Disease relevance of Angioplasty, Transluminal, Percutaneous Coronary

• As compared with t-PA therapy for acute myocardial infarction, immediate PTCA reduced the combined occurrence of nonfatal reinfarction or death, was associated with a lower rate of intracranial hemorrhage, and resulted in similar left ventricular systolic function [1].
• We performed percutaneous transluminal coronary angioplasty as an emergency procedure in 60 patients with unstable angina pectoris that was refractory to treatment with maximally tolerated doses of beta-blockers, calcium antagonists, and intravenous nitroglycerin [2].
• Percent diameter stenosis after PTCA was 39 +/- 18% in the heparin group and 40 +/- 20% in the heparin+antithrombin III group (NS) [3].
• Silent myocardial ischemia in Kawasaki disease: evaluation of percutaneous transluminal coronary angioplasty by dobutamine stress testing [4].
• Pretreatment with adenosine is remarkably effective (even more effective than ischemic preconditioning) and could be used prophylactically to attenuate ischemia in selected patients undergoing PTCA of the left anterior descending coronary artery [5].

Psychiatry related information on Angioplasty, Transluminal, Percutaneous Coronary

• RESULTS: Women treated with pravastatin had a risk reduction of 43% for the primary end point (p = 0.035), 46% for combined coronary events (p = 0.001), 48% for PTCA (p = 0.025), 40% for CABG (p = 0.14) and 56% for stroke (p = 0.07) [6].
• In conclusion, this study shows that PFA-100 may be helpful in the decision making for additional antiaggregant therapy before PTCA or in monitoring long-term GPIIb/IIIa receptor antagonist treatment [7].

High impact information on Angioplasty, Transluminal, Percutaneous Coronary

• Intracranial bleeding occurred more frequently among patients who received t-PA than among those who underwent PTCA (2.0 vs. 0 percent, P = 0.05) [1].
• Eight hours before PTCA, the oral dipyridamole was replaced with intravenous dipyridamole at a dosage of 10 mg per hour for 24 hours, and oral aspirin was continued [8].
• CONTEXT: The direct thrombin inhibitor bivalirudin has been associated with better efficacy and less bleeding than heparin during coronary balloon angioplasty but has not been widely tested during contemporary percutaneous coronary intervention (PCI) [9].
• CONCLUSIONS: Creatine kinase elevation following elective PTCA is associated with increased late cardiac mortality [10].
• Furthermore, markers of leukocyte activation - in particular, increased expression of the beta2-integrin Mac-1 (alphaMbeta2, or CD11b/CD18), which is responsible for firm leukocyte adhesion to platelets and fibrinogen on denuded vessels - predict restenosis after PTCA [11].

Chemical compound and disease context of Angioplasty, Transluminal, Percutaneous Coronary

• BACKGROUND--Heparin needs the plasma protein antithrombin III to function as an inhibitor of thrombin, and local antithrombin III deficiency might therefore limit the antithrombotic effectiveness of heparin during percutaneous transluminal coronary angioplasty [3].
• Those who had angiography earlier and did not have restenosis (> or = 50% loss of gain at PTCA plus > or = 50% luminal diameter stenosis) also had angiography at 6 months [12].
• Changing features of anginal pain after PTCA suggest a stenosis on a different artery rather than restenosis [13].
• The results of this study indicate that there is no permanent dysfunction of global or regional myocardial mechanics, myocardial blood flow, or lactate metabolism after PTCA with four to six coronary occlusions of 40 to 60 sec [14].
• The respective numbers in the fosinopril and the control groups were for death, 0 and 0; myocardial infarction, 0 and 0; coronary artery bypass graft surgery, 1 and 3; repeat PTCA, 35 and 35; recurrent signs of ischemia necessitating early repeat coronary angiography and managed medically, 6 and 7; and none of the above, 111 and 106 [15].

Biological context of Angioplasty, Transluminal, Percutaneous Coronary

• In 7 control patients, PTCA caused a rise in platelet surface expression of P-selectin and glycoprotein IIb/IIIa, which was maximal 5 minutes after PTCA, indicating increased platelet activation despite treatment with aspirin, glyceryl trinitrate, and heparin [16].
• Progressive vasoconstriction (defined as a loss of diameter that was reversed by intracoronary nitroglycerin) was observed after PTCA in the dilated and distal segments (10 of 10 patients) but not in the control segment [17].
• The response of left ventricular function, coronary blood flow, and myocardial lactate metabolism during percutaneous transluminal coronary angioplasty (PTCA) was studied in a series of patients undergoing the procedure [14].
• Maximal vasodilation was induced immediately before and 15 minutes after PTCA by intracoronary administration of papaverine, and digital angiographic studies were performed [18].
• A collateral flow index (CFI; no unit) expressing collateral flow relative to normal anterograde flow was determined using coronary wedge pressure or Doppler measurements through sensor-tipped PTCA guide wires [19].

