Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present a patient with two rare disorders, recurrent vasospastic angina leading to cardiac transplant and acute aortic occlusion. The patient had recurrent episodes of coronary vasospasm presenting with unstable angina, acute myocardial infarction, and sudden cardiac death in spite of adequate therapy with nitrates and calcium-channel blockers. He went on to have a cardiac transplant. The patient later presented with acute aortic occlusion with concomitant renal and mesenteric artery spasm. The circumstances of the presentation raise the possibility of a generalized vasospastic predisposition that is responsible for both events. Smoking, the only known major risk factor other than atherosclerosis, was noted to be temporally related to both events in our patient.
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PMID:Refractory vasospasm with a malignant course. 1067 6

There are many patients with vasospastic angina who have minor atherosclerosis, and in Japan the majority of them are male. No data exist concerning sex differences in patients with coronary spastic angina, so the present study sought to clarify the clinical characteristics between male and female patients with vasospastic angina. Between April 1991 and June 1998, 204 consecutive patients were diagnosed with vasospastic angina and of these, 26 (12.7%) were female. An acetylcholine test was performed with incremental doses of 20, 50, and 80 microg injected into the right coronary artery and 20, 50, and 100 microg into the left coronary artery. Ergonovine was injected in a total dose of 40 microg into the right coronary artery and 64 microg into the left coronary artery. Coronary spasm was defined as 99% or more luminal narrowing accompanied by ischemic changes on ECG. Compared with male patients, female patients had less organic stenosis (12 vs 33%, p<0.05), less history of smoking (15 vs 85%, p<0.01), and fewer focal spasms (31 vs 64%, p<0.01). There were no other differences between the 2 groups. In conclusion, Japanese female patients with vasospastic angina had the characteristics of diffuse provoked spasm, less organic stenosis, and less history of smoking, but only 1 in 10 of all patients with vasospastic angina are female.
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PMID:Clinical characteristics of female patients with coronary spastic angina: comparison with male patients. 1087 31

Endothelins (ET) comprise a group of substances which are produced and have a regulatory function in different systems of the organism. The main cardiovascular ET is ET-1 which is so far the most potent vasoconstrictor substance. ET is important in the early stages of atherosclerosis as it is a strong chemical attractant of monocytes and macrophages and causes endothelial and vasomotor dysfunction. In later stages of atherosclerosis it can affect the firmness and integrity of the fibrous part of the atherosclerotic plaque. During myocardial infarction the ET level rises and this leads to vasoconstriction and reduction of the fibrillation threshold. In coronary angioplasty (PTCA) the ET-1 level rises depending on the applied mechanical stress. ET can participate in the formation of the neointima and the development of restenosis. ET increases also immediately after an aortocoronary bypass (CABG) and after reperfusion. Higher ET levels were found in patients with a positive ECG and echocardiographic loading test. In the latter after CABG normalization of ET was found. Raised ET levels were recorded also in patients where a coronary vasospasm can be provoked, in Prinzmetal's angina pectoris, coronary syndrome X, atrial tachystimulation. In unstable angina pectoris big-ET is elevated, the increase of the ET-1 level is not unequivocal. Stable angina pectoris does not affect ET-1. In the treatment of atherosclerosis for the selective ETA blocker reduction of the number and size of macrophage and foam cells was proved. In acute myocardial infarction a favourable effect for the non-selective ETA/ETB blocker and for the selective ETA blocker was found. In the treatment of restenosis after PTCA blockers of selective ETB receptors and inhibitors of endothelin converting enzyme seem hopeful. Th non-selective ETA/ETB blocker bosentan is in the stage of clinical tests and seems to be safe and perspective.
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PMID:[Endothelins and ischemic heart disease]. 1095 65

The objective of the present study was to investigate the differences between coronary hyperresponsiveness without ischemia and vasospastic angina in an ergonovine provocation test using multivariate analysis. We have sometimes experienced a more than 50% narrowing response of vascular diameter without ischemia in a coronary response to ergonovine. We studied 107 patients with less than 50% stenosis in a coronary arteriogram. Their vascular responses to ergonovine were measured and the patients were divided into three groups, as follows: Group 1 had 50% or less vascular narrowing response without ischemia; Group 2 had a vascular hyperresponsiveness of more than 50% narrowing response without ischemia; and Group 3 experienced a hyperresponsiveness with ischemia. The degree of coronary response was found to be related to smoking, inpaired glucose tolerance (IGT) and the Gensini score by multiple regression analysis. A multiple logistic analysis revealed that the Gensini score and smoking were significant predictive factors for Group 3 (odds ratio: 1.20 and 8.97). The only factor different between Group 2 and Group 1 was gender. The coronary hyperresponsiveness to ergonovine without ischemia differs from vasospastic angina in the degree of coronary atherosclerosis and smoking habits. The patients with hyperresponsiveness had similar characteristics to those with atypical chest pain rather than vasospastic angina, except for a gender difference.
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PMID:Differences between coronary hyperresponsiveness to ergonovine and vasospastic angina. 1098 46

