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)

We evaluated the effect of high versus low loading doses of clopidogrel in patients with stable angina pectoris who underwent percutaneous coronary intervention (PCI) on periprocedural events, in-hospital complications, and 30-day outcomes. The recommended loading dose of clopidogrel for patients with PCI is currently 300 mg. Recent studies have suggested that 600 mg may decrease periprocedural complications in patients with unstable angina. However, whether this holds for patients with stable angina pectoris is unknown. We reviewed records of 445 patients with stable angina pectoris who underwent PCI and were loaded with 300 mg (n = 126) or 600 mg (n = 319) of clopidogrel immediately before the procedure. Study end points were periprocedural ischemic events, bleeding complications, and a composite of major adverse cardiac events at 30 days. Baseline characteristics and procedural indexes were similar between groups. Major in-hospital complications were recorded in 2 patients in the 600-mg group and in no patient in the 300-mg group (p = 1.00). Postprocedural increase of cardiac enzymes (troponin I, p = 0.91; creatinine kinase-MB, p = 0.395) and major bleeding (0.6% vs 0%, p = 1.00) were comparable, as was 30-day major adverse cardiac events (1.2% vs 0%, p = 0.56). Multivariate analysis did not identify any risk decrease for periprocedural myocardial infarction with 600 mg of clopidogrel (odds ratio 2.68, 95% confidence interval 0.74 to 9.78, p = 0.135). In conclusion, in patients with stable angina pectoris, a 300-mg clopidogrel loading dose, when given immediately before PCI, is sufficient. Although 600 mg was clinically safe, it was not associated with fewer periprocedural events and improved 30-day outcomes compared with 300 mg.
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PMID:Clopidogrel loading dose (300 versus 600 mg) strategies for patients with stable angina pectoris subjected to percutaneous coronary intervention. 1656 1

Cell-free DNA that originates from cell death, circulates in peripheral blood. There are indications that the infarcted myocardium contributes to an increase of cell-free DNA levels. Our aims were to quantify levels of cell-free DNA in patients with acute myocardial infarction (AMI) and examine their correlation with myocardial markers and with postinfarction (PI) clinical course. Thirteen patients (age 57 +/- 16 year) admitted with AMI and who underwent thrombolysis with reteplase within 6 h from the onset of chest pain were studied. PB samples were collected on admission and for 5 consecutive days. Creatine kinase (CK) and troponin I (TnI) were measured on admission and every 8 h for 3 consecutive days. Clinical events were recorded throughout the hospitalization period. Cell-free DNA levels were also measured in 30 healthy controls. Log-transformed mean (+/-SE) of maximum free DNA values in patients higher than controls (6873 +/- 357 g.e./mL verses 4112 +/- 234 g.e./mL, P < 0.0001). Log-transformed maximum values of CK and TnI were correlated with log-transformed free DNA values of first (r = 0.62, P = 0.02/r = 0.68, P = 0.01) and second (r = 0.57, P = 0.04/r = 0.72, P = 0.0053) PI day. Nine patients (group A) had an uncomplicated PI clinical course and four patients (group B) had recorded events (three with angina and one death). Free DNA levels on the second PI day were higher in group B than group A (1298.0 +/- 796.0 g.e./mL verses 244.6 +/- 257.7 g.e./mL, P = 0.003). In conclusion, free DNA levels are significantly higher in patients with AMI than in controls and may play a role in the prognosis of these patients.
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PMID:Cell-free DNA levels as a prognostic marker in acute myocardial infarction. 1710 21

Fifty patients with stable angina pectoris entered a randomized, double-blind study and were assigned to receive celecoxib (200 mg 2 times daily) or placebo 7 days before percutaneous coronary intervention (PCI). Results showed that detection of markers of myocardial injury above the upper normal limit was significantly lower in the celecoxib than in the placebo group: 12% versus 35% for creatine kinase-MB (CK-MB; p = 0.001), 20% versus 48% for troponin I (p = 0.0004), and 22% versus 51% for myoglobin (p = 0.0005). Myocardial infarction by CK-MB determination was less commonly seen after PCI in the celecoxib than in the placebo group (5% vs 18%, p = 0.025). Postprocedural peak levels of CK-MB (2.9 +/- 18 vs 7.5 +/- 18 ng/ml, p = 0.0002) were also significantly lower in the celecoxib than in the placebo group. No significant side effect was reported by the 2 groups of patients. In conclusion, pretreatment with celecoxib 200 mg 2 times daily for 7 days significantly decreased procedural myocardial injury in elective PCI. These findings indicate that the antiphlogistic action of cyclo-oxygenase-2 inhibition may provide a friendly protection to ischemic cardiomyocytes.
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PMID:Safety and efficacy of short-term celecoxib before elective percutaneous coronary intervention for stable angina pectoris. 1712 50

