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
Query: EC:2.7.10.2 (
focal adhesion kinase
)
44,029
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The study comprises 375 patients who had received an endocardial pacemaker electrode primarily. A stylet electrode of the Medtronic type was used in 165 patients and of the Elema type in 79 patients. Elema's flexible electrode model 588
EMT
was used in 131 patients. The total number of electrode complications was surprisingly high. In 92 out of the 375 patients, 141 serious episodes of pacing failure occurred during the observation period of from 6 to 42 months. The complication rate increased with pacemaker function time. The stylet electrodes gave the highest complication rate. The choice of vein for introducing the electrode into the heart seems not to affect the complication rate significantly. Nor did the initial threshold value of stimulation influence the complication rate to any marked degree. The pacemaker manufacturers have devoted much effort to producing long-life impulse generators but there is also a great need for well-functioning long-life electrodes.
Scand J Thorac
Cardiovasc
Surg Suppl 1978
PMID:Complications with permanent endocardial electrode systems. A comparison between two types of electrodes. 36 24
In this case report of a patient presenting with an acute inferior wall myocardial infarction, the infarct conduit was a saphenous vein graft. Extraction atherectomy using the
TEC
successfully reestablished patency and reversed the patient's clinical symptoms. Extraction atherectomy is a feasible procedure during acute coronary events and deserves further investigation.
Cathet
Cardiovasc
Diagn 1992 Jun
PMID:Extraction atherectomy during myocardial infarction in a patient with prior coronary artery bypass surgery. 160 99
The presence of amidases cleaving the tripeptide VAL.LEU.
ARG
.pNA, and liberating from human plasma kininogen substance(s) able to contract uterine smooth muscle and to lower blood pressure (uterus contracting and hypotensive activity), has been demonstrated in vascular and muscle tissues from normally perfused and ischaemic areas of dog hearts. Studies were carried out on blood free preparations of coronary arteries and veins and normally perfused and ischaemic ventricle. All the tissues were found to contain both acid optimum (pH 6) and alkaline optimum (pH greater than 9) enzymes forming uterus contracting substance (UCS, bioassayed on isolated uterus of rats in oestrus), the highest levels of both activities being found in arterial tissues and the least in ventricle. Enzyme levels in ischaemic or normally perfused ventricle did not differ significantly. Gel filtration (Sephacryl, S-300) of coronary artery extracts gave one peak each of acid optimum enzyme with a molecular weight of 38,300 +/- 800 daltons and alkaline optimum enzyme with a molecular weight of 92,100 +/- 4000 daltons. Both acid and alkaline enzyme fractions cleaved the tripeptide substrate with pH optima identical to those for UCS formation. The acid optimum activity, both of UCS formation and tripeptide cleavage, was inhibited by pepstatin but not by aprotinin or soybean trypsin inhibitor (SBTI). The alkaline optimum activity was inhibited by aprotinin and SBTI but not pepstatin. Both acid and alkaline optimum enzymes released a hypotensive agent from a plasma protein substrate. The molecular weight and response to inhibitors of the acid optimum enzyme were similar to a cathepsin, and those of the alkaline optimum enzyme were similar to plasma kallikrein.
Cardiovasc
Res 1989 Feb
PMID:Enzymes in normally perfused and ischaemic dog hearts which release a substance with kinin like activity. 277 62
A report is presented of 1253
EMT
588 endocardial leads implanted in 1063 patients. The electrode surface area was large (47 mm2) in the 473 leads implanted during 1962-1973, and small (8-12 mm2) in the 780 leads implanted in 1974-1981. Replacement of 245 leads was necessary, in 187 cases due to lead failure and in 58 because of problems with normally functioning leads, such as infection. The highest lead failure rate occurred within the first 6 months after implantation, and was mostly caused by displacement and threshold increase. The dominating cause of late failure was lead lesion. The cumulative lead survival rates for the first and the second series were 88 and 94%, respectively after 1 year, 80 and 91% after 5 years, and 72 and 84% after 9 years. The polyethylene insulation proved to be the most vulnerable part of this lead. Insulation lesions could result in corrosion and/or fracture of the steel conductors. The chronic thresholds were largely stable.
