RESUMEN
OBJECTIVES: The purpose of this study was to determine the prevalence, characteristics and the predictive value of nonsustained ventricular tachycardia (VT) for subsequent death and arrhythmic events after acute myocardial infarction (AMI). BACKGROUND: Nonsustained VT has been linked to an increased risk for sudden death in coronary patients. It is unknown whether this parameter can be used for selection of high-risk patients to receive an implantable defibrillator for primary prevention of sudden death in patients shortly after AMI. METHODS: In 325 consecutive infarct survivors, 24-h Holter monitoring was performed 10+/-6 days after AMI. All patients underwent coronary angiography, determination of left ventricular function and assessment of heart rate variability (HRV). Mean follow-up was 30+/-22 months. RESULTS: There was a low prevalence (9%) of nonsustained VT shortly after AMI. Nonsustained VT together with depressed left ventricular ejection fraction (LVEF) was found in only 2.4% of patients. During follow-up, 25 patients reached one of the prospectively defined end points (primary composite end point of cardiac death, sustained VT or resuscitated ventricular fibrillation; secondary end point: arrhythmic events). Kaplan Meier event probability analyses revealed that only HRV, LVEF and status of the infarct-related artery were univariate predictors of death or arrhythmic events. The presence of nonsustained VT carried a relative risk of 2.6 for the primary study end point but was not a significant predictor if only arrhythmic events were considered. On multivariate analysis, only HRV, LVEF and the status of the infarct artery were found to be independently related to the primary study end point. CONCLUSIONS: There is a low prevalence of nonsustained VT shortly after AMI. Only 2% to 3% of all infarct survivors treated according to contemporary guidelines demonstrate both depressed LVEF and nonsustained VT. The predictive value of nonsustained VT for subsequent mortality and arrhythmic events is inferior to that of impaired autonomic tone, LVEF or infarct-related artery patency. Accordingly, the use of nonsustained VT to select patients for primary implantable cardioverter/defibrillator prevention trials shortly after AMI appears to be limited.
Asunto(s)
Fibrinolíticos/uso terapéutico , Infarto del Miocardio/complicaciones , Taquicardia Ventricular/epidemiología , Terapia Trombolítica , Adulto , Anciano , Angiografía Coronaria , Muerte Súbita Cardíaca/epidemiología , Electrocardiografía Ambulatoria , Femenino , Estudios de Seguimiento , Frecuencia Cardíaca , Humanos , Incidencia , Masculino , Persona de Mediana Edad , Infarto del Miocardio/diagnóstico , Infarto del Miocardio/tratamiento farmacológico , Valor Predictivo de las Pruebas , Prevalencia , Pronóstico , Estudios Prospectivos , Ventriculografía con Radionúclidos , Volumen Sistólico , Taquicardia Ventricular/diagnóstico , Taquicardia Ventricular/etiologíaRESUMEN
INTRODUCTION: Tilt table testing is widely used in the management of patients with neurocardiogenic syncope. However, the exact pathophysiologic mechanism of this disorder is still under debate. Likewise, therapy of these patients continues to represent a challenge in many cases. Therefore, the present study aimed to gain further insight into the pathophysiology of this syndrome and to examine easily accessible clinical parameters that can improve therapy selection. METHODS AND RESULTS: In 16 patients with neurocardiogenic syncope, changes in endogenous catecholamine concentrations were determined during repeated tilt table testing before and during treatment with metoprolol. Tachycardia preceded syncope in 8 of 10 responders compared to only 1 of 6 nonresponders (P < 0.05). In responders, the relative increase in epinephrine levels averaged 197% +/- 51% during drug-free tilting and 75% +/- 33% during repeated testing while on beta-blocker therapy (P < 0.05). In nonresponders, there was a smaller relative increase in epinephrine averaging 137% +/- 35% at baseline tilt. During repeated tilt testing, a similar increase was observed in these patients with recurrent syncope (156% +/- 104%; P = NS compared to baseline). CONCLUSION: In patients with neurocardiogenic syncope who show both an increase in epinephrine concentration during tilt test and sinus tachycardia prior to the onset of symptoms, beta-blocker treatment is very effective. These findings confirm the major role of sympathetic activation as a trigger of syncope. Particularly, heart rate changes at the onset of syncope may allow early identification of patients responding to antiadrenergic therapy.