Cases reported "Coronary Vasospasm"

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1/120. A case of vasospastic angina presenting Brugada-type ECG abnormalities.

    An electrophysiological study and a provocative test of coronary artery spasm was attempted in a 68-year-old man who was having syncopal attacks and chest pain. His electrocardiogram had the characteristics of brugada syndrome and ventricular fibrillation (VF) was induced by programmed electrical stimulation. ST-segment elevation became exaggerated by procainamide, which could not prevent the induction of VF. coronary angiography revealed no stenotic lesions, and spasm in the left coronary artery was induced by intracoronary administration of acetylcholine with similar chest pain to that experienced before. Under treatment with diltiazem and flecainide, which suppressed the induction of VF, the patient experienced no recurrence of symptoms despite persistent ST-segment elevation. No previous reports have described coronary spasm associated with Brugada-type ECG abnormalities, and patients with syncope should be evaluated carefully.
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2/120. coronary vasospasm associated with uncontrolled carcinoid tumour.

    We report on a 74-year-old carcinoid patient who, following acute myocardial infarction (MI) and percutaneous transluminal coronary angioplasty, suffered recurrent episodes of chest pain and ST-segment elevation on ECG. This was accompanied by elevation of urinary 5-hydroxy-indole acetic acid. A review of the patient's file revealed that during the 3 weeks prior to the MI, she had been treated inadvertently with a fivefold lower dosage of octreotide. Following the correction of octreotide dosage, episodes of chest pain resolved immediately. We therefore suggest that this patient suffered from recurrent coronary vasospasm due to uncontrolled carcinoid tumour.
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3/120. coronary artery bypass grafting for spontaneous coronary artery dissection: a case report and a review of the literature.

    A 37 year-old woman underwent coronary angiography because of chest pain at rest. Selective coronary angiography demonstrated dissection and stenosis with a filling delay from the left main trunk to the left anterior descending coronary artery. The patient was successfully managed with urgent coronary artery bypass grafting. Spontaneous coronary artery dissection is relatively rare and threatens both elderly and young patients with acute coronary disturbances. patients can be divided etiologically into three groups. The first was comprised of those in the postpartum period. The second was those with atherosclerotic coronary artery disease, and the third was those associated with coronary vasospasm. Dissections are frequently fatal and most of the known cases have been diagnosed at autopsy. Only a few cases have been documented by coronary angiography, and operative cases of spontaneous coronary artery dissection have rarely been reported.
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4/120. acetylcholine- and ergonovine-induced coronary microvascular spasm reflected by increased coronary vascular resistance and myocardial lactate production.

    diagnosis of coronary microvascular spasm remains largely speculative because it has been mostly based on chest pain and electrocardiographic ST-segment shift with slow filling of contrast medium into the coronary artery. A patient with resting chest pain and normal coronary angiograms underwent provocative tests with intracoronary acetylcholine (ACh) and ergonovine. During the tests, coronary diameter and flow velocity in the left anterior descending (LAD) coronary artery were measured with quantitative coronary angiography and intracoronary Doppler guide wire, respectively. vascular resistance of the LAD and lactate production were determined separately. With injections of 100 microg of ACh and 20 microg of ergonovine, chest pain occurred with ST-segment elevation in the precordial leads in the absence of epicardial coronary spasm. Coronary vascular resistance increased by 2.2- and 1.6-fold of the baseline value with ACh and ergonovine, respectively. Myocardial lactate production was noted during the ST-segment elevation. Coronary microvascular spasm was verified by the increment in coronary vascular resistance and myocardial lactate production with concomitant ST-segment elevation in the presence of normal coronary angiograms.
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5/120. Coronary artery spasm induced by carotid sinus massage.

    A 60 year old man with a history of frequent episodes of chest pain and dizziness was referred for evaluation of coronary artery disease. He had no significant coronary artery stenosis at baseline coronary angiography. A carotid sinus massage was performed for evaluation of carotid sinus hypersensitivity in the patient. Both heart rate and blood pressure decreased a little, and returned to baseline level immediately after carotid sinus massage. However, 2.5 minutes after carotid sinus massage, ECG showed ST segment elevation in leads II, III, and aVF. Four minutes after carotid sinus massage, he had chest pain with a progressive elevation in the ST segment in the same leads, when he had 99% focal spasm in the right coronary artery. The vasospasm induced by carotid sinus massage was reproducible over several minutes and resolved spontaneously. Coronary artery spasm may be provoked by the enhanced vagal activation due to carotid sinus massage.
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6/120. Endothelial nitric oxide synthase gene mutation and human leukocyte antigen analyzed in three cases of familial vasospastic angina pectoris.

