title: [Arrhythmia risk stratification in patients with heart failure according to drug treatment and its effects].
abstract: Despite therapeutic advances in heart failure treatment, this syndrome still presents a poor prognosis, with a relevant mortality due to both systolic dysfunction progression and sudden death. Sudden cardiac death appears to be relatively more frequent in less compromised patients (NYHA functional class I) but in absolute numbers it is more frequent in more functionally compromised patients. The ability to predict sudden cardiac events with current available tests is poor, with the possible exception of electrophysiological test in ischemic cardiomyopathy. The risk of sudden death is proven to be increased in more advanced cardiac dysfunction and frequently the acute event can be precipitated by ischemia. Therefore the best approach in the prevention of sudden cardiac death may well be the proper treatment of ischemia and cardiac dysfunction. Beta-blockers have demonstrated a favorable effect in the prevention of sudden cardiac death. ACE-inhibitors can significantly reduce global death in heart failure patients, but their impact on sudden death appears to be limited. The same may be true for angiotensin II blockers. Diuretics have generally been demonstrated to increase sudden death, possibly via electrolyte imbalance; this may explain why spironolactone has a pronounced impact in reducing sudden death. Inotropes, in spite of their good effect on refractory heart failure and their usefulness in the compassionate care of terminally ill heart failure patients, have demonstrated an increase in sudden cardiac death. The same holds true for digoxin, in spite of its ability to reduce death due to heart failure deterioration. Antiarrhythmic drugs, with the possible exception of amiodarone, have demonstrated an unfavorable effect on sudden death incidence.
authors.affiliation: U.O. di Cardiologia, Clinica ed Insufficienza Cardiaca, Istituto Clinico Humanitas, Via Manzoni, 56 20089 Rozzano, MI. edoardo.gronda@humanitas.it
authors.forename: E
authors.initials: E
authors.lastname: Gronda
authors.forename: M
authors.initials: M
authors.lastname: Mangiavacchi
authors.forename: B
authors.initials: B
authors.lastname: Andreuzzi
authors.forename: A
authors.initials: A
authors.lastname: Municinò
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000638:Amiodarone / Q000627:therapeutic use; D000804:Angiotensin II / Q000037:antagonists & inhibitors; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D001145:Arrhythmias, Cardiac / Q000209:etiology* / Q000517:prevention & control; D002316:Cardiotonic Agents / Q000627:therapeutic use; D016757:Death, Sudden, Cardiac / Q000209:etiology / Q000517:prevention & control; D004232:Diuretics / Q000627:therapeutic use; D006333:Heart Failure / Q000150:complications* / Q000188:drug therapy* / Q000401:mortality; D006801:Humans; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use; D009203:Myocardial Infarction / Q000517:prevention & control; D010138:Pacemaker, Artificial; D011379:Prognosis; D016032:Randomized Controlled Trials as Topic; D012306:Risk; D018570:Risk Assessment; D013148:Spironolactone / Q000627:therapeutic use; D014665:Vasodilator Agents / Q000627:therapeutic use
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000889:Anti-Arrhythmia Agents; D002316:Cardiotonic Agents; D004232:Diuretics; D000451:Mineralocorticoid Receptor Antagonists; D014665:Vasodilator Agents; D000804:Angiotensin II; D013148:Spironolactone; D000638:Amiodarone