Ventricular arrhythmias: Overview in patients with heart failure and cardiomyopathy

INTRODUCTION — Ventricular arrhythmias, including premature ventricular complexes or beats, ventricular premature complexes or beats, ventricular tachycardia, and ventricular fibrillation, are common in patients with heart failure (HF) and cardiomyopathy, both ischemic and nonischemic in nature [1-3].

The etiology and types of arrhythmias, clinical presentation, diagnosis, and management of ventricular arrhythmias in patients with HF and/or cardiomyopathy will be reviewed here. The secondary and primary prevention of sudden cardiac death in these patients, including a review of the causes of death in HF, and the importance of ventricular arrhythmias in other causes of cardiomyopathy, such as hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy, are discussed separately. (See "Secondary prevention of sudden cardiac death in heart failure and cardiomyopathy" and "Primary prevention of sudden cardiac death in patients with cardiomyopathy and heart failure with reduced LVEF" and "Hypertrophic cardiomyopathy: Risk stratification for sudden cardiac death" and "Arrhythmogenic right ventricular cardiomyopathy: Treatment and prognosis".)

TYPES OF ARRHYTHMIA

Premature ventricular complexes (PVCs) — PVCs occur in 70 to 95 percent of patients with heart failure (HF), and they may be frequent (including bigeminy or trigeminy) and complex (ie, multifocal, couplets, or triplets/nonsustained ventricular tachycardia) [4-7]. (See "Premature ventricular complexes: Clinical presentation and diagnostic evaluation" and "Premature ventricular complexes: Treatment and prognosis".)

Among patients with cardiomyopathy, PVCs may be clinically significant for the following reasons:

●PVCs (particularly when complex, ie, multifocal, couplets [ie, two PVCs in a row], or triplets [ie, three PVCs in a row, often called nonsustained VT]) may be predictors of more malignant arrhythmias and sudden cardiac death (SCD). In patients with a prior myocardial infarction (MI), PVCs are associated with an increased risk of death. By contrast, PVCs do not appear to be associated with a worse prognosis in patients with nonischemic cardiomyopathy, although data are limited [8].

●PVCs can cause symptoms, usually palpitations. Symptoms are generally mild, and most patients require no specific therapy. Beta blockers can help to control symptoms (particularly palpitations related to the post-extrasystolic potentiation of myocardial contractility) although they will not usually suppress the PVCs, but most patients with HF and cardiomyopathy already have an indication for a beta blocker.

●Because of the proarrhythmic risks of antiarrhythmic drugs (which are particularly increased in patients with HF) other than beta blockers, these medications are not used in the routine treatment of PVCs. In the rare circumstance in which a patient is severely symptomatic despite beta blockers, amiodarone or dofetilide appears to be safe in patients with HF, and radiofrequency catheter ablation may also be an option.

●In rare cases, very frequent PVCs cause a reduction in left ventricular ejection fraction or even less frequently exacerbate left ventricular (LV) dysfunction. In such cases, radiofrequency catheter ablation is a safe and possibly an effective therapy that can reduce the number of PVCs and often restore LV function toward normal. (See "Arrhythmia-induced cardiomyopathy", section on 'Frequent ventricular ectopy'.)

Nonsustained ventricular tachycardia — Runs of nonsustained ventricular tachycardia (NSVT) have been observed on ambulatory monitoring in 50 to 80 percent of patients with HF or cardiomyopathy [4,7,9]. We define NSVT as three or more consecutive ventricular beats at a rate of greater than 100 beats/minute with a duration of less than 30 seconds (or self-terminating) and no associated hemodynamic collapse. The clinical significance of NSVT can be considered in a similar manner to that of PVCs:

●NSVT may be predictive of future malignant arrhythmias and mortality. An association between NSVT and mortality has been shown in patients with ischemic and hypertrophic cardiomyopathy but not in most other forms of cardiomyopathy. (See "Incidence of and risk stratification for sudden cardiac death after myocardial infarction".)

●Among 1080 patients with class III and IV HF in the PROMISE study, the frequency of NSVT was a significant independent predictor of both sudden and non-sudden death mortality [4].

