Roberts, W. C. (2018). “Cardiac rupture during acute myocardial infarction diagnosed clinically.” Coron Artery Dis 29(2): 95-96.
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Rencuzogullari et al. from Kars, Izmir, and Istanbul, Turkey, compared clinical observations in 33 patients with cardiac rupture during acute myocardial infarction (AMI) to observations in 1630 patients, also with AMI but without clinical evidence of cardiac rupture. Compared with the patients without cardiac rupture, those with rupture had a greater percent in Kilip classes II–IV: higher leukocyte counts, higher levels of C-reactive protein, creatinine kinase MB, and peak troponin I; higher frequencies of the thrombus in the left anterior descending coronary artery, higher basal syntax scores, and syntax II percutaneous coronary intervention scores. The systolic blood pressures, glomerular filtration rates, left ventricular ejection fractions, and hemoglobin values were lower. Many of these relations have not been described previously in patients with AMI and cardiac rupture compared with those with AMI but without cardiac rupture. All patients in their study underwent percutaneous coronary intervention, a procedure that may have effects on some of these factors. What are some potential and real problems with this clinical study? Cardiac rupture during AMI is not easily diagnosed clinically, particularly when the rupture site is the left ventricular free wall, the most common rupture site during AMI. Some cases in this clinical study classified as cardiac rupture probably did not have cardiac rupture, and some cases classified as no cardiac rupture probably did have cardiac rupture. Autopsies were not done in any of their patients or, if so, the results of such studies were not reported. Autopsy or surgery, in actuality, may be the only means of accurately diagnosing cardiac rupture if it involves the left ventricular free wall. A relatively high early survival rate (nearly 50% at 30 days) in their rupture cases also raises some doubt of the accuracy of their diagnosis of rupture during life. The type of cardiac rupture was not specified by these authors, namely whether it involved the left ventricular free wall or ventricular septum or a papillary muscle. The latter two are far less frequent than the former and the former is much more difficult to diagnose clinically than the latter two. It might be useful to compare some findings in autopsy-documented cases of cardiac rupture secondary to AMI to autopsy-documented cases of AMI without cardiac rupture. Table 1 summarizes a number of studies 2–15 performed by me and my colleagues, and Table 2 focuses on factors distinguishing cardiac rupture cases from nonruptured autopsy cases during AMI 2–I15. I suspect that some of the observations of the present authors that are at variance with previous principles learned in patients studied at autopsy with cardiac rupture during AMI are probably related to errors in diagnosis of cardiac rupture. As mentioned, left ventricular free wall rupture is by far the most common site of cardiac rupture during AMI and it is often impossible to get an echocardiogram recorded to search for hemopericardium before the fatality occurs. Nevertheless, the authors made a valiant attempt to diagnose cardiac rupture clinically and to compare numerous variables to their nonrupture cases. Such studies are not easy particularly when the ‘instruments of precision’ are less than ideal when diagnosing cardiac rupture secondary to AMI clinically. (Excerpt from text, p. 95; no abstract available.)
