Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151744 (myocardial ischemia)
31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In general, anginal symptoms diminish with time in patients with vasospastic angina. We assessed changes in coronary vascular tone (CVT) in patients with vasospastic angina over a 4-year period to evaluate the time course of spastic activity. Vasospastic angina was evaluated in 39 patients in whom occlusive spasm was evoked by selective intracoronary injection of ergonovine maleate (ERG-S) 48 h after stopping all coronary vasodilator drugs. These patients had no organic coronary stenosis and developed no stenosis during follow-up. ERG-S was repeated 3 times at 2-year intervals. CVT was determined at each ERG-S study using the equation: CVT = 1-(coronary artery diameter before ERG-S/coronary artery diameter after intracoronary injection of isosorbide dinitrate). Thirty-four patients (87%) had no angina pectoris at the second ERG-S study and 28 (72%) had none at the third. Coronary spasm was induced in 25 patients at the second ERG-S study and in 20 at the third. The overall CVT was shown to decrease at each successive ERG-S study (p < 0.01). There was no correlation between changes in CVT and anginal symptoms or the coronary spasm induction rate. These results demonstrate that CVT decreases over time in patients with vasospastic angina, suggesting that myocardial ischemia may improve spontaneously.
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PMID:Evolution of coronary vascular tone in vasospastic angina. 915 68

Fluctuations of spasmodicity have been reported in affected vessels in patients with vasospastic angina, but the incidence of spasmodicity induced by pharmacologic agents on both vessels with spasm and vessels without induced spasm has not been investigated. Repeated spasm provocation tests by acetylcholine or ergonovine were performed at 13.1 +/- 9.9 month intervals (3-50 months) in 111 vessels of 50 patients with ischemic heart disease, consisting of 19 old myocardial infarction and 31 angina pectoris, who did not undergo angioplasty or have signs of advancing atherosclerosis. Spasm was defined as present when more than 90 percent stenosis was accompanied by the appearance of usual chest pain or significant electrocardiographic changes. Ninety-six vessels (86.5%), 65 without spasm and 31 with spasm, revealed coincident responses and the remaining 15 vessels contrary reacted. The coincidence rate of spasmodicity in patients at intervals of within 24 months (90.2%) was significantly higher (p < 0.05) than that at intervals of over 24 months apart (70.4%). The spasm coincidence rate was 67.3% in the vessels with provoked spasm by either the first or second tests. Only one (0.9%) out of the 111 vessels showed obvious progressive atherosclerosis during this study. The majority of vessels showed identical spasmodicity within 2 years. In conclusion, coronary spasmodicity might remain unchanged for at least 2 years despite medication with calcium channel blockers and isosorbide dinitrate.
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PMID:[Is coronary spasmodicity unchangeable?: a study with acetylcholine or ergonovine in patients with ischemic heart disease]. 936 54

One hundred twenty-four patients with lung cancer undergoing operation in our hospital were prospectively studied on evaluation of the ischemic heart disease before operation. They performed master double electrocardiogram and exercised T1 scintigram before operation. The patient with positive master double electrocardiogram and/or exercised T1 scintigram was taken into high risk group. All patients in high risk group performed coronary angiography. This high risk group consisted of 37 patients (29.8%), including 6 single vessel disease (4.8%), 2 double vessel disease (1.6%), and 1 triple vessel disease (0.8%). Preoperative revascularization was done 8 patients (6.5%). These revascularization patients had uneventful course during and after lung operation. However 2 cases of vasospastic angina (VSA) occurred in non-risk group during operation. It was impossible to anticipate VSA before lung operation in our series. Therefore our preoperative evaluation and care of organic ischemic heart disease was effective in preventing cardiac complications.
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PMID:[Prospective study on evaluation of the ischemic heart disease for preoperative patients with lung cancer]. 963 41

