Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 58-year-old woman suffering from congestive heart failure caused by a mechanical pulmonary valve thrombosis was operated on with a pulmonary allograft. She had experienced pulmonary valvotomy and resection of infundibular stenotic muscle for congenital pulmonary stenosis at the age of 23 years old. She got congestive heart failure caused by pulmonary regurgitation, and underwent pulmonary valve replacement with a St. Jude Medical (SJM) valve when she was 48 years old. She suffered from episodes of a thrombosed SJM valve in 1984 and 1993. Each time, thrombolytic treatment with urokinase or recombinant tissue-type plasminogen activator was effective. She suffered from the third episode of SJM valve thrombosis in January 1994. As thrombolytic treatment was not effective this time, the thrombosed SJM valve was resected and her pulmonary root was reconstructed with a cryopreserved pulmonary allograft. Postoperative course was uneventful, and she now enjoys her life without anticoagulant therapy.
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PMID:[Pulmonary root reconstruction with a cryopreserved pulmonary allograft for mechanical pulmonary valve thrombosis]. 805 35

Valve thrombosis is one of the most serious complications after prosthetic valve replacement. We report the use of tissue-type plasminogen activator (t-PA) in the treatment of a patient with thrombosed aortic and mitral valves. Thrombolysis resulted in immediate hemodynamic improvement and resolution of congestive heart failure, thereby avoiding surgical intervention. Based on our experience, thrombolysis with t-PA is an effective alternative in the treatment of thrombosed prosthetic valves.
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PMID:Tissue-type plasminogen activator (t-PA) lysis of aortic and mitral valve thrombosis. 834 79

Increased T-wave amplitude is one of the earliest electrocardiographic (ECG) changes following coronary artery occlusion. Therefore, higher T waves in the presenting electrocardiogram should represent earlier time to treatment and thus be associated with lower mortality following thrombolytic therapy. However, T-wave amplitude has never been evaluated as a prognostic marker in this setting. We examined clinical outcomes in 3,317 patients with acute myocardial infarction (AMI) who underwent thrombolysis in the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO-I) Study. Patients were classified as either those with high T waves or those with low T waves. Higher T waves were defined as those >98th percentile of the upper limit of normal. T-wave amplitude was also evaluated as a continuous variable according to infarct location (maximum T-wave amplitude) and as the amount of excess T-wave amplitude above normal (excess T-wave amplitude). Patients with higher T waves had lower 30-day mortality than those without (5.2% vs 8.6%, p = 0.001) and were less likely to develop congestive heart failure (15% vs 24%, p <0.001) or cardiogenic shock (6.1% vs 8.6%, p = 0.023). Higher maximum T-wave amplitude and excess T-wave amplitude were predictive of lower 30-day mortality (chi-square = 67, p <0.001 and chi-square = 33, p <0.001, respectively). These differences remain significant after controlling for other prognostic baseline ECG variables. In addition, T-wave amplitude added prognostic significance after controlling for time to treatment. T-wave amplitude, an often-overlooked component of the electrocardiogram, can add significant prognostic information in initial evaluation of patients with AMI.
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PMID:Higher T-wave amplitude associated with better prognosis in patients receiving thrombolytic therapy for acute myocardial infarction (a GUSTO-I substudy). Global Utilization of Streptokinase and Tissue plasminogen Activator for Occluded Coronary Arteries. 960 45

Circadian patterns of risk for cardiac events and their implications for prevention and treatment of cardiovascular conditions are discussed. Sympathovagal tone, a major biological determinant of circadian variation in cardiovascular function, is modulated through circadian patterns of sleep-wake activity. The influence of neurohumoral activity on cardiovascular function is manifested by 24-hour variability in heart rate, blood pressure, and vasomotor tone. Platelet aggregation and plasminogen-activator inhibitor-1 activity peak around the time of awakening. Conversely, endogenous plasminogen activator exhibits a nadir around the time of awakening. Studies of patterns of occurrence of cardiac disorders such as acute myocardial infarction, sudden cardiac death, stroke, and ventricular arrhythmia show an increased occurrence during the period surrounding awakening. These patterns are consistent with observed circadian patterns in cardiovascular function. Diabetes, left ventricular dysfunction, and congestive heart failure may contribute to alterations in patterns of occurrence of cardiac events. Factors such as race, sex, and age may lead to alterations in circadian variation in cardiovascular function. Unusual physical exertion, stress, and anger may act as triggers of an event at any time of day. The circadian patterns of cardiac events follow the natural fluctuations in endogenous physiological processes, with a vulnerable period consistently observed in the early morning; dynamic assessment of markers of cardiovascular function may assist in determining the extent of disease progression and in selecting cardiovascular therapies.
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PMID:Circadian variations in cardiovascular function and their relation to the occurrence and timing of cardiac events. 982 43

