Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heparin is a parenteral antithrombotic agent with efficacy in the treatment and prevention of venous thromboembolic disease and in preinfarctional angina. Accumulating evidence also suggests that heparin is useful in the prevention of coronary artery reocclusion after thrombolytic therapy for acute myocardial infarction, and in the prevention of left ventricular mural thrombosis after anterior wall myocardial infarction. Heparin appears to offer only marginal benefit in reducing mortality when given in combination with thrombolytic therapy and aspirin for acute myocardial infarction. When used for prevention of venous thromboembolism in moderate risk patients, heparin should be given subcutaneously in a dose of 5000 U every 12 hours for 5 to 7 days or until the patient is ambulatory. In higher risk patients, such as those undergoing total hip replacement, heparin should be given subcutaneously every 12 hours in a dose to prolong the activated partial thromboplastin time (aPTT) by 4 to 5 seconds into the upper normal range. When used to treat active venous thromboembolism or the peri-infarctional state, heparin should be given by intravenous infusion with loading and maintenance doses to consistently prolong the aPTT to between 1.5- and 2.5-fold the control value (mean of laboratory's normal range). If constant intravenous infusion is not possible, the drug should be given subcutaneously every 12 hours to consistently prolong the aPTT between 1.5 and 2.5 times control. This regimen is also recommended in pregnant women with venous thromboembolic disease or mechanical heart valves.
 ...
PMID:Heparin therapy. Regimens and treatment considerations. 128 May 66

To clarify the pathogenesis of an impending infarction and to investigate the difference between the pathogenesis of an acute myocardial infarction and an impending infarction, we have performed percutaneous transluminal coronary angioscopy in 13 patients with an impending infarction and in 13 patients with an acute myocardial infarction. As a result, coronary thrombi were observed in 12 of the 13 patients with an impending infarction, and a similar frequency of thrombi was observed in the patients with an acute myocardial infarction. Further, grayish white thrombi were observed in 9 of 12 patients with an impending infarction, but no such thrombi were noted in those with an acute myocardial infarction. Reddish thrombi, however, were observed in all patients with acute myocardial infarction, whereas such thrombi were observed in only 3 of 12 patients with an impending infarction. Informatively, occlusive thrombi occurred more frequently in patients with an acute myocardial infarction than in those with an impending infarction. As a thrombus plays an important role in an impending infarction, we also evaluated the effect of anticoagulant and thrombolytic therapy for an impending infarction in 79 patients. The incidence of recurrent angina and a subsequent acute myocardial infarction were significantly higher in non-heparin-treated patients and in thrombolytic-treated patients than in heparin-treated patients. In conclusion, a thrombus plays an important role in the pathogenesis of an impending infarction and in an acute myocardial infarction, though the characteristics of the thrombus differ in each instance. This difference may account for the differing results of thrombolytic therapy. Heparin was found an effective treatment for myocardial ischemia in an impending infarction.
 ...
PMID:The pathogenesis of an impending infarction and its treatment--an angioscopic analysis. 145 40

The pathogenesis, clinical manifestations and diagnosis, and drug and nondrug therapies of unstable angina pectoris are reviewed. Coronary-artery plaque fissure and rupture, with subsequent platelet aggregation and thrombosis, are the primary underlying stimuli for unstable angina. Unstable angina has been defined as consisting of new-onset angina; angina that is increasing in frequency, intensity, or duration (crescendo angina); or angina at rest. The diagnosis of unstable angina is based on the clinical presentation, electrocardiographic findings, the lack of evidence of myocardial infarction (MI), exercise testing, and coronary angiography. I.V. nitroglycerin is the cornerstone of medical therapy for unstable angina, it relieves chest pain and has a short onset of action. I.V. nitroglycerin, however, has not been shown to reduce the occurrence of MI or death, and its beneficial effects may decrease over time. Aspirin reduces the occurrence of MI and death in patients with unstable angina, but the ideal dosage has not been established. Heparin may reduce the frequency of angina and MI, but its effect on mortality is unknown. Nifedipine has produced beneficial effects in small trials, whereas larger trials have suggested that the drug has deleterious effects when used in the treatment of unstable angina. Verapamil and diltiazem may be effective in relieving chest pain. Calcium-channel blockers have generally not been proved to reduce the risk of MI and death. Data evaluating the efficacy of beta-adrenergic blockers as monotherapy for unstable angina are lacking; these drugs should not be used in patients with vasospastic or Prinzmetal's angina. Thrombolytic therapy has produced mixed results when used in the treatment of unstable angina. Nondrug therapies for unstable angina include intra-aortic balloon counterpulsation, percutaneous transluminal coronary angioplasty, and coronary-artery bypass surgery. Numerous drug and nondrug therapies may be employed in the treatment of unstable angina pectoris.
 ...
PMID:Advances in the treatment of unstable angina pectoris. 179 19