The authors treated 10 patients with microvascular angina (MVA) manifesting angina pectoris, ST segment elevation suggestive of transmural myocardial ischemia, and no epicardial arterial obstruction. Since such patients frequently showed abnormal responses to oral glucose loading, the authors investigated the glucose and insulin responses to glucose loading in 10 MVA patients, 25 patients with vasospastic angina (VAP), 25 patients with effort angina (EAP), and 25 control subjects. Insulinogenic index, peripheral insulin activity [= 10(4)/(peak glucose x insulin at glucose peak)], glucose area, and insulin area were calculated. The MVA group included two patients with impaired glucose tolerance and two newly diagnosed diabetic patients. These proportions were similar to those in the VAP and EAP groups. Glucose levels at 30 to 180 min and insulin levels at 90 to 120 min in the MVA group were higher than in the control group. Peak glucose, glucose area, peak insulin, and insulin area were higher in the MVA group than in the control group (p<0.01). Those in the VAP and EAP groups were also higher. Insulin/glucose ratio at 120 min was higher, peripheral insulin activity, lower, in the disease groups than in the control group (p<0.05). The MVA patients showed a hyperglycemic and hyperinsulinemic response to oral glucose loading, as did the patients with EAP and VAP. Enhanced insulin response to oral glucose loading may also contribute to the pathogenesis of MVA.
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PMID:Enhanced insulin response to oral glucose load in patients with angina pectoris associated with ST segment elevation in the absence of epicardial coronary arterial obstruction. 978 46

There are only a few reports concerning coexistent hypertrophic cardiomyopathy (HCM) and vasospastic angina. Clinical characteristics in patients with both diseases have not been clarified yet. This study was designed to elucidate the relationship between chest pain and coronary vasospasm in HCM patients and to delineate clinical characteristics in patients with both HCM and coronary vasospasm. First, 36 patients with HCM underwent acetylcholine provocation test for coronary vasospasm and were divided into two groups on the basis of presence or absence of coronary vasospasm. Next, the following risk factors for coronary artery disease were compared between the two groups: hypertension, smoking, hyperlipidemia, diabetes mellitus, and hyperuricemia. Coronary vasospasm was induced in 10 (28%) of 36 patients with HCM. There were no significant differences in age and male gender between the two groups. Smoking was more prominent in HCM patients with than without coronary vasospasm (80% vs 35%, p<0.05), but there were no differences in the prevalence of other risk factors between the two groups. In conclusion, coronary vasospasm appears to play a significant role in the etiology of myocardial ischemia in Japanese patients with HCM, and smoking might be a major risk factor for coexistence of HCM and coronary vasospasm.
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PMID:Clinical characteristics in Japanese patients with coexistent hypertrophic cardiomyopathy and coronary vasospasm. 978 50

The relationship between autonomic nervous system activity (ANA) and coronary vasoreactivity during transient myocardial ischemia was determined in patients with vasospastic angina (VA). ANA was measured by power spectral analysis of heart rate variability and humoral factors following intravenous infusion of insulin in 24 patients with VA and 6 control patients. Nine (38%) of the VA patients had significant ST segment depression (STD), and 4 of these patients had symptomatic STD. The frequency of anginal episodes in the 9 patients with VA and STD was significantly greater than that in the 15 VA patients without STD (3.4 +/- 3.1 vs 0.5 +/- 0.8 episodes/week, p < 0.05). The increase in the LF/HF ratio 30 min after insulin injection in patients with STD was significantly greater than that in patients without STD (34 +/- 31% vs 4 +/- 34%, p < 0.05). All of the patients with VA and STD had significant coronary vasospasm in response to the infusion of < or = 20 micrograms of acetylcholine, higher levels of nocturnal parasympathetic activity, and greater norepinephrine production in response to insulin stimulation than the VA patients without STD. These findings suggest that increased vagal tone and hyperreactivity to adrenergic stimulation may trigger vasospasm in patients with VA.
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PMID:Coronary hyperreactivity to adrenergic stimulation and increased nocturnal vagal tone trigger coronary vasospasm. 980 51

