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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial infarction (MI) is the result of acute coronary occlusion and the prognosis depends on the infarct size. In experimental studies, infarct size is reduced by early coronary reperfusion which may be obtained by intravenous thrombolytic therapy. This simple, rapid and widely used technique is the clinical treatment of choice. The diagnosis of MI must be confirmed by clinical and electrocardiographic findings. The clinical history is important because the value of reperfusion when started after the 6th hour after the onset of chest pain is questionable. However, it is often difficult to determine the beginning of MI when preceded by unstable angina. Contraindications to thrombolytic therapy must be carefully excluded irrespective of the thrombolytic agent because of the risk of haemorrhage. This must be weighed up against the risk of the MI itself. Therefore, age is not a systematic exclusion criterion. The choice of thrombolytic is based on the efficacy, mode of administration and cost. Heparin therapy at effective doses is associated in all cases to prevent reocclusion. Aspirin is given orally. The association of a calcium inhibitor or a betablocker may also be considered. Reperfusion and ischaemia may give rise to arrhythmias and haemodynamic changes which have to be rapidly corrected. Haemorrhagic complications during thrombolysis are treated according to the severity and time of onset by blood transfusion sometimes associated with a plasmin inhibitor. Reocclusion is an indication for emergency coronary angioplasty but in some cases repeat thrombolytic therapy may be beneficial. When the MI is extensive, rapid transfer to a cardiological centre with catheter facilities is advisable.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Thrombolytic therapy of myocardial infarction: practical management]. 153 Apr 12

Multiple clinical trials have demonstrated that thrombolytic treatment early in the course of acute myocardial infarction significantly reduces mortality. Patients under 75 years of age who have had chest pain for no longer than six hours and who demonstrate ST-segment elevation on electrocardiogram are the best candidates for this therapy. Recent studies suggest that there is little difference in effectiveness among streptokinase, alteplase and anistreplase. However, streptokinase is 10 times less expensive than the other agents and causes fewer intracranial bleeds, the major serious adverse effect of thrombolytic therapy. An advantage of anistreplase is that it can be given in a five-minute bolus injection, compared with a one-hour infusion for streptokinase and a three-hour infusion for alteplase. Thrombolytic therapy is contraindicated in patients with known pregnancy, active internal bleeding, uncontrolled hypertension, aortic dissection, intracranial neoplasm or a history of hemorrhagic stroke. Heparin should be administered with both alteplase and streptokinase. Aspirin, beta blockers, nitrates and lidocaine are useful adjunctive therapies in the setting of an acute myocardial infarction.
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PMID:Thrombolytic therapy in acute myocardial infarction. 173 49

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.
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PMID:Advances in the treatment of unstable angina pectoris. 179 19

The efficacy and safety of intravenous administration of recombinant tissue-type plasminogen activator (rt-PA, made by Boehringer Ingelheim Corp.) was investigated in 10 patients with acute myocardial infarction (AMI). The rt-PA was given as a bolus dose of 10 mg followed by an infusion of 50 mg, 20 mg and 20 mg in successive hours. Heparin and aspirin were given to all the patients. The time interval from the onset of chest pain to thrombolysis was from 2.3 to 6.1 h with mean of 3.9 h. Coronary angiography, performed before administration of rt-PA and every 30 minutes thereafter, demonstrated total coronary occlusion (grade O) in 9 patients and grade 1 in 1 at baseline study. The infarct-related coronary artery were LAD in 5, RCA in 3 and LCX in 2. At 90 minutes after infusion of rt-PA reperfusion of the infarct-related artery was observed in 7 patients, the success rate was 70%. In one case the infarct-related LCX was not opened at 90 minutes, but it was reperfused at 170 minutes, after intracoronary administration of 10 mg of rt-PA. The total dose in this case was 130 mg. During 30 days of hospitalization death occurred in only one case with cardiogenic shock, in whom the infarct-related RCA was not reperfused by rt-PA but was successfully recanalized by PTCA. The patient died from rupture of the left ventricle on the 4th day. No patient had clinical evidence of reinfarction. Follow-up angiography in 2 patients showed that the arteries reperfused initially were patent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Intravenous recombinant tissue-type plasminogen activator in acute myocardial infarction]. 181 88

Feasibility of home Heparin infusion in the management of deep vein thrombophlebitis (DVT) was assessed in 15 patients. Patients with chest pain, dyspnea, bleeding tendencies, immediate postoperative state, and lack of reliable care giver were excluded. Five patients received the entire course of Heparin infusion at home and 10 were initially started on Heparin in the hospital. Regular assessment and monitoring of blood coagulation parameters were performed by a visiting home nurse clinician in consultation with the attending physician. Eleven physicians were involved in this management and made a total of six physician home visits. Results showed improvement in all but one patient, who had advanced malignancy and resistant thrombophlebitis and who eventually died. No complications occurred among the patients studied. Patient and family surveys indicated a high degree of satisfaction and preference for this modality of care. Analysis of cost indicated a 48% savings compared with similar treatment administered in a hospital setting.
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PMID:Home heparin infusion in the management of deep vein thrombophlebitis. 225 4

