Clinical pathologic correlates in acute myocardial infarction

C. M. Bloor, W. R. Roeske, R. A. O'Rourke

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

Abstract

In this patient population representing all patients dying after myocardial infarction who had infarct size determined at autopsy, there was a lack of correlation between infarct size and variety of clinical data including heart rates, systolic blood pressure or radiographic heart size at the time of admission. Furthermore, the MIRU class on admission (class I-IV) did not correlate significantly with the extent of infarct at the time of autopsy. In contrast to the lack of correlation from any clinical variables, the authors concluded that total (old plus new) infarct size at autopsy was indeed related to the extent of coronary atherosclerosis present at autopsy. Patients with a history of prior myocardial infarction or with left ventricular aneurysms died with a greater total (old plus new) infarct size. These data suggest that a larger total infarct is necessary to produce mortality in patients who have compensatory changes from an old infarct. The patients expiring with only a new infarct frequently have the complications of left ventricular or septal rupture. These patients died with infarct sizes which averaged 15% of left ventricular mass. The use of autopsy infarct size provides an important tool for validation of many methods that are currently involved in reducing infarct size, determined in vivo. These data suggest that infarct size correlates most highly with the extent of coronary atherosclerosis and not with the clinical variables associated with poor prognosis in an unselected population of postmyocardial infarction patients.

Original languageEnglish (US)
Pages (from-to)14-24
Number of pages11
JournalAdvances in Cardiology
VolumeVOL.23
StatePublished - Jan 1 1978
Externally publishedYes

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Fingerprint Dive into the research topics of 'Clinical pathologic correlates in acute myocardial infarction'. Together they form a unique fingerprint.

Cite this