The application of selected histochemical and immunohistochemical markers and procedures to the diagnosis of early myocardial damage

Abstract

Histochemical (= HIS) methods (haematoxylin-eosin, luxol fast blue, chromotrope aniline blue) and various immunohistochemical (= IH) markers (myoglobin, desmin, fibrinogen, complement C5b-9) were applied in parallel to test the efficiency, specificity and sensitivity for the recognition of early ischemic myocardial damage. The whole series was subgrouped into cardiac deaths (N = 35) and controls (N = 13). Cardiac deaths were sub-divided into 3 groups: 1. infarction visible in gross examination (N = 15), 2. coronary thrombosis without infarction (N = 11), 3. stenosing coronary atherosclerosis without infarction (N = 9). The control group (group 4) consisted of unnatural deaths with presumed short agonal periods (N = 13). Group 1 cases usually exhibited extended coagulation necrosis of the diffuse type and the contraction type in combination (1 exception). Group 2 showed mainly a patchy type of coagulation necrosis and contained 1 cases where all methods failed to react and 3 more cases where only the HIS methods failed to react. Group 3 and 4 were associated with a disseminated type of single and/or grouped fibre necrosis. In addition, the average reaction strengths showed a decrease from group 1 to group 4 which was more pronounced in the HIS reactions compared with the IH reactions. One case in group 1 showing negative IH reactions cannot be explained. Positive IH reactions observed in a few cases in group 2 contrasting with negative HIS reactions would indicate a greater sensitivity of this methodology and this interpretation also applies to groups 3 and 4. From pathophysiological considerations, the positive cases in groups 3 and 4 can be well explained.(ABSTRACT TRUNCATED AT 250 WORDS)

Markers of cardiac oxidative stress and altered morphology after intraperitoneal cocaine injection in a rat model

“…In the present study, the only myocardial lesion found corresponded to "contraction band necrosis" or "coagulative myocytolysis" or "Zenker necrosis": the two latter terms prove to be more precise due to the presence of different types of contraction bands and they indicate a necrosis of the myocardial cells in a hypercontracted state (tetanic death) characterised by rhexis of the myofibrillar apparatus, anomalous hypereosinophilic cross-bands formed by segments of hypercontracted sarcomeres with extremely thickened Z lines, as shown ultrastructurally [32,33,34,35]. Within chronological limits, the present findings confirm the conclusions of the previous human study [7]: a. Cocaine-related adrenergic overactivity does not induce extensive myocardial necrosis and thus per se is unable to explain the cardiac arrest.…”

Immunohistochemical expression of fibronectin and C5b-9 in the myocardium in cases of fatal ethanol intoxication

“…In each case, immunohistochemical reactions with the antibodies fibronectin (Polyclonal Rabbit Anti-Human, DAKO Deutschland GmbH, Hamburg, Germany) and C5b-9 (Monoclonal Mouse Anti-Human, DAKO Deutschland GmbH, Hamburg, Germany) of both cardiac ventricles (free wall of the right ventricle (RV), anterior and/or posterior wall of the left ventricle (LV)) were prepared as described elsewhere [13,14]. A blind investigation of the slides was performed by two different observers with final consensual evaluation.…”

A Forensic Pathological Approach to Sudden Cardiac Death

“…The finding of contraction band necrosis, even if microfocal, could be an important histological signal for interpreting the cause of death and the natural history of a disease in any single patient. In particular, in a sudden death resulting from myocardial infarction that is otherwise not detectable histologically (26)(27)(28), the finding of contraction band necrosis could be the marker explaining cardiac arrest as secondary to adrenergic stress. However, one must remember that in people who die suddenly and unexpectedly, the frequency of a myocardial infarction is about 20% as shown in resuscitated and electrocardiographically monitored patients (9).…”