Necrotic myocardium

Nuclear imaging techniques, like single photon emission tomography (SPECT) and positron emission tomography (PET), directly assess myocardial perfusion, cell membrane integrity, cellular metabolism, and the molecular mechanisms of ischemic viable or necrotic myocardium, thereby indicating revascularization procedures or not. 

Siegel RJ, Said JW, Shell WE, Corson G, Fishbein MC. Identification and localization of creatine Idnase B and M in normal, ischemic and necrotic myocardium an immunohistochemical study. J Mol Coll Cardiol 1984 16 95-103. 

Fig. 7. Myocardium of male rat fed HEAR oil (22.3% erucic acid) and killed on day 112. Part of a fibrous connective tissue scar replacing necrotic myocardium. H E. x272. Bar = 50 xm.

Performing a standard coronary CTA, CT density values within the myocardium can give insight into pathologic ischemia of the myocardium, i.e., hypoperfusion or myocardial infarction, both reflected by a reduced CT density or hypoattenuation. Ischemic changes in the myocardium after coronary arterial occlusion consist of disruption of cell membrane function and integrity and increased permeability of small vessel walls. In contrast-enhanced CT, the initial area of low attenuation primarily reflects myocardial edema, i.e., a pronounced water content of the myocardium, which is followed by infiltration of inflammatory cells. Subsequently, necrotic myocardium is replaced by fibrous and/or fatty... 

At low concentrations, the catecholamines, epinephrine, and norepinephrine exert positive inotropic effects on the myocardium. High concentrations, however, can cause cardiac lesions (Balazs and Ferrans, 1978 Inoue et al., 1998). Even physiologic concentrations, when extended over time, lead to cardiac damage as shown by Szakacs and Melhnan (1960). The LD50 of norepinephrine in rats is 680 mg/kg, but at doses as low as 0.02 mg/kg, focal necrotic lesions are produced. 

On admission, some 36 h after the incident, local necrotic lymphadenopathy was present and gastrointestinal haemorrhage ensued with hypo-volaemic shock and renal failure death occurred on the third day. At autopsy, there was evidence of pulmonary oedema and haemorrhagic necrosis of the small bowel haemorrhages were observed in the lymph nodes local to the injection site, in the myocardium, testicles and pancreas. 

After intravenous injection in patients, Tc-(Sn)-pyrophosphate accumulates in regions of active osteogenesis, and also in injured myocardium, mainly in necrotic tissue (Buja et al. 1977). Uptake in infarcted myocardium in experimental model (dog) was reported as 4.4% injected dose (ID)/g, compared with 0.31% in normal myocardial tissue (Bevan et al. (1980). 

Roine et a/. (1960) were the first to report myocardial lesions in male rats fed HEAR oil. These workers conducted histological examinations on thyroid, heart, liver, spleen, kidneys, adrenal, stomach, small intestine, large intestine, aorta, and striated muscle and found lesions only in the myocardium. They described lesions that they felt resembled toxic myocarditis (interstitial edema, with variable numbers of fibroblasts, histiocytes, lymphocytes, plasma cells and neutrophils, cloudy swelling, and loss of striation of muscle fibers). Small necrotic foci were also reported. The number of sections examined from each heart or the plane of the sections was not described. Lesions were found in rats receiving 70 calorie % HEAR oil only, and not in rats fed 50 calorie % HEAR oil or less, or in the soybean oil fed controls. The number of rats per treatment was relatively low (5-9) and the duration of the feeding trial relatively short (6-7 weeks). 

Cardiac scintigraphy can be used to obtain parameters of cardiac perfusion and function. 99mTc-pyrophosphate can be used to assess acute myocardial infarction. In the case of myocardial infarction the agent localizes in the area of necrotic tissue, forming an intense spot of radioactivity. Global uptake of activity in the ventricular myocardium usually represents some other cardiac disease. 

A late uptake of contrast media after first pass in the myocardium of patients after infarction has already been observed in CT similar to MR about 20 years ago (Masuda et al. 1984). It is rather likely that this kind of myocardial enhancement may correspond to interstitial uptake of contrast media within necrotic myocytes, 6 weeks to 3 months after onset. The optimal point of time for scanning may be in between 5 and 10 min after first pass of the contrast media (Huber et al. 1981). 

In atherosclerosis, fatty material and cholesterol are deposited inside the lumen of medium- and large-sized blood vessels (arteries). Eventually, the plaque can rupture, triggering the formation of a blood clot. If the blood clot develops in the brain, it can cause a stroke if it develops in a coronary artery, it can cause a vessel occlusion and consequently a heart attack the supply of nutrients and oxygen to the heart muscle is reduced and the contractile muscle cells (cardiomyocytes) die within the blood-deprived myocardium. The tissue becomes necrotic and cardiac performances are impaired. 

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