Electrical Instability Heralding Worsening Heart Failure in a Patient With Nonischemic Dilated Cardiomyopathy

A patient with idiopathic dilated cardiomyopathy and New York Heart Association (NYHA) class II heart failure (HF) underwent prophylactic implantation of an implantable cardioverter-defibrillator (ICD) with home monitoring capability. Three months later he had an episode of asymptomatic nonsustained ventricular tachycardia (NSVT), which heralded worsening HF within 3 weeks. After a period of electrical and clinical stability he had 2 episodes of asymptomatic self-terminating ventricular tachycardia/ventricular fibrillation (VT/VF), which again preceded clinical decompensation by 3 weeks. This report shows that the development of asymptomatic nonsustained VT/VF may predict HF exacerbation and that home-monitoring capabilities might alert the physician to the need for closer follow-up (weekly nurse visits, frequent blood pressure and weight measurements, and up-titration of medications, especially β-blockers and angiotensin-converting enzyme inhibitors) and possibly earlier, more aggressive therapy if these measures fail (inotropic support, need for listing for heart transplant). Decompensated congestive HF (CHF) remains a major cause of morbidity, mortality, and soaring health care costs. Current clinical predictors of impending HF exacerbation (eg, weight gain, edema, dyspnea) occur relatively late in the course of cardiac decompensation and, thus, have limited utility. Hence, it is important to identify novel markers of impending HF exacerbation in order to better prevent disease progression. Ideally, these markers would occur very early, prior to the onset of hemodynamic deterioration and clinical decompensation. While the presence of NSVT is not a clinically robust independent marker of increased mortality or risk of arrhythmic death,1,2 studies have shown that patients with ischemic and nonischemic cardiomyopathy who receive ICD shocks have a poor long-term prognosis.3–5 However, asymptomatic, nonsustained VT/VF has not been studied as a predictor of impending HF exacerbation, primarily due to the difficulty in reliably and continuously detecting these subclinical rhythms over extended periods of time. However, with the current availability of remote telemonitoring systems in patients with ICDs, one can continuously monitor electrical parameters and prospectively relate them to the development of HF exacerbations. In this report we describe a patient in whom nonsustained asymptomatic VT/VF, detected by home monitoring, heralded impeding HF exacerbation by several weeks. A 51-year-old man with idiopathic dilated cardiomyopathy diagnosed in 2001, hypertension, mild renal insufficiency (baseline creatinine, 1.6 mg/dL), and NYHA class II HF underwent ICD implantation for primary prophylaxis. He had no history of prior cardiac arrest or syncope but was hospitalized once in the past 12 months for HF exacerbation (in November 2004, during Thanksgiving due to noncompliance with diet). At the time of implant, his blood pressure was 94/62 mm Hg and heart rate was 54 beats per minute (bpm). He had normal first and second heart sounds with II/VI pan-systolic murmur and normal jugular venous pressure and his chest was clear to auscultation. His abdomen was not distended and he had trace lower extremity edema. His medications included carvedilol 25 mg twice a day, lisinopril 20 mg once a day, simvastatin 40 mg once a day, aspirin 81 mg once a day, eplerenone 25 mg once a day, furosemide 100 mg twice a day, digoxin 0.125 mg once a day, and colchicine 0.6 mg once a day. Electrocardiography findings showed sinus bradycardia, left anterior fascicular block, and a QRS width of 104 ms. Two-dimensional echocardiography revealed 4-chamber enlargement, moderate mitral regurgitation, and an ejection fraction of 10%. A single-chamber ICD with home telemonitoring (Lexos VR-T; Biotronik, Inc, Berlin, Germany) was implanted in July 2005. The patient had an uneventful course during the 3 months following the procedure. He did not have any ventricular ectopy during that time. In October 2005, his ICD detected an episode of NSVT and transmitted a message informing the physician of the event. On device interrogation, the patient was found to have an episode of fast NSVT that terminated prior to receiving therapy (13 beats, cycle length 284 ms) (Figure 1). The baseline programming parameters were VVI with backup pacing at 40 bpm and he was paced only 8% of the time and no changes were made. The patient was at his baseline functional status (NYHA class II), and he completely denied any worsening HF symptoms. His electrolyte and digoxin levels were normal (potassium, 4.4 mm/L; magnesium, 2.1 mg/dL), and he did not have any evidence of volume overload. Given his clinical stability, he remained on the same medical regimen. Intracardiac electrography and