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)

Risk stratification of patients with acute coronary syndromes (ACS) is pivotal for correct allocation of health resources and for maximizing the benefit of available treatment modalities. However, clinical and electrocardiographic indicators of high risk lack sufficient sensitivity for the detection of major cardiac events. The complementary information provided by the measurement of different biomarkers is believed to be very useful. Specifically, elevations of cardiac troponin I (cTnI) and T (cTnT) are strongly associated with a high-risk profile both at short- and long-term. This has been definitely demonstrated in many studies as well as in cumulative meta-analysis. The role of different biomarkers, such as those reflecting activation of hemostasis and the presence of inflammation, is however less defined. At the moment, no study has prospectively evaluated these biomarkers in the whole spectrum of unselected patients with ACS. It is also unclear whether these biomarkers add independent prognostic value to the clinical and electrocardiographic indicators of adverse outcome and whether they offer additional information when compared to each other. The Early Prognostic Value of Biochemical Markers of Myocardial Damage, Activation of Hemostatic Mechanism and Inflammation in Acute Ischemic Syndromes (EMAI) study has been prospectively designed to solve these issues. In this study, we have evaluated the prognostic value of cTnI and cTnT, D-dimer, prothrombin fragment 1+2 (F1+2), thrombin-antithrombin complex (TAT) and C-reactive protein (CRP) in patients with ACS at the time of admission. We have enrolled in 31 Italian Coronary Care Units 1971 patients with rest anginal pain within 12 h from admission and electrocardiographic evidence of myocardial ischemia. Of these, 730 patients resulted to have ST-segment elevation myocardial infarction eligible for a reperfusion strategy and 1241, an acute coronary syndrome without persisting ST-segment elevation. Primary outcome measure of the study is the composite of death and non-fatal MI within 30 days from admission, which has occurred in 8.9% of the study population.
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PMID:Cardiac markers and risk stratification: an integrated approach. 1155 47

The cardiac troponins have been shown to provide prognostic information allowing risk stratification of patients with acute coronary syndromes (ACS). The benefit of early percutaneous coronary intervention (PCI) in this setting has been highlighted by the FRISC II study. We assessed the pattern of release of cardiac troponin I (cTnI) following PCI in patients with ACS and evaluated its prognostic value for major adverse cardiac events (MACE): death, Q-wave myocardial infarction (QWMI), and repeat revascularization at follow-up. cTnI was sampled at baseline and 6, 14, and 24 hr following PCI in 73 patients presenting with unstable and post-MI angina. Clinical follow-up was obtained in all 73 patients at a mean period of 43 +/- 19.9 weeks (range, 11-68 weeks). Patients were stratified into two groups according to whether cTnI remained unchanged or fell below baseline 24 hr post-PCI (group 1, n = 47) or increased above baseline 24 hr following PCI (group 2, n = 26). MACE occurred in 4 (8.5%) of patients in group 1 (QWMI = 1, CABG = 1, re-PCI = 2) and in 19 (73%) of patients in group 2 (death = 1, QWMI = 2, CABG = 2, re-PCI = 14; chi-square = 32.34, P < 0.0001). The positive predictive value of rising cTnI within 24 hr following PCI for MACE at follow-up was 0.73 and the negative predictive value was 0.92 (specificity = 83%, sensitivity = 86%; odds ratio = 29.18, 95% CI = 7.62-110.64, P < 0.0001). cTnI is an inexpensive and widely applicable tool that offers reliable prognostic information for the risk stratification of patients undergoing coronary revascularization in the setting of acute coronary syndromes and may identify a group of patients at particular risk of repeat PCI.
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PMID:Cardiac troponin I for risk stratification following percutaneous coronary artery intervention in acute coronary syndromes. 1179 93

