Abstract
Heart failure (HF) is a complex clinical syndrome in which structural/functional myocardial abnormalities result in symptoms and signs of hypoperfusion and/or pulmonary or systemic congestion at rest or during exercise. More than 80% of deaths in patients with HF recognize a cardiovascular cause, with most being either sudden cardiac death (SCD) or death caused by progressive pump failure. Risk stratification of SCD in patients with HF and preserved (HFpEF) or reduced ejection fraction (HFrEF) represents a clinical challenge. This review will give an update of current strategies for SCD risk stratification in both HFrEF and HFpEF.
Highlights
Heart failure (HF) is a complex clinical syndrome in which structural/functional myocardial abnormalities result in symptoms and signs of hypoperfusion and/or pulmonary or systemic congestion at rest or during exercise [1].Currently, 5.7 million people in the United States have HF, and approximately 45% of them have systolic dysfunction [2]
In patients with ischemic dilated cardiomyopathy, a reduction of global longitudinal strain (GLS) has been independently associated with sudden cardiac death (SCD), appropriate ICD therapy, and ventricular arrhythmias [35], Haugaa et al have showed, in an observational study including 94 patients with nonischemic dilated cardiomyopathy [36], that an increase of GLS it is associated with a high risk of arrhythmic events
Microvolt T-wave alternans (MTWA) is a beat-to-beat fluctuation of T-wave amplitude and morphology, that has been associated with increased susceptibility for sustained ventricular arrhythmia [68], early studies showed that TWA was a powerful electrocardiographic tool in predicting SCD in patients, in cohorts with ischemic and non-ischemic cardiomyopathy [69,70]
Summary
Heart failure (HF) is a complex clinical syndrome in which structural/functional myocardial abnormalities result in symptoms and signs of hypoperfusion and/or pulmonary or systemic congestion at rest or during exercise [1]. In patients with systolic dysfunction after a myocardial infarction, non-arrhythmic SCD frequently occurs during the first four to six weeks and is due to mechanical complication of myocardial infarction (i.e., rupture of the left ventricular free wall; rupture of the interventricular septum; and the development of acute mitral regurgitation) [19]. It seems that the proportions of arrhythmic and non-arrhythmic SCD cases become equivalent approximately one month after the acute coronary syndrome. Irrespective of HF etiology and LVEF, in patients with advanced HF, arrhythmias are triggered primarily by pump failure with about 60% of such patients that have severe bradyarrhythmias or electromechanical dissociation as the underlying cause for their SCD [27]
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