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 American College of Cardiology/American Heart Association Task Force on Practice Guidelines has published recommendations on the diagnosis and treatment of patients with known or suspected unstable angina and non-ST-segment elevation myocardial infarction. The acute ischemia pathway presented in these guidelines encompasses both an early invasive strategy and an early conservative strategy. There are now 4 randomized, controlled trials that have compared the routine early invasive strategy with the selective-invasive or ischemia-guided strategy (Thrombolysis in Myocardial Infarction [TIMI] IIIB, Veterans Affairs Non-Q-Wave Infarction Strategies in Hospital [VANQWISH], Fragmin and Fast Revascularization During Instability in Coronary Artery Disease [FRISC] II, and Treat Angina with Aggrastat and Determine Cost of Therapy with an Invasive or Conservative Strategy [TACTICS]-TIMI 18). The most relevant of these studies to current clinical practice are the FRISC II and TACTICS-TIMI 18 studies. The data from these studies indicate that ST-segment depression or elevated levels of troponin or the MB isoenzyme of creatinine kinase are markers of increased risk and that such patients would benefit from early revascularization. However, the data further suggest that aggressive antiplatelet, antithrombin, and anti-ischemic therapies are also important. Although FRISC II and TACTICS-TIMI 18 support an early invasive approach in most patients (ie, intermediate- and high-risk patients) with non-ST-segment elevation acute coronary syndromes (ACS), all 4 trials support a more conservative approach in those without electrocardiographic changes or enzyme elevations, notably the use of intensive antiplatelet, antithrombotic, and anti-ischemic therapy combined with careful clinical assessment and provocative testing. Patients then undergo catheterization and revascularization only if spontaneous angina occurs or if there is electrocardiographic, enzymatic, or other objective evidence of stress-induced myocardial ischemia. We conclude that tailoring the early initial therapy in hospital to the level of risk is essential to optimizing efficacy and clinical outcomes in this challenging, but common group of ACS patients.
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PMID:Interpreting new treatment guidelines for non-ST-segment elevation acute coronary syndromes. 1169 15

Plasma levels of haemostasis factors (HFs) such as fibrinogen, tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1) and D-dimer may be markers of arteriosclerosis for the following reasons: There seems to be no difference in levels of HFs between patients with longstanding stable angina and those with an isolated myocardial infarction. HF levels are generally positively associated with subclinical arteriosclerosis as determined by ankle-arm index and carotid ultrasonography in asymptomatic individuals. Levels of most HFs are positively associated with inflammation, which is an essential part of the initiation and progression of the disease. A rough classification is assigned to the associations found in under (2) and (3). Fibrinogen is strongly associated with subclinical arteriosclerosis and with inflammation; Factor VII is not, while an intermediate group is formed by, for instance, von Willebrand Factor (vWF), Factor VIII (F VIII), t-PA, PAI-1, and D-dimer. Also, the associations of HFs with cardiovascular events follow a similar pattern. Fibrinogen is a strong and consistent risk factor in several studies, Factor VII is not, and a similar intermediate group as mentioned under (2) and (3) exists. It suggests that the risk of cardiovascular events in relation to HF levels is explained by their identity as markers of arteriosclerosis. A causal association between HF levels and the disease is not proven. Out of the HF, the markers of coagulation such as thrombin-antithrombin complex and of fibrinolysis such as D-dimer are more likely to act causally. Increased levels indicate that they are markers of arteriosclerosis, but in addition, they may reflect a low-grade, continuous formation and subsequent lysis of fibrin in the disease. As the latter reflects an increased tendency to thrombosis, a causal association of levels of markers of coagulation and fibrinolysis with arteriosclerosis, although not yet proven, seems likely.
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PMID:Levels of haemostatic factors, arteriosclerosis and cardiovascular disease. 1261 75

Is a "routine invasive" or "selective invasive" strategy the best approach for patients with non-ST-segment elevation acute coronary syndrome (ACS)? A "selective invasive" strategy incorporates ischemia-guided use of aggressive medical therapy followed by angiography and revascularization for angina or stress-induced myocardial ischemia. The "routine invasive" strategy (cardiac catheterization followed by percutaneous coronary intervention within 24 to 48 h of symptom-onset) is frequently employed, but no randomized, controlled trials have demonstrated improved clinical outcomes. Recently, the second Fragmin and fast Revascularization during InStability in Coronary artery disease (FRISC-II) and the Treat angina with Aggrastat and determine Cost of Therapy with an Invasive or Conservative Strategy-Thrombolysis in Myocardial Infarction (TACTICS TIMI-18) trials found significant reductions in death, recurrent myocardial infarction, or hospitalization for biomarker-positive ACS. Also, the third Randomized Intervention Trial of unstable Angina (RITA-3) recently reported a halving of refractory angina and reduction in the use of antianginal medication with early intervention. Early trials failed to demonstrate the superiority of the "routine invasive" approach, presumably because of fewer revascularizations, unavailability of stents, and more recent use of glycoprotein IIb/IIIa inhibitors and low-molecular-weight heparins. The FRISC-II, TACTICS TIMI-18, and RITA-3 studies indicate that higher-risk patients benefit from early revascularization, but that aggressive antiplatelet, antithrombin, and anti-ischemic therapy are also important. While all three trials support an "early invasive" approach in intermediate- and high-risk patients, other trials support a more "conservative" approach in those without electrocardiographic changes or enzyme elevations. Optimal management should incorporate both strategies.
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PMID:"Routine invasive" versus "selective invasive" approaches to non-ST-segment elevation acute coronary syndromes management in the post-stent/platelet inhibition era. 1264 49

