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Biomedical subjects

Moses S Elisaf

Publications and source records attributed to Moses S Elisaf.

At least 19 recordsLinked to original sources
PubMed2006

Prevalence of vascular disease in metabolic syndrome using three proposed definitions.

BACKGROUND: There are a number of definitions available for the diagnosis of the metabolic syndrome (MetS). The MetS-associated increase in cardiovascular disease (CVD) risk may depend on the definition used. AIM: To investigate which of the 3 recently proposed definitions of MetS [the National Cholesterol Education Program-Adult Treatment Panel-III (NCEP-ATP-III), the International Diabetes Federation (IDF) and the American Heart Association/National Heart Lung and Blood Institute (AHA/NHLBI)] is related to excessive CVD risk and thus may be more appropriate to implement in clinical practice. METHODS: A cross-sectional analysis of a representative sample of Greek adults (n=9669). RESULTS: The age-adjusted CVD prevalence was 11.4% in the whole study population, 23.3% in the NCEP-ATP-III (+) subjects, 22.6% in AHA/NHLBI (+) subjects and 18.3% in IDF (+) subjects [p<0.001 for the comparison between the whole study population and all MetS groups and p<0.0001 for the comparison between IDF (+) and either NCEP-ATP-III (+) or AHA/NHLBI (+) MetS]. However, the CVD prevalence was only 11.2% in the IDF (+) but NCEP-ATP-III (-)/AHA/NHLBI (-) MetS subjects [p<0.0001 vs. either NCEP-ATP-III (+) or AHA/NHLBI (+)], which was not different compared with the whole study population. Furthermore, subjects with NCEP ATP III (+) or AHA/NHLBI (+) MetS but not diabetes (DM) had a persistently higher prevalence of CVD compared with the whole study population. However, there was no significant difference regarding CVD prevalence between the whole study population and IDF (+)/DM (-) MetS subjects. CONCLUSIONS: CVD prevalence was increased in the presence of MetS irrespective of the definition used. However, this increase was more pronounced when the NCEP-ATP-III and AHA/NHLBI criteria were implemented compared with the IDF definition. Furthermore, the IDF definition included a large proportion of subjects who did not have increased CVD prevalence compared with the whole study population. These findings may have implications regarding which definition should we use to diagnose the MetS.

Adult↗
PubMed2006

Elevated serum uric acid levels in metabolic syndrome: an active component or an innocent bystander?

Elevated serum uric acid (SUA) levels are commonly seen in patients with the metabolic syndrome (MetS). Several mechanisms, both direct and indirect, connect the increased SUA levels with the established diagnostic criteria of MetS. It is possible that the increased cardiovascular disease risk associated with the MetS is partially attributed to elevated circulating SUA concentration. Several drugs used in the treatment of MetS may alter SUA levels. Thus, lifestyle measures together with the judicious selection of drugs for the treatment of hypertension, dyslipidemia, and insulin resistance associated with MetS may result in a reduction of SUA levels and possibly cardiovascular disease risk. This review summarizes the pathophysiologic association between SUA and MetS and focuses on the prevention of hyperuricemia and its cardiovascular consequences.

Animals↗
PubMed2006

Upper gastrointestinal haemorrhage complicating antiplatelet treatment with aspirin and/or clopidogrel: where we are now?

A large number of patients require antiplatelet therapy (mainly aspirin and/or clopidogrel). Recent studies suggest that the combination of these agents is useful in patients with acute coronary syndrome and after percutaneous coronary intervention with stent placement. On the other hand, bleeding complications, most of which arise from the upper gastrointestinal (UGI) tract, can limit the use of antiplatelet drugs. Clopidogrel appears to be associated with fewer UGI side effects and bleeding compared with aspirin. However, a history of previous UGI bleeding is a major risk factor for clopidogrel-associated bleeding. The use of proton-pump inhibitors (PPIs) decreases the rate of UGI bleeding in patients receiving aspirin or clopidogrel. Furthermore, a recent study suggested that the administration of low-dose aspirin plus high-dose esomeprazole (a potent PPI) was associated with fewer episodes of UGI bleeding than clopidogrel alone in patients with a history of recent UGI haemorrhage. However, this study had several limitations and its results should be cautiously extrapolated into clinical practice. The combination of aspirin plus clopidogrel increases the risk of UGI bleeding. Unfortunately, there are no data on the effect of PPI prophylaxis in this setting. Available evidence suggests that where aspirin and/or clopidogrel are to be started or continued in patients with a recent history of UGI ulceration or bleeding (after ulcer healing and eradication of H. pylori infection), treatment with a PPI is a useful precaution. The patients should also be carefully monitored for recurrence of UGI bleeding.

