Association between excess catecholamine synthesis and polymorphic premature ventricular contraction.

BACKGROUND: The reasons for the etiology of premature ventricular contractions (PVCs) are not specifically known. Many patients are resistant to medical treatment, and a factor that would predict response to medical treatment cannot be identified. This study aims to investigate if a high catecholamine level results in polymorphic PVC. METHODS: This study was obtained by prospective data registry analysis. A total of 100 patients, 50 from the PVC group, and 50 from the control group have been evaluated. The participants who were included in the patient group had a polymorphic PVC of 5% or more in their 24-h Holter evaluations. Metanephrine showing the level of adrenaline and normetanephrine, showing the level of noradrenaline levels have been measured from these urine samples. RESULT: There was no difference between the two groups in terms of biochemical and essential characteristics. Normetanephrine level has been significantly higher in the PVC group compared to the control group (323.9 ± 208.9 µg to 129.25 ± 67.88 µg; p < 0.001). Similarly, metanephrine level has also been higher in the PVC group (124.75 ± 82.43 µg to 52.615 ± 36,54 µg; p < 0.001). A positive and moderate correlation has been identified between the number and ratio of PVC and the metanephrine and normetanephrine levels. CONCLUSION: In this study, we found that the catecholamine levels were higher in the polymorphic PVC group than in the healthy volunteers. Also, an increase in the number and rate of PVC has been observed as the catecholamine levels increased. CLINICAL TRIAL REGISTRATION: Urine Levels of Metanephrine and Normetanephrine in Patients With Frequent PVC; ClinicalTrials.gov number NCT03447002.

Is electrophysiological study a novel predictor for permanent pacemaker implantation after transcatheter aortic valve implantation?

Background/aim: Despite advancements in valve technology and increased clinical experience, complications related to conduction defects after transcatheter aortic valve implantation (TAVR) have not improved as rapidly as expected. In this study, we aimed to predict the development of complete atrioventricular (AV) block and bundle branch block during and after the TAVR procedure and to investigate any changes in the cardiac conduction system before and after the procedure using electrophysiological study. Materials and methods: A total of 30 patients who were scheduled for TAVR at our cardiovascular council were planned to be included in the study. TAVR was performed on patients at Erciyes University Medical Faculty Hospital as a single center between May 2019 and August 2020 Diagnostic electrophysiological study was performed before the TAVR procedure and after its completion. Changes in the cardiac conduction system during the preprocedure, intra-procedure, and postprocedure periods were recorded. Results: Significant increases in baseline cycle length, atrial-His (AH) interval, his-ventricular (HV) interval and atrioventricular (AV) distance were observed before and after the TAVR procedure (p = 0.039, p < 0.001, p = 0.018, p < 0.001, respectively). During the TAVR procedure, the preprocedural HV interval was longer in patients who developed AV block and bundle branch block compared to those who did not and this difference was statistically significant (p = 0.024). ROC curve analysis revealed that a TAVR preprocedure HV value >59.5 ms had 86% specificity and 75% sensitivity in detecting AV block and bundle branch block (AUC = 0.83, 95% CI: 0.664-0.996, p = 0.013). The preprocedure HV distance was 98 ± 10.55ms in the group with permanent pacemaker implantation and the mean value in the group without permanent pacemaker implantation was 66.27 ± 15.55 ms, showing a borderline significant difference (p = 0.049). Conclusion: The prolongation of HV interval in patients with AV block and bundle branch block suggests that the block predominantly occurs at the infra-hisian level. Patients with longer preprocedural HV intervals should be closely monitored for the need for permanent pacemaker implantation after the TAVR procedure.

Systemic immune inflammation index: a novel predictor for coronary collateral circulation.

