Transmyocardial fibrinolytic activity in patients with unstable angina pectoris

William C. Daniel, Robert S. Meidell, L. David Hillis, Richard A. Lange

Research output: Contribution to journalArticle

Abstract

Objectives: This study was performed to investigate local (transmyocardial) fibrinolytic activity in patients with unstable angina. Background: Previous studies have reported decreased intrinsic fribrinolytic activity - increased systemic plasminogen activator inhibitor-1 (PAI-1) activity and/or decreased systemic tissue plasminogen activator (t-PA) activity - in patients with acute myocardial infarction. In contrast, the role of intrinsic fibrinolytic activity in patients with unstable angina is not well understood. Methods: We studied 67 consecutive patients (52 men and 15 women, aged 38-82 years) undergoing cardiac catheterization for chest pain within 24 h of acute presentation: 17 with unstable angina, 33 with stable angina, and 17 with atypical chest pain with angiographically normal coronary arteries. In each, blood samples were obtained simultaneously from the aorta and coronary sinus for measurement of t-PA and PAI-1 activities. Results: There was no difference in coronary sinus or systemic (aortic) t-PA activity among the three groups. The coronary sinus t-PA activity was 0.092 ± 0.054, 0.088 ± 0.038, and 0.080 ± 0.050 IU/ml in the control, unstable angina, and stable angina groups, respectively [not significant (NS)], and the aortic t- PA activity was 0.114 ± 0.053, 0.099 ± 0.057, and 0.090 ± 0.056 IU/ml in the control unstable angina, and stable angina groups, respectively (NS). Similarly, there was no difference in coronary sinus or systemic (aortic) PAI-1 activity among the three groups: the coronary sinus PAI-1 activity was 8.2 ± 2.0, 7.4 ± 2.0, and 8.0 ± 2.5 AIU/ml in the control, unstable angina, and stable angina groups, respectively (NS). The aortic PAI-1 activity was 7.8 ± 2.1, 7.2 ± 1.4, and 8.0 ± 1.8 AIU/ml in the control, unstable angina, and stable angina groups, respectively (NS). Conclusions: Although it has been suggested that alterations in local (transmyocardial) t- PA and PAI-1 activities may be of pathophysiologic importance in the genesis of unstable angina, our data show no difference in transmyocardial fibrinolytic activity in patients with unstable angina, stable angina, and noncardiac chest pain.

Original languageEnglish (US)
Pages (from-to)45-49
Number of pages5
JournalCoronary Artery Disease
Volume7
Issue number1
StatePublished - 1996
Externally publishedYes

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Unstable Angina
Stable Angina
Plasminogen Activator Inhibitor 1
Coronary Sinus
Tissue Plasminogen Activator
Chest Pain
Cardiac Catheterization
Aorta
Coronary Vessels
Myocardial Infarction

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Daniel, W. C., Meidell, R. S., Hillis, L. D., & Lange, R. A. (1996). Transmyocardial fibrinolytic activity in patients with unstable angina pectoris. Coronary Artery Disease, 7(1), 45-49.

Transmyocardial fibrinolytic activity in patients with unstable angina pectoris. / Daniel, William C.; Meidell, Robert S.; Hillis, L. David; Lange, Richard A.

In: Coronary Artery Disease, Vol. 7, No. 1, 1996, p. 45-49.

Research output: Contribution to journalArticle

Daniel, WC, Meidell, RS, Hillis, LD & Lange, RA 1996, 'Transmyocardial fibrinolytic activity in patients with unstable angina pectoris', Coronary Artery Disease, vol. 7, no. 1, pp. 45-49.
Daniel, William C. ; Meidell, Robert S. ; Hillis, L. David ; Lange, Richard A. / Transmyocardial fibrinolytic activity in patients with unstable angina pectoris. In: Coronary Artery Disease. 1996 ; Vol. 7, No. 1. pp. 45-49.
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abstract = "Objectives: This study was performed to investigate local (transmyocardial) fibrinolytic activity in patients with unstable angina. Background: Previous studies have reported decreased intrinsic fribrinolytic activity - increased systemic plasminogen activator inhibitor-1 (PAI-1) activity and/or decreased systemic tissue plasminogen activator (t-PA) activity - in patients with acute myocardial infarction. In contrast, the role of intrinsic fibrinolytic activity in patients with unstable angina is not well understood. Methods: We studied 67 consecutive patients (52 men and 15 women, aged 38-82 years) undergoing cardiac catheterization for chest pain within 24 h of acute presentation: 17 with unstable angina, 33 with stable angina, and 17 with atypical chest pain with angiographically normal coronary arteries. In each, blood samples were obtained simultaneously from the aorta and coronary sinus for measurement of t-PA and PAI-1 activities. Results: There was no difference in coronary sinus or systemic (aortic) t-PA activity among the three groups. The coronary sinus t-PA activity was 0.092 ± 0.054, 0.088 ± 0.038, and 0.080 ± 0.050 IU/ml in the control, unstable angina, and stable angina groups, respectively [not significant (NS)], and the aortic t- PA activity was 0.114 ± 0.053, 0.099 ± 0.057, and 0.090 ± 0.056 IU/ml in the control unstable angina, and stable angina groups, respectively (NS). Similarly, there was no difference in coronary sinus or systemic (aortic) PAI-1 activity among the three groups: the coronary sinus PAI-1 activity was 8.2 ± 2.0, 7.4 ± 2.0, and 8.0 ± 2.5 AIU/ml in the control, unstable angina, and stable angina groups, respectively (NS). The aortic PAI-1 activity was 7.8 ± 2.1, 7.2 ± 1.4, and 8.0 ± 1.8 AIU/ml in the control, unstable angina, and stable angina groups, respectively (NS). Conclusions: Although it has been suggested that alterations in local (transmyocardial) t- PA and PAI-1 activities may be of pathophysiologic importance in the genesis of unstable angina, our data show no difference in transmyocardial fibrinolytic activity in patients with unstable angina, stable angina, and noncardiac chest pain.",
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AU - Daniel, William C.

