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)

Myocardial infarction results from a platelet-rich occlusive coronary thrombus. Platelet membrane glycoprotein IIb/IIIa plays an important role in platelet adhesion and aggregation. Two polymorphisms of the gene encoding the IIIa subunit. PLA1 and PLA2, have been identified. We investigated the frequency of these polymorphisms in 114 consecutive patients with a history of angina-like chest pain admitted for coronary arteriography. Forty-three of these patients had previously suffered a myocardial infarction. The PLA2 polymorphism was found in 21% of the patients with previous myocardial infarction and in 27% of the patients with angina-like chest pain but no previous myocardial infarction (p = 0.634). There was also no significant association with the extent of coronary disease. There is no evidence, therefore, from this study of an association between the PLA polymorphisms and the occurrence of myocardial infarction.
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PMID:Coronary thrombosis and the platelet glycoprotein IIIA gene PLA2 polymorphism. 971 40

Hepatocyte growth factor (HGF), a cytokine involved in tissue regeneration, angiogenesis and lateral vessel growth, is secreted as a biological-inactive, single-chain precursor named pro-HGF. In case, of tissue injury pro-HGF is proteolytically cleaved at the extracellular locus by serine proteases. Results obtained from in vitro experiments showed that urokinase-type plasminogen activator (uPA) and tissue-type plasminogen activator (tPA) can cleave single-chain HGF. In this study we measured serum HGF levels in patients with acute myocardial infarction (MCI). Two groups of patients were compared. One group (n = 7) was treated with a conventional therapy and the other group (n = 7) was subjected to a thrombolytic therapy with recombinant tissue-type plasminogen activator (rtPA). Serum samples were collected at time of admission and subsequently 12-16 hours, 20-30 hours and 50-60 hours after onset of chest pain. At admission and before administration of rtPA, serum HGF levels peaked at 16.8 +/- 2.2 ng/ml in the lysed group and at 20.7 +/- 6.5 ng/ml in the non-lysed group. Levels then continuously declined, reaching lowest values 50-60 hours after onset of chest pain (3.2 +/- 1.3 ng/ml in the group treated with rtPA versus 4.4 +/- 0.9 ng/ml in the non-lysed group). No statistical significant difference could be detected between the two groups at any time. We suggest that serine proteases other than tPA are involved in HGF activation in vivo.
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PMID:Hepatocyte growth factor plasma levels after myocardial infarction are not affected by recombinant tissue-type plasminogen-activator therapy. 1070 4

In acute myocardial infarction (AMI), immediate beta-blocker therapy reduces the incidence of reinfarction and recurrent chest pain in patients receiving tissue plasminogen activator (t-PA). Data from the Thrombolysis in Myocardial Infarction (TIMI)-2 trial also raises the possibility that such therapy may reduce the rate of intracranial hemorrhage (ICH). We reviewed data obtained from 60,329 patients treated with t-PA who were enrolled in the National Registry of Myocardial Infarction 2. Of the 60,329 in the study cohort, 23,749 patients (39.4%) were treated with immediate beta-blocker therapy and 542 patients (0.9%) developed an ICH. In a multivariate model that included all covariates known to be associated with the development of ICH, immediate beta-blocker therapy was associated with a 31% reduction in the ICH rate (odds ratio 0.69, 95% confidence intervals 0.57 to 0.84). Thus, in the present study, the use of immediate beta-blocker therapy in patients with AMI treated with t-PA was associated with a significant reduction in ICH. This finding supports the observations made in the TIMI 2 trial and serves to reinforce the recommendations made by the American College of Cardiology/American Heart Association task force that immediate beta-blocker therapy should be administered to all patients with AMI who do not have contraindications to this therapy.
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PMID:Intracranial hemorrhage rates and effect of immediate beta-blocker use in patients with acute myocardial infarction treated with tissue plasminogen activator. Participants in the National Registry of Myocardial Infarction-2. 1107 95

An 82 year old man was admitted to hospital with unstable angina pectoris. There was a long history of minor symptoms suggesting reflux disease, with a small diaphragmatic hernia. One day after admission the patient complained of severe chest pain. An acute inferior-posterior myocardial infarction was diagnosed on ECG, and thrombolytic treatment with alteplase (rt-PA) was initiated. Within a few hours total dysphagia occurred, caused by haemorrhagic oesophagitis. The haematoma resolved spontaneously within about 10 days. The patient was discharged three weeks later after full resolution of the dysphagia.
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PMID:Complete dysphagia after thrombolytic treatment for myocardial infarction. 1108 74

The goal of this study was to examine the relationship between contrast agent type (ionic vs. nonionic) and angiographic, electrocardiographic, and clinical outcomes after thrombolytic administration. Ionic or nonionic contrast agents were selected in a nonrandomized fashion for 90-min angiography and percutaneous coronary intervention (PCI) following thrombolytic administration in the TIMI 14 trial [tissue plasminogen activator (tPA) or reteplase (rPA) vs. low-dose lytic + abciximab]. There was no relationship between contrast agent type and overall patency, rate of TIMI grade 3 flow, or corrected TIMI frame counts (CTFCs) in open culprit arteries and in post-PCI patency rates or post-PCI CTFCs. In patients treated with ionic contrast, ejection fractions at 90 min were slightly but significantly lower (56.2 +/- 16.5, n = 122, vs. 59.8 +/- 14.4, n = 322; P = 0.02), chest pain duration was longer (2.8 +/- 4.1 hr, n = 255, vs. 1.7 +/- 3.6, n = 550; P = 0.0003), and complete ST segment resolution was less frequent (41.5% vs. 50.8%; P = 0.04). While there was no difference in epicardial blood flow, ionic contrast agent use was associated with poorer ST segment resolution, longer chest pain duration, and poorer ejection fractions, perhaps as a result of microvascular dysfunction.
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PMID:Impact of contrast agent type (ionic versus nonionic) used for coronary angiography on angiographic, electrocardiographic, and clinical outcomes following thrombolytic administration in acute myocardial infarction. 1132 10