Scand J Thorac
Cardiovasc
Surg 1988
PMID:A 20-year study of endocardial pacing lead EMT 588. Lead durability and nature of failure. 338 42
To explore endothelium-dependent relaxation and the L-arginine (L-ARG)-nitric oxide (NO) pathway during chronic hypoxia, we examined isolated rings from large conduit pulmonary arteries and aorta from rats exposed to either room air (N), 3-week hypoxia (H), or 3-week H followed by 72-h recovery to normoxia (room air). We examined the vasodilatory actions of acetylcholine (ACh), ionophore A23187, and endothelin-3 (ET-3) on extrapulmonary left and right branches of pulmonary arteries and thoracic aorta precontracted by phenylephrine (PE 10(-6) M). Endothelium-dependent relaxation of N rat pulmonary arteries and aorta to ACh and A23187 was abolished in the presence of L-NG nitroarginine methyl ester (L-NAME 10(-4) M) or methylene blue (MB 10(-5) M) but was suppressed only partially by NG-monomethyl-L-arginine (L-NMMA 5 x 10(-4) M). In pulmonary arteries but not in aorta, ET-3 induced endothelium-dependent relaxation that was suppressed by L-NAME, MB, and L-NMMA. Pulmonary arteries from H rats did not relax with ET-3. As compared with those of N rats, they exhibited less relaxation to ACh and A23187, (47 +/- 3 vs. 89 +/- 2 and 53 +/- 2 vs. 85 +/- 4%, p < 0.001, respectively) but exhibited similar relaxation to the nonendothelium-dependent vasodilator linsidomine. In contrast, endothelial-relaxation did not differ between N and H rat aorta.2+ pretreatment with L-
ARG
.
J
Cardiovasc
Pharmacol 1993 Dec
PMID:Loss of endothelium-dependent relaxation in proximal pulmonary arteries from rats exposed to chronic hypoxia: effects of in vivo and in vitro supplementation with L-arginine. 750 10
We studied the effects of adenosine (AD) and its analogues, 5'-N-ethylcarboxamidoadenosine (NECA) and 2-chloroadenosine (CAD) on membrane potential of porcine coronary artery with an without endothelium, conducting experiments with addition of indomethacin (10(-5) M) to rule out involvement of prostanoids. Average resting membrane potential (RMP) in porcine coronary artery was -51.1 +/- 0.2 and -50.3 +/- 0.2 mV, with and without endothelium, respectively. AD agonists at 10(-5) M caused a significant increase in RMP to -69.5 +/- 0.2 mV for AD, to -82.2 +/- 0.3 mV for CAD, and to -81.2 +/- 0.3 mV for NECA in porcine coronary arteries with intact endothelium. Moreover, AD agonists at 10(-5) M caused a smaller but significant increase in RMP to -54.3 +/- 0.2 mV for AD, -56.1 +/- 0.1 mV for CAD, and -61.1 +/- 0.2 mV for NECA without endothelium. The average RMP for human coronary artery with and without endothelium was -66.1 +/- 0.5 and -64.0 +/- 0.4, respectively. Qualitatively, similar effects of AD and its analogues were observed in two human coronary arteries. The AD receptor antagonist, 8-sulfophenyltheophylline (8-SPT, 10(-5) M) blocked hyperpolarization caused by AD and its analogues with and without endothelium both in porcine and human coronary arteries. The hyperpolarization caused by CAD and NECA in porcine coronary artery was attenuated in part by the nitric oxide (NO) synthase inhibitors N-monomethyl-L-arginine (L-NMMA, 10(-5) M) and N-nitro-L-arginine methylester (L-NAME, 10(-5) M), and the effect of L-NAME was reversed by L-arginine (L-
ARG
, 10(-4) M).(ABSTRACT TRUNCATED AT 250 WORDS)
J
Cardiovasc
Pharmacol 1995 Feb
PMID:Role of endothelium in hyperpolarization of coronary smooth muscle by adenosine and its analogues. 775 49
Coronary perforation is a rare, but potentially catastrophic, complication of percutaneous coronary intervention. A retrospective review of the Cardiology Quality Assurance Database was performed for all percutaneous coronary interventions (n = 8,932) at William Beaumont Hospital from October 1988 to December 1992. Coronary artery perforation was reported in 35 patients (0.4%), including after percutaneous transluminal coronary angioplasty (PTCA, 11/7,905, 0.14%), transluminal extraction coronary atherectomy (
TEC
, 6/420, 1.3%), directional coronary atherectomy (DCA, 1/249, 0.25%), and excimer laser coronary angioplasty (ELCA, 5/242, 2%); and none after high-speed mechanical rotational atherectomy with the Rotablator (MRA, 0/116, 0%). Perforations were classified by coronary angiography as free perforations (n = 10), contained perforations (n = 17), or other types of perforation (n = 8). Although perforation was apparent in 32 (91%) of 35 angiograms, delayed cardiac tamponade occurred in 3 patients (9%), despite the absence of angiographic evidence for perforation at the time of the procedure. Causes of perforation were the guidewire in 7 (20%), an interventional device in 26 (74%), and indeterminate in 2 (6%). Complex B2 or C lesions accounted for 83% of perforations. Final treatment included conservative therapy (reversal of anticoagulation and/or PTCA) in 22 (63%) and surgical intervention (with or without bypass surgery) in 13 (37%). Serious clinical complications included cardiac tamponade in 6 (17%), blood transfusion in 12 (34%), myocardial infarction in 9 (26%), and death in 3 (9%).