Aspirin↗
PubMed2006

Combined treatment with angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers: a review of the current evidence.

Several studies have shown that angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers are useful in the treatment of hypertension, cardiovascular disease, chronic heart failure, and some types of nephropathy. In this context, dual renin-angiotensin system blockade with both angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers may be more effective than treatment with each agent alone. Many clinical trials have demonstrated the beneficial effect of this combined treatment on proteinuria, hypertension, heart failure, and cardiovascular events. Moreover, these studies demonstrated that dual renin-angiotensin system blockade is generally safe and well tolerated. Long-term studies are under way to confirm these effects and also investigate the effectiveness of dual renin-angiotensin system blockade on cerebrovascular disease and prevention of type 2 diabetes mellitus. These studies are expected to define the optimal use of combination treatment in everyday clinical practice. This review considers the most important clinical trials that evaluated the effect of dual renin-angiotensin system blockade on blood pressure, heart failure, and renal function.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2006

The effect of apolipoprotein E polymorphism on the response to lipid-lowering treatment with atorvastatin or fenofibrate.

Although the effect of apolipoprotein E gene polymorphism on the response to treatment with statins has been studied, the results are conflicting. Moreover, little is known about the possible effect of apolipoprotein E alleles on the response to treatment with fibrates. The purpose of this study was to evaluate the effect of apolipoprotein E polymorphism on lipid-lowering response to treatment with atorvastatin and fenofibrate in patients with different types of dyslipidemia. The study population included 136 patients with heterozygous familial hypercholesterolemia (type IIA dyslipidemia) treated with atorvastatin (20 mg/day) and 136 patients with either primary hypertriglyceridemia (type IV dyslipidemia) or mixed hyperlipidemia (type IIB dyslipidemia) treated with micronized fenofibrate (200 mg/day). Overall, no significant associations were detected between apolipoprotein E genotype and response to treatment with atorvastatin. In patients treated with fenofibrate, significant associations were noted between apolipoprotein E genotype and changes in apolipoprotein B, apolipoprotein E and triglyceride levels. Specifically, in apolipoprotein E2, apolipoprotein E3, and apolipoprotein E4 individuals, apolipoprotein B reductions were 22%, 17%, and 8%, respectively (P = .003); apolipoprotein E reductions were 45%, 20%, and 15%, respectively (P = .006); whereas triglyceride reductions reached 53%, 36%, and 33%, respectively (P = .033). In conclusion, apolipoprotein E genotype had no significant effect on the response to treatment with atorvastatin in patients with heterozygous familial hypercholesterolemia, but in patients with primary hypertriglyceridemia or mixed hyperlipidemia, there was a clear association between apolipoprotein E genotype and response to treatment with fenofibrate.

Adult↗
PubMed2006

Effect of multifactorial treatment on non-alcoholic fatty liver disease in metabolic syndrome: a randomised study.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome (MetS). There is no established treatment for NAFLD. AIM: To evaluate a multifactorial intervention in the treatment of NAFLD. METHODS: A prospective, open-label, randomised study in non-diabetic patients (n = 186) with MetS (follow-up: 54 weeks). All patients had both biochemical and ultrasonographic evidence of NAFLD at baseline. Other causes of liver disease were excluded. Patients received lifestyle advice and treatment for hypertension (mainly inhibitors of the renin-angiotensin system), impaired fasting glucose (metformin), obesity (orlistat) and dyslipidaemia [randomly allocated to atorvastatin 20 mg/day (n = 63) or micronised fenofibrate 200 mg/day (n = 62) or both drugs (n = 61)]. Liver ultrasonography was assessed at baseline and at the end of the study. RESULTS: At the end of treatment, 67% of patients on atorvastatin, 42% on fenofibrate and 70% on combination treatment no longer had biochemical plus ultrasonographic evidence of NAFLD (p < 0.05 vs. baseline for all comparisons). The percentage of patients who no longer had evidence of NAFLD was significantly higher (p < 0.009) in the atorvastatin and combination groups compared with the fenofibrate group. This effect was independently related to drug treatment, as well as to reductions in high-sensitivity C-reactive protein, waist circumference, body weight, triglycerides, low-density lipoprotein-cholesterol, total cholesterol, systolic blood pressure and glucose. Four patients discontinued treatment because of adverse effects. CONCLUSIONS: Multifactorial intervention in MetS patients with both biochemical and ultrasonographic evidence of NAFLD offsets surrogate markers of NAFLD (i.e. elevated aminotransferase plus echogenic liver).

