An 82-year-old woman with a history of mild hypertension reported fatigue on strenuous exertion since adolescence that was not investigated. The fatigue had worsened progressively until it was triggered by minimal exertion over the previous year.

Echocardiography performed at another center revealed a dilated left ventricle with non-hypertrophied walls, global systolic dysfunction (ejection fraction 37%) but no wall motion abnormalities, mild mitral regurgitation and left atrial dilatation. She also presented moderate tricuspid regurgitation, moderate pulmonary hypertension (estimated at 49 mmHg) and marked dilatation of the pulmonary artery (47 mm).

The patient was referred to our department to exclude ischemic etiology; cardiac catheterization showed no apparent coronary disease.

A grade II/VI systolic–diastolic murmur was audible at the upper left sternal border that was not explained by previous studies. Transthoracic echocardiography was repeated (Figure 1), which confirmed the previous findings, but also showed continuous turbulent flow at the level of the pulmonary artery bifurcation, from the aorta towards the trunk and right branch of the pulmonary artery; it was also visible in suprasternal view (Figures 2–4). A diagnosis was made of patent ductus arteriosus (PDA).

Figure 1.

M-mode echocardiogram, left parasternal long-axis view, showing dilated left ventricle with end-diastolic diameter of 69 mm and end-systolic diameter of 49 mm.

Figure 2.

Color Doppler echocardiogram, left parasternal short-axis view, showing dilated pulmonary artery and flow from aorta to pulmonary artery.

Figure 3.

Color Doppler echocardiogram, suprasternal view, showing flow from aorta to pulmonary artery. AO: aorta; ap: pulmonary artery.

Figure 4.

Echocardiogram, left parasternal short-axis view at the pulmonary valve level. Pulsed Doppler study immediately distal to the pulmonary valve guided by color Doppler (above), showing systolic flow through the pulmonary valve (narrow arrow) against a background of systolic–diastolic flow from aorta to pulmonary artery (wide arrow).

In view of the patient's age, it was decided to optimize medical therapy. Her condition improved and she now has fatigue on moderate exertion.

This case of PDA is unusual for being diagnosed so late in life. The patient's left ventricular dysfunction was probably due to increased flow caused by the PDA, which was the only pathological condition identified apart from mild hypertension. The elevated pulmonary artery pressure resulting from the PDA probably reduced the shunt, which is now weak and turbulent.

The authors have no conflicts of interest to declare.