AIM: Recently, a new inflammatory and prognostic marker has emerged called as Systemic Immune Inflammation Index (SII). In the current study, we searched the relation between SII and Coronary Collateral Circulation (CCC) formation in stable Coronary Artery Disease (CAD). MATERIALS & METHODS: 449 patients with stable CAD who underwent coronary angiography and documented coronary stenosis of 95% or more in at least one major coronary vessel were included in the study. The study patients were divided into two groups according to the Rentrop score as well CCC (Rentrop 2-3) and bad CCC (Rentrop 0-1). Blood samples for SII and other laboratory parameters were gathered from all the patients on admission. The SII score was formulized as platelet × neutrophil/lymphocyte counts. RESULTS: Patients, who had developed bad CCC had a higher C-reactive protein (CRP), neutrophil/lymphocyte ratio (NLR), platelets/lymphocyte ratio (PLR) and SII levels compared to those who had developed well CCC (p < 0.001, for all). Multivariate logistic regression analysis showed that high levels of SII was an independent predictor of bad CCC (OR: 1.005, 95% confidence interval (CI): 1.003-1.006, p < 0.001) together with dyslipidemia, high levels of CRP and NLR. In Receiver Operator Characteristic curve (ROC) analysis, the optimal cutoff value of SII to predict poor CCC was found to be 729.8, with 78.4% sensitivity and 74.6% specificity (area under ROC curve = 0.833 (95% CI: 0.777-0.889, p < 0.001). CONCLUSION: We have demonstrated that SII, a novel cardiovascular risk marker, might be used as one of the independent predictors of CCC development.

Relationship between thiol, disulphide volume and contrast-induced nephropathy in acute coronary syndrome patients treated with percutaneous coronary intervention.

BACKGROUND: This study aimed to evaluate thiol disulphide volume for the risk of contrast-induced nephropathy (CIN) in patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI). METHODS: A total of 638 patients with ACS were enrolled in the study. CIN was defined as an increase in serum creatinine level of ≥0.5 mg/dL or ≥25% above baseline within 72 h after the procedure. Patients were divided into two groups: patients with and without CIN. Demographics, clinical risk factors, angiographic and laboratory parameters, CIN incidence, thiol, disulphide, and CHA2DS2-VASc score were compared between the two groups. RESULTS: Native thiol, total thiol, and disulphide at baseline were significantly lower in patients who developed CIN compared to those who did not. Also, the CHA2DS2-VASc score was found to be higher in patients with CIN than those without CIN. In receiver operating characteristic analysis showed that at a cutoff of <342.1, the value of native thiol exhibited 82% sensitivity and 80% specificity for detecting CIN. Total thiol< 383.1 calculated on admission had an 80% sensitivity and 80% specificity in predicting CIN. CONCLUSION: Our study suggested that the thiol disulphide volume on admission was independently associated with the development of CIN after PCI in patients with ACS.

New onset atrial fibrilation and risk faktors in COVID-19.

BACKGROUND: There is limited data concerning the prevalence of arrhythmias, particularly atrial fibrillation (AF), which may develop as a consequence of direct myocardial injury and the inflammatory state existing in COVID-19. METHODS: This single-center study included data concerning 658 COVID-19 patients, who were hospitalized in our institute, between April 20th, 2020 and July 30th, 2020. Demographic data, findings of the imaging studies, and laboratory test results were retrieved from the institutional digital database. RESULTS: New onset AF (NOAF) was identified in 33 patients (5%). Patients who developed AF were older (72.42 ± 6.10 vs 53.78 ± 13.80, p < 0.001) and had higher frequencies of hypertension and heart failure compared to patients without NOAF (p < 0.001, for both). The CHA2DS2-VASc score was higher in patients, who developed NOAF, compared to those who did not during hospitalization for COVID-19 (p < 0.001). Subjects, who developed NOAF during hospitalization, had a higher leukocyte count, neutrophil / lymphocyte ratio (NLR), C-reactive protein, erythrocyte sedimentation rate, and procalcitonin levels compared to those without NOAF (p < 0.001 for all comparisons). Diffuse lung infiltration was also more frequent in COVID-19 patients, who developed NOAF, during hospitalization (p = 0.015). Multivariate logistic regression analysis demonstrated that age, CHA2DS2-VASc score, CRP, erythrocyte sedimentation rate, and presence of diffuse lung infiltration on thorax CT were predictive for NOAF. CONCLUSION: The prevalence of NOAF in hospitalized COVID-19 patients is higher than the general population. Age, CHA2DS2-VASc score, C-reactive protein, erythrocyte sedimentation rate, and presence of diffuse lung infiltration on thorax CT may be used to identify patients at high risk for development of NOAF. Especially among these parameters, the presence of diffuse lung infiltration on thorax CT it was the most powerful independent predictor of NOAF development.

