Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The problems involved in the treatment, the criterion for selective initial treatment, and the relationship between the treatment and the prognosis were studied in 48 patients with unstable angina pectoris, based on coronary arteriographic findings, left ventricular performance, coronary circulation and myocardial energetics with various interventional observations. Among these patients 43.7% initially responded to medication and 56.3% did not. In newly developed angina at rest, the effectiveness of an isolated sustained administration of isosorbide dinitrate (ISDN) or Ca2+ antagonist (nifedipine) was 100%, while in the changing pattern type of effort angina, the effectiveness of nifedipine was 71.4%, being higher than that of other drugs. As for coronary circulation, nifedipine, having different effects from ISDN, acted directly on resistance vessels and increased the endocardium/epicardium blood flow ratio by its powerful preload-unloading effect. Percutaneous transluminal coronary angioplasty (PTCA) was performed on 5 patients with unstable angina pectoris (USP). A completely asymptomatic condition, significant dilatation and improvement of coronary circulation were obtained after PTCA. The prognosis of UAP was not good with a mortality rate of 21%. Therefore, initial intensive medical therapies and the earliest stabilization of the patients' conditions are also important. The mechanism of the resistance to medical treatment is an important problem to be solved in the near future. In addition to the validity of the definitions of this disease, the appropriate long-term management must also be considered.
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PMID:Concepts for the initial management of patients with unstable angina pectoris--from the viewpoint of coronary arteriography, coronary circulation and cardiac performance including various interventional studies. 622 Jan 67

Coronary angiographic findings were compared in patients who presented with acute myocardial infarction (AMI, n = 75), unstable angina pectoris (UAP, n = 36), or stable angina pectoris (SAP, n = 36) for > or = 2 years without evidence of any previous acute event and with an angiogram within 2 years of the initial symptoms. Angiograms were evaluated blindly for severity, extent (depending on the percentage of each coronary segment showing atherosclerosis), and pattern (discrete, < 3 loci of narrowings involving < 50% of any segment; diffuse, anything exceeding this). Patients in the SAP group had more narrowed arteries (2.4 +/- 0.7 vs 1.3 +/- 0.6 [p < 0.02] and 1.4 +/- 0.6 [p < 0.02]), more stenoses (6.0 +/- 3.3 vs 2.1 +/- 1.5 [p < 0.01] and 2.6 +/- 1.7 [p < 0.05]) and occlusions (1.3 +/- 1.1 vs 0.7 +/- 0.6 [p = 0.05] and 0.3 +/- 0.5 [p < 0.02]), and a greater extent index (0.9 +/- 0.5 vs 0.5 +/- 0.3 [p < 0.02] and 0.5 +/- 0.3 [p < 0.02]) than those in the AMI and UAP groups. Furthermore, a discrete pattern was less prevalent in patients with UAP than in those with SAP or AMI (3% vs 40% [p < 0.02] and 25% [p < 0.05], respectively). In conclusion, patients who present with acute coronary syndromes have less extensive atherosclerosis than those who present with chronic stable angina. Therefore, in the former group, coronary atherosclerosis appears to be more susceptible to ischemic stimuli responsible for acute coronary syndromes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of coronary angiographic narrowing in stable angina pectoris, unstable angina pectoris, and in acute myocardial infarction. 761 11

UAP is a frequent manifestation of ischaemic heart disease; it is intermediary between stable angina and myocardial infarction and sudden death resp. The hospitalization mortality is 5%, approximately 15% of the patients with UAP develop myocardial infarction. The aim of UAP treatment is: 1. prevention of ischaemic episodes, 2. prevention of infarction and 3. control or elimination of risk factors, to improve the long-term prognosis in these patients. As antianginal drugs in UAP as a routine calcium antagonists, beta-blockers and nitrates are used. A very important part in the treatment of UAP is played by antithrombotic and thrombolytic treatment as in this disease rupture or fissure of plaques and subsequent thrombus formation is important. Non-occlusive thrombi are present in 80% in UAP, while in infarctions they are present in 21%. Rupture of an atherosclerotic plaque leads to thrombocyte activation, release of tissue thromboplastin and activation of the coagulation system aspirin inhibits platelet function and thus reduces thromboxane A2 formation. Heparin affects the coagulation process in UAP, reduces the number of anginal attacks and protects from the development of infarction. Treatment of UAP with streptokinase and rt-PA has no great advantages, when compared with heparin. Surgical treatment of UAP has somewhat better results than conservative treatment. Coronary angioplasty is an ideal solution in UAP when one or two arteries are damaged.
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PMID:[The present status of treatment of unstable angina pectoris]. 807 49

Emergency CABG for acute coronary syndrome (ACS) was studied. Sixty patients had CABG for medically refractory UAP, 78 patients for AMI and 8 patients for post-infarction angina (PIA). In UAP group 7 patients (12%) died postoperatively, mainly due to perioperative myocardial infarction (PMI) and operative complications. In AMI group, 26 patients (33%) died, 14 of them due to myocardial failure. The operative mortality was extremely high in shock-state patients group (48%) and cardiac pulmonary arrest state patients group (85%). Operative result was poor in those patients whose infarct-related artery was not recanalized preoperatively. Operative mortality was 13% in PIA group. It was concluded that the reduction of mortality of those patients required much refined myocardial preservation technique and powerful mechanical assist system to support the postoperative myocardial failure.
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PMID:[Emergency coronary artery bypass grafting for acute coronary syndrome]. 1044 54

