Variant angina pectoris caused by coronary artery spasm

A 58 year old man presented with Prinzmetal's variant angina. Recurrent ventricular tachyarrhythmias, uncontrolled by various medical regimens, prompted cardiac catheterization. At catheterization a congenital anomaly of the coronary circulation was demonstrated, consisting of a single coronary artery. During coronary angiography, arterial spasm occurred associated with chest pain and ventricular ectopic beats. This was relieved by the acute administration of sublingual nitrates. Subsequently, despite the frequent administration of nitroglycerin and isosorbide dinitrate, chest pain and ventricular tachycardia continued to occur sporadically. Because of this, saphenous vein bypass surgery was performed. After an initial symptom-free interval, the chest pain recurred. Recatheterization revealed complete occlusion of the distal circumflex artery at the insertion of the implanted saphenous vein. The use of aortocoronary saphenous vein bypass grafting for relief of symptomatic coronary arterial spasm is questioned.     

Spontaneous coronary artery spasm in variant angina is caused by a local hyperreactivity to a generalized constrictor stimulus

To assess whether spontaneous coronary artery spasm in patients with variant angina results from local coronary hyperreactivity to a generalized constrictor stimulus or from a stimulus generated only at the site of the hyperreactive segment, the behavior of spastic and nonspastic coronary segments was studied in six patients with variant angina in whom focal coronary spasm developed spontaneously during cardiac catheterization. None of the patients had critical (greater than 50% luminal diameter reduction) organic coronary stenoses. Coronary diameters were measured by computerized quantitative arteriography during control, spontaneous spasm and ergonovine-induced spasm and after intracoronary nitrates were given. During spontaneous spasm, the luminal diameter of spastic and both proximal and distal nonspastic coronary segments was significantly reduced from control values, 64.2%, 13.2% and 14.8%, respectively. Average diameter reduction of unrelated arteries was 12.3%. Ergonovine, which was also administered to four patients, provoked focal spasm at the same site as spontaneous spasm. During intravenous ergonovine, luminal diameter of spastic segments was reduced by 91.5%, that of nonspastic proximal segments by 17.8% and that of nonspastic distal segments by 11.5%. Luminal diameter of unrelated arteries during ergonovine-induced spasm was reduced by 17.7%. Constriction of spastic segments was greater during ergonovine-induced spasm (p less than 0.05), whereas the extent of diameter reduction of nonspastic segments was not significantly different during spontaneous spasm and ergonovine-induced spasm. Intracoronary isosorbide dinitrate dilated spastic and nonspastic coronary segments to a similar extent from control (20.7%, 18% and 16.5%, respectively; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)     

Microvascular angina accompanied by epicardial coronary artery spasm

A case of microvascular angina accompanied by coronary artery spasm is described. A 54-year-old woman had anginal pain at rest and during exercise. Both exercise testing and rapid atrial pacing caused significant ST depression in the inferior and all precordial leads. Exercise thallium myocardial scintigraphy was negative despite similar ST depressions. Coronary angiography revealed insignificant stenoses of the left anterior descending coronary artery after the injection of nitrate. Intracoronary acetylcholine provoked diffuse spasm of the artery with concurrent myocardial lactate production. Coronary flow reserve assessed with papaverine was 2.75. The combined use of amlodipine and high-dose nicorandil was effective for the treatment of angina.     

Clinical characteristics and prognosis of patients with postinfarction angina caused by coronary artery spasm

Clinical features and the course of 15 patients with postinfarction angina caused by coronary artery spasm are described. Episodes of postinfarction angina in the patients recurred at rest in the early recovery phase and were accompanied by transient ST-segment elevation. The area where ST-segment elevations were demonstrated on a 12-lead ECG always included the leads with newly developed abnormal Q waves. Pain resolved spontaneously or after sublingual nitroglycerin in several minutes. Holter ECGs during a 24-h period demonstrated frequent episodes of ST-segment elevation that were not always associated with chest pain. Treatment with calcium antagonist and/or nitrates effectively suppressed angina, and only one patient developed reinfarction. The patient's subjective symptoms were abolished by diltiazem and isosorbide dinitrate. A Holter ECG of the patient revealed silent ST-segment elevations before and after the reinfarction and an increase of the drugs completely suppressed the recurrence of silent ischemic ECG changes. Coronary arteriograms were obtained from 8 patients, which demonstrated more than 75% segmental stenosis on one coronary artery in 5 patients and no significant obstruction in the remaining 3. All patients performed a treadmill exercise stress test before discharge and most demonstrated excellent tolerance. All patients experienced no form of chest pain for an average of 25 months follow-up under medication. We conclude that among patients with postinfarction angina, those cases caused by coronary artery spasm have a relatively good prognosis.     

