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Biomedical subjects

C Stefanadis

Publications and source records attributed to C Stefanadis.

At least 19 recordsLinked to original sources
PubMed2006

CLimate Impacts on Myocardial infarction deaths in the Athens TErritory: the CLIMATE study.

OBJECTIVE: To evaluate the impact of meteorological variables on daily and monthly deaths caused by acute myocardial infarction (AMI). METHODS: All death certificate data from the Athens territory were analysed for AMI deaths in 2001. Daily atmospheric temperature, pressure and relative humidity data were obtained from the National Meteorological Society for Athens for the same year. RESULTS: The total annual number of deaths caused by AMI was 3126 (1953 men) from a population of 2,664,776 (0.117%). Seasonal variation in deaths was significant, with the average daily AMI deaths in winter being 31.8% higher than in summer (9.89 v 7.35, p < 0.001). Monthly variation was more pronounced for older people (mean daily AMI deaths of people older than 70 years was 3.53 in June and 7.03 in December; p < 0.001) and of only marginal significance for younger people. The best predictor of daily AMI deaths was the average temperature of the previous seven days; the relation between daily AMI deaths and seven-day average temperature (R(2) = 0.109, p < 0.001) was U-shaped. Considering monthly AMI death rates, only mean monthly humidity was independently associated with total deaths from AMI (R(2) = 0.541, p = 0.004). CONCLUSION: Ambient temperature is an important predictor of AMI mortality even in the mild climate of a Mediterranean city like Athens, its effects being predominantly evident in the elderly. Mean monthly humidity is another meteorological factor that appears to affect monthly numbers of AMI deaths. These findings may be useful for healthcare and civil protection planning.

Adult↗
PubMed2006

Increased coronary sinus blood temperature: correlation with systemic inflammation.

BACKGROUND: Recent studies have shown that patients with single vessel coronary artery disease (CAD) suffering from acute coronary syndromes (ACS) have increased coronary sinus (CS) blood temperature compared with the right atrium (RA). The aim of this study was to investigate whether there is a correlation between systemic inflammatory indexes and CS temperature and whether there is a difference in CS temperature between patients with single vs. multivessel disease. MATERIALS AND METHODS We included consecutive patients scheduled for coronary angiography for recent-onset chest pain evaluation. We measured C-reactive protein (CRP) levels in the study population. Coronary sinus and RA blood temperature measurements were performed by a 7F thermography catheter. DeltaTau was calculated by subtracting the RA from the CS blood temperature. RESULTS: The study population comprised 53 patients with ACS, 25 patients with stable angina (SA) and 22 subjects without CAD (control group). DeltaTau was greater in patients with ACS and with SA compared with the control group (0.22 +/- 0.10 degrees C, 0.18 +/- 0.04 degrees C vs. 0.14 +/- 0.07 degrees C, P < 0.01 for both comparisons). The ACS group had greater DeltaTau compared with the SA group, although the difference did not reach statistical significance (P = 0.09). Eighteen (39.1%) out of 46 patients with multivessel disease had three-vessel disease and 28 (60.8%) had two-vessel disease. DeltaTau between patients with multivessel and single vessel disease was similar (0.22 +/- 0.01 degrees C, 0.19 +/- 0.01 degrees C, P = 0.17). The levels of CRP were well correlated with DeltaTau (R = 0.35b, P < 0.01). CONCLUSIONS: Systemic inflammation is well correlated with CS temperature; thus, an inflammatory process could be the underlying mechanism for increased heat production from the myocardium.

Aged↗
PubMed2005

Clinical appraisal of arterial stiffness: the Argonauts in front of the Golden Fleece.

Interest in evaluating arterial elastic properties has grown in parallel with the widespread availability of non-invasive methods for assessing arterial stiffness. A clinically useful diagnostic index must be pathophysiologically relevant, must be readily measurable, and must indicate the severity of the disease and predict the corresponding risk. Interventional modification of this index must parallel disease regression and benefit prognosis. The current evidence for the clinical value of estimating arterial stiffness (mainly of large, elastic-type arteries, such as the aorta and the carotids) in the contemporary era of cardiovascular medicine is reviewed.

Antihypertensive Agents↗
PubMed2005

Endothelial function and inflammation in coronary artery disease.

