Heart lesions

In developed countries endocarditis is present in 1/1000 hospital admissions or 1-2 cases per million population. An increasing number of endocarditis cases are associated with intravascular device infections and the placement of prosthetic valves thus, endocarditis can be acquired during hospital stay. Men are afflicted more often than females, and most patients are >50 years of age. Pre-existing heart lesions predispose to bacterial endocarditis if they are accompanied by (thrombotic) alterations of the endocardial surface or blood flow such that bacteria... 

Patients with the non-obstructive form of hypetrophic cardiomyopathy should not undergo septal ablation. Patients with congential anomalies of the mitral valve apparatus, associated heart lesions (e.g., advanced multivessel coronary artery disease) requiring surgical correction, unfavorable distribution of septal hypertrophy with mild proximal thickening, basal septal wall thickness < 18 mm, or anatomically unsuitable septal perforators should not be candidates for septal ablation. 

Heart lesions consisting of focal myocytolysis with or without fibrosis and/or calcification were consistently observed in mice receiving the highest dosage of DMH and also in one-third of those receiving the intermediate dose (Table X). The dose response relation is relatively strong (P <. 001) but no evidence was found that pathology in the heart was affected by dietary protein. 

Adverse effects are uncommon. Patients taking penicillin prophylaxis are liable to have penicillin-resistant viridans type streptococci in the mouth, so that during even minor dentistry, e.g. scaling, there is a risk of bacteraemia and thus of infective endocarditis with a penicillin-resistant organism in those with any residual rheumatic heart lesion. The same risk applies to urinary, abdominal and chest surg-... 

Cardiovascular effects in animals were investigated by histopathological examination in one study. Intermittent 90-day dermal exposure to 500 mg/kg/day of 1,1,1-trichloroethane (uncovered) had no effect on heart weight or the incidence of heart lesions in rabbits (Torkelson et al. 1958). A NOAEL derived from this study is recorded in Table 2-3. Much higher doses may be required to produce effects by the dermal route high vapor concentrations were required to produce cardiotoxic effects by inhalation exposure, and percutaneous absorption of 1,1,1-trichloroethane is much slower and less complete than pulmonary absorption. 

Hoffman, J. I. E., Rudolph, A. M., and Heymann, M. A. (1981). Pulmonary vascular disease with congenital heart lesions Pathologic features and causes. Circulation 64,... 

Cobalt is an essential element. Its deficiency can result in pernicious anemia. It is present in vitamin B12. Excessive intake of this element may result in polycythemia or overproduction of erythrocytes and heart lesions. Exposure to its dusts can produce cough and respiratory irritation. Chronic inhalation of its dusts or fumes can decrease pulmonary functions and may cause diffuse nodular fibrosis and other pulmonary diseases. Skin contact may induce dermal hypersensitivity reactions, producing an allergy-type dermatitis. 

Diet Strain of male rat" Length of feeding-(weeks) Heart lesions Ref. ... 

In order to eliminate one of the variables, i.e., the level of fat in the diet, HEAR oil was diluted with either sunflower oil (Abdellatif and Vies, 1973) or a 3 to 1 lard/corn oil mixture (Beare-Rogers et al., 1972b), and the level of fat in the diet was maintained at a constant level. In both experiments, as the proportion of HEAR oil increased, so did the incidence of heart lesions... 

Fig. 1). It is, however, interesting to observe that whereas with lard/corn oil control diets there was a zero incidence of heart lesions, when sunflower oil diets were used as controls, the heart lesion incidence was 29%. This suggests that myocardial necrosis can be reduced quite effectively by saturated fatty acids, while a mixture of polyunsaturated fatty acids, as in sunflower oil, is not as effective. It must be kept in mind, however, that in these two experiments both the rat strain and the experimental feeding period were different. Wistar rats were fed the sunflower oil mixtures for 32 weeks, while the Sprague-Dawley rats were fed the lard/corn oil mixtures for only 16 weeks. 

It is quite evident from the results in Table III that male rats fed diets containing high levels of HEAR oil will develop myocardial necrosis. These heart lesions can also be produced by feeding an equal mixture of trierucin and sunflower oil at 60 calorie % (Abdellatif and Vies, 1973) with a level of 22 1 in the oil of about 42% (Table V). Subsequently, this finding was confirmed when rats were fed olive oil interesterified with erucic acid to give a mixture which contained 30% 22 1 (Beare-Rogers, 1975). 

