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 aim of the study was to evaluate which pattern of coagulation indicators characterizes unstable angina and, particularly, its relationship with short-term prognosis. Forty patients with unstable angina (UA Group) at admission in the intensive care unit, 40 patients with chronic stable effort angina (SEA Group), and 20 age- and sex-matched healthy controls were studied. Blood coagulation indicators were fibrinogen, prothrombin fragment F1 + 2 (F1 + 2), thrombus precursor protein (TpP), and D-dimer. C reactive protein (CRP) and cardiac Troponin I (cTnI) have also been determined and compared. Patients in the UA Group were followed for in-hospital adverse events (sudden death, acute myocardial infarction and angina refractory to medical therapy). CRP, D-dimer and cTnI plasma levels were significantly lower in the SEA Group than in the UA Group; the same trend was found for fibrinogen and F1 + 2 plasma levels, although not statistically significant. The TpP was similar in all groups. The control group showed the lowest levels for all indicators. Within the UA Group, 17 patients developed adverse events during hospitalization; F1 + 2, D-dimer, cTnI and CRP plasma levels were higher in these patients than in those with good outcome. Relative risks for adverse events associated with the highest tertile of D-dimer, cTnI, and CRP plasma levels were 8.4 (95% confidence interval, 1.5-48.9), 6.7 (95% confidence interval, 1.1-38.6) and 5.2 (95% confidence interval, 1.1-25.2), respectively. D-Dimer is significantly increased in patients with unstable angina and, in particular, in those who develop an adverse event.
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PMID:Coagulation indicators in chronic stable effort angina and unstable angina: relationship with acute phase reactants and clinical outcome. 1194 39

The purpose of the study was to measure the blood level of thrombus precursor protein (TpP), a soluble fibrin monomer, in patients with stable exertional angina (SEA) and healthy people. The study included the examination of 33 patients with SEA (functional class II and III) and 29 practically healthy volunteers (control group). The detection of TpP in blood plasma was performed by solid-phase immune-enzyme analysis ("sandwich" type) using commercial diagnosticum "Kit" ("ABS", USA) and a microplate reader "IEMS Analyzer\Dispenser, with automatic result calculation in "Logistic fif" mode. TpP level in patients with SEA on the average was slightly higher than in control group, but the difference was not significant. TpP blood level was independent of the patients' gender, age, angina functional class and an old myocardial infarction. TpP blood level in patients with SEA depended on the duration of the illness, and proved to be significantly higher (compared with that in control group) in patients with SEA during the first 5 years of the illness, i.e. at early stages of CHD. Solid-phase immune-enzyme analysis ("sandwich" type) is a highly informative and affordable clinical method. TpP level in patients with SEA on the average was slightly higher than in healthy people (1.21 +/- 0.06 mkg/ml and 1.01 +/- 0.12 mkg/ml, respectively), but the difference was significant only in patients during the first 5 years of having SEA (1.41 +/- 0.11 mkg/ml).
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PMID:[The soluble fibrin monomer in patients with instable angina]. 1588 36

The purpose of the study was to determine the level of thrombus precursor protein (TrP) in patients with acute coronary syndrome (ACS). Twenty-six patients with ACS and anginal pain experienced during 2 to 12 hours (7.2 +/- 1.3 hours), admitted to cardiological intensive care unit, were enrolled in the study. Five ml of blood were sampled from a cubital vein of all the patients during the phase of the most intensive pain. TrP blood levels were measured with ELISA, Enzyme-Linked Immunoadsorbent Assay. The control group consisted of 29 healthy volunteers and 22 patients with stable exertional stenocardia. A significant increase in TpR (7.2 +/- 1.45 mcg/ml) was noted in the ACS patients as early as during the first 6 hours, vs. the healthy controls (1.01 +/- 0.12 mcg/ml) and the patients with stable stenocardia (1.21 +/- 0.06 mcg/ml), p < 0.01. A high level of TrP in the ACS patients could be noted earlier than a diagnostically significant increase in creatine phosphokinase level. No direct correlation was observed between the TrP level and the dynamics of such indices of the procoagulatory hemocoagulation chain as fibrinogen, prothrombin index, and active partial thromboplastin time. The results of the study demonstrate that the measurement of TrP level is highly informative when the intensity of intravascular blood coagulation in ACS patients is to be evaluated, which can be used to clarify indications to anticoagulation therapy. The enzyme immune method of TrP detection in the plasma of ACS patients can be recommended for clinical application.
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PMID:[Thrombus precursor protein (soluble monomeric protein) in patients with acute coronary syndrome]. 1720 43

Amyloidosis covers a group of disorders that can manifest in virtually any organ system in the body and is thought to be secondary to misfolding of extracellular proteins with subsequent deposition in tissues. The precursor protein that is produced in excess defines the specific amyloid type. This requires histopathological confirmation using Congo-red dye with its characteristic demonstration of green birefringence under cross-polarized light. There are three main types of amyloidosis associated with cardiac involvement: light-chain (AL), familial or senile (ATTR), and secondary (AA) amyloidosis. The frequency of cardiac involvement and prognosis varies among each type. Amyloid cardiomyopathy commonly manifests as heart failure and the presenting features are usually dyspnoea, oedema, angina, pre-syncope and syncope. The diagnosis of cardiac amyloidosis is very hard and can easily be misdiagnosed. Although the imaging studies (such as echocardiography and cardiovascular magnetic resonance) may guide the diagnosis, tissue biopsy is needed for confirmation. Management of cardiac amyloidosis initially is to treat the underlying heart failure. Pacemaker implantation is usually required in patients with any conduction abnormalities. Transplantation is the next step with worsening heart failure. However, the aim of any treatment in amyloidosis, irrespective of type, is to prevent further deposition of amyloid while managing concurrent symptoms. In this manuscript, we will discuss the pathogenesis of cardiac amyloidosis, diagnostic methods and management options.
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PMID:Cardiac amyloidosis: pathogenesis, clinical context, diagnosis and management options. 2870 53