●NSVT is often asymptomatic, but some patients experience palpitations, lightheadedness, presyncope, or dyspnea. Because many of the symptoms that may be attributed to NSVT are vague and nonspecific, it is important to try to correlate symptoms to episodes of NSVT before initiating therapy. In patients with symptoms due to NSVT, options include beta blockers (for which most patients already have an indication), catheter ablation, and, in rare cases of severe and refractory symptoms, amiodarone or dofetilide. In patients with an ischemic cardiomyopathy, the occurrence of nonsustained polymorphic ventricular tachycardia (VT) may be the result of active ischemia. (See "Nonsustained ventricular tachycardia: Clinical manifestations, evaluation, and management".)

●In rare cases, very frequent NSVT can contribute to or exacerbate LV dysfunction. (See "Arrhythmia-induced cardiomyopathy", section on 'Ventricular arrhythmias'.)

Accelerated idioventricular rhythm — An accelerated idioventricular rhythm (AIVR), which has also been called "slow VT," arises below the atrioventricular (AV) node (within the ventricular myocardium) and has, by definition, a rate between 60 and 100 beats/minute. When the AIVR is an accelerated rhythm, there is AV dissociation present, but the rate of the QRS complexes is faster than the atrial rate. AIVR occurs in approximately 8 percent of patients with HF or cardiomyopathy [10]. It also occurs in up to 50 percent of patients during an acute MI, most commonly in patients undergoing revascularization (ie, a reperfusion arrhythmia). Most episodes of AIVR are transient and require no treatment. (See "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features", section on 'Accelerated idioventricular rhythm'.)

Sustained VT or VF — In contrast to the high prevalence of PVCs and NSVT in patients with HF or cardiomyopathy, sustained VT (monomorphic or polymorphic) is unusual, occurring in ≤5 percent of patients [4,7,9]. Patients with spontaneous sustained VT or resuscitated ventricular fibrillation (VF) are at high risk for SCD [11,12]. Patients with HF or cardiomyopathy (especially with an LVEF ≤35 percent) who are survivors of SCD due to unstable VT or VF, with or without recurrent stable sustained VT, are typically treated with an implantable cardioverter-defibrillator for secondary prevention. (See "Secondary prevention of sudden cardiac death in heart failure and cardiomyopathy".)

PATHOGENESIS — There are multiple factors responsible for ventricular arrhythmias in patients with heart failure (HF) and cardiomyopathy. These include:

●Underlying structural myocardial disease

●Mechanical factors

●Neurohormonal factors

●Electrolyte abnormalities

●Myocardial ischemia

●Drugs

Underlying structural myocardial disease — Extensive myocardial damage and fibrosis (including scar from prior myocardial infarction), myocardial infiltration or inflammation, or the loss of cell-to-cell coupling in patients with dilated cardiomyopathy provides the proper substrate for reentry, the mechanism thought to be responsible for most ventricular arrhythmias.

A focal mechanism may also contribute to ventricular arrhythmia in patients with a nonischemic cardiomyopathy, probably from an ectopic focus or triggered activity arising from either early afterdepolarizations or delayed afterdepolarizations, without evidence of reentry.

Mechanical factors — Mechanical factors that can alter the electrophysiologic properties (electromechanical feedback) of myocardial tissue in HF include an increase in wall stress and left ventricular dilation [13,14]. It has been shown that a stretching of atrial or ventricular myocardium can enhance automaticity and result in arrhythmia. Since regions of the heart differ in mechanical function, electromechanical feedback that can cause PVCs may result in an increase in dispersion of action potential duration and membrane recovery. These effects can increase the incidence of arrhythmias, particularly sustained VT or VF. Among 311 patients in the SOLVD (Studies of Left Ventricular Dysfunction) trial, for example, there was a direct correlation between left ventricular end-diastolic volume and the prevalence of ventricular arrhythmia [15].

Neurohormonal factors — HF results in the activation of the sympathetic nervous and renin-angiotensin systems and withdrawal of parasympathetic tone, resulting in increased heart rate, reduced heart rate variability, and depressed baroreceptor sensitivity.

