A class I treatment the benefits greatly outweigh the risks. In a Class II treatment the benefits outweigh the risks by a smaller margin. In a class III treatment the benefits and risks are close, and in a class IV treatment, the risks outweigh the benefits. Here is how the task force viewed various treatments for arrhythmias.

Recommendations for Permanent Pacing in Sinus Node Dysfunction (SND)

CLASS I

1. Permanent pacemaker implantation is indicated for SND with documented symptomatic bradycardia, including frequent sinus pauses that produce symptoms. (Level of Evidence: C) (Kay, Estioko, & Wiener, 1982; Kusumoto & Goldschlager, 1996; Rasmussen, 1981)
2. Permanent pacemaker implantation is indicated for symptomatic chronotropic incompetence. (Level of Evidence: C) (Kay, Estioko, & Wiener, 1982; Kusumoto & Goldschlager, 1996; Rasmussen, 1981; Linde-Edelstam et al., 1992; Gammage et al., 1991)
3. Permanent pacemaker implantation is indicated for symptomatic sinus bradycardia that results from required drug therapy for medical conditions. (Level of Evidence: C)

CLASS IIa

1. Permanent pacemaker implantation is reasonable for SND with heart rate less than 40 bpm when a clear association between significant symptoms consistent with bradycardia and the actual presence of bradycardia has not been documented. (Level of Evidence: C) Kay, Estioko, & Wiener, 1982; Kusumoto & Goldschlager, 1996; Rasmussen, 1981; Shaw, Holman, & Gowers, 1980; Dreifus, Michelson, & Kaplinsky, 1983; Rubenstein et al., 1972)
2. Permanent pacemaker implantation is reasonable for syncope of unexplained origin when clinically significant abnormalities of sinus node function are discovered or provoked in electrophysiological studies. (Level of Evidence: C) (Fisher, 1981, Reiffel & Kuehnert, 1994)

CLASS IIb

1. Permanent pacemaker implantation may be considered in minimally symptomatic patients with chronic heart rate less than 40 bpm while awake. (Level of Evidence: C) (Kay, Estioko, & Wiener, 1982; 1996; Rasmussen, 1981; Linde-Edelstam et al., 1992; Shaw, Holman, & Gowers, 1980; Dreifus, Michelson, & Kaplinsky, 1983; Rubenstein et al., 1972)

CLASS III

1. Permanent pacemaker implantation is not indicated for SND in asymptomatic patients. (Level of Evidence: C)
2. Permanent pacemaker implantation is not indicated for SND in patients for whom the symptoms suggestive of bradycardia have been clearly documented to occur in the absence of bradycardia. (Level of Evidence: C)
3. Permanent pacemaker implantation is not indicated for SND with symptomatic bradycardia due to nonessential drug therapy. (Level of Evidence: C)

Recommendations for Acquired Atrioventricular (AV) Block in Adults

CLASS I

1. Permanent pacemaker implantation is indicated for third-degree and advanced second-degree AV block at any anatomic level associated with bradycardia with symptoms (including heart failure) or ventricular arrhythmias presumed to be due to AV block. (Level of Evidence: C) (Dreifus, Michelson, & Kaplinsky, 1983; Friedberg, Donoso, & Stein, 1964; British Pacing and Electrophysiology Group, 1991; Kastor, 1975)
2. Permanent pacemaker implantation is indicated for third-degree and advanced second-degree AV block at any anatomic level associated with arrhythmias and other medical conditions that require drug therapy that results in symptomatic bradycardia. (Level of Evidence: C) (Dreifus, Michelson, & Kaplinsky, 1983; Friedberg, Donoso, & Stein, 1964; British Pacing and Electrophysiology Group, 1991; Kastor, 1975)
3. Permanent pacemaker implantation is indicated for third-degree and advanced second-degree AV block at any anatomic level in awake, symptom-free patients in sinus rhythm, with documented periods of asystole greater than or equal to 3.0 seconds (Ector, Rolies, & De Geest, 1983) or any escape rate less than 40 bpm, or with an escape rhythm that is below the AV node. (Level of Evidence: C)(Kay, Estioko, & Wiener, 1982; Shaw, Holman, & Gowers, 1980)
4. Permanent pacemaker implantation is indicated for third-degree and advanced second-degree AV block at any anatomic level in awake, symptom-free patients with atrial fibrillation (AF) and bradycardia with 1 or more pauses of at least 5 seconds or longer. (Level of Evidence: C)
5. Permanent pacemaker implantation is indicated for third-degree and advanced second-degree AV block at any anatomic level after catheter ablation of the AV junction. (Level of Evidence: C) (Gallagher et al., 1982; Langberg et al., 1989)
6. Permanent pacemaker implantation is indicated for third-degree and advanced second-degree AV block at any anatomic level associated with postoperative AV block that is not expected to resolve after cardiac surgery. (Level of Evidence: C) (Kim et al., 2001; Kastor, 1975; Glikson et al., 1997; Koplan et al., 2003)
7. Permanent pacemaker implantation is indicated for third-degree and advanced second-degree AV block at any anatomic level associated with neuromuscular diseases with AV block, such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb dystrophy (limb-girdle muscular dystrophy), and peroneal muscular atrophy, with or without symptoms. (Level of Evidence: B) (Perloff et al., 1984; Hiromasa et al., 1987; Stevenson et al., 1990; James & Fisch, 1963; Roberts, Perloff, & Kark, 1979; Charles et al., 1981; James, 1962)
8. Permanent pacemaker implantation is indicated for second-degree AV block with associated symptomatic bradycardia regardless of type or site of block. (Level of Evidence: B) (Strasberg et al., 1981)
9. Permanent pacemaker implantation is indicated for asymptomatic persistent third-degree AV block at any anatomic site with average awake ventricular rates of 40 bpm or faster if cardiomegaly or left ventricular (LV) dysfunction is present or if the site of block is below the AV node. (Level of Evidence: B) (British Pacing and Electrophysiology Group, 1981; Shaw et al., 1985)
10. Permanent pacemaker implantation is indicated for second- or third-degree AV block during exercise in the absence of myocardial ischemia. (Level of Evidence: C) (Chokshi et al., 1990; Barold & Mugica, 1991)

