Cardiomyopathy implantable cardioverter-defibrillator

Abstract Two thirds of the nearly half a million deaths per year in the United States due to sudden cardiac death (SCD) is attributed to coronary artery disease (CAD) and most commonly results from untreated ventricular tachyarrhythmias. Patients with ischemic cardiomyopathy and left ventricular dysfunction are at highest risk for SCD, but this still defines only a small subset of patients who will suffer SCD. Multiple lines of evidence now support the superiority of implantable cardioverter defibrillator (ICD) therapy over antiarrhythmic therapy for both primary and secondary prevention of SCD in advanced ischemic heart disease. Optimization of ICD therapy in advanced ischemic cardiomyopathy includes preventing right ventricular pacing as well as the use of highly effective anti-tachycardia pacing to reduce the number of shocks. While expensive, ICD therapy has been shown to compare favorably to the accepted standard of hemodialysis in cost effectiveness analyses. 

In a 62-year-old man with dilated cardiomyopathy and an implantable cardioverter defibrillator for ventricular tachycardia, microvolt T wave alternans differed when amiodarone was added (55). The onset heart rate with T wave alternans was lower and the alternans voltage higher with amiodarone than without it. 

Strickberger SA, Hummel JD, Bartlett TG, et al. Amiodarone versus implantable cardioverter-defibrillator randomized trial in patients with nonischemic dilated cardiomyopathy and asymptomatic nonsustained ventricular tachycardia. AMIOVIRT. J Am Coll Cardiol 2003 41 1707-1712. 

Patients with hypertrophic cardiomyopathy (HCM) who are at high risk for sudden cardiac death should receive an implantable cardioverter-defibrillator (ICD). 

FIGURE 18-4. Treatment algorithm for hypertrophic cardiomyopathy. ACEI = angiotensin-converting enzyme inhibitor NSVT = nonsustained ventricular tachycardia ICD = implantable cardioverter-defibrillator LV = left ventricular SCD = sudden cardiac death. 

FIGURE 1.6 Kaplan-Meier estimates of death from any cause in patients with both ischemic and nonischemic cardiomyopathy randomized to amiodarone, placebo, or implantable cardioverter-defibrillator therapy in SCD-HeFT. (From Ref. 29, with permission.)... 

Roes SD, Borleffs CJ, van der Geest RJ, Westenberg JJ, Marsan NA, Kaandorp TA et al. Infarct tissue heterogeneity assessed with contrast-enhanced MRl predicts spontaneous ventricular arrhythmia in patients with ischemic cardiomyopathy and implantable cardioverter-defibrillator. Circulation Cardiovascular Imaging. 2009 2(3) 183-190. 

Coirado, D., et al, Implantable cardioverter-defibrillator therapy for prevention of sudden death in patients with arrhythmogenic right ventricular cardiomyopathy/ dysplasia. Circulation, 2003. 108(25) p. 3084-91. 

Gomick CC, Hauser RG, Ahnquist AK, and Maron BJ. Unpredictable implantable cardioverter-defibrillator pulse generator failure due to electrical overstress causing sudden death in a young high-risk patient with hypertrophic cardiomyopathy. Heart Rhythm 2005 2 681-683. 

A potential case of an interaction between quinidine and flucloxacillin was demonstrated in a 63-year-old patient with recently diagnosed dilated cardiomyopathy who was admitted to the hospital with polymorphic ventricular tachycardia and ventricular fibrillation episodes induced by bradycardia. The patient was on a heart failure regimen of furosemide, spironolactone and perindopril, and was initiated on oral quinidine in the hospital for the prevention of ventricular arrhythmias. The patient s temporary pacemaker lead was removed and an implantable cardioverter-defibrillator was placed due to continued ventricular fibrillation. The next day, the patient became febrile. Culture of pacemaker lead tip and blood cultures were positive for S. aureus. Flucloxacillin and rifampin were initiated, but rifampin was discontinued due to the development of renal insufficiency and liver test abnormalities. These were normalised after rifampin was discontinued. The patient required continuous pacing to prevent ventricular tachycardia episodes, and quinidine was increased to 2800 mg per day (maximum daily dose). Quinidine plasma levels were subtherapeutic at 1.1 mg/L. The authors speculate that this interaction was due to quinidine being a substrate of Pgp and CYP3A4, and flucloxacillin s ability to induce these enzymes. While this may be a potential mechanism, the authors do not comment on how long the patient received rifampin. Rifampin is also a CYP3A4 inducer and could have been parf of fhe reason for fhe decrease in quinidine level [46 ]. 

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