Neurohormonal activation can promote arrhythmia formation via a variety of mechanisms:

●Catecholamines are arrhythmogenic by virtue of their ability to enhance automaticity, precipitate triggered activity, and alter conduction and refractoriness, which may promote reentry.

●Angiotensin II can indirectly promote arrhythmia formation via low potassium or magnesium levels, resulting from potassium and magnesium loss in the urine. It can also potentiate the effects of the sympathetic nervous system through central or peripheral actions.

●Both systems may be arrhythmogenic because the associated vasoconstriction alters loading conditions, affecting wall stress and mechanical factors as described above.

Electrolyte abnormalities — Patients with HF often have electrolyte abnormalities, particularly diuretic-induced hypokalemia and hypomagnesemia, which may be directly arrhythmogenic [16]. Hyperkalemia, as may occur with the use of ACE inhibitors or ARBs, results in slowing of conduction through the myocardium, which may also be a precondition for arrhythmia. In addition, stimulation of beta-2 receptors by circulating epinephrine can transiently lower the plasma potassium concentration by enhancing potassium entry into cells. In the SOLVD trial, for example, non-potassium-sparing diuretic use at baseline was associated with a lower serum concentration of potassium and a higher incidence of arrhythmic death compared with no diuretic use (3.1 versus 1.7 deaths per 100 patient-years) [17]. (See "Use of diuretics in patients with heart failure".)

Myocardial ischemia — Myocardial ischemia, through its effects on electrolyte shifts, acidosis, heterogeneity of electrophysiologic properties, and other mediators, may lead to alteration in the electrophysiologic milieu, including regional alterations in conduction and refractoriness and enhanced automaticity. These alterations may be enhanced by hypokalemia, increased catecholamine levels, digitalis, and antiarrhythmic agents. While monomorphic ventricular tachycardia (VT) is not usually due to active ischemia, polymorphic VT or ventricular fibrillation (VF) are often ischemia-induced arrhythmias.

Drugs — The drugs used to treat HF can directly or indirectly precipitate arrhythmia formation.

●Diuretic-induced electrolyte disturbances may be directly arrhythmogenic.

●Drugs may be proarrhythmic by prolonging the QT interval (table 1) (eg, antiarrhythmic medications, certain antifungal and antibiotic agents, certain psychoactive drugs, etc) and predisposing to acquired long QT syndrome and polymorphic VT (which, associated with QT prolongation, is termed torsades de pointes). (See "Acquired long QT syndrome: Clinical manifestations, diagnosis, and management".)

●Phosphodiesterase inhibitors – Phosphodiesterase inhibitors are positive inotropic agents that increase intracellular calcium, which can increase cyclic AMP and precipitate afterdepolarizations, resulting in triggered activity. They can also exacerbate ventricular arrhythmias by inducing ischemia [18]. A number of trials have shown that one such agent, milrinone, increased the frequency of all forms of spontaneous arrhythmia [19-21] and, in a long-term survival trial (PROMISE), was associated with a 20 percent excess in mortality compared with placebo [22].

●Sympathomimetic drugs – Studies with sympathomimetic agents (eg, dobutamine, albuterol) have shown an increased frequency of ventricular arrhythmias and/or increased mortality [23]. The use of sympathomimetic drugs is also associated with an increased incidence of hospitalization for arrhythmia, especially atrial fibrillation, VT, and VF [24].

●Digoxin – There have been conflicting data on the effect of digoxin on the frequency and clinical significance of arrhythmias in HF. Two relatively large studies found that digoxin did not significantly affect the frequency of ventricular arrhythmias in patients with congestive HF [21,25]. Conversely, other studies in patients with HF after acute myocardial infarction (MI) reported an excess mortality in patients who had complex ventricular arrhythmias who were treated with digitalis [26,27]; however, other reports did not confirm this increased risk in post-MI patients [28,29].