Involvement of AVP in several pathological states is now established and specific modulation of the different AVP receptor subtypes (V1a, V1b and V2) offers new clinical perspectives for treating major diseases. Recent years have marked a turning point with the design and the use of the first nonpeptide vasopressin receptor antagonists expressing various selectively profile. In that field, we report here the characterization of SR 121463A a highly selective, orally-active antagonist of vasopressin V2 receptors in several models in vitro and in vivo. This compound displayed competitive nanomolar affinity for V2 receptors in various species including man and exhibited a highly selective AVP V2 profile. In vitro, SR 121463A potently antagonized AVP-stimulated adenylyl cyclase activity in human kidney preparations (Ki = 0.26 +/- 0.04 nM) without any intrinsic agonistic effect. In normally-hydrated rats, SR 121463A induced dose-dependent powerful and long-lasting aquaresis after intravenous (0.003 to 0.3 mg/kg) or oral (0.03 to 10 mg/kg) administration. The action of SR 121463A is purely aquaretic with no changes in urine Na+ and K+ excretions unlike that of known diuretic agents such as furosemide or hydrochlorothiazide. In vasopressin-deficient Brattleboro rats, SR 121463A is devoid of any V2 antidiuretic agonist properties. In addition, this compound potently antagonized DDAVP extrarenal V2 effects on hemostasis factor release (FVIII, vW and t-PA) in dogs (ID50 approximately 10 micrograms/kg i.v.). Thus, SR 121463A is the most potent and selective, orally-active V2 antagonist yet described. It is a useful ligand for exploring V2 receptors and the therapeutical usefulness of pure V2 aquaretic agents in several water-retaining diseases and congestive heart failure.
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PMID:Nonpeptide antagonists for vasopressin receptors. Pharmacology of SR 121463A, a new potent and highly selective V2 receptor antagonist. 1002 34

The usefulness and safety of intravenous thrombolytic therapy were investigated in 298 patients older than 65 years (145 males, 153 females, mean age 78 years) with acute myocardial infarction from 1984 to 1993. These patients were divided into 2 groups of 88 patients younger than 74 years (Group A) and 210 patients older than 75 years (Group B). Seventy patients received thrombolytic therapy with urokinase (UK) or tissue-plasminogen activator [t-PA (UK96 X 10(4)U: 57 patients, t-PA 30-40 X 10(4)U/kg: 12, UK + t-PA: 1)] within 6 hours after the onset of acute myocardial infarction (Group TL). Two hundred twenty-eight patients received conventional therapy (Group C). There were no differences in the frequencies of the site of myocardial infarction, Killip class, admission within 6 hours after the onset of acute myocardial infarction or thrombolytic therapy between the 2 age groups. In-hospital mortality was significantly higher in Group B than in Group A (43% vs 24%, p < 0.01). In Groups A and B, in-hospital mortality was 20% lower in Group TL compared with Group C (20% vs 25% in Group A, 36% vs 45% in Group B). In Group B, the mortality from pump failure including shock and congestive heart failure was half in Group TL compared with Group C (13% vs 30%). Cardiac rupture was found in 11 patients of Group TL and 7 patients of Group C. Therefore, the mortality from cardiac rupture was fivefold higher in Group TL compared with Group C (8% vs. 1.6% in Group A, 20% vs 3.6% in Group B). Of 11 patients with cardiac rupture in Group TL, 8 patients suffered rupture in the early phase within 12 hours after the onset of acute myocardial infarction and the tear was present near the center of infarcted area in all 7 autopsy cases. The case of recanalization of the infarct-related coronary artery in Group TL revealed moderate to massive hemorrhagic infarction at autopsy. This indicates that the mechanisms involved in cardiac rupture are different in thrombolytic therapy and conventional therapy. Intravenous thrombolytic therapy is effective for the reduction of mortality from pump failure in elderly patients with acute myocardial infarction older than 75 years. However, it must be evaluated as one of the risk factors of cardiac rupture in elderly patients.
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PMID:[Usefulness and safety of intravenous thrombolytic therapy for elderly patients with acute myocardial infarction: relationship with cardiac rupture]. 1022 95

In acute myocardial infarction may increase the synthesis of cytokines, which can enlarge the myocardial lesion owing to their direct toxic action on myocytes or induction of inflammatory changes that lead to myocardiofibrosis. All this may quickening the appearance of congestive heart failure after myocardial infarction. The aim of the study was examination of tumor necrosis factor (TNF-alpha) and interleukin 6 (IL-6) plasma levels in patients with acute myocardial infarction and analysis of correlation between concentrations of these cytokines and myocardial lesions during infarction. The study was made in 94 patients admitted to the Department of Cardiology with acute myocardial infarction (AMI). Of these, 40 were women aged from 41 to 85 (mean 67 years) and 54 were men aged from 39 to 86 (mean 63 years). Anterior AMI was diagnosed in 40 patients, inferior AMI was diagnosed in 54 patients. 63 patients underwent the thrombolytic therapy, reperfusion appeared in 45 patients, 24 patients were excluded from the thrombolytic therapy. Control group consisted of 28 healthy persons aged from 35 to 76 (mean 61 years). Blood samples for determination of TNF-alpha and IL-6 plasma levels were taken just after admission prior to the treatment. Then patients were taken streptokinase or tissue-type plasminogen activator with typical doses. Blood samples for determination of cytokines were obtained in 3. and 7. day after treatment. TNF-alpha and IL-6 plasma levels were determined with radioimmunological assay. Creatine kinase activity were monitored in patients with AMI as well as ejection fraction was checked in echocardiography in 3. and 7. day after treatment. We showed increased plasma levels of TNF-alpha and IL-6 in patients with AMI with maximum in 3. day of infarction. Concentrations of cytokines were higher in patients with anterior AMI than in patients with inferior AMI. In anterior infarction concentrations of cytokines were significantly lower after thrombolytic therapy with reperfusion than after treatment without reperfusion. There is a correlation between infarct size and concentrations of TNF-alpha and IL-6.
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PMID:[Levels of tumor necrosis factor (TNF-alpha) and interleukin 6 (IL-6) in serum of patients with acute myocardial infarction]. 1069 95

