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)

From the clinical standpoint a cardiomyopathy can be classified as primitive when other causes, i.e. ischemic, infiltrative, systemic diseases, can be ruled out. Initial symptoms usually include a progressive dyspnea and fatigue with tachycardia in a patient previously healthy. Congestive heart failure may be the initial manifestation. Angina is often present, not only because of coronary heart disease. Auscultatory findings usually include a gallop rhythm with a third heart sound, not rarely a four-sound gallop. Blood test to evaluate renal and liver function should be performed. The dosage of troponin I and/or troponin T, plasma renin activity, brain natriuretic peptide or endothelins has recently gained some reputation to indicate prognosis, but there is no reason to believe that these measures are superior to cardiopulmonary stress test.
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PMID:[Dilated cardiomyopathy: role of clinical and laboratory evaluation]. 1202 82

To evaluate the supplemental value of serial troponin I (Trp) measurements when combined with a clinical model composed of six clinical parameters in predicting in-hospital adverse event rates, a total of 118 consecutive patients admitted over a 23-month period with intermediate- or high-risk unstable angina or non-Q wave myocardial infarction (MI) as defined by AHCPR criteria who had coronary angiography within 72 hours of hospitalization were studied. Presenting clinical characteristics were graded using a previously validated variation of the Braunwald criteria (RUSH model). The RUSH model clinical score includes six clinical parameters: age, diabetes, intravenous nitroglycerin, pre-admission calcium-channel and beta-blocker, ST depression and post-MI angina (< 2 weeks), and creates an estimated probability of MI or death. The RUSH model was compared to serial Trp levels drawn at 6-hour intervals (0, 6 and 12 hours). An abnormal Trp value was defined as > 2.0 mg/dl. Outcome measures included death, MI, recurrent chest pain and new ST or T changes and enzyme elevation. One death, 23 MIs and 24 other adverse clinical events occurred. The event group had a RUSH score predictive of 12.7 12.4% risk and the no-event group had a score of 13.2 10.2% risk (p = 0.64). The Trp positive group had a clinical score predicting 14.2 13.2% risk and the Trp negative group had a score of 11.7 9.3% risk (p = 0.21). Patients with elevated Trp had an adverse event rate of 32/50 (64%) vs. 21/68 (31%) in patients with normal Trp (p < 0.0004). Elevated Trp had 60.4% sensitivity and 72.3% specificity, odds ratio of 3.97 (1.71 9.33), as well as 64% positive and 69.1% negative predictive values for predicting adverse events. Thus, there was significant incremental value to adding Trp to the clinical score when predicting outcomes in patients with intermediate- and high-risk clinical scores. When Trp was abnormal, it was useful when predicting higher risk; if Trp was normal, it was useful predicting lower but still elevated risk. Consequently, in a population selected for intermediate and high risk, the presence or absence of elevated Trp I is a sensitive and specific additive predictor to clinical score to predict need for revascularization and adverse in-hospital outcomes, as suggested in current guidelines.
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PMID:Supplemental value of troponin I combined with a clinical risk model to predict in-hospital events in intermediate and high risk patients with acute coronary syndromes. 1236 14

Early exercise testing (first 24 hours) was evaluated in the stratification of patients seen in the emergency room for chest pain. One hundred and forty-two consecutive patients without ischemia in the ECG or troponin I elevation were included. Ninety-two patients were discharged after the exercise testing (group I, 82 negative and 10 inconclusive test results) and 50 patients were hospitalized (group II, 29 positive and 21 inconclusive test results). In group I, cardiac events (unstable angina and non-fatal infarction) occurred in the next 30 days of follow-up in 2 patients with inconclusive test results; no cardiac events occurred in patients with negative test results. In group II, unstable angina was diagnosed in 30 patients and 3 presented recurrent angina. There were no complications during exercise testing. In conclusion, early exercise testing is safe and useful in the stratification of patients seen in the emergency room for chest pain. Only patients with negative test results should be discharged early.
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PMID:[Value of early exercise stress testing in a chest pain unit protocol]. 1238 83

