Circulation, Vol 73, 749-757, Copyright © 1986 by American Heart Association
H Fujiwara, T Onodera, M Tanaka, T Fujiwara, DJ Wu, C Kawai and Y Hamashima
Hemorrhagic acute myocardial infarction (AMI) was studied after selective
intracoronary thrombolysis (SICT) in 30 patients undergoing autopsy.
Urokinase, 240,000 to 1,200,000 U, was selectively injected into the
infarct-related coronary artery at 2 to 9 hr (4 +/- 2 hr) after the onset
of AMI. The infarct-related coronary artery showed complete occlusion in
21, 99% stenosis in eight, and 90% stenosis in one patient before SICT.
After SICT, complete occlusion was seen in only five, 99% stenosis in 22,
and 90% stenosis in three patients. Twenty-eight patients had transmural
infarction and the other two had subendocardial infarction. Macroscopically
and microscopically, the degree of hemorrhage was classified as no, slight,
moderate, or marked bleeding and the hemorrhagic infarction was defined as
moderate or marked diffuse bleeding in the infarct area. According to the
interval from SICT to death, patients were also classified into stage I
(early acute stage, 1 to 4 hr after SICT and 4 to 13 hr after the onset of
AMI; n = 7), stage II (late acute stage, 9 hr to 11 days after SICT and 15
hr to 11 days after the onset of AMI; n = 18), or stage III (old infarction
stage, over 17 days after AMI and SICT; n = 5). There were no significant
differences with respect to the frequency of recanalization, the time from
the onset of AMI to SICT, the dose of urokinase, or other clinical
parameters among patients at the three stages. Only the hearts of patients
in stage II showed hemorrhagic infarction, and it was found in 15 of 18 of
these hearts.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
A clinicopathologic study of patients with hemorrhagic myocardial infarction treated with selective coronary thrombolysis with urokinase
This article has been cited by other articles:
 |
|
 |
|
  H. Fonge, K. Vunckx, H. Wang, Y. Feng, L. Mortelmans, J. Nuyts, G. Bormans, A. Verbruggen, and Y. Ni Non-invasive detection and quantification of acute myocardial infarction in rabbits using mono-[123I]iodohypericin {micro}SPECT Eur. Heart J., January 2, 2008; 29(2): 260 - 269. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G R Rhydwen, S Charman, and P M Schofield Influence of thrombolytic therapy on the patterns of ventricular septal rupture after acute myocardial infarction Postgrad. Med. J., July 1, 2002; 78(921): 408 - 412. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Asanuma, K. Tanabe, K. Ochiai, H. Yoshitomi, K. Nakamura, Y. Murakami, K. Sano, T. Shimada, R. Murakami, S. Morioka, et al. Relationship Between Progressive Microvascular Damage and Intramyocardial Hemorrhage in Patients With Reperfused Anterior Myocardial Infarction : Myocardial Contrast Echocardiographic Study Circulation, July 15, 1997; 96(2): 448 - 453. [Abstract] [Full Text]
|
|
|
|
|
|
S. V. Pislaru, L. Barrios, T. Stassen, L. Jun, C. Pislaru, and F. Van de Werf Infarct Size, Myocardial Hemorrhage, and Recovery of Function After Mechanical Versus Pharmacological Reperfusion : Effects of Lytic State and Occlusion Time Circulation, July 15, 1997; 96(2): 659 - 666. [Abstract] [Full Text]
|
|
|
|
|
|
Y. Ohnishi, M. C. Butterfield, J. E. Saffitz, B. E. Sobel, P. B. Corr, and J. A. Goldstein Deleterious Effects of a Systemic Lytic State on Reperfused Myocardium : Minimization of Reperfusion Injury and Enhanced Recovery of Myocardial Function by Direct Angioplasty Circulation, August 1, 1995; 92(3): 500 - 510. [Abstract] [Full Text]
|
|
|
|
 |
|
 T. Tomaru, Y. Uchida, H. Sonoki, M. Tsukamoto, and T. Sugimoto The Thrombolytic Effects of Native Tissue-Type Plasminogen Activator (AK-124) on Experimental Canine Coronary Thrombosis Angiology, May 1, 1989; 40(5): 429 - 435. [Abstract] [PDF]
|
|