CLASS IIa

1. Permanent pacemaker implantation is reasonable for persistent third-degree AV block with an escape rate greater than 40 bpm in asymptomatic adult patients without cardiomegaly. (Level of Evidence: C) (Dreifus, Michelson, & Kaplinsky et al., 1983; Friedberg, Donoso, & Stein, 1964; Gadboys, Wisoff, & Litwak, 1964; British Pacing and Electrophysiology Group, 1991; Barold & Mugica, 1991; Kastor, 1975)
2. Permanent pacemaker implantation is reasonable for asymptomatic second-degree AV block at intra- or infra-His levels found at electrophysiological study. (Level of Evidence: B) (Strasberg et al., 1981; British Pacing and Electrophysiology Group, 1991; Shaw et al., 1985)
3. Permanent pacemaker implantation is reasonable for first- or second-degree AV block with symptoms similar to those of pacemaker syndrome or hemodynamic compromise. (Level of Evidence: B) (Barold, 1996; Kim et al., 1993)
4. Permanent pacemaker implantation is reasonable for asymptomatic type II second-degree AV block with a narrow QRS. When type II second-degree AV block occurs with a wide QRS, including isolated right bundle-branch block, pacing becomes a Class I recommendation. (See Section 2.1.3, “Chronic Bifascicular Block” in the original guideline document.) (Level of Evidence: B) (Barold, 1996; British Pacing and Electrophysiology Group, 1991; Zipes, 1979; Kastor, 1975)

CLASS IIb

1. Permanent pacemaker implantation may be considered for neuromuscular diseases such as myotonic muscular dystrophy, Erb dystrophy (limb-girdle muscular dystrophy), and peroneal muscular atrophy with any degree of AV block (including first-degree AV block), with or without symptoms, because there may be unpredictable progression of AV conduction disease. (Level of Evidence: B) (Perloff et al., 1984; Hiromasa et al., 1987; Stevenson et al., 1990; James & Fisch, 1963; Roberts, Perloff & Kark, 1979; Charles et al., 1981; James, 1962)
2. Permanent pacemaker implantation may be considered for AV block in the setting of drug use and/or drug toxicity when the block is expected to recur even after the drug is withdrawn. (Level of Evidence: B) (Zeltser et al., 2004; Shohat-Zabarski et al., 2004)

CLASS III

1. Permanent pacemaker implantation is not indicated for asymptomatic first-degree AV block. (Level of Evidence: B) (Mymin et al., 1986) (See Section 2.1.3, “Chronic Bifascicular Block” in the original guideline document.)
2. Permanent pacemaker implantation is not indicated for asymptomatic type I second-degree AV block at the supra-His (AV node) level or that which is not known to be intra- or infra-Hisian.(Level of Evidence: C) (Strasberg et al., 1981)
3. Permanent pacemaker implantation is not indicated for AV block that is expected to resolve and is unlikely to recur (McAlister, et al., 1989) (e.g., drug toxicity, Lyme disease, or transient increases in vagal tone or during hypoxia in sleep apnea syndrome in the absence of symptoms). (Level of Evidence: B) (Shohat-Zabarski et al., 2004; McAlister et al., 1989)

Recommendations for Permanent Pacing in Chronic Bifascicular Block

CLASS I

1. Permanent pacemaker implantation is indicated for advanced second-degree AV block or intermittent third-degree AV block. (Level of Evidence: B) (Friedberg, Donoso, & Stein, 1964; Gadboys, Wisoff, & Litwak, 1964; Johansson, 1966; Hindman et al., 1978; Donmoyer, DeSanctis, & Austen, 1967; Edhag & Swahn, 1976)
2. Permanent pacemaker implantation is indicated for type II second-degree AV block. (Level of Evidence: B) (Dhingra et al., “The significance,” 1974; Donoso, Adler, & Friedberg, 1964; Ranganathan et al., 1972; Dhingra et al.,”Syncope,” 1974)
3. Permanent pacemaker implantation is indicated for alternating bundle-branch block. (Level of Evidence: C) (Josephson, 1993)

CLASS IIa

1. Permanent pacemaker implantation is reasonable for syncope not demonstrated to be due to AV block when other likely causes have been excluded, specifically ventricular tachycardia (VT). (Level of Evidence: B) (Fisch, Zipes, & Fisch, 1980; McAnulty et al., 1982; Kulbertus & Collignon, 1969; DePasquale & Bruno, 1973; Denes, 1977; McAnulty et al., 1978; Peters et al., 1979; Scheinman et al., 1982; Morady et al., 1984; Click et al., 1987; Ezri et al., 1983; Twidale et al., 1988; Englund et al., 1995; Scheinman et al., 1977; Probst et al., 1979; Dhingra et al., 1979; Cheng, 1971; Dhingra et al., “Syncope,” 1974; Brignole et al., 2001)
2. Permanent pacemaker implantation is reasonable for an incidental finding at electrophysiological study of a markedly prolonged HV interval (greater than or equal to 100 milliseconds) in asymptomatic patients. (Level of Evidence: B) (Scheinman et al., 1982)
3. Permanent pacemaker implantation is reasonable for an incidental finding at electrophysiological study of pacing-induced infra-His block that is not physiological. (Level of Evidence: B) (Dhingra et al., 1979)

CLASS IIb

1. Permanent pacemaker implantation may be considered in the setting of neuromuscular diseases such as myotonic muscular dystrophy, Erb dystrophy (limb-girdle muscular dystrophy), and peroneal muscular atrophy with bifascicular block or any fascicular block, with or without symptoms. (Level of Evidence: C) (Perloff et al., 1984; Hiromasa et al., 1987; Stevenson et al., 1990; James & Fisch, 1963; Roberts, Perloff, & Kark, 1979; Charles et al., 1981; James, 1962)

CLASS III

1. Permanent pacemaker implantation is not indicated for fascicular block without AV block or symptoms. (Level of Evidence: B) (McAnulty et al., 1982; McAnulty et al.,1978; Scheinman et al., 1982; Scheinman et al., 1977)
2. Permanent pacemaker implantation is not indicated for fascicular block with first-degree AV block without symptoms. (Level of Evidence: B) (McAnulty et al., 1982; McAnulty et al.,1978; Scheinman et al., 1982; Scheinman et al., 1977)

