Petra M Gorter

University Medical Center Utrecht, Utrecht, Utrecht, Netherlands

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Publications (10)35.05 Total impact

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    ABSTRACT: Insulin resistance is accompanied by a cluster of metabolic changes, often referred to as metabolic syndrome. Metabolic syndrome is associated with an increased cardiovascular risk in patients with manifest arterial disease. We investigated whether insulin resistance is associated with an increased risk for cardiovascular events in patients with manifest arterial disease without known diabetes and whether this can be explained by the components of the metabolic syndrome or by inflammation. Prospective cohort study in 2611 patients with manifest arterial disease without known diabetes. Homeostasis model of insulin resistance (HOMA-IR) was used to quantify insulin resistance. The relation of HOMA-IR with cardiovascular events (vascular death, myocardial infarction or stroke) and all cause mortality was assessed with Cox regression analysis. In additional models adjustments were performed for the single components constituting the metabolic syndrome and for inflammation. HOMA-IR increases with the number of metabolic syndrome components (mean HOMA-IR ± SD in groups with 0, 1, 2, 3, 4 and 5 metabolic syndrome components: 1.4 ± 0.7; 1.8 ± 1.2; 2.4 ± 1.5; 3.1 ± 1.8; 4.0 ± 2.6; and 5.6 ± 3.6 respectively). High HOMA-IR was independently associated with an increased risk of cardiovascular events (tertile 2 vs. 1 HR 1.92; 95%CI 1.20-3.08) (tertile 3 vs.1 HR 1.78; 95%CI 1.10-2.89) and with all cause mortality (tertile 2 vs. 1 HR 1.80; 95%CI 1.04-3.10) (tertile 3 vs.1 HR 1.56; 95%CI 0.88-2.75). These relations were not influenced by the individual components of metabolic syndrome or by inflammation. In patients with manifest arterial disease without known diabetes, insulin resistance increases with the number of metabolic syndrome components, and elevated insulin resistance increases the risk of new cardiovascular events.
    Cardiovascular Diabetology 11/2011; 10:100. · 4.21 Impact Factor
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    ABSTRACT: Abdominal obesity and its associated metabolic consequences are major determinants for the development of vascular disease. Fat tissue close to arteries may also directly affect atherogenesis. The study examined whether intra-abdominal fat accumulation is an independent determinant of infrarenal aortic diameter in patients with clinically evident arterial disease. The relationship between metabolic syndrome and infrarenal aortic diameter was also assessed in this patient group. Cross-sectional study was done of 2726 patients with clinically evident arterial disease enrolled in the Second Manifestations of ARTerial Disease (SMART) study. Intra-abdominal fat was measured with ultrasonography and by measuring waist circumference. Metabolic syndrome was defined according to the Adult Treatment Panel III. The maximal anteroposterior diameter of the infrarenal aorta was measured using ultrasonography. The relation between intra-abdominal fat, metabolic syndrome, and infrarenal aortic diameter was determined with linear regression analyses and adjusted for age, sex, height, and smoking. Infrarenal aortic diameters (mm) increased across quartiles of intra-abdominal fat derived by ultrasonography (quartile 4, 19 +/- 7 mm vs quartile 1, 17 +/- 5 mm; adjusted beta, 1.34; 95% confidence interval [CI], 0.73-1.94) and across quartiles of waist circumference (quartile 4, 19 +/- 7 mm vs quartile 1, 17 +/- 5 mm; adjusted beta, 1.43; 95% CI, 0.82-2.04). Patients with metabolic syndrome had slightly larger infrarenal aortic diameters (18 +/- 7 mm vs 17 +/- 6 mm; adjusted beta, 0.70; 95% CI, 0.27-1.13) compared with those without metabolic syndrome. Intra-abdominal fat accumulation and metabolic syndrome are associated with larger infrarenal aortic diameters in patients with clinically evident arterial disease. These data may indicate a role for intra-abdominal fat in the development of larger aortic diameters.
