Abstract

Sirs, A 69-year-old caucasian man was admitted to the Emergency Department for worsening dyspnea (NYHA II–III) and paroxysmal nocturnal dyspnea. The symptoms had appeared in the last months and had progressively worsened through the last 6 weeks. He referred no angina or syncope. The patient’s clinical history was absolutely negative and he reported none of the major cardiovascular risk factors. A physical exam was essentially unremarkable except for the presence of bilateral basal crepitations and mild bilateral ankle edema. Blood pressure was 100/ 60 mmHg. An ECG showed atrial fibrillation with a ventricular rate of 130/min and no sign suggestive of acute ischemia. Blood analysis showed elevated creatinine (1.6 mg/dl) and BNP (750 pg/ml). All other parameters, including C-reactive protein, were normal. Therapy with loop diuretics, 100 mg aspirin and amiodarone was started. On the first day after admission, the patient was asymptomatic and his heart rate was 90/min, and ECG showed atypical atrial flutter with irregular AV conduction. Echocardiography showed a dilated left ventricle (end-diastolic volume 130 ml) with global hypokinesia and an ejection fraction of 25%. Both atria were dilated, and there was a mild to moderate (secondary) mitral insufficiency. On day 5 after admission, a cardiac magnetic resonance and a coronary angiography excluded the presence of coronary artery disease, prior myocardial infarction and of signs suggestive of myocarditis. Left and right heart catheterization showed data compatible with heart failure (Table 1), and moderate to severe mitral regurgitation. The patient was discharged with a diagnosis of dilated cardiomyopathy and was prescribed amiodarone, spironolactone (25 mg o.d.), low-dose b-blockers (carvedilol 6.25 mg b.i.d), angiotensin converting enzyme (ACE)-inhibitors (ramipril 2.5 mg o.d.), low-molecular weight heparin (followed by oral anticoagulants). An electrophysiology examination was scheduled for the next 6 weeks. Further, since the patient appeared to be hemodynamically stable after initiating therapy with the above drugs, hydralazine (25 mg b.i.d.) and the oral organic nitrate pentaerythrityl tetranitrate (PETN, 50 mg t.i.d) were also added. Six weeks later, the patient was admitted again for the scheduled electrophysiology examination and follow-up right heart catheterization. He had scrupulously followed the therapy prescribed and had been essentially asymptomatic since discharge, and his mean heart rate was 80/ min. At this time, echocardiography, as well as left and right heart catheterization showed a marked improvement in the parameters of left ventricular performance (Table 1; Fig. 1). The mitral regurgitation was only mid-grade. The patient underwent the electrophysiology examination and successful cavotricuspid isthmus ablation. We describe a case of dilated cardiomyopathy in which medical treatment with a combination of antineurohormonal drugs and nitrate/hydralazine led to a dramatic improvement in symptoms and hemodynamic variables. Organic nitrates are widely used in the therapy of patients with chronic congestive heart failure, especially in North America [1], and the coadministration with the vasodilator and antioxidant [2] hydralazine has been associated with improvements in exercise tolerance, left ventricular size, systolic function, ischemia, cardiac remodeling [3] and, ultimately, mortality in African Americans [4]. Of note, this benefit appears to be T. Gori (&) T. Munzel 2. Medizinische Klinik, Universitatsmedizin der Johannes Gutenberg-Universitat Mainz, Mainz, Germany e-mail: tommaso.gori@ukmainz.de; tomgori@hotmail.com

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