Anti-Obesity Agents↗
PubMed2006

Treating to target patients with primary hyperlipidaemia: comparison of the effects of ATOrvastatin and ROSuvastatin (the ATOROS study).

OBJECTIVES: In a 24-week, open-label, randomized, parallel-group study, we compared the efficacy and metabolic effects, beyond low density lipoprotein cholesterol (LDL-C)-lowering, of atorvastatin (ATV) and rosuvastatin (RSV) in cardiovascular disease-free subjects with primary hyperlipidaemia, treated to an LDL-C target (130 mg/dL). METHODS: After a 6-week dietary lead-in period, patients were randomized to RSV 10 mg/day (n = 60) or ATV 20 mg/day (n = 60). After 6 weeks on treatment the dose of the statin was increased (to RSV 20 mg/day or ATV 40 mg/day) if the treatment goal was not achieved. A control group of healthy volunteers (n = 60) was also included for the validation of baseline serum and urinary laboratory parameters. The primary outcome was the percentage of patients reaching the LDL-C goal; secondary outcomes were changes in lipid and non-lipid metabolic parameters. RESULTS: A total of 45 patients (75.0%) in the RSV-treated group and 43 (71.7%) in the ATV-treated group achieved the treatment target at the initial dose. Both regimens were generally well tolerated and there were no withdrawals due to treatment-related serious adverse events. Similar significant reductions in total cholesterol, LDL-C, apolipoprotein (apo) B, triglycerides, apoB/apoA1 ratio, fibrinogen and high-sensitivity C-reactive protein levels were seen. RSV had a significant high density lipoprotein cholesterol (HDL-C)-raising effect and showed a trend towards increasing apoA1 levels. Glycaemic control and renal function parameters were not influenced by statin therapy. ATV, but not RSV, showed a significant hypouricaemic effect. CONCLUSIONS: RSV and ATV were equally efficacious in achieving LDL-C treatment goals in patients with primary hyperlipidaemia at the initial dose and following dose titration. RSV seems to have a significantly higher HDL-C-raising effect, while ATV lowers serum uric acid levels.

Atorvastatin↗
PubMed2006

Plasma lipoprotein(a) levels and LDL-cholesterol lowering response to statin therapy in patients with heterozygous familial hypercholesterolemia.

Familial hypercholesterolemia (FH) is characterised by elevated plasma LDL-cholesterol levels and premature ischemic heart disease. Statin therapy is mandatory in order to prevent atherosclerosis in patients with heterozygous FH. Both genetic and environmental factors affect the statin-induced LDL-cholesterol lowering effect in patients with heterozygous FH. Recently published data suggest that plasma lipoprotein(a) levels may affect the efficacy of statin therapy in patients with nephrotic syndrome. However, no data are available concerning the effect of lipoprotein(a) levels on the efficacy of statin therapy in patients with heterozygous FH. This report demonstrates negative correlation between plasma lipoprotein(a) levels and the LDL-cholesterol lowering effect of statin therapy in 49 patients with heterozygous FH.

Anticholesteremic Agents↗
PubMed2005

Serum lipoprotein(a) levels and apolipoprotein(a) isoform size and risk for first-ever acute ischaemic nonembolic stroke in elderly individuals.