Evidence supports the central role of endothelium and inflammation in all phases of the atherosclerotic process. Clinical studies have shown their prognostic potential for the development of ischaemic events and for adverse outcome after acute coronary syndromes. Reduction in inflammatory levels and improving endothelial function by traditional and novel treatment strategies were associated with a proportional reduction in cardiovascular events. However, randomised controlled trials are required to explore further whether drugs targeting the inflammatory process and endothelial function will constitute a reasonable adjunctive treatment for patients with coronary artery disease.

Biomarkers↗
PubMed2005

Apolipoprotein E polymorphism is not associated with lipid levels and coronary artery disease in Greek patients with familial hypercholesterolaemia.

Familial hypercholesterolaemia is a genetic disorder characterised by high low-density lipoprotein (LDL) cholesterol concentrations, which frequently gives rise to premature coronary artery disease (CAD). The clinical expression of familial hypercholesterolaemia is highly variable even in patients carrying the same LDL receptor gene mutation. This variability may be due to environmental and other genetic factors. Apolipoprotein E (Apo-E) has been extensively studied for its effects on the phenotype of familial hypercholesterolaemia. In this study we examined the influence of Apo-E genotype on lipid parameters and the incidence of CAD in 93 Greek patients with familial hypercholesterolaemia. Apo-E E2, E3 and E4 allele frequencies were 0.06, 0.86 and 0.09 respectively. The levels of total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides, apolipoproteins A and B and lipoprotein alpha did not differ significantly among carriers and non-carriers of the E4 allele. The prevalence of CAD and hypertension did not differ either. Our results suggest that the E4 allele is not associated with lipid levels or with the prevalence of CAD among familial hypercholesterolaemia patients of the Greek population.

Adult↗
PubMed2005

The controversial role of serum uric acid in essential hypertension: relationships with indices of target organ damage.

The role of serum uric acid (SUA) in the context of adverse cardiovascular events in hypertensive subjects is controversial. Additionally, the relationship between SUA and indices of target organ damage is not well defined in this setting. Towards this end, we studied 842 consecutive nondiabetic patients with stage I-II essential hypertension (office blood pressure=148/95 mmHg, aged 53.4 years), referred to our outpatient hypertensive unit within a period of 4 years. According to the urinary albumin excretion (UAE), the study population was classified into those with microalbuminuria [MA(+), UAE=20-200 mg/24 h, n=222] and those without MA [MA (-), UAE< 20 mg/24 h, n=620]. Moreover, according to the presence of left ventricular hypertrophy (LVH) the participants were subdivided into two additional groups: [LVH (+), n=305 and LVH (-), n=537]. SUA levels were higher by 0.4 mg/dl, (P=0.04) in group MA (+) compared with the group MA (-), while no difference was observed between groups LVH (+) and LVH (-) (P=NS). In the entire population, SUA was correlated with body mass index (BMI) (r=0.17, P<0.001), waist/hip ratio (r=0.3, P<0.001), office systolic blood pressure (SBP) (r=0.14, P<0.05), triglycerides levels (r=0.25, P<0.001), UAE (r=0.35, P<0.001) and HDL (r=-0.26, P<0.001). Multiple regression analysis demonstrated that SUA was significantly related with BMI, office SBP and UAE (P<0.05). In conclusion, increased SUA levels are associated with MA but not with LVH in essential hypertensive subjects. Whether these inter-relationships may elucidate the clinical positioning of augmented SUA in this setting remains to be clarified in future studies.

Albuminuria↗
PubMed2005

The J-shape effect of alcohol intake on the risk of developing acute coronary syndromes in diabetic subjects: the CARDIO2000 II Study.

