this study, the prevalence of first-degree AV block increased at age 50 years in both ethnic groups and gradually increased with advancing age. The peak in African-American patients occurred in the 10th decade of life, whereas the peak in Caucasian patients was in the 9th decade of life.[8]

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Prognosis

The prognosis for isolated first-degree AV block usually is very good. Progression from isolated first-degree heart block to high-degree block is very uncommon.[9] Patients with first-degree AV block and infranodal blocks, however, are at increased risk for progression to complete AV block.

Heart block in children with Lyme carditis tends to resolve spontaneously, with median recovery in 3 days (range, 1-7 days).[10]

Cheng et al found that first-degree heart block is associated with increased long-term risks of atrial fibrillation, pacemaker implantation, and all-cause mortality.[11] Their community-based cohort included 7575 individuals from the Framingham Heart Study who underwent baseline routine 12-lead ECG in 1968-1974 and were followed prospectively through 2007.

Traditionally, first-degree AV block has been considered a benign condition. However, epidemiological data from the Framingham Study have shown that first-degree AV block is associated with increased risk of all-cause mortality in the general population. Compared with individuals whose PR intervals were 200 msec or shorter, those with first-degree AV block had a 2-fold adjusted risk of atrial fibrillation, a 3-fold adjusted risk of pacemaker implantation, and a 1.4-fold adjusted risk of all-cause mortality.[11] Each 20-msec increment in PR interval was associated with an adjusted hazard ratio (HR) of 1.11 for atrial fibrillation, 1.22 for pacemaker implantation, and 1.08 for all-cause mortality.[12]

A study by Uhm et al of 3816 patients indicated that in the presence of hypertension, patients with first-degree AV block have a greater risk of developing advanced AV block, atrial fibrillation, and left ventricular dysfunction than do hypertensive patients with a normal PR interval.[13]

Crisel showed that patients with stable coronary artery disease who had a PR of 220 msec or more had a significantly higher risk of reaching the combined end point of heart failure or cardiovascular death over a follow-up of 5 years.[14]

The Korean Heart Failure registry selected 1,986 patients with acute heart failure in sinus rhythm and divided them into 4 groups, depending on the presence of first-degree AV block and/or QRS prolongation. During the median follow-up of 18.2 months, overall death rate was highest in patients who had both first-degree AV block and prolonged QRS. This group also showed worst outcomes regarding the requirement of invasive managements during the index admission, in-hospital mortality, post discharge death/rehospitalization, and cardiac device implantation.[15]

In an analysis of the COMPANION Trial, 1520 patients fulfilling criteria for cardiac resynchronization therapy (CRT) implant were assigned to normal (PR < 200 msec) or prolonged (PR ≥200 msec) AV delay and cohorts were compared within the optimal pharmacologic therapy and CRT groups regarding an endpoint of all-cause mortality or heart failure hospitalization. CRT was compared with optimal pharmacologic therapy in normal and prolonged PR interval groups. Randomization to CRT was associated with a reduction in the endpoint in all patients; the strength of the association was greater for those with first-degree AV block versus normal PR intervals. This analysis demonstrated that the deleterious effect of first-degree AV block in patients with systolic dysfunction, heart failure, and wide QRS complexes be attenuated by CRT.[16]

These studies suggest that first-degree AV block is not necessarily a benign condition; in patients with chronic systolic heart failure and wide QRS, CRT may attenuate its deleterious effect.

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Contributor Information and Disclosures
Author

Jamshid Alaeddini, MD, FACC, FHRS Director, Cardiac Electrophysiology Services, Lake Health System

Jamshid Alaeddini, MD, FACC, FHRS is a member of the following medical societies: American College of Cardiology, American Heart Association, Heart Rhythm Society

Disclosure: Nothing to disclose.

Coauthor(s)

Jamshid Shirani, MD Director of Cardiology Fellowship Program, Director of Echocardiography Laboratory, Director of Hypertrophic Cardiomyopathy Clinic, St Luke's University Health Network

Jamshid Shirani, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society of Echocardiography, Association of Subspecialty Professors, American College of Cardiology, American College of Physicians, American Heart Association

Disclosure: Nothing to disclose.

Theodore J Gaeta, DO, MPH, FACEP Clinical Associate Professor, Department of Emergency Medicine, Weill Cornell Medical College; Vice Chairman and Program Director of Emergency Medicine Residency Program, Department of Emergency Medicine, New York Methodist Hospital; Academic Chair, Adjunct Professor, Department of Emergency Medicine, St George's University School of Medicine

Theodore J Gaeta, DO, MPH, FACEP is a member of the following medical societies: American College of Emergency Physicians, New York Academy of Medicine, Society for Academic Emergency Medicine, Council of Emergency Medicine Residency Directors, Clerkship Directors in Emergency Medicine, Alliance for Clinical Education

Disclosure: Nothing to disclose.

Michael D Levine, MD Assistant Professor, Department of Emergency Medicine, Section of Medical Toxicology, Keck School of Medicine of the University of Southern California

Michael D Levine, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, American College of Medical Toxicology, American Medical Association, Phi Beta Kappa, Society for Academic Emergency Medicine, Emergency Medicine Residents' Association

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Brian Olshansky, MD Professor Emeritus of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Brian Olshansky, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society

Disclosure: Speaker, consultant, DSMB for: Lundbeck; Daiichi Sankyo, Amarin, On-X, Biotronik.

Chief Editor

Jeffrey N Rottman, MD Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society

Disclosure: Nothing to disclose.

Additional Contributors

Eddy S Lang, MDCM, CCFP(EM), CSPQ Associate Professor, Senior Researcher, Division of Emergency Medicine, Department of Family Medicine, University of Calgary Faculty of Medicine; Assistant Professor, Department of Family Medicine, McGill University Faculty of Medicine, Canada

Eddy S Lang, MDCM, CCFP(EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Canadian Association of Emergency Physicians

Disclosure: Nothing to disclose.

References
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The PR interval is 0.24 seconds (240 ms) in this patient with asymptomatic first-degree atrioventricular block.
ECG in a patient with first-degree heart block.
ECG in patient with first-degree heart block.
 
 
 
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