Recommendations for Permanent Pacing After the Acute Phase of Myocardial Infarction (MI)

CLASS I

1. Permanent ventricular pacing is indicated for persistent second-degree AV block in the His-Purkinje system with alternating bundle-branch block or third-degree AV block within or below the His-Purkinje system after ST-segment elevation MI. (Level of Evidence: B) (Ranganathan et al., 1972; Col & Weinberg, 1972; Ritter et al., 1976; Ginks et al., 1977; Domenighetti & Perret, 1980; Lamas et al., 1986)
2. Permanent ventricular pacing is indicated for transient advanced second- or third-degree infranodal AV block and associated bundle-branch block. If the site of block is uncertain, an electrophysiological study may be necessary. (Level of Evidence: B) (Col & Weinberg, 1972; Ritter et al., 1976)
3. Permanent ventricular pacing is indicated for persistent and symptomatic second- or third-degree AV block. (Level of Evidence: C)

CLASS IIb

1. Permanent ventricular pacing may be considered for persistent second- or third-degree AV block at the AV node level, even in the absence of symptoms. (Level of Evidence: B) (Shaw, Holman, & Gowers, 1980)

CLASS III

1. Permanent ventricular pacing is not indicated for transient AV block in the absence of intraventricular conduction defects. (Level of Evidence: B) (Col & Weinberg, 1972)
2. Permanent ventricular pacing is not indicated for transient AV block in the presence of isolated left anterior fascicular block. (Level of Evidence: B) (Ginks et al., 1977)
3. Permanent ventricular pacing is not indicated for new bundle branch block or fascicular block in the absence of AV block. (Level of Evidence: B) (Hindman et al., 1978; Col & Weinberg, 1972)
4. Permanent ventricular pacing is not indicated for persistent asymptomatic first-degree AV block in the presence of bundle branch or fascicular block. (Level of Evidence: B) (Col & Weinberg, 1972)

*These recommendations are consistent with the “ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction” (Antman et al., 2004).

Recommendations for Permanent Pacing in Hypersensitive Carotid Sinus Syndrome and Neurocardiogenic Syncope

CLASS I

1. Permanent pacing is indicated for recurrent syncope caused by spontaneously occurring carotid sinus stimulation and carotid sinus pressure that induces ventricular asystole of more than 3 seconds. (Level of Evidence: C) (Brignole et al., 1992; Brignole et al., 1991)

CLASS IIa

1. Permanent pacing is reasonable for syncope without clear, provocative events and with a hypersensitive cardioinhibitory response of 3 seconds or longer. (Level of Evidence: C) (Brignole et al., 1992)

CLASS IIb

1. Permanent pacing may be considered for significantly symptomatic neurocardiogenic syncope associated with bradycardia documented spontaneously or at the time of tilt-table testing. (Level of Evidence: B) (Sutton et al., 2000; Ammirati, Colivicchi, & Santini, 2001; Connolly et al., 2003; Sheldon et al., 1998)

CLASS III

1. Permanent pacing is not indicated for a hypersensitive cardioinhibitory response to carotid sinus stimulation without symptoms or with vague symptoms. (Level of Evidence: C)
2. Permanent pacing is not indicated for situational vasovagal syncope in which avoidance behavior is effective and preferred. (Level of Evidence: C)

Recommendations for Pacing After Cardiac Transplantation

CLASS I

1. Permanent pacing is indicated for persistent inappropriate or symptomatic bradycardia not expected to resolve and for other Class I indications for permanent pacing. (Level of Evidence: C)

CLASS IIb

1. Permanent pacing may be considered when relative bradycardia is prolonged or recurrent, which limits rehabilitation or discharge after postoperative recovery from cardiac transplantation. (Level of Evidence: C)
2. Permanent pacing may be considered for syncope after cardiac transplantation even when bradyarrhythmia has not been documented. (Level of Evidence: C)

Recommendations for Permanent Pacemakers That Automatically Detect and Pace to Terminate Tachycardias

CLASS IIa

1. Permanent pacing is reasonable for symptomatic recurrent supraventricular tachycardia (SVT that is reproducibly terminated by pacing when catheter ablation and/or drugs fail to control the arrhythmia or produce intolerable side effects. (Level of Evidence: C) (Peters et al., 1985; Fisher et al., 1987; Den et al., 1984; Saksena et al., 1986; Barold et al., 1987)

CLASS III

1. Permanent pacing is not indicated in the presence of an accessory pathway that has the capacity for rapid anterograde conduction. (Level of Evidence: C)

Recommendations for Pacing to Prevent Tachycardia

CLASS I

1. Permanent pacing is indicated for sustained pause-dependent VT, with or without QT prolongation. (Level of Evidence: C) (Eldar et al., 1987; Eldar et al., 1992)

CLASS IIa

1. Permanent pacing is reasonable for high-risk patients with congenital long-QT syndrome. (Level of Evidence: C) (Eldar et al., 1987; Eldar et al., 1992)

CLASS IIb

1. Permanent pacing may be considered for prevention of symptomatic, drug-refractory, recurrent AF in patients with coexisting SND. (Level of Evidence: B) (Lamas et al., 2000; Saksena et al., 1996; Saksena et al, 1998)

CLASS III

1. Permanent pacing is not indicated for frequent or complex ventricular ectopic activity without sustained VT in the absence of the long-QT syndrome. (Level of Evidence: C) (Fisher et al., 1987)
2. Permanent pacing is not indicated for torsade de pointes VT due to reversible causes. (Level of Evidence: A) (Moss & Robinson, 1992; Viskin et al., 1996)

Recommendation for Pacing to Prevent Atrial Fibrillation

CLASS III

1. Permanent pacing is not indicated for the prevention of AF in patients without any other indication for pacemaker implantation. (Level of Evidence: B) (Knight et al., 2005)

Recommendations for Cardiac Resynchronization Therapy in Patients With Severe Systolic Heart Failure

CLASS I

1. For patients who have left ventricular ejection fraction (LVEF) less than or equal to 35%, a QRS duration greater than or equal to 0.12 seconds, and sinus rhythm, cardiac resynchronization therapy (CRT) with or without an ICD is indicated for the treatment of NYHA functional Class III or ambulatory Class IV heart failure symptoms with optimal recommended medical therapy. (Level of Evidence: A) (Abraham et al., 2002; Bristow et al., 2004; Cleland et al., 2005; Hunt, 2005)