The objective of this study was to determine the safety of the glycoprotein IIb/IIIa receptor inhibitor eptifibatide in patients at high risk for adverse clinical outcomes and to determine risk factors for eptifibatide-associated bleeding. Consecutive patients (n = 175) who presented with an acute coronary syndrome and who were at high risk for adverse clinical outcomes were prospectively observed for eptifibatide-associated bleeding, which was classified according to Thrombolysis in Myocardial Infarction (TIMI) and Global Use of Strategies to Open Occluded arteries (GUSTO) criteria. High risk was defined as unstable angina or non-Q-wave myocardial infarction with at least one of the following: left ventricular ejection fraction < 40%, diabetes mellitus, ST segment depression or transient ST segment elevation, serum [troponin I] > 2.5 ng/mL, and recurrent angina symptoms after initiation of conventional antianginal therapy. Bleeding incidences in the patients in this study were compared with those in the 4722 eptifibatide-treated patients in the Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) trial. Compared to PURSUIT patients, the population in this study was similar in age but had a higher proportion of females, African Americans, hypertension, diabetes, prior myocardial infarction, heart failure, and revascularization. Bleeding incidences in this study's patients were similar to or lower than those in the PURSUIT population: TIMI major 1.1% versus 10.8%, TAMI minor 12.6% versus 13.1%, GUSTO severe 1.7% versus 1.5%, GUSTO moderate 3.9% versus 11.3%, and GUSTO mild 19.7% versus 26.1%. Renal dysfunction was an independent risk factor for TIMI (odds ratio = 9.1 ([95% CI= 1.6-52.5]) and GUSTO (odds ratio = 6.1 [95% CI = 1.2-30.0]) bleeding. In conclusion, despite being at higher risk for adverse outcomes, patients administered eptifibatide according to this study's institutional guidelines had comparable or lower bleeding rates than in the PURSUIT trial. Renal dysfunction is an independent risk factor for eptifibatide-induced bleeding.
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PMID:Bleeding associated with eptifibatide targeting higher risk patients with acute coronary syndromes: incidence and multivariate risk factors. 1246 32

Myocardial Blush Grade (MBG) is an angiographic method of assessing myocardial microcirculation and provides independent risk stratification among patients with normal TIMI 3 flow. Although the beneficial effect of abciximab on microvascular perfusion is well established, the efficacy of eptifibatide in the prevention of platelet aggregation and distal microembolization is less proven. After a pharmacologic shift by our institution towards the use of eptifibatide in patients with unstable angina presenting for PCI, we sought to evaluate our experience by retrospectively comparing the effect on myocardial perfusion between abciximab and eptifibatide following PCI in stable angina or acute coronary syndrome. Microcirculatory perfusion was reviewed in 101 consecutive patients (23 stable angina, 61 unstable angina, 17 non-q MI) undergoing PTCA/stenting. This comparison was between the last group of 51 patients who routinely received standard bolus and infusion of abciximab and the first group of 50 patients who began receiving standard bolus and infusion of eptifibatide. Baseline characteristics between the two groups were balanced, except for more patients with previous CABG in the eptifibatide group. Angiograms were evaluated by 2 blinded independent reviewers for MBG as follows: 0, no blush; 1, minimal blush; 2, moderate blush; and 3, normal blush. TIMI 3 flow was seen in 98 patients. MBG scores were not significantly different in the abciximab group (67% MBG 3; 31% MBG 2; 2.0% MBG 0 1) than in the eptifibatide group (58% MBG 3; 36% MBG 2; 6.0% MBG 0 1); p = 0.34. Patients with prior PTCA/stenting had lower MBG scores (0 2) compared to patients without prior PTCA (58% vs 31%; p = 0.03). There were significantly lower MBG scores in all patients with prior PTCA or CABG compared to patients without (55% vs 30%; p = 0.03). MBG scores significantly and inversely correlated with peak troponin I levels (r = -0.18, one-tailed p = 0.04). The similarity in myocardial perfusion between abciximab and eptifibatide suggests that both compounds are equally effective in reducing platelet aggregation and microembolization during mechanical reperfusion. Lower MBG scores in patients with prior PTCA or revascularization may be explained by irreversible microvascular dysfunction resulting from distal microembolization during the previous procedure. Lower MBG scores in patients with higher troponin I levels may reflect more frequent microemboli and microinfarcts during an ischemic event. Larger prospective studies need to be performed to validate these findings.
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PMID:Preservation of myocardial microcirculation during mechanical reperfusion for myocardial ischemia with either abciximab or eptifibatide. 1294 5