Heparin is a commonly used drug in critical care. In this case study we describe a relatively unknown and unforeseen event whereby the administration of heparin to prevent thrombus formation paradoxically resulted in clot formation. Heparin-induced thrombocytopenia and thrombosis syndrome developed in a 36-year-old woman initially admitted to the coronary care unit with complaints of chest pain. We explore the theoretic basis of this syndrome as an immune-mediated response, along with the mechanisms leading to this syndrome as an immune-mediated response, along with the mechanisms leading to the clinical features and the difficulties associated with diagnosis treatment. In view of the frequent use of heparin and nurses' responsibility for recognizing the untoward effects of medications they administer, this case study is useful in gaining insight into a relatively unknown phenomenon.
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PMID:Heparin-induced thrombocytopenia and thrombosis syndrome: a case study. 240 14

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.
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PMID:Comparative study of heparin and antiplatelets in treatment of preinfarction angina. 266 Sep 91

In a double-blind trial of streptokinase for acute myocardial infarction, 219 consecutive patients presenting with infarction within four hours (mean, 3.0 +/- 0.8) of the onset of chest pain were randomly assigned to treatment with streptokinase (1.5 million units) or placebo, given intravenously over 30 minutes. The primary end point of the study was left ventricular function in patients with first infarctions. Patients who could undergo beta-blockade also received intravenous propranolol. Heparin (for 48 hours) and a combination of low-dose aspirin and dipyridamole were administered to both groups until cineangiography was performed at three weeks. In the patients with first infarctions treated with streptokinase, the left ventricular ejection fraction was 6 percentage points higher (streptokinase vs. placebo, 59 +/- 10.5 vs. 53 +/- 13.5 percent; P less than 0.005), with benefit to patients with either anterior infarction (57 +/- 11.9 vs. 49 +/- 15.9 percent; P less than 0.05) or inferior infarction (60 +/- 9.1 vs. 55 +/- 11.3 percent; P less than 0.05). Left ventricular function was improved regardless of whether concomitant propranolol was given. Survival (at 30 days) was improved with streptokinase: 2 deaths occurred among 79 patients who received this drug, as compared with 12 deaths among 93 patients who received placebo (2.5 vs. 12.9 percent, P = 0.012). Rates of reinfarction (streptokinase vs. placebo, 3 vs. 1 percent) and requirements for surgery or angioplasty (7 vs. 5 percent) were similar in the two groups. We conclude that administration of intravenous streptokinase (1.5 million units) to patients with a first myocardial infarction results in improved left ventricular function and short-term survival.
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PMID:Effect of intravenous streptokinase on left ventricular function and early survival after acute myocardial infarction. 288 18

The optimal approach to management of patients after thrombolytic therapy for acute myocardial infarction (AMI) is unclear. The role of anticoagulation with heparin was evaluated in 75 consecutive patients who received intravenous streptokinase for AMI. Heparin therapy was titrated to keep the partial thromboplastin time (PTT) between 90 and 120 seconds. Seventeen episodes of definite myocardial ischemia (associated with reversible electrocardiographic changes) were observed in 13 patients. When episodes of probable myocardial ischemia are included (typical chest pain relieved by nitroglycerin or associated with more than a 15-mm Hg change in blood pressure but without electrocardiographic changes), 52 episodes occurred in 28 patients. Four episodes of definite and 4 of probable myocardial ischemia occurred within 24 hours of discontinuation of heparin. Analysis of the level of anticoagulation as assessed by PTT at the time of the ischemic events shows that ischemia occurred more often at lower PTTs. Nine hemorrhagic complications occurred, all within 24 hours of streptokinase infusion. In 4 patients bleeding was believed to be major and heparin administration was discontinued; 2 patients with gastrointestinal bleeding required blood transfusions. Our data suggest that after thrombolytic therapy for AMI, the level of anticoagulation is inversely related to the frequency of recurrent ischemic events; that discontinuation of heparin is frequently associated with ischemia; and that administration of heparin is associated with a low incidence of hemorrhagic complications.
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PMID:Role of heparin after intravenous thrombolytic therapy for acute myocardial infarction. 381 72

Thrombin has been suggested as one of the main pharmacologic targets in unstable coronary syndromes. Electrocardiographic signs of ischemia during continuous monitoring convey prognostic information in these patients. This study assessed the anti-ischemic and clinical effects of the novel low-molecular weight thrombin inhibitor inogatran in patients with unstable angina and non-Q-wave infarction without persistent ST-segment elevation on hospital admission. Within 24 hours of the last episode of chest pain, 324 patients were randomized to 72 hours of treatment with inogatran or heparin. Continuous ST-segment analysis with computerized vectorcardiography was used to monitor ischemia for 24 hours. The occurrence of cardiac events during the first 7 days were studied and compared with ischemic episodes during the initial 24 hours. The heparin-treated patients had less episodes of ischemia (ST vector magnitude [ST-VM]: 1 +/- 2.6 vs 2 +/- 4.5, p < 0.001 and ST change vector magnitude [STC-VM]: 3 +/- 4.7 vs 6 +/- 7.6, p < 0.001) than the patients receiving inogatran. This was paralleled by a lower incidence of the combined end point of death, nonfatal infarction, refractory or recurrent angina during the first 7 days for the heparin-treated patients (35%) compared with the inogatran-treated patients (50%) (p < 0.05). Patients who had episodes of ischemia in spite of anti-ischemic therapy were at increased risk of all events studied. Heparin is more effective than inogatran in suppressing myocardial ischemia and clinical events at short-term follow-up. Continuous ST-segment monitoring with vectorcardiography identifies nonresponders who are at an increased level of risk.
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PMID:Heparin is more effective than inogatran, a low-molecular weight thrombin inhibitor in suppressing ischemia and recurrent angina in unstable coronary disease. Thrombin Inhibition in Myocardial Ischemia (TRIM) Study Group. 957 50


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