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:C0002962 (angina)
21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heparin has been used intensively in the treatment of acute myocardial infarction and preinfarction angina (PA) at full doses as a single drug by us. However, heparin may be used at smaller doses for similar purposes. These doses are not exactly anticoagulant, even though they reduce blood hypercoagulability, and act mainly in an antithrombotic capacity. We studied 529 patients with acute myocardial infarction, of whom 262 were treated with subcutaneous heparin at low doses (5000 IU every 12 h) and 267 received conventional therapy without antithrombotic drugs. Heparin used was Heparina (Abbott) and Liquemine (Roche), in vials with the equivalence 1 cm3 = 50 mg = 5000 IU. Blood rheologic factors (thromboelastography, platelet adhesiveness, total blood viscosity, and number of platelets) were determined in all patients, those treated with heparin at low doses and also the control group, before and after the 30-day treatment period. Diagnosis was based on clinical symptoms, laboratory studies, and electrocardiogram examination. In both the 262 patients treated with heparin at low doses and in the control group of 267 patients, baseline values of rheological factors were high. After 30 days (i.e., after study completion) these high values which are statistically significant compared with normal values, with p less than 0.0001 for both groups, remained constant in the control group who did not receive heparin. On the contrary, in the group treated with heparin at low doses, all these factors changed. Heparin provides protection against thrombosis by increasing the negative charge of the vessel wall and by other reactions at the endothelial surface. Heparin requires a plasmatic component called antithrombine III.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of acute myocardial infarction with subcutaneous heparin at low doses. 282 17

Angina presents itself to us as a continuous spectrum of ischemic syndromes. The disease is multifactorial, and within the same patient different pathophysiological mechanisms may occur at different times and in succession. Several factors may be causative at a particular moment of the disease process and the very next moment a different mechanism may prevail or spontaneous improvement may occur. Among these are stable atheroma with episodic increased vasomotor tone, fissured plaques with intraluminal and/or intraintimal thrombus, thrombocyte aggregation in greater than 70% intraluminal narrowing from ulcerated plaques, as well as frank spasm of vessels without major atherosclerosis. Consequently, there will never be one therapy for every case of (un)stable angina nor will there ever be a best therapy for all. Rather, a stepped approach appears the most likely to be successful. This begins with bed rest and requires vasodilator therapy with nitrates and/or Ca2+ antagonists and beta blockade. If this triple therapy does not "cool" the symptoms within 6-12 hours, semiurgent arteriography is indicated. Depending on the pathophysiology found, thrombolytic therapy with streptokinase or tissue plasminogen activator, percutaneous transluminal coronary angioplasty (PTCA), or coronary artery bypass grafting (CABG) must be carried out early. Heparin in the short term and aspirin in the long term protect best against late complications. The moment is now here when infarction or death after an attack of angina pectoris should be rare.
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PMID:Calcium antagonists for angina pectoris. 289 19

We tested the usefulness of aspirin (325 mg twice daily), heparin (1000 units per hour by intravenous infusion), and a combination of the two in the early management of acute unstable angina pectoris in a double-blind, randomized, placebo-controlled trial involving 479 patients. The patients entered the study as soon as possible after hospital admission (at a mean [+/- SD] of 7.9 +/- 8.0 hours after the last episode of pain), and the study was ended after 6 +/- 3 days, when definitive therapy had been selected. Major end points--refractory angina, myocardial infarction, and death--occurred in 23, 12, and 1.7 percent of the 118 patients receiving placebo, respectively. Heparin was associated with a decrease in the occurrence of refractory angina (P = 0.002). The incidence of myocardial infarction was significantly reduced in the groups receiving aspirin (3 percent; P = 0.01), heparin (0.8 percent; P less than 0.001), and aspirin plus heparin (1.6 percent, P = 0.003), and no deaths occurred in these groups. There were too few deaths overall to permit evaluation of the effect of treatment on this end point. The combination of aspirin and heparin had no greater protective effect than heparin alone but was associated with slightly more serious bleeding (3.3 vs. 1.7 percent). We conclude that in the acute phase of unstable angina, either aspirin or heparin treatment is associated with a reduced incidence of myocardial infarction, and there is a trend favoring heparin over aspirin. Heparin treatment is also associated with a reduced incidence of refractory angina.
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PMID:Aspirin, heparin, or both to treat acute unstable angina. 263 52