The term X syndrome is used to indicate a group of patients who present anginous symptoms and ischemic-type electrocardiographic alterations which appear during exercise tolerance tests, dipiridamol tests or Holter's dynamic monitoring where coronary ultrasonography reveals no evident coronary lesions, vasospastic angina, arterial hypertension and/or diabetes mellitus, block of the left branch when resting or exercising, cardiomyopathy or valvulopathy. The highest incidence is in females with a mean age of around 50. A reduced reserve of coronary flow, highlighted both in response to vasodilatators or rapid stimulation and by positron emission tomography (PET), underlies this syndrome. It is thought to be caused by a dysfunction of the coronary microcirculation which consists in a deficit of the endothelium-dependent vasodilatory mechanisms, probably also owing to the accumulation of vasoconstrictive type substances, like endothelin-1. In addition to a dysfunction of the coronary microcirculation, one widely backed hypothesis concerns the existence of an altered perception of painful symptoms in patients with X syndrome: the anomalous constriction of prearteries might cause an increased release of adenosine, able to provoke angina despite the scarce signs of myocardial ischemia in terms of the metabolic or functional profile. From a therapeutic point of view, treatment of these patients is often ineffective: treatment should be based on the use of nitrates, calcium-antagonists or beta-blockers, if necessary moving on to other forms of therapy (aceinhibitors, xanthine methylate, estrogens, alphablockers, imipramine); the simultaneous use of tranquillizers may be useful in view of the anxious personality often characteristic of these patients.
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PMID:[Syndrome X and microvascular angina]. 988 62

To understand the effect of hyperventilation (HV) stress in patients with spastic angina, left ventricular (LV) contraction was analyzed by quantitative phase analysis. The study was performed on 36 patients with spastic angina pectoris, including vasospastic angina pectoris (VspAP: 16 patients) and variant angina pectoris (VAP: 20 patients). First-pass radionuclide ventriculography (first-pass RNV) was performed at rest and after HV stress, and standard deviation of the LV phase distribution (SD) was analyzed. The SD was lower in patients with VspAP than in VAP (12.8+/-1.4 degrees vs. 14.6+/-2.2 degrees, p < 0.005) at rest. After HV stress, the SD (HVSD) tended to increase in VspAP patients (62.5%), whereas the SD decreased in VAP patients (70%). Due to HV stress, the percentage change in SD (%SD) in VspAP patients was 8.9+/-23.7% whereas that in VAP patients was -9.1+/-17.3% (p < 0.01). Moreover, phase histograms were divided into HVSD increase and HVSD decrease groups. The HVSD increase group had a decrease of HVEF, but the HVSD decrease group tended to have more decreased HVEF than the HVSD increase group. These results indicate that spastic angina pectoris patients show various responses to HV stress. The HVSD increase group might have additional myocardial ischemia due to regional coronary spasm. In contrast, in the HVSD decrease group severe LV dysfunction or diffuse wall motion abnormality might have been generated, and this caused a reduction in the SD value. Phase analysis would therefore add new information regarding electrocardiographically silent myocardial ischemia due to coronary spasm, and HV stress might increase sensitivity for the detection of abnormalities in quantitative phase analysis, especially in VspAP patients.
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PMID:Phase changes caused by hyperventilation stress in spastic angina pectoris analyzed by first-pass radionuclide ventriculography. 1020 43

A 41-year-old-man without previous ischemic heart disease, developed a severe anaphylactic reaction. After administration of epinephrine (0.5 mg) the patient complained of chest pain. The electrocardiogram showed an elevation of ST segment in inferior leads. Myocardial necrosis was ruled out. Coronary arteriography disclosed normal coronary arteries. Eight months later, the patient developed severe chest pain during physical activity. ST elevation was again seen in inferior leads. ECG changes disappeared, when sublingual nitroglycerin was administered. A diagnosis of vasospastic angina was made. Exercise test was negative, during treatment with calcium-blocking agents. The patient subsequently remain free of symptoms taking medication. The physiological mechanisms of vasospastic angina and precipitating factors are discussed.
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PMID:[An adrenaline-induced vasospasm as the form of presentation of variant angina]. 1021 70

Vasospastic angina is rarely observed during cancer treatment. The present report describes two males with lung cancer, aged 73 and 61, who developed vasospastic angina during combination treatment of cisplatin-containing chemotherapy and thoracic irradiation. As both patients have smoked and their ages are typical for patients with coronary artery disease, such events may be incidental. However, oncologists should be aware of the possible development of myocardial ischemia during or following administration of antineoplastic agents, especially in elderly patients with pre-existing coronary risk factors or a history of thoracic radiotherapy.
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PMID:Vasospastic angina likely related to cisplatin-containing chemotherapy and thoracic irradiation for lung cancer. 1039 83


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