Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was designed to test if prophylactic intravenous nifedipine or nitroglycerine could reduce myocardial damage after cardiopulmonary bypass. 45 patients scheduled for elective coronary artery bypass grafting were divided at random into three groups: Group 1: control; group 2: nifedipine (0.25 microgram/kg/min); group 3: nitroglycerine (1.5 micrograms/kg/min). Infusion period reached from the beginning of anaesthesia until crossclamp of the aorta. Myocardial damage was estimated by troponin T (TnT), CK-MB and ST-segment analysis of the ECG. TnT is a cardiospecific protein from the contractile apparatus of striated muscle cells. TnT-levels might provide a very sensitive marker of small amounts of cardiac muscle necrosis. It was tested with an ELISA/one-step sandwich-assay with streptavidin-technology [9]. Criteria for ischemia in the ST-segment analysis were (according to Smith et al. [19]): ST-depression > 1 mm from baseline or ST-elevation > 2 mm from baseline at J-point + 60 ms. Statistical interpretation was done by one- and two-factorial analyses of variance (including multivariate analyses of variance). Correlation between two variables was tested by regression analysis. A level of p < 0.05 was taken for indicating statistical significance. Biometrical data, circulation data and data from cardiopulmonary bypass were without significant differences among all groups (Tables 1 and 2). Starting from normal values (< 0.05 ng/ml) TnT significantly rose in all groups immediately after cardiopulmonary bypass and remained elevated until the forth day after operation (values between 0.4 and 0.6 microgram/ml) (Figure 1).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cardiac protection in heart surgery interventions by preventive drug administration before extracorporeal circulation. Studies with troponin T as a parameter for perioperative myocardial damage]. 830 54

In 963 patients, participating in a randomized study of low molecular weight heparin in unstable coronary artery disease and followed for 5 months, troponin T was determined. In the 766 patients with a pre-discharge exercise test both troponin T level and exercise test response were independent predictors of prognosis. Cardiac death or myocardial infarction occurred in 5, 9 and 13% of the patients with a maximal troponin T level of < 0.06 (n = 154), 0.06-0.2 (n = 175) and > or = 0.2 microgram.l-1 (n = 437), respectively. Based on exercise tolerance and occurrence of ST depression, patients with a low (n = 361), intermediate (n = 325) and high risk (n = 80) exercise test response were identified. In these, death or myocardial infarction occurred in 5, 13 and 29%, respectively. The combination of troponin T and the exercise test response allowed an even better categorization into low (n = 84), intermediate (n = 406) and high (n = 276) risk groups with 1, 7 and 20% death or myocardial infarction, respectively. Among those 197 patients unable to perform an exercise test the incidence was 3, 16 and 27% in patients with troponin T < 0.06, 0.06-0.2 and > or = 0.2 microgram.l-1, respectively. Thus, troponin T determinations and pre-discharge exercise tests alone and combined are valuable for risk assessment in unstable coronary artery disease.
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PMID:Risk stratification in unstable coronary artery disease. Additive value of troponin T determinations and pre-discharge exercise tests. FRISK Study Group. 915 41

Clinical assessment of patients with acute coronary syndromes is routinely employed for risk stratification and selection of treatment strategies. Both, patients risk and treatment options vary in unstable angina, non-Q-wave infarction and massive Q-wave infarction. Clinical symptoms and admission ECG are the key elements in the daily work-up of chest pain patients. However, absent or nonconclusive ECG changes, even in patients with confirmed acute myocardial infarction, and high variability of clinical symptoms, particularly in elderly patients, limit their diagnostic value and their precision for risk stratification of acute coronary syndromes. Additional diagnostic testing such as 24 hours Holter ECG depicting prolonged episodes of ST-segment depression, and radio-nuclide tomography using Tc-Sestamibi improves accuracy of risk assessment. However, in clinical practise these techniques are not readily available. Troponins, particularly cardiac specific troponin T, are paramount for risk stratification of acute coronary syndromes, either alone, or in combination with admission ECG or a predischarge exercise stress test. Stratifying individuals into high, intermediate, and low risk for death and subsequent cardiac events may aid to improve outcomes by tailored use of a more aggressive therapy in these subjects.
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PMID:Strategies for clinical assessment of patients with suspected acute coronary syndromes. 1038

Skinned fibers prepared from rabbit fast and slow skeletal and cardiac muscles showed acidotic depression of the Ca2+ sensitivity of force generation, in which the magnitude depends on muscle type in the order of cardiac>fast skeletal>slow skeletal. Using a method that displaces whole troponin-complex in myofibrils with excess troponin T, the roles of Tn subunits in the differential pH dependence of the Ca2+ sensitivity of striated muscle were investigated by exchanging endogenous troponin I and troponin C in rabbit skinned cardiac muscle fibres with all possible combinations of the corresponding isoforms expressed in rabbit fast and slow skeletal and cardiac muscles. In fibers exchanged with fast skeletal or cardiac troponin I, cardiac troponin C confers a higher sensitivity to acidic pH on the Ca2+ sensitive force generation than fast skeletal troponin C independently of the isoform of troponin I present. On the other hand, fibres exchanged with slow skeletal troponin I exhibit the highest resistance to acidic pH in combination with either isoform of troponin C. These results indicate that troponin C is a determinant of the differential pH sensitivity of fast skeletal and cardiac muscles, while troponin I is a determinant of the pH sensitivity of slow skeletal muscle.
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PMID:Roles of troponin isoforms in pH dependence of contraction in rabbit fast and slow skeletal and cardiac muscles. 1039 29

