So Doctor...Why Did I Have That Operation?

Coronary artery vasospasm may be observed in 3–4% of diagnostic coronary angiography procedures.¹ It is more likely to occur in younger females who are heavy smokers and who present with rest pain.² In addition to occurring spontaneously, coronary spasm may be induced by the angiographic catheter tip. The right coronary artery is more commonly involved, whereas spasm of the left main coronary artery is rare. Differentiation of spasm from fixed obstructive coronary lesions is crucial, as treatment strategies are different. This can be difficult, particularly in more distal spasm. We describe a case of a patient presenting with rest angina and a strongly positive exercise stress test whose coronary angiography demonstrated an apparent severe left main coronary lesion. This led to expeditious surgical revasculariztion. However, the patient presented with ongoing symptoms and follow-up angiography, employing sublingual nitroglycerin, showed that the left main coronary stenosis was only mild. Case Report. A 59-year-old woman with a history of hypercholesterolemia (fasting total cholesterol of 6.8 mmol/L) and cigarette smoking (for 43 years), was admitted following 3 bouts of chest pain occurring at rest in one day. The episodes were brief (less than 5 minutes) and described as central chest heaviness radiating to the neck and left arm. She had no other cardiovascular or associated systemic symptoms. Her clinical examination was unremarkable. Serial electrocardiograms and troponin I levels were all normal. An exercise stress test was strongly positive, with chest tightness and widespread ST-segment depression of > 3 mm during stage II of the standard Bruce protocol (exercise duration 4 minutes 39 seconds). Coronary angiography was performed without the administration of nitroglycerin. The left main coronary artery was engaged with a 6 French (Fr) Judkins left 4 catheter and the right coronary artery with a Judkins right 4. Angiography revealed a severe ostial left main coronary artery stenosis (Figures 1 A and B), with an ostial right coronary artery lesion of moderate stenosis. Left ventricular systolic function was normal. She was surgically revascularized with an internal mammary graft (IMA) to the anterior descending artery (2 mm vessel) and saphenous vein grafts (SVG) to the large diagonal and the posterior descending coronary arteries. She was discharged on aspirin 150 mg and simvastatin 40 mg daily. At 10 months, she experienced further exertional chest pain. An exercise stress test showed evidence of inducible ischemia at a moderate workload: 1–1.5 mm inferolateral ST-segment depression at 6 minutes 44 seconds of the standard Bruce protocol. It was elected to treat her medically. Two years following surgery, she remained symptomatic and a repeat exercise stress test provoked chest pain, but no electrocardiographic ischemic changes. Repeat coronary angiography with administration of sublingual nitroglycerin revealed that the left main coronary artery was only mildly narrowed (Figure 1 C and D). There were no flow-limiting lesions in her other native coronary arteries. The IMA graft was diffusely, severely narrowed. The SVG to the posterior descending artery was occluded and that to the diagonal branch was patent. Three years later, she remains asymptomatic and is on aspirin 75 mg, atenolol 25 mg, and simvastatin 80 mg daily. She had stopped smoking, and her total cholesterol is 4.3 mmol/L. Discussion. Coronary spasm is thought to be related to endothelial dysfunction and impaired nitric oxide release.^3–5 Altered autonomic regulation, particularly at the site of atherosclerotic disease, may contribute.^4,6–11 This leads to the so-called vasospastic or Prinzmetal’s angina. The angiographic catheter tip may induce coronary spasm. While the mechanism is not defined, mechanical irritation by the catheter may trigger a myogenic reflex or cause alterations in autonomic regulation.^12,13 Left main coronary artery spasm is uncommon. It may be associated with Prinzmetal’s angina,^5,14–16 or be due to catheter tip irritation during angiography.^6,17 In addition, it may be induced by administration of intracoronary ergonovine¹⁸ and has been observed in cocaine users¹⁹ and in patients with hyperthyroidism.²⁰ Vasospastic angina may have a cyclic pattern, with periods of remission.6 It may be worse in the early morning,^21–24 paralleling circadian variation in both the sympathetic activity^10,25 and the vasodilator response to intracoronary nitrates.⁷ Exercise may induce coronary spasm in some patients with vasospastic angina, but exercise stress testing may be negative in up to 50% of patients.^7,26–29 The prognosis is generally good,^30,31 even though arrhythmogenic death may occur with severe multivessel spasm.^7,32 Vasodilator therapy is the mainstay of treatment, although percutaneous revascularization of associated obstructive lesions has been undertaken. Sympathetic denervation has also been tried in some caess.³³ There are several reports of coronary spasm (spontaneous or catheter-induced) inadvertently diagnosed as fixed stenosis.^13,17,34,35 This patient demonstrated severe catheter-induced spasm of the left main coronary artery. Her prior rest angina and positive stress tests may represent spontaneous or exercise-induced spasm on a background of mild atherosclerotic coronary disease. In keeping with the condition, she continued to experience angina and had a positive stress test after surgical revascularization. Any lesion at or near the catheter tip should be re-evaluated following intracoronary vasodilator administration. Other clues that the lesion may be vasospastic in nature include lack of significant obstructive atherosclerotic disease elsewhere in the coronary arteries and lesions in middle-aged females who are heavy smokers. It is our practice to routinely administer nitroglycerin by the sublingual or intracoronary route before coronary angiography. If a vasodilator had been administered at the time of initial angiography in this patient, unnecessary revascularization surgery would have been avoided.

1. Harding MB, Leithe ME, Mark DB, et al. Ergonovine maleate testing during cardiac catheterization: A 10-year perspective in 3,447 patients without significant coronary artery disease or Prinzmetal’s angina. J Am Coll Cardiol 1992;20:107–111. 2. Caralis DG, Deligonul U, Kern MJ, Cohen JD. Smoking is a risk factor for coronary spasm in young women. Circulation 1992;85:905–909. 3. Kugiyama, Yasue H, Odumura K, et al. Nitric oxide activity is deficient in spasm arteries of patients with coronary spastic angina. Circulation 1996;94:266–272. 4. Lanza GA, Pedrotti P, Pasceri V, et al. Autonomic changes associated with spontaneous coronary spasm in patients with variant angina. J Am Coll Cardiol 1996;28:1249–1256. 5. Wiener L, Kasparian H, Duca P, et al. Spectrum of coronary arterial spasm: Clinical, angiographic and myocardial metabolic experiences in 29 cases. Am J Cardiol 1976;38:945–955. 6. Persin GA, Matthai WH Jr. Catheter-induced spasm of the left main coronary. J Invasive Cardiol 2000;12:158–161. 7. Yassue H, Omote S, Takizawa A, et al. Circadian variation of exercise capacity in patients with Prinzmetal’s variant angina: Role of exercise induced coronary arterial spasm. Circulation 1979;59:938–948. 8. Tuchiya T, Okumura K, Yasue H, et al. Heart period variability in patients with variant angina. Am J Cardiol 1996;77:932–936. 9. Yoshio H, Shimizu M, Sugihara N, et al. Assessment of autonomic nervous activity by heart rate spectral analysis in patients with variant angina. Am Heart J 1993;125:324–329.