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Results for “Angina Pectoris, Variant”

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At least 1,099 records · Page 61Linked to original sources
PubMed1997

Iodine-123 metaiodobenzylguanidine cardiac imaging to identify and localize vasospastic angina without significant coronary artery narrowing.

OBJECTIVES: We assessed the ability of iodine-123 metaiodobenzylguanidine (MIBG) imaging to identify and localize coronary spasm and determined the most useful method of MIBG analysis in vasospastic angina without significant coronary narrowing. BACKGROUND: Various noninvasive methods have been used to detect vasospastic angina, but they are not very sensitive in patients with sporadic attacks. MIBG imaging has recently been proposed as a useful tool for detecting vasospastic angina. METHODS: Normal limits of both visual and quantitative analysis of two-dimensional polar maps (bull's-eyes) for MIBG imaging were at first established in 59 normal subjects. For optimal criteria of visual analysis, we established regional differences in abnormal MIBG defect scores. An abnormal region of the bull's-eye was defined as an area > 2 SD below normal. An abnormal regional washout rate was defined as < 0%. Using these criteria, we prospectively evaluated 104 patients with suspected vasospastic angina. Visual, bull's-eye and regional washout rate analyses were compared for overall detection of the disease and for individual vessel involvement. RESULTS: Overall sensitivity by these methods was 30%, 42% and 76%, respectively. Washout rate analysis showed a significantly higher sensitivity than the other two methods. Specificity was 78%, 72% and 87%, respectively. The sensitivity of detecting spasm-induced coronary artery with washout rate analysis was 82% for the left anterior descending (LAD), 76% for the right (RCA) and 69% for the circumflex (Cx) coronary arteries. The sensitivity of visual analysis was 29%, 15% and 35%, respectively; that for bull's-eye analysis was 34%, 54% and 41%, respectively. Washout rate analysis showed a significantly higher sensitivity for LAD spasm than for the other two methods and a higher sensitivity for RCA and Cx spasms than for visual analysis. CONCLUSIONS: Regional washout rate analysis of MIBG imaging is a highly accurate technique for determining the presence and location of coronary artery spasm.

3-Iodobenzylguanidine↗
PubMed1997

Nitric oxide-mediated flow-dependent dilation is impaired in coronary arteries in patients with coronary spastic angina.

OBJECTIVES: This study sought to examine whether flow-dependent dilation is impaired at the site of coronary artery spasm in patients with coronary spastic angina. BACKGROUND: Physiologic stimuli such as exercise and exposure to cold have been shown to cause an increase in coronary blood flow, leading to flow-dependent dilation of coronary arteries in normal subjects, but cause coronary constriction in patients with coronary spastic angina. METHODS: A maximal increase in blood flow was induced selectively in the left anterior descending coronary artery (LAD) by infusion of adenosine through a Doppler flow catheter tip in the midportion of the LAD in 10 patients with coronary spastic angina, all with angiographically demonstrated spasm of the LAD, and in 11 control patients. Coronary artery diameter at the proximal site of the LAD (exposed to increased flow but not to adenosine) was measured by quantitative angiography. RESULTS: Flow-dependent dilation of the proximal LAD was found to be less in spasm arteries than in control arteries. Infusion of NG-monomethyl-L-arginine (L-NMMA) in the proximal LAD suppressed flow-dependent dilation in control arteries but had no significant effect on spasm arteries. The dilator response to nitroglycerin was not impaired in spasm coronary arteries. CONCLUSIONS: Our results indicate that flow-dependent coronary dilation is impaired in spasm arteries, partly due to a deficiency in endothelial nitric oxide bioactivity, which in turn may contribute to the increase in coronary tone during physiologic stimuli in patients with coronary spastic angina.

Adenosine↗
PubMed1998

Vitamin C attenuates abnormal vasomotor reactivity in spasm coronary arteries in patients with coronary spastic angina.