Role of dyslipidemia in early vascular aging syndrome

Background/aim: Arterial stiffness, known as a predictor of early vascular aging, was defined as the main determinant of cardiovascular mortality and morbidity. However, the relationship between lipid profile and increased arterial stiffness is not clear. The aim of this study is to investigate the relationship between lipid profiles and increased arterial stiffness in patients with early vascular aging syndrome. Materials and methods: A total of 1582 participants ­504 (31.8%) of were male and the mean age was 52.8 ±14.2 years­ were included in the study . Patients who applied to the hospital for various reasons and who had undergone 24-h blood pressure Holter monitoring were included in this study. Patients were divided into four groups according to pulse wave velocity (PWV) quartiles (Q1 (<6.3), Q2 (6.3­7.4), Q3 (7.5­8.8), Q4 (>8.8)). Results: We found that in the highest PWV group, patients had higher systolic blood pressure (SBP), diastolic blood pressure (DBP), glucose, blood urea nitrogen (BUN), creatinine, urinary albumin excretion (UAE), uric acid(UA), total cholesterol (TC), low-density lipoprotein ( LDL-C), triglycerid (TG), and non- high-density lipoprotein (HDL-C ) levels. Additionally, diabetes mellitus (dm), age, non-HDL-C, and TG/ HDL-C levels were detected as independent risk factors of increased PWV in ordinal logistic regression analysis. Conclusion: Our study demonstrates that lipid parameters are strongly correlated with increased PWVvalue and early vascular aging. In daily clinical practice, TG\HDL-C ratio, known as atherogenic index, might be used routinely for predicted of early vascular aging and subclinical atherosclerosis.

Effect of nondipper hypertension on coronary artery disease progression in patients with chronic coronary syndrome

Background/aim: It has been suggested that there is a significant progress in coronary artery disease (CAD) by many pathophysiological mechanisms. Nondipper hypertension (NDH) has been shown to have higher target organ damage and have a higher rate of cardiovascular mortality and morbidity. In this study, we investigated the effect of nondipper hypertension on the progression of coronary atherosclerosis. Materials and methods: A total of 186 patients who underwent coronary angiography twice between 6 months and 3 years were included in the study. Coronary angiography was repeated on the admission day due to angina or positive exercise test and the patients were divided into groups. Results: Progression of coronary artery disease was detected in 58 of 186 patients. Seventy-one of the total patients were found to be nondipper hypertensive. Nondipper hypertension, hypertension, diabetes mellitus, low-density lipoprotein, and total cholesterol were found to be effective in the progression of CAD. Among these parameters, it was seen that nondipper hypertension and hyperlipidemia were the most important independent risk factors. Conclusion: Coronary artery disease is a progressive disease, and this progression depends on many reasons. In our study, we showed that nondipper hypertension is a new parameter that is effective in CAD progression.

An investigation of the relationship between arterial aortic stiffness and coronary slow flow that was detected during coronary angiography.