Unstable coronary artery disease is in most cases associated with plaque rupture, activation of the coagulation system and subsequent intracoronary thrombus formation which may cause myocardial cell damage. The aim of the present analysis was to assess the relation between troponin T, markers of coagulation activity, i.e. prothrombin fragment 1+2, thrombin-antithrombin complex, soluble fibrin and D-dimer, and ischemic events, i.e. death, myocardial (re-)infarction or refractory angina. 320 patients with unstable coronary artery disease were randomized to 72 hours infusion with inogatran, a low molecular weight direct thrombin inhibitor, or unfractionated heparin. Patients with elevated troponin levels had higher levels of prothrombin fragment 1+2, soluble fibrin and D-dimer before, during, and at 24 hours after cessation of anticoagulant treatment. These troponin-positive patients tended to have worse short-term clinical outcome, without relation to markers of coagulation activity. Troponin-negative patients with unchanged or early increased thrombin generation during treatment had a cluster of ischemic events within 24 hours after cessation of the study drug. The 30-day ischemic event rate was 19 % in troponin-negative patients with unchanged or early increased prothrombin fragment 1+2, and 5.7 % in patients with decreased prothrombin fragment 1+2, p=0.006, and similarly 15 % in troponin-negative patients with unchanged or early increased thrombin-antithrombin complex and 4.5 % in patients with decreased thrombin-antithrombin complex, p=0.02. In conclusion, in unstable coronary artery disease a troponin elevation indicates higher risk and higher coagulation activity. However, among the troponin negative patients, with a lower risk and lower coagulation activity, a part of the patients seem to be non-responders to treatment with a thrombin inhibitor expressed as unchanged or raised coagulation activity and a raised risk of ischemic events early after cessation of treatment.
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PMID:Myocardial damage, coagulation activity and the response to thrombin inhibition in unstable coronary artery disease. 1496 Nov 68

In the last decade, a variety of novel anticoagulant and antiplatelet agents that improve outcomes in patients undergoing percutaneous coronary revascularization have emerged. During the next decade, continued refinements in catheter-based device technology should lead to further increases in the number of interventional procedures. The use of optimal antithrombotic strategies is pivotal in reducing adverse events among patients undergoing percutaneous coronary intervention (PCI). Our purpose is to review the current evidence regarding the efficacy of available adjunctive anticoagulant and antiplatelet agents in treating patients undergoing percutaneous coronary revascularization. It should be borne in mind that patients undergoing PCI in the midst of an acute coronary event require a different level of coagulation and platelet aggregation inhibition than low-risk patients undergoing elective PCI for stable angina pectoris. Similarly, generalizing antithrombotic regimen safety data to a wide spectrum of catheter-based therapeutic devices should be avoided. A level of anticoagulation that is safe and effective for angioplasty and stent placement may not be sufficient for devices with longer intracoronary dwell times such as brachytherapy catheters. In light of current evidence, activated clotting times should be targeted in the 200- to 250-second range during elective PCI and in the 250- to 300-second range when intervening on a higher-risk lesion, such as one with an angiographically visible thrombus or in patients presenting with an acute coronary syndrome (ACS).Low-dose enoxaparin sodium is an attractive antithrombin strategy in PCI because it is intrinsically adjusted for renal function, age, and concomitant glycoprotein (GP) IIb/IIIa antagonist use. Other low-molecular weight heparins have also been studied as adjunctive anticoagulants during cardiac catheterization. For example, in pilot studies, dalteparin sodium was shown to have a good safety profile when used alone or in combination with abciximab during PCI.A wealth of data supports the use of a GP IIb/IIIa antagonist in patients presenting with ACS, especially those with high-risk features such as elevated cardiac markers; the systematic use of GP IIb/IIIa inhibitors in this population is therefore encouraged. Overall, the use of GP IIb/IIIa inhibitors reduces the incidence of thrombotic complications following PCI, is associated with a mortality benefit, but has no impact on the risk of restenosis.
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PMID:Interventional cardiovascular pharmacotherapy: current issues. 1572 40

