FIGURE 17-1 Telemetry monitor recording from the fourth day after the patient’s acute myocardial infarction (MI). Nonsustained ventricular tachycardia (NSVT) is demonstrated on the telemetry strip.

CASE EXPLANATION AND OVERVIEW

This patient has had an episode of NSVT 4 days after an acute anterior myocardial infarction (MI) in the setting of LV dysfunction documented on echocardiogram. Management considerations for this patient include determining the prognostic significance of his NSVT and determining whether further therapy is indicated either while he is still an inpatient or during outpatient follow-up.

Historically, NSVT has been defined in a number of ways based on the duration and rate of the observed arrhythmia.¹ The standard definition is three or more consecutive ventricular premature depolarizations at a rate of at least 100 beats/min, lasting up to a maximum duration of 30 seconds before spontaneous termination.² The rate cutoff of 100 beats/min is based on the observation that tachycardias slower than this rate do not generally confer adverse prognostic significance in patients who have a history of MI.³

The prevalence and prognostic significance of NSVT in a given patient depends upon the presence and extent of structural heart disease. Up to 3% of asymptomatic patients with no evidence of heart disease have been shown to experience runs of NSVT over the course of 24 hours of monitoring, but the prognostic significance of this finding remains unclear.⁴ In contrast, NSVT occurring in patients who have suffered an MI or have a history of idiopathic dilated cardiomyopathy,⁵ valvular heart disease such as mitral valve prolapse,⁶ longstanding hypertension and left ventricular hypertrophy,⁷ and hypertrophic cardiomyopathy⁸ is more common and may function as an independent predictor of mortality under certain situations. However, this does not mean that NSVT independently predicts arrhythmic death. NSVT in the post-MI period, such as that which occurred in the Case Presentation, portends a worse overall prognosis, but the incidence of sudden cardiac death (SCD) in patients with NSVT is not increased out of proportion to the increase in total mortality in this patient population.

In the following sections, we will outline the prognostic significance and management considerations of NSVT in patients with a history of MI.

ETIOLOGY AND PATHOPHYSIOLOGY

Unlike sustained tachyarrhythmias, NSVT is usually not associated with symptoms in patients with structural heart disease (because most episodes are brief); rather, it is usually discovered incidentally during electrocardiographic monitoring. Early studies that identified NSVT as a risk factor for the development of sudden death in patients with a recent MI were based on the observation that ventricular fibrillation in the acute phase of MI was often preceded by escalating frequency of ventricular ectopy and NSVT. Later studies demonstrated an association between the presence of NSVT discovered in the early postinfarction period and risk of SCD in patients with reduced left ventricular ejection fraction (LVEF).⁹ With rare exception, most data suggest that NSVT within the first 48 hours after an MI does not carry prognostic significance.¹⁰ By contrast, NSVT occurring after the first 48 hours after an MI has been linked with an increased risk of both SCD and total mortality in pre-reperfusion era studies,¹¹ and NSVT was accordingly used as a qualifying characteristic in early implantable cardioverter-defibrillator (ICD) trials in patients with prior MI and LV systolic dysfunction.^12,13 It is important to note, however, that the increased risk of SCD in patients with NSVT is due to the increased risk of total mortality in these patients and not due to any specific predilection to sustained ventricular arrhythmias. Indeed, in a subgroup analysis of the first 1480 patients enrolled in the MUSTT study, Buxton et al found that electrocardiographic characteristics of spontaneous NSVT in patients with coronary artery disease cannot differentiate between patients with and those without sustained VT inducible by programmed stimulation.^14,15 In these patients, NSVT portends a worse overall prognosis, but the risk of SCD is not increased out of proportion to the risk of total mortality. A post-hoc analysis of the relation of LVEF and inducible VT to mode of death in MUSTT-enrolled patients (who all had significant LV dysfunction and spontaneous asymptomatic NSVT) demonstrated a significantly higher risk of mortality in those patients whose LVEF was <30%, regardless of the presence or absence of inducible sustained VT that might predict risk for VT. In these patients, it is the presence and severity of heart failure that serves as a major determinant of total mortality. Furthermore, the percent of total mortality accounted for by arrhythmic events was similar regardless of whether the LVEF was <30% or ≥30% and would likely also be similar whether or not there was a history of documented NSVT.¹⁶

In the reperfusion era, the presence of NSVT has become a less significant risk stratification tool following an MI, as newer data have not identified an independent association between NSVT and worse prognosis in many situations.^17,18 In the absence of other risk factors such as low LVEF, NSVT predicts neither inducibility of sustained monomorphic VT nor total mortality in patients post-MI. The reason for this is probably multifactorial and has to do with the fact that early reperfusion strategies and the ubiquitous use of β-blocker therapy have reduced both the incidence of NSVT and postinfarction scar burden even in patients who do have NSVT.

MANAGEMENT

The patient described in the Case Presentation has been noted to have asymptomatic NSVT in the setting of an LVEF estimated to be between 35% and 40% after his acute MI. The first question is whether this observation portends worse prognosis. As discussed in the previous section, the more significant issue is his LV dysfunction (reflected both by EF and clinical evidence of heart failure), and he will require optimal medical management and follow-up echocardiography as an outpatient to determine his long-term total mortality. Demonstrating persistent LV dysfunction during follow-up 2 to 3 months after his MI is likely to have greater prognostic utility than observing episodes of NSVT. If LV dysfunction persists in the months-to-years after his MI, his total mortality risk will be higher, but his risk of SCD requires other prognostic variables for accurate risk stratification. Unfortunately, while the LVEF correlates with overall survival, it tells us nothing about how patients die (suddenly versus nonsuddenly).

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