伴λ波的冠状动脉痉挛性心绞痛致意识丧失1例

λ波是一个心室除复极均有异常的心电图波形,为独立的猝死高危心电图标志。λ波可由冠状动脉急性严重缺血引起,需要临床医师高度重视,本文报道1例冠状动脉痉挛引起意识丧失伴随λ波的临床病例。     

Stent deformity caused by coronary artery spasm.

Previous studies have shown that coronary stents have radial strength above the pressure induced by coronary artery spasm. This case report describes a stent deformity caused by coronary artery spasm during percutaneous coronary intervention.     

A case of painless myocardial injury probably caused by coronary artery spasm]

A 53-year-old male was admitted to the hospital due to electrocardiographic ST-segment elevation in V1-4 with ST-segment depression in the inferior leads, which suggested acute myocardial infarction. He had a cough and a slight fever without chest pain. Serum creatine kinase and its myocardial band were slightly elevated but creatine kinase value did not exceed twice the normal upper limit. Emergent coronary arteriography (CAG) revealed intact coronary arteries. The CAG in a chronic stage again revealed intact coronary arteries. Intracoronary administration of acetylcholine of 100 micrograms to the left coronary artery and 50 micrograms to the right coronary artery provoked diffuse spasm in the right and left coronary arteries. The electrocardiogram (ECG) during the right coronary artery spasm revealed ST-segment depression in the inferior leads with ST-segment elevation in V2 and V3, which resembled the ECG finding at the time of the patient's admission. With intracoronary isosorbide dinitrate, the spasm and ST-segment elevation were resolved. These findings strongly suggest that coronary spasm can cause myocardial injury indicated by a slight elevation of serum creatine kinase value.     

Molsidomine prevention of coronary artery spasm caused by alkalosis

A test provocation of coronary artery spasm by alkalosis was used to evaluate a possible anti-coronary artery spasm effect of molsidomine. The rapid infusion of an alkaline buffer followed by maximal voluntary hyperventilation in 10 patients with angina at rest led to the appearance of angina pain and significant, transient ischaemic changes of the ST segment, due to alkalosis induced coronary spasm. A second provocation test was performed under the same conditions, 24 hours later, after the prior administration of 4 mg of molsidomine. Molsidomine prevented the development of coronary artery spasm in 8 of the 10 patients in the study group. These preliminary results justify further clinical evaluation of molsidomine in the treatment of vasospastic angina.     

Catheter-induced spasm of the left main coronary artery

Catheter-induced spasm of the left main coronary artery is rare during catheterization. We present several cases in which the occurrence of both ostial left main and right coronary spasm suggests that multiple sites of spasm may be a clue to this important diagnosis.     

Occluding spasm of the total left coronary artery during coronary angiography

Catheter-induced coronary artery spasms are rare during diagnostic coronary angiography, and they occur more often after PTCA because of local vessel wall injury. These spasms are rapidly reversible after administration of nitroglycerine and are normally no cause of serious complications. We report about a catheter-induced occlusive spasm of the entire left anterior descending and circumflex coronary artery in a 56-year-old patient with coronary double-vessel disease, 70% restenosis of the LAD, and a history of two coronary angiographic procedures and one PTCA without any complication. The spasm occurred immediately after the intubation of the left main stem with a 9F PTCA guiding catheter before the coronary guide wire or balloon was advanced into the LAD. Cardiac resuscitation was necessary due to acute left heart failure. The spasm was spontaneously reversible, but reproducible. Therefore, life-threatening coronary artery spasm can occur during coronary angiography or PTCA, but the tendency of spontaneous spasm relief seems to be high.     

Cardiogenic shock caused by severe coronary artery spasm immediately after coronary stenting

Coronary artery spasm is common during percutaneous coronary intervention and is easily relieved by intracoronary administration of vasodilators. We report the case of a patient who had severe, protracted, generalized spasm of the entire left coronary artery system during coronary artery stenting. The spasm, which was unresponsive to intracoronary vasodilators administered via guiding catheter, resulted in pulmonary edema and cardiogenic shock. Local injection of nitroglycerin via a transit catheter in the coronary artery eventually resolved the spasm and reversed the cardiogenic shock. To our knowledge, this is the 1st report of such a case in the English-language medical literature.     

A case of acute myocardial infarction following intracoronary thrombi caused by coronary artery spasm]

A 65-year-old man underwent coronary angiography (CAG) after 10 hours from the onset of myocardial infarction. We observed large Thrombi at the filling defect in the proximal site and mid-portion of the right coronary artery. CAG showed that they had disappeared completely without residual stenosis on the 4th day. In addition to this segmental spasms developed spontaneously at the proximal site of a thrombus accompanied by ST elevation, but these spasms recovered after intracoronary infusion of isosorbide dinitrate on the 26th day CAG. Thus, our case indicates that acute myocardial infarction may be caused by secondary coronary artery thrombosis and accompanying coronary artery spasm.