Thrombolysis in postinfarction angina

Pamela Ouyang, Edward Shapiro, Sidney O. Gottlieb

Research output: Contribution to journalArticle

Abstract

Postinfarction angina carries a poor prognosis, with a 20-70% incidence of recurrent myocardial infarction (MI) or death within the subsequent 3-6 months. The pathophysiologic mechanisms causing postinfarction angina may include thrombus, complex coronary arterial lesions that form a nidus for thrombus formation, inadequate collateral supply following acute MI, or intimal endothelial dysfunction. The role of thrombus has been established in the pathophysiology of Q-wave MI, and thrombolytic treatment of patients presenting with acute transmural MI has been shown to salvage left ventricular function and to reduce mortality. However, thrombolytic therapy for the acute MI does not reduce the incidence of recurrent ischemia or infarction, as is evident from the 18-26% incidence of recurrent ischemia reported in the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) and Thrombolysis in Myocardial Infarction (TIMI) trials. In the Gruppo Itaiiano per lo Studio della Streptochinasi nell Infarto Miocardico (GISSI) study the incidence of reinfarction was documented as 4% in the streptokinase group, which was actually significantly greater than in the placebo group (2%). In a randomized placebo-controlled study of thrombolysis for postinfarction angina, 29 patients were randomized to placebo (P group, n = 17) or to thrombolytic therapy (T group, n = 12). Patient groups were similar with respect to age, location of MI, ejection fraction, severity of coronary artery disease, and antianginal therapy. Patients underwent coronary angtography 6 ± 1 days postinfarction. Filling defects consistent with intracoronary thrombus was seen in 11 of 12 T group patients and in 11 of 17 P group patients prior to treatment. Lysis occurred in 7 of 11 T patients and 1 of 11P (p <0.02). Holter-detected silent ischemia was compared pre- and posttherapy. Of patients with pretherapy Holter studies, silent ischemia occurred in 8 of 15 P patients (1.7 ± 0.33 episodes/24 hr, lasting 27.9 ± 12.1 min/24 hr) and in 2 of 9 T patients (0.6 ± 0.4 episodes/24 hr lasting 9.4 ± 3.1 min/24 hr). There was no significant change in the amount of silent ischemia following therapy in either group. Clinical ischemic events occurred in 3 of 12 T patients and in 5 of 17 P patients (no difference between the 2 groups). This study showed that thrombus was commonly seen in patients with postinfarction angina, and thrombolytic therapy could successfully lyse the clot 6 days postinfarction. However, despite achieving successful thrombolysis, in patients who were already receiving an intensive antianginal regimen for postinfarction angina, thrombolytic therapy did not result in an improvement in Holter-detected or clinical ischemia.

Original languageEnglish (US)
JournalThe American Journal of Cardiology
Volume68
Issue number7
DOIs
StatePublished - Sep 3 1991

Fingerprint

Myocardial Infarction
Ischemia
Thrombolytic Therapy
Thrombosis
Placebos
Incidence
Tunica Intima
Streptokinase
Therapeutics
Angioplasty
Left Ventricular Function
Infarction
Coronary Artery Disease
Cohort Studies
Mortality

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Thrombolysis in postinfarction angina. / Ouyang, Pamela; Shapiro, Edward; Gottlieb, Sidney O.

In: The American Journal of Cardiology, Vol. 68, No. 7, 03.09.1991.

