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Biomedical subjects

Asterios Karagiannis

Publications and source records attributed to Asterios Karagiannis.

At least 19 recordsLinked to original sources
PubMed2007

The role of renin-angiotensin system inhibition in the treatment of hypertension in metabolic syndrome: are all the angiotensin receptor blockers equal?

The metabolic syndrome (MetS) is a strong predictor of cardiovascular morbidity and mortality, as well as new Type 2 diabetes. MetS consists of visceral obesity, elevated blood pressure, impaired glucose metabolism, atherogenic dyslipidaemia (elevated triglycerides and low levels of high-density lipoprotein cholesterol), as well as other metabolic abnormalities. The underlying pathophysiology seems to be largely, but not uniquely, attributable to insulin resistance. Existing antihypertensive drugs were designed to lower blood pressure rather than to modify the metabolic abnormalities associated with hypertension. This review considers the role of renin-angiotensin system inhibition and especially the use of angiotensin receptor blockers (ARBs) in the treatment of hypertension in MetS. There are differences among ARBs. Among them is the uricosuric effect of losartan. Furthermore, telmisartan may function as a partial agonist of the peroxisome proliferator-activated receptor-gamma (PPAR-gamma).

Angiotensin Receptor Antagonists↗
PubMed2006

Effect of statin treatment on renal function and serum uric acid levels and their relation to vascular events in patients with coronary heart disease and metabolic syndrome: a subgroup analysis of the GREek Atorvastatin and Coronary heart disease Evaluation (GREACE) Study.

BACKGROUND: Metabolic syndrome (MetS) is associated with increased risk for both vascular and chronic kidney disease. Whether statins ameliorate these risks is not established. METHODS: This post hoc analysis of the GREek Atorvastatin and Coronary heart disease (CHD). Evaluation (GREACE) examines the effect of statins on estimated glomerular filtration rate (e-GFR) and serum uric acid (SUA) levels and their relation to vascular events in CHD patients with MetS. MetS patients were divided into two groups: Group A (n = 365) received lifestyle advice, target-driven treatment with statins (mainly atorvastatin) and treatment for hypertension and elevated glucose. Group B (n = 347) received the same except for statins. Patients without MetS were divided into those who received treatment similar to Group A and Group B [Groups C (n = 504) and D (n = 384), respectively]. All patients were followed for 3 years. RESULTS: A total of 12.1% of patients in Group A experienced a vascular event vs 28% in Group B; risk ratio (RR) 0.43, 95% confidence interval (CI) 0.20-0.64, P < 0.0001, while in those without MetS (Group C vs Group D), the respective RR was 0.59, 95% CI 0.41-0.79, P < 0.0001. In Group A, e-GFR increased by 13.7% and SUA levels fell by 8.9%, while in Group B e-GFR was reduced by 5.8% and SUA increased by 4.3% (P < 0.005). Stepwise regression analysis showed that these changes were independently related to vascular events. CONCLUSION: Among CHD patients, those with MetS benefited more from statin treatment than those without MetS. This benefit could be partially attributed to favourable changes in e-GFR and SUA levels probably induced by statin treatment.

Aged↗
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

Vascular endothelial growth factor and nitric oxide serum levels in arterial hypertension.

Vascular endothelial growth factor (VEGF) is a specific mitogen for endothelial cells and an inducer of the angiogenic procedure. Endothelial nitric oxide (NO) is a potent vasodilator. Because both are implicated in vascular function, it is possible that they would be significantly affected in arterial hypertension. The aim of the study was the investigation of the levels of the two substances in blood serum and their potential relation in patients with untreated essential arterial hypertension compared to healthy individuals. VEGF levels were found 129.1 +/- 135.9 pg/mL in a group of 28 untreated hypertensive patients vs. 209.0 +/- 133.3 pg/mL in a group of 28 healthy individuals (p = 0.008). Nitrites and nitrates levels (as an indirect index of calculating NO levels) were also lower in hypertensive patients than in healthy individuals (19.8 +/- 9.7 micromol/L vs. 29.6 +/- 15.9 micromol/L, p = 0.014). A positive correlation between NOx (nitrites and nitrates levels) and VEGF was found in healthy individuals (r = 0.55, p = 0.003), but there was no correlation in hypertensive patients. The significant decrease of serum VEGF and NO in arterial hypertension and the existence of a correlation between the two substances in healthy subjects that did not exist in the hypertensive patients are findings that need evaluation.

