A beneficial effect of 3-year spironolactone therapy supplementing atenolol therapy on the remodeling of atria and ventricles in a patient with permanent atrial fibrillation.

Permanent atrial fibrillation (AF) is a chronic dysrhythmia that over time promotes electrical and structural remodeling of atria and ventricles. Lack of the hemodynamically effective systole of atria synchronized with the systole of ventricles and a consequent chaotic rhythm of the ventricles result in the volumetric overload of the cardiac chambers, reduced diastolic filling and reduced stroke volume [1]. These changes are followed by a decrease in renal perfusion, activation of the adrenergic and renin– angiotensin–aldosterone (RAAS) systems. Aldosterone (ALD) concentrations are elevated in patients with persistent AF. Long lasting AF leads to interstitial fibrosis, monocytic infiltration, degeneration and atrophy of atrial myocytes, atrial and ventricular remodeling and, finally, to heart failure. Therapy with ALD induces cell proliferation and myocardial fibrosis. It may promote inflammation, oxidative stress and autonomic system dysfunction as well [2, 3]. Recent reports, some of them controversial, suggest that suppression of RAAS activity by ACE-inhibitors and angiotensin receptor antagonists may prevent the development or recurrence of AF, and inhibit atrial and ventricular remodeling [4]. We present the case of a young patient with permanent AF lasting 7 years with signs of progressive atrial and left ventricular remodeling, inhibited successfully by spironolactone—an ALD antagonist. Patient J.P., aged 39, was admitted to the II Ischemic Heart Disease Department in September 1997. AF was diagnosed. There were no symptoms of heart failure or hypertension. He had the symptoms of an upper respiratory tract infection 1 month prior to the admission. General weakness and palpitation occurred in the course of the disease. Myocarditis was excluded. After antithrombotic treatment, electrical cardioversion was performed three times without successful conversion. Due to episodes of second degree type II atrio-ventricular block, a VVI type pacemaker was implanted. The patient has been treated with 50 mg atenolol and coumarine since the discharge in 1997. No other diseases have been diagnosed. His functional status was in the NYHA II class. Progressive atrial and left ventricle remodeling was observed in echocardiographic examinations performed annually since 1997 by two independent cardiologists. Spironolactone was introduced in a daily dose of 25 mg in February 2004 in addition to previous treatment. An increase in the left ventricle ejection fraction and inhibition of atria and ventricles remodeling were observed in March 2005 and 2007 examinations (Table 1). The patient has a permanent form of AF since 1997, is clinically stable, NYHA I class, blood pressure and laboratory examinations results are normal. His exercise tolerance is good. Atrial fibrillation itself may perpetuate the development of structural atrial alterations by the increased expression of ACE, by the number of AT1-receptors in cardiomyocytes and ALD action. Angiotensin II and ALD promote activation of fibroblasts and collagen accumulation, which lead to atrial R. Dąbrowski (&) H. Szwed II Ischemic Heart Disease Department, Institute of Cardiology, Spartańska 1, 02-637 Warsaw, Poland e-mail: [email protected]