In a population-based case-control study, we investigated the association of acute ischaemic stroke with lipoprotein(a) (Lp(a)) levels and apolipoprotein (Apo) (a) isoform size in subjects aged older than 70 years. A total of 163 patients with a first-ever-in-a-lifetime acute ischaemic/nonembolic stroke and 166 controls were included. Compared to controls, stroke patients exhibited higher Lp(a) concentrations (median value, 12.2 mg/dl versus 6.4 mg/dl, p < 0.001) and a higher frequency of small Apo(a) isoforms (44.2% versus 29.5%, p < 0.01). Multivariate logistic regression analysis showed a significant association of acute ischaemic stroke with Lp(a) levels [adjusted odds ratio (OR), 1.37, 95% CI (1.12-1.67); p = 0.002], and small Apo(a) isoform size [OR, 1.74 (1.10-3.03); p = 0.04]. Compared to subjects with Lp(a) levels in the lowest quintile, those within the highest quintile had a 3.2-times adjusted risk to suffer an acute ischaemic/nonembolic stroke (1.60-6.62, 95% CI; p < 0.001). Furthermore, analysis of interaction between lipid variables revealed that in the presence of elevated Lp(a) levels the inverse relationship between HDL-cholesterol levels and ischaemic stroke was negated [OR, 1.01 (1.00-1.03); p = 0.015]. Our study suggests that determination of Lp(a) levels and Apo(a) isoform size may be important in identifying elderly individuals at risk of ischaemic stroke independently of other risk factors and concurrent metabolic derangements.

Aged↗
PubMed2005

Components of the metabolic syndrome and risk for first-ever acute ischemic nonembolic stroke in elderly subjects.

BACKGROUND AND PURPOSE: Metabolic syndrome (MetSyn) represents a constellation of lipid and nonlipid risk factors for cardiovascular disease and is a recognized target for increased behavioral therapy. OBJECTIVE: The association between acute ischemic/nonembolic stroke and the MetSyn in elderly individuals was assessed in a population-based case-control study in the prefecture of Ioannina, Greece. STUDY POPULATION: A total of 163 patients aged older than 70 years admitted with first-ever-in-a-lifetime acute ischemic/nonembolic stroke and 166 controls were included. RESULTS: The prevalence of MetSyn (defined according to NCEP/ATP III criteria) was high in stroke patients (46.0% versus 15.7%, P<0.001). Compared with controls as a group (with and without MetSyn), stroke patients with the MetSyn showed higher concentrations of triglycerides, lipoprotein(a), uric acid, and fibrinogen, and lower high-density lipoprotein (HDL) cholesterol and apolipoprotein A-I levels. In logistic regression analysis, crude and adjusted odd ratios (ORs) for MetSyn were 5.33 (95% confidence interval [CI], 2.91 to 9.79; P<0.0001) and 2.59 (95% CI, 1.24 to 5.42; P=0.012), respectively. The analysis of interaction between MetSyn and its individual components revealed significant associations with abdominal obesity (adjusted OR, 2.74; 95% CI, 1.15 to 6.50; P=0.02), hypertension (OR, 2.03; 95% CI, 0.91 to 4.49; P=0.08), high fasting glucose levels (OR, 2.95; 95% CI, 1.19 to 7.35; P=0.02), high triglyceride (OR, 5.55; 95% CI, 2.71 to 11.37; P<0.0001]), and low HDL cholesterol (OR, 5.42; 95% CI, 2.85 to 10.30; P<0.0001). Notably, in stroke patients with the MetSyn the inverse relationship between HDL cholesterol levels and ischemic stroke was negated (OR, 1.04; 95% CI, 1.02 to 1.05; P<0.0001). CONCLUSIONS: MetSyn is associated with an increased risk for acute ischemic/nonembolic stroke in elderly subjects with significant contributions from its individual components. In the presence of MetSyn, HDL cholesterol loses its protective role against ischemic stroke.

Aged↗
PubMed2005

Risk factors for first-ever acute ischemic non-embolic stroke in elderly individuals.

BACKGROUND: Stroke is a leading cause of mortality and subsequent serious long-term physical and mental disability among survivors. In the elderly, ischemic stroke accounts for more than 80% of all strokes. OBJECTIVES: To identify major risk factors for a first-ever acute ischemic/non-embolic stroke in individuals older than 70 years. METHODS: A population-based case-control study of patients admitted to the University Hospital of Ioannina, Epirus, Greece, due to first-ever ischemic/non-embolic stroke from March 1997 to January 2002. All patients were subjected to brain CT and had their serum lipids and biochemical metabolic parameters determined within 24 h from the onset of symptoms. RESULTS: A total of 163 (aged>70 years) consecutive stroke patients and 166 apparently healthy volunteers were studied. An atherogenic lipid profile and metabolic disturbances were more prevalent in the patient group than in stroke-free controls. Multivariate logistic regression analysis identified diabetes mellitus (odds ratio (OR), 1.92; 95% CI, 1.02-3.63), triglycerides (TG) (OR, 1.16; 95% CI, 1.09-1.22), HDL-cholesterol (OR, 0.57; 95% CI, 0.43-0.76), apo A-I (OR, 0.80; 95% CI, 0.70-0.92), lipoprotein(a) [LP(a)] (OR, 1.51; 95% CI, 1.25-1.79), uric acid (OR, 1.30; 95% CI, 1.06-1.59) albumin (OR, 0.38; 95% CI, 0.20-0.70) fibrinogen (OR, 1.10; 95% CI, 1.05-1.13) and the metabolic syndrome (OR 2.48, 95% CI, 1.16-5.29) as significantly associated with ischemic/non-embolic stroke. CONCLUSION: Ischemic non-embolic stroke in the elderly is associated with dyslipidemia and several predictor metabolic factors, which could be substantially modified by lifestyle changes and therapeutic intervention.