AU - Meidell, Robert S.

AU - Hillis, L. David

AU - Lange, Richard A.

PY - 1996

Y1 - 1996

N2 - Objectives: This study was performed to investigate local (transmyocardial) fibrinolytic activity in patients with unstable angina. Background: Previous studies have reported decreased intrinsic fribrinolytic activity - increased systemic plasminogen activator inhibitor-1 (PAI-1) activity and/or decreased systemic tissue plasminogen activator (t-PA) activity - in patients with acute myocardial infarction. In contrast, the role of intrinsic fibrinolytic activity in patients with unstable angina is not well understood. Methods: We studied 67 consecutive patients (52 men and 15 women, aged 38-82 years) undergoing cardiac catheterization for chest pain within 24 h of acute presentation: 17 with unstable angina, 33 with stable angina, and 17 with atypical chest pain with angiographically normal coronary arteries. In each, blood samples were obtained simultaneously from the aorta and coronary sinus for measurement of t-PA and PAI-1 activities. Results: There was no difference in coronary sinus or systemic (aortic) t-PA activity among the three groups. The coronary sinus t-PA activity was 0.092 ± 0.054, 0.088 ± 0.038, and 0.080 ± 0.050 IU/ml in the control, unstable angina, and stable angina groups, respectively [not significant (NS)], and the aortic t- PA activity was 0.114 ± 0.053, 0.099 ± 0.057, and 0.090 ± 0.056 IU/ml in the control unstable angina, and stable angina groups, respectively (NS). Similarly, there was no difference in coronary sinus or systemic (aortic) PAI-1 activity among the three groups: the coronary sinus PAI-1 activity was 8.2 ± 2.0, 7.4 ± 2.0, and 8.0 ± 2.5 AIU/ml in the control, unstable angina, and stable angina groups, respectively (NS). The aortic PAI-1 activity was 7.8 ± 2.1, 7.2 ± 1.4, and 8.0 ± 1.8 AIU/ml in the control, unstable angina, and stable angina groups, respectively (NS). Conclusions: Although it has been suggested that alterations in local (transmyocardial) t- PA and PAI-1 activities may be of pathophysiologic importance in the genesis of unstable angina, our data show no difference in transmyocardial fibrinolytic activity in patients with unstable angina, stable angina, and noncardiac chest pain.

AB - Objectives: This study was performed to investigate local (transmyocardial) fibrinolytic activity in patients with unstable angina. Background: Previous studies have reported decreased intrinsic fribrinolytic activity - increased systemic plasminogen activator inhibitor-1 (PAI-1) activity and/or decreased systemic tissue plasminogen activator (t-PA) activity - in patients with acute myocardial infarction. In contrast, the role of intrinsic fibrinolytic activity in patients with unstable angina is not well understood. Methods: We studied 67 consecutive patients (52 men and 15 women, aged 38-82 years) undergoing cardiac catheterization for chest pain within 24 h of acute presentation: 17 with unstable angina, 33 with stable angina, and 17 with atypical chest pain with angiographically normal coronary arteries. In each, blood samples were obtained simultaneously from the aorta and coronary sinus for measurement of t-PA and PAI-1 activities. Results: There was no difference in coronary sinus or systemic (aortic) t-PA activity among the three groups. The coronary sinus t-PA activity was 0.092 ± 0.054, 0.088 ± 0.038, and 0.080 ± 0.050 IU/ml in the control, unstable angina, and stable angina groups, respectively [not significant (NS)], and the aortic t- PA activity was 0.114 ± 0.053, 0.099 ± 0.057, and 0.090 ± 0.056 IU/ml in the control unstable angina, and stable angina groups, respectively (NS). Similarly, there was no difference in coronary sinus or systemic (aortic) PAI-1 activity among the three groups: the coronary sinus PAI-1 activity was 8.2 ± 2.0, 7.4 ± 2.0, and 8.0 ± 2.5 AIU/ml in the control, unstable angina, and stable angina groups, respectively (NS). The aortic PAI-1 activity was 7.8 ± 2.1, 7.2 ± 1.4, and 8.0 ± 1.8 AIU/ml in the control, unstable angina, and stable angina groups, respectively (NS). Conclusions: Although it has been suggested that alterations in local (transmyocardial) t- PA and PAI-1 activities may be of pathophysiologic importance in the genesis of unstable angina, our data show no difference in transmyocardial fibrinolytic activity in patients with unstable angina, stable angina, and noncardiac chest pain.

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