CLASS IIa

1. For patients who have LVEF less than or equal to 35%, a QRS duration greater than or equal to 0.12 seconds, and AF, CRT with or without an ICD is reasonable for the treatment of NYHA functional Class III or ambulatory Class IV heart failure symptoms on optimal recommended medical therapy. (Level of Evidence: B) (Cazeau et al., 2001; Hunt, 2005)
2. For patients with LVEF less than or equal to 35% with New York Heart Association (NYHA) functional Class III or ambulatory Class IV symptoms who are receiving optimal recommended medical therapy and who have frequent dependence on ventricular pacing, CRT is reasonable. (Level of Evidence: C) (Hunt, 2005)

CLASS IIb

1. For patients with LVEF less than or equal to 35% with NYHA functional Class I or II symptoms who are receiving optimal recommended medical therapy and who are undergoing implantation of a permanent pacemaker and/or ICD with anticipated frequent ventricular pacing, CRT may be considered. (Level of Evidence: C) (Hunt, 2005)

CLASS III

1. CRT is not indicated for asymptomatic patients with reduced LVEF in the absence of other indications for pacing. (Level of Evidence: B) (Abraham et al., 2002; Bristow et al., 2004; Cleland et al., 2005; Hunt, 2005)
2. CRT is not indicated for patients whose functional status and life expectancy are limited predominantly by chronic noncardiac conditions. (Level of Evidence: C) (Hunt, 2005)

Recommendations for Pacing in Patients With Hypertrophic Cardiomyopathy (HCM)

CLASS I

1. Permanent pacing is indicated for SND or AV block in patients with HCM as described previously (see Section 2.1.1, “Sinus Node Dysfunction,” and Section 2.1.2, “Acquired Atrioventricular Block in Adults” in the original guideline document). (Level of Evidence: C)

CLASS IIb

1. Permanent pacing may be considered in medically refractory symptomatic patients with HCM and significant resting or provoked LV outflow tract obstruction. (Level of Evidence: A) As for Class I indications, when risk factors for SCD are present, consider a DDD implantable cardioverter defibrillator (ICD) (see Section 3, “Indications for Implantable Cardioverter-Defibrillator Therapy” in the original guideline document). (Fananapazir et al., 1994; Nishimura et al., 1997; Kappenberger et al., 1997; Maron et al., 1999; Nishimura et al., “Effect of,” 1996; Nishimura et al., “Dual-chamber,” 1996)

CLASS III

1. Permanent pacemaker implantation is not indicated for patients who are asymptomatic or whose symptoms are medically controlled. (Level of Evidence: C)
2. Permanent pacemaker implantation is not indicated for symptomatic patients without evidence of LV outflow tract obstruction. (Level of Evidence: C)

Recommendations for Permanent Pacing in Children, Adolescents, and Patients With Congenital Heart Disease

CLASS I

1. Permanent pacemaker implantation is indicated for advanced second- or third-degree AV block associated with symptomatic bradycardia, ventricular dysfunction, or low cardiac output. (Level of Evidence: C)
2. Permanent pacemaker implantation is indicated for SND with correlation of symptoms during age-inappropriate bradycardia. The definition of bradycardia varies with the patient’s age and expected heart rate. (Level of Evidence: B) (Kay, Estioko, & Wiener, 1982; Ector, Rolies, & De Geest, 1983; Beder et al., 1983; Kelly et al., 2001)
3. Permanent pacemaker implantation is indicated for postoperative advanced second- or third-degree AV block that is not expected to resolve or that persists at least 7 days after cardiac surgery. (Level of Evidence: B) (Strasberg et al., 1981; Lillehei et al., 1963)
4. Permanent pacemaker implantation is indicated for congenital third-degree AV block with a wide QRS escape rhythm, complex ventricular ectopy, or ventricular dysfunction. (Level of Evidence: B) (Michaelsson, Jonzon, & Riesenfield , 1995; Moak et al., 2001; Villain et al., 2006)
5. Permanent pacemaker implantation is indicated for congenital third-degree AV block in the infant with a ventricular rate less than 55 bpm or with congenital heart disease and a ventricular rate less than 70 bpm. (Level of Evidence: C) (Pinsky et al., 1982; Jaeggi et al., 2002)

CLASS IIa

1. Permanent pacemaker implantation is reasonable for patients with congenital heart disease and sinus bradycardia for the prevention of recurrent episodes of intra-atrial reentrant tachycardia; SND may be intrinsic or secondary to antiarrhythmic treatment. (Level of Evidence: C) (Silka et al., 1990; Stephenson et al., 2003; Pfammatter et al., 1995)
2. Permanent pacemaker implantation is reasonable for congenital third-degree AV block beyond the first year of life with an average heart rate less than 50 bpm, abrupt pauses in ventricular rate that are 2 or 3 times the basic cycle length, or associated with symptoms due to chronotropic incompetence. (Level of Evidence: B) (Dewey, Capeless, & Levy, 1987; Sholler & Walsh, 1989)
3. Permanent pacemaker implantation is reasonable for sinus bradycardia with complex congenital heart disease with a resting heart rate less than 40 bpm or pauses in ventricular rate longer than 3 seconds. (Level of Evidence: C)
4. Permanent pacemaker implantation is reasonable for patients with congenital heart disease and impaired hemodynamics due to sinus bradycardia or loss of AV synchrony. (Level of Evidence: C) (Cohen et al., 2001)
5. Permanent pacemaker implantation is reasonable for unexplained syncope in the patient with prior congenital heart surgery complicated by transient complete heart block with residual fascicular block after a careful evaluation to exclude other causes of syncope. (Level of Evidence: B) (Villain et al., 2006; Banks, Jenson, & Kugler, 2001; Gross et al., 2006; Villain et al., 2003)