OBJECTIVES: This study sought to examine effect of vitamin C, an antioxidant, on the abnormal vasomotor reactivity in spasm coronary arteries. BACKGROUND: Oxygen free radicals generated in the arterial walls have been shown to cause endothelial vasomotor dysfunction. METHODS: Responses of the epicardial arterial diameters of the left coronary arteries to the intracoronary infusion of acetylcholine (ACh) (10 and 50 microg/min) were measured by quantitative coronary angiography before and during combined intracoronary infusion of vitamin C (10 mg/min) or saline as a placebo in 32 patients with coronary spastic angina and in 34 control subjects. RESULTS: Vitamin C infusion suppressed the constrictor response of the epicardial diameter to ACh in spasm coronary arteries but had no significant effect in the control coronary arteries (percent change in distal diameter in response to 10 microg/min of ACh [constriction (-), dilation (+), mean +/- SEM] before vitamin C: -8.2 +/- 2.9% in spasm arteries, +8.4 +/- 2.9%* in control arteries; during vitamin C: +0.2 +/- 3.8%* in spasm arteries, +7.2 +/- 1.3%* in control arteries [*p < 0.01 vs. spasm arteries before vitamin CI). The coronary sinus-arterial difference in plasma thiobarbituric acid reactive substances during ACh infusion, an indicator of lipid peroxidation in coronary circulation, was higher in patients with coronary spastic angina than in control subjects (p < 0.01) but was suppressed in patients with coronary spastic angina to comparable levels in control subjects by combined infusion of vitamin C. Saline infusion had no effect. CONCLUSIONS: The results indicate that vitamin C attenuates vasomotor dysfunction in epicardial coronary arteries in patients with coronary spastic angina. Oxygen free radicals may at least in part play a role in the abnormal coronary vasomotor reactivity in response to ACh in spasm coronary arteries.

Acetylcholine↗
PubMed1998

Vitamin E administration improves impairment of endothelium-dependent vasodilation in patients with coronary spastic angina.

OBJECTIVES: We examined the effects of oral administration of vitamin E, an antioxidant, on endothelium-dependent vasodilation in patients with coronary spastic angina. BACKGROUND: We have recently reported that endothelium-dependent vasodilation is impaired in patients with coronary spastic angina (CSA). Furthermore, it is known that oxidative stress may play an important role in the impairment of endothelium-dependent vasodilation in cardiovascular diseases. METHODS: With the ultrasound technique, flow-dependent vasodilation of the brachial arteries during reactive hyperemia was examined before and after treatment for a month with either oral administration of vitamin E (alpha-tocopherol acetate, 300 mg/day) or placebo, which is randomly assigned, in patients with CSA (n=60). RESULTS: Before treatment, patients with CSA had impaired flow-dependent vasodilation, lower plasma levels of alpha-tocopherol and higher plasma levels of thiobarbituric acid reactive substances (TBARS), as compared with age- and sex-matched control subjects (n=60) (flow-dependent vasodilation: 3.1+/-1.8 vs. 7.1+/-2.5%, p < 0.001; alpha-tocopherol levels: 8.9+/-1.8 vs. 10.8+/-1.8 microg/ml, p < 0.001). In patients with CSA, treatment with vitamin E restored flow-dependent vasodilation (3.1+/-1.7 vs. 8.3+/-2.0%, p < 0.001), and this improvement was associated with the decreases in plasma TBARS levels and anginal attacks. CONCLUSIONS: The results indicate that vitamin E treatment improved endothelium-dependent vasodilation and decreased plasma TBARS levels in patients with CSA. Thus, increased oxidative stress may contribute to endothelial dysfunction and anginal attacks in patients with CSA.

Adult↗
PubMed2002

Circadian variation of basal total vascular tone and chronotherapy in patients with vasospastic angina pectoris.

Vasospastic angina pectoris (VSA) is an anginal attack which occurs characteristically between night and early morning. The aim of this study was to clarify the cause of VSA. The subjects consisted of 16 patients with VSA, 18 patients with effort angina (EAP) and 15 healthy individuals, who were used as the control group. Subjects were attached to an ambulatory blood pressure monitor and a non-invasive continuous cardiac output monitor concurrently, over a 24-hour period. Mean blood pressure (MBP), and cardiac index (CI) were measured. Then basal total vascular tone (TVT) was calculated as follows: basal TVT = (MBP/CI) x 1,332 dyne/sec/cm5. The decrement of CO was greater during sleeping hours as compared with the decrement of the MBP in the VSA group. Nocturnal basal TVT was significantly greater in the VSA group than in the EAP group or the control group. The increased nocturnal basal TVT was significantly suppressed by long acting calcium antagonists to the level of the EAP and the control groups. The treatment also decreased the frequency of ischemic attacks.

