Pulmonary arterial aneurysms

424

tion of the involved coronary arteries. This failure provides an additional support to the theory that spasm may constitute one of the primary events in the pathogenesis of myocardial infarction related to cocaine addiction.

pressure, tachycardia and alpha-receptor mediated vasoconstriction can cause myocardial infarction in patients with severe underlying coronary obstruction. Thrombotic occlusion of epicardial coronary arteries has been the only angiographic finding in some patients, and thrombolytic therapy was successful when applied [1,3]. An alpha-adrenergic mediated increase in platelet aggregability has been suggested to explain these cases [2]. About one-third of the reported patients with cocaine-related myocardial infarction had angiographically normal epicardial arteries [ 11. This finding, together with the absence of evidence of plaque rupture, supports the theory of cocaine-induced spasm as the primary event of infarction in cocaine users. Ergonovine has failed to provoke focal spasm in any case, but Lange et al. [4] have demonstrated the induction of coronary vasoconstriction by a low dose of intranasal cocaine, which is potentiated by beta-blockers, reaching total occlusion in one case [5]. Both patients we present here received thrombolytic therapy, but it failed to achieve repermeabiliza-

International Journal of Cardiology, 35 (1992) 424-426 0 1992 Elsevier Science Publishers B.V. All rights reserved

CARD10

References Isner JM, Chokshi SK. Cardiac complications of cocaine abuse. Annu Rev Med 1991;42:133-138. Hueter DC. Cardiovascular effects of cocaine. JAMA 1987;257:978-980. Smith III HWB, Liberman HA, Brody SL, Battey LL, Donohue BC, Morris DC. Acute myocardial infarction temporally related to cocaine use. Ann Intern Med 1987;107: 13-18. Lange RA, Cigarroa RG. Yancy CW et al. Cocaine-induced coronary artery vasoconstriction. N Engl J Med 1989;321: 1557-1562. Lange RA, Cigarroa RG, Flores ED et al. Potentiation of cocaine induced coronary vasoconstriction by beta-adrenergic blockade. Ann Intern Med 1990;112:897-903.

0167-5273/92/$05.00

01459

Pulmonary arterial aneurysms Pradeep Vaideeswar and J.R. Deshpande Department of Pathology, Seth G.S. Medical College and K.E.M. Hospital, Parel, Bombay, India (Received

8 August

1991; revision

accepted

4 December

1991)

Over a period of 12 years, two cases of pulmonary arterial aneurysms were encountered in our autopsy data of 13 cases of congenital heart defects with right-sided infective endocarditis. Pulmonary arterial aneurysms are rare lesions and may be categorized as central or peripheral. Although early reports implicated tuberculosis as a major aetiologic factor, pulmonary arterial aneurysms are generally associated with congenital heart disease. Key words: Pulmonary endocarditis

arterial aneurysm; Congenital

Correspondence to: Dr. Pradeep Bombay 400 050, India.

Vaideeswar,

B-85, Kamal

heart disease; Pulmonary

Pushpa,

Gen. Arunkumar

hypertension;

Vaidya

Nagar,

Bandra

Right-sided

Reclamation

infective

(West),

Introduction

Pulmonary arterial aneurysms are rare lesions most frequently associated with congenital heart disease. The reported causative factors include tuberculosis, syphilis, infective endocarditis, pulmonary hypertension, cystic medionecrosis, generalized arteritis and thoracic trauma [l]. Pulmonary arterial aneurysms may either be central (involving the pulmonary trunk or its right and left branches) or peripheral (arising from segmental or intra-pulmonary branches) [2]. In a 12-year period (1978-19891, we encountered 19 cases of right-sided infective endocarditis at autopsy. Thirteen of these cases were associated with congenital heart disease (Table 1). Two of these had pulmonary arterial aneurysms. Both were mycotic in nature, one being peripheral while the other had both central and peripheral aneurysms. Case 1