Unstable angina and non-Q-wave myocardial infarction (MI) are common and costly clinical events, but there is considerable uncertainty about optimal clinical management of these syndromes. We developed a prediction rule to help clinicians determine which patients with unstable angina or non-Q-wave MI are likely to "fail" medical therapy and ultimately require cardiac catheterization within 6 weeks of presentation. Subjects were 733 patients presenting with unstable angina or non-Q-wave MI enrolled in the TIMI IIIB trial and randomized to initial medical management. We developed a prediction rule based on logistic regression analysis of baseline data from history, physical examination, electrocardiogram, and blood studies. The outcome of interest was "failure" of medical therapy, defined as need for coronary catheterization within 42 days. Significant predictors of "failing" medical therapy included ST segment depression >or= .1 mV (odds ratio, OR, = 2.7, 95% confidence interval, CI, 1.8-4.1), accelerated angina in the prior 2 months (OR = 1.8, 95% CI 1.2-2.6), nitrate use in the prior week (OR = 1.6, 95% CI 1.1-2.2), exertional angina in the prior 2 months (OR = 1.6, 95% CI 1.1-2.2), and cardiac troponin I (cTnI) >or= 0.4 ng/mL (OR = 1.4, 95% CI 1.1-1.9). We used these variables to build a risk score by assigning point values based on these ORs. The risk score had a moderate ability to predict which patients would subsequently fail medical therapy and undergo cardiac catheterization (c = 0.682). Out of a total risk score of 13, failure of medical therapy occurred in 86% of patients who had a risk score >or= 8 (n = 111), 78% of patients who had a risk score >or= 6 (n = 240), and 72% of patients who had a risk score >or= 4 (n = 438). At scores of < 2 (n = 88), 40% of patients failed medical therapy. Although the management of unstable angina is in constant evolution, clinicians will always be faced with determining which patients should be managed most invasively. The simple prediction rule we present can be applied to patients with unstable angina or non-Q-wave MI at the time of presentation to predict which patients have a high probability of failing medical therapy. Such a rule may be useful for identifying patients who should be considered for early cardiac catheterization.
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PMID:Which patients with unstable angina or non-Q-wave myocardial infarction should have immediate cardiac catheterization? A clinical decision rule for predicting who will fail medical therapy. 1246 84

Serum cardiac troponin I (cTnI) is a highly specific marker for myocardial damage in patients with chronic renal insufficiency (CRI), unlike creatine kinase myocardial band fraction (CK-MB), which may be elevated in the absence of myocardial injury in patients with CRI. We studied 116 consecutive CRI patients (serum creatinine +/- 1.8 mg/dL, not on dialysis) with normal baseline cTnI levels who underwent successful percutaneous coronary intervention (PCI). Patients were divided into two groups: group 1, elevated postprocedural cTnI (n = 50), and group 2, normal cTnI (n = 66). Patients with elevated cTnI were older and had a higher incidence of postinfarction angina and lower creatinine clearance compared to patients who did not have cTnI elevation. Atheroablative devices (rotational and directional atherectomy and excimer laser coronary angioplasty) were more frequently used in group 1 patients (27.1% vs. 18.5%; P = 0.04). In-hospital mortality, cardiac mortality, and Q-wave myocardial infarction rates did not differ between the two groups. At 12-month follow-up, total mortality rates were significantly higher in group 1 (28.0% vs. 9.9%; P = 0.002). Multivariate analysis showed that cTnI was an independent predictor of late mortality (OR = 2.26; CI = 1.07-4.77; P = 0.03). Thus, in patients with CRI, elevated cTnI levels after successful PCI is an important predictor of poor long-term outcome. Our data suggest that patients with cTnI elevation > 3 times above normal values are particularly at higher risk.
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PMID:Prognostic value of cardiac troponin I elevation after percutaneous coronary intervention in patients with chronic renal insufficiency: a 12-month outcome analysis. 1183 43

Nicorandil is a K(ATP) channel opener used to treat angina. It is cardioprotective and a vasodilator. We conducted a prospective, randomized, double-blind, placebo-controlled study to assess oral nicorandil in patients undergoing coronary artery bypass grafting (CABG) with cardiopulmonary bypass (CPB). Twenty-two patients received nicorandil (10 mg twice a day) and 23 patients received placebo. Haemodynamic data were recorded before induction of anaesthesia (T0), 5 and 20 min after starting mechanical ventilation (T1, T2), before aortic cannulation (T3), after 30 min of CPB (T4), 10 min after CPB (T5) and after 3, 8 and 18 h in the intensive care unit (T6, T7, T8). Serum proteins (creatine kinase metabolite and cardiac troponin I) were measured before and 8 and 18 h after surgery. Haemodynamic values did not differ between the two groups. There was no tachycardia during the study, no significant difference in hypotensive episodes, ST segment changes and no changes in cardiac enzymes. Myocardial infarction after surgery was similar in the two groups. Vasoactive therapy was similar in the two groups. Nicorandil can be continued safely up to premedication without deleterious haemodynamic consequences, but a myocardial protective effect of nicorandil in CABG surgery was not found.
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PMID:Safety of oral nicorandil before coronary artery bypass graft surgery. 1187 85

