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At least 19 recordsLinked to original sources
PubMed1991

[Continuous measurement of coronary sinus oxygen saturation in patients with effort angina and vasospastic angina].

Coronary sinus oxygen saturation (CSO2-Sat) was measured continuously using a fiberoptic catheter system during interventional catheterization, i.e., pacing stress test and ergonovine provocation test to determine whether such measurement can detect myocardial ischemia. Subjects consisted of 24 patients who underwent routine cardiac catheterization; 14 patients with effort angina, 3 with old myocardial infarction and 3 with valvular heart disease were assigned to pacing stress test, and 4 with vasospastic angina were assigned to ergonovine provocation test. The results were as follows: 1. Among 14 patients with effort angina, ischemic electrocardiographic changes occurred in 10 patients during pacing stress test. Of these 10 patients, CSO2-Sat decreased in 8 with ischemic electrocardiographic changes. All patients with decrease in CSO2-Sat had significant left coronary artery stenosis. CSO2-Sat continued to decrease throughout intervention and never came back to the baseline. Decrease in CSO2-Sat was more than 5% in most of the cases. 2. In all patients with vasospastic angina, coronary vasospasm was induced by the ergonovine provocation test. CSO2-Sat declined (> 5%) gradually, preceding anginal pain and ischemic ST segment changes. The present study suggests that continuous monitoring of coronary sinus oxygen saturation may be useful in detecting myocardial ischemia at its early stage, except for patients with right coronary artery disease.

Adolescent↗
PubMed1999

[Cardiac events in vasospastic angina: site and morphology of coronary artery spasm is related to the long-term prognosis of vasospastic angina].

To determine whether the site and morphology of coronary artery spasm provoked with acetylcholine can predict the long-term prognosis of vasospastic angina, coronary artery spasm (more than 90% narrowing) provoked with acetylcholine was studied in 66 consecutive patients (56 males, 10 females, mean age 56 +/- 9 years) with vasospastic angina. All patients were followed for 6.7 +/- 0.9 years and the incidence of cardiac events such as sudden death, myocardial infarction or worsened unstable angina was compared with the site and morphology of provoked spasm. The site of spasm was regarded as proximal when spasm occurred in the proximal site of 3 major coronary arteries which was designated as segment 1, 6 or 11, according to the classification of the American Heart Association, and distal in other segments. The morphology of spasm was classified into 3 types, focal (12 cases, localized more than 90% narrowing with adjoining parts constricting less than 25%), diffuse (17 cases, diffuse more than 90% narrowing), and intermediate (37 cases, localized more than 90% narrowing with adjoining parts constricting 25-90%). The site of spasm was classified into 2 types, the proximal group (24 cases) and the distal group (42 cases). Cardiac events occurred in 7 patients during the follow-up period: sudden death in 2, myocardial infarction in 2, and worsened unstable angina in 3. As to the site of spasm, the incidence of cardiac events was 21% (5/24 patients) in the proximal group, significantly higher than 5% (2/42) in the distal group (p < 0.05). As to the site of spasm, the incidence of cardiac events was 41% (5/12) in the focal group, significantly higher than 3% (1/37) in the intermediate group and 6% (1/17) in the diffuse group (p < 0.001). The presence of proximal and focal coronary artery spasm was associated with a significantly higher incidence of cardiac events. The site and morphology of coronary artery spasm provoked with acetylcholine is related to the long-term prognosis of vasospastic angina.

Acetylcholine↗
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↗
PubMed1986

Comparison of risk factors in vasospastic angina without significant fixed coronary narrowing to significant fixed coronary narrowing and no vasospastic angina.