Unstable angina patients should be hospitalized and treated with antianginal drugs to control their symptoms and with aspirin or heparin to reduce the risk of myocardial infarction. Heparin is probably preferable to aspirin acutely, because it also reduces the risk of refractory angina. However, aspirin therapy should be started before heparin is discontinued, to prevent the rebound in symptoms, and continued long-term. Unless specifically contraindicated, coronary arteriography should be performed to identify patients who might benefit from coronary bypass surgery or angioplasty. Control of risk factors is important for long-term outcome.
 ...
PMID:Newer concepts in the treatment of unstable angina pectoris. 195 Nov 1

399 out of 474 inpatients with unstable angina were monitored for 48 h and 97 of these were found to be refractory to conventional antianginal treatments and entered a randomised double-blind study. With the initial protocol heparin infusion or bolus were compared with aspirin; with a modified protocol, heparin infusion, the best of these three treatments, was compared with alteplase. Patients were monitored for 3 days after starting treatment and then observed clinically for 4 more days. On the first days of treatment heparin infusion significantly decreased the frequency of angina (by 84-94%), episodes of silent ischaemia (by 71-77%), and the overall duration of ischaemia (by 81-86%). Heparin bolus and aspirin were not effective. Alteplase caused small (non-significant) reductions on the first day only. Only minor bleeding complications occurred.
 ...
PMID:Effect of heparin, aspirin, or alteplase in reduction of myocardial ischaemia in refractory unstable angina. 196 13

We studied the effects of heparin, given as 12,500 units intravenously, on cardiac metabolism during catheterization of the coronary sinus at rest and during repeated rapid atrial pacing in 8 patients with stable angina pectoris, positive stress tests and coronary arterial disease and in 8 patients with normal coronary arteries without objective signs of ischemic heart disease. Heparin did not influence angina, ST-segment depression or myocardial lactate production induced by pacing in the group with diseased coronary arteries. In both groups, heparin increased the arterial levels (70%) and the myocardial uptake (40-50%) of free fatty acids, the latter only during non-ischemic conditions. Myocardial net uptakes of glucose, lactate and glutamate and the release of alanine were reduced by heparin in the subjects with normal coronary arteries but not in those with ischemic heart disease. Myocardial oxygen consumption was unchanged. In the patients with normal coronary arteries, the levels of free fatty acid in the arteries were positively related to myocardial uptake of fatty acids and the release of citrate but inversely related to cardiac uptake of lactate and glucose. These relations were lacking in the patients with diseased coronary arteries. The metabolic effects of heparin on the heart, therefore, were diminished in patients with ischemic heart disease when compared to controls. This is probably due to an altered regulation of substrate preference in ischemic hearts.
 ...
PMID:Cardiac metabolic effects of heparin differentiate between patients with normal and stenotic coronary arteries. 197 Aug 7

A randomized, placebo-controlled, double-blinded trial was performed to evaluate the usefulness of empiric therapy with a calcium antagonist in patients who undergo coronary angioplasty. A total of 201 patients were randomized to placebo or to high-dose diltiazem (mean dose, 329 mg/day). Treatment began 24 hours before angioplasty. Restenosis was assessed by percent area stenosis as determined by quantitative angiographic techniques before, immediately and 1 year after angioplasty. All patients also received aspirin and dipyridamole before angioplasty. Heparin and verapamil were administered intravenously during the procedure. The 2 groups were similar with respect to age, extent of coronary artery disease, smoking history, and baseline lipid levels. Procedural complications, including death (1 vs 1), Q-wave infarction (0 vs 3), acute occlusion (5 vs 5) and focal spasm (0 vs 0), were not significantly different in the diltiazem and placebo patients, respectively. Freedom from all acute complications was noted in 85% of patients in both groups. One-year angiographic follow-up was obtained in 60% of patients. Restenosis rates were similar: 36% in the diltiazem group and 32% in the placebo group (p = 0.30). The incidence of late cardiac events (death, Q-wave myocardial infarction, recurrent angina or coronary bypass graft surgery) was similar in the 2 groups. Thus, diltiazem did not influence the overall restenosis rate or prevent late events after coronary angioplasty.
 ...
PMID:Effects of diltiazem on complications and restenosis after coronary angioplasty. 199 61