Research output: Contribution to journalArticle

@article{5181985eb5334a7983e9a86196f68d5c,
title = "Thrombolysis in postinfarction angina",
abstract = "Postinfarction angina carries a poor prognosis, with a 20-70{\%} incidence of recurrent myocardial infarction (MI) or death within the subsequent 3-6 months. The pathophysiologic mechanisms causing postinfarction angina may include thrombus, complex coronary arterial lesions that form a nidus for thrombus formation, inadequate collateral supply following acute MI, or intimal endothelial dysfunction. The role of thrombus has been established in the pathophysiology of Q-wave MI, and thrombolytic treatment of patients presenting with acute transmural MI has been shown to salvage left ventricular function and to reduce mortality. However, thrombolytic therapy for the acute MI does not reduce the incidence of recurrent ischemia or infarction, as is evident from the 18-26{\%} incidence of recurrent ischemia reported in the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) and Thrombolysis in Myocardial Infarction (TIMI) trials. In the Gruppo Itaiiano per lo Studio della Streptochinasi nell Infarto Miocardico (GISSI) study the incidence of reinfarction was documented as 4{\%} in the streptokinase group, which was actually significantly greater than in the placebo group (2{\%}). In a randomized placebo-controlled study of thrombolysis for postinfarction angina, 29 patients were randomized to placebo (P group, n = 17) or to thrombolytic therapy (T group, n = 12). Patient groups were similar with respect to age, location of MI, ejection fraction, severity of coronary artery disease, and antianginal therapy. Patients underwent coronary angtography 6 ± 1 days postinfarction. Filling defects consistent with intracoronary thrombus was seen in 11 of 12 T group patients and in 11 of 17 P group patients prior to treatment. Lysis occurred in 7 of 11 T patients and 1 of 11P (p <0.02). Holter-detected silent ischemia was compared pre- and posttherapy. Of patients with pretherapy Holter studies, silent ischemia occurred in 8 of 15 P patients (1.7 ± 0.33 episodes/24 hr, lasting 27.9 ± 12.1 min/24 hr) and in 2 of 9 T patients (0.6 ± 0.4 episodes/24 hr lasting 9.4 ± 3.1 min/24 hr). There was no significant change in the amount of silent ischemia following therapy in either group. Clinical ischemic events occurred in 3 of 12 T patients and in 5 of 17 P patients (no difference between the 2 groups). This study showed that thrombus was commonly seen in patients with postinfarction angina, and thrombolytic therapy could successfully lyse the clot 6 days postinfarction. However, despite achieving successful thrombolysis, in patients who were already receiving an intensive antianginal regimen for postinfarction angina, thrombolytic therapy did not result in an improvement in Holter-detected or clinical ischemia.",
author = "Pamela Ouyang and Edward Shapiro and Gottlieb, {Sidney O.}",
year = "1991",
month = "9",
day = "3",
doi = "10.1016/0002-9149(91)90394-Z",
language = "English (US)",
volume = "68",
journal = "American Journal of Cardiology",
issn = "0002-9149",
publisher = "Elsevier Inc.",
number = "7",

}

TY - JOUR

T1 - Thrombolysis in postinfarction angina

AU - Ouyang, Pamela

AU - Shapiro, Edward

AU - Gottlieb, Sidney O.

PY - 1991/9/3

Y1 - 1991/9/3

N2 - Postinfarction angina carries a poor prognosis, with a 20-70% incidence of recurrent myocardial infarction (MI) or death within the subsequent 3-6 months. The pathophysiologic mechanisms causing postinfarction angina may include thrombus, complex coronary arterial lesions that form a nidus for thrombus formation, inadequate collateral supply following acute MI, or intimal endothelial dysfunction. The role of thrombus has been established in the pathophysiology of Q-wave MI, and thrombolytic treatment of patients presenting with acute transmural MI has been shown to salvage left ventricular function and to reduce mortality. However, thrombolytic therapy for the acute MI does not reduce the incidence of recurrent ischemia or infarction, as is evident from the 18-26% incidence of recurrent ischemia reported in the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) and Thrombolysis in Myocardial Infarction (TIMI) trials. In the Gruppo Itaiiano per lo Studio della Streptochinasi nell Infarto Miocardico (GISSI) study the incidence of reinfarction was documented as 4% in the streptokinase group, which was actually significantly greater than in the placebo group (2%). In a randomized placebo-controlled study of thrombolysis for postinfarction angina, 29 patients were randomized to placebo (P group, n = 17) or to thrombolytic therapy (T group, n = 12). Patient groups were similar with respect to age, location of MI, ejection fraction, severity of coronary artery disease, and antianginal therapy. Patients underwent coronary angtography 6 ± 1 days postinfarction. Filling defects consistent with intracoronary thrombus was seen in 11 of 12 T group patients and in 11 of 17 P group patients prior to treatment. Lysis occurred in 7 of 11 T patients and 1 of 11P (p <0.02). Holter-detected silent ischemia was compared pre- and posttherapy. Of patients with pretherapy Holter studies, silent ischemia occurred in 8 of 15 P patients (1.7 ± 0.33 episodes/24 hr, lasting 27.9 ± 12.1 min/24 hr) and in 2 of 9 T patients (0.6 ± 0.4 episodes/24 hr lasting 9.4 ± 3.1 min/24 hr). There was no significant change in the amount of silent ischemia following therapy in either group. Clinical ischemic events occurred in 3 of 12 T patients and in 5 of 17 P patients (no difference between the 2 groups). This study showed that thrombus was commonly seen in patients with postinfarction angina, and thrombolytic therapy could successfully lyse the clot 6 days postinfarction. However, despite achieving successful thrombolysis, in patients who were already receiving an intensive antianginal regimen for postinfarction angina, thrombolytic therapy did not result in an improvement in Holter-detected or clinical ischemia.