To determine the importance of usual risk factors of coronary artery disease (CAD) in patients with coronary artery spasm, 40 patients with vasospastic angina (VA), normal or nearly normal coronary arteries and without previous myocardial infarction were compared with 2 control groups of 40 patients each, matched for age and sex: 1 group with CAD and 1 without heart disease. Ninety percent of patients with VA were cigarette smokers and 70% were heavy smokers (more than 20 cigarettes daily), compared with 53% and 33% in patients with CAD (p less than 0.001) and 30% and 15% in those without heart disease (p less than 0.001). Except for cigarette smoking, the risk factor profile of patients with VA appeared more like the profile of patients without heart disease than that of patients with CAD. The results suggest that cigarette smoking may play a role in CAD independent of atherosclerosis and possibly favoring coronary artery spasm.

Adult↗
PubMed1995

Progression and regression of coronary stenosis in the long-term follow-up of vasospastic angina.

BACKGROUND: Whether focal vasospasticity plays a pathogenic role in the progression or regression of coronary atherosclerosis is unknown. To determine whether evidence for such a role exists, we studied long-term changes in coronary luminal measurements in patients with vasospastic angina. METHODS AND RESULTS: Quantitative coronary angiography and repeated ergonovine provocation tests were performed 45 +/- 16 months apart in 30 patients. All patients had vasospastic anginal symptoms and coronary spasm on the initial provocation test. On the 30 patients, 16 had persistent symptoms of vasospastic angina and showed coronary spasm at the same site on the follow-up angiogram (group 1), while the remaining 14 whose vasospastic anginal symptoms disappeared at follow-up demonstrated a negative response to ergonovine on the follow-up tests (group 2). There was no significant difference in patients' baseline characteristics between the two groups. Long-term changes in minimal (MLD) and mean (MEAN) luminal diameter were measured (in millimeters) after administration of isosorbide dinitrate in 19 spastic and 93 nonspastic segments in group 1 and in 17 previously spastic and 81 nonspastic segments in group 2. Both MLD and MEAN were measured in 210 coronary segments of the 30 patients at baseline and after administration of ergonovine and isosorbide dinitrate by use of a computer-based quantitative coronary angiography system. Stenosis progression and regression of individual lesions were defined as a change in MLD of > or = 0.40 mm. In group 1, both the MLD and MEAN of 19 spastic segments were significantly smaller (progression) at follow-up compared with the initial angiogram (MLD, 2.21 +/- 0.54 initially versus 1.95 +/- 0.65 at follow-up, P < .01; MEAN, 2.80 +/- 0.56 initially versus 2.56 +/- 0.58 at follow-up, P < .01), whereas the MLD and MEAN of 93 nonspastic segments in group 1 were not significantly different between the initial and follow-up angiograms (MLD, 2.47 +/- 0.67 initially versus 2.44 +/- 0.69 at follow-up, P = NS; MEAN, 2.96 +/- 0.69 initially versus 2.91 +/- 0.68 at follow-up, P = NS). In group 2, the MLD of the 17 previously spastic segments significantly improved (regression) at follow-up (MLD, 1.99 +/- 0.68 initially versus 2.24 +/- 0.54 at follow-up, P < .05); the MLD and MEAN of the 81 nonspastic segments were not significantly different (MLD, 2.36 +/- 0.59 initially versus 2.39 +/- 0.60 at follow-up, P = NS; MEAN, 2.81 +/- 0.58 initially versus 2.81 +/- 0.61 at follow-up, P = NS). In group 1, significant stenosis progression of individual lesions was observed more frequently at spastic than nonspastic segments (6 of 19 versus 10 of 93, P < .05), whereas stenosis regression was observed in no spastic and 3 nonspastic segments (P = NS). In group 2, stenosis progression was observed at 1 previously spastic segment and 4 nonspastic segments (P = NS), while significant stenosis regression of individual lesions was seen more commonly in previously spastic than nonspastic segments (6 of 17 versus 7 of 81, P < .01). CONCLUSIONS: These results have demonstrated in patients an association between persistent vasospastic activity and progression of atherosclerosis and an association between cessation of vasospastic activity and regression of atherosclerosis.

Adult↗
PubMed1999

Mental stress test is an effective inducer of vasospastic angina pectoris: comparison with cold pressor, hyperventilation and master two-step exercise test.