AIM: Increased intimal thickness in coronary arteries, extensive calcification, and atheromatous plaque that does not cause luminal irregularities in a significant portion of the patients with coronary slow flow (CSF). Arterial stiffness is an indicator for atherosclerosis. We aimed to investigate the relation between coronary slow flow phenomenon (CSFP) and arterial stiffness. METHOD: Total of 73 patients were included in the study, and a control group was formed with 64 individuals. Aortic stiffness index ß (ASIß) and pulse wave velocity (PWV) were used as the determinant of arterial stiffness in all analyses. RESULT: Pulse wave velocity values were significantly higher in the coronary slow flow group than the control group (P < .001). PWV, aortic stiffness index ß (ASIß) values were found to be significantly higher in the CSF group. ASIß value was 3.4 ± 1.0 in CSF patients and 2.2 ± 0.6 in the control group (P < .001). Receiver operating characteristic curve (ROC) analysis showed that PWV predicted coronary slow flow with 97% sensitivity and 90% specificity for 7.15 cutoff value. And aortic stiffness index was found to predict coronary slow flow with 83% sensitivity and 75% specificity for 2.63 cutoff value. CONCLUSION: Our findings prove that coronary slow flow phenomenon should be considered a subgroup of coronary artery diseases and that increased PWV is an indicator of CSFP.

Management of Renal Artery Occlusion during Endovascular Aortic Repair.

A 67-year-old man was admitted to the emergency unit with abdominal pain. An infrarenal aortic aneurysm with a diameter of 70 millimeters was detected by computed tomography. In the catheter laboratory, graft stents were implanted into the infrarenal aorta. Total occlusion of the right renal artery was seen in angiography. The graft stent was punctured with a 30° angled Brockenbrough catheter, and another stent was implanted.

Risk factors for coronary artery disease in young patients with stable angina pectoris

Background/aim: We aimed to investigate the relationship between risk factors and the presence of coronary artery disease (CAD) in a young population with stable angina pectoris (SAP). Materials and methods: A total of571 individuals younger than 60 years old, admitted to the outpatient clinic with chest pain and referred for coronary angiography between January 2015 and December 2017, were included in the study. All clinical and biochemical parameters were documented in the hospital records. Coronary angiography of patients was monitored from records. The individuals were divided into two groups. The patient group consisted of 363 individuals with at least one-vessel stenosis of ≥70%, and the control group consisted of 208 individuals with normal coronary angiography. We compared the traditional and nontraditional risk factors of these two groups in terms of the presence of CAD. Results: Prevalence of male sex and smoking were higher in the patient group, and the prevalence of hypertension and diabetes were similar in the two groups. In the patient group, mean age, blood cholesterols, serum gamma-glutamyltransferase, hemoglobin, and white blood cell and lymphocyte levels were higher, while estimated glomerular filtration rate (eGFR), high-density lipoprotein cholesterol (HDL-C), platelets, and neutrophil/lymphocyte and platelet/lymphocyte ratios were lower. Low eGFR and HDL-C levels, older age, male sex, smoking, and high levels of low-density lipoprotein cholesterol and lymphocytes were independent risk factors for the presence of CAD in young patients. Conclusion: Contrary to studies performed in the elderly, traditional and nontraditional risk factors could not exactly predict the presence of CAD in a young population with SAP.

The effect of prophylactic migraine treatment on arterial stiffness.

BACKGROUND: Migraine is a common type of primary headache predominantly seen in women. This study aimed to evaluate endothelial function in patients with migraine using pulse wave velocity (PWV). METHODS: The study included 73 patients with newly diagnosed migraine and 80 healthy subjects. All patients and controls underwent baseline transthoracic echocardiography and PWV measurements. Patients were randomized to three groups to receive propranolol, flunarizine or topiramate, and the measurements were repeated at the end of 1 month. RESULTS: The newly diagnosed migraine patients and the control group exhibited no differences in baseline clinical characteristics, and the measurements showed that PWV was 7.4 ± 1.0 m/s in the patient group and 6.0 ± 1.0 m/s in the control group (p < 0.001). The same measurements were repeated during a control visit at the end of 1 month. Following treatment, a significant decrease was observed in PWV in all patient groups compared to baseline (p < 0.001). Subgroup analysis showed significantly decreased PWV in all drug groups, with the most prominent decrease in the topiramate group. CONCLUSIONS: The increased PWV demonstrated in migraine patients in this study stands out as an additional parameter elucidating endothelial dysfunction in these patients. Decreasing the number of migraine attacks with prophylactic treatment may reduce PWV and decrease cardiovascular risk in long-term follow-up.