The largest trial evaluating the efficacy of digoxin in HF, the DIG trial, randomly assigned approximately 6800 patients with HF to digoxin or placebo; all patients were also treated with an angiotensin converting enzyme inhibitor and, if necessary, a diuretic [30]. Digoxin was associated with an increase in non-HF cardiac mortality, which included a trend towards increased mortality from arrhythmia. This trend counterbalanced the fewer deaths from progressive HF in patients treated with digoxin, leading to no effect on overall patient survival. (See "Cardiac arrhythmias due to digoxin toxicity", section on 'Digoxin-induced arrhythmias'.)

For patients who take digoxin, periodic monitoring of serum levels should be performed, as higher serum digoxin levels have been associated with worse outcomes. (See "Treatment with digoxin: Initial dosing, monitoring, and dose modification", section on 'Monitoring serum digoxin'.)

CLINICAL MANIFESTATIONS — The type and intensity of symptoms, if present, will vary depending upon the type and duration of the ventricular arrhythmia along with the patient’s overall clinical status and significant comorbid conditions.

●Patients with ventricular premature beats who notice symptoms typically present with palpitations or dizziness, though the vast majority of patients experience few or no symptoms. (See "Premature ventricular complexes: Clinical presentation and diagnostic evaluation", section on 'Symptoms'.)

●Patients with nonsustained ventricular tachycardia (NSVT) who notice symptoms typically present with one or more of palpitations, chest pain, shortness of breath, or syncope/presyncope. (See "Nonsustained ventricular tachycardia: Clinical manifestations, evaluation, and management", section on 'History and associated symptoms'.)

●Patients with sustained VT may briefly experience the onset of symptoms prior to the abrupt loss of consciousness and sudden cardiac arrest if VT results in hemodynamic collapse. For patients without immediate sudden cardiac arrest, the type and intensity of symptoms are similar to NSVT and will vary depending upon the rate and duration of sustained monomorphic VT along with the presence and severity of underlying heart disease and the presence or absence of significant comorbid conditions. (See "Sustained monomorphic ventricular tachycardia: Clinical manifestations, diagnosis, and evaluation", section on 'History and associated symptoms'.)

Syncope in the setting of severe cardiomyopathy and HF requires special consideration. Although these patients may have syncope due to any of the usual causes, they are more likely than other patients to have an arrhythmic etiology. Thus, syncope in this population requires careful evaluation. This evaluation sometimes includes an electrophysiology study, both to exclude the possibility of a bradyarrhythmic cause and to attempt to induce ventricular arrhythmias. Patients in whom no etiology of syncope is found are said to have unexplained syncope. Extended ambulatory ECG monitoring (with an event recorder, patch monitoring, or implantable loop recorder) is often used to establish the etiology for unexplained syncope. Syncope is associated with an increased risk of sudden cardiac death in patients with HF and cardiomyopathy, even if an arrhythmic cause cannot be identified [31-34]. (See 'Diagnostic evaluation' below.)

Sleep disordered breathing (SDB), presenting as either obstructive sleep apnea or central sleep apnea syndrome (including Cheyne-Stokes breathing) occurs commonly in patients with HF and is associated with increased cardiac mortality. In a study of 283 patients with HF (170 with no or mild SDB, and 113 with untreated SDB) who already had an implantable cardioverter-defibrillator (ICD), time periods to first monitored ventricular arrhythmias (VT or ventricular fibrillation) and to first appropriate ICD therapy were significantly shorter in patients with SDB [35]. (See "Sleep-disordered breathing in heart failure", section on 'Arrhythmias'.)

DIAGNOSTIC EVALUATION — An electrocardiogram (ECG) should be part of the standard evaluation for any patient with suspected premature ventricular complexes (PVCs), nonsustained ventricular tachycardia (NSVT), or sustained VT. The diagnostic evaluation beyond an ECG will vary depending upon the particular arrhythmia in question and the patient’s prior investigations, but additional testing may include one or more of ambulatory ECG monitoring, exercise testing, echocardiography, and invasive electrophysiology (EP) studies. The diagnostic evaluation of PVCs, NSVT, and sustained VT is discussed in detail separately. (See "Premature ventricular complexes: Clinical presentation and diagnostic evaluation", section on 'Additional testing' and "Nonsustained ventricular tachycardia: Clinical manifestations, evaluation, and management", section on 'Diagnostic evaluation' and "Sustained monomorphic ventricular tachycardia: Clinical manifestations, diagnosis, and evaluation", section on 'Additional diagnostic evaluation'.)