Pathologic and experimental evidence indicates that platelet activation and fibrin formation contribute to the pathogenesis of angina pectoris, coronary vasospasm and myocardial infarction. Detection of localized intravascular platelet activation and fibrin formation in vivo by selective blood sampling requires catheters that do not induce coagulation ex vivo. We studied the effect of heparin bonding of catheter surfaces on activation of the coagulation system by cardiovascular catheters. Woven Dacron, polyvinylchloride, and polyurethane catheters were tested and compared with identical catheters with heparin-bonded surfaces in 47 patients undergoing percutaneous cardiac catheterization. Platelet activation was measured by radioimmunoassay of plasma platelet factor 4 (PF4), beta-thromboglobulin (BTG), and thromboxane B2 (TXB2) in blood samples withdrawn through catheters, and fibrin formation was assessed by determination of fibrinopeptide A (FPA) levels. In blood samples collected through conventional catheters, FPA, PF4, BTG, and TXB2 levels were markedly elevated; blood sampling through heparin-bonded catheters had no significant effect on FPA, PF4, BTG, or TXB2 levels. Scanning electron microscopy disclosed extensive platelet aggregates and fibrin strands adherent to the surface of conventional catheters but not to heparin-bonded catheter surfaces. This study demonstrates that (1) collection of blood samples through cardiovascular catheters causes artifactual elevation of FPA, PF4, BTG, and TXB2 levels, and (2) heparin-bonded catheter surfaces effectively prevent catheter-induced platelet alpha-granule release and fibrin formation on catheter surfaces. Heparin-bonded catheters will facilitate investigation of the role of intravascular coagulation in coronary artery disease by eliminating catheter-induced fibrin formation and platelet activation.
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PMID:Effect of heparin bonding on catheter-induced fibrin formation and platelet activation. 623 7

Early restenosis in over 30% of cases limits the benefits of percutaneous transluminal coronary angioplasty (PTCA). The mechanisms that underlie restenosis are uncertain, although experimental evidence suggests that the renin-angiotensin system is involved in the vascular response to angioplasty. An insertion(I)/deletion(D) polymorphism in the angiotensin-converting enzyme (ACE) gene, which influences plasma ACE level, has been associated with an increased risk of myocardial infarction in those with the DD genotype. To investigate whether this polymorphism influences the risk of restenosis after PTCA, 233 patients who underwent single-vessel angioplasty in the Subcutaneous Heparin and Angioplasty Restenosis Prevention (SHARP) study were genotyped for the I/D polymorphism and pre-PTCA, post-PTCA, and 4-month clinical and quantitative angiographic data were compared in the three genotype groups. The groups, (II 53, ID 117, and DD 63) were well matched for baseline clinical and both pre- and post-PTCA angiographic features. At 4-month follow-up there was no significant difference between the genotype groups with respect to any of the quantitative angiographic criteria of restenosis: minimal luminal diameter at the site of the angioplasty (DD 1.35 [SE 0.10] mm, ID/II 1.43 [0.05] mm, difference -0.08 [95% CI -0.30 to 0.14]), numbers of subjects with more than 50% diameter stenosis (DD 49%, ID/II 46%, relative risk 1.06 [0.79 to 1.43]), or the number of subjects with more than 50% loss of the acute diameter gain after PTCA (DD 54%, ID/II 43%, 1.26 [0.94 to 1.67]). Likewise, there was no difference in the number of subjects with angina or a positive exercise stress test. We conclude that, in patients undergoing elective PTCA, the I/D polymorphism in the ACE gene does not influence the extent of restenosis, and typing for the polymorphism will not be a useful predictor of risk before the procedure.
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PMID:Insertion/deletion polymorphism in the angiotensin-converting enzyme gene and risk of restenosis after coronary angioplasty. 772 97

A discrete fall in the ACT (activated coagulation time) has been observed in patients with known activation of the coagulation cascade. Injury to the coronary artery resulting in thrombin activation, whether spontaneous as in the case of acute myocardial infarction or planned as with percutaneous transluminal coronary angioplasty (PTCA), may therefore be reflected in a change in ACT values. We reviewed the records of patients undergoing PTCA at St. Luke's Episcopal Hospital/Texas Heart Institute from January 1990 through December 1992 for information regarding ACT values and clinical events. A total of 469 patients, whose record contained adequate information for study inclusion, were divided into four separate groups: acute myocardial infarction (group I, n = 62), unstable angina with heparin therapy that was withdrawn at least 4 hr prior to PTCA (group II, n = 102), unstable angina with heparin therapy continued until the time of PTCA (group III, n = 154), and stable angina undergoing elective PTCA (group IV, n = 151). Heparin was discontinued 12-15 hr after the procedure in all but group I where anticoagulation was often maintained up to 72 hr. ACT values were measured prior to the PTCA procedure (baseline), after the initial heparin bolus of 10,000 U (postheparin) and approximately 12-18 hr after the procedure (heparin withdrawal).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Activated clotting times in acute coronary syndromes and percutaneous transluminal coronary angioplasty. 772 56