Hepatocyte growth factor (HGF) is an endothelial cell specific growth factor involved in the repair of endothelial cells and collateral formation, however, the role for coronary artery disease is still unknown. We measured serum HGF level in various coronary artery diseases to examine the clinical significance. Serum HGF level was measured using the enzyme-linked immunosorbent assay method in patients with stable effort angina pectoris (n = 26), old myocardial infarction (n = 18), unstable angina pectoris (UAP; n = 10) and acute myocardial infarction (AMI; n = 21). As a control group, we selected 11 patients with neurocirculatory asthenia. Blood samples from peripheral veins were collected at cardiac catheterization before heparin administration. In the AMI group, blood samples were also collected at 48, 72 hr, 1, 2, 3 and 4 weeks from the peripheral veins and 48 and 72 hr after reperfusion from the coronary sinus. Serum HGF level was significantly higher in the UAP (0.41 +/- 0.12 ng/ml, p < 0.001) and AMI groups (0.38 +/- 0.26 ng/ml, p < 0.05) compared to the control group (0.19 +/- 0.09 ng/ml). Serum HGF level peaked 48 hr after reperfusion in both the peripheral veins (0.42 +/- 0.16 ng/ml) and coronary sinus (0.58 +/- 0.23 ng/ml) in the AMI group, with a significantly higher level in the coronary sinus than the peripheral veins (p < 0.05). No significant correlation between peak HGF level in the peripheral veins and peak creatine kinase (CK), CK-MB, ejection fraction and cardiac index was observed. Serum HGF was elevated in acute coronary syndrome, indicating advanced endothelial cell damage. HGF is produced, at least partially, in the heart in patients with AMI. Serum HGF level may be useful to detect endothelial cell damage rather than myocardial cell damage.
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PMID:[Changes of serum hepatocyte growth factor in coronary artery disease]. 1083 75

We analyzed the concentrations of interleukins (IL)-6, IL-10, IL-12, and IL-18, interferon (IFN)-gamma, and high-sensitivity C-reactive protein (hsCRP) in 40 patients with unstable angina (UAP), 39 patients with stable angina (SAP), and 52 age- and gender-matched controls. Compared with the control group, IL-12 concentrations were significantly higher in both the SAP and UAP groups, especially in the UAP group, and the IL-18 concentrations tended to be higher in the UAP group. Conversely, IL-10 concentrations were significantly lower in the SAP and UAP groups. Both IL-6 and hsCRP concentrations were significantly higher in the UAP group. The levels of hsCRP were positively correlated with inflammatory or proinflammatory cytokines (IL-6, IL-12, and IL-18), and negatively correlated with anti-inflammatory cytokine (IL-10). Moreover, the levels of IL-12 were positively correlated with IL-18, and negatively correlated with IL-10, and the results revealed the T-helper 1 dominant state. These results suggested that the inflammatory response was strongly associated with coronary atherosclerosis and angina pectoris, and that the T-helper 1 dominance may play an important role in these diseases.
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PMID:Concentrations of interleukins, interferon, and C-reactive protein in stable and unstable angina pectoris. 1508 94

This study evaluates transcoronary changes in neutrophil and platelet activation and conjugate formation in patients with angina pectoris secondary to coronary artery disease. We examined parameters of neutrophil and platelet activation as well as the neutrophil-platelet conjugate formation in patients who underwent diagnostic coronary angiography. Thirty-nine patients with chest pain referred for cardiac catheterization were studied (23 patients with unstable angina pectoris [UAP] and 16 with stable angina pectoris [SAP]). Before coronary angiography, blood samples were obtained simultaneously from the aortic root and coronary sinus to assess leukocyte (CD11b) and platelet (CD62P) activation and leukocyte-platelet conjugates. There was a 94% increase in CD62-expressing platelets from the aorta to the coronary sinus in patients with UAP compared with a 49% increase in patients with SAP. The percentage of neutrophil-platelet conjugates increased by 22% in patients with UAP compared with a 16% decrease in those with SAP (p <0.01). In contrast, monocyte-platelet binding across the coronary bed increased to a similar degree in both groups. This study demonstrates an increase in neutrophil-platelet conjugates across the coronary circulation in UAP, compatible with a higher activation state in both cell types.
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PMID:Comparison of coronary artery specific leukocyte-platelet conjugate formation in unstable versus stable angina pectoris. 1496 12