    Journal of Vascular Surgery 08/2008; 48(1):114-20. · 2.88 Impact Factor
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    ABSTRACT: Fat surrounding coronary arteries might aggravate coronary artery disease (CAD). We investigated the relation between epicardial adipose tissue (EAT) and pericoronary fat and coronary atherosclerosis and coronary artery calcium (CAC) in patients with suspected CAD and whether this relation is modified by total body weight. This was a cross-sectional study of 128 patients with angina pectoris (61 +/- 6 years of age) undergoing coronary angiography. EAT volume and pericoronary fat thickness were measured with cardiac computed tomography. Severity of coronary atherosclerosis was assessed by the number of stenotic (> or =50%) coronary vessels; extent of CAC was determined by the Agatston score. Patients were stratified for median total body weight (body mass index [BMI] 27 kg/m(2)). Overall, EAT and pericoronary fat were not associated with severity of coronary atherosclerosis and extent of CAC. In patients with low BMI, those with multivessel disease had increased EAT volume (100 vs 67 cm(3), p = 0.04) and pericoronary fat thickness (9.8 vs 8.4 mm, p = 0.06) compared with those without CAD. Also, patients with severe CAC had increased EAT volume (108.0 vs 69 cm(3), p = 0.02) and pericoronary fat thickness (10.0 vs 8.2 mm, p value = 0.01) compared with those with minimal/absent CAC. In conclusion, EAT and pericoronary fat were not associated with severity of coronary atherosclerosis and CAC in patients with suspected CAD. However, in those with low BMI, increased EAT and pericoronary fat were related to more severe coronary atherosclerosis and CAC. Fat surrounding coronary arteries may be involved in the process of coronary atherosclerosis, although this is different for patients with low and high BMIs.
    The American Journal of Cardiology 08/2008; 102(4):380-5. · 3.21 Impact Factor
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    ABSTRACT: Adipose tissue surrounding coronary arteries may contribute to the development of coronary atherosclerosis given its localisation and potential for local production of inflammatory cytokines. We compared various measurements for quantifying epicardial adipose tissue (EAT) and peri-coronary fat using cardiac CT. Additionally, we estimated their relationship with obesity and metabolic syndrome in patients suspected of coronary artery disease (CAD). EAT and peri-coronary fat measurements were performed on cardiac multi-slice CT scans in 60 patients (aged 50-70 years) referred for coronary angiography. EAT was measured as thickness on the right ventricular free wall, as area at the base of the ventricles, and as volume. Peri-coronary fat was assessed as thickness and cross-sectional area surrounding the three main coronary arteries. Linear regression analysis was used to assess the relation of EAT and peri-coronary fat with obesity and metabolic syndrome (ATPIII criteria). Volumetric EAT measurements showed good reproducibility with low coefficients of variation (CVs) varying between 3.0% and 5.0%. Measurements of EAT and peri-coronary fat thickness and area were moderately reproducible (CVs 11.0-23.4%). The amount of EAT and peri-coronary fat (per standard deviation) was related with obesity (BMI > or =30 kg/m(2)) (beta 1.24; 95% CI 0.66; 1.81) and metabolic syndrome (beta 0.81; 95% CI 0.28; 1.33). Volumetric quantification of EAT using cardiac CT is highly reproducible compared to more simple measurements as EAT and peri-coronary fat thickness and area. The quantity of EAT and peri-coronary fat is related with the presence of obesity and metabolic syndrome in patients suspected of CAD.