Adult↗
PubMed1997

Unexpected hemoglobin electrophoresis results following red cell exchange in a sickle cell anemia patient with acute chest syndrome.

Acute chest syndrome is a well described complication of sickle cell anemia. It is characterized by fever, pulmonary infiltrates, pleuritic chest pain and abnormal pulmonary auscultation. Transfusion therapy, either simple transfusion of red blood cells or a total red blood cell exchange, is a cornerstone therapy for these patients. Exchange transfusion is preferred when an acute reduction of the hemoglobin S (HbS) concentration is the therapeutic goal since it allows one to rapidly reduce the percent HbS without increasing blood viscosity or volume (Wayne, Kevy and Nathan, Blood 1993; 81:1109-1123). Hemoglobin electrophoresis may be used to monitor the effectiveness of the exchange in decreasing HbS. The post-exchange HbS electrophoresis results which were obtained in this case initially caused confusion. In this report we discuss the findings and the reasons why such results may be occasionally expected in future similar situations.

Anemia, Sickle Cell↗
PubMed2002

Brugada syndrome: a case report of an unusual association with vasospastic angina and coronary myocardial bridging.

This report describes a case of an unusual association between vasospastic angina, coronary myocardial bridging, and Brugada syndrome. The patient complained of chest pain followed by rhythmic palpitation and syncope. Brugada syndrome ECG markers were documented with transient ST-segment elevation in lateral leads. A coronary angiogram showed a myocardial bridging in the left anterior descending artery and coronary vasospasm was reproduced after intracoronary ergonovine injection in the circumflex coronary artery. Ventricular fibrillation was induced by programmed electrical stimulation. The described association can be important because interaction between ischemia and Brugada syndrome electrophysiological substrate could modulate individual susceptibility to life-threatening ventricular tachyarrhythmias.

Angina Pectoris, Variant↗
PubMed2002

Class I antiarrhythmic drug and coronary vasospasm-induced T wave alternans and ventricular tachyarrhythmia in a patient with Brugada syndrome and vasospastic angina.

A 50-year-old man presented with a history of transient chest pain and palpitations. The 12-lead ECG at rest showed normal sinus rhythm. A slight ST segment elevation was observed in leads V1 to V3. During hospitalization, atrial fibrillation developed, and oral pilsicainide was administered. Thirty minutes after the drug was given, the ECG showed marked ST segment elevation in leads V1 to V3, and T wave alternans became visible in leads V2 and V3. Self-terminating ventricular tachycardia was initiated following frequent ventricular premature complexes, which showed a left bundle branch block pattern. The coronary angiogram was normal, but in the provocation test of vasospastic angina, acetylcholine administration into the left coronary artery resulted in complete occlusion of the left anterior descending and circumflex arteries. Marked ST segment elevation developed in leads I, aVL, and V3 to V6 concomitant with visible QT/T alternans in leads V4 and V5, and ventricular tachyarrhythmia was initiated. Brugada syndrome and vasospastic angina coexisted in this patient, and T wave alternans can be used as a predictor of ventricular tachyarrhythmias in such patients.

Acetylcholine↗
PubMed1980

[Non-invasive method for recognition of coronary artery spasm: 201thallium sequential scintigraphy of the myocardium after ergotamine provocation (author's transl)].

For evaluation of coronary artery spasm 201thallium sequential scintigraphy of the myocardium after ergotamine provocation was performed in 10 patients with recurrent angina pectoris at rest and normal exercise ECG. In 9 out of the 10 patients ergotamine administration in the same dosage was repeated during the coronary angiography. A reversible defect in the 201thallium scintigram representative of regional myocardial ischaemia developed in 9 patients after ergotamine. Only in 4 out of the 9 patients angina pectoris and ST elevation were present at the same time. In all cases coronary spasm after ergotamine was demonstrable in the coronary angiogram; in the 4 patients with ergotamine-induced Prinzmetal angina pectoris it consisted of complete vascular occlusion, in the asymptomatic patients of incomplete vascular narrowing of a higher degree. In all cases the spasm could be relieved by ergotamine antidotes within a few minutes.

Adult↗