Minor myocardial injury (MMI), identified by elevated serum levels of cardiac markers, is not uncommon after successful, uncomplicated elective percutaneous coronary intervention (PCI) in patients with stable angina. Serum cardiac troponin, especially cardiac troponin I (cTnI), are more sensitive than serum creatine kinase - MB in detecting MMI. Occlusion of small side-branch vessels, visualized by angiography, may explain the mechanism of the MMI in some, but not all patients. Occlusion of small intramyocardial vessels, not visualized by angiography, might be the mechanism of MMI in these patients. Recent reports have shown that cardiac troponin I elevation after successful, uncomplicated elective PCI in patients with stable angina may be a marker of adverse long-term outcome. Also, it has recently been reported that increased serum C-Reactive protein (CRP) is common in patients with stable angina and is a significant and independent determinant of MMI after uncomplicated elective PCI, indicating involvement of the systemic inflammatory state in the etiology of this periprocedural myocardial injury. An intense inflammatory response is expected following PCI in patients with increased baseline CRP levels, which can cause small vessel occlusion and/or microembolization that will lead to troponin elevation. With these findings in mind, and with the observation that increased risk associated with systemic inflammation can be reduced with certain preventive therapies, CRP may help to identify those who would benefit most from these pharmacological therapies before coronary interventions.
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PMID:Percutaneous coronary intervention in the context of systemic inflammation: more injury and worse outcome. 1294 45

A teaching hospital is working with the Victorian State Government and universities, integrating cost-effectiveness evidence into clinical practice guidelines (CPGs), protocols and pathways for respiratory and cardiology interventions. Acute myocardial infarction (AMI) findings are reported. Results will stimulate cost-effective practice and inform medical associations, federal and state governments and international organisations developing CPGs. Published CPGs by the American College of Cardiology/American Heart Foundation for AMI in 1999 are reviewed by a large interdisciplinary hospital-based committee given cost-effectiveness evidence. Levels of evidence criteria rating on methodological rigor for effectiveness and costs are applied. National Health and Medical Research Council (NHMRC) grades of recommendation criteria for combinations of relative effectiveness versus relative costs and cut-off points are used. Extrapolating results between countries was addressed by applying the OECD's health purchasing power parity series. Recommendations for revisions to United States guidelines and for local application are formulated. United States Guidelines require updating: Regarding angioplasty, percutaneous transluminal coronary angioplasty (PTCA) is cost-effective for men aged 60 years relative to recombinant tissue plasminogen activator (tPA), with additional cost per life year saved of 274 ecu. PTCA with discharge after 3 days is cost-effective in low-risk AMI. Regarding GP IIb/IIIa drugs, Abciximab during intervention incurred equal mean hospital costs for placebo, abciximab bolus, and abciximab bolus+infusion with incremental 6-month cost for the latter treatment costing 293 US dollars per patient. Agent recouped almost all initial therapy costs with significant benefits. Incremental cost of abciximab per event prevented is 3,258 US dollars. Tirofiban was compared to placebo after high-risk angioplasty for AMI or unstable angina. Tirofiban decreased the rate of hospital deaths, myocardial infarction, revascularisation at 2 days by 36% relative to placebo (8% vs. 12%) without increased cost. Clinical benefits were similar at 30 days. Tirofiban+heparin+aspirin was compared to heparin+aspirin. Tirofiban arm resulted in net savings of 33,418 ecu per 100 patients for the first 7 days of treatment. Regarding thrombolytics, tPA is more cost-effective than streptokinase. Incremental costs for each life saved when streptokinase is substituted by recombinant tissue plasminogen are 31%, 45%, 97% higher in Germany, Italy and the United States than in the United Kingdom. Regarding anticoagulants, enoxaparin is a promising alternative to unfractionated heparin for hospitalised patients with non-Q-wave myocardial infarction or unstable angina, saving 1,485 Canadian dollars per patient over 12 months with 10% reduction in 1 year risk of death, myocardial infarction or recurrent angina. Regarding antiarrhymics, the cost-effectiveness of no amiodarone, amiodarone for patients with depressed heart rate variability (DHRV), and amiodarone for patients with DHRV plus positive programmed ventricular stimulation (PPVS) for high-risk post-AMI was investigated. Amiodarone for DHRV+PPVS patients was dominated by a blend of the two alternatives. Compared to no amiodarone, the incremental cost-effectiveness of amiodarone for DHRV patients was 39,422 US dollars per quality adjusted life year gained. Amiodarone for DHRV is the most appropriate. Other CPG updates concern serum markers, for example, cardiac troponin I assay (c-Tnl), cost advantages of ad hoc angioplasty and secondary prevention through antioxidants and pravastatin. Australian costs are reported later in the paper.
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PMID:Integrating cost-effectiveness evidence into clinical practice guidelines in Australia for acute myocardial infarction. 1560 15