AB - Postinfarction angina carries a poor prognosis, with a 20-70% incidence of recurrent myocardial infarction (MI) or death within the subsequent 3-6 months. The pathophysiologic mechanisms causing postinfarction angina may include thrombus, complex coronary arterial lesions that form a nidus for thrombus formation, inadequate collateral supply following acute MI, or intimal endothelial dysfunction. The role of thrombus has been established in the pathophysiology of Q-wave MI, and thrombolytic treatment of patients presenting with acute transmural MI has been shown to salvage left ventricular function and to reduce mortality. However, thrombolytic therapy for the acute MI does not reduce the incidence of recurrent ischemia or infarction, as is evident from the 18-26% incidence of recurrent ischemia reported in the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) and Thrombolysis in Myocardial Infarction (TIMI) trials. In the Gruppo Itaiiano per lo Studio della Streptochinasi nell Infarto Miocardico (GISSI) study the incidence of reinfarction was documented as 4% in the streptokinase group, which was actually significantly greater than in the placebo group (2%). In a randomized placebo-controlled study of thrombolysis for postinfarction angina, 29 patients were randomized to placebo (P group, n = 17) or to thrombolytic therapy (T group, n = 12). Patient groups were similar with respect to age, location of MI, ejection fraction, severity of coronary artery disease, and antianginal therapy. Patients underwent coronary angtography 6 ± 1 days postinfarction. Filling defects consistent with intracoronary thrombus was seen in 11 of 12 T group patients and in 11 of 17 P group patients prior to treatment. Lysis occurred in 7 of 11 T patients and 1 of 11P (p <0.02). Holter-detected silent ischemia was compared pre- and posttherapy. Of patients with pretherapy Holter studies, silent ischemia occurred in 8 of 15 P patients (1.7 ± 0.33 episodes/24 hr, lasting 27.9 ± 12.1 min/24 hr) and in 2 of 9 T patients (0.6 ± 0.4 episodes/24 hr lasting 9.4 ± 3.1 min/24 hr). There was no significant change in the amount of silent ischemia following therapy in either group. Clinical ischemic events occurred in 3 of 12 T patients and in 5 of 17 P patients (no difference between the 2 groups). This study showed that thrombus was commonly seen in patients with postinfarction angina, and thrombolytic therapy could successfully lyse the clot 6 days postinfarction. However, despite achieving successful thrombolysis, in patients who were already receiving an intensive antianginal regimen for postinfarction angina, thrombolytic therapy did not result in an improvement in Holter-detected or clinical ischemia.

UR - http://www.scopus.com/inward/record.url?scp=0026009310&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026009310&partnerID=8YFLogxK

U2 - 10.1016/0002-9149(91)90394-Z

DO - 10.1016/0002-9149(91)90394-Z

M3 - Article

C2 - 1892059

AN - SCOPUS:0026009310

VL - 68

JO - American Journal of Cardiology

JF - American Journal of Cardiology

SN - 0002-9149

IS - 7

ER -