JOURNAL OF THE AMERICAN GERIATRICS SOCIETY Copyright © 1975 by the American Geriatrics Society

Vol. XXIII. No.7 Printed in U.S.A.

Patent Ductus Arteriosus in Old Age I. SYRKIS, MD, I. MACHTEY, MD* and M. SAGIV, MD

Departments of Medicine and Pathology, Hasharon Hospital, Petah-Tiqua, Israel ABSTRACT: An unusual case of patient ductus arteriosus (PDA) in a 78-year-old man is presented. The patient was known to have PDA since the age of 30, but it had remained well compensated until shortly before death. He had undergone some difficult operations successfully, and had no specific pulmonary complaints. Death at age 78 was caused by arteriosclerotic heart disease following myocardial infarction. Autopsy revealed a smooth patent ductus arteriosus with no perforation. The survival of a PDA patient to such advanced age is a comparatively rare occurrence. Patent ductus arteriosus usually is observed

parasternal areas. Both systolic and diastolic murmurs (grade 3/6) were heard over the second intercostal space, left of the sternum; they were of the so-called machinery type. A systolic ejection murmur (grade (3/6) was heard over the apex and in the area of Erb. The second sound was accentuated. The third sound was muffled. The blood pressure was 160/80 mm Hg. There was 2+ pitting edema of the ankles. The liver and spleen were not palpable. The patient complained of diffuse abdominal pains of an indefinite nature. An iron-deficiency anemia was found. Blood urea and electrolyte levels were normal and liver function tests gave normal results. A chest roentgenogram showed that the heart was enlarged in comparison with its size when the patient had been hospitalized with acute myocardial infarction. There was also congestion of the lungs, particularly around the hili. Fluoroscopic examination of the heart disclosed normal pulsation in the aorta, which was enlarged along its entire length. These pulsations also were seen in the main pulmonary artery. The x-ray picture indicated patent ductus arteriosus with a left-to-right shunt. In addition to this congenital heart defect, there was arteriosclerotic heart disease (ASHD), the diagnosis being based upon the previous myocardial infarction as well as the LBBB. The patient was treated for congestive heart failure, with some improvement. Five months later, the patient was re-admitted because of sudden weakness, nausea and

in the very young. According to the literature,

only rarely have such patients reached an advanced age. Therefore, it seemed pertinent to report a case of this anomaly in a septuagenarian. CASE REPORT A 78-year-old man, known since his 30's to have a patent ductus arteriosus, was admitted to our hospital. His first admission to our department had been in 1961, because of melena; an additional episode of melena occurred a year later. Barium x-ray examination of the gastrointestinal tract showed a duodenal ulcer, a diaphragmatic hernia of the stomach, and many diverticuli of the colon. There was also a stone in the left ureter. A subtotal gastrectomy with vagotomy was performed without complications and, in the same year, a herniotomy. In 1965 he underwent prostatectomy because of marked prostatic hypertrophy. At the beginning of 1970, he had an acute myocardial infarction. At the end of 1970, congestive heart failure developed. An electrocardiogram showed atrial fibrillation, not previously diagnosed, and a left bundle-branch block (LBBB), which had been present for several years. Examination of the heart disclosed a diffuse uplift in the apical and

* Address: Head, Department of Medicine, Hasharon Hospital, Petah-Tiqva, Israel. 333



Fig. 1. Short ductus arteriosus (da) between aorta (ao) and pulmonary artery (pa). Black arrowhead shows the site of "jet lesion. "

Fig. 2. Fibrotic opening of ductus arteriosus (da) as seen from pulmonary artery (pa). Arrowheads show the "jet lesion."

diaphoresis. His sensorium was clouded. Electrocardiographic tracings demonstrated the previously documented LBBB as well as multiple ventricular extrasystoles. Suddenly, ventricular tachycardia dominated the picture; the pulse rate rose to 150 per minute. He was treated first with procainamide (Pronestyl), and later with ajmaline (Gilurythmal) and potassium chloride. Another electrocardiogram showed substantial widening of the QRS complex and a


bradycardia of 40 per minute. The systolic blood pressure had dropped to 50 mm Hg. Hydrocortisone was started intravenously, with potassium chloride and bicarbonate; later, glucagon was added. The patient improved. His pulse rate and blood pressure rose to normal and the QRS complex returned to its previous width. However, the signs of congestive heart failure had increased markedly. On the next day, the steep drop in blood pressure and pulse