AIMS: To identify the threshold of alcohol consumption above which the balance of risk and benefit becomes adverse in diabetic subjects. METHODS: We studied demographic, lifestyle, dietary and clinical information in 216 hospitalized diabetic patients (171 men, 63 +/- 9 years old, 45 women, 67 +/- 5 years old) with a first event of an acute coronary syndrome (ACS) and 196 frequency matched (age-sex) diabetic controls, without any clinical evidence of coronary heart disease. Alcohol consumption was quantified and a measure for the comparisons was predetermined to be a wine glass (100 ml of wine, 12 g of ethanol) and its alcohol equivalents. RESULTS: Alcohol consumption was associated with an age-adjusted J-shape relationship with total cholesterol, blood pressure and smoking (all P < 0.001). A J-shape association was also found between alcohol intake and the risk of ACS (OR = 2.54-2.43 x (alcohol intake) + 0.80 x (alcohol intake)2, R2 = 0.96, P < 0.001), adjusted for several risk factors and interactions between alcohol intake and smoking status, job and familial stress, and low income. In particular, low alcohol consumption (< 12 g/day) was associated with a 47% (OR = 0.53, 95% CI 0.28-0.97) reduction of the prevalence of ACS, while a higher intake (12-24 and > 24 g/day) increased the prevalence by 2.7-fold (OR = 2.72, 95% CI 1.39-5.38) and 5.4-fold (OR = 5.44, 95% CI 1.21-24.55), respectively. CONCLUSIONS: Alcohol intake is a significant predictor of coronary events. Low-to-moderate intake seems to be associated with a reduction in the prevalence of ACS in diabetes, whereas higher consumption is associated with an increase in lipids and blood pressure levels, and also the risk of developing ACS.

Age Factors↗
PubMed2005

The epidemiology of Type 2 diabetes mellitus in Greek adults: the ATTICA study.

AIMS: Individuals with Type 2 diabetes are at high risk for coronary heart disease, and may benefit from aggressive lifestyle modification. We evaluated the prevalence of Type 2 diabetes, in a Greek adult population, in relation to physical activity and dietary habits. METHODS: From May 2001 to December 2002, we randomly enrolled 1514 men and 1528 women, with no evidence of cardiovascular or any other chronic disease. The sampling was stratified by the age and gender distribution of the general population in the greater area of Athens (census 2001). Diabetes was defined according to the established American Diabetes Association criteria. Dietary habits were assessed through a validated food frequency questionnaire and a diet score was developed, in which higher values suggest greater adherence to the Mediterranean diet. Weekly energy expenditure was assessed by considering frequency, duration and intensity of sports-related physical activity during a usual week. RESULTS: After age adjustment for the Greek adult population (2001 census), the projected prevalence of Type 2 diabetes was 7.6% in men and 5.9% in women. A significant proportion of diabetic subjects (24% of men and 30% of women) were unaware of their condition. Moreover, a 10-unit increase in the diet score was associated with 21% lower odds of diabetes (P < 0.05), while individuals taking light physical activity were at 35% lower odds ratio of diabetes compared with sedentary individuals (P < 0.05). CONCLUSIONS: Diabetes mellitus is common in our population, with approximately 1 in 5 individuals with Type 2 diabetes being unaware of their condition. The lifestyle approach described here may contribute significantly to the reduction in the prevalence of diabetes, at a population level.

Adolescent↗
PubMed2005

Effects of atorvastatin on reactive hyperaemia and the thrombosis-fibrinolysis system in patients with heart failure.

OBJECTIVE: To investigate the effects of short term atorvastatin treatment on forearm vasodilatory response to reactive hyperaemia (RH%) and on components of the thrombosis-fibrinolysis system (antithrombin III, proteins and S, factors V and VII, von Willebrand factor, tissue plasminogen activator (tPA), and plasminogen activator inhibitor (PAI-1)) in patients with heart failure. PATIENTS AND METHODS: 35 patients with heart failure were enrolled in this study; 17 patients received atorvastatin 10 mg/day and 18 patients received no statin for four weeks. Forearm blood flow (FBF) was measured by venous occlusion strain gauge plethysmography. RH% and forearm vasodilatory response to nitrate were defined as the percentage change of FBF from rest to the maximum flow during reactive hyperaemia and after nitrate administration, respectively. Plasma concentrations of antithrombin III, protein C, protein S, factor V, factor VII, von Willebrand factor, tPA, and PAI-1 were determined before and after treatment. RESULTS: Maximum hyperaemic FBF remained unchanged in both groups. Baseline FBF was slightly but not significantly decreased in the atorvastatin treated group. RH% was significantly increased only in the atorvastatin treated group, from mean (SD) 42.44 (18.9)% to 83.7 (36.1)% (p < 0.01). Plasma concentrations of antithrombin III (from mean (SD) 81.7 (11.37)% to 73.5 (13.8)%), protein C (from mean (SD) 88.3 (26.9)% to 63.9 (25.0)%), factor V (from mean (SD) 126.2 (33.4)% to 94.9 (29.8)%), tPA (from median (25th-75th percentile) 11.68 (8.60-20.95) ng/ml to 10.30 (8.65-15.12) ng/ml), and PAI-1 (from median (25th-75th percentile) 3.10 (2.15-4.40) IU/l to 1.90 (0.75-3.0) IU/l) were significantly decreased in the atorvastatin treated group (p < 0.05) but not in the control group. Plasma concentrations of von Willebrand factor, factor VII, and protein S remained unaffected in both groups. CONCLUSION: Atorvastatin did not change the maximum hyperaemic flow, although it decreased plasma concentrations of antithrombin III, protein C, factor V, tPA, and PAI-1 in patients with heart failure. Therefore, short term treatment with atorvastatin may affect the expression of both endothelium and liver derived components of the thrombosis-fibrinolysis system in patients with heart failure.

