Relation of plasma lipoprotein(a) to infarct artery patency in survivors of myocardial infarction

David J. Moliterno, Richard A. Lange, Robert S. Meidell, John E. Willard, Carla C. Leffert, Robert D. Gerard, Eric Boerwinkle, Helen H. Hobbs, L. David Hillis

Research output: Contribution to journalArticle

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Abstract

Background. In the minutes to days after myocardial infarction, endogenous lysis of an occlusive coronary arterial thrombus occurs in most subjects. Compared with those in whom thrombolysis does not occur, those with antegrade flow in the infarct artery have improved left ventricular performance, less left ventricular dilatation, and improved survival. This study was performed to assess intrinsic hemostasis and fibrinolysis in survivors of myocardial infarction with or without antegrade perfusion of the infarct artery. Methods and Results. In 105 survivors of infarction (75 men, 30 women; age, 30 to 80 years) not given thrombolytic therapy, coronary angiography revealed a patent (group 1, n=52) or occluded (group 2, n=53) infarct artery. Plasma concentrations of plasminogen, fibrinogen, tissue plasminogen activator activity, plasminogen activator inhibitor activity, cholesterol, triglycerides, and lipoproteins, including lipoprotein(a) (Lp[a]), were measured in blood procured 23±13 (mean±SD) months after infarction. Groups 1 and 2 were similar in age, sex, race, cardioactive medications, infarct artery, extent of coronary artery disease, and left ventricular performance. Of the plasma constituents assayed, the groups were similar except that Lp(a) averaged 18.5±21.7 mg/dL in group 1 and 49.1±44.8 mg/dL in group 2 (P<.001). This difference was evident in both Caucasian (n=65) (P=.009) and African American (n=40) (P=.01) subjects. Conclusions. Survivors of myocardial infarction who failed to recanalize the infarct artery have higher plasma Lp(a) concentrations than those with a patent infarct artery. Lp(a) may inhibit intrinsic fibrinolysis.

Original languageEnglish (US)
Pages (from-to)935-940
Number of pages6
JournalCirculation
Volume88
Issue number3
StatePublished - Sep 1993

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Lipoprotein(a)
Survivors
Arteries
Myocardial Infarction
Fibrinolysis
Infarction
Plasminogen Inactivators
Plasminogen
Thrombolytic Therapy
Tissue Plasminogen Activator
Hemostasis
Coronary Angiography
African Americans
Fibrinogen
Coronary Artery Disease
Dilatation
Triglycerides
Thrombosis
Perfusion
Survival

Keywords

  • Apolipoproteins
  • Fibrinolysis
  • Thrombolysis

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Moliterno, D. J., Lange, R. A., Meidell, R. S., Willard, J. E., Leffert, C. C., Gerard, R. D., ... Hillis, L. D. (1993). Relation of plasma lipoprotein(a) to infarct artery patency in survivors of myocardial infarction. Circulation, 88(3), 935-940.

Relation of plasma lipoprotein(a) to infarct artery patency in survivors of myocardial infarction. / Moliterno, David J.; Lange, Richard A.; Meidell, Robert S.; Willard, John E.; Leffert, Carla C.; Gerard, Robert D.; Boerwinkle, Eric; Hobbs, Helen H.; Hillis, L. David.

In: Circulation, Vol. 88, No. 3, 09.1993, p. 935-940.

Research output: Contribution to journalArticle

Moliterno, DJ, Lange, RA, Meidell, RS, Willard, JE, Leffert, CC, Gerard, RD, Boerwinkle, E, Hobbs, HH & Hillis, LD 1993, 'Relation of plasma lipoprotein(a) to infarct artery patency in survivors of myocardial infarction', Circulation, vol. 88, no. 3, pp. 935-940.
Moliterno DJ, Lange RA, Meidell RS, Willard JE, Leffert CC, Gerard RD et al. Relation of plasma lipoprotein(a) to infarct artery patency in survivors of myocardial infarction. Circulation. 1993 Sep;88(3):935-940.
Moliterno, David J. ; Lange, Richard A. ; Meidell, Robert S. ; Willard, John E. ; Leffert, Carla C. ; Gerard, Robert D. ; Boerwinkle, Eric ; Hobbs, Helen H. ; Hillis, L. David. / Relation of plasma lipoprotein(a) to infarct artery patency in survivors of myocardial infarction. In: Circulation. 1993 ; Vol. 88, No. 3. pp. 935-940.
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abstract = "Background. In the minutes to days after myocardial infarction, endogenous lysis of an occlusive coronary arterial thrombus occurs in most subjects. Compared with those in whom thrombolysis does not occur, those with antegrade flow in the infarct artery have improved left ventricular performance, less left ventricular dilatation, and improved survival. This study was performed to assess intrinsic hemostasis and fibrinolysis in survivors of myocardial infarction with or without antegrade perfusion of the infarct artery. Methods and Results. In 105 survivors of infarction (75 men, 30 women; age, 30 to 80 years) not given thrombolytic therapy, coronary angiography revealed a patent (group 1, n=52) or occluded (group 2, n=53) infarct artery. Plasma concentrations of plasminogen, fibrinogen, tissue plasminogen activator activity, plasminogen activator inhibitor activity, cholesterol, triglycerides, and lipoproteins, including lipoprotein(a) (Lp[a]), were measured in blood procured 23±13 (mean±SD) months after infarction. Groups 1 and 2 were similar in age, sex, race, cardioactive medications, infarct artery, extent of coronary artery disease, and left ventricular performance. Of the plasma constituents assayed, the groups were similar except that Lp(a) averaged 18.5±21.7 mg/dL in group 1 and 49.1±44.8 mg/dL in group 2 (P<.001). This difference was evident in both Caucasian (n=65) (P=.009) and African American (n=40) (P=.01) subjects. Conclusions. Survivors of myocardial infarction who failed to recanalize the infarct artery have higher plasma Lp(a) concentrations than those with a patent infarct artery. Lp(a) may inhibit intrinsic fibrinolysis.",
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T1 - Relation of plasma lipoprotein(a) to infarct artery patency in survivors of myocardial infarction

