Tevfik Gürmen

The Relationship Between Chronic Kidney Disease and SYNTAX Score

Chronic kidney disease (CKD) is associated with increased risk of cardiovascular disease and death. We evaluated the association between CKD and severity of coronary artery stenosis by calculating SYNTAX Score in patients with left main coronary artery and/or 3-vessel coronary artery disease. Coronary angiograms of 217 patients were assessed. Chronic kidney disease was staged using the estimated glomerular filtration rate (eGFR, mL/min per 1.73 m2) prior to coronary angiography. Patients were divided into 5 groups according to the National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF KDOQI) Clinical Practice Guidelines (14). Patients with eGFR >90 mL/min per 1.73 m2 (group 1), patients with eGFR 60 to 89 mL/min per 1.73 m2 (group 2), patients with eGFR 30 to 59 mL/min per 1.73 m2 (group 3), patients with eGFR >15 to < 30 per 1.73 m2 and dialysis patients with eGFR < 15 per 1.73 m2 were combined as group 4. The risk of significant lesion complexity increased progressively with decreasing kidney function (P = .001). Estimated glomerular filtration rate was a strong predictor of higher SYNTAX Score.

Impact of Rosuvastatin on Contrast-Induced Acute Kidney Injury in Patients at High Risk for Nephropathy Undergoing Elective Angiography

Although statins have been shown to prevent contrast-induced acute kidney injury in patients with acute coronary syndromes, the benefit of statins is not known for patients at high risk for nephropathy who undergo elective coronary angiography. Two hundred twenty consecutive statin-naive patients with chronic kidney disease (estimated glomerular filtration rate <60 ml/min/1.73 m(2)) who underwent elective coronary or peripheral angiography were randomly assigned to receive rosuvastatin (40 mg on admission, followed by 20 mg/day; n = 110) or no statin treatment (control group, n = 110). Contrast-induced acute kidney injury was defined by an absolute increase in serum creatinine of ≥0.5 mg/dl or a relative increase of ≥25% measured 48 or 72 hours after the procedure. Contrast-induced acute kidney injury occurred in 15 patients (7.2%), 9 (8.5%) in the control group and 6 (5.8%) in the rosuvastatin group (p = 0.44). The incidences of adverse cardiovascular and renal events (death, dialysis, myocardial infarction, stroke, or persistent renal damage) were similar between the two groups at follow-up. In conclusion, rosuvastatin did not reduce the risk for contrast-induced acute kidney injury or other clinically relevant outcomes in at-risk patients who underwent coronary and peripheral vascular angiography.

Chronic Kidney Disease as a Predictor of Coronary Lesion Morphology

Coronary artery disease (CAD) is the main cause of death in patients with chronic kidney disease (CKD). We investigated whether CKD stage affected coronary lesion morphology in patients with established CAD. Coronary angiograms of 264 patients were evaluated. Chronic kidney disease was staged using the estimated glomerular filtration rate (eGFR) from the serum creatinine prior to coronary angiography. Patients were divided into 3 groups: dialysis or severe decrease in GFR <30 mL/min per 1.73 m2 (group 1; n = 60), patients with moderate kidney failure (group 2; n = 116), and patients with normal renal function or mild decrease in GFR (group 3; n = 88). The likelihood of CAD and lesion complexity increased with decreasing eGFR (P = .001). Patients with CKD also had more significant CAD. The risk of significant coronary obstruction and lesion complexity increased progressively with decreasing eGFR. The eGFR may predict lesion complexity among patients with CKD undergoing coronary angiography.

Relationship Between Increased Serum Resistin Level and Severity of Coronary Artery Disease

Resistin, which is derived from the gene of RSTN, belongs to a family of cysteine-rich secretory proteins called resistin-like molecules (RELMs). Increased serum resistin levels are associated with coronary artery disease (CAD) and the risk of cardiovascular death. Patients (n = 214) with an initial diagnosis of stable angina pectoris, unstable angina pectoris, and myocardial infarction without ST-segment elevation and referred to catheter laboratory for coronary angiography were enrolled in the study. We aimed to investigate the relationship between increased serum resistin level and CAD. The severity of CAD was calculated by the Gensini scoring system. In conclusion, we established a significant correlation between serum resistin levels and CAD (P = .010). Also, serum resistin levels correlated with the Gensini score that represents the severity of CAD angiographically (P = .010).

Relationship between serum endothelin-1 level and spontaneous reperfusion in patients with acute myocardial infarction.

AimSpontaneous reperfusion (SR) was associated with better clinical outcomes and lower incidence of major adverse cardiovascular events. Endothelin-1 (ET-1) is a potent endothelium-derived vasoconstrictor peptide and elevated systemic ET-1 levels predict a poor prognosis in patients with ST-segment elevation myocardial infarction (STEMI). We aimed to investigate the relationship between systemic ET-1 plasma levels and SR in a group of STEMI patients treated with a primary percutaneous coronary intervention (PCI). Methods and resultsWe measured ET-1 levels acutely (within the first 6 h) in 33 STEMI patients with SR and 45 STEMI patients with non-SR presenting with their first STEMI who underwent primary PCI. Blood samples for ET-1 plasma level measurement were drawn after vascular puncture before angiography in the catheterization laboratory from the peripheral vein.The mean age of the patients was 56.1±13.3 years in the SR group and 57.4±11.4 years in the non-SR group. The circulating level of ET-1 was considerably higher in the non-SR patients than in the SR patients (0.81±0.2, 1.0±0.3, P=0.004). On multivariable logistic regression analysis, the ET-1 level was the only significant predictor of SR (P=0.01).The receiver operating characteristic curve analysis showed that the ET-1 level at admission is an indicator of SR, with an area under the curve of 0.62. ConclusionThis study shows that in patients admitted with ST-elevation acute myocardial infarction, ET-1 plasma levels are related to angiographic SR before primary PCI.

