Abstract
The sialic acid/glycosaminoglycan ratio was determined in 35 coronary artery ectasia patients and 35 control subjects to determine the possible role of fluoride in the etiology of the disease. The coronary artery ectasia patients and controls were selected from subjects who underwent coronary angiography. The mean serum sialic acid level was significantly lower in patients with coronary artery ectasia (CAE) than in controls (340.3±28.6 vs. 427.0±15.9 ug/mL, respectively; p<0.001). The mean serum glycosaminoglycan level was significantly higher in patients with CAE than in controls (5,013.1±158.6 vs. 3,833.6±237.1 ug/mL, respectively; p<0.001). The sialic acid/glycosaminoglycan ratio in patients with coronary artery ectasia was significantly lower than in controls (0.068±0.007 vs. 0.111±0.005; p<0.001). There was more than 38.7% reduction in this ratio in patients with CAE when compared with controls. We demonstrated that chronic fluoride exposure has an important role in pathogenesis of coronary artery ectasia.
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Delayed fatal hyperkalemia in a patient with acute fluoride intoxication.
A 19-year-old man presented with acute fluoride poisoning. Initially his serum electrolytes were normal, but two hours later he developed ECG evidence of hyperkalemia followed by refractory ventricular fibrillation, suggesting that hyperkalemia may be important in the cardiotoxicity of acute fluoride intoxication. Treatment of fluoride-induced hyperkalemia consists of removal of
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Association between fluoride exposure and cardiometabolic risk in peripubertal Mexican children.
Highlights Fluoride has been added to table salt in Mexico to reduce dental caries. Human studies of fluoride exposure and metabolic syndrome are rare. We examined the association between fluoride and cardiometabolic risk factors. Fluoride may increase the risk of cardiometabolic disorders in Mexican girls. BACKGROUND: Several animal studies have suggested
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Acute fluoride toxicity: The influence of acid-base status.
The influence of preexisting acid-base disturbances on acute fluoride toxicity was studied in anesthetized rats. Metabolic acidosis was induced by the administration of NH4Cl and alkalosis by NaHCO3. Fluoride was infused i.v. until death occurred. One experiment involved intact animals (n = 18); another study used nephrectomized animals (n =
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Cardiopulmonary response to sodium fluoride infusion in the dog
Because humans are occasionally acutely exposed fluoride (F-), and cardiac and especially pulmonary to high levels of tissue accumulate higher concentrations of F- than do the other soft tissues, the present study was undertaken to investigate the effects of acute exposure to toxic plasma levels of F- on cardiopulmonary hemodynamics. Anesthesized
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Effects of melatonin and epiphyseal proteins on fluoride-induced adverse changes in antioxidant status of heart, liver, and kidney of rats
Several experimental and clinical reports indicated the oxidative stress-mediated adverse changes in vital organs of human and animal in fluoride (F) toxicity. Therefore, the present study was undertaken to evaluate the therapeutic effect of buffalo (Bubalus bubalis) epiphyseal (pineal) proteins (BEP) and melatonin (MEL) against F-induced oxidative stress in heart,
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Fluoride & Arteriosclerosis
Healthy arteries are flexible and elastic, allowing efficient transfer of blood and nutrients from the heart to the rest of the body. Arteriosclerosis refers to a stiffening of the arteries, including loss of elasticity. This is a slow, progressive disease that may begin early in life from damage to the
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Fluoride, Blood Pressure and Hypertension
Individuals with blood pressure readings that exceed 140/90 are considered hypertensive. Hypertension can increase the risk of stroke, heart attack, heart failure, aortic aneurysms, and peripheral arterial disease. An association between increased fluoride in ground water and increased prevalence of hypertension has been observed, especially among adult males (Amini et
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Fluoride & Myocardial Damage
Structural damage to the heart resulting from fluoride toxicity has been observed in numerous human and animal studies. The general features of this damage include cloudy swelling, vacuolization or vacuolar degeneration, hemorrhages, interstitial edema, fibrous necrosis, dissolution of nuclei, and thickening of the vessel walls in the heart muscle (Basha
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Fluoride & Arterial Calcification
The major change involved with cardiovascular disease is development of atherosclerosis in critical arteries, which is partially characterized by vascular calcification. The level of coronary artery calcification is thought to be the most important indicator of future cardiovascular events. Increased arterial calcifications have frequently been reported in those with skeletal fluorosis
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Fluoride & Electrocardiogram Abnormalities
An electrocardiogram (ECG) is a diagnostic test that measures the electrical activity of the heart. An ECG can reveal heart rate, heart rhythym (i.e. steady or irregular), and the strength and timing of the heart’s natural electrical signals. ECGs are described in terms of “waves” (e.g. amplitude and duration). Problems
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