EP studies can demonstrate the mechanisms of induced or spontaneous arrhythmias and characterize the function of the sinus node, the AV node, and the His-Purkinje system. Thus, EP studies can assist in the diagnosis of unexplained symptoms (eg, palpitations or syncope) and arrhythmias. NSVT can be an indication for EP study and possible implantable cardioverter-defibrillator (ICD) therapy in selected patients with a prior myocardial infarction (MI) and ischemic cardiomyopathy who do not otherwise meet criteria for prophylactic ICD implantation. The ability to induce ventricular arrhythmias is not predictive of sudden cardiac death risk in patients with nonischemic cardiomyopathy. Thus, EP testing does not have a role in risk stratification in these patients.

In contemporary patient management, however, EP studies are used only in a small minority of patients, typically in the following situations:

●Patients with structural heart disease and syncope of uncertain etiology (especially if NSVT is present).

●Patients with a remote MI and NSVT who do not otherwise meet criteria for prophylactic ICD implantation (eg, left ventricular ejection fraction [LVEF] ≥35 percent).

●Patients with nonischemic cardiomyopathy and NSVT who do not otherwise meet criteria for prophylactic ICD implantation (eg, LVEF ≥35 percent).

●Patients with cardiomyopathy felt to be at high risk, but who are in a "waiting period" prior to ICD implantation (eg, newly diagnosed nonischemic cardiomyopathy and NSVT).

DIAGNOSIS — The diagnosis of sustained ventricular tachycardia (VT) should be suspected in a patient who presents with either sudden cardiac arrest, syncope, or sustained palpitations, particularly in a patient with a known history of structural heart disease. The diagnosis of nonsustained VT (NSVT) or premature ventricular complexes (PVCs) is more commonly suspected in a patient with intermittent palpitations, which may or may not be associated with other symptoms.

The diagnosis of sustained VT, NSVT, or PVCs is typically confirmed following review of an ECG acquired during the arrhythmia. The ECG in patients with VT (sustained or nonsustained) will show a wide QRS complex tachycardia often with the presence of AV dissociation (manifest as an atrial rate slower than the ventricular rate), while the ECG in patients with PVCs will show one or more isolated PVCs . (See "Wide QRS complex tachycardias: Approach to the diagnosis" and "Sustained monomorphic ventricular tachycardia: Clinical manifestations, diagnosis, and evaluation", section on 'Diagnosis'.)

MANAGEMENT — The management of ventricular arrhythmias in patients with heart failure (HF) and cardiomyopathy is multifaceted and includes:

●HF management

●Arrhythmia control

●Consideration of an implantable cardioverter-defibrillator (ICD) for primary or secondary prevention of sudden cardiac death (SCD)

Heart failure therapy — Patients with HF and ventricular arrhythmias should have their HF treated aggressively.

Standard therapy for HF due to systolic dysfunction consists of the following:

●A beta blocker such as carvedilol, metoprolol succinate, or bisoprolol

●An angiotensin receptor neprilysin inhibitor (ARNI), angiotensin converting enzyme (ACE) inhibitor or an angiotensin II receptor blocker (ARB)

●An aldosterone antagonist in selected patients

●Diuretics if there is evidence of fluid overload or to prevent recurrent fluid overload

In addition, digoxin and intravenous inotropic agents (eg, milrinone, dobutamine) are occasionally used for acute symptom control, while diuretics are given for congestive symptoms. Many of these drugs can affect the incidence of arrhythmic death in patients with HF or cardiomyopathy.

Some of the key points of various HF therapies will be discussed here, while more extended discussions can be found in the related topics.