    A 50-year-old woman with rest angina underwent cardiac catheterization; coronary angiography in the presence of acetylcholine revealed 99% coronary spasm of the proximal left anterior descending artery. The patient's 82-year-old mother was also admitted to hospital with rest angina. Her Holter electrocardiogram showed ST-segment elevation during the attack at rest and coronary angiography showed 99% spasm of the right coronary artery and 90% spasm of the left coronary artery. Both women complained of chest pain during the spasm, which was accompanied by ST-segment depression. The 62-year-old brother of the original patient was also found to have coronary spasm of the left coronary artery. Human leukocyte antigen was analyzed in the 2 women: A2, B51, CW1, DR8 and DQ1 were common factors. A Glu298Asp point mutation of the endothelial nitric oxide synthase gene was investigated in both parents, their 2 daughters and 2 sons, but was not detected in the 3 patients, and was detected only in the 90-year-old father who did not suffer from angina. Nor was the T-786-C mutation found in the 3 cases. Other causes of familial spasm need to be elucidated.
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7/120. Uncommon and dynamic changes detected by 123I-15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid myocardial single photon emission computed tomography in a stunned myocardium induced by coronary microvascular spasm.

    A 55-yr-old man underwent surgery. Soon after the procedure was finished, the patient complained of chest pain, and the electrocardiogram showed increase in the ST-segment in some leads. Emergency angiography showed normal coronary arteries, but there was asynergy in the left ventricle, and delayed filling of contrast medium was observed in the LCA. An intracoronary infusion of isosorbide dinitrate did not improve the delayed filling of contrast medium or ST segment increase in the electrocardiogram. Soon after nicorandil was injected into the LCA, the patient's symptoms, electrocardiogram, and delayed filling of contrast medium dramatically improved. On the second day, initial imaging by 123I-BMIPP myocardial SPECT showed a moderate increase in tracer uptake in the apico-anteroseptal region and a moderate decrease in tracer uptake in the lateral region, in which the first left ventriculography showed akinesis, and delayed imaging revealed a moderate increase in tracer uptake in the apical region and a high washout of 123I-BMIPP in the anteroseptal and lateral regions. On the sixth day, initial imaging by 123I-BMIPP myocardial SPECT showed a moderate decrease in tracer uptake in the apical and lateral regions and a mild decrease in tracer uptake in the anteroseptal region, and delayed imaging revealed a moderate increase in tracer uptake in the apical region and a high washout of 123I-BMIPP in the anteroseptal and lateral regions. By the 30th day, 123I-BMIPP myocardial SPECT had normalized. We consider that these dynamic changes in 123I-BMIPP myocardial SPECT imaging may reflect metabolic changes in fatty acids in the ischemic state, the size of the triacylglycerol pool, and the degree of turnover in the triacylglycerol pool.
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8/120. Successful management of intractable coronary spasm with a coronary stent.

    Although the long-term survival of patients suffering from coronary spasm is usually excellent, serious complications can develop, such as disabling pain, myocardial infarction, ventricular tachyarrhythmias, atrioventricular block and sudden cardiac death. A 40-year-old man who had intractable chest pain from coronary artery spasm suffered ventricular fibrillation and an acute anterior myocardial infarction upon first admission. The patient underwent a coronary angiogram, which revealed a spontaneous focal spasm at the proximal left anterior descending coronary artery (LAD). He was treated by the combination of nitrate and calcium channel blocker, but continued to complain of severe chest pain despite intensive medical therapy and he had to be treated in the emergency room 5 times during an 8-month follow-up period. An ergonovine coronary angiogram was performed and an intracoronary ultrasound examination, which revealed a focal spasm at the same site of the proximal LAD with a small amount of localized eccentric atheromatous plaque. A coronary artery stent was placed in the proximal LAD and his symptoms resolved. A follow-up coronary angiogram was performed 3 years after stenting and the stent remained patent without any in-stent restenosis or spasm.
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9/120. Anteroapical stunning and left ventricular outflow tract obstruction.

    Dynamic left ventricular outflow tract (LVOT) obstruction is typically observed in the setting of hypertrophic cardiomyopathy. It has also been reported with concentric LV hypertrophy, excessive sympathetic stimulation, and acute myocardial infarction. We describe 3 patients with chest discomfort after emotional stress, who had pronounced abnormalities on electrocardiograms, insignificant obstructive coronary disease and hemodynamic instability with LVOT obstruction, and regional wall motion abnormalities. Suppression of contractility with beta-blockers resulted in resolution of the gradient and in clinical improvement. On follow-up, functional recovery was excellent, and ventricular function had normalized. The conditions and mechanisms that may produce this sequence of events are discussed. The most probable scenario is that an acute ischemic insult secondary to vasospasm, LV stunning, and acute geometric remodeling produced a substrate for LVOT obstruction that was exacerbated by basal LV hypercontractility. The importance of this observation is that routine treatment of cardiogenic shock cannot be used and that conservative management results in excellent prognosis.
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10/120. cardiopulmonary resuscitation during coronary vasospasm induced by tilt table testing.

    A 65-year-old man presented to our institution with recurrent episodes of early morning chest discomfort and near syncope. An ergonovine provocation test documented a diagnosis of coronary vasospastic angina. Using our investigation of the syncope, a head-up tilt table test provoked a severe episode of coronary vasospasm that resulted in a life-threatening cardiac event. The present case reminds us that an elevation of ST segments on the electrocardiogram during tilt testing should be promptly managed as an attack of coronary vasospasm.
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