Cathet
Cardiovasc
Diagn 1994 Jul
PMID:Perforations after percutaneous coronary interventions: clinical, angiographic, and therapeutic observations. 1128 14
Our objectives were to determine procedural success, clinical complications, and follow-up restenosis rates after rotational burr and transluminal extraction atherectomy of coronary artery and saphenous vein graft ostial stenoses. Balloon angioplasty of ostial lesions has been associated with low rates of success and high rates of clinical complications and restenosis compared to nonostial lesions. Atherectomy, due to its ability to excise (extraction atherectomy) or pulverize (rotational atherectomy) atheroma and the internal elastic lamina, may result in improved procedural outcome. We retrospectively studied 101 patients with ostial stenoses treated by rotational burr and transluminal extraction atherectomy over a 3-yr period. Quantitative angiography and clinical follow-up were reviewed to determine success, complication, and restenosis rates. Rotational burr (n = 29) and transluminal extraction (n = 72) atherectomy were associated with high procedural success (93% and 90%, respectively) and a low incidence of complications (6.9% and 4.2%, respectively). Post-atherectomy angiographic success was low (52% and 69%, respectively) and required adjunctive balloon angioplasty in 85% of patients overall. This lower success rate likely reflects device undersizing as the overall post-atherectomy artery to device ratio was near unity (0.95). The rates of angiographic ostial restenosis remain high (39.1% and 65.9%, respectively, P < 0.05). The high rate of restenosis after transluminal extraction atherectomy was due to the higher rate of restenosis in saphenous vein grafts (80%) compared to
TEC
treated coronary arteries (59%). When only coronary artery lesions were compared, there was no significant difference between atherectomy device groups with respect to restenosis rates or late loss.(ABSTRACT TRUNCATED AT 250 WORDS)
Cathet
Cardiovasc
Diagn 1994 Apr
PMID:Success, complications, and restenosis following rotational and transluminal extraction atherectomy of ostial stenoses. 805 62
The migration of arterial vascular smooth muscle cells (VSMC) is thought to play a central role in atherogenesis and restenosis. The migration of several other cell types, including monocytes, T-lymphocytes and endothelial cells is also involved in the development of the mature atherosclerotic lesion. Several defined growth factors, cytokines and extracellular matrix components which are released at the sites of lesions have been implicated in the regulation of migration of VSMC and other lesion-associated cells. Platelet-derived growth factor BB-homodimer of PDGF (PDGF-BB) is strongly implicated in neo-intima formation in vivo and is the most potent known chemoattractant for VSMC in vitro. Dynamic interactions between cell surface adhesive receptors (integrins) for ECM components, organisation of the actin cytoskeleton and the turnover of focal adhesions are all key processes in cell locomotion and migration. The signal transduction pathways which mediate the chemotactic effects of PDGF-BB and other migration factors on VSMC are unknown, but several classes of cellular components are implicated including components associated with focal adhesions, small GTP-binding proteins of the rho family, and certain substrates of the PDGF beta-receptor. Tyrosine phosphorylation of the novel focal adhesion-associated protein tyrosine kinase, p125
focal adhesion kinase
(p125FAK), is regulated by integrins and by several factors which alter actin cytoskeletal organisation. Recent findings suggest that tyrosine phosphorylation of p125FAK and other focal adhesion-associated proteins may be implicated in the chemotactic response of VSMC to PDGF-BB. The migratory response to PDGF-BB may be dependent on both ligand isoform bio-availability and on receptor-isotype expression as well as on down-stream signalling events. Ultimately, cell migration in vivo will be determined by a complex array of diverse extracellular molecules organised in intercellular paracrine/autocrine networks as well as multiple interacting intracellular signal transduction pathways.
Cardiovasc
Res 1995 Oct
PMID:Signalling mechanisms in the regulation of vascular cell migration. 857 3
Percutaneous revascularization of thrombus containing saphenous vein grafts is associated with a high incidence of acute complications. This case report describes successful revascularization of an occluded vein graft employing angioscopically guided sequential urokinase infusion,
TEC
atherectomy and stent implantation.
Cathet
Cardiovasc
Diagn 1995 Dec
PMID:Efficacy of angioscopy in determining the effectiveness of intracoronary urokinase and TEC atherectomy thrombus removal from an occluded saphenous vein graft prior to stent implantation. 871 86
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