Acute Disease↗
PubMed2005

Thyroid substitution therapy induces high-density lipoprotein-associated platelet-activating factor-acetylhydrolase in patients with subclinical hypothyroidism: a potential antiatherogenic effect.

BACKGROUND: Subclinical hypothyroidism (SH) has been associated with an increased risk of ischemic heart disease, which has been partly attributed to lipid abnormalities. Human plasma platelet-activating factor acetylhydrolase (PAF-AH) is an enzyme associated with lipoproteins (both low-density lipoproteins [LDL], and high-density lipoproteins [HDL]). Plasma paraoxonase 1 (PON1) is an esterase exclusively associated with HDL. OBJECTIVE: To evaluate qualitative changes in lipoprotein metabolism with respect to PAF-AH and PON1 activities in patients with SH before and after the restoration of euthyroidism. DESIGN AND METHODS: We determined the PAF-AH activity in plasma and on HDL and PON1 activities as well as the lipid profile patients with SH at baseline and after 6 months of levothyroxine substitution therapy. Thirty normolipidemic healthy individuals comprised the control group. RESULTS: Compared to controls, patients with SH showed higher levels of total cholesterol, LDL cholesterol, triglycerides, and apolipoprotein B. Triglycerides were significantly reduced after levothyroxine treatment. Patients with SH exhibited higher plasma baseline PAF-AH activity (63.0 +/- 16.5 versus 44.3 +/- 9.5 nmol/mL per minute p < 0.0001) and lower baseline HDL associated PAF-AH (2.9 +/- 1.1 versus 3.6 +/- 0.9 nmol/mL per minute p = 0.02) compared to the control group. PON1 activities were similar in both groups. Levothyroxine treatment had no effect on plasma PAF-AH activity or PON1 activities but resulted in a significant elevation of HDL-associated PAF-AH activity (from 2.9 +/- 1.1 to 3.5 +/- 1.0 nmol/mL per minute, p = 0.003). CONCLUSIONS: Patients with SH exhibit increased plasma PAF-AH activity and low HDL-associated PAF-AH activity. Levothyroxine induces a significant increase in HDL-PAF-AH activity. This action may represent a potential antiatherogenic effect of thyroid replacement therapy.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed2005

Alterations in electrolyte equilibrium in patients with acute leukemia.

BACKGROUND AND AIM: A wide array of disturbances in electrolyte equilibrium is commonly seen in patients with acute leukemia (AL). These abnormalities present a potential hazard in these patients, as that of enhancing the cardiotoxic effects of certain chemotherapeutic regimens. The literature dealing with AL-related electrolyte abnormalities and their interactions in leukemic patients was reviewed. DATA SYNTHESIS: Sources included MEDLINE and EMBASE. The search strategy was based on the combination of 'acute leukemia', 'electrolyte abnormalities', 'acid-base disorders', 'potassium', 'sodium', 'magnesium', 'calcium', and 'phosphorus'. References of retrieved articles were also screened. A decrease in serum potassium, mainly owing to lysozyme-induced tubular damage, appears to be one of the most frequent and potentially hazardous abnormalities. Other clinically significant metabolic perturbations include hyponatremia and hypercalcemia. CONCLUSION: A broad spectrum of electrolyte abnormalities is encountered in the clinical setting of AL, which are related to the disease process per se and/or to the therapeutic interventions. Clinicians should be vigilant for early detection and appropriate management of these disorders before the initiation of chemotherapy regimens as well as during treatment.

Acid-Base Imbalance↗