The purpose of this study was to compare cardiac markers in the pericardial fluid and serum in order to evaluate preoperative myocardial injury. Thirty patients were divided into three groups. The first group (AVR; n=10) received an aortic valve replacement. The second group (SA; n=10) included patients with stable angina who underwent elective coronary artery bypass grafting (CABG). The third group (ACS; n=10) included patients with acute coronary syndrome who underwent urgent CABG. Pericardial fluid and venous samples were taken after opening the pericardium and 24 h postoperatively. Serum and pericardial concentration of troponin I (cTnI), creatine kinase (CK), its MB isoenzyme (CK-MB) and myoglobin were determined. Preoperative pericardial cTnI was significantly (P<0.01) higher than in serum in all groups. Preoperative pericardial CK, CK-MB and myoglobin were significantly (P<0.01) lower than in serum in groups AVR and SA. Preoperative pericardial and serum cTnI were significantly higher in the ACS than in AVR and SA groups (P<0.01). Postoperative pericardial concentration of all markers was significantly higher (P<0.01) than in serum in all groups. We conclude that preoperative pericardial accumulation of cTnI may reflect subclinical injury which may not be demonstrated by the usual laboratory tests.
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PMID:Biochemical markers of myocardial injury in the pericardial fluid of patients undergoing heart surgery. 1825 49

We present a case of a male patient who was admitted to the cardiology department with a diagnosis of NSTEMI (deep negative T waves in all precordial leads). Two weeks earlier he was hospitalised because of a stroke caused by thrombosis of the left carotid artery. He had no angina. An ECHO showed a normal myocardial contractility of the left ventricle. The concentration of troponin I was also normal. No coronary artery stenosis was revealed in coronary angiography. We present a review of studies devoted to ECG changes in patients with stroke.
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PMID:[ECG changes in patients with stroke]. 1928 85

Exercise-induced ST-segment elevation in lead aVR accompanied by ST-segment elevation in lead V1 might be a specific finding of left main coronary artery (LMCA) stenosis. Lead aVR and lead v1 ST segment elevation has been reported, during an attack of chest pain, in patients with LMCA disease with ST segment depression in leads V3, V4 and V5 (with maximal depression in V4). ST-segment elevation in lead aVR in patients with angina at rest can be related to transmural ischemia of the basal part of the interventricular septum, frequently due to LMCA or multivessel coronary disease too. 3-vessel coronary artery disease (CAD) and LMCA disease show a frequent combination of leads with abnormal ST segments during chest pain with ST-segment depression in leads I II V4-V6, and ST-segment elevation in lead aVR. When ST-segment status in lead aVR combines with troponin T, ST-segment elevation in lead aVR and positive troponin T on admission are useful predictors of LMCA or 3-vessel CAD. We present a case of acute myocardial infarction with significant left main coronary artery stenosis, significant 3-vessel coronary artery disease and elevated troponin I at admission in an 83-year-old Italian woman. Also this case focuses attention on the importance of the recognition of the patterns suspected for LMCA and/or 3-vessel coronary disease.
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PMID:Acute myocardial infarction with significant left main coronary artery stenosis, significant 3-vessel coronary artery disease and elevated troponin-I at admission. 1935 9

There are not enough clinical data about centenarians with acute myocardial infarction (AMI) undergoing percutaneous coronary intervention (PCI). A 104-year-old woman exhibited sharp chest pain and severe dyspnea. In routine examinations, her electrocardiogram showed 1-3 mm ST-segment elevation from V1 to V4 leads, the cardiac enzymes were also elevated: creatine kinase (CK)-MB was 45.7 U/L, and cardiac specific troponin I was 40 microg/L. A two-dimensional echocardiography showed anteroseptal akinesia with severely depressed left ventricular function, 38% ejection fraction. She primarily refused to receive percutaneous coronary intervention (PCI) considering her old age, and she was given a dual anti-platelet medications (low molecular heparin and frusemide). Three days later, due to continuously deteriorating angina pectoris and dyspnea, she was treated with PCI. A diagnostic percutaneous transradial coronary angiography revealed 95% stenosis in the proximal left anterior descending artery (LAD) with 90% stenosis at the origin of diagonal one. A percutaneous coronary intervention for the LAD lesion was successfully performed, and the final angiogram showed a good coronary flow without residual stenosis. The dual anti-platelet medications had to be ceased due to the upper gastrointestinal bleeding after one week and Tongguan Capsule (Chinese medicine composed with Radix Astragali, Radix Salviae Miltiorrhiae, etc.) was administered continuously. The six-month follow-up displayed a high level quality of life for the centenarian woman with the absence of angina pectoris and dyspnea. The case reinforces the importance of PCI for very elderly patients with AMI even centenarian people and reveals the possibility that Tongguan Capsule can be used to replace dual anti-platelet medication with the reduction of bleeding complications.
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PMID:Combined therapy with Chinese medicine and percutaneous transradial coronary intervention for a centenarian patient with acute myocardial infarction. 1956 19