Heparin-induced Extracorporeal LDL-Precipitation (HELP) is an effective procedure for the elimination of both plasma LDL and fibrinogen. In 10 adult patients with severe type II hyperlipoproteinemia, a single HELP treatment of 3 1 plasma led to an acute decrease in the average plasma viscosity (PV) from 1.30 to 1.1 mPas. At the same time, an even more marked decrease in the mean erythrocyte aggregation rate from a pathological value of 7.9% to a value of 3.7% (normal range less than 5%) was observed. Long-term studies on five patients demonstrated a lasting improvement in these two haemorheological variables. The acute rheological changes were also accompanied by an improvement in polarographically determined muscle oxygen tension. Mean oxygen tension values measured in both the m.biceps brachii and the m.tibialis anterior in five patients before and after a single HELP treatment increased from 30 +/- 4 to 37 +/- 7 mmHg and from 27 +/- 2 to 31 +/- 3 mmHg respectively. These results may provide an explanation for the rapid improvement in patients' clinical symptoms such as angina pectoris and in stress electrocardiogram which have been observed during HELP therapy.
 ...
PMID:Improved haemorheology associated with a reduction in plasma fibrinogen and LDL in patients being treated by heparin-induced extracorporeal LDL precipitation (HELP). 249 59

Examinations were performed in 153 consecutive patients with myocardial infarction (MS), which were divided into two groups. Group I (21 persons) consisted of patients with echocardiographically diagnosed left ventricular mural thrombus, and in group II were patients without evidence of thrombi. Significantly more patients with anterior myocardial infarction were in the the group I, whereas those with inferior MI in the group II. Increased left ventricular wall contractility index and considerably percentage of dyskinesis, mostly of the apex region were stated in the group I. 15 patients (71%) of the group I were treated with heparin, but only 4 of them within 4 hours from the beginning of angina pain. In 4 patients of the group I (19%) thromboembolic complications occurred: in 1 patient during proper anticoagulant therapy and in 3 others without treatment with heparin. Thus mural thrombi were observed in majority in patients with anterior myocardial infarction and were localized in a diskinetic region. Echocardiograms of patients with mural thrombi testified to greater than in others left ventricular function impairment. Heparin administration during first hours of myocardial infarction seemed to lower the incidence of mural thrombi and probably thrombembolic complications.
 ...
PMID:[Left ventricular mural thrombi in myocardial infarction in echocardiographic studies and clinical observations]. 263 38

Heparin, aspirin with dipyridamole or placebo were given to 266 patients with pre-infarction angina treated with isosorbide dinitrate, beta blockers and nifedipidine. The number of patients who developed acute myocardial infarction (MI) in the next 72 hours was comparable in all 3 groups. However, patients on heparin developed only 3.2% (2 out of 61) Q MI compared with 20% (20 out of 100, p = 0.005) taking dipyridamole with aspirin and 19% (20 out of 105 on placebo, p = 0.006). Infarctions of patients treated with heparin as assessed by peak of serum creatine kinase (CK) were also smaller (810 +/- 538 IU/1) than in groups taking antiplatelets (1229 +/- 829 IU/1, p = 10.048) or placebo (1417 +/- 919 IU/1, p = 0.009). We defined a subgroup at high risk patients who had prolonged chest pain longer than 45 min and ECG changes with ST segment depression more than 1 mm within 6 hours of admission: 55% of these patients developed acute infarction in the following 72 hours. Aggressive management including coronary angiography and fibrinolysis should be considered in well equipped centers for patients with evolving coronary thrombus in a general hospital, heparin infusion should be part of routine treatment as patients on heparin developed smaller infarctions.
 ...
PMID:Comparative study of heparin and antiplatelets in treatment of preinfarction angina. 266 Sep 91


1 2 3 4 Next >>