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Biomedical subjects

M Elisaf

Publications and source records attributed to M Elisaf.

At least 19 recordsLinked to original sources
PubMed2006

Statins and solid organ transplantation.

Dyslipidaemia is common in solid organ transplant recipients and its presence is associated with chronic rejection and accelerated atherosclerosis, leading to an increased prevalence of cardiovascular disease (CVD). CVD is a major cause of morbidity and mortality in transplant recipients. It is therefore of interest and clinical value to introduce agents that effectively and safely reduce the incidence of this outcome. In the present review we consider the potential benefits of statin administration in adults who have undergone solid organ (mainly renal, heart and liver) transplantation, as well as in paediatric transplant patients. We also briefly review the effects of combination therapy with ezetimibe and statins in this population. Overall, statins are efficient and safe drugs for the management of dyslipidaemias in transplant populations, and in most trials they had a beneficial effect on long-term survival rates, CVD events and rejection rates. The transplanted population is different from other patient groups, mostly due to concomitant immunosuppressive therapy. Statins, at an appropriate dosage, should be prescribed to dyslipidaemic transplanted patients but they should be closely monitored for adverse effects.

Adolescent↗
PubMed2005

The predictive value of lipid markers in vascular disease.

Lipid markers are well established predictors of vascular disease. The most frequently measured lipid variables are total cholesterol, high density lipoprotein cholesterol, low density lipoprotein cholesterol and triglycerides. In this review we consider the predictive value of these variables and other more specialised related tests. We also discuss the effect of lipid altering drugs on these markers. The interaction of other vascular risk factors and the lipid effects of non-lipid altering drugs (e.g. blood pressure lowering agents) are also briefly described. Similarly, we discuss the effects of lipid lowering drugs on non-lipid vascular risk factors. Finally, we briefly consider the effect of altering the lipid profile on surrogate markers and events associated with atherosclerosis.

Animals↗
PubMed2005

Effect on serum uric acid levels of drugs prescribed for indications other than treating hyperuricaemia.

Beyond allopurinol and the well-established uricosuric drugs, several other agents can decrease serum uric acid (SUA) levels, such as losartan, fenofibrate and some non-steroidal anti-inflammatory drugs (NSAIDs). Some of these drugs increase renal urate excretion. Hyperuricaemia and gout are common problems (at least 1% of Western men are affected by gout). Raised SUA levels increase the incidence of acute gout and renal calculi. Hyperuricaemia may also predict an increased risk of vascular events. Therefore, lowering SUA levels is of clinical relevance. In this review we consider the effect on SUA levels of drugs that are prescribed for indications other than treating hyperuricaemia. These drugs may obviate the need for specific treatment (e.g. allopurinol) aimed at lowering SUA levels. Furthermore, because hyperuricaemic patients may already be on several drugs (e.g. due to associated dyslipidaemia, hypertension and/or arthritis) compliance may be improved by avoiding additional medication. The potential for adverse effects associated with polypharmacy would also be decreased.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2004

Enterococcus casseliflavus bacteremia. Case report and literature review.

Motile Enterococci are rare causes of enterococcal bacteremia, usually in immunocompromised patients. We describe a case of polymicrobial bacteremia, including Enterococcus casseliflavus, Escherichia coli, and Morganella morganii, in an 80-year old woman, shortly after a liver biopsy performed to exclude cholangiocarcinoma. We further discuss the unique genetic characteristics and the clinical significance of such isolates, such as their intrinsic resistance to vancomycin, and the low virulence exhibited clinically. Further workup on the mechanisms of motile Enterococci resistance to vancomycin could probably yield useful information in achieving new ways of facing resistance attributed to the more usual, and malignant Enterococci.

Aged↗
PubMed2004

Effect of statins and ACE inhibitors alone and in combination on clinical outcome in patients with coronary heart disease.

We assessed the 'synergy' of statins and angiotensin-converting enzyme inhibitors (ACEI) in reducing vascular events in patients with coronary heart disease (CHD). The GREek Atorvastatin and CHD Evaluation (GREACE) Study, suggested that aggressive reduction of low density lipoprotein cholesterol to 2.59 mmol/l (<100 mg/dl) significantly reduces morbidity and mortality in CHD patients, in comparison to undertreated patients. In this post hoc analysis of GREACE the patients (n=1600) were divided into four groups according to long-term treatment: Group A (n=460 statin+ACEI), B (n=420; statin, no ACEI), C (n=371;no statin, on ACEI), and D (n=349; no statin, no ACEI). Analysis of variance was used to assess differences in the relative risk reduction (RRR) in 'all events' (primary end point) between groups. During the 3-year follow-up there were 292 cardiovascular events; 45 (10% of patients) in group A, 61 (14.5%) in group B, 91 in group C (24.5%) and 95 events in group D (27%). The RRR (95% confidence interval (CI) in the primary end point in group A was 31%, (95% CI -48 to -6%, P=0.01) in comparison to group B, 59% (95% CI -72 to -48%, P<0.0001) to group C and 63% (95% CI -74 to -51%, P<0.0001) to group D. There was no significant difference in RRR between groups C and D (9%, CI -27-10%, P=0.1). Other factors (eg the blood pressure) that can influence clinical outcome did not differ significantly between the four treatment groups. In conclusion, the statin+ACEI combination reduces cardiovascular events more than a statin alone and considerably more than an ACEI alone. Aggressive statin use in the absence of an ACEI also substantially reduced cardiovascular events. Treatment with an ACEI in the absence of a statin use reduced clinical events in comparison to patients not treated with an ACEI but not significantly, at least in these small groups of patients.