    Atherosclerosis 05/2008; 197(2):896-903. · 3.71 Impact Factor
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    ABSTRACT: To determine whether peri-coronary epicardial adipose tissue (EAT) is associated with vascular risk factors and coronary atherosclerosis. In this study, 573 healthy post-menopausal women underwent a cardiac CT scan to assess coronary calcification. Peri-coronary EAT thickness was measured in the areas of right coronary artery (RCA), left anterior descending (LAD) artery, and left circumflex (LCX) coronary artery. Average EAT thickness was 16.5 +/- 4.3 mm (range 5.9-34.6) in the RCA area, 6.4 +/- 2.2 mm (range 2.0-14.0) in the LAD area, and 10.8 +/- 3.0 mm (range 2.8-29.1) in the LCX area. Overall average thickness was 11.2 +/- 2.2 mm (range 5.4-19.1). EAT was positively related to age (P = 0.002). In age-adjusted linear regression models, EAT was positively related to weight (P< 0.001), waist circumference (P< 0.001), waist-to-hip ratio (P< 0.001), body mass index (P< 0.001), glucose (P< 0.001), triglycerides (P = 0.001), use of anti-hypertensive drugs (P = 0.007), and systolic blood pressure (P = 0.034), and inversely to HDL cholesterol (P = 0.005). In multivariable models, age, weight, waist circumference, smoking, and glucose were the main determinants of EAT. EAT showed a graded relation with coronary calcification (P = 0.026). EAT is strongly related to vascular risk factors and coronary calcification. Our findings support the hypothesis that EAT affects coronary atherosclerosis and possibly coronary risk.
    European Heart Journal 04/2008; 29(6):777-83. · 14.10 Impact Factor
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    ABSTRACT: Patients with Type 2 diabetes and coronary heart disease (CHD) have an excess cardiovascular risk. The relationship of both other sites [cerebrovascular disease, peripheral arterial disease (PAD)] and the extent of clinically evident cardiovascular disease (CVD) with the occurrence of new cardiovascular events have not been investigated previously in patients with diabetes. We aimed to quantify this relationship and to assess the additional influence of atherosclerotic burden. From 1996 to 2005, 776 patients with Type 2 diabetes with (n = 458) and without (n = 318) clinically evident CVD were followed prospectively for cardiovascular events (cardiovascular death, non-fatal ischaemic stroke or myocardial infarction). CVD was classified according to the site (cerebrovascular disease, CHD, PAD); the extent of atherosclerosis was expressed as the number of affected sites. Carotid intima-media thickness and albuminuria were used as markers of atherosclerotic burden. Compared with patients with diabetes without CVD, the hazard ratio (HR) for a cardiovascular event was 3.8 (95% confidence interval 1.7, 8.5), adjusted for age, gender and potential confounders, in those with cerebrovascular disease, 4.3 (1.9, 9.5) in those with CHD, and 4.6 (2.1, 10.2) in those with PAD. Findings were similar after additional adjustment for atherosclerotic burden. Adjusted HR was 3.4 (1.6, 6.9) for patients with diabetes with one affected site and 6.6 (3.0, 14.3) for those with two or more sites. Patients with Type 2 diabetes and cerebrovascular disease, CHD or PAD have strongly increased risks for future cardiovascular events which are comparable. This risk increases markedly with the number of different cardiovascular sites affected and is irrespective of atherosclerotic burden.