Scientists from the University of Guelph (McCutcheon et ai, 1976) repeated the earlier study by Abdellatif and Vies (1973) and found that erucic acid will increase heart lesions irrespective of the source of erucic acid, i.e., whether from a HEAR oil or from a non-Brass/ca source, such as nasturtium seed (Tropaeolum majus) (Table V). They reported that removal of linolenic acid (18 3) from a simulated HEAR oil which contained 28.7% 22 1 resulted in a significant reduction in the severity of heart lesions. On the other hand, increasing the level of linoleic acid (18 2) in a HEAR oil or a simulated HEAR oil had no apparent effect. These results suggest that there may be an interaction of erucic and linolenic acid, or that linolenic acid predisposes the heart to lesions. 

Reference for severity categories of heart lesions 1, Abdellatif and Vies (1973) mild (1), moderate (2), definite (3), and severe (4) cellular and/or fibrotic scars 1, McCutcheon et al. (1976) fresh (1) and old (2) myocardial necrosis and microvascular alterations (3) 3, Astorg and Levillain (1979) histiocytes (1), granules (2), and granules and necrosis (3). 

In studies with HEAR oils mainly two strains of albino rats, Sprague-Daw-ley and Wistar, have been used. There appears to be little difference in heart lesion response to HEAR oil between these two strains. Hulan et al. (1977) observed that male Chester Beatty (hooded) rats were resistant to the formation of myocardial necrosis. A subsequent study showed that this strain of rat did not develop a higher incidence of heart lesion with HEAR oil (26% 22 1) than with corn oil (Kramer et ai, 1979). These results were confirmed (Clan-dinin and Yamashiro, 1980), and suggest that the cardiac lesions are strain specific. 

Test oil % Fat in diet % 22 1 in oil Strain Sex Time on diet (weeks) Heart lesions Ref."... 

Ziemlanski et al. (1972) fed HEAR oil, hydrogenated HEAR oil, and a number of experimentally produced margarines to rats and produced heart lesions, which they referred to as histiocytic granulomas. These lesions consisted of small necrotic foci, surrounded by histiocytic granulomas and focal fibrosis. They found no myocardial lesions in rats fed a standard diet (7% fat) for 7 and 12 months. 

Clandinin and Yamashiro (1980) have recently pointed out that if the methionine per calorie ratio is calculated for rat diets containing 20% casein and 20% fat (4500 kcal/kg ME), the diet is apparently deficient in methionine. However, these workers were not able to demonstrate a consistent improvement in weight gains when rats were fed the diet supplemented with methionine. An experiment carried out in this laboratory indicated that methionine supplementation did improve weight gains but the choline level of the diet had no effect. Neither the choline nor the methionine status of the diet affected the incidence or severity of heart lesions (Farnworth et a ., 1982a). 

E. The Relationship of Dietary Fatty Acids to Heart Lesions. 453... 

As indicated in Table III, female rats of all strains are less susceptible to the development of myocardial lesions than male rats fed control or rapeseed oil containing diets. In general, male rats of the albino strain have a higher incidence and severity of myocardial lesions when fed isocaloric amounts of LEAR oils than when fed other vegetable oils. The incidence and severity of heart lesions are similar in female rats fed control or LEAR oils. 

The duration of most experiments reported to date is 16 to 26 weeks. The results of Table V show the reason for this. Almost no myocardial lesions were observed when weanling rats were fed experimental diets for 4 weeks lesions began to appear after 8 weeks and were quite evident at 16 weeks. Further feeding up to 1 year continues to increase the incidence and severity of heart lesions even more, but at a somewhat slower rate as shown in Fig. 1. If we assume the lifespan of the rat to be 36 months, then a maximum number of lesions have developed when rats have reached about 10 percent of their life-span. 

The results show that the incidence of heart lesions in male rats is not altered by increasing the level of protein from 20 to 25% (Beare-Rogers et a., 1974), or by substituting different quality proteins, i.e., casein vs. a casein-soybean meal mixture (Vies etai, 1976). Some recent publications suggest that the methionine content in the rat diets may be deficient if casein is fed as the only source of protein and that methionine deficiency increases the incidence of heart lesions (Clandinin and Yamashiro, 1980, 1982). Different results were obtained by Farnworth et al. (1982c), who found that the addition of methionine to casein-containing diets improved the growth of rats but that the incidence of heart lesions was not affected. 

The data in Table VII to XI summarize the available published data from different research centers on heart lesions in male rats produced by feeding diets rich in LEAR and control oils. 

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