Spontaneous coronary artery dissection associated with oral contraceptive use

Spontaneous coronary artery dissection associated with oral contraceptive use

International Journal of Cardiology 48 (1995) 195-198 ELSEVIER Spontaneous coronary artery dissection associated with oral contraceptive use M.N. Az...

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International Journal of Cardiology 48 (1995) 195-198

ELSEVIER

Spontaneous coronary artery dissection associated with oral contraceptive use M.N. Azam*, D.H. Roberts, W.F.W.E. Logan Department of Cardiology,

Victoria Hospital,

Whinney Heys Road, Blackpool. Lancashire FY3 8NR. United Kingdom

Received 5 September 1994;accepted 10 November 1994

Abstract

A 39-year-old woman presentedwith acute myocardial infarction due to spontaneous dissection of the left anterior descending artery. This was treated conservatively. She had been on combined oral contraceptive pills from the age of 22. Repeat coronary angiography 7 months later revealed spontaneous complete healing. Keywork Spontaneous coronary dissection; Oral contraceptive

Spontaneous coronary artery dissection is a rare and often fatal disorder. Although no single aetiology has clearly beenestablished, there is a higher prevalence in otherwise healthy women in the peripartum period and LAD is involved in approximately 80?/ of patients [1,2]. We report the first case associated with chronic use of oral contraceptives. A 39-year-old Caucasian woman was admitted with a history of crushing chest pain radiating to the left arm and neck, shortness of breath and sweating. She had previously been in excellent health and had never smoked. There was no family history of cardiovascular diseases. She had no children. From the time she was 22 she had been on combined oral contraceptive pills, initially of * Corresponding author.

high oestrogen content but later changed to reduced oestrogen content (Ovranette: ethinyloestradiol 30 pg + levonorgestrel 150 pg). Electrocardiogram at admission showed ST segment elevation consistent with acute anterior wall myocardial infarction. She was treated with streptokinase, aspirin and atenolol, but chest pain continued for some hours and required intravenous nitrates and diamorphine. Shedeveloped primary ventricular fibrillation which responded to DC shock. Her subsequent hospital stay was uneventful and 7 days later she was discharged. The oral contraceptive pill was withdrawn. Five weekslater shewas readmitted with acute left ventricular failure and treated with diuretics and an ACE inhibitor. Atenolol was withdrawn. Eleven weeks later she was readmitted with further chest pain and acute myocardial infarction was exclud-

0167.5273/95/X%50 0 1995Elsevier Science Ireland Ltd. All rights reserved SSDI 0167-5273(94)02238-E

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(b)

Fig. I. (a) Left coronary angiogram (RAO projection) showing coronary dissection of the left anterior descending artery (arrow). Then is a thin radiokent line as a result of partial separation of the intima and tilling of the dissection channel with thrombus. (b) b!I coronary angiogram (RAO projection) showing delayed emptying of the left anterior descending artery (arrow).

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Fig. 2. Repeat left coronary angiogram (ROA projection) showing spontaneous complete healing.

ed. Coronary angiography was performed which showed normal right, left main and circumflex coronary arteries. The left anterior descending artery revealed marked coronary dissection (Fig. la) with delayed emptying (Fig. lb). Left ventricular angiography showed good left ventricular function with apical hypokinesis. As the dissection channel appeared to contain thrombus she was treated with coumarin and bypass grafting was withheld. She has had no further chest pain. An exercisetolerance test was subsequently performed in which she had no symptoms, a good exercise capacity and normalisation of the inverted anterior T waves. Sevenmonths later repeat coronary angiography revealed normal coronary arteries with no signs of vessel lumen irregularity, thrombus or dissection (Fig. 2). An inherent structural defect in the coronary artery has been implicated as the basis for spontaneous dissection. Both cystic medial necrosis or eosinophilic infiltration [3] of the adventitia may be responsible for these structural changes although pre-existing atherosclerotic disease may also play a role. Whether this structural defect is

secondary to hormonal factors has not been clearly established. The largest group experiencing coronary dissection, however, are women in the peripartum period [l], suggesting that hyperoestrogenism may be of prime importance. A case occurring in a man with cirrhosis of the liver (also associatedwith hyperoestrogenism) supports this view [4]. This case suggests that chronic contraceptive use with high dose oestrogen may predisposeto similar coronary structural fragility. While early coronary bypass surgery may be lifesaving in coronary dissection (by restoring flow beyond the obstruction and minimising the chance of extension) [2] there are a number of long-term survivors who have not undergone such an operation [5]. This suggeststhat patients with spontaneous dissection that is not immediately fatal may survive with medical treatment alone. This case supports this belief as the vascular structural defect responsible showed spontaneous healing. Further exogenousoestrogen should be avoided in such case by switching the patient to nonhormonal contraception and advising against pregnancy.

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References [l] Alvarez J, Deal CW. Spontaneous dissection of the left main coronary artery: casereport and review of the literture. Aust NZ J Med 1991; 21: 891-892. [2] Thayer JO, Healy RW, Maggs PR. Spontaneous coronary artery dissection. Ann Thorac Surg 1987; 44: 97-102. [3] Robinson PG, Mayers DL. Spontaneous dissection of

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left anterior descendingcoronary artery. Am J Med 1983; 74: 4%. ]41 Black MD, Catzavelos C, Boyd D, Walley VM. Simultaneous spontaneous dissections in the three coronary arteries. Can J Cardiol 1991; 7: 34-36. 151 Nishikawa H, Nakanishi S, Nishiyama S, Nisshimura S, Seki A, Yamaguchi H. Primary coronary artery dissection observed at coronary angiography. Am J Cardiol 1988;61: 645-648.