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

Dyslipidaemia, hypercoagulability and the metabolic syndrome.

The metabolic syndrome is a clustering of risk factors including central obesity, insulin resistance, dyslipidaemia and hypertension. This syndrome is associated with increased risk of cardiovascular disease and is a common early abnormality in the development of type 2 diabetes. The pathogenesis of the syndrome has multiple origins. Obesity and sedentary lifestyle coupled with genetic factors interact to produce the syndrome. Here, we consider two components of the metabolic syndrome, dyslipidaemia and hypercoagulability.

Adipose Tissue↗
PubMed2005

Targeting vascular risk in patients with metabolic syndrome but without diabetes.

There are no prospective data on the effect of a multitargeted treatment approach on cardiovascular disease (CVD) risk reduction in nondiabetic patients with metabolic syndrome (MetS). Furthermore, the optimal hypolipidemic drug treatment in these patients remains controversial. In this prospective, randomized, open-label, intention-to-treat, and parallel study, 300 nondiabetic patients with MetS, free of CVD at baseline, were studied for a period of 12 months. Age- and sex-matched subjects without MetS (n = 100) acted as controls. All patients received lifestyle advice and a stepwise-implemented drug treatment of hypertension, impaired fasting glucose, and obesity. For hypolipidemic treatment, the patients were randomly allocated to 3 treatment groups: atorvastatin (n = 100, 20 mg/d), micronized fenofibrate (n = 100, 200 mg/d), and both drugs (n = 100). Clinical and laboratory parameters, including the lipid profile and C-reactive protein (CRP), were assessed at the baseline and at the end of the study. The primary end point was the proportion of patients not having MetS or its component features at the end of the 12-month treatment period. The secondary end points were the difference in 10-year CVD risk (Prospective Cardiovascular Munster risk calculator) and the degree of CRP reduction. By the end of the study, 76% of the patients no longer had MetS, and 46% had only one diagnostic MetS factor. The estimated 10-year (Prospective Cardiovascular Munster) risk of all patients with MetS at baseline was 14.6%. This was reduced in the atorvastatin group to 6.4%, in the fenofibrate group to 9.2%, and in the combination group to 5.5% (P < .0001 for all vs baseline). The 10-year risks of the atorvastatin and combination groups were not different from that of the control group (5.0%). C-reactive protein was significantly reduced in all treatment groups, with the atorvastatin and combination groups having the greatest reduction (65% and 68%, respectively, P < .01 vs the fenofibrate group, 44%). Lipid values were significantly improved in all 3 treatment groups, with those on the combined treatment attaining lipid targets to a greater extent than those in the other 2 groups. A target-driven and intensified intervention aimed at multiple risk factors in nondiabetic patients with MetS substantially offsets its component factors and significantly reduces the estimated CVD risk. The atorvastatin-fenofibrate combination had the most beneficial effect on all lipid parameters and significantly improved their CVD risk status. Atorvastatin and combination treatment were more effective than fenofibrate alone in reducing CRP levels.

Aged↗
PubMed2005

Gonadal dysfunction in systemic diseases.

Gonadal function is significantly affected in many acute and chronic systemic diseases. As the function of the testes and the ovaries is determined by the integrity of the hypothalamic-pituitary-gonadal axis, it is obvious that a systemic disease may affect one or more levels of the axis in such a manner that the gonadal dysfunction may have various clinical and laboratory manifestations. In this brief review, the most common disturbances seen in the main systemic diseases will be discussed.

Cardiovascular Diseases↗
PubMed2004

Acute renal failure due to tumor lysis syndrome in a patient with non-Hodgkin's lymphoma.

Tumor lysis syndrome is characterized by multiple metabolic derangements resulting from the release of intracellular components into the bloodstream due to abrupt malignant cell death, spontaneously or following antineoplastic therapy. The syndrome is characterized by hyperkalemia, hyperuricemia, hyperphosphatemia, and hypocalcemia, while deposition of uric acid and calcium phosphate crystals may result in acute renal failure, which is often exacerbated by concomitant intravascular volume depletion. A case of tumor lysis syndrome complicated by acute renal failure in a patient with non-Hodgkin's lymphoma is reported and the pathophysiology, the clinical features, and the treatment options are discussed.