Prognostic assessment of unstable angina pectoris is a common clinical problem for physicians. Markers of myocardial cell injury, serial electrocardiographic findings and ST segment monitoring are mainly studied for prognosis. We investigated the relation between myocardial injury and the value of cardiac troponin T and QT interval dispersion in hospitalized unstable angina patients. This is a prospective study that includes adult patients admitted to an emergency department with Braunwald class IIIB unstable angina pectoris. Eighty-six patients were enrolled in the study (mean age of 57 +/- 12 years, 63 males and 23 females). Cardiac troponin T was assayed and QT dispersion calculated from surface ECG. Fifty-eight patients with troponin T < 0.1 ng/ml and 28 patients with troponin T levels > or = 0.1 formed group 1 and group 2, respectively. There were no significant differences in sex, age, history of coronary revascularization or ECG findings such as ST depression and T inversions between the two groups. The QT dispersion was significantly greater in patients with elevated cardiac troponin T levels (77 +/- 18 msec vs 38 +/- 13 mse; p < 0.014). Because QT interval dispersion exhibited an association with cardiac troponin T levels, it may be used as a non-invasive marker of ischemic injury in patients with unstable angina.
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PMID:QT interval dispersion: non-invasive marker of ischemic injury in patients with unstable angina pectoris? 1113 66

Protein kinase C (PKC)-mediated phosphorylation of cardiac troponin I (cTnI) and troponin T (cTnT) has been shown to diminish maximum activation of myofilaments. The functional role of cTnI phosphorylation has been investigated. However, the impact of cTnT phosphorylation on myofilament force is not well studied. We tested the effect of endogenous PKC activation on steady-state tension development and Ca(2+) sensitivity in skinned fiber bundles from transgenic (TG) mouse hearts expressing fast skeletal TnT (fsTnT), which naturally lacks the PKC sites present in cTnT. The 12-O-tetradecanoylphorbol 13-acetate (TPA) treatment induced a 29% (46.1 +/- 2.5 vs. 33.4 +/- 2.6 mN/mm(2)) reduction in maximum tension in the nontransgenic (NTG) preparations (n = 7) and was inhibited with chelerythrine. However, TPA did not induce a change in the maximum tension in the TG preparations (n = 11). TPA induced a small but significant (P < 0.02) increase in Ca(2+) sensitivity (untreated pCa(50) = 5.63 +/- 0.01 vs. treated pCa(50) = 5.72 +/- 0.01) only in TG preparations. In TG preparations, (32)P incorporation was not evident in TnT and was also significantly diminished in cTnI, compared with NTG. Our data indicate that incorporation of fsTnT into the cardiac myofilament lattice blunts PKC-mediated depression of maximum tension. These data also suggest that cTnT may play an important role in amplifying the myofilament depression induced by PKC-mediated phosphorylation of cTnI.
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PMID:Transgenic incorporation of skeletal TnT into cardiac myofilaments blunts PKC-mediated depression of force. 1117 42

This article summarizes the design and findings -- both at 3 months and at 1 year follow-up -- of the Fragmin during Instability in Coronary Artery Disease (FRISC) II trial. This multicentre randomized trial compared both an early invasive with an early non-invasive stategy, and prolonged treatment with dalteparin as opposed to placebo, in patients with unstable coronary artery disease. The results show that an early invasive strategy with coronary angiography and, if appropriate, revascularization procedures within 7 days after admission reduces the subsequent rate of mortality and myocardial infarction. The benefits of the invasive treatment were noticeably more marked in patients with any high-risk indicator -- for example, male gender, age above 65 years, previous severe angina, or signs of ischaemia (ST depression on ECG) or of myocardial damage (elevated levels of troponin T). Treatment with dalteparin reduced the risk of death and myocardial infarction in high-risk (i.e. troponin-positive) patients, particularly during the first month of treatment. However, continuation with dalteparin therapy after revascularization procedures conferred no benefit. It is concluded that extended treatment with dalteparin is useful as a bridge to revascularization in this high-risk subgroup of patients with unstable coronary artery disease.
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PMID:Low-molecular-weight heparin as a bridge to timely revascularization in unstable coronary artery disease -- an update of the Fragmin during Instability in Coronary Artery Disease II Trial. 1125 53