BACKGROUND: Cold pressor, hyperventilation and exercise stress tests were usually used for inducing an angina attack in patients with vasospastic angina pectoris. We induced vasospastic angina attack using the mental calculation stress test, and compared the results with those using other stress tests. SUBJECTS AND METHODS: Subjects were 29 patients with vasospastic angina pectoris. Their ages were 60.8+/-8.4 years. Coronary vasospasm was induced by an acetylcholine infusion test during coronary angiography. The mental stress test was performed as follows; after memorizing six digits numbers, they repeated these numbers in reverse for 5 min, and performed serial subtraction of 17 from 1000 for 5 min. Blood pressure, heart rate and ECG were recorded every 1-5 min during the mental stress test. The serum concentrations of epinephrine and norepinephrine were measured before and during the mental stress test. We compared these results with those obtained using cold pressor, hyperventilation and the Master two-step exercise stress test. RESULTS: (1) Eight of the 29 patients (28%) showed ischemic ST-T change, which was caused by the mental stress test. (2) The increase in norepinephrine was greater in patients with an ST-T change than without an ST-T change (0.11+/-0.06 vs. 0.04+/-0.04 ng/ml, P<0.01). (3) The incidence of the ST-T change caused by the mental stress test (28%) was similar to the cold pressor test (27%) and greater than that caused by the hyperventilation test (13%). The incidence of ST-T change caused by the Master two-step test was 55%. CONCLUSIONS: The mental stress test is an effective inducer of vasospastic angina attack, and attack may be induced by neurohumoral vasoconstrictive reflex and/or increased left ventricular afterload.

Acetylcholine↗
PubMed1995

Vasospastic angina in two sisters.

Vasospastic angina was observed in two sisters. The 52-year-old younger sister presented with rest angina at midnight and in the early morning. The coronary arteriogram showed no significant organic stenosis. Vasospasm to the left anterior descending and right coronary arteries was induced by the intracoronary administration of acetylcholine. The 57-year-old elder sister complained of rest and effort angina. Her coronary arteriogram was also normal. Vasospasm to the left circumflex and right coronary arteries was provoked by acetylcholine. In both cases, human leukocyte antigen DQw3 was negative. In the present cases, genetic factors may partly contribute to the mechanism of vasospastic angina.

Acetylcholine↗
PubMed1996

Impaired glucose tolerance with late hypersecretion of insulin during oral glucose tolerance test in patients with vasospastic angina.

OBJECTIVES: This study tested whether patients with vasospastic angina have impaired glucose tolerance or impaired insulin response. BACKGROUND: Hyperinsulinemia has been demonstrated in patients with coronary artery disease and syndrome X. METHODS: We performed an oral glucose tolerance test (75 g) in 30 patients with vasospastic angina in whom severe coronary vasospasm was induced by acetylcholine and in a matched group of 30 patients with atypical chest pain in whom no significant vasospasm was induced. The responses of insulin and glucose were compared between the two groups. No subjects had overt diabetes mellitus, hypertension, dyslipidemia, obesity or angiographically detected significant baseline coronary stenosis. Venous blood samples were taken during fasting and at 30, 60, 120 and 180 min after glucose load to obtain plasma glucose and immunoreactive insulin levels. RESULTS: Impaired glucose tolerance was detected in the 19 (63%) of 30 patients with vasospastic angina and in none of 30 patients with atypical chest pain (p < 0.001). The immunoreactive insulin levels at 60 and 120 min as well as the interval to peak insulin level were significantly greater in patients with vasospastic angina (p < 0.001). Among patients with vasospastic angina, those with acetylcholine-induced multivessel coronary vasospasm showed a significantly higher sum of insulin concentrations than those with single-vessel spasm (p < 0.01). During induction of coronary spasm, 10 patients with vasospastic angina presented ventricular arrhythmias. The sum of insulin concentrations was significantly greater in patients with than in those without ventricular arrhythmias. CONCLUSIONS: Patients with vasospastic angina exhibited a high incidence of impaired glucose tolerance and delayed and significantly higher insulin responses. These findings suggest that impaired glucose tolerance with late hypersecretion of insulin may contribute to the pathogenesis of severe coronary vasospasm.