After successful percutaneous coronary interventions (PCI), elevations of cardiac enzymes are not rare, but it is still not clear whether those elevations are associated with adverse late outcome. The purpose of the study was to investigate the relation between cardiac troponin I (cTn-I) increase after successful percutaneous intervention and late outcome. The study consisted of 100 consecutive patients (mean age 56 +/-9.8, 84% male) who had successful elective coronary balloon angioplasty with or without stent implantation. Patients with stable angina (n=54) and unstable angina (n=46) were included in the study. Blood samples for measurement of cTn-I were taken before and immediately after the procedure, and every 6 hours for the first 24 hours. Patients with preprocedural cTn-I elevation were excluded from the study. Postprocedural cTn-I elevation was detected in 34 patients (34%, troponin (+) group) and cTn-I levels were normal in 66 patients (66%, troponin (-) group). Logistic regression analysis showed that intervention in patients with unstable angina, stent implantation following balloon dilation, and maximal inflation pressure were the predictors of cTn-I elevation (p=0.035, p=0.038, and p=0.014, respectively). During the prospective follow-up period for 21 +/-7.5 months, the incidence of major cardiac events including recurrent angina, acute myocardial infarction, death, and revascularization were not different in patients with and without cTn-I elevation. Overall, major cardiac events occurred in 9 patients (26%) in the troponin (+) group and in 13 patients (20%) in the troponin (-) group. Kaplan-Meier survival analysis showed that cTn-I elevation was not an important correlate of overall cardiac events (log-rank: 1.66, p=0.19). The authors conclude that postprocedural cTn-I elevation is related to unstable angina, stent implantation following predilation, and inflation pressure, and there is no association with minor myocardial injury occurring after successful percutaneous coronary intervention and late adverse cardiac events.
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PMID:Cardiac troponin I increase after successful percutaneous coronary angioplasty: predictors and long-term prognostic value. 1651 23

The aim of the study was to evaluate whether markers of myocardial injury and ischemia are helpful in detecting coronary artery disease (CAD) in patients with stable angina. Venous blood was obtained before and after a bicycle exercise test in 47 outpatients with suspected CAD for measurement of cardiac troponin I (cTnI), heart-type fatty acid binding protein, and glycogen phosphorylase BB. Patients with a coronary artery stenosis >/=70% in diameter (n = 33) were compared with patients with coronary narrowing <50% (controls, n = 14). None of the markers increased after bicycle exercise testing. cTnI measured before and after exercise was higher in the CAD group than in controls (p <0.001). The area under the curve for diagnosis was greater when the cTnI value was detectable than with stress testing alone. In conclusion, baseline cTnI was of value in detecting CAD and also during follow-up in predicting the need for further revascularization.
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PMID:Usefulness of detectable levels of troponin, below the 99th percentile of the normal range, as a clue to the presence of underlying coronary artery disease. 1771 17

The transient receptor potential vanilloid (TRPV1) channels expressed in sensory afferent fibers innervating the heart may be activated by protons or endovanilloids released during myocardial ischemia (MI), leading to angina. Although our previous in vitro data indicate that TRPV1 activation may preserve cardiac function after ischemia-reperfusion injury, the underlying mechanisms are largely unknown. To test the hypothesis that TRPV1 modulates inflammatory and early remodeling processes to prevent cardiac functional deterioration after myocardial infarction, TRPV1-null mutant (TRPV1(-/-)) and wild-type (WT) mice were subjected to left anterior descending coronary ligation or sham operation. The infarct size was greater in TRPV1(-/-) than in WT mice (P<0.001) 3 days after MI, and the mortality rate was higher in TRPV1(-/-) than in WT mice (P<0.05) 7 days after MI. The levels of plasma cardiac troponin I; cytokines, including tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6; chemokines, including monocyte chemoattractant protein-1 and macrophage inflammatory protein-2; and infiltration of inflammatory cells, including neutrophils, macrophages, and myofibroblasts; as well as collagen contents, were greater in TRPV1(-/-) than in WT mice (P<0.05) in the infarct area on days 3 and 7 after MI. Changes in left ventricular geometry led to increased end-systolic and -diastolic diameters and reduced contractile function in TRPV1(-/-) compared with WT mice. These data show that TRPV1 gene deletion results in excessive inflammation, disproportional left ventricular remodeling, and deteriorated cardiac function after MI, indicating that TRPV1 may prevent infarct expansion and cardiac injury by inhibiting inflammation and abnormal tissue remodeling.
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PMID:Transient receptor potential vanilloid gene deletion exacerbates inflammation and atypical cardiac remodeling after myocardial infarction. 1911 47


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