Aged↗
PubMed2004

The effect of statins versus untreated dyslipidaemia on renal function in patients with coronary heart disease. A subgroup analysis of the Greek atorvastatin and coronary heart disease evaluation (GREACE) study.

BACKGROUND: Little is known about statins in the prevention of dyslipidaemia induced renal function decline. The secondary coronary heart disease (CHD) prevention GREACE study suggested that dose titration with atorvastatin (10-80 mg/day, mean dose 24 mg/day) achieves the national cholesterol educational programme treatment goals and significantly reduces morbidity and mortality, compared with usual care. AIMS: To report the effect of statin on renal function compared with untreated dyslipidaemia in both treatment groups. METHODS/RESULTS: All patients had plasma creatinine values within the reference range < 115 micro mol/litre (13 mg/litre). The on study creatinine clearance (CrCl), as estimated (for up to 48 months) by the Cockroft-Gault formula, was compared within and between treatment groups using analysis of variance to assess differences over time. Patients from both groups not treated with statins (704) showed a 5.2% decrease in CrCl (p < 0.0001). Usual care patients on various statins (97) had a 4.9% increase in CrCl (p = 0.003). Structured care patients on atorvastatin (783) had a 12% increase in CrCl (p < 0.0001). This effect was more prominent in the lower two quartiles of baseline CrCl and with higher atorvastatin doses. After adjustment for 25 predictors of all CHD related events, multivariate analysis revealed a hazards ratio of 0.84 (confidence interval 0.73 to 0.95; p = 0.003) with every 5% increase in CrCl. CONCLUSIONS: In untreated dyslipidaemic patients with CHD and normal renal function at baseline, CrCl declines over a period of three years. Statin treatment prevents this decline and significantly improves renal function, potentially offsetting an additional factor associated with CHD risk.

Aged↗
PubMed2004

Uric acid levels and vascular disease.

There is evidence showing that serum uric acid (SUA) levels predict the risk for vascular events. For example, up to 29% of the reduction in the primary composite endpoint seen in the LIFE trial (favouring losartan versus atenolol) can be attributed to a fall in SUA levels. We also discuss the findings of the GREACE study (treating to target with atorvastatin versus 'usual' care) in relation to SUA levels. In this brief comment we extend this argument to consider the SUA-lowering effect of other drugs commonly prescribed in patients with vascular disease (e.g. statins, fibrates and antihypertensive agents). A judicious use of drugs (alone or in combination) will result in small reductions in SUA levels. These changes may translate into a substantial reduction in the risk of vascular events. Results retrieved from completed trials together with new prospective findings will support or refute the proposed association between lowering SUA levels and reducing vascular morbidity and mortality.

Diuretics↗
PubMed2003

Acid-base and electrolyte abnormalities observed in patients receiving cardiovascular drugs.

Cardiovascular drugs can cause a variety of acid-base and electrolyte abnormalities that need to be considered when clinicians manage the large number of patients who receive these agents. Diuretic-induced metabolic alkalosis is the most common acid-base disorder observed and is associated with hypokalemia. Drug-induced hyperkalemia is the most important cause of increased potassium levels in everyday clinical practice. Multifactorial-origin diuretic-induced hyponatremia is mostly due to thiazides and should be carefully managed. This review focuses on the pathogenetic mechanisms as well as on the treatment of these metabolic derangements that are commonly encountered in patients who receive cardiovascular drugs.

Acid-Base Imbalance↗
PubMed2002

Genetic polymorphisms of the apolipoprotein A-IV in a Greek population and their relation to plasma lipid and lipoprotein levels.

Apolipoprotein (apo) A-IV is a protein component of triglyceride-rich lipoproteins and high-density lipoproteins (HDL). In this study, two common genetic polymorphisms of the apoA-IV gene [codons 347(allele A and T) and 360 (allele 1 and 2)] were investigated in Greek patients with hyperlipidaemia and in healthy individuals matched for age, sex and smoking habits. In both study populations we evaluated the effect of these polymorphic sites on lipid and lipoprotein plasma levels and the body mass index (BMI). The frequencies of the 1/1 and 1/2 genotypes in codon 360 were 0.94 and 0.06 in hyperlipidemic patients and 0.92 and 0.08 in the control population, respectively. The frequencies of the A/A, A/T and T/T genotypes in codon 347 were 0.62, 0.34 and 0.04 in hyperlipidemic patients and 0.59, 0.33 and 0.08 in the control population, respectively. None of the above genotype frequency differences between the study populations reached statistical significance. The control population was not affected by any polymorphism of the apo A-IV gene. Hyperlipidaemic patients, carriers of the allele 2 (1/2 genotype), had significantly lower plasma triglyceride levels than carriers of the allele 1 (p = 0.03). Genetic variation in codon 347 had no influence on lipid and lipoprotein plasma levels. None of the polymorphisms at codons 360 and 347 affected the BMI. In conclusion, this study describes for the first time the genotype frequencies for polymorphic sites in codons 360 and 347 of the apo A-IV gene in a Greek population and suggests that the presence of the allele 2 is associated with lower plasma triglyceride levels in hyperlipidaemic patients.

Apolipoproteins A↗