Adult↗
PubMed1994

Angina-linked syncope and lack of calcium antagonist therapy predict cardiac arrest before definitive diagnosis of vasospastic angina.

BACKGROUND: Several prognostic factors have been identified in patients with vasospastic angina; however, factors that would predict potentially fatal cardiac arrest during the period between the onset of angina and its definitive diagnosis remain unknown. We investigated the predictive value of the clinical findings that are available when a patient is hospitalized after a cardiac arrest but before a definitive diagnosis of vasospastic angina is made. METHODS: We compared the clinical findings in 11 patients who experienced cardiac arrest before vasospastic angina was definitively diagnosed (group I) with 81 patients with vasospastic angina without cardiac arrest (group II). The definitive diagnosis of vasospastic angina was made on the basis of results of coronary spasm provocation test or ECGs during spontaneous attacks, or both. RESULTS: The incidence of angina-linked syncope was significantly higher in group I than in group II (six out of 11 versus nine out of 81, P < 0.005). Significantly fewer group I patients were receiving calcium antagonists than group II patients (three out of 11 versus 63 out of 81, P < 0.005). Serious arrhythmias were significantly more common in group 1 than in group II (seven out of 11 versus 12 out of 81, P < 0.005). Logistic regression analysis of the eight clinical variables available when first seen in the hospital indicated that angina-linked syncope and the lack of calcium antagonist therapy were independently related to risk of cardiac arrest. CONCLUSIONS: From the clinical findings available, a history of angina-linked syncope and lack of calcium antagonist therapy were found to be independent predictors of cardiac arrest before a definitive diagnosis had been made. Patients who have suspected vasospastic angina may benefit from early treatment with calcium antagonists if they have a history of angina-linked syncope.

Aged↗
PubMed2007

Vasospastic angina in a 13-year-old female patient whose only symptom was toothache.

Vasospastic angina was confirmed in a 13-year-old female patient at autopsy. The patient's only symptom was recurrent toothache, which began when she was 10 years old. In November 2000, she was evaluated at our medical center; however, all examinations were judged normal. Six months later, she suffered a severe toothache. She went to school the next morning after the symptoms improved. She lost consciousness at school and was given cardiopulmonary resuscitation but could not be revived. At autopsy, her three coronary vessels showed marked intimal hyperplasia, and multiple focal myocardial infarctions were observed in the lateral wall of the left ventricle. The patient's only clinical symptom was toothache and none of the physicians realized that this was caused by angina. Vasospastic angina begins at a young age and is one of the causes of sudden death in adolescents.

Adolescent↗
PubMed1999

The role of alcohol dehydrogenase 2 and aldehyde dehydrogenase 2 genotypes in alcohol-induced vasospastic angina.

Alcohol ingestion often provokes attacks in patients with vasospastic angina. Type 2 aldehyde dehydrogenase (ALDH2) deficiency, which is based on a single point mutation (Glu487Lys) of the ALDH2 gene, is common in the Japanese population, but rare among the Caucasian population. We investigated how the genotype of ALDH2 affects the characteristics of alcohol-induced vasospastic angina. Ninety-one patients with vasospastic angina who had ingested alcohol daily or occasionally were studied. Patients had been diagnosed as vasospastic angina by a provocation test with an intracoronary injection of ergonovine or acetylcholine during coronary angiography. The Glu487Lys mutation was detected by allele specific PCR. We interviewed the patients to obtain information concerning the relationship between alcohol ingestion and anginal attacks. Alcohol ingestion induced attacks in 16 of 66 patients without the Glu487Lys mutation, 8 of 22 in heterozygotes, and 1 of 3 in mutant homozygotes. The intervals between alcohol ingestion and the onset of anginal attacks were shorter in homozygotes (0.17 hours) and heterozygotes (1.5+/-0.6 hours) for ALDH2*2 than in normal homozygotes for ALDH2*1 (5.4+/-0.6 hours). The amount of ethanol which induced attacks was significantly greater in normal homozygotes than in homozygotes (11 ml) and heterozygotes (42.5+/-7.1 ml) for ALDH2*2 (96.1+/-13.4 ml in normal patients). The frequency of anginal attacks induced by alcohol ingestion did not differ between ALDH deficient and normal homozygotes. In ALDH deficient patients, however, anginal attacks were induced by a smaller amount of alcohol immediately after its ingestion. Thus, the ALDH2 genotype modifies the characteristics of the anginal attacks as a co-factor for the induction of vasospastic angina after alcohol ingestion.

