Prodromata in Acute Myocardial Infarction

Solomon, Herbert; Edwards, Adrian L.; Killip, Thomas

doi:10.1161/01.cir.40.4.463

Cited by 130 publications

(20 citation statements)

References 19 publications

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“…There were similarities between cues from past symptoms and current physiological cues with chest pain being the most prominent cue and the neurological signs of headache and diaphoresis next in frequency. These findings were similar to those of Solomon et al (1969) and Zeiner-Henriksen (1972). In addition, subjects also found the activities of relaxation and cessation of work as helpful and over-exertion as harmful.…”

Section: Discussion and Implications For Future Studysupporting

confidence: 81%

Internal and External Cues Identified as Helpful or Harmful by Myocardial Infarction Patients

Miller¹

1981

West J Nurs Res

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Section: Discussion and Implications For Future Studysupporting

confidence: 81%

Internal and External Cues Identified as Helpful or Harmful by Myocardial Infarction Patients

Miller¹

1981

West J Nurs Res

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“…One additional patient underwent elective CABG after 21 days. In the rt-PA group, one patient underwent semiurgent 10,19,20 Over 90% of patients with unstable angina have significant fixed atherosclerotic coronary disease. Proposed mechanisms for the development of the syndrome include coronary vasospasm, progression of atherosclerosis, and platelet aggregation.2' This has led to the use of nitrates, calcium antagonists, /3-blocking agents, and antiplatelet drugs for the treatment of unstable angina.…”

Section: Resultsmentioning

confidence: 99%

A randomized, blinded, placebo-controlled trial of recombinant human tissue-type plasminogen activator in patients with unstable angina pectoris.

Gold¹,

Johns²,

Leinbach³

et al. 1987

Circulation

133

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Twenty-four patients with unstable angina pectoris, defined as chest pain at rest with transient ST segment deviation of at least 1 mm, were randomly assigned to blinded treatment with either placebo or intravenous recombinant human tissue-type plasminogen activator (rt-PA). Before randomization, all patients were treated with oral 13-blockers, calcium antagonists, nitrates, and continuous intravenous heparin for a monitoring period of 12 to 28 hr. After this monitoring period the 24 patients were randomly assigned to receive either placebo or 1.75 mg/kg intravenous rt-PA given over 12 hr at a rate of 0.75 mg/kg over 1 hr, 0.5 mg/kg over 4 hr, and 0.5 mg/kg over 7 hr. One patient, assigned to receive placebo, developed acute myocardial infarction after randomization but before receiving the study drug. Ischemic events were recorded during a hospital follow-up period of at least 4 days unless a further intervention was indicated or the coronary angiogram was normal. The follow-up period was 7 5 days (mean + SD) after the placebo infusion and 8 ± 4 days after the infusion of rt-PA. Unstable angina pectoris persisted after the completion of the infusion in six of 11 patients receiving placebo and only one of 12 patients receiving rt-PA (p < .03). Coronary angiography, performed 38 ± 19 hr after the infusion, demonstrated subocclusive thrombus in eight of 11 patients receiving placebo but in none of 11 patients treated with rt-PA (p < .002). One patient on rt-PA refused coronary angiography. Persistence of unstable angina pectoris correlated significantly with the presence of intracoronary thrombus (p < .003). The infusion of rt-PA caused a decrease of fibrinogen to 66 ± 19% after 1 hr, to 65 ± 21% after 5 hr, and to 64 ± 29% after 12 hr. Oozing at puncture sites was not observed in patients receiving placebo but was seen in eight of 12 patients treated with rt-PA. In three patients on rt-PA, bleeding complications necessitated termination of the infusion within 5, 8, and 11 hr after onset. Thus, in this group of patients with unstable angina pectoris, intravenous infusion of rt-PA appeared to lyse subocclusive intracoronary thrombi. The removal of intracoronary thrombus by rt-PA was associated with reduction of the severity of resting angina. The decision for further intervention could then be made on the basis of residual coronary occlusion.

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“…In the literature, prevalence of chronic angina prior to infarction ranges from 25% to 50% [14][15][16] . These differences may be attributed to diverse definitions of chronic angina and different populations studied.…”

Section: Discussionmentioning

confidence: 99%

Acute Myocardial Infarction: The First Manifestation of Ischemic Heart Disease and Relation to Risk Factors

Manfroi

Peukert²,

Berti³

et al. 2002

Arq. Bras. Cardiol.

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Objective -To assess the association between cardiovascular risk factors and acute myocardial infarction as the first manifestation of ischemic heart disease, correlating them with coronary angiographic findings. Methods - (RR=0.19; P=0.04) and left ventricular hypertrophy (RR=0.27; 95% CI=0, P=0.03). The remaining risk factors were not statistically significant. Conclusion -Prevalence of acute myocardial infarction as the first manifestation of ischemic

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Prodromata in Acute Myocardial Infarction

Cited by 130 publications

References 19 publications

Internal and External Cues Identified as Helpful or Harmful by Myocardial Infarction Patients

Internal and External Cues Identified as Helpful or Harmful by Myocardial Infarction Patients

A randomized, blinded, placebo-controlled trial of recombinant human tissue-type plasminogen activator in patients with unstable angina pectoris.

Acute Myocardial Infarction: The First Manifestation of Ischemic Heart Disease and Relation to Risk Factors

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