    Diabetic Medicine 01/2008; 24(12):1352-60. · 3.24 Impact Factor
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    P.M. Gorter
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    ABSTRACT: The work in this thesis focused on the relationship between presence of insulin resistance and advanced vascular damage in patients with manifest atherosclerotic vascular disease, and on the occurrence of (new) vascular events in insulin resistant patients with and without evident vascular disease. Also, the relationship between adipose tissue (abdominal fat and fat surrounding coronary arteries) and atherosclerotic vascular damage was examined. Patients with evident vascular disease or high insulin resistance (e.g. patients with metabolic syndrome or type 2 diabetes) are particularly prone to develop (new) vascular diseases. We demonstrated that metabolic syndrome, the clustering of vascular risk factors associated with insulin resistance, was highly prevalent (46%) in patients with manifest arterial disease. Also, an elevated level of insulin resistance was associated with an increased prevalence of albuminuria in patients with arterial disease. This association was only partly mediated by components of metabolic syndrome. High insulin resistance was not associated with an increased carotid intima-media thickness. Thus, insulin resistance may play a role in different stages of the atherosclerotic process. Another study showed that diabetic patients with cerebrovascular disease, coronary heart disease or peripheral arterial disease had a similar three- to fourfold higher risk of new vascular events, compared with diabetic patients without vascular disease. Diabetic patients with two or more clinical manifestations of atherosclerosis at different vascular sites had an even higher cardiovascular risk. Counting the number of sites of evident vascular disease, irrespective of the type of vascular disease, may help to simply identify those patients with diabetes type 2 particularly at very high risk for new macrovascular complications from a generally high-risk diabetic population. In case of obesity, an imbalanced production of pro- and anti-inflammatory cytokines by abdominal fat not only induces insulin resistance and consequently metabolic syndrome, but also leads directly to the development of endothelial dysfunction and progression of atherosclerosis. We found that infrarenal aortic diameter was larger in patients with more intra-abdominal fat compared to those with less intra-abdominal fat, suggesting that intra-abdominal fat may play a role in the process of aortic dilatation. Also, there is growing evidence that the adipose tissue directly surrounding the coronary arteries may affect atherogenesis from ‘outside to inside’ by the local release of a large number of pro-inflammatory factors. We determined the reproducibility of various measurements (thickness, area, volume) for quantifying epicardial adipose tissue (EAT) and peri-coronary fat using cardiac CT scans of patients undergoing coronary angiography (CAG). Volumetric quantifications of EAT were highly reproducible (coefficient of variations (CVs) 3%-5%) compared to thickness and area measurements of EAT and peri-coronary fat (CVs 11%-23%). EAT and peri-coronary fat accumulations were both associated with obesity and presence of metabolic syndrome in these patients. EAT volume and peri-coronary fat thickness were not associated with the severity of coronary atherosclerosis and extent of CAC in the whole study population. Nonetheless, in patients with a BMI <27 kg/m2, those with multi-vessel disease had higher EAT volume and peri-coronary fat thickness than those without coronary artery disease. Also, patients with severe or extensive CAC had higher EAT volume and peri-coronary fat thickness compared to those with minimal or absent CAC.
    01/2008;
  • Atherosclerosis Supplements - ATHEROSCLER SUPPL. 01/2007; 8(1):134-134.
  • Atherosclerosis Supplements - ATHEROSCLER SUPPL. 01/2006; 7(3):335-335.
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    ABSTRACT: Metabolic syndrome patients are at increased risk for developing cardiovascular morbidity and mortality. The increasing prevalence of the metabolic syndrome in various asymptomatic populations has been well documented, however, limited information is available about the prevalence in manifest atherosclerotic vascular disease patients. The aim of this study is to determine the overall and gender-specific prevalence of the metabolic syndrome and its components in these patients. This cross-sectional survey of 1117 patients, aged 18-80 years, mean age 60+/-10 years, comprised patients with coronary heart disease (n=527), cerebrovascular disease (n=258), peripheral arterial disease (n=232) or abdominal aortic aneurysm (n=100). Metabolic syndrome was defined by Adult Treatment Panel III. The prevalence of the metabolic syndrome in the study population was 46%: 58% in PAD patients, 41% in CHD patients, 43% in CVD patients and 47% in AAA patients. Overall, women had a higher prevalence than men (56% versus 43%). Age did not influence the metabolic syndrome prevalence; crude odds ratios (crude OR) 1.00 (95% CI: 0.99-1.02). Our results demonstrate a high prevalence of the metabolic syndrome in patients with manifest atherosclerotic vascular disease. Screening for metabolic syndrome in patients with high risk for new vascular incidents may identify patients with even higher vascular risk and may direct anti-atherosclerotic treatment in order to prevent new vascular incidents in the same or another vascular bed.
    Atherosclerosis 05/2004; 173(2):363-9. · 3.71 Impact Factor