Percutaneous coronary intervention vs. optimal medical therapy – the other side of the coin: medication adherence

Although many studies have examined medication adherence in patients with coronary artery disease (CAD), no prospective trial has compared medication adherence between patients treated with percutaneous coronary intervention (PCI) or with optimal medical therapy (OMT) in real life. This study sought to compare the adherence to evidence‐based secondary preventive medications in patients with documented CAD treated with PCI and OMT, or OMT alone.

Increased secretion of insulin during oral glucose tolerance test can be a predictor of stent restenosis in nondiabetic patients

Insulin is known to stimulate proliferation and migration of vascular smooth muscle cells. As the predominant mechanism of restenosis after stent implantation is neointimal tissue proliferation, one can expect a relationship between hyperinsulinemia and restenosis in these patients. The aim of this study was to determine whether hyperinsulinemia during oral glucose tolerance test is a predictor of the development of restenosis after stent implantation in nondiabetic patients. We prospectively studied 52 nondiabetic patients with effort angina who underwent elective stent implantation for single‐vessel coronary artery disease. In order to increase the statistical power of the study, numerous exclusion criteria were applied. All patients were subjected to a 75 g oral glucose tolerance test a day before the stent implantation and underwent follow‐up angiography 6 months later. Plasma insulin levels in fasting (6.77 ± 1.57 vs. 5.36 ± 1.35 μU/ml; P = 0.005), at 30 min (102.48 ± 10.6 vs. 47.74 ± 12.75 μU/ml; P = 0.001), 1 hr after (120.23 ± 14.1 vs. 63.08 ± 12.62 μ/ml; P = 0.001), 2 hr after (63.58 ± 8.64 vs. 34.88 ± 6.82 μ/ml; P = 0.001), and 3 hr after (25.71 ± 5.65 vs. 23.02 ± 4.61 μ/ml; P = 0.04) loading were significantly higher in patients with stent restenosis than in patients without stent restenosis. Insulin area and insulin area/glucose area were also significantly higher in patients with stent restenosis than in patients without (219.5 ± 23.8 vs. 118.9 ± 21.8, P = 0.001, and 0.62 ± 0.09 vs. 0.33 ± 0.06, P = 0.001, respectively). By multiple logistic regression analysis, insulin area during oral glucose tolerance test was found to be an independent predictor of stent restenosis (OR = 1.12; 95% CI = 1.01–1.25; P = 0.031). In conclusion, nondiabetic patients with hyperinsulinemia during oral glucose tolerance test have a high risk for restenosis after stent implantation, and performing this simple test before intervention may be useful for the prediction of stent restenosis. Cathet Cardiovasc Intervent 2003;58:306–312.

Laboratory signs of aspirin response in haemodialysis patients.

Abstract Introduction. Aspirin is effective in the secondary prevention and high-risk primary prevention of cardiovascular events. However, clinical and laboratory evidence demonstrates diminished or no response to aspirin in some patients. This study was designed to assess aspirin response in haemodialysis patients. Methods. We prospectively enrolled 78 haemodialysis patients (28 female; 58.4 ± 12.6 years old) and 79 patients (29 female; 58.4 ± 10.6 years old) with normal renal function (glomerular filtration rate (GFR) >60 mL/min/1.73 m2). All subjects in both the haemodialysis patient group and the control group were taking aspirin (80–300 mg) for at least 30 days and were not taking other antiplatelet agents. Platelet function was assessed by arachidonic acid-induced aggregometry with a Multiplate analyser (Dynabyte Medical, Munich, Germany). Multiplate electrode aggregometry values below 300 AU were applied as a cut-off for response to aspirin. Results. Aspirin non-response was two-fold more prevalent in haemodialysis patients (42.3%) than in patients with normal renal function (21.5%), and this difference was statistically significant (p = 0.005). The two groups were similar in terms of sex, age, tobacco use, the presence of diabetes mellitus, and platelet count. Conclusions. The frequency of aspirin non-response as defined in this study was higher in haemodialysis patients than in patients with normal renal function. However, larger subsets of patients are needed to confirm the present study.

Chronic total occlusion of left circumflex artery after radiofrequency ablation of left ventricular outflow tract tachycardia

In this report, we present a 22-year-old female patient referred to our institution for evaluation of anginal chest pain. Her medical history revealed two ablation procedures of the left ventricular outflow tract tachycardia performed 1 month a part, 2 years ago. Coronary angiography revealed chronic total occlusion of the proximal left circumflex artery. To our knowledge, this is the first report of ablation-related chronic total occlusion of a coronary artery.

Admission Hyperglycemia and TIMI Frame Count in Primary Percutaneous Coronary Intervention

We evaluated the relationship between admission blood glucose levels and estimated coronary flow by the thrombolysis in myocardial infarction (TIMI) frame count (TFC) method in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (pPCI). The TFC of 121 consecutive patients with STEMI were evaluated after pPCI. Patients with admission glucose levels >198 mg/dL (11 mmol/L) were defined as hyperglycemic. Hyperglycemia was observed in 36 (29.8%) patients. The TFC was significantly higher in patients with hyperglycemia (70.75 [10-96] vs 56.87 [8-100], P = .04). No-reflow frequency was higher in the hyperglycemia group (44.4% vs 23.5%, P = .02). In multivariate linear regression analysis admission glucose was an independent predictor of high TFC (B = 0.21, P = .02). Our findings suggest that admission blood glucose is a predictor of TFC which reflects coronary blood flow.