marker channel of nonsustained ventricular tachycardia detected by home monitoring. HV indicates high-voltage electrography (superior vena cava coil to tip); V, right ventricular bipolar electrography. Within 4 weeks, however, he developed significant dyspnea despite full compliance with diet and medical therapy. The patient was hospitalized for worsening HF, and a right heart catheterization revealed a pulmonary capillary wedge pressure of 27 mm Hg, pulmonary artery pressure of 67/38 mm Hg, and a cardiac index of 1.8 L/min/m2. He was listed for transplant, and intravenous milrinone was initiated with subsequent improvement in symptoms. He was discharged home on continuous milrinone infusion and did well for the following 3 weeks, but, in early December, his device detected and transmitted an episode of self-terminating VF (22 beats, cycle length 224 ms) (Figure 2) and an episode of NSVT (14 beats, cycle length 278 ms). The patient was seen in the clinic and again he denied any new symptoms or signs of worsening HF. He was compliant with his diet and medications and did not have evidence of volume overload. No changes were made in his regimen. Intracardiac electrocardiography and marker channel (as above) of self-terminating ventricular fibrillation detected by home monitoring. Three weeks later, the patient complained of lightheadedness and was found to be hypotensive (blood pressure, 66/46 mm Hg; heart rate, 105 bpm). The carvedilol dosage was reduced, but increased weight gain and dyspnea progressed despite increased diuretics. He was subsequently admitted with decompensated HF. The milrinone was increased and he was placed on an intravenous furosemide drip. His condition improved following 3 weeks of inpatient therapy; however, the improvement was transient and he was readmitted within 2 weeks with recurrent severe decompensation. An intra-aortic balloon pump was inserted and this was soon followed by left ventricular assist device implantation and ultimately heart transplantation. Sudden cardiac death is the most common cause of death in patients with NYHA class II/III HF, while most patients with NYHA class IV HF die of pump failure.6 Although asymptomatic ventricular arrhythmias have been associated with a poor prognosis in some studies,7–9 they do not independently increase mortality after adjustment for LV ejection fraction.1,2 It is well known that worsening HF can lead to ICD shocks10,11 and that the development of ICD shocks in patients with ischemic cardiomyopathy is associated with increased long-term HF hospitalization and mortality.3 However, a direct link between individual episodes of asymptomatic nonsustained VT/VF (not requiring shocks) and subsequent HF decompensation has not been described in these patients. Similarly, while multiple shocks due to VT clusters portend a poor prognosis in patients with dilated cardiomyopathy,4,5 the significance of asymptomatic VT/VF in these patients has not been well studied. Furthermore, there is no data demonstrating that episodes of asymptomatic nonsustained VT/VF are predictive of impending HF exacerbation. This is in large part due to the fact that monitoring systems capable of real-time detection and early physician notification, thereby allowing prospective follow-up, have not been available until recent times. While milrinone infusion could have caused the patient’s NSVT prior to his second decompensation, the NSVT still heralded his clinical deterioration by several weeks. This report demonstrates that asymptomatic nonsustained VT/VF can herald impeding HF exacerbation and that the onset of the electrical instability may precede clinical decompensation by several weeks. Large-scale outcome studies using home monitoring technology are needed to determine whether asymptomatic nonsustained VT/VF may be a marker of impending HF. In addition, other characteristics of the ventricular ectopy detected by telemonitoring systems (ie, premature ventricular complex burden, VT cycle length) may also carry predictive value. This is of utmost importance because current clinical markers of impending HF occur late in the course decompensation. Thus, there is an acute need to identify novel markers that occur at an early stage before severe deterioration occurs. Early and aggressive preventative treatment of HF exacerbation requires identification of novel markers of impending decompensation. While no firm conclusions can be drawn on the basis of one patient, this report provides evidence that asymptomatic NSVT detected by home monitoring technology may herald impending HF exacerbation and that the onset of the electrical instability may precede clinical decompensation by several weeks. Large randomized studies using home monitoring technologies are needed to demonstrate this point. Acknowledgments: The author would like to acknowledge Dr Joseph G. Akar for helping in editing the manuscript.