Alcohol Dehydrogenase↗
PubMed1997

Insulin resistance as an independent risk factor for carotid artery wall intima media thickening in vasospastic angina.

Studies have shown the presence of insulin resistance together with compensatory hyperinsulinemia in vasospastic angina as well as obstructive coronary artery disease. There is growing evidence that the development of coronary atherosclerosis may be closely related to systemic atherosclerosis as well as coronary spasm. However, no information is available about the possible relationship between insulin resistance and the existence of carotid atherosclerosis in vasospastic angina without segmental stenosis or luminal irregularities in coronary angiograms. To evaluate the independent effect of insulin resistance on carotid intima media thickening, we performed insulin sensitivity tests (steady-state plasma glucose method) on 40 patients with vasospastic angina and 24 control subjects with angiographically intact coronary arteries. Both oral glucose tolerance tests and lipid analyses were performed. Using B-mode ultrasonography, we assessed intima media thickness and plaque formation of common carotid arteries in these subjects. The steady-state plasma glucose level in the vasospastic angina group was about twofold higher than that of the control group, confirming the presence of insulin resistance in patients with vasospastic angina. The patients with vasospastic angina showed a significant increase in the average intima media thickness of the carotid wall and frequency of plaque formation, although they were comparable to the control subjects in risk factors other than insulin resistance. The intima media thickness was correlated with age (r = .62, P < .001), 2-hour insulin area (r = .45, P < .01), and steady-state plasma glucose level (r = .68, P < .0001) in patients with vasospastic angina. Similar correlations were observed in the control subjects. Multiple regression analyses of data indicated that 67% of the variation in the intima media thickness could be accounted for by age, steady-state plasma glucose level, and cigarette-years in vasospastic angina. In addition, differences in IMT were independently related to vasospastic angina. These results suggest that insulin resistance in association with compensatory hyperinsulinemia may be an important pathogenic factor for the development of coronary artery spasms and systemic early atherosclerosis.

Adult↗
PubMed1992

[Evaluation of coronary hemodynamics and exercise 201Tl-myocardial scintigraphy in patients with vasospastic angina].

To clarify the coronary hemodynamics and myocardial perfusion in patients with vasospastic angina, we performed exercise-201Tl-myocardial scintigraphy (planar and SPECT) in 72 patients and left coronary digital subtraction angiography (DSA) in 37 patients without significant organic coronary artery stenosis. Coronary artery spasm was documented by coronary angiography in all patients. Fifty-four patients (75%) developed exercise-induced 201Tl-myocardial perfusion defect on SPECT. 201Tl pulmonary uptake (L/H) was significantly increased in patients with vasospastic angina. Especially, L/H was higher in patients with multiple small perfusion defect on 201Tl-SPECT, so that exercise-induced left ventricular dysfunction existed in patients with vasospastic angina and especially in cases with multiple small perfusion defect on 201Tl-SPECT. The left coronary circulation time (CCT) was prolonged in patients with vasospastic angina. The mechanism of prolonged CCT is still unknown, but we suspected that prolonged CCT was induced by increased peripheral coronary vascular resistance in patients with vasospastic angina. It was concluded that the peripheral coronary circulation was disturbed in patients with vasospastic angina, but its abnormal coronary circulation had no relation to location of spasm-induced vessels. We concluded that impaired coronary microcirculation was taken a part of pathophysiology in vasospastic angina.

