Coronary artery spasm is localized to a segment of epicardial coronary artery; in most patients, it is superimposed on the angiographically detectable atherosclerotic lesion.1,12 However, it can also occur in coronary arteries that lack angiographic evidence of an atherosclerotic lesion.2 In most patients, coronary artery spasm may be successfully treated with nitrates and calcium channel blockers, but some patients continue to have recurrent episodes of vasospastic angina with serious complications including myocardial infarction and arrhythmogenic sudden cardiac death.3,4 We present a patient with recurrent episodes of vasospastic angina and serious complications of coronary artery spasm including ventricular fibrillation and myocardial infarction who was treated with coronary stenting at the site of ergonovine-induced coronary vasospasm where the coronary artery appeared angiographically normal, i.e., without evidence of an atherosclerotic lesion. Case Report. A 53-year-old male with a history of vasospastic angina suffered an acute anterior myocardial infarction one month before he was admitted to our hospital for invasive diagnostics. Six months earlier, he had been admitted to our Cardiac Care Unit with signs of vasospastic angina complicated with ventricular fibrillation. Coronary angiography performed at that time disclosed normal coronary arteries without any detectable atherosclerotic lesions and normal left ventricular function. He was a heavy cigarette smoker (40 cigarettes/day) and his total cholesterol (6.1 mmol/L) and triglyceride levels (3.0 mmol/L) were elevated. Physical exam, chest radiography and routine laboratory tests were normal. Resting electrocardiogram (ECG) showed sinus rhythm, normal QRS complex, no ST and T abnormalities, and no rhythm disturbances. Submaximal Bruce treadmill exercise stress test was negative for myocardial ischemia. Two-dimensional echocardiography showed a mild hypokinesia of the anteroseptal region of the left ventricle. Coronary arteriography again revealed normal coronary arteries (Figure 1) and ergonovine maleate provocation at doses of 50, 100 and 200 µg in 3-minute intervals was subsequently performed. The coronary artery in which ergonovine was administered was chosen on the basis of the leads showing ST-segment elevation on the electrocardiogram during vasospastic angina attacks. Coronary artery spasm developed at the dose of 200 µg ergonovine in the proximal part of the left anterior descending coronary artery (Figure 2), which was relieved by intracoronary nitroglycerine. Due to clear demonstration of coronary artery spasm previously accompanied by serious complications and the fact that vasospastic anginal attacks could not be prevented by full medical therapy, we decided to perform coronary stenting. After intracoronary administration of 200 µg of nitroglycerine, direct stent placement was performed at the site of ergonovine-induced coronary spasm. After placement of a 3.0 x 10 mm Tenax-XR coronary stent (Biotronik, Berlin, Germany), the patient developed chest pain with ST elevation. Coronary angiography revealed coronary artery spasm proximal to the site of stent placement, which was treated with the placement of another coronary stent (3.0 x 10 mm Tenax-XR just proximal to the position of the first coronary stent). After placement of the second stent, the patient was free of symptoms and final angiogram showed an excellent result (Figure 3). Six months later, the patient was free of symptoms related to coronary vasospasm, but he started to experience mild anginal episodes during exertion. Control coronary angiography revealed diffuse in-stent restenosis (Figure 4), which was successfully treated by conventional balloon (3.5 x 20 mm) angioplasty (Figure 5). The patient was discharged, and in the short-term follow-up, he was free of both vasospastic as well as effort-induced anginal attacks. Discussion. Previous, mostly anecdotal reports, have suggested the potential role and effectiveness of coronary angioplasty and stenting for treatment of medically uncontrolled coronary vasospasm. Studies regarding angioplasty for the treatment of coronary vasospasm5,6 showed fair angiographic results, but high restenosis rates (between 35–50%) have been documented. With the introduction of coronary stenting, which generally decreased the rate of restenosis, several authors7–11 reported on the usefulness of coronary stenting in the treatment of medically uncontrolled coronary vasospasm. In the largest series of 9 patients, Gaspardone et al.9 showed that stent placement represented a valid alternative therapeutic option, effective in preventing anginal attacks in 6 out of 9 patients in the medium-term follow-up. Asymptomatic in-stent restenosis developed in 1 patient. A common feature of previous reports on stenting for coronary vasospasm is that all patients presented with angiographically defined atherosclerotic lesions ranging from 36–65% luminal narrowing. In this case, coronary stenting was used for the treatment of coronary artery spasm in a patient with an angiographically normal coronary artery, showing that the effectiveness of coronary stenting for the treatment of coronary vasospasm may be extrapolated to patients without angiographic evidence of coronary stenosis. Thus, implantation of a stent at the site of coronary vasospasm superimposed on either a normal or mild atherosclerotic lesion, definitely carries two possible side effects, including development of coronary vasospasm next to stent implantation location and development of in-stent restenosis. In summary, coronary stenting of medically uncontrolled coronary vasospasm is a valid and effective therapeutic option, but side effects of coronary stenting in this condition, including vasospasm next to stent implantation and in-stent restenosis, may occur.
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