Acute precipitants of NSVT include MI, cardiac surgery, electrolyte and metabolic abnormalities, antiarrhythmic drugs, QT prolongation, and pulmonary edema. NSVT
caused by an acute precipitant often resolves promptly with resolution of the precipitating condition. Chronic treatment depends on the continued presence of the arrhythmia, patient age, heart disease, and symptoms. After patient stabilization and after correction of potential precipitants, evaluation and long-term therapy should be considered if NSVT persists.
The prognostic significance of NSVT that occurs early after an acute MI remains uncertain (see Fig. 3D). Monomorphic NSVT after acute MI has been reported to occur in as few as 1% and as many as 75% of the patients. In a recent report, 10 ± 6 d after an acute MI, (52) 9% of 325 consecutive patients had NSVT. The predictive value of NSVT increases the further out from MI it occurs. Initially, conservative management is generally indicated: beta-blocker therapy (but not titrated to suppress NSVT), assessment of ischemia, and determination of left ventricular function. Revascularization should be undertaken if indicated. If NSVT persists and impaired left ventricular function (LVEF <0.4) is present, electrophysiology testing for risk stratification should be considered. Potential causes of polymorphic NSVT include ischemia, electrolyte disturbance, drug pro-arrhythmia, and coronary reperfusion (see Fig. 3D). Supplementation with magnesium sulfate may reduce ventricular ectopy, but data on improved survival are questionable. Lidocaine, or any antiarrhythmic drug, does not appear to improve survival when given acutely or chronically.
Limited data address the prognostic significance of NSVT in acute infarction. In one study of 112 patients with NSVT within 72 h of an acute MI, in-hospital VF occurred more frequently in the NSVT group (9% vs 0% in the control group; p < 0.001), but total mortality during hospitalization and after discharge did not differ significantly (39). Multivariate analysis identified time from presentation to occurrence of NSVT as an important predictor of mortality (p < 0.0001). The increased relative risk of NSVT first became significant at 13 h from presentation; this risk increased as the interval from presentation to occurrence of NSVT increased. The risk plateaued at 24 h with a relative risk of 7.5. Contrary to prevailing clinical opinion, NSVT that occurs in the setting of acute MI may have important prognostic significance. Notably, in this group, beta-blocker usage at hospital discharge was also significant predictor of survival (p < 0.0001).
In a report of 185 patients with ventricular arrhythmias after coronary-bypass graft (CABG) surgery, 108 had NSVT (97). NSVT did not predict early mortality, and usually disappeared late after the operation. If NSVT is present preoperatively, and the LVEF is <0.40, postoperative monitoring for NSVT is recommended. If NSVT persists, a postoperative electrophysiology test should be considered, although recent CABG excluded patients from enrolling in MADIT and MUSTT (98). If noncardiac surgery is planned and NSVT is present, the patient's symptoms, chronicity of the problem, medical regimen, and underlying heart disease should be considered. Ischemia and a progression of cardiac disease should be excluded prior to surgery. If the LVEF is <0.40 in the setting of CAD, EP testing should be considered preoperatively. If there is an inducible sustained ventricular tachyarrhythmia, ICD implantation should be considered prior to elective surgery. If there is new-onset NSVT after cardiac surgery, without an acute change in cardiac condition, the prognostic significance is unclear. Beta-blocker therapy may be useful in this setting. In many patients, NSVT resolves spontaneously within 7-14 d. If NSVT persists in the setting of left ventricular dysfunction, an electrophysiology test is indicated, with ICD implantation if positive.
The prognosis is generally excellent in patients with idiopathic VT (IVT). Idiopathic NSVT usually arises from the RVOT (repetitive monomorphic, or exercise-induced) (see Fig. 3K) or the left ventricular apical septum ("Bellehassen's" tachycardia) (98a). The 12-lead ECG characterization of the morphology of the NSVT is useful to determine the location of the NSVT if ablative therapy is considered. If NSVT is an incidental finding in a patient with no known heart disease, an appropriate evaluation includes an echocardiogram and a treadmill test. Given the excellent prognosis in the absence of structural heart disease, therapy is usually directed at symptoms. If tachycardia is frequent or incessant, however, patients may be at risk of tachycardia-induced cardiomyopathy, and therapy should be recommended. Idiopathic RVOT tachycardia frequently responds to a beta-blocker, and idiopathic left ventricular VT may be more responsive to verapamil. If ineffective and/or intolerable symptoms occur, other drugs to consider include propafenone or flecainide (second-line), sotalol (third-line), and amiodarone. Ablation is a highly effective therapy for these patients, and should also be considered a first-line therapy. Referral to an electrophysiologist is recommended for these patients. Optimal management of patients with atypical forms of IVT is not clear (see Fig. 3I).
