NSVT is one of several risk factors for sudden death and death resulting from heart disease, but by itself, NSVT has little predictive value (35-37). In combination with specific conditions (acute MI, hypertrophic cardiomyopathy, impaired left ventricular function caused by CAD or LQTS), NSVT can be a major concern (38-42). In a "normal" population, NSVT recorded on a Holter monitor is associated with a significantly higher risk of early death, although causality has not clearly been established. Some studies show as much as a doubling in mortality and an association with CAD ultimately diagnosed (36). However, other studies have yielded contradictory results (43). In patients with CHF, some studies have linked NSVT with a higher risk of death (3,44-46). The GESICA trial showed that NSVT imparted an excess mortality risk of 69% (15,16). In the CHF STAT trial, NSVT was associated with an insignificant trend toward worsened survival (14,47). In another trial, NSVT was associated with higher pulmonary-artery pressures, higher pulmonary wedge pressures, and more pronounced sympathetic activation (47A). These data suggest that the NSVT may be a marker for a more diseased heart, which results in a poorer outcome.
In contrast to patients with heart failure, NSVT has consistently been shown to be a marker of risk for death for patients with CAD and reduced left ventricular ejection fraction (LVEF) (48) (see Fig. 4). These patients have a doubling or tripling in risk
of sudden cardiac death (49). Even a single 3-beat recording of NSVT on a 24-h Holter monitor has prognostic significance. When the LVEF is <0.35, mortality can exceed 20% in 2-yr follow-up, clearly greater than if no NSVT is present. In this population, the length and frequency of the episodes have not reproducibly been linked to prognosis, although recent data from the MUSTT trial indicates that NSVT runs >8 beats are associated with a poorer prognosis (50,51). The presence of NSVT in patients with CAD and impaired left ventricular function (LVEF <0.40 or 0.35) remains a nonspecific marker for sudden and total cardiac death. To this end, other prognostic markers have been considered to further define risk.
The prognostic significance of NSVT during the acute phase of a myocardial infarction is controversial even if impaired left ventricular function is present (39,52). In patients with hypertrophic cardiomyopathy, NSVT has been associated with higher risk for cardiac death in some, but not all studies (53). Some series suggest that NSVT imparts a several-fold increase in mortality in hypertrophic cardiomyopathy. Exercise-induced NSVT can have prognostic importance (8,54-61). While it may be caused by a benign condition ("idiopathic VT") (62), it can be associated with arrhythmogenic right ventricular dysplasia, LQTS, an aberrant coronary artery, hypertrophic cardiomy-opathy or dilated cardiomyopathy. An athlete with NSVT requires restriction from athletics until the problem is evaluated fully and treated based on the Bethesda guidelines (62a).
Refining risk in patients with cardiac disease may extend beyond the diagnosis of NSVT, symptoms of CHF, and presence of ventricular dysfunction. Other risk-stratifiers currently being investigated include heart-rate variability (HRV), signal-averaged electrocardiography (SAECG), baroreflex responses, spectral turbulence, QT dispersion, and T-wave alternans (TWA). Even if better predictors become available, the magnitude of absolute-risk "high" enough to warrant ICD implantation must be defined.
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