In order to evaluate peripheral endothelial function in patients with vasospastic angina (VSA), we measured flow-mediated dilation (FMD) of the brachial artery in patients with VSA and compared it with FMD in patients without VSA. Endothelial dysfunction is considered one of the mechanisms underlying VSA. However, its exact role remains to be clarified. The study included 30 patients with positive spasm-provocational test results without evidence of significant coronary stenosis (VSA group) and 30 patients with negative spasm-provocational test results without evidence of significant coronary stenosis (control group). In each patient, brachial artery diameter responses to hyperemic flow and glyceryl trinitrate spray were measured using high-resolution ultrasound. The carotid intima-media thickness was also measured as a marker of systemic atherosclerosis. FMD was lower in the VSA group (4.8+/-0.5%) compared with the control group (9.4+/-0.7%, P<0.0001). In the VSA group, FMD was not affected by coronary risk factors or the presence of atherosclerotic changes on coronary angiography. Glyceryl trinitrate-induced dilation did not differ between the two groups. The intima-media thickness was comparable between the VSA (0.85+/-0.04 mm) and control groups (0.81+/-0.05 mm). These findings indicated that peripheral endothelial function is impaired only in the VSA group, whereas the atherosclerotic changes were similar in the two groups. We conclude that endothelial dysfunction may be an independent factor responsible for the development of VSA.
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PMID:Endothelial dysfunction is an independent factor responsible for vasospastic angina. 1172 60

Rho-kinase has been identified as one of the effectors of the small GTP-binding protein Rho. Accumulating evidence has demonstrated that the Rho/Rho-kinase-mediated pathway plays an important role in various cellular functions, not only in vascular smooth muscle contraction but also in actin cytoskeleton organization, cell adhesion and motility, cytokinesis, and gene expressions, all of which may be involved in the pathogenesis of arteriosclerosis/atherosclerosis. Indeed, animal experiments have demonstrated that Rho-kinase inhibitors effectively suppress coronary artery spasm and that long-term inhibition of Rho-kinase inhibits the development of coronary arteriosclerotic lesions and even causes regression of coronary vascular lesions in vivo. Recent clinical studies also have demonstrated the inhibitory effect of a Rho-kinase inhibitor on coronary artery spasm in patients with vasospastic angina and on exercise-induced myocardial ischemia in patients with stable effort angina with adequate safety. It is possible that Rho-kinase is also involved in the pathogenesis of other forms of cardiovascular diseases. Thus, Rho-kinase could be regarded as a novel therapeutic target in treatment of cardiovascular diseases.
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PMID:Rho-kinase as a novel therapeutic target in treatment of cardiovascular diseases. 1186 9

Coronary artery calcification (CAC) was assessed by cinefluoroscopy and its extent was scored (CAC score) in 2,163 consecutive patients undergoing coronary angiography, based on the angiographic and clinical data, the patients were categorized into 8 types of coronary artery disease (CAD). The CAC score was lowest in angiographically normal subjects (0.12+/-0.60) and highest in patients with silent myocardial ischemia (14.31+/-8.61). Risk factors for CAC were advanced age, male sex (at age <80 years), hypertension, diabetes mellitus, and a high grade of organic coronary stenosis. The CAC score in patients with acute coronary syndrome (unstable angina+acute myocardial infarction; 5.48+/-7.42) was significantly lower than that in those with chronic CAD (silent ischemia+stable angina; 9.72+/-8.73; p<0.0001), but was still higher than that in normal subjects or those with vasospastic angina (0.92+/-2.88; p<0.0001). The results indicate that CAC is a manifestation of coronary atherosclerosis and its appearance depends on the pathological type of ischemic heart disease. Fixed stenosis with a slow and chronic process tends to be associated with CAC. The clinical implication of extensive CAC in acute coronary syndrome compared with normal subjects should be further investigated.
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PMID:Clinical significance of coronary calcification. 1203 Mar 43