CLASS IIb

1. Permanent pacemaker implantation may be considered for transient postoperative third-degree AV block that reverts to sinus rhythm with residual bifascicular block. (Level of Evidence: C) (Krongrad, 1978)
2. Permanent pacemaker implantation may be considered for congenital third-degree AV block in asymptomatic children or adolescents with an acceptable rate, a narrow QRS complex, and normal ventricular function. (Level of Evidence: B) (Sholler & Walsh, 1989; Michaelsson, Jonzon, & Riesenfield, 1995)
3. Permanent pacemaker implantation may be considered for asymptomatic sinus bradycardia after biventricular repair of congenital heart disease with a resting heart rate less than 40 bpm or pauses in ventricular rate longer than 3 seconds. (Level of Evidence: C)

CLASS III

1. Permanent pacemaker implantation is not indicated for transient postoperative AV block with return of normal AV conduction in the otherwise asymptomatic patient. (Level of Evidence: B) (Weindling et al., 1988; Krongrad, 1978)
2. Permanent pacemaker implantation is not indicated for asymptomatic bifascicular block with or without first-degree AV block after surgery for congenital heart disease in the absence of prior transient complete AV block. (Level of Evidence: C)
3. Permanent pacemaker implantation is not indicated for asymptomatic type I second-degree AV block. (Level of Evidence: C)
4. Permanent pacemaker implantation is not

The US Stroke death map shows the concentration of stroke deaths is spread more evenly across the full breadth of the old south.

Heart failure is only one of several possible underlying causes of the broader issue of circulatory failure in  which an abnormality of some component of circulation is responsible for inaequate cardiac output.  Circulatory failure can arise from heart failure, or from insufficient blood volume, low concentrations of oxygenated hemoglobin in arterial blood, or other circumstance that prevent an otherwise healthy heart from adequately meeting the metabolic needs of the body.

The assessment of left ventricular hypertrophy in hypertension

Abstract

The presence of left ventricular hypertrophy (LVH) in hypertension, as detected by the electrocardiogram or echocardiography, is associated with an increased risk of mortality and morbidity several times above and beyond the risk of hypertension alone. The LIFE (Losartan Intervention For Endpoint reduction in hypertension) study confirmed that pharmacological agents, which reduce LVH, confer further reduction in morbidity and mortality. This makes the identification of patients with LVH all the more important. In this article we describe the various methods available to diagnose the presence of LVH in patients with hypertension, and consider their strengths and their place in clinical practice and in research.

Introduction

Hypertension is associated with an increased risk of morbidity and mortality as a result of an increase in the incidence of myocardial infarcts, strokes, cardiac and renal failure, as well as sudden death . The presence of evidence of left ventricular hypertrophy (LVH) on the electrocardiogram (ECG) increases the risk of mortality and morbidity several times above and beyond the risk of the hypertension alone . Echocardiography provides a more sensitive test for identifying LVH and elevated left ventricular mass (LVM), as measured by M-mode echocardiography, which is also associated with increased cardiovascular risk . The two tests identify different populations of patients with LVH and the combination of the two tests provides additive prognostic information   The ECG criteria of LVH identify a group of hypertensive patients with a particularly high LVM . This is clinically relevant as there is an incremental relationship between LVM index and cardiovascular risk. Interestingly, the continuous relationship between LVM index and cardiovascular risk is present even in the quintiles below the upper limit of normal for LVM index, as measured by echocardiography (125 g/m² for men and 110 g/m² for women) .There is recent evidence that regression of LVM, through pharmacological intervention, reduces the cardiovascular risk   Furthermore, the LIFE (Losartan Intervention For Endpoint reduction in hypertension) study confirmed that pharmacological agents that reduce LVH above and beyond lowering of blood pressure (BP), confer further reduction in morbidity and mortality It is therefore important to identify patients with LVH, both for prognosis and for tighter BP control. Currently, the European Society of Hypertension guidelines recommend that an ECG should be performed to assess for the presence or absence of LVH based on the Sokolow–Lyons or the Cornell Product criteria. They recommend echocardiography, using M-mode to measure wall thickness and calculate LVM index, when treatment decisions are uncertain, to refine the classification of the overall risk

This article describes the various methods available to diagnose the presence of LVH in patients with hypertension, both in the context of clinical practice and research. The optimal method should be easy to perform, inexpensive, widely available and accurate. We consider how the various methods compare.

The electrocardiogram

The ECG is easy to perform, widely available and inexpensive. It is usually the first test to detect LVH, on the basis of numerous validated criteria of variable complexity. The sensitivity of these criteria varies in published studies depending on the severity of hypertension and hence prevalence of LVH in the cohort being studied   However, these criteria generally have high specificities but low sensitivities . In the validation studies of these criteria, the sensitivity has been reported to be as high as 50% in severely diseased necropsy populations, to as low as 6–17% in Cornell and Framingham studies . Some of these criteria are simple to use, like the Sokolow–Lyon voltage criterion which is based on voltage amplitude of leads SV₁ + RV₅ or RV₆ , or the Lewis index voltage criterion which is based on voltage amplitudes in leads I and III [(RI – RIII) + (SIII - SI) >= 17 mm]  The Cornell voltage criterion is another simple, gender-specific criterion, and is based on the voltage amplitude sum of R in lead aVL plus S in lead V₃ being >= 28 mm for men and >= 20 mm for women   Other criteria are more complex and are based on scoring several ECG findings, such as the Romhilt–Estes score, which is based on a point system where six different criteria are awarded a different number of points with a maximum of 13 points and two cut-off values of 4 and 5 points, with the 5-point cut-off value being more and specific [ The Romhilt–Estes score was validated with very high sensitivity and specificity in 90 severely hypertrophied hearts from post-mortems   The Perugia score is another composite criterion that requires positivity in one of three different criteria: Cornell with a cut-off >= 24 mm for men; Romhilt–Estes score with a cut-off value of 5 points; and left ventricular strain pattern . In a study by Verdecchia et al. the Perugia score was associated with the highest rate of cardiovascular events and mortality when compared with Cornell voltage, Romhilt–Estes score, left ventricular strain and Sokolow–Lyon criteria in a 10-year follow-up.In the LIFE study, two ECG LVH criteria were used to confirm regression of LVH: Cornell product criterion and Sokolow–Lyon voltage criterion . The Cornell product criterion is based on the product of the Cornell voltage, with the addition of a 8 mm adjustment for females, and the QRS duration [(RaVL + SV₃) × QRS duration] > 2440 mm/ms . Based on the LIFE study, the European Society of Hypertension guidelines recommend the use of the Sokolow–Lyon voltage and the Cornell product criteria for the assessment of LVH. However, the LIFE study investigators selected a partition value for the Sokolow–Lyon voltage criterion of 38 mm for both men and women. It is recognized that there are gender differences in QRS duration and voltage measurements, which are not completely accounted for by differences in body size and LVM, and hence gender-specific partition values are important . Recent data suggest that the partition value for the Sokolow–Lyon voltage criterion should be 34 mm for females and 38 mm for males   This postulates that the use of a single partition value of 38 mm in the LIFE study may have resulted in a lower sensitivity at detecting LVH in females.