July 1975


recurred. Then Cheyne-Stokes respiration developed, and finally cardiac arrest. Attempts at resuscitation were of no avail. Laboratory determinations in the final stage showed a bilirubinemia of 1.2 mg/100 ml; (transaminase) SGOT 205 units, SGPT 150 units; alkaline phosphatase, initially 4.0 BesseyLowry units and later 11.0 units; serum urea nitrogen 100 mg/100 ml; and serum electrolytes normal. Autopsy. The heart was enlarged (760 gm). The right auricle and ventricle were dilated. The wall of the left ventricle was thickened (2 em), with pronounced trabeculation of the myocardium and diffuse fibrosis of the endocardium. The pulmonary artery was dilated and its diameter was equal to that of the aorta. The main arteries of the lungs were also dilated. Between the left pulmonary artery and the aorta and just below the left subclavian artery was a patent ductus arteriosus, 1 ern in length and nearly 3 mm in diameter (Fig. 1). At the aortic end it opened at the bottom of a small dimple, and at the other end a small conus protruded into the lumen of the pulmonary artery. A fibrotic "jet lesion" was visible on the wall of the left pulmonary artery facing the opening of the ductus arteriosus (Fig. 2). The duct was patent throughout its whole length and x-ray examination revealed that it was not calcified. Microscopic examination showed that the duct was made up of dense connective tissue without any sign of thrombosis and recanalization. The anterior wall of the left ventricle of the heart showed extensive postinfarction scarring and a fresh myocardial infarction involving also the conduction system. The lungs showed severe chronic emphysema and bronchiectasis with widespread fibrosis and many heart-failure cells in the alveoli. Moderate to severe athersclerotic changes were found in the kidneys, the aorta, and the arteries of virtually all the organs examined. DISCUSSION The chief complications which might be expected in a case of patent ductus arteriosus (PDA) are: pulmonary hypertension, endartentis of the duct, and congestive heart failure. The endarteritis is a form of proliferative tissue

which appears at the pulmonary opening of the duct and may extend from there toward the heart valve. Patent ductus arteriosus may be one of two types, according to the diameter of the aperture. The larger type leads to pulmonary hypertension and right ventricular hypertrophy, with recurrent pulmonary infection which adversely affects survival. The second type of PDA is smaller and narrower and usually does not produce complications. The PDA in our patient belonged to the latter category, and therefore he was able to reach a ripe old age despite the pulmonary changes. The clinical cardiac symptoms and signs were not caused by his congenital defect, but rather by arteriosclerotic heart disease, to which also the LBBB probably was attributable (as this block usually is not found in simple PDA). The oldest male PDA patient reported in the literature was 90 years of age (1) and the oldest woman was 85 (2). PDA is more common in women than in men, and the women survive longer. Fairley and Goodwin (3), in their series of PDA patients, found that only 5 per cent reached the age of 60, and all of these were women. Men tend to have more complications, and at a younger age than the women (3). The reason for this is unknown. Elderly men with such a defect usually are treated conservatively rather than surgically. The oldest woman to be operated upon, according to the literature, was 72 years of age; she had severe congestive heart failure due to PDA, but the operation was successful (4). In the case presented here, the chief point of interest is the fact that the patient reached the age of 78 without the development of clinical complications which could be attributed directly to his congenital heart disease. REFERENCES 1. White PO, Mazurkie SJ and Boschelti AE: Patency

of the patent ductus arteriosus at 90, New England JMed 280: 146,1969. 2. Bain ewC: Longevity in patent ductus arteriosus, Brit Heart J 19: 574, 1957. 3. Fairley, GH and Goodwin JF: Patent ductus arteriosus in adult life, Brit J Dis Chest 53: 263, 1959. 4. Hornsten TR, Hellerstein HK and Ankeney JL: Patent ductus arteriosus in a 72-year-old woman, JAMA 199: 580, 1967.


Patent ductus arteriosus in old age.

An unusual case of patient ductus arteriosus (PDA) in a 78-year-old man is presented. The patient was known to have PDA since the age of 30, but it ha...
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