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Hemodynamically Tolerable VT

The management of patients with CAD or nonischemic dilated cardiomyopathy who present with hemodynamically tolerable VT with no or minimal symptoms is controversial. Studies that evaluate the effectiveness of the ICD in reducing mortality for this group of patients are few. A subset of patients who initially present with hemodynamically tolerable VT treated with drug or ablative therapy may subsequently present with a lethal ventricular event, for which ICD therapy may be useful. We suggest that the treatment strategy for these patients should be based on four guiding principles: 1) the status of left ventricular function; 2) the frequency of arrhythmic recurrences; 3) the inducibility of poorly tolerated arrhythmias; and 4) the outcome of a detailed discussion with the patient in which treatment options and risks are outlined. Left ventricular dysfunction is a poor prognostic variable. Mechanisms of death for patients with cardiomyopathies include both ventricular tachyarrhythmias and progressive CHF. Although the MUSTT trial was a primary prevention study, extrapolating the data to post-infarct patients with sustained tolerable VT suggests that ICD implantation for patients with EF <40% is appropriate (31,32). Inducibility of poorly tolerated arrhythmias during electrophysiology testing before and after drug or ablative therapy suggests a higher-risk population.

The management of patients with EF >40% and tolerable VT in the setting of ischemic or nonischemic heart disease is more difficult. Patients with frequent VT episodes need drug or catheter ablative therapy to prevent frequent recurrences. We have been pleased with the outcome of ablation for frequent stable VT; and advocate the approach over chronic drug administration. A final decision should be made on an individual basis after a discussion of options between the patient and physician.

Summary of Secondary Prevention in Patients With Hemodynamically Tolerable VT

The management of patients with ischemic or nonischemic dilated cardiomyopathy with tolerable VT should be approached on an individual basis. Extrapolating from primary prevention studies, it is appropriate to implant defibrillators in post-infarct patients with EF <40%. Patients with an EF >40% should be managed based on the frequency of VT occurrences. Those patients with frequent arrhythmias should be considered for catheter ablative therapy. Inducibility of more rapid VT suggests the need for ICD therapy.

VT in the Setting of Other Cardiac Disorders

Monomorphic VT occurs in other cardiac disorders associated with myocardial disease or fibrosis. These include arrhythmogenic RV dysplasia (ARVD), hypertrophic cardiomyopathy, incisional VT related to prior ventriculotomy, infiltrative cardiac disorders (sarcoid, amyloid, or malignancy), and inflammatory disorders (myocarditis). The underlying disease should be treated. Factors that should be considered in the management of these patients include: 1) the overall prognosis; 2) left ventricular function and associated prognostic variables; 3) VT tolerability; and 4) the documented effectiveness of different therapeutic options for the specific disorder.

Arrhythmogenic RV dysplasia. Arrhythmogenic RV dysplasia (ARVD) was first described by Fontaine in 1977 (45). Pathologically, it is associated with fatty infiltration of the right ventricle. The disease has a slight male preponderance. The underlying

BASELINE- NSR ARVD TACHYCARDIA

BASELINE- NSR ARVD TACHYCARDIA

Fig. 8.12-lead ECG recording of sinus rhythm (left) and VT (right) from a patient with arrhythmogenic right ventricular dysplasia. Note the right precordial T-wave inversion in the sinus rhythm tracing and the spontaneous VPD which matches the VT morphology. NSR = normal sinus rhythm, ARVD = arrhythmogenic right ventricular dysplasia.

Fig. 8.12-lead ECG recording of sinus rhythm (left) and VT (right) from a patient with arrhythmogenic right ventricular dysplasia. Note the right precordial T-wave inversion in the sinus rhythm tracing and the spontaneous VPD which matches the VT morphology. NSR = normal sinus rhythm, ARVD = arrhythmogenic right ventricular dysplasia.

mechanism for VT is believed to be reentry. Because the tachycardia typically arises from the RV, it gives rise to a left bundle-branch block (LBBB) morphology with a variable frontal axis, depending upon the site of involvement (Fig. 8). Poor R-wave progression in the precordial leads is expected. The characteristic resting ECG shows right atrial enlargement, right axis deviation, incomplete RBBB, inverted T waves in the right precordial leads and an epsilon wave in lead V1. The epsilon wave represents slow conduction in the dysplastic RV free wall (46). Treatment options include drugs (beta-blockers, Type 1 and 3 antiarrhythmic agents), catheter ablation (46a), surgery, and ICD implantation.

Hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy is a primary cardiac disease characterized by right or left ventricular hypertrophy (LVH), or both in the absence of another cardiac or systemic cause for hypertrophy. The majority of cases are caused by autosomal dominant inherited mutations in genes encoding cardiac sarcomeric proteins. Rhythm abnormalities include atrial fibrillation (AF), heart block, pre-excitation, VT, and sudden death. VT occasionally originates from left ventricular apical aneurysms in patients with midcavitary obliteration or from the interventricular septum in patients with left ventricular outflow-tract (LVOT) obstruction (47,48). Several risk factors are associated with sudden death, including: 1) severe and diffuse hypertrophy; 2) NSVT; 3) inducible VT/VF; 4) history of syncope; and 5) family history of sudden death. Although prophylactic therapy with amiodarone is associated with a significant reduction in sudden death rate in patients with hypertrophic cardiomy-

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