A Sokolow–Lyon product criterion, based on the product of the Sokolow–Lyon voltage and the QRS duration [(SV₁ + RV₅ or RV₆) × QRS duration], has been described , with gender-specific partition values of 4000 mm/ms in males and 3000 mm/ms in females suggested recently  Both Sokolow–Lyon product and Cornell product criteria are thought to be more sensitive at detecting LVH than their respective voltage criteria

The ECG criteria, however, have significant inter-study variability, which makes them less reliable for temporal follow-up in individual patients . The large numbers recruited into studies such as LIFE overcome this problem.

Echocardiography

Echocardiography is also relatively easy to perform and widely available. It is more expensive than the ECG but provides additional information on the structure and function of the heart and valves. Both M-mode and two-dimensional (2-D) echocardiography are used in the measurement of LVM. M-mode has the advantage of superior endocardial definition, as the high frame rate improves the resolution. It is the most widely used echocardiography method to measure LVM because it was the first to be validated and because it is relatively simple and quick. The M-mode method measures the left ventricle (LV) in one dimension and assumes a prolate ellipsoid shape for the LV with a ratio of long to short axis lengths of 2: 1 The calculation of LVM is based on a mathematical formula, LVM = 0.8(1.04[(LVIDD + PWTD + IVSTD)³ - (LVIDD)³]) + 0.6 g, as modified by Devereux et al. using the American Society of Echocardiography (ASE) convention, where LVIDD is left ventricle internal dimension in diastole, PWTD is posterior wall thickness in diastole and IVSTD is intraventricular septal thickness in diastole. This modified formula was validated on necropsy findings in 52 subjects

However, the accuracy and reproducibility of M-mode at measuring LVM has been debated. This is a result of the potential for variations in measured wall thickness, depending on the ultrasound beam angle to the LV wall and the assumption that the wall thickness is uniform throughout the LV. In addition, the assumed prolate ellipsoid shape of the LV is no longer valid in patients with LVH . Furthermore, LVM as measured by M-mode echocardiography relies on linear measurements of wall thickness which, when cubed, increases the standard deviation (SD) by a factor of 2–3. As elevated LVM is defined as mean + 2SD, M-mode echocardiography will underestimate the prevalence of LVH in hypertensive cohorts Finally, the cubing of the measurements for LV wall thickness amplifies any errors of such measurements, resulting in a significant variation of LVM estimates compared to direct measurement by three-dimensional (3-D) cardiac magnetic resonance imaging (MRI)

Two-dimensional echocardiography is thought to be more accurate and reproducible than the M-mode method .Two-dimensional echocardiography takes into account the length of the LV as well as the myocardial wall thickness, but is limited by the lower frame rate and hence lower resolution. It is important to ensure that the LV apical view is not foreshortened, as it would change the length of the LV and hence the LVM. Two-dimensional echocardiography relies on mathematical formulae to estimate the LVM but there is no cube function in these formulae and hence measurement errors are not magnified. However, it still assumes a prolate ellipsoid shape of the LV and a uniform LV wall thickness. Two-dimensional echocardiography is less widely used to estimate the LVM than M-mode echocardiography, as it is more time consuming and it is more difficult to obtain images of suitable quality.

Tissue harmonic imaging (THI) is a relatively new ultrasound imaging modality with an improved resolution in comparison to fundamental imaging, which is the standard ultrasound imaging modality. THI improves the image quality and the detection of the endocardial border, and has been shown to be superior at measuring ejection fractions compared to fundamental imaging .Because of the improved image quality, THI is becoming the default imaging modality in some echocardiography units. However, THI overestimates M-mode echocardiography measurements of LV wall thickness as well as M-mode LVM .Normal ranges for echocardiography should be updated to take account of the shift to THI.

Indexed left ventricular mass

There are a few indexes to correct for body size. These are height, weight and body surface area (BSA). These different indexes result in different prevalence of LVH in the population under investigation .Indexation to BSA reduces variability due to body size and gender, and is the most widely used method in the literature .but it can underestimate LVM at the upper end of the distribution .Indexation of LVM to height is thought to be more accurate in the obese. Regression models for height^2.7 provide the most accurate estimation for LVH and cardiovascular risk .The association between obesity and hypertension makes this relevant.
Geometric patterns

Different geometric forms of LVH have been adopted to classify the maladaptive responses of the LV in hypertension . LV geometry is classified into four exclusive groups on the basis of LVM and relative wall thickness: concentric hypertrophy (increased mass and increased relative wall thickness), eccentric hypertrophy (increased mass and normal relative wall thickness), concentric remodelling (normal mass and increased relative wall thickness) and normal geometry (normal mass and normal relative wall thickness). Krumholz et al. investigated 3200 patients from the Framingham study, indexing LVM to height, and found that patients with concentric hypertrophy (defined by thickness of the septum or the posterior wall divided by the LV radius at end-diastole >= 0.45) have a higher rate of cardiovascular events and mortality compared to patients with eccentric hypertrophy. Further studies by Verdecchia et al. found a higher risk, beyond LVM indexed to BSA, for concentric remodelling, but no additional risk for those already identified as having concentric hypertrophy. This implies that simply measuring the LV wall thickness and LV radius offers the same, if not possibly more, prognostic information as measuring LVM.