An 1 l-year-old male child presented with increased precordial activity and progressively increasing dyspnoea since the age of one year. Cross-sectional echocardiography revealed a large sub-aortic ventricular septal defect with vegetations on the pulmonary valve. The patient underwent surgery for closure of the defect and removal of vegetations. The patient died on the 4th post-operative day. At autopsy, the pulmonary valve, which had two leaflets, was partially destroyed by polypoidal vegetations. Vegetations were also seen in the pulmonary trunk together with a small 1 cm saccular aneurysm. The lower lobe of the right lung had a large aneurysmal cavity 10 X 8 cm (Fig. 11, filled

TABLE

Fig. 1. Right lung, lower lobe with aneurysmal

cavity

filled

with thrombus.

with organized thrombus. A small segment of the intrapulmonary artery was identified in the fibrotic wall of the aneurysmal sac. There was severe pulmonary hypertension with plexogenic pulmonary arteriopathy.

1

Congenital heart disease with right-sided infective endocarditis. Type of congenital No. of Valves affected heart disease caSeS Tricuspid Pulmonary Others Ventricular septal defect Fallot’s tetralogy Tricuspid atresia Atrioventricular septal defect * Prosthetic * * Acquired

6 5 1

3 5 _

3 1 -

1* I**

1

1

-

-

mitral valve. left ventricle

-

right atrium

communication.

Fig. 2. Partly destroyed pulmonary artery. forming wall of the aneurysmal sack (elastic Van Gieson x 63).

426 Case 2

Another interesting observation is the link between mycotic aneurysms and pulmonary hypertension [5]. Septic emboli could lodge in the wall of the pulmonary vessel already under stress due to pulmonary hypertension leading to aneurysmal formation. Both cases reported here had evidence of severe pulmonary hypertension in the form of plexogenic arteriopathy. This, associated with infection, has in all probability predisposed to the development of pulmonary arterial aneurysms.

A 27-year-old male presented with pleuritic chest pain, cough and dyspnoea. The clinical impression was ventricular septal defect with right mid-zone consolidation. The patient died before any detailed investigation could be carried out. At autopsy, there was a 7 x 5 mm sub-arterial ventricular septal defect with infective endocarditis of the pulmonary valve, which had two leaflets. The middle lobe of the right lung was occupied by an aneurysm 5 cm in diameter, filled with blood clots and thrombus. Part of the elastic pulmonary artery could be identified in hyalinized connective tissue forming the aneurysmal wall (Fig. 2). As in the previous case, the lung vasculature showed changes of severe pulmonary hypertension.

We are grateful to the Dean, Seth G.S. Medical College, Bombay, for granting us the permission to publish this article.

Discussion

References

Several reviews have emphasized the rarity of pulmonary arterial aneurysms. Groedel estimated the ratio of pulmonary to aortic aneurysms as 1: 250 [3]. Deterling and Clagett, reviewing a series of 10,971 autopsies over a period of 100 years recorded only 8 cases [4] and divided them into central and peripheral types. Half the cases confirmed on autopsy are associated with congenital heart disease [l]. The two cases reported here were associated with congenital lesions complicated by right-sided infective endocarditis. Both the aneurysms were mycotic. Mycotic pulmonary arterial aneurysms mostly arise in the segmental arteries and are often multiple and bilateral [S].

Acknowledgement

1 Butto Fouad, LRV Jr. Pulmonary arterial aneurysms, a

pathologic study of 5 cases. Chest 1987;91:237-241. 2 Murphy JP, Adyanthaya AV, Adams PR et al. Peripheral pulmonary artery aneurysm in a patient with limited respiratory reserve: controlled resection using cardiopulmonary bypass. Ann Thorac Surg 1987;43:323-325. 3 Groedel FM. Arieurysm of the pulmonary artery. Radiology 1939;33:219-232. 4 Deterling RA, Clagett OT. Aneurysm of the pulmonary artery: review of literature and report of a case. Am Heart J 1941;34:411-499. 5 Kaufmann SL, Lynfield J, Hennigar, CR. Mycotic aneurysms of intrapulmonary arteries. Circulation 1967;35: 90-99.