Retinal vein occlusion (RVO) is a multifactorial disease involving vessel damage, stasis, viscosity and thrombosis. Conflicting findings on hereditary thrombophilic risk factors have been reported and their impact on RVO features remains to be defined. The aim of the present study was to evaluate the prevalence of hereditary thrombophilic risk factors (HTRF) and characteristics of RVO in patients with or without HTRF. The design of the study was a prospective, observational case series. Two hundred and thirty-four patients with RVO were included consecutively. A French healthy population of the same region was studied as control group. The HTRF studied were protein C (PC), protein S (PS) and antithrombin (AT) deficiencies, factor V Leiden (FVL) and factor II 20210A polymorphisms. Chi-Square was used for comparison with the healthy subjects and between RVO patient with and without HTRF according to localisation (branch vs. central), type of RVO (ischemic or non-ischemic), recurrence, age at first event and classical vascular risk factors. Twenty-two patients had HTRF (12 FV Leiden heterozygotes, 9 FII 20210A heterozygotes and 1 PS deficiency). No AT or PC deficiency was detected. Frequencies of PS deficiency, FVL and FII 20210A allele were similar to the reference population as well as to published data in the general caucasian population. Eighty-six patients experienced their first episode before the age of 60 years. Systemic hypertension, glaucoma and angina were significantly less frequent in patients with RVO before 60 years. Fourteen of the 22 patients with one HTRF (64%) experienced their first episode of RVO before the age of 60 years compared to 72 of 212 without HTRF (34%) (p = 0.006). Heterozygote status for FV Leiden was significantly more frequent in patients who had experienced their first episode of RVO before 60 years (p = 0.027). In conclusion, this study suggests a role of FV Leiden in the occurrence of RVO in patients younger than 60 years who exhibit fewer acquired vascular risk factors than in older patients.
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PMID:Increased prevalence of factor V Leiden in patients with retinal vein occlusion and under 60 years of age. 1611 92

Osteoprotegerin (OPG) is a member of the tumour necrosis factor superfamily and is involved in the regulation of bone metabolism and vascular calcification. Increased serum OPG levels have been reported in patients with stable angina pectoris and survivors of myocardial infarction with heart failure. The purpose of the present study was to determine serum OPG levels in young survivors of acute myocardial infarction (MI), and the relationship between OPG, homocysteine, sCD40L and coagulation factors in blood. Fifty-eight patients with verified MI, 40-60 years of age, were recruited 1-4 years after the acute event into an age- and sex- matched case control study with controls recruited from the general population. Serum OPG levels were similar in cases (2.41 ng/ml, 2.11-2.77 ng/ml) (mean, 95% CI) and controls (2.43 ng/ml, 2.11-2.79 ng/ml) (p = 0.92). Significant correlation between OPG and homocysteine was found in patients (r = 0.30, p = 0.02) and controls (r = 0.35, p = 0.007). A significant negative correlation was found between OPG and sCD40L in patients (r = -0.51, p < 0.001), but not in controls (r = 0.001, p = 0.96). No associations were found between serum OPG and markers of coagulation activation. The present study shows that serum OPG level was not increased in young survivors of uncomplicated myocardial infarction. Serum OPG levels were not associated with thrombin generation assessed by thrombin-antithrombin complexes (TAT), but a positive association between serum OPG and homocysteine was found.
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PMID:Serum osteoprotegerin in young survivors of myocardial infarction. 1667 81

Improvements in the management of haemophilia have led to a significant increase in the life expectancy of haemophilia patients, which is now close to the life expectancy in the general male population. Therefore, age-related conditions, especially cardiovascular disease (CVD), have become increasingly common in these patients. The management of CVD, especially that of coronary artery disease (CAD), acute coronary syndrome (ACS) and atrial fibrillation (AF), is particularly challenging in patients with haemophilia due to the need to find an adequate balance between bleeding and ischemic risk, requiring close coordination between cardiologists and haemophilia specialists. However, specific recommendations and relevant literature and data are scarce. Therefore, we propose pragmatic and practical therapeutic suggestions, based on the available literature and our own experience, for the management of ACS, stable angina and AF in patients with haemophilia. Overall, evidence and experience suggest that they should be treated much in the same way as the general CVD population, following standard guidelines, while choosing available treatment options known to be associated with low rates of bleeding complications. Treatments advocated for patient with haemophilia include antiplatelet therapy (aspirin and P2Y12 inhibitors), antithrombin therapy such as heparin or bivalirudin, glycoprotein IIb/IIIa inhibitors (GPIIb/IIIa inhibitors), transradial cardiac catheterization, and use of bare metal (BMS) or drug-eluting stents (DES). Antithrombotic agents with shorter half-lives that are reversible or have an antidote offer a safer choice in this setting. In addition, optimal clotting factor replacement therapy should be tailored to the increased risk of bleeding associated with invasive procedures and antithrombotic therapies, particularly during the acute phase of ACS.
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PMID:Management of cardiovascular disease in haemophilia. 2374 27


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