An Unusual Case of Acquired Dilated Cardiomyopathy Due to Long-Standing Patent Ductus Arteriosus.

Patent ductus arteriosus (PDA) is a common congenital cardiac condition in neonates. Its frequency is substantially higher in preterm infants, and it is frequently associated with other congenital heart defects. Its persistence into adulthood has become increasingly uncommon due to advances in neonatal screening, echocardiographic diagnosis, and timely therapeutic intervention. The hemodynamic burden imposed by PDA depends on the magnitude of the left-to-right shunt and may result in both short- and long-term complications. While small shunts may remain asymptomatic throughout life, moderate and large shunts can cause pulmonary congestion, cardiac volume overload, organ hypoperfusion, and even death, early in life. When left untreated, particularly in small-to-moderate defects that may not initially meet the criteria for intervention, chronic shunting may progressively result in pulmonary hypertension and heart failure. In adults, heart failure related to PDA is usually associated with preserved or moderately reduced left ventricular ejection fraction (LVEF), whereas severe systolic dysfunction and acquired dilated cardiomyopathy are exceptionally rare. Here, we present the case of a 70-year-old male who was admitted with progressive dyspnea, orthopnea, dry cough, and bilateral lower extremity edema over one month. His medical history included PDA diagnosed in childhood, without intervention or regular follow-up. On admission, physical examination revealed signs of acute heart failure, including tachypnea, jugular venous distension, pulmonary congestion, and marked peripheral edema. Cardiac auscultation demonstrated a prominent second heart sound and systolic murmurs consistent with mitral and tricuspid regurgitation, and a characteristic continuous, "machinery" murmur suggestive of PDA. Electrocardiography showed sinus rhythm with frequent atrial and ventricular premature beats, poor R-wave progression in the precordial leads, and nonspecific ST-T abnormalities in the limb leads. Chest radiography demonstrated cardiomegaly, pulmonary vascular congestion, alveolar edema, and bilateral pleural effusions. Laboratory evaluation revealed elevated natriuretic peptide levels and mildly increased high-sensitivity cardiac troponin I, consistent with the setting of acute heart failure. Transthoracic echocardiography revealed dilation of all four chambers and severe biventricular systolic dysfunction, with an LVEF of 25%, mild mitral and tricuspid insufficiency, and increased systolic pressure in the pulmonary artery. A moderate left-to-right shunt was found. Evaluation by coronary angiography ruled out obstructive coronary artery disease. Further assessment with cardiac magnetic resonance imaging demonstrated a persistent communication between the aortic isthmus and the main pulmonary artery, confirming PDA. A diagnosis of acquired dilated cardiomyopathy secondary to long-standing left-to-right shunt, likely precipitated by frequent atrial and ventricular arrhythmias, was established. Although the patient was a candidate for transcatheter percutaneous ductal closure, he declined any intervention, and optimized guideline-directed medical therapy was initiated. This case represents an exceptionally rare presentation of PDA in adulthood and highlights the importance of lifelong medical surveillance in patients with congenital heart defects.