Background and Purpose-The value of warfarin in preventing stroke in patients with chronic atrial fibrillation is well established. However, the prevalence of such treatment generally lags behind actual requirements. The aim of this study was to evaluate doctor-and/or patient-related demographic, clinical, and echocardiographic factors that influence decision for warfarin treatment. Methods-Between 1990 and 1998, 1027 patients were discharged with chronic or persistent atrial fibrillation. This population was composed of (1) patients with cardiac prosthetic valves (nϭ48), (2) those with increased bleeding risks (nϭ152), (3) physically or mentally handicapped patients (nϭ317), and (4) the remaining 510 patients, the main study group who were subjected to thorough statistical analysis for determining factors influencing warfarin use.

Objectives: To determine the prevalence of hypomagnesaemia and hypermagnesaemia, to discern various factors associated with abnormal serum magnesium, and to estimate prognostic significance of serum magnesium aberrations in patients with congestive heart failure. Design: Observational study. Setting: Medical department of a university hospital (tertiary referral centre). Patients: 404 consecutive patients admitted with congestive heart failure as one of the diagnoses and previously treated with furosemide (frusemide) for at least three months. Main outcome measures: Clinical, biochemical, and electrocardiographic variables were analysed with respect to serum magnesium aberrations. Following discharge, mortality rates, including sudden death, were registered. Results: Hypomagnesaemia was found in 50 patients (12.3%) and 20 (4.9%) were hypermagnesaemic. Female sex (p < 0.04), diabetes mellitus (p < 0.006), hypocalcaemia (p = 0.03), hyponatraemia (p < 0.05), malignant disease (p = 0.05), and high fever (p = 0.05) were statistically associated with hypomagnesaemia. Renal failure, severe congestive heart failure, and high dose furosemide treatment (> 80 mg/day) were associated with hypermagnesaemia (p < 0.001, p = 0.05, and p < 0.03, respectively). Hypermagnesaemic patients were older and weighed less. On follow up (median duration 43 months), 169 (41.8%) died, with 22 (13%) sudden deaths. Mortality was highest with hypermagnesaemia, lowest with normomagnesaemia, and intermediate with hypomagnesaemia. After adjustment for renal failure, old age, and severity of congestive heart failure, hypomagnesaemia but not hypermagnesaemia emerged as being significantly associated with shorter survival (p = 0.009). No statistical association was found between sudden death and magnesium concentrations. Conclusions: While hypermagnesaemia seems to represent a prognostic marker only, hypomagnesaemia appears to have an adverse pathophysiological effect. The subgroup of patients at risk for hypomagnesaemia requires frequent serum magnesium determinations and magnesium replacement for as long as hypomagnesaemia persists. M agnesium is the second most abundant intracellular cation after potassium. Ninety nine per cent of total body magnesium is located intracellularly, so that less than 1% is restricted to the serum. Magnesium plays a key role in a variety of enzymatic reactions. Thus more than 300 enzyme systems, including all ATPases, are magnesium dependent. In addition to energy-requiring metabolic processes and anaerobic phosphorylation, magnesium is involved in protein and DNA synthesis as well as in transmembrane transport mechanisms.

Heart failure (HF) is a prevalent syndrome resulting in a high mortality rate. HF may be associated with zinc deficiency through a reduction in dietary intake, decreased absorption due to gastrointestinal edema, impaired motility or intestinal zinc losses. Diseases concomitant with HF such as diabetes mellitus (DM) and hypertension may enhance zinc deficiency. Medications given for HF may affect zinc metabolism in different ways. It was shown that thiazides may cause zincuria and a decrease in tissue zinc concentration. There is conflicting evidence about furosemide, even though patients with chronic furosemide treatment showed low tissue zinc levels in autopsies. Treatment with angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) resulted in zincuria and zinc deficiency, but this outcome was not consistent in all studies. Beta-blockers did not alter plasma zinc concentration. Matrix metalloproteinases (MMPs) and ACE are zinc-containing enzymes, which play a role in the process of remodeling in HF. It was shown that ACE inhibitors may inhibit the activity of different MMPs. The exact interrelationship between HF, zinc-containing enzymes, zinc deficiency and the clinical manifestation of HF has to be investigated.