Cardiac sarcolemmal (SL) cis-unsaturated fatty acid sensitive phospholipase D (cis-UFA PLD) is modulated by SL Ca(2+)-independent phospholipase A(2) (iPLA(2)) activity via intramembrane release of cis-UFA. As PLD-derived phosphatidic acid influences intracellular Ca(2+) concentration and contractile performance of the cardiomyocyte, changes in iPLA(2) activity may contribute to abnormal function of the failing heart. We examined PLA(2) immunoprotein expression and activity in the SL and cytosol from noninfarcted left ventricular (LV) tissue of rats in an overt stage of congestive heart failure (CHF). Hemodynamic assessment of CHF animals showed an increase of the LV end-diastolic pressure with loss of contractile function. In normal hearts, immunoblot analysis revealed the presence of cytosolic PLA(2) (cPLA(2)) and secretory PLA(2) (sPLA(2)) in the cytosol, with cPLA(2) and iPLA(2) in the SL. Intracellular PLA(2) activity was predominantly Ca(2+) independent, with minimal sPLA(2) activity. CHF increased cPLA(2) immunoprotein and PLA(2) activity in the cytosol and decreased SL iPLA(2) and cPLA(2) immunoprotein and SL PLA(2) activity. sPLA(2) activity and abundance decreased in the cytosol and increased in SL in CHF. The results show that intrinsic to the pathophysiology of post-myocardial infarction CHF are abnormalities of SL PLA(2) isoenzymes, suggesting that PLA(2)-mediated bioprocesses are altered in CHF.
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PMID:Redistribution and abnormal activity of phospholipase A(2) isoenzymes in postinfarct congestive heart failure. 1117 77

Patients with persistent ST segment elevation after fibrinolysis are at high risk for death and congestive heart failure, even if normal epicardial flow has been restored. In the TIMI 14 trial, combination therapy with abciximab plus reduced-dose alteplase enhanced the speed and efficacy of epicardial reperfusion. We also found that combination therapy provided an additional benefit in terms of myocardial reperfusion, as evidenced by greater ST resolution on serial 12-lead electrocardiograms. Specifically, the proportion of patients with complete (> or =70%) ST resolution was higher among patients receiving combination therapy than in those treated with alteplase alone (59% vs 37%; p < 0.0001). Even among patients with normal (TIMI grade 3) epicardial blood flow, combination therapy was associated with a significantly greater likelihood of complete ST resolution than was fibrinolysis alone (69% vs 44%; p = 0.0002). In conclusion, combination reperfusion therapy improved myocardial (microvascular) reperfusion, independent of epicardial flow, suggesting an additional mechanism by which abciximab may improve outcomes in patients with acute MI.
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PMID:ST-Segment resolution as a marker of epicardial and myocardial reperfusion after thrombolysis: insights from the TIMI 14 and in TIME-II trials. 1126 39

Regulation of vascular tone by the endothelium is abnormal in patients with heart failure and contributes to the characteristic peripheral vasoconstriction and increased afterload. This endothelial dysfunction is mediated through several endothelium-derived factors, including nitric oxide; there is an important interplay between the endothelium and the renin angiotensin system. The benefits of ACE inhibition in heart failure relate, in part, to a reduction in ischemic events which may be mediated by improvements in endothelial function and the endothelium derived fibrinolytic parameters: tissue plasminogen activator (t-PA) and its inhibitor, plasminogen activator inhibitor type 1 (PAI-1). In addition to potential improvements in the regulation of vasomotion, ACE inhibitor therapy may increase bradykinin induced t-PA release and/or reduce angiotensin II mediated PAI-1 release. Recent evidence suggests that both angiotensin II type 1 receptor (AT(1)) antagonism and ACE inhibition improve basal fibrinolytic parameters in patients with heart failure which may facilitate the acute endogenous fibrinolytic response. 1999 by CHF, Inc.
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PMID:The renin angiotensin system and endothelial dysfunction in chronic heart failure: role of endogenous fibrinolysis. 1218 94


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