here have been previous cases of left-sided heart failure soon after successful electrical cardioversion, 1-8 but the mechanism of this curious phenomenon has not yet been clarified completely. One possible cause is that left atrial mechanical activity recovers much more slowly than that of the right atrium. 1 The underlying cardiovascular disorders of these patients were rheumatic heart disease, hypertrophic cardiomyopathy, ischemic heart disease, and congenital heart disease. We present an intriguing case of restrictive cardiomyopathy that developed right-sided dominant heart failure whenever atrial fibrillation (AF) was converted to sinus rhythm spontaneously or by electrical cardioversion. We report the interesting hemodynamic profile during both AF and sinus rhythm that suggests the possible mechanism of right-sided heart failure, and the therapy that has successfully controlled recurrence of heart failure in this patient.
Case ReportA 44-year-old woman was referred to hospital in March, 2000 complaining of palpitation, heaviness in the right upper quadrant and dyspnea on exertion after a palpitation. She had had some cardiac disease diagnosed by her home doctor at 16 years of age, and had experienced occasional palpitations thereafter. At 38 years old, she sometimes felt a heaviness in the right upper quadrant, and had dyspnea when she tried to continue her work in this condition. At 40 years old, the frequency of the palpitation attacks increased
Circulation Journal Vol.67, November 2003and she was diagnosed as paroxysmal AF the next year. Medication did not control the symptoms. When the AF was converted to sinus rhythm, the feeling of heaviness in the right upper quadrant developed, with a significant increase in hepatic enzymes. In contrast, these symptoms improved during AF. The patient had also had hypothyroidism since the age of 40 years, but had become euthyroid without medication. Her mother also had had AF since the age of 40 years and after one episode of cardiac failure, she was diagnosed as cardiomyopathy.On admission, the present patient's height was 147 cm, and her weight was 53 kg. Her blood pressure was 106/66 mmHg and the pulse rate was 125 beats/min and irregular. The third heart sound was audible. The liver was palpable with tenderness 2 fingerbreadths below the xiphoid process. There was no apparent edema and her palpebral conjunctivae were not anemic.Chest X-ray revealed a cardiothoracic ratio of 60% and mild lung congestion (Fig 1). The ECG showed atrial flutter -fibrillation at a heart rate 143 beats/min with incomplete right bundle branch block and evident left ventricular hypertrophy (Fig 1).Laboratory tests revealed elevated hepatic enzymes (aspartate aminotransferase 59 U/L, alanine aminotransferase 79 U/L, -glutamyl transpeptidase 79 U/L), possibly because of liver congestion, and serum atrial natriuretic peptide (ANP) (200 pg/ml) and brain natriuretic peptide (BNP) (657 pg/ml) concentrations were also increased. Serum thyroid stimulating hormone (TSH) was mildly elevated (free...