Aged↗
PubMed2005

Effects of vitamin C on intracoronary L-arginine dependent coronary vasodilatation in patients with stable angina.

OBJECTIVE: To assess the effects of intravenous vitamin C administration on the vasomotor responses to intracoronary L-arginine infusion in epicardial coronary arteries. METHODS: 28 patients with coronary artery disease and stable angina were enrolled in the study. Eight patients received intracoronary infusions of 150 micromol/min L-arginine before and after intravenous infusion of vitamin C, 10 patients received intracoronary infusions of 150 micromol/min L-arginine before and after intravenous infusion of normal saline, and 10 patients received intracoronary normal saline before and after intravenous infusion of vitamin C. The diameter of proximal and distal coronary artery segments was measured by quantitative angiography. RESULTS: Infusion of L-arginine caused significant dilatation of both proximal (4.87 (0.96)%, p < 0.01 v normal saline) and distal (6.33 (1.38)%, p < 0.01 v normal saline) coronary segments. Co-infusion of vitamin C and L-arginine dilated proximal coronary segments by 8.68 (1.40)% (p < 0.01 v normal saline, p < 0.01 v L-arginine) and distal segments by 13.07 (2.15)% (p < 0.01 v normal saline, p < 0.01 v L-arginine). Intravenous infusion of vitamin C caused a borderline increase in proximal and distal coronary segment diameters (1.93 (0.76)% and 2.09 (1.28)%, respectively, not significant). CONCLUSIONS: L-arginine dependent coronary segment vasodilatation was augmented by the antioxidant vitamin C in patients with coronary artery disease. Thus, vitamin C may have beneficial effects on nitric oxide bioavailability induced by L-arginine.

Angina Pectoris↗
PubMed2004

FH clinical phenotype in Greek patients with LDL-R defective vs. negative mutations.

BACKGROUND: Familial hypercholesterolaemia (FH) is caused by mutations in the low-density lipoprotein receptor gene and the gene encoding apolipoprotein B-100, affecting one in 500 individuals. METHODS: One hundred and eighty-three Greek FH patients were screened for mutations on the LDLR and ApoB genes. RESULTS: We identified mutations in 67 probands and 11 relatives. Sixteen mutations located in eight different exons and the promoter of the LDLR were discovered. Among them 10 were missense mutations (C6W, S265R, A370T, Q363P, D365E, V408M, A410T, A517T, G528D, G571E), two were nonsense mutations (Q363X and C660X), three were splice defects (2140 + 5G-->A and 2140 + 9C-->T, 1706 - 10G-->A), and one was a nucleotide substitution (- 45delT) on the promoter. None of the subjects carried any apoB mutation. The detection rate of mutations in this study was 43%. From the above mutations, A410T, A519T and the splice site defects 2140 + 9C-->T were detected for the first time in the Greek population. Among them V408M, G528D, C6W and S265R account for 73% of heterozygous FH probands. V408M mutation is more common in Central West, while C6W is more common in Central East. Separating the patients into two groups (receptor defective and receptor negative) we found that the receptor negative group had higher levels of total cholesterol, low-density lipoprotein cholesterol and higher prevalence of tendon xanthomas compared with the receptor-defective group. DISCUSSION: The homogenous molecular basis of familial hypercholesterolaemia in Greece facilitates the application of a DNA diagnostic strategy based on the origin of the patient. The early mutation analysis would add valuable information on the severity of the disease.

Apolipoprotein B-100↗