The following are key points to remember about the management of ventricular arrhythmias and the prevention of sudden cardiac death (SCD):

1. SCD accounts for about 25% of the 17 million deaths due to cardiovascular diseases every year in the world. The SCD rate ranges from 1.40 per 100,000 person-years in women to 6.68 per 100,000 person-years in men. Approximately 50% of cardiac arrests occur in individuals without a known heart disease, but most suffer from undiagnosed ischemic heart disease.
2. An autopsy is recommended to investigate the cause of sudden death. Histological examination and blood analysis for toxicology and molecular pathology are recommended in all victims. Targeted post-mortem genetic analysis should be considered if a specific inheritable channelopathy or cardiomyopathy is suspected.
3. Family screening of first-degree relatives of victims of sudden death is an important intervention to identify individuals at risk, advise on available treatment, and adequately prevent sudden death. The diagnosis of an inheritable arrhythmogenic disorder is established in up to 50% of families with a sudden arrhythmic death syndrome victim.
4. It is recommended that public access defibrillation be established at sites where cardiac arrest is relatively common (e.g., schools, sports stadiums, large stations, casinos, etc.) or at sites where no other access to defibrillation is available (e.g., trains, cruise ships, airplanes, etc.).
5. Physical examination and resting 12-lead electrocardiogram (ECG) should be considered for pre-participation screening in younger athletes. Careful history taking to uncover underlying cardiovascular disease, rhythm disorder, syncopal episodes, or family history of SCD is recommended in adult athletes. Upon identification of ECG abnormalities suggestive of structural heart disease, echocardiography and/or cardiac magnetic resonance imaging is recommended.
6. Post-resuscitation care should be performed in high-volume expert centers capable of offering primary coronary interventions, electrophysiology, cardiac assist devices, cardiac and vascular surgery, and therapeutic hypothermia.
7. Early (before discharge) assessment of left ventricular ejection fraction (LVEF) is recommended in all patients with acute myocardial infarction (MI). Re-evaluation of LVEF 6–12 weeks after MI is recommended to assess the potential need for primary prevention implantable cardioverter-defibrillator (ICD) implantation. Early (<40 days) ICD implantation or the temporary (<40 days) use of a wearable cardioverter defibrillator (WCD) may be considered in cases of pre-existing LVEF impairment, incomplete revascularization, and arrhythmia occurring >48 hours after the onset of the acute coronary syndrome.
8. ICD placement is recommended in patients with documented ventricular fibrillation or hemodynamically unstable ventricular tachycardia (VT) in the absence of reversible causes or within 48 hours after MI who have a reasonable expectation of survival with a good functional status >1 year. Sustained monomorphic VT in patients with previous MI is less likely to be affected by revascularization. Myocardial revascularization is unlikely to prevent recurrent SCD in patients with extensive myocardial scarring and markedly depressed LVEF.
9. Electrophysiologic study with programmed ventricular stimulation should be considered in survivors of an MI with preserved LV function and otherwise unexplained syncope.
10. Optimal pharmacological therapy with angiotension-converting enzyme inhibitors (or, when intolerant, angiotensin-receptor blockers), beta-blockers, and mineralocorticoid receptor antagonists is recommended in patients with heart failure with systolic dysfunction (LVEF ≤35%–40%) to reduce total mortality and SCD.
11. Cardiac resynchronization therapy is recommended to reduce all-cause mortality in patients with an LVEF ≤35% and left bundle branch block despite at least 3 months of optimal pharmacological therapy, and who are expected to survive at least 1 year with good functional status.
12. A new calculator for risk stratification for patients with hypertrophic cardiomyopathy (http://doc2do.com/hcm/webHCM.html) has been endorsed. In contrast with the recently released hypertrophic cardiomyopathy guidelines, however, the authors of this guideline document did not incorporate a Class III recommendation for ICD therapy for patients with an estimated risk of sudden death <4% at 5 years.
13. ICDs should be considered in patients with light-chain amyloidosis or hereditary transthyretin-associated amyloidosis who experience sustained ventricular arrhythmia and have a life expectancy with good functional status of >1 year.
14. ICD implantation in addition to beta-blockers with or without flecainide is recommended in patients with a diagnosis of cathecholaminergic polymorphic VT who experience a cardiac arrest, recurrent syncope, or polymorphic/bidirectional VT despite optimal therapy.
15. Catheter ablation of right ventricular outflow tract (RVOT) VT or premature ventricular contractions (PVCs) is recommended in symptomatic patients and/or in patients who failed beta-blockers, or in patients with a decline in LV function due to high RVOT-PVC burden. Treatment with sodium channel blockers (class IC agents) is recommended in symptomatic patients with LVOT/aortic cusp/epicardial VT/PVC. Catheter ablation of LVOT/aortic cusp/epicardial VT/PVC by experienced operators after failure of one or more sodium channel blockers (class IC agents) or in patients not wanting long-term antiarrhythmic drug therapy should be considered in symptomatic patients.
16. The following are some drugs associated with an increased risk of torsades de pointes in susceptible individuals: quinolones, azithromycin, macrolide antibiotics erythromycin and clarithromycin, the co-administration of renin-angiotensin inhibitors, and co-trimazole (known is the United States as Trimethoprim/sulfamethoxazole).
17. Evaluation of the QT interval before initiation of treatment and during titration of dose with antipsychotic drugs should be considered.
18. Obstructive sleep apnea associated with a reduced mean nocturnal oxygen saturation <93% and a lowest nocturnal oxygen saturation <78% were independent risk factors for SCD (p = 0.0001). A circadian pattern of ventricular arrhythmia and a higher rate of SCD during sleep time (midnight to 6 a.m.) have been demonstrated.

Keywords: Acute Coronary Syndrome, Adrenergic beta-Antagonists, Amyloidosis, Angiotensin Receptor Antagonists, Anti-Arrhythmia Agents, Antipsychotic Agents, Arrhythmias, Cardiac, Athletes, Cardiac Resynchronization Therapy, Cardiomyopathy, Hypertrophic, Catheter Ablation, Death, Sudden, Cardiac, Defibrillators, Implantable, Echocardiography, Electrocardiography, Electrophysiology, Hypothermia, Induced, Heart Arrest, Heart Failure, Mineralocorticoid Receptor Antagonists, Myocardial Infarction, Myocardial Revascularization, Primary Prevention, Sleep Apnea, Obstructive, Sodium Channel Blockers, Syncope, Tachycardia, Ventricular, Torsades de Pointes, Ventricular Premature Complexes

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