The physiopathological mechanisms resulting in increased left ventricular pressures in acute cardiac failure with normal systolic function are not well understood. Although coronary artery disease is commonly associated with acute episodes, the diagnostic value of troponin I measurement and the prevalence of ischaemia as the predisposing factor are not known. Twenty coronary patients (mean age 77 +/- 9 years) in acute cardiac failure with left ventricular ejection fractions of 50% or over and without angina, were studied retrospectively. The diagnostic value of troponin I (cTnI, AxSYM, method) was assessed by comparing with a control group of 16 acute cardiac failure patients without coronary disease. The frequency of hypertension and diabetes in the coronary group was 50 and 45% respectively. At the time of investigation, the pulmonary capillary and systemic arterial pressures were comparable in the coronary patients irrespective of the cTnl value. At threshold levels of 0.5 microgram/l, cTnl had a specificity of 100% and confirmed ischaemia in 60% of the coronary patients. Ischaemia was the commonest predisposing factor for increased cardiac pressures. Over a 268 +/- 101 days follow-up period, half the coronary patients were readmitted for acute cardiac failure and a third of them died. The authors conclude that silent ischaemia is a common predisposing factor for acute cardiac failure in coronary patients with normal systolic function and troponin I measurement is a useful diagnostic help.
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PMID:[Silent ischemia and acute cardiac insufficiency with normal systolic function: diagnostic value of troponin I measurement]. 1457 38

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

The aim of this study was to show clinical benefit of simultaneous determinations of troponin I (cTnI) and high sensitivity C-reactive protein (hsCRP) at early diagnosis in the group of patients with stenocardia admitted to the Emergency Unit of 5-th Military Hospital in Krakow. The study group consisted of 38 (51.3%) patients with acute myocardial infarction (AMI) and 36 (48.6%) with unstable angina pectoris. ROC function analysis for cTnI (cutoff value 0.69 ng/mL) and hsCRP (3.33 mg/L) indicated significant amelioration of diagnostic sensitivity into 84.9% at early diagnostics of AMI in group of patients with acute coronary syndrome (ACS). Moreover, studies of mutual relationship between elevated levels of hsCRP and cTnI concentrations have shown a remarkably positive correlation (r = 0.90; p < or = 0.01) in the group of patients with AMI.
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PMID:[The role of serum troponin I and high sensitivity C-reactive protein concentrations in early diagnosis of acute coronary syndrome in patients admitted to Emergency Unit]. 1580 96

We examined the cardiotoxicity in 153 patients treated with capecitabine and oxaliplatin in two prospective trials for advanced colorectal cancer. Ten patients (6.5%) developed cardiac events. One patient (0.7%) had sudden death, one patient developed cardiac failure with raised troponin I while another developed ventricular tachycardia (VT). The remaining seven patients (4.6%) experienced angina and three of the seven patients had raised troponin I, one of which developed ventricular fibrillation. Eight events occurred within cycle 1 (median cycle 1 day 10). Four patients with angina and one patient with VT recovered on stopping capecitabine, four patients required additional medical management and the remaining patient died suddenly at home. Patients with ischaemic heart disease appeared to be at increased risk. Physicians and patients need to be aware of these complications, so that prompt discontinuation of treatment and appropriate interventions may be instituted.
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PMID:The frequency and pattern of cardiotoxicity observed with capecitabine used in conjunction with oxaliplatin in patients treated for advanced colorectal cancer (CRC). 1597

The aim of this study was to evaluate diagnostic usefulness of serum amyloid A (SAA) in diagnosis of acute myocardial infarction (AMI) in group of patients with stenocardia. The study was carried out in group of 62 patients admitted to Emergency Unit of 5-th Military Hospital in Krakow. The study group consisted of 24 (38.7%) patients with unstable angina pectoris and 38 (61.3%) with acute myocardial infarction. It was found that SAA concentration significantly increases in patients with AMI: 136.0 +/- 220.6 mg/L versus 7.38 +/- 8.8 mg/L in unstable angina pectoris (p < or = 0.009). Studies of mutual relations between SAA levels and cardiac markers have shown a remarkably positive correlation between SAA and troponin I (r = 0.39; p < or = 0.01) and negative correlation between SAA concentrations and platelet count decrease (r = -0.55; p < or = 0.01).
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PMID:[The role of serum amyloid A in the early diagnosis of acute coronary syndrome]. 1605 13


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