Despite medical treatment, including diuretics and angiotensin-converting enzyme inhibitors, his condition irreversibly deteriorated beyond repair. RV function, measured with scintigraphy, indicated a marked deterioration from 50% to 20% ( Table 1). In 1998, SPECT imaging demonstrated a clear dilation of the RV ( Figure 2). The QRS gradually widened, from 90 ms in 1989 to 200 ms in 1998, and the QTc fluctuated between 338 and 410 ms ( Figure 1A– 1C, Table 1). These signs led to a definitive ACM diagnosis. However, progressively, over 24 years of follow-up, the right ventricle (RV) became dilated ( Figure 2) and the T waves became negative in leads V 1 to V 3 ( Figure 1A). Sotalol (240 mg/day) reduced the symptoms. Two years later, he experienced palpitations and unsustained ventricular tachycardia. The patient underwent automatic defibrillator implantation and was treated with nadolol. The patient had normal results on an echocardiogram, cardiac computed tomography scan, phase-analysis SPECT angio-scintigraphy ( Figure 2), and an exercise stress test. C: Plot shows how the durations of the corrected QT (ms, black, left axis) and QRS (ms, red, right axis) evolved in the index patient. B: Short premature ventricular beats that triggered ventricular fibrillation in 19. A: Twelve-lead electrocardiograms performed at the time of the initial event ( left), 4 years later ( middle), and 9 years later ( right). Electrocardiograms and electrical characteristics.
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