Association of red blood cell distribution width levels with severity of coronary artery disease in patients with non-ST elevation myocardial infarction.

OBJECTIVES: The aim of this study was to evaluate the association of the levels of red blood cell distribution width (RDW) with the severity of atherosclerosis and to determine whether or not the RDW level on admission is an independent predictor of all-cause mortality in patients with non-ST elevation myocardial infarction (NSTEMI). MATERIALS AND METHODS: A total of 335 consecutive patients with NSTEMI were enrolled in this study. The patients were divided into high (n = 105) and low (n = 230) SYNTAX groups. The high SYNTAX group was defined as patients with a value in the third tertile (SYNTAX score, SXscore ≥12), while the low SYNTAX group was defined as those with a value in the lower 2 tertiles (SXscore <12). The high RDW group (n = 152) was defined as patients with RDW >14.25% and the low RDW group (n = 183) as those with RDW ≤14.25%. All-cause mortality was followed up to 38 months. RESULTS: The mean follow-up period was 18 ± 11 months. The RDW levels of patients were significantly higher in the high SYNTAX group than in the low SYNTAX group (15.2 ± 1.8 vs. 14.2 ± 1.2, p < 0.001). Pearson's coefficients were used to determine the degree of association between RDW levels and SXscore and also between RDW levels and high-sensitivity C-reactive protein. There was a significant correlation between RDW levels and SXscore (r = 0.460, p < 0.001). Also, there was a significant correlation between RDW levels and high-sensitivity C-reactive protein (r = 0.180, p = 0.001). All-cause mortality rate was not significantly different between the high and low RDW groups (log-rank, p = 0.621). CONCLUSION: RDW levels were independently associated with high SXscore but were not associated with long-term mortality in NSTEMI patients.

Mean platelet volume levels predict pulmonary artery hypertension in patients with atrial septal defect.

INTRODUCTION: Some reports have shown increased platelet aggregation and activation in patients with pulmonary artery hypertension (PAH). Mean platelet volume (MPV) is a simple and easy method of assessing platelet function. We aimed to investigate the mean platelet volume levels in patients with atrial septal defect (ASD) and the association between MPV levels and pulmonary artery hypertension. METHOD: One hundred and forty consecutive patients (42 males and mean age 35 +/- 9 y) and forty healthy controls (15 males and mean age 35 +/- 4 y) were enrolled in the study between December 2008 and February 2011. RESULTS: The ASD group demonstrated a significantly higher right ventricular size and pulmonary artery pressure than the control group (42 +/- 4 mm vs. 36 +/- 3 mm and 43 +/- 12 mmHg vs. 32 +/- 11 mmHg; P < 0.001 and P < 0.001, respectively). MPV levels were higher in the ASD group than the control group (9.3 +/- 1.2 fl vs. 8.6 +/- 0.8 fl, P < 0.001). There was a significant, positive correlation between MPV and systolic pulmonary artery pressure (PAP) (r = 0.542 and P < 0.001) in the ASD group. MPV was also significantly correlated with right ventricular size but not ASD diameter in the ASD group (r = 0.441, P < 0.001 and r = 0.126, P = 0.268, respectively). In receiver operating characteristics curve analysis, the cut-off value of MPV levels was > 8.7 fl and had 82% sensitivity and 63% specificity in predicting pulmonary artery hypertension. CONCLUSION: In the present study, we found that MPV levels, an indicator of platelet activation, were significantly higher in patients with ASD and correlated with systolic pulmonary artery pressure and right ventricular diameter.

Elevated hyaluronan levels in patients with rheumatic mitral stenosis and pulmonary arterial thromboembolism.