High-sensitivity C-reactive protein predicts future cardiovascular events in both healthy individuals and patients with unstable and stable coronary syndromes. Few data are available about the incidence and the relation to inflammation of troponin elevation following percutaneous coronary intervention (PCI), a potential predictor of longterm outcome. We sought to confirm the impact of embolization on long-term outcome and evaluate the ability of baseline inflammation to predict troponin elevation induced by PCI. We prospectively analyzed 200 patients treated by PCI for stable or Braunwald IIA class unstable angina. The patients were recruited between January 1997 and May 1999, and the population was followed during a mean follow-up of 32 months. Major adverse cardiac events (MACEs) were defined as the occurrence of death, myocardial infarction or recurrent angina requiring repeat PCI, or coronary artery bypass grafting. During the follow-up period, 58 MACEs were observed. By multivariate analysis, independent predictors for the occurrence of MACEs were unstable angina and troponin I level after PCI (P < 0.0001 for both). No correlation was found between baseline inflammation and significant troponin I elevation post PCI and by multivariate analysis, no biological variable was a predictor of troponin I elevation post PCI. Baseline inflammation cannot predict onset of minor myonecrosis damage (expressed by troponin elevation) induced by PCI, a significant predictor of long-term outcome in this setting.
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PMID:Baseline inflammation is not predictive of periprocedural troponin elevation after elective percutaneous coronary intervention. 1962 98

Both randomized and observational studies have suggested that pretreatment with statins may reduce the incidence of periprocedural myocardial infarction (PMI) in patients with stable angina during elective percutaneous coronary intervention (PCI). The purpose of this randomized study (Clinical Trial Registration No. NCT00469326) was to investigate the effect of 2-day atorvastatin therapy on the incidence of PMI in patients with stable angina pectoris undergoing elective PCI. A total of 200 patients with stable angina pectoris who were not taking statins and who had been referred for PCI were enrolled and randomized (ratio 1:1) to a 2-day pretreatment regimen with atorvastatin 80 mg/day and subsequent PCI or immediate PCI. The serum concentration of creatine kinase-MB mass and troponin I were measured before and 16 to 24 hours after PCI. The incidence of PMI was assessed using established criteria. Of the patients, 10% in the atorvastatin group and 12% in the control group had a postprocedural creatine kinase-MB mass elevation > or =3 times the upper limit of normal (p = 0.65). The incidence of PMI as determined by the postinterventional release of troponin I > or =3 times the upper limit of normal was 17% in the atorvastatin group and 16% in the control group (p = 0.85). The median creatine kinase-MB mass peak after PCI was 1.46 ng/ml (interquartile range 0.83 to 2.52) in the atorvastatin group and 1.40 ng/ml (interquartile range 0.90 to 2.54) in the control group (p = 0.70). The median peak troponin I level after PCI was 0.100 ng/ml (0.096 to 0.385) in the atorvastatin group and 0.100 ng/ml (0.60 to 0.262) in the control group (p = 0.54). On multivariate analysis, the only independent predictor of PMI was patient age (odds ratio 1.09, 95% confidence interval 1.025 to 1.159, p = 0.006). In conclusion, in the present study 2-day pre-PCI therapy with atorvastatin did not reduce the occurrence of PMI in patients with stable angina pectoris undergoing elective PCI.
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PMID:Effect of two-day atorvastatin pretreatment on the incidence of periprocedural myocardial infarction following elective percutaneous coronary intervention: a single-center, prospective, and randomized study. 1969 35

Multiple landmark clinical trials have demonstrated the beneficial effects of statin therapy for primary and secondary prevention of cardiovascular disease, but the exact timing of how early to treat relative to acute presentation has been less clear. The benefits of statin in cardiovascular disease can be explained not only by their lipid-lowering potential but also by non-lipid-related mechanisms, called pleiotropic effects. Percutaneous coronary intervention (PCI) can result in myocardial injury that is reflected by an increase in creatine kinase-MB and troponin I isoenzymes with worsened long-term prognosis following PCI. Observational studies suggested that pretreatment with statins might reduce the incidence of myocardial infarction after coronary intervention and prevent myocardial injury. Thus, several randomized controlled trials were conducted. They showed that pretreatment with statin before elective PCI reduces periprocedural myocardial injury in patients with stable angina. Moreover, short-term high-dose statin administration before coronary procedures also improves clinical outcome in patients with acute coronary syndromes and/or high preprocedural C-reactive protein levels. Thus, this evidence strongly supports routine utilization of high-dose statins as adjuvant pharmacological therapy before percutaneous coronary revascularization.
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PMID:Preprocedural statin therapy to prevent myocardial damage in percutaneous coronary intervention: a review of randomized trials. 2021 6


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