AU - Moliterno, David J.

AU - Lange, Richard A.

AU - Meidell, Robert S.

AU - Willard, John E.

AU - Leffert, Carla C.

AU - Gerard, Robert D.

AU - Boerwinkle, Eric

AU - Hobbs, Helen H.

AU - Hillis, L. David

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N2 - Background. In the minutes to days after myocardial infarction, endogenous lysis of an occlusive coronary arterial thrombus occurs in most subjects. Compared with those in whom thrombolysis does not occur, those with antegrade flow in the infarct artery have improved left ventricular performance, less left ventricular dilatation, and improved survival. This study was performed to assess intrinsic hemostasis and fibrinolysis in survivors of myocardial infarction with or without antegrade perfusion of the infarct artery. Methods and Results. In 105 survivors of infarction (75 men, 30 women; age, 30 to 80 years) not given thrombolytic therapy, coronary angiography revealed a patent (group 1, n=52) or occluded (group 2, n=53) infarct artery. Plasma concentrations of plasminogen, fibrinogen, tissue plasminogen activator activity, plasminogen activator inhibitor activity, cholesterol, triglycerides, and lipoproteins, including lipoprotein(a) (Lp[a]), were measured in blood procured 23±13 (mean±SD) months after infarction. Groups 1 and 2 were similar in age, sex, race, cardioactive medications, infarct artery, extent of coronary artery disease, and left ventricular performance. Of the plasma constituents assayed, the groups were similar except that Lp(a) averaged 18.5±21.7 mg/dL in group 1 and 49.1±44.8 mg/dL in group 2 (P<.001). This difference was evident in both Caucasian (n=65) (P=.009) and African American (n=40) (P=.01) subjects. Conclusions. Survivors of myocardial infarction who failed to recanalize the infarct artery have higher plasma Lp(a) concentrations than those with a patent infarct artery. Lp(a) may inhibit intrinsic fibrinolysis.

AB - Background. In the minutes to days after myocardial infarction, endogenous lysis of an occlusive coronary arterial thrombus occurs in most subjects. Compared with those in whom thrombolysis does not occur, those with antegrade flow in the infarct artery have improved left ventricular performance, less left ventricular dilatation, and improved survival. This study was performed to assess intrinsic hemostasis and fibrinolysis in survivors of myocardial infarction with or without antegrade perfusion of the infarct artery. Methods and Results. In 105 survivors of infarction (75 men, 30 women; age, 30 to 80 years) not given thrombolytic therapy, coronary angiography revealed a patent (group 1, n=52) or occluded (group 2, n=53) infarct artery. Plasma concentrations of plasminogen, fibrinogen, tissue plasminogen activator activity, plasminogen activator inhibitor activity, cholesterol, triglycerides, and lipoproteins, including lipoprotein(a) (Lp[a]), were measured in blood procured 23±13 (mean±SD) months after infarction. Groups 1 and 2 were similar in age, sex, race, cardioactive medications, infarct artery, extent of coronary artery disease, and left ventricular performance. Of the plasma constituents assayed, the groups were similar except that Lp(a) averaged 18.5±21.7 mg/dL in group 1 and 49.1±44.8 mg/dL in group 2 (P<.001). This difference was evident in both Caucasian (n=65) (P=.009) and African American (n=40) (P=.01) subjects. Conclusions. Survivors of myocardial infarction who failed to recanalize the infarct artery have higher plasma Lp(a) concentrations than those with a patent infarct artery. Lp(a) may inhibit intrinsic fibrinolysis.

KW - Apolipoproteins

KW - Fibrinolysis

KW - Thrombolysis

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