INTRODUCTION: The role of hyaluronan (HA) was previously demonstrated in patients with idiopathic pulmonary arterial hypertension (PAH). Mitral stenosis (MS) and pulmonary arterial thromboembolism (PTE) are important health problems that can cause pulmonovascular pathology. Pulmonary arterial hypertension develops especially in untreated patients with severe MS and most of patients with PTE. However, there is no data about HA levels in patients with MS and PTE. In this study, we investigated HA levels in patients with rheumatic MS and PTE. METHOD: Study population was divided into three groups. MS group consisted of 18 patients with moderate or severe MS. PTE group consisted of 16 patients with PTE. Control group consisted of 15 subjects without cardiac and pulmonary disease. Percutaneous mitral balloon valvuloplasty (PMV) was performed on all patients in MS group. Mitral gradients and systolic pulmonary arterial pressure (sPAP) were measured in all patients. HA levels were measured at baseline and first month after PMV. RESULTS: Mean sPAP±SD (mmHg) was 23±3 in the control group, 44±9 in the MS group and 66±11 in the PTE group (p<0.001). Baseline serum HA levels were significantly correlated with sPAP(echo) (r=0.332 p=0.03) and sPAP(cath) (r=0.559, p=0.007). Serum HA levels (ng/ml) in MS were significantly higher compared to controls [39±14 vs 24±11; p=0.01]. Patients in PTE group had the highest HA levels (61±21; p<0.001). Serum HA levels were significantly decreased at the first month after PMV in patients with MS [MS group: 39±14 (ng/ml), after PMV: 31±8; p=0.03]. CONCLUSION: This is the first article showing that both MS and PTE can cause increased serum HA levels. HA levels were decreased with PMV procedure in patients with MS.

Evaluation of the Renal and Cardiovascular Effects of Long-Term Tolvaptan Treatment in Autosomal Dominant Polycystic Kidney Disease.

INTRODUCTION: Cardiovascular diseases constitute a significant cause of morbidity and mortality in individuals with autosomal dominant polycystic kidney disease (ADPKD). This study aimed to assess the long-term effects of tolvaptan on the kidneys and heart in rapidly progressing ADPKD. METHODS: Among 354 patients diagnosed with ADPKD, 58 meeting the eligibility criteria for tolvaptan were included in the study. The study comprised two groups with similar demographic and clinical characteristics: 29 patients receiving tolvaptan treatment and 29 in the control group. Several included genetic analysis, magnetic resonance imaging, and echocardiography. Clinical and cardiac changes were recorded in both groups after a 3-year follow-up. RESULTS: Tolvaptan treatment demonstrated a significant reduction in the rate of eGFR decline compared to the control group. Furthermore, it was observed that tolvaptan could prevent the development of cardiac arrhythmias by inhibiting an increase in QTc interval and heart rate. CONCLUSION: These findings suggest that, in addition to slowing kidney progression in ADPKD management, tolvaptan may potentially benefit in preventing cardiac complications.

Elevated plasma hyaluronan levels in pulmonary hypertension.

Pulmonary arterial hypertension (PAH) is a progressive disease, with a poor prognosis. The pathophysiologic mechanism of PAH is unknown, but may involve both tissue remodeling and inflammatory processes. Hyaluronan (HA) is a large glycosaminoglycan polymer and a major component of the extracellular matrix. In the present study, we measured plasma HA levels in PAH associated with systolic congestive heart failure (CHF, n = 16) or chronic obstructive pulmonary disease (COPD, n = 18). The control group was consisted of 14 healthy individuals without pulmonary or cardiovascular disease. Plasma HA levels (ng/mL) were determined in all patients by an enzyme linked HA binding assay. Pulmonary arterial pressure (PAP) was calculated in echocardiography (mmHg). Pulmonary arterial pressures were significantly higher in CHF and COPD (CHF: 55.0 ± 11 mmHg and COPD: 62.5 ± 21 mmHg, p < 0.001 for each), compared to the control group (25.4 ± 5.9 mmHg). Plasma HA levels were significantly higher in CHF (73.0 ± 37.5 ng/ml, p = 0.007) and COPD (87.3 ± 53.2 ng/ml, p = 0.001) compared to control patients (26.2 ± 8.4 ng/ml). There was no significant difference in plasma HA levels between the CFH and COPD groups (p = 0.690). In COPD, plasma HA levels were significantly correlated with PAP, left atrium diameter. There was no significant correlation between plasma HA levels and age or with echocardiography parameters in CHF. Both CHF and COPD are associated with increased plasma HA levels. Elevated plasma HA may contribute to the development of PAH.

