Heart muscle necrosis

Heart muscle begins to die within 20-40 minutes if blood flow is not restored, and necrosis is irreversible if the coronary vessel remains occluded for more than 4-6 hours. 

It has long been known that Se deficiency results in a form of muscular dystrophy in lambs and calves and it has been shown that a complex relationship exists between the metabolism of Se, vitamin E and the polyunsaturated fatty acids. Until recently, however, no evidence had been obtained of Se deficiency in humans. Now a disease known as Keshan disease, which is responsive to Se, has been found in certain areas of China. It takes the form of a patchy necrosis of the heart muscle and is regarded as a geochemical disease resulting from a deficiency of Se in the soil and hence in the staple diet. 

Gatz and Houchin found that the degenerative processes in the heart muscle of E deficient rabbits resembled those in skeletal muscle. In the cardiac tissue which showed considerable increase of oxygen consumption the capillaries and other vessels were prominent and distended with blood. Constriction bands developed around some fibers. The view of the authors is that muscle metabolism in vitamin E deficiency becomes increased prior to the appearance of necrosis. 

Unidentified Hyaline sclerosis and calcification of blood vessels Necrosis of heart muscle Cardiac aneurysm Liver damage (32, 36, 37, 49) (36, 37) (37) (36, 37, 49)... 

Various syndromes associated with hypereosinophilia involve skeletal muscle. There is a rare form of polymyositis which is characterized by this feature (defined as exceeding 1,500 eosinophils/mm for at least six months). Clinical presentation includes skin changes, heart and lung involvement, and peripheral neuropathy as well as proximal myopathy. The condition must be distinguished from trichinosis and other parasitic infections associated with hypereosinophilia. Muscle biopsy findings are interstitial and perivascular infiltrates in which eosinophils predominate but are accompanied by lymphocytes and plasma cells, and occasional muscle fiber necrosis. Fascitis may also be associated with hypereosinophilia (Shulman s syndrome). This condition is characterized by painful swelling of skin and soft tissues of trunk and extremities and weakness of limb muscles. Biopsy of muscle... 

Sodium and fluid retention, congestive heart failure in susceptible patients, potassium loss, hypokalemic alkalosis, hypertension Muscle weakness, steroid myopathy, loss of muscle mass, vertebral compression fractures, aseptic necrosis of humeral and femoral heads, pathologic fracture of long bones, osteoporosis Peptic ulcer with possible perforation and hemorrhage, pancreatitis, abdominal distension, ulcerative esophagitis... 

In 1957, Schwartz and associates showed that the toxic element selenium was also a nutritional factor essential for prevention of the death of liver cells in rats.527 Liver necrosis would be prevented by as little as 0.1 ppm of selenium in the diet. Similar amounts of selenium were shown to prevent a muscular dystrophy called "white muscle disease" in cattle and sheep grazing on selenium-deficient soil. Sodium selenite and other inorganic selenium compounds were more effective than organic compounds in which Se had replaced sulfur. Keshan disease, an often fatal heart condition that is prevalent among childen in Se-deficient regions of China, can be prevented by supplementation of the diet with NaSe03.528 Even the little crustacean "water flea" Daphnia needs 0.1 part per billion of Se in its water.529... 

The findings of toxic effects in the heart, stomach, blood, muscles, and kidneys of humans who were dermally exposed to chromium compounds is suggestive of distribution to these organs (see Section 2.2.3.2). Fourteen days after a salve containing potassium chromate(VI) was applied to the skin of an individual to treat scabies, appreciable amounts of chromium were found in the blood (2-5 mg/100 mL), urine (8 mg/L), feces (0.61 mg/100 g), and stomach contents (0.63 mg/100 mL) (Brieger 1920). The preexisting condition of scabies or the necrosis caused by the potassium chromate could have facilitated its absorption. A transient increase in the levels of total chromium in erythrocytes and plasma was observed in subjects immersed in a tank of chlorinated water containing potassium dichromate(VI) (Corbett et al. 1997). 

Transaminases Alanine aminotransferase (ALT) Aspartate aminotransferase (AST) Liver, heart, skeletal muscle 0 0 lU/L 0 0 lU/L Raised levels indicate hepatocyte damage/necrosis ALT is more liver specific but has a longer half-life, so less sensitive May be normal in compensated liver cirrhosis... 

Tacrolimus causes acute reversible renal dysfunction in renal [661-663,667], hver [290,664-666,679,680], heart [681-683] and pulmonary [684, 685] transplant recipients and in patients with immunologically mediated diseases [686]. Tacrolimus-induced GFR and RBF decrease is associated with an important increase in renal vascular resistance, both in humans and rodents [63,679,687-692]. Calcium channel blockers improved renal function in TAC-treated liver transplant recipients [693] and in animal models of TAC nephrotoxicity [689,694-6%]. Tacrohmus acute nephrotoxicity, similar to CSA, shows normal renal histology or non-specific changes such as isometric cytoplasmic vacuolation in tubular epithelial cells, microcalcification, giant mitochondria and lysosomes, and necrosis and early hyahnosis of individual smooth muscle cells in the afferent arterioles, which revert with drug reduction or discontinuation [697-699]. 

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