PubMed · 13615778
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O TORGERSEN. 1958-11-15. [Diagnostic errors in epidemiological studies].. https://pubmed.ncbi.nlm.nih.gov/13615778/
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Until recently the physiological role of magnesium was essentially ignored. However, with the development of new technologies to measure the intracellular free concentration of magnesium ([Mg2+]i), the biologically important fraction, there has been an explosion of interest in the molecular, biochemical, physiological and pharmacological functions of magnesium. In addition improved methods for assessing magnesium status in the clinic have contributed to the further understanding of magnesium regulation in health and disease. Magnesium deficiency is now considered to contribute to many diseases and the role for magnesium as a therapeutic agent is being tested in numerous large clinical trials. This review focuses on clinical manifestations associated with magnesium deficiency and highlights the clinical significance of hypermagnesemia. Specific clinical conditions in which magnesium deficiency has been implicated to play a pathophysiological role, namely hypertension, ischemic heart disease, arrhythmias, prec-eclampsia, asthma and critical illness will be discussed and the possible therapeutic role of magnesium will be considered. Although there is still much to be learnt regarding the exact role of magnesium in clinical medicine, there are two conditions where magnesium is now considered the therapeutic agent of choice, pre-eclampsia and torsades de pointes. Future research, both at the fundamental and clinical levels, will certainly facilitate our understanding of how magnesium contributes to pathological processes and under what circumstances it should be used therapeutically.
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We investigated the effect that carotid plaque area (CPA) and intima media thickness (IMT) measurements have on risk stratification in 95 patients with intermediate Framingham scores (6% to 19%). The risk status of each patient was adjusted to be low, intermediate, or high based on the results of carotid ultrasound. After carotid testing, 44% (IMT) and 45% (CPA) of the intermediate-risk patients were stratified as low risk, and 22% (IMT) and 40% (CPA) were stratified as high risk. Using the threshold values derived from our laboratory, 28% (IMT) and 45% (CPA) of patients were stratified as low risk, and 35% (IMT) and 27% (CPA) were identified as high risk. These tests adjust the risk strata of >/=63% of patients deemed as having intermediate risk by Framingham scores.