The lack of benefit of a combination of an angiotensin receptor blocker and calcium channel blocker on contrast-induced nephropathy in patients with chronic kidney disease.

AIM: Contrast-induced nephropathy (CIN) is a relatively common and serious complication, which occurs after the administration of contrast materials to patients. Although the pathophysiology of CIN is not exactly understood, ischemia of the medulla, oxidative stress, and direct toxicity of the contrast material are some of the factors that are implicated for the pathogenesis of CIN. To date, the only therapy that reduces the risk of CIN is volume expansion. There are conflicting results about the roles of angiotensin receptor blockers (ARB) and calcium channel blockers (CCB) in studies on CIN. For this reason the aim of this study was to compare the efficiency of the prophylactic use of amlodipine/valsartan plus hydration versus hydration only for the prevention of CIN in patients undergoing coronary angiography (CAG). PATIENTS AND METHODS: We prospectively enrolled 90 patients whose baseline serum creatinine levels were under 2.1 mg/dL and who were scheduled for CAG. Patients were divided into two groups. Group I (n = 45), consisted of patients who received amlodipine/valsartan plus hydration, group II (n = 45) consisted of patients who received only hydration. The patients in group I were given amlodipine/valsartan 5/160 mg once a day for a total of 3 days, starting one day before CAG and continuing on the day of and the day after the procedure. A 1 mL/kg/h sodium chloride infusion was administered for a total of 24 h, starting 12 h before the procedure and 12 h after, in all patients. The baseline serum creatinine (Scre) level was obtained before the procedure and repeated 48 h after. CIN was defined as an increase of ≥0.5 mg/dL or an increase of >25% in baseline Scre on the second day after CAG. RESULTS: The baseline clinical characteristics of the treatment groups were similar. Baseline Scre was 1.13 ± 0.33 in group I and 1.07 ± 0.23 mg/dL in group II (p = 0.31). There was a significant difference between the Scre levels 48 h after CAG between the two groups (1.18 ± 0.33-1.05 ± 0.23) (p = 0.03). The reason for this was the increase of Scre in group I. CIN occurred in 17.8% (8/45) of patients in group I and in 6.7% (3/45) of patients in group II (p = 0.197). In the diabetic subgroup, CIN occurred in 10.5% (2/19) of patients taking amlodipine/valsartan and in none of the patients in group II (p = 0.486). The Mehran scores of the patients who developed CIN were significantly higher than those patients who did not develop CIN. CONCLUSION: Amlodipine/valsartan therapy plus hydration did not reduce the risk of CIN in chronic kidney disease (CKD) Stage 2 patients who underwent elective CAG using a low-osmolar nonionic contrast medium. This is because there was a decrease in the glomerular filtration rate (GFR) using the Levey Modification of Diet in Renal Disease (MDRD) formula in the amlodipine/valsartan group and CIN occurred at a higher frequency in this group; ARBs and CCBs may be withheld before CAG in high-risk patients.

An investigation of tenascin-C levels in rheumatic mitral stenosis and their response to percutaneous mitral balloon valvuloplasty.