●Beta blockers – A substantial part of the survival benefit seen with beta blockers in patients with HF is due to a significant reduction in SCD [36-38]. As examples, there were significantly fewer SCDs in trials using carvedilol. In the MERIT-HF trial, there were significantly fewer SCDs (3.9 versus 6.6 percent) and fewer deaths from worsening of HF (1.5 versus 2.9 percent) with metoprolol compared with placebo, while in CIBIS-II, the survival benefit from beta blocker therapy was primarily due to a reduction in SCD (3.6 versus 6.3 percent), with only a nonsignificant trend toward fewer deaths from HF [36].

●ACE inhibitors and ARBs – ACE inhibitors improve survival in all stages of HF. However, there are conflicting data as to whether ACE inhibitors reduce SCD. A meta-analysis of trials of 15,104 patients within 14 days of an acute myocardial infarction found that ACE inhibitor therapy modestly but significantly reduced the risk of SCD (odds ratio 0.80, absolute benefit approximately 1.4 percent) [39]. However, as noted above, 45 percent of patients who died suddenly in AIRE had severe or worsening HF prior to their death, and only 39 percent of sudden deaths were thought to be due to arrhythmia [40].

The ARBs appear to be as or perhaps slightly less beneficial than ACE inhibitors in patients with HF [41]. The major ARB trial CHARM noted a clear survival benefit but did not report data on SCD [42]. ELITE II, which directly compared losartan with captopril, found a higher rate of SCD with losartan that was not statistically significant [41]. This might suggest that ARBs alone are unlikely to have a major impact on SCD in HF patients. Conversely, however, the addition of ARB to ACE inhibitor therapy in patients with HF in the CHARM-Added trial was found to reduce the rate of SCD, as well as the rate of death from worsening HF [43].

●Angiotensin receptor neprilysin inhibitors (ARNI) – For some patients, an ARNI such as sacubitril-valsartan can be substituted in place of ACE inhibitor (or single-agent ARB) therapy for patients who have tolerated an ACE inhibitor or ARB. However, some experts recommend the ARNI sacubitril-valsartan as initial oral therapy (in place of ACE inhibitor or single-agent ARB) in hemodynamically stable patients.

●Aldosterone antagonists – The aldosterone antagonists spironolactone and eplerenone significantly reduce overall mortality and SCD in patients with advanced HF [44,45]. They also reduce the frequency of VPBs and nonsustained ventricular tachycardia (NSVT) [46]. These benefits may reflect a reduction in aldosterone effect on the heart and/or the maintenance of a higher serum potassium concentration.

●Cardiac resynchronization therapy – Cardiac resynchronization therapy appears to reduce the incidence of ventricular tachyarrhythmias in patients with HF and cardiomyopathy. This is discussed in greater detail separately. (See "Cardiac resynchronization therapy in heart failure: Indications and choice of system".)

Arrhythmia control — The initial management of a patient with sustained VT depends on the hemodynamic stability of the patient (algorithm 1). Emergency management is required in unstable patients, typically with electrical cardioversion and occasionally antiarrhythmic medications. Additional time may be spent determining the etiology and treating any underlying precipitating factors in patients who are hemodynamically stable (although treatment for such patients should usually be promptly administered). Subsequent management of the patient will be guided by the initial presentation (ie, hemodynamically stable or unstable) and the initial approach to treatment [47]. A full discussion of the treatment of sustained VT is presented separately. (See "Sustained monomorphic ventricular tachycardia in patients with structural heart disease: Treatment and prognosis", section on 'Treatment'.)

Patients with symptomatic NSVT or PVCs should usually be treated with beta blockers as the initial therapy. While beta blockers do not usually reduce the frequency of these arrhythmias, they may be effective for reducing or eliminating symptoms. For patients who have very frequent, symptomatic NSVT or PVCs not controlled by medications, catheter ablation can be effective for reducing or eliminating associated symptoms. Antiarrhythmic medications are generally reserved for patients with severely symptomatic NSVT despite therapy with beta blockers who are not candidates for catheter ablation of the VT. A full discussion of the treatment of NSVT and PVCs is presented separately. (See "Nonsustained ventricular tachycardia: Clinical manifestations, evaluation, and management", section on 'Treatment'.)