Acute Kidney Injury↗
PubMed2004

Lack of an association between angiotensin-converting enzyme gene insertion/deletion polymorphism and ischaemic stroke.

BACKGROUND AND PURPOSE: Numerous factors have been reported to influence the pathogenesis of stroke. The angiotensin I-converting enzyme (ACE) gene is a candidate gene for atherosclerotic-related diseases. In the present study, the association between the polymorphism of the ACE gene and ischaemic stroke was investigated. METHODS: Using polymerase chain reaction techniques, 100 patients (48 males, age 69.3 +/- 9.7 years) with cerebral infarction and 100 age- and sex-matched controls were divided into the following three ACE genotypes [deletion (D) and insertion (I)]: II, ID and DD. RESULTS: There was no evidence of any association between the ACE gene polymorphism and the presence of ischaemic stroke (odds ratio 0.874, 95% confidence interval 0.386-1.973). CONCLUSIONS: The DD genotype in the human ACE gene does not appear to be a risk factor for ischaemic stroke. Further evaluation in a larger population study is required to examine the possibility of an increased risk of ischaemic stroke in DD homozygotes.

Aged↗
PubMed2004

Lack of an association between angiotensin converting enzyme gene polymorphism and peripheral arterial occlusive disease.

Numerous factors have been reported to influence the pathogenesis of atherosclerosis. The angiotensin I converting enzyme (ACE) gene is a candidate gene for atherosclerotic-related disease. In the present study, the association between the polymorphism of the ACE gene and peripheral arterial occlusive disease (PAOD) was investigated. Using polymerase chain reaction techniques, 100 patients (age 66.7 +/- 7.7 years) with PAOD and 100 age-matched controls were divided into the three ACE genotypes: II, ID and DD (Insertion I and Deletion D). There was no evidence of any association between ACE gene polymorphism and the presence of PAOD (odds ratio 0.759; 95% confidence interval 0.418-1.377). These results indicate an absence of association between DD genotype and PAOD. Further evaluation in a larger population study is required to examine the possibility of an increased risk of PAOD in DD homozygotes.

Aged↗
PubMedDate not supplied

The unilateral measurement of blood pressure may mask the diagnosis or delay the effective treatment of hypertension.

Several studies have indicated the presence of significant interarm blood pressure (BP) differences; this could result in misclassification of BP status. Nevertheless, the findings of these studies were not consistent. This prospective, observational study investigated the presence and magnitude of interarm BP differences and determined the influence of age, gender, arm circumference, smoking, being hypertensive or diabetic, or having a previous history of cardiovascular disease in these differences. The study included 384 subjects, who were patients, ward visitors, and members of the nursing staff of this Department. BP measurements were recorded simultaneously in both arms by using 2 validated, fully automated oscillometric electronic devices. There were significant differences between the right arm and left arm systolic BP (p < 0.0005), between right arm and left arm diastolic BP (p < 0.05), and between right arm and left arm pulse pressure (p = 0.006). The mean interarm differences in systolic and diastolic BP measurements were 1.2 +/-5.0 mm Hg and 0.4 +/-4.2 mm Hg, respectively. There were 13 subjects (3.4%) and 4 subjects (1.04%) with an interarm systolic and diastolic BP difference of > 10 mm Hg, respectively, and a single patient with both interarm systolic and diastolic BP differences of > 10 mm Hg (0.26%). None of the studied demographic or clinical characteristics was a significant predictor of interarm systolic and diastolic BP differences. The authors conclude that significant interarm systolic and diastolic BP differences are frequently present. Therefore, the unilateral measurement of BP may mask the diagnosis or delay the effective treatment of hypertension. It is thus recommended that BP should be simultaneously measured in both arms at the initial consultation and the higher of the 2 readings should be used to guide further management decisions.

Age Factors↗
PubMedDate not supplied

Treatment of recurrent gastrointestinal haemorrhage in a patient with von Willebrand's disease with administration of octreotide LAR and propranolol.

We report a patient with von Willebrand' s disease who had had recurrent and life-threatening bleeding from the gastrointestinal tract. Despite extensive investigation, no apparent cause of haemorrhage was identified. He was successfully treated with combined administration of octreotide LAR (long-acting release) and propranolol. This is the first report on the successful use of octreotide LAR in a patient with von Willebrand' s disease.

Journal Article↗