OBJECTIVE: The purpose of this study was to evaluate the tenascin-C levels in severe rheumatic mitral stenosis before and after percutaneous mitral balloon valvuloplasty (PMBV). SUBJECTS AND METHODS: Forty patients with severe mitral stenosis requiring PMBV and 20 age-matched healthy subjects were included in the study. The mitral valve areas, mitral gradients and systolic pulmonary artery pressure (sPAP) were measured by echocardiography. The sPAP values and mitral gradients were also measured by catheterization before and after PMBV. The blood tenascin-C levels were measured before PMBV and 1 month after the procedure. RESULTS: The echocardiographic mean mitral gradients had a significant decrease after PMBV (11.7 ± 2.8 vs. 5.6 ± 1.7 mm Hg; p < 0.001) and also those of catheterization (13.9 ± 4.4 vs. 4.0 ± 2.4 mm Hg; p < 0.001). Mitral valve areas increased significantly after PMBV (from 1.1 ± 0.1 to 1.8 ± 0.2 cm(2), p < 0.001). Tenascin-C levels decreased significantly in patients after PMBV (from 15.0 ± 3.8 to 10.9 ± 3.1 ng/ml; p < 0.001). Tenascin-C levels were higher in patients with mitral stenosis before PMBV than in healthy subjects (15.0 ± 3.8 and 9.4 ± 2.9 ng/ml; p < 0.001, respectively). There were no significant differences between patients with mitral stenosis after PMBV and healthy subjects (10.9 ± 3.1 and 9.4 ± 2.9 ng/ml; p = 0.09, respectively). There was a significant positive correlation between tenascin-C levels and sPAP (r = 0.508, p < 0.001). In multivariant analysis, tenascin-C predicted mitral stenosis (p = 0.004, OR: 2.31). CONCLUSIONS: Tenascin-C was an independent predictor for rheumatic mitral stenosis.

Relationship Between the Progression of Coronary Artery Disease and Pulse Pressure Index: A Cross-Sectional Work.

This study sought to analyze the relationship between pulse pressure (PP) index (PPI) (PP/systolic blood pressure; a less variable and objective form of PP) and coronary artery disease (CAD) progression. A registry of 193 patients was evaluated to show CAD progression by comparing current vs previous (6 months to 3 years prior) angiograms. One day after the second angiogram, we conducted ambulatory blood pressure measurements on the patients. Of the 193 patients, 65 (34%) had CAD progression. The PP and PPI were significantly higher in the progression than in the non-progression group (55 ± 12 vs. 51 ± 10 mmHg, P = .02 and .47 ± .06 vs. .42 ± .05, P = .004, respectively). Also, the PP and PPI were independently predictive of CAD progression (OR = 1.03, P = .03 and OR = 6.47, P = .01, respectively). Moreover, the correlation of PPI with low-density lipoprotein cholesterol and glycosylated hemoglobin was greater than their correlation with PP. In addition, PPI predicted CAD progression better than PP (area under the curve [AUC] = .649 vs. .574, P = .03). Elevated PP and PPI may be associated with the progression of CAD. PPI seems more successful in predicting CAD progression than PP.

Predictive Values of Systemic Immune-Inflammation Index in New-Onset Atrial Fibrillation Following Coronary Artery Bypass Grafting.

INTRODUCTION: We investigated the relationship between the newly-defined systemic immune-inflammation index and the new-onset atrial fibrillation in patients undergoing coronary artery bypass grafting. METHOD: This study included 392 patients who underwent coronary artery bypass grafting. We divided the participants into two groups as those with and without new-onset atrial fibrillation. Prior to coronary artery bypass grafting, we evaluated blood samples, including systemic immune-inflammation index, and other laboratory parameters of the patients. We formulized the systemic immune-inflammation index score as platelet × neutrophil/lymphocyte counts. RESULTS: The findings revealed that new-onset atrial fibrillation occurred in 80 (20.4%) of 392 patients during follow-ups. Such patients had higher systemic immune-inflammation index, neutrophil/lymphocyte ratio, and C-reactive protein levels than those who did not develop new-onset atrial fibrillation (P<0.001, P<0.001, P=0.010, respectively). In receiver operating characteristic curve analysis, systemic immune-inflammation index levels > 712.8 predicted new-onset atrial fibrillation with a sensitivity of 85% and a specificity of 61.2% (area under the curve: 0.781, 95% confidence interval: 0.727-0.835; P<0.001). CONCLUSION: Overall, systemic immune-inflammation index, a novel inflammatory marker, may be used as a decisive marker to predict the development of atrial fibrillation following coronary artery bypass grafting.