Bidirectional or polymorphic NSVT in a young individual, even if there is no apparent heart disease, may be life-threatening (see Fig. 3J). Treatment with a beta-blocker may be effective. Similarly, the presence of nonsustained PVT in a patient with congenital LQTS requires initial treatment with a beta-blocker and referral to an electrophysiologist. These patients are now being treated with ICDs more frequently when a significant risk of sudden cardiac death is suspected (98b). Discontinuation of the offending agent, and avoidance of QT-prolonging drugs in the future, are frequently sufficient in patients with acquired LQTS.
An exacerbation of heart failure can trigger NSVT. Treatment with intravenous (iv) inotropic agents, diuretics, digoxin, and antiarrhythmic drugs may trigger or exacerbate ventricular arrhythmias. Toxid and metabolic disturbances (e.g., hypoxia, hypokalemia, or acidosis) may be contributory. Pharmacologic therapy should be optimized in all of these patients.
NSVT is not rare in patients with ischemic cardiomyopathy (see Figs. 2A, 3A). If there are no symptoms, a SAECG or other noninvasive marker (such as TWA or HRV) may give further prognostic information when the ejection fraction is greater than 0.40, but there is no evidence thus far that any therapy—pharmacologic or ICD—will improve the prognosis in this patient group. In general, the noninvasive tests are relatively nonspecific and insensitive. Beta-blockers are recommended unless contraindications exist. If there are severe symptoms associated with NSVT, beta-adrenergic blockers sotalol or amiodarone (started in the hospital) may be needed to suppress frequent recurrences. If the LVEF is <0.40, patients should be referred for electrophysiology testing, with ICD implantation if positive. Screening for NSVT in this cohort is reasonable. It is still premature to suggest that all patients with NSVT, CAD and impaired left ventricular function require ICD implantation.
The best long-term therapy for NSVT in patients with dilated (i.e., nonischemic) cardiomyopathy (see Figs. 3B, 3G) is a matter of debate, because of conflicting data. Based on available data, asymptomatic NSVT does not require antiarrhythmic therapy for suppression or protection. Ongoing ICD trials such as DEFINITE may help to define the efficacy of ICD implantation (91c) in this setting. Preliminary results of the AMIOVERT trial suggest no benefit to ICD implantation compared with amiodarone (91d). If there are symptomatic episodes of NSVT, empiric treatment with amiodarone is reasonable. This may improve symptoms; the effect on prognosis is unclear. Few data guide the management of patients with infiltrative cardiomyopathies and NSVT.
NSVT can potentially forecast a malignant, life-threatening ventricular arrhythmia, and occurs in 10-20% of patients with hypertrophic cardiomyopathy (see Fig. 3H). It is premature to suggest that ICD implantation is needed in all asymptomatic patients with hypertrophic cardiomyopathy and NSVT. No specific antiarrhythmic therapy is recommended, but restriction from athletics is mandatory and a beta-adrenergic blocker is the recommended first-line option. Amiodarone has been used in some patients with NSVT. ICD implantation is controversial in this patient population for NSVT, although the trend is to implant "high-risk" patients (98c). Electrophysiology testing is of no proven benefit in this setting. NSVT may indicate higher mortality than patients without VT, but no drug therapy has been proven to improve survival.
If there are severe symptoms or family history of sudden death, an ICD should be considered. If there are episodes of frequent NSVT, a beta-blocker is an appropriate initial therapy. If symptoms persist, sotalol or amiodarone may be beneficial. The implantation of an ICD may be appropriate, but little data exists.
Few data guide the management of patients with NSVT in the setting of acute myocarditis (98d). The fact that many patients will have significant or even complete recovery of ventricular function tempers enthusiasm for very early ICD implantation.
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