Cardiovascular (CV) calcification is known as sub-clinical atherosclerosis and is recognised as a predictor of CV events and mortality. As yet there is no treatment for CV calcification and conventional CV risk factors are not consistently correlated, leaving clinicians uncertain as to optimum management for these patients. For this reason, a review of studies investigating diet and serum levels of macro- and micronutrients was carried out. Although there were few human studies of macronutrients, nevertheless transfats and simple sugars should be avoided, while long chain ω-3 fats from oily fish may be protective. Among the micronutrients, an intake of 800 μg/day calcium was beneficial in those without renal disease or hyperparathyroidism, while inorganic phosphorus from food preservatives and colas may induce calcification. A high intake of magnesium (≥380 mg/day) and phylloquinone (500 μg/day) proved protective, as did a serum 25(OH)D concentration of ≥75 nmol/L. Although oxidative damage appears to be a cause of CV calcification, the antioxidant vitamins proved to be largely ineffective, while supplementation of α-tocopherol may induce calcification. Nevertheless other antioxidant compounds (epigallocatechin gallate from green tea and resveratrol from red wine) were protective. Finally, a homocysteine concentration >12 µmol/L was predictive of CV calcification, although a plasma folate concentration of >39.4 nmol/L could both lower homocysteine and protect against calcification. In terms of a dietary programme, these recommendations indicate avoiding sugar and the transfats and preservatives found in processed foods and drinks and adopting a diet high in oily fish and vegetables. The micronutrients magnesium and vitamin K may be worthy of further investigation as a treatment option for CV calcification.
A review of the predictive ability of arterial and valvular calcification has shown an additive effect of calcification in more than 1 location in predicting mortality and coronary heart disease, with mitral annual calcification being a particularly strong predictor. In individual arteries and valves there is a clear association between calcification presence, extent and progression and future cardiovascular events and mortality in asymptomatic, symptomatic and high risk patients, although adjustment for calcification in other arterial beds generally renders associations non-significant. Furthermore, in acute coronary syndrome, culprit plaque is normally not calcified. This would tend to reduce the validity of calcification as a predictor and suggest that the association with cardiovascular events and mortality may not be causal. The association with stroke is less clear; carotid and intracranial artery calcification show little predictive ability, with symptomatic plaques tending to be uncalcified.
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