Three-dimensional echocardiography

Three-dimensional echocardiography had been limited by time-consuming sequential acquisition of multiple 2-D image planes using transoesophageal or transthoracic approaches, as well as time-consuming post-processing to reconstruct 3-D datasets from multiple 2-D images. While 3-D echocardiography improved the intra- and interobserver variability of the LVM measurements compared to M-mode and 2-D echocardiography , with its accuracy reported to be close to that of cardiac MRI   the technique remained limited to a few research centres. However, recently 3-D echocardiography has advanced significantly, with the introduction of second-generation real-time 3-D technology. The second-generation matrix array probes, with 3000 simultaneously active ultrasound elements, have solved the acquisition difficulties, while advances in computer technology and analysis software have shortened the duration of post-processing  . Quantification of LVM using real-time 3-D echocardiography was found to be highly reproducible and to have excellent correlation with cardiac MRI  In contrast to M-mode and 2-D echocardiography, 3-D echocardiography does not rely on geometrical assumptions for calculating LVM   One remaining limitation for 3-D echocardiography is the acoustic windows in some subjects.

Cardiac magnetic resonance imaging

At the present time, cardiac MRI is relatively expensive, not widely available and requires more expertise than echocardiography. However, it has been shown to be the most accurate and reproducible tool for the estimation of LVM  This has been validated in animal studies  and was demonstrated to be more accurate and reproducible than M-mode and 2-D echocardiography measurements . Cardiac MRI provides a spatially defined 3-D dataset at multiple levels throughout the heart, and hence the measurement of the LVM does not require geometric assumptions about the shape of the LV. The excellent contrast between blood and myocardial tissue and the high spatial resolution mean that the endocardial and epicardial contours are easily defined ( . Currently two pulse sequences are in common use: the segmented k-space turbo gradient echo (TGE) technique and the steady-state free precession technique (SSFP). LVM measurements using these two pulse sequences have been compared and a systematic difference was found between them, with the SSFP pulse sequence yielding smaller LVM measurements than TGE   Hence, it is important to use a normal range that corresponds to the MRI pulse sequence in use

Low standard deviation left ventricular mass

The sensitivity of the ECG criteria for detecting LVH depends on the severity of hypertension and hence the prevalence of LVH in the cohort being studied   The prevalence of elevated LVM is also dependent on the severity of hypertension in the population being studied. However, it is also dependent on the methodology of calculating the LVM. The M-mode echocardiography method has a high SD, which is the result of the ‘cube function’ in the mathematical formula, which magnifies the SD . For example, the SD of the mean LVM index calculated using M-mode echocardiography for a cohort of normal individuals was 21 g/m² for men and 19 g/m² for women   The equivalent SD for cardiac MRI using TGE pulse sequence, where there is no such ‘cube function’, was 9.1 g/m² for men and 7.7 g/m² for women . The larger SD of LVM index by M-mode echocardiography results in a higher upper limit of normal (based on the upper 95th percentile of the distribution; mean + 2SD)  . This leads to subjects with milder degrees of elevated LVM falling within the normal range of M-mode echocardiography. This may explain why Schillaci et al. found an increased cardiovascular risk even in individuals below the upper limit of normal of LVM index using M-mode echocardiography. To detect individuals with milder degrees of LVH, the LVM needs to be obtained using a method with a low SD such as 2-D echocardiography, 3-D echocardiography or 3-D cardiac MRI . An alternative ‘low SD’ method is to assess the geometric patterns of the structural remodelling of the LV by measuring wall thickness and wall thickness: internal radius ratio

Implications for research

The LIFE study, where all patients had LVH on ECG, confirmed that LVH regression results in improved outcomes, independent of BP reduction Demonstration of LVH regression using ECG criteria of LVH in the LIFE study was only possible as it was a very large cohort. Demonstration of LVM regression using M-mode or 2-D echocardiographic methods also requires relatively large cohorts of patients because of the relatively high observer and interstudy variability [59]. Precise measurement of LVM using cardiac MRI or 3-D echocardiography means that a much smaller sample size is needed to detect changes in LVM. It is calculated that the number of subjects needed for such studies using cardiac MRI is as little as a tenth of the number required to do the same study using M-mode echocardiography [59]. Cardiac MRI or 3-D echocardiography should be the techniques of choice in clinical trials investigating LVM regression where the accuracy of LVM measurements will allow for the accurate detection of small degrees of change in LVM in small cohorts of patients, particularly when recruitment of large numbers of patients is not possible.

Implications for clinical practice

In clinical practice the ECG is usually the first test performed to assess for the presence of LVH. Patients who are ECG LVH positive may not require further prognostic assessment as the ECG criteria have high specificity and they identify the subgroup of patients with the highest LVM and the highest risk . However, a normal ECG does not exclude the presence of LVH, and these patients should be investigated further. The M-mode echocardiography method remains the most widely available technique and will detect all but the mildest degrees of LVH. A precise estimate of LVM or serial follow-up in an individual patient may not be accurate in view of the observer variability and the fact that any error in measurement is cubed in the M-mode method of measuring LVM. de-Simone et al. calculate that the probability of a true change in LVM over time would be detected by the same observer only if the change in LVM is greater than 18% of the initial value. The geometric classification, which depends on simple measurements of wall thickness and LV radius using M-mode, or 2-D measurements when M-mode measurements are not possible, may suffice to give an accurate and reproducible assessment of the degree and the geometric type of LVH, with the same, if not possibly more, prognostic information as measuring LVM   with the added advantage of increased sensitivity and hence the detection of individuals with milder degrees of LVH. The use of echocardiography to investigate LVH has the additional advantage of providing a quick and accurate assessment of the valves and LV systolic and diastolic function.

Cost implications

The acquisition time of the cardiac MRI scan for LVM using the most recent techniques can be as short as 3 min and the semi-automated contour detection for LVM can be achieved within a minute. The speed and accuracy of cardiac MRI may make LVM measurement using cardiac MRI cost effective in clinical practice in the near future. However, second-generation real-time 3-D echocardiography systems are likely to become more widely available in the near future. This new technology will have the accuracy and reproducibility approaching that of cardiac MRI, while maintaining a cost advantage, as well as being more patient friendly. In clinical practice, cardiac MRI may be reserved for patients with limited acoustic windows or in subjects with deformed ventricles . In the meantime, the ECG, M-mode and 2-D echocardiography remain the most cost-effective methods that are widely available in clinical practice to date

People with chronic chest pain who are not in big danger of a heart attack now may have even less reason to rush into an artery-opening angioplasty: There’s more evidence drugs should be tried first and often are just as effective.