Prevention of SCD — Patients who have been resuscitated from sudden cardiac arrest (due to either sustained VT or ventricular fibrillation) are candidates for, and generally should receive, an ICD for secondary prevention of SCD. Patients who present with sustained VT in the setting of cardiomyopathy and patients with NSVT and/or syncope and inducible sustained ventricular arrhythmia at electrophysiology testing should also generally receive an ICD for secondary prevention. Additionally, many patients with HF and cardiomyopathy (and left ventricular ejection fraction ≤35 percent) are candidates for ICD implantation as primary prevention of SCD. Secondary and primary prevention of SCD in HF and cardiomyopathy are discussed separately. (See "Secondary prevention of sudden cardiac death in heart failure and cardiomyopathy" and "Primary prevention of sudden cardiac death in patients with cardiomyopathy and heart failure with reduced LVEF".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Arrhythmias in adults" and "Society guideline links: Heart failure in adults" and "Society guideline links: Ventricular arrhythmias".)

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Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient education: Ventricular tachycardia (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Background – Ventricular arrhythmias, including premature ventricular complexes (PVCs), ventricular tachycardia (VT), and ventricular fibrillation (VF), are common in patients with heart failure (HF) and cardiomyopathy, occurring in up to 95 percent of this population. (See 'Types of arrhythmia' above.)

●Pathogenesis – Multiple factors may be responsible for ventricular arrhythmias in patients with HF and cardiomyopathy, including underlying structural heart disease, mechanical factors, neurohormonal factors, electrolyte disturbances, myocardial ischemia, and medications. (See 'Pathogenesis' above.)

●Clinical manifestations – The type and intensity of symptoms, if present, will vary depending upon the type and duration of the ventricular arrhythmia along with the patient’s overall clinical status and significant comorbid conditions. Patients may experience few or no symptoms with PVCs or short runs of nonsustained VT, or may present with syncope or sudden cardiac arrest due to sustained VT or VF. (See 'Clinical manifestations' above.)

●Diagnostic evaluation – An ECG should be part of the standard evaluation for any patient with suspected PVCs, VT, or VF. The diagnostic evaluation beyond an ECG will vary depending upon the particular arrhythmia in question and the patient’s prior investigations, but additional testing may include one or more of ambulatory ECG monitoring, exercise testing, echocardiography, and invasive electrophysiology studies. (See 'Diagnostic evaluation' above.)

●Management – The management of ventricular arrhythmias in patients with HF and cardiomyopathy is multifaceted and includes HF therapy, arrhythmia control, and consideration of an implantable cardioverter-defibrillator (ICD) for primary or secondary prevention of sudden cardiac death (SCD).

•Heart failure – Standard therapy for HF due to systolic dysfunction consists of a beta blocker; an angiotensin receptor neprilysin inhibitor, angiotensin converting enzyme inhibitor, or an angiotensin II receptor blocker (ARB); and in selected patients, an aldosterone antagonist. Digoxin and other inotropic agents are occasionally used for symptom control, while diuretics are given for congestive symptoms. (See 'Heart failure therapy' above.)

•Arrhythmia control – The initial management of a patient with sustained VT depends on the hemodynamic stability of the patient (algorithm 1), with emergency management required in unstable patients. Subsequent management of VT will be guided by the initial presentation (ie, hemodynamically stable or unstable) and the initial approach to treatment. Patients with symptomatic NSVT or PVCs should usually be treated with beta blockers as the initial therapy. (See 'Arrhythmia control' above.)

•Prevention of SCD – Patients who have been resuscitated from sudden cardiac arrest (due to either sustained VT or VF) are candidates for, and generally should receive, an ICD for secondary prevention of SCD. Additionally, many patients with HF and cardiomyopathy (and left ventricular ejection fraction ≤35 percent) are candidates for ICD implantation as primary prevention of SCD. (See "Secondary prevention of sudden cardiac death in heart failure and cardiomyopathy" and "Primary prevention of sudden cardiac death in patients with cardiomyopathy and heart failure with reduced LVEF".)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Leonard Ganz, MD, FHRS, FACC, who contributed to an earlier version of this topic review.