Anatomical context of Angioplasty, Transluminal, Percutaneous Coronary

• Thallium-201 imaging may be used to help determine the distribution and amount of myocardium in jeopardy and the success of revascularization after percutaneous transluminal coronary angioplasty [20].
• Thromboxane A2 stimulation of smooth muscle cells contributes to the development of vascular lesions after percutaneous transluminal coronary angioplasty [21].
• Neutrophil surface expression of CD11b (alpha subunit of Mac-1) significantly increased at 24 h (P < 0.01) to 48 h (P < 0.001) after PTCA in the coronary sinus blood in patients with restenosis but the change showed less significant in patients without restenosis [22].
• In both P/P and p/p melanoblasts and melanocytes cultured with 2.0 mM L-Tyr for 14 days, slight increases in contents of eumelanin marker, pyrrole-2,3,5-tricarboxylic acid (PTCA) and pheomelanin marker, aminohydroxyphenylalanine (AHP) were observed [23].
• CONCLUSIONS: Our chimeric DNA-RNA hammerhead ribozyme targeting PDGF A-chain mRNA inhibited neointima formation in rat carotid artery after balloon injury with specific inhibition of expression of PDGF A-chain mRNA, suggesting that this ribozyme may be useful for therapy of restenosis of coronary artery after PTCA [24].

Associations of Angioplasty, Transluminal, Percutaneous Coronary with chemical compounds

• Aspirin and dipyridamole in the prevention of restenosis after percutaneous transluminal coronary angioplasty [8].
• Quantitative coronary measurements were made at 3, 15, and 30 min after PTCA, and then after intracoronary (IC) nitroglycerin, in coronary segments distal to the dilated lesion (distal) and in a nonmanipulated vessel (control) [25].
• Coronary stenting decreases restenosis in lesions with early loss in luminal diameter 24 hours after successful PTCA [26].
• METHODS AND RESULTS: GP IIb/IIIa receptor blockade, impedance (5 microg/mL collagen), and turbidimetric aggregation (5 and 20 micromol/L ADP) measurements were obtained on 14 PTCA patients who received the standard bolus plus a 12-hour infusion of abciximab [27].
• Myocardial perfusion imaging with thallium-201 to evaluate patients before and after percutaneous transluminal coronary angioplasty [20].

Gene context of Angioplasty, Transluminal, Percutaneous Coronary

• CONCLUSIONS: The increase in TxA(2) during PTCA is primarily COX-1 dependent, and aspirin alone is effective in suppressing its formation [28].
• Percent change in the expression of CD18 at 48 h after PTCA (from baseline) and that of CD11b were correlated (r = 0.73, p = 0.0008) in patients with restenosis [29].
• Optimal suppression of thromboxane A(2) formation by aspirin during percutaneous transluminal coronary angioplasty: no additional effect of a selective cyclooxygenase-2 inhibitor [28].
• On the other hand, plasma MCP-1 levels did not change significantly during a 24-h observation period after PTCA [30].
• Plasma MMP-2/TIMP-2 ratio and MMP-2 activity in the coronary sinus showed significant increases 4 and 24 h after PTCA [31].

Analytical, diagnostic and therapeutic context of Angioplasty, Transluminal, Percutaneous Coronary

• INTERVENTIONS: All 43 patients received acute reperfusion therapy: 21 patients received intravenous tissue plasminogen activator, and 22 patients underwent primary percutaneous transluminal coronary angioplasty [32].
• BACKGROUND: The Emory Angioplasty Versus Surgery Trial (EAST) is a randomized trial that compares, by intention to treat, the clinical outcome and costs of percutaneous transluminal coronary angioplasty (PTCA) and coronary surgery for multivessel coronary artery disease [33].
• CONCLUSIONS: In patients with successful PTCA but reduced luminal diameter demonstrated by repeat angiography at 24 hours, the Gianturco-Roubin stent appears to reduce angiographic restenosis at follow-up [26].
• The criteria for restenosis were that the quantitative coronary angiography at 6 months show a > 30% increase in narrowing at the stenosis site or loss of at least half of the gain achieved at the time of PTCA and final restenosis with < 50% luminal diameter remaining [34].
• We studied the effectiveness of percutaneous transluminal coronary angioplasty (PTCA) in patients with silent myocardial ischemia detected by dobutamine stress 99mTc myocardial scintigraphy (TMS), body surface mapping (BMS), and signal-averaged ECG late potentials (ELP) [4].

References