Aged↗
PubMed1985

Autonomic hyperactivity in patients with vasospastic angina.

To evaluate the role of the autonomic nervous system in vasospastic angina, plasma catecholamine and cyclic nucleotide levels were measured and the pilocarpine test was performed in 19 patients with vasospastic angina, 14 patients with nonvasospastic angina and 7 control subjects who were hospitalized patients without heart disease. Diurnal and nocturnal levels of plasma catecholamines were significantly higher in patients with angina pectoris, especially in patients with vasospastic angina, as compared with those of controls. In addition, an increase in plasma catecholamines preceded the onset of spontaneous and pilocarpine induced anginal attacks associated with significant increases in plasma catecholamines in patients with vasospastic angina. On the other hand, while nifedipine significantly suppressed both spontaneous and pilocarpine induced anginal attacks, the increase in plasma catecholamines remained. These results indicate that increased activity and responsiveness of the sympathetic nervous system may possibly contribute to the development of vasospastic angina on the basis of parasympathetic hyperactivity.

Angina Pectoris↗
PubMed1987

Hyperventilation thallium-201 myocardial imaging for the diagnosis of vasospastic angina.

In seven patients with vasospastic angina, a transient myocardial perfusion defect was demonstrated on Tl-201 myocardial imaging after hyperventilation (HV). The development of spasm on one or more coronary arteries after HV was confirmed by later coronary arteriographic studies, with the perfusing area of the coronary arteries being compatible with the scintigraphic location of the defect. Repeated 12-lead electrocardiograms failed to establish the diagnosis in one of the seven patients. It is concluded that HV Tl-201 myocardial imaging provides invaluable information in establishing a diagnosis of vasospastic angina.

Adult↗
PubMed1989

Clinical characteristics of sudden cardiac death in patients with vasospastic angina.

Of 383 patients with vasospastic angina who were followed for a period of 3.2 +/- 0.1 years, 9 (2%) died suddenly from cardiac causes. Calcium antagonists had been given to 98% of our patients. Only one patient who died suddenly had a fixed coronary stenosis of 75% or greater. Eight of the 9 patients showed ST segment elevation during anginal attack at rest, and 3 patients showed ST segment elevation at both anterior and inferior leads. Sudden death occurred in 6 of 41 patients (12.5%) who were documented to have multivessel coronary spasm, but in only 3 of 342 patients (1%) who had single vessel spasm (p less than 0.01). Serious arrhythmia occurred during anginal episode in 3 of 9 patients who died suddenly (53%) and in 52 of 374 who did not (14%). These results suggest that the frequency of sudden cardiac death was rather low in Japanese patients with vasospastic angina. The risk of sudden death was increased in patients with multivessel spasm and serious arrhythmia during anginal attacks but not these with fixed coronary stenosis.

Adult↗
PubMed1987

Clinical characteristics associated with myocardial infarction, arrhythmias, and sudden death in patients with vasospastic angina.

A total of 349 patients with vasospastic angina were followed in eight centers in Japan for a period of 3.4 +/- 0.1 years (mean +/- SE). Ninety-eight percent of patients were treated with calcium blockers. Twenty-one episodes of myocardial infarction occurred in 18 patients (5%), including two fatal myocardial infarctions. The rate of myocardial infarction was higher (p less than .01) in patients with a fixed stenosis of 90% or greater than in patients with a fixed stenosis of less than 90% or normal coronary arteries. Myocardial infarctions occurred predominantly during hospital stays or at a time when the frequency of vasospastic angina increased. There were five sudden deaths (2%). Only one patient suffering sudden death had a fixed stenosis of 75% or greater. Serious arrhythmias were noted in 49 patients (14%). The risk of arrhythmias did not depend on the presence of a fixed stenosis of 75% or greater. These results suggest that cardiac events are rather infrequent in Japanese patients with vasospastic angina who are receiving treatment with calcium blockers and that the presence of a severe fixed stenosis markedly increases the risk of myocardial infarction but not the risk of arrhythmias.

Adult↗