The current study was designed to investigate the number and affinity of platelet thromboxane A2/prostaglandin H2 (TxA2/PGH2) receptors in patients with unstable angina and, if any, the role played by the increased thrombin formation that is a common finding in these patients. Measurements taken during active unstable angina but not those taken during inactive angina showed an increase number (p < 0.001), without changes in affinity, of platelet TxA2/PGH2 receptors, evaluated as the binding capacity of iodine 125-PTA-OH, a stable TxA2 analogue. Moreover patients with active angina had higher plasma concentrations of fibrinopeptide A (FPA) (p < 0.0001), which were significantly related to the number of platelet TxA2/PGH2 receptors (r = 0.76; p < 0.01). Heparin infusion but not aspirin treatment promptly normalized the number of TxA2/PGH2 receptors and significantly reduced plasma FPA concentrations. In an in-vitro study thrombin in a concentration similar to that found in vivo significantly increased the number of platelet TxA2/PGH2 receptors (p < 0.01), whereas heparin did not affect TxA2/PGH2 receptors. These results have important therapeutic implications and indicate the preferential use of heparin rather than aspirin during the acute phase of unstable angina.
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PMID:Increased number of thromboxane A2-prostaglandin H2 platelet receptors in active unstable angina and causative role of enhanced thrombin formation. 773 75

The primary drugs utilized in the treatment of angina pectoris include organic nitrates, beta-adrenoceptor antagonists, Ca2+ antagonists, and the antithrombotic agents aspirin and heparin. Not all of these drugs are useful in every form of angina, and treatment is symptomatic rather than curative. In stable effort angina, beta-blockers, Ca2+ antagonists, and organic nitrates provide relief from angina pain and improve exercise tolerance primarily through their ability to decrease oxygen demand. The antiplatelet action of aspirin may decrease the incidence of myocardial infarction in these patients. Ca2+ channel blockers and organic nitrates are the drugs of choice for variant angina. These vasodilators restore blood flow by relieving the coronary vasospasm that triggers the ischemic episode. In unstable angina, aspirin and heparin reduce the risk of myocardial infarction, and aspirin increases survival. Heparin and nitrates alleviate angina pain, and under some circumstances beta-blockers and Ca2+ antagonists have a role in the relief of pain.
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PMID:Pharmacologic therapy of angina pectoris. 778 75

Although a functional role of coronary collaterals has been continuously debated, we observed the following facts in our studies during intracoronary thrombolytic therapy: (a) Myocardial ischemia is important for the development of collateral circulation, (b) collaterals can perfuse the infarcted myocardium, and (c) the presence of collaterals prevents the left ventricular aneurysm formation in acute myocardial infarction, even when the amount of the salvaged tissue is small. Thus, coronary collaterals are not merely markers of severe ischemia but help to preserve the functional integrity of the myocardium in the presence of coronary obstruction. We then attempted to promote collateralization to treat patients with angina pectoris. Patients with chronic stable effort angina were treated with heparin followed by treadmill exercise twice a day for 10 days. Treadmill capacity was found to improve in association with an increase in coronary collateral circulation. Heparin treatment of ischemic patients was found to be a noninvasive alternative to percutaneous transluminal coronary angioplasty and coronary bypass surgery for patients who are not candidates for invasive procedures.
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PMID:Effect of coronary collateral circulation on myocardial ischemia and ventricular dysfunction. 794 75

Non-Q wave myocardial infarction is associated with a high recurrence rate of ischaemic events (angina and infarction). The artery responsible for the infarction is usually patent but stenosed and seems to be the cause of these complications. This prospective multicenter series of 66 patients treated by Heparin, Aspirin, Diltiazem and undergoing coronary angiography during the hospital period studied the artery responsible for the infarction and the value of coronary angiography in this setting. Several conclusions were drawn from the results: the precise diagnosis of the artery responsible for the infarct may be difficult (14%); the left circumflex artery or one of its branches is often implicated (47%); non-Q wave infarction is a various and heterogeneous group, including: infarctions located on small branch arteries, "warning" ischaemic episodes in the left anterior descending artery territory. definitive infarction of the left circumflex artery territory; nevertheless, this group is an intermediate state between Q wave infarction and unstable angina (low occlusion rate 26% and angiographic lesional appearances similar to those of unstable angina); early coronary angiography (48-72 h) seems to be useful to improve prevention of ischaemic recurrences by adequate revascularisation.
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PMID:[Role of coronary angiography in infarction without Q wave. Results of a prospective angiographic study]. 802 68


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