We performed BMIPP myocardial SPECT and Tl myocardial SPECT in patients with unstable angina (UAP) and stable effort angina (SAP), and compared the results for the two groups. Our subjects were 30 patients with the UAP and 25 patients with the SAP. The early and delayed images of the BMIPP were obtained with patients at rest. The early image of the Tl alone was obtained with patients at rest. We calculated severity score (SS) using the polar map based on SPECT short-axis image on the both myocardial SPECT. And, we calculated % uptake of the responsible coronary lesion and regional washout rate (WR) on myocardial SPECT with BMIPP. On coronary angiogram, no difference in % diameter stenosis was seen between the two groups. On myocardial SPECT with Tl, no difference in the SS was seen between the two groups. However, on myocardial SPECT with BMIPP, the SS was significantly higher score in the UAP group than in the SAP group. And, on myocardial SPECT with BMIPP, the % uptake and the WR were significant lower values in the UAP group than in the SAP group. Even if the two groups have almost the same level of myocardial perfusion disorder, the UAP group may have severer myocardial fatty-acid metabolic disorder than the SAP group, because the defects in BMIPP were significantly severer in the UAP group.
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PMID:[Comparison between unstable angina pectoris and stable effort angina pectoris by using 123I-BMIPP and 201Tl myocardial SPECT]. 1517 54

The complement system is part of the host defence response. However, considerable evidence suggests that complement plays an important role in the pathophysiology of ischemic heart disease. The aim of this study was to evaluate complement activation in patients with all forms of acute coronary syndromes (ACS) and to examine the relationship between the degree of complement activation and myocardial injury. The study population included 152 subjects (26 females): 82 with ACS (35 acute myocardial infarction (AMI), 22 non-Q wave MI (NQMI), 25 unstable angina (UAP)) (Group A), 35 stable angina (SA) (Group B), and 35 healty control subjects (Group C). Complement 3 (C3), Complement 4 (C4), C-reactive protein (CRP), troponin I (TnI) as well as creatine kinase MB (CK-MB) were evaluated. Patients' blood samples were taken on admission (day 1) and after 2, 3 and 7 days in group A. However, only one measurement was performed in the groups B and C. Plasma C3 and C4 peak levels were significantly higher in patients with AMI (141+/-29 and 35+/-11 mg/dl) and NQMI (136+/-13 and 35+/-7 mg/dl) than in patients with SA (128+/-14 and 27+/-10 mg/dl) and the control subjects (114+/-22 and 22+/-7 mg/dl) (p<0.03). Also, C3 and C4 serum levels in patients with SA and UAP (126+/-16 and 31+/-7 mg/dl) were significantly higher than those in control subjects (p<0.01, p<0.03, respectively). At 1-week follow-up, there were no significant differences between the plasma levels of C3 and C4 in patients with UAP (p>0.05). However, plasma levels of C3 and C4 were significantly different between days in patients with AMI and NQMI (p<0.0001). Plasma C3 and C4 levels in ACS showed a relationship with peak CK-MB and Tn I levels (p<0.01). Plasma CRP level in ACS showed positive correlation with C3 (p<0.01) and C4 (p<0.001). In this study, we determined that plasma C3 and C4 levels were elevated in ACS and SA. Although C3 and C4 were higher in ACS and SA, the systemic levels of inflammatory markers in patients with SA and UAP were lower than those found in the AMI and NQMI groups. The relationship between C3, C4 levels and ACS further suggests that the complement activation is related to necrosis within the myocardium.
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PMID:Complement activation in acute coronary syndromes. 1579 59

Risk stratification at presentation with acute coronary syndromes (ACS) on the basis of the TIMI risk score for unstable angina and non-ST-elevation myocardial infarction (UAP/NSTEMI) identifies patients at high risk of recurrent cardiac events and those who benefit from more aggressive treatment strategy. We hypothesised the following: (a) that a high TIMI risk score brings a greater degree of acute changes in endothelial damage/dysfunction (circulating endothelial cells [CECs], von Willebrand factor [vWf]), inflammation (interleukin-6, IL-6) and blood thrombogenicity (plasma tissue factor, TF); and (b) that these indices are higher in those with high TIMI risk score who experienced recurrent cardiac event at day 14 and day 30. TIMI risk scores were determined at admission and 48 hours later in 88 ACS patients (60 male, age 67+/-12 yrs) with UAP or NSTEMI. CECs, IL-6 and TF levels were measured at both time points and the acute change (delta) calculated. Patients were split into high (score > or =4) or low (<4) TIMI score groups. The composite end point of death, myocardial infarction, and refractory angina requiring revascularisation following 14 and 30 days' follow-up was ascertained. Fifty-eight patients with high TIMI risk score (mean 4.7) had significantly higher baseline and 48 h CEC, vWf, IL-6,TF and deltaTF levels, compared to low TIMI risk score (mean 2.4) patients (all p<0.05). Multivariate Cox regression analysis adjusted for clinical variables and TIMI risk score expressed as either continuous or categorical variable identified baseline CECs and deltavWf levels (both p< or =0.01) as independent predictors of subsequent cardiac events at both 14 days and 30 days. TIMI risk score for UA/NSTEMI identifies those patients with more profound vascular insult, inflammation and thrombogenicity that, in the 'high risk' patient group, predicts short-term outcomes, although vascular damage was the more sensitive predictor. These indices may further refine global risk stratification for short-term adverse cardiac events in these patients.
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PMID:Plasma markers of endothelial damage/dysfunction, inflammation and thrombogenesis in relation to TIMI risk stratification in acute coronary syndromes. 1636 52


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