The slim early advantage for angioplasty at relieving pain in these non-emergency cases starts to fade within six months and vanishes after three years, according to a new report from a landmark heart study.

That is sooner than the five years doctors estimated last year after their first analysis of the study. The new information comes from patients’ own reports of how they fared after treatment. Results are in Thursday’s New England Journal of Medicine.

The number of angioplasties has been falling since the first results from this big study came out in 2007, according to new figures from an American College of Cardiology database.

Angioplasty remains the top treatment for people having a heart attack or hospitalized with worsening symptoms. It involves using a tiny balloon to flatten a clog and propping the artery open with a mesh tube called a stent.

However, at least a third of angioplasties are done on people not in imminent danger, to relieve chest pain. These patients are no more likely to die or suffer a heart attack if initially treated with drugs alone, the big 2,287-patient study revealed.

Still, angioplasty’s fans tout it as a quick fix that improves quality of life. That benefit is fairly small and short-lived, compared to good medication use alone, the new report found.

Researchers did followup health surveys of about 70 percent of the study’s participants. At the start, 78 percent had chest pain.

Three months after treatment, 53 percent of patients who had angioplasties plus drug treatment and 42 percent of the drugs-alone patients were free of chest pain. Both groups continued to improve, and the gap started to narrow within six months. After three years, their scores on chest pain, quality-of-life and treatment satisfaction did not significantly differ.

“Patients get better,” regardless of which initial treatment they have, said study leader Dr. William Weintraub of Christiana Care Health System in Newark, Del.

One exception: Those who started out with more severe chest pain fared better with angioplasty. And not everyone did well on drugs alone — about one-third ultimately needed an angioplasty or heart bypass surgery.

The study was funded by the U.S. Department of Veterans Affairs, the Medical Research Council of Canada and a host of drug companies. Many of the researchers have consulted for drug makers, and many of the study’s critics have consulted for stent makers.

People in the study were properly tested to ensure they were medically stable, said Dr. Spencer King, a cardiologist at St. Joseph’s Heart and Vascular Institute in Atlanta and past president of the cardiology college.

“My greatest fear” is that some patients now may be given medications without adequate testing to show angioplasty can safely be delayed, he said.

The study patients also received an ideal mix of medicines, potentially including aspirin, cholesterol-lowering statins, nitrates, ACE inhibitors, beta-blockers and calcium channel blockers.

Not all patients do, especially when doctors are paid more to do an angioplasty than for the many office visits needed to get the meds right.

“It’s a tricky business and it requires a lot of close followup,” said Dr. W. Douglas Weaver, a heart specialist at Henry Ford Health System in Detroit and president of the cardiology college.

About 1 million angioplasties are done in the United States each year.

The number started to decline before the study came out, because of safety worries about certain stents, and continued to fall after it, said Dr. Ralph Brindis, a California heart specialist who heads the cardiology college’s cardiovascular data registry.

The proportion of angioplasties done on people with chronic but stable chest pain dropped from 18 percent in early 2005 to just over 15 percent by March 2008, the registry shows. Started 10 years ago, it now includes information on about 530,000 angioplasties per year — roughly 60 percent of the national total.

Air pollution levels do not need to be very high to cause harm, researchers report in the Aug. 25 issue of the Journal of the American College of Cardiology. Air pollution — even at levels deemed “acceptable” by the Environmental Protection Agency — leads to short- and long-term injury to the heart and blood vessels, increases rates of heart disease-related hospitalizations, and can even cause death.

“There doesn’t have to be an environmental catastrophe for air pollution to cause injury,” Boris Z. Simkhovich, MD, PhD, a senior research associate at the Heart Institute of the Good Samaritan Hospital and an assistant professor of research medicine at the Keck School of Medicine, University of Southern California, says in a news release. “We’re talking about very modest increases. Air pollution can be dangerous at levels that are within the accepted air quality standards.”

Air quality levels in the U.S. are based on five major pollutants: ground-level ozone, particle pollution (including smoke from wildfires and emissions from vehicles and power plants), carbon monoxide, sulfur dioxide, and nitrogen dioxide. The air quality index (AQI) runs from 0 to 500. The higher the number, the more toxic the air and the greater the health concern. An AQI under 100 is generally considered acceptable.

Data documenting the ill effects of air pollution dates back more than a century. In 1872, one of the first air-pollution studies detailing the toxic components of urban air was published.

Recent studies show that the ultrafine particles found in polluted air can pass into a person’s bloodstream and travel to the heart, where they can cause an inflammatory response. This may reduce the ability of the heart to pump blood effectively to the body, raise blood pressure, and diminish blood flow through coronary arteries — the vital blood vessels which supply the heart with its oxygen and nutrient supply. Exposure to pollutants can also predispose individuals to experience irregular heartbeats.

Simkhovich and colleagues published their report after reviewing data from numerous studies regarding air pollution’s dangerous health effects. The researchers write in the journal report that the evidence “unequivocally indicate[s] pollution is directly linked to the adverse cardiovascular outcomes in the general population, and effects are seen at levels at or below existing air quality standards.

Specifically, both animal and human studies have shown that breathing in bad air:

* Affects heart rate and blood pressure
* Disrupts blood vessel function
* Interferes with blood clotting
* Speeds up the development of atherosclerosis (clogged arteries)

Long-term studies involving a large group of people have linked spikes in air pollution to emergency hospital admissions due to heart attacks, chest pain, heart failure, and even heart-related death.

The elderly and people with existing heart disease or diseases that damage the blood vessels (such as diabetes) are especially vulnerable to the harmful heart-related effects of air pollution. In the U.S., air quality index levels over 100 are considered dangerous for sensitive individuals, such as those with heart or lung disease.

“Patients with cardiovascular disease shouldn’t exercise outside on days with increased air pollution levels. On very polluted days, they should consider staying inside, and during the winter, they should limit exposure to fireplace smoke,” Robert A. Kloner, MD, PhD, director of research at the Heart Institute of the Good Samaritan Hospital and a professor of medicine at the Keck School of Medicine, University of Southern California, says in a news release. “Of course, the real solution is to reduce air pollution.”

The term cardiology is derived from the Greek word καρδιά (transliterated as kardia and meaning heart or inner self)

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