Diagnosis and risk stratification of patients with acute coronary syndromes remain extremely important in order to avoid unnecessary hospitalizations on the one hand, and to improve prognosis of these patients on the other. For diagnosis of acute coronary syndromes, an ECG should be obtained at rest, troponin T and I should be measured on admission and again 6 to 12 h later, and myoglobin or CK-MB should be determined in patients with recent syndromes and those with recurring ischemia. Risk should be assessed upon admission and repeatedly during the hospital stay. Early risk indicators are: age, male sex, previous manifestation of coronary artery disease, history of left ventricular dysfunction or congestive heart failure and ongoing chest pain, as well as ST depression, transient ST segment elevation, and elevated levels of troponin T or I. Longer term risk assessment in unstable coronary artery disease includes rest and stress echocardiography, exercise ECG, thallium scintigraphy, as well as coronary angiography and left ventriculography. Markers of high long-term risk are old age, prior history of myocardial infarction, diabetes, elevated levels of C-reactive protein, and the extent of coronary artery disease and left ventricular dysfunction.
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PMID:Diagnosis and risk stratification in patients with acute coronary syndromes according to ESC guidelines. 1156 70

Acute myocardial infarction (AMI) is one of many causes of electrocardiographic ST segment elevation (STE) in ED chest pain (CP) patients; at times, the electrocardiographic diagnosis may be difficult. Coexistent ST segment depression has been reported to assist in the differentiation of non-infarction causes of STE from AMI-related ST segment elevation. The objective was to determine the effect of AMI diagnosis on the presence of STD among ED CP patients with electrocardiographic STE. Adult CP patients with electrocardiographic STE in at least 2 anatomically distributed leads were reviewed for the presence or absence of ST segment depression in at least 1 lead and separated into 2 groups, both with and without ST segment depression. A comparison of the 2 groups was performed in 2 approaches: all STE patients and then only with STE patients who lacked confounding electrocardiographic pattern (bundle branch block [BBB], left ventricular hypertrophy [LVH], or right ventricular paced rhythm [VPR]). All patients in the study underwent prolonged observation in the ED (at least 8 hours) with 3 serial troponin T determinations and 3 electrocardiograms (ECG). AMI was diagnosed by abnormal serum troponin T values (>0.1 mg/dL); electrocardiographic STE diagnoses of non-AMI causes were determined by medical record review. There were 171 CP patients with STE were entered in the study with 112 (65.5%) individuals show ST segment depression. When considering all study patients, ST segment depression was present at statistically equal rates in AMI and non-AMI situations (P = NS). The sensitivity, specificity, positive predictive value, and negative predictive value for the electrocardiographic diagnosis of AMI were 63%, 34%, 30%, and 67%, respectively. Patients with confounding patterns (LVH 46, BBB 19, and VPR 6) were removed from the analysis group, leaving 100 patients for analysis; 38 of these patients had ST segment depression. When considering this group of study patients, ST segment depression was present significantly more often in AMI patients (P <.0001). The sensitivity, specificity, positive predictive value, and negative predictive value for the electrocardiographic diagnosis of AMI were 69%, 93%, 93%, and 71%, respectively. Clinical diagnoses were as follows: 56 AMI, 50 USAP, and 65 noncoronary syndrome. When all CP patients with electrocardiographic STE are considered, the presence of ST segment depression is not helpful in distinguishing AMI from non-AMI. If one considers only patterns which lack electrocardiographic ST segment depression caused by altered intraventricular conduction, the presence of ST segment depression strongly suggests the diagnosis of AMI. In these cases, reciprocal ST segment depression is of considerable value in establishing the electrocardiographic diagnosis of STE AMI.
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PMID:Reciprocal ST segment depression: impact on the electrocardiographic diagnosis of ST segment elevation acute myocardial infarction. 1178 11

Striated muscle tropomyosin (TM) interacts with actin and the troponin complex to regulate calcium-mediated muscle contraction. Previous work by our laboratory established that alpha- and beta-TM isoforms elicit physiological differences in sarcomeric performance. Heart myofilaments containing beta-TM exhibit an increased sensitivity to calcium that is associated with a decrease in the rate of relaxation and a prolonged time of relaxation. To address whether the carboxyl-terminal, troponin T binding domain of beta-TM is responsible for these physiological alterations, we exchanged the 27 terminal amino acids of alpha-TM (amino acids 258 -284) for the corresponding region in beta-TM. Hearts of transgenic mice that express this chimeric TM protein exhibit significant decreases in their rates of contraction and relaxation when assessed by ex vivo work-performing cardiac analyses. There are increases in the time to peak pressure and a dramatic increase in end diastolic pressure. In myofilaments, this chimeric protein induces depression of maximum tension and ATPase rate, together with a significant decrease in sensitivity to calcium. Our data are the first to demonstrate that the TM isoform-specific carboxyl terminus is a critical determinant of sarcomere performance and calcium sensitivity in both the whole heart and in isolated myofilaments.
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PMID:Functional importance of the carboxyl-terminal region of striated muscle tropomyosin. 1269 96


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