Direct PTCA is a treatment of choice in patients with acute myocardial infarction with ST segment elevations (STEMI). Fibrinolysis remains important modality of treatment in these patients. Currently, there are more then 100 tissue plasminogen activator mutants available with different fibrin specificity. In a clinical practice, tissue-type plasminogen activator (t-PA), recombinant tissue-type plasminogen activator (rt-PA), tenecteplase (TNK-tPA) and lanoteplase (n-PA) are most important examples. Fibrinolytic treatment in STEMI patients should be used in patients presenting in first 4 hours after beginning of chest pain, when it is sure, that direct PTCA cannot be started within next 90 minutes. Concomittant therapy of acute STEMI patients consists of anticoagulans, antiplatelet and antiagregatory treatment.
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PMID:[Fibrinolytic therapy in acute myocardial infarct]. 1463 19

To determine whether tenecteplase (TNK-t-PA), a bioengineered variant of tissue-type plasminogen activator (t-PA) designed to accelerate thrombolysis, exhibits favorable properties compared with those of alteplase, 266 men were studied </=6 hours after the onset of symptoms and signs of acute myocardial infarction. The primary end point was the rapidity of recanalization as judged from analysis of serial changes in the concentrations in blood of isoforms of creatine kinase-MM in serially obtained blood samples. Additional end points included enzymatically estimated infarct size and mortality. Patients were treated quite promptly after the onset of symptoms. The interval from the onset of chest pain to recanalization seen with TNK-t-PA was 208 +/- 10 (SE) minutes compared with 237 +/- 9 minutes seen with alteplase (p = 0.04). Thirty-day mortality was low with the use of the 2 agents (2%). TNK-t-PA appears to induce recanalization more rapidly than alteplase, and thrombolysis initiated early after the onset of symptoms is associated with remarkably low mortality.
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PMID:Comparison of rapidity of coronary recanalization in men with tenecteplase versus alteplase in acute myocardial infarction. 1519 14

We report a case of spontaneous coronary artery dissection (SCAD) causing acute myocardial infarction, which was complicated by vasospastic angina (VA). The patient received intravenous administration of t-PA. Emergency coronary angiography demonstrated narrowing of the left anterior descending artery (LAD) due to SCAD. During hospitalization, the patient suffered chest pain, and ECG showed ST elevation in the inferior leads. Sublingual administration of nitroglycerin provided temporary remission. Coronary stent implantation was performed electively using intravascular ultrasound imaging. This is the first reported case of SCAD associated with vasospasm in a non-culprit coronary artery during the hospitalization.
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PMID:Intravascular ultrasound-guided coronary artery stenting for spontaneous coronary artery dissection in a case of acute myocardial infarction associated with vasospasm in a non-culprit coronary artery during the hospitalization. 1684 65

Cell-free DNA that originates from cell death, circulates in peripheral blood. There are indications that the infarcted myocardium contributes to an increase of cell-free DNA levels. Our aims were to quantify levels of cell-free DNA in patients with acute myocardial infarction (AMI) and examine their correlation with myocardial markers and with postinfarction (PI) clinical course. Thirteen patients (age 57 +/- 16 year) admitted with AMI and who underwent thrombolysis with reteplase within 6 h from the onset of chest pain were studied. PB samples were collected on admission and for 5 consecutive days. Creatine kinase (CK) and troponin I (TnI) were measured on admission and every 8 h for 3 consecutive days. Clinical events were recorded throughout the hospitalization period. Cell-free DNA levels were also measured in 30 healthy controls. Log-transformed mean (+/-SE) of maximum free DNA values in patients higher than controls (6873 +/- 357 g.e./mL verses 4112 +/- 234 g.e./mL, P < 0.0001). Log-transformed maximum values of CK and TnI were correlated with log-transformed free DNA values of first (r = 0.62, P = 0.02/r = 0.68, P = 0.01) and second (r = 0.57, P = 0.04/r = 0.72, P = 0.0053) PI day. Nine patients (group A) had an uncomplicated PI clinical course and four patients (group B) had recorded events (three with angina and one death). Free DNA levels on the second PI day were higher in group B than group A (1298.0 +/- 796.0 g.e./mL verses 244.6 +/- 257.7 g.e./mL, P = 0.003). In conclusion, free DNA levels are significantly higher in patients with AMI than in controls and may play a role in the prognosis of these patients.
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PMID:Cell-free DNA levels as a prognostic marker in acute myocardial infarction. 1710 21

We investigated the efficacy and safety of intrapleural instillation of recombinant tissue plasminogen activator (Alteplase) in 120 patients with complicated pleural effusion (CPE) or empyema. These 120 patients had failed simple chest tube placement and conventional medical treatment. The patients included 52 with empyema, 41 with CPE, 10 with hemothorax, and 17 with complicated malignant pleural effusions. A total of 345 doses of Alteplase were instilled intrapleurally in these patients, with doses ranging from 10 to 100 mg daily. Most patients required 3 to 4 doses of alteplase. After Alteplase therapy, complete resolution of CPE/empyema occurred in 102 patients (85%), partial resolution in 10 patients (8%), and failure to respond in 8 patients (7%). All patients who failed to respond to Alteplase treatment had either chronic empyema or empyema associated with lung abscesses. Adverse effects of Alteplase therapy were chest pain in 7 patients (6%) and bleeding at the chest tube site in 2 patients (2%).
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PMID:Efficacy and safety of intrapleural instillation of alteplase in the management of complicated pleural effusion or empyema. 1766 8


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