We are always exposed to oxidative stress, when oxygen is used for production of energy for our daily activity. Mild to moderate oxidative stress affects intracellular signal transduction, accelerating the protective system for oxidation; thereby inflammatory cytokines are produced leading to increased levels of acute phase proteins. Vascular endothelial cells protect the vessels from oxidative stress, however, when they are damaged by shear stress to the vascular wall, oxidation spreads into the subendothelial matrix, leading to oxidation of low-density lipoproteins(LDL) accumulated there. Oxidized LDL is easily and abundantly taken up into macrophages via the scavenger receptors such as LOX-1, which leads to the formation of atherosclerosis. Markers for oxidative stress in vivo are being sought for prevention and treatment of cardiovascular diseases. There are a number of parameters as candidates, and among them, we chose biopyrrins, oxidative products of bilirubin, and have studied their role in coronary heart diseases. Urinary excretions of biopyrrins are significantly elevated in patients with coronary arterial stenosis and with ischemic changes on electrocardiogram. Similar finding have been obtained in patients with vasospastic angina. These findings suggest that markers for oxidative stress will be a good laboratory test for evaluation of coronary heart diseases.
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PMID:[Cardiovascular diseases and oxidative stress]. 1269 Jun 30

Macrophages play a major role in the development of vascular lesions in atherogenesis. The cells express Fc gamma RIIIa (CD16) identical to that in NK cells, but with a cell type-specific glycosylation. The Fc gamma RIIIa molecules are released from the cell surface on activation, and these soluble forms (sFc gamma RIIIa) are present in plasma. We measured sFc gamma RIIIaM phi in plasma by Immuno-PCR with newly-developed anti-Fc gamma RIII mAb, MKGR14 (mIgM), which recognizes Fc gamma RIIIaM phi specifically. In healthy donors, the level of sFc gamma RIIIaM phi increased with age, and was positively correlated with LDL-cholesterol to HDL-cholesterol ratios and LDL-cholesterol, but negatively with HDL-cholesterol. In addition, the sFc gamma RIIIaM phi level was related to the number of risk factors for atherosclerosis and correlated with carotid maximum intima-media thickness in subjects for annual medical checkup. The sFc gamma RIIIaM phi level was significantly increased in patients with coronary artery disease (CAD) with atherosclerosis, but not in patients with vasospastic angina (VSA) or intact coronary artery, compared with age-matched healthy donors. The sFc gamma RIIIaM phi level was related to the number of significant coronary artery stenoses, and positively correlated with LDL-cholesterol to HDL-cholesterol ratios and lipoprotein (a), but negatively with HDL-cholesterol. These findings suggest that the macrophages are activated during the incipient stage of atherosclerosis, and that sFc gamma RIIIaM phi may serve as predictive marker for atherosclerosis.
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PMID:[Soluble Fc gamma RIIIa derived from macrophages]. 1467 89

Because atherosclerotic vascular lesions stimulate platelets, the platelets release serotonin (5-hydroxytryptamine, aka 5-HT). We therefore measured 5-HT concentrations not only in platelet-poor plasma but also in whole blood as a means of assessing vascular lesions. The plasma concentration of 5-HT tended to increase with age, whereas that in whole blood decreases. Therefore the ratio of the plasma to the whole-blood concentration of 5-HT (P/WB) increases with age. This may be a result of the activation of platelets in older subjects with atherosclerotic vascular damage. Patients who underwent coronary angiography (CAG) were classified into 4 groups according to diagnosis: effort-induced angina pectoris (eAP), old myocardial infarction (OMI), vasospastic angina pectoris (VSAP), and unstable angina (uAP). The mean plasma 5-HT concentration was significantly (P <.01) greater in patients with eAP, uAP, OMI, and VSAP than in healthy controls, whereas the concentration in whole blood was lower in patients with eAP than in healthy controls. When the P/WB ratios were calculated, the mean levels in all disease groups were significantly higher than that in the healthy controls. These findings suggested that 5-HT is released into the plasma from the platelets and that the concentration in the platelets decreases in patients with atherosclerosis.
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PMID:The ratio of plasma to whole-blood serotonin may be a novel marker of atherosclerotic cardiovascular disease. 1525 5


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