The Role of Pan-Immune-Inflammation Value in Determining the Severity of Coronary Artery Disease in NSTEMI Patients.

BACKGROUND: Even though medication and interventional therapy have improved the death rate for non-ST elevation myocardial infarction (NSTEMI) patients, these patients still have a substantial residual risk of cardiovascular events. Early identification of high-risk individuals is critical for improving prognosis, especially in this patient group. The focus of recent research has switched to finding new related indicators that can help distinguish high-risk patients. For this purpose, we examined the relationship between the pan-immune-inflammation value (PIV) and the severity of coronary artery disease (CAD) defined by the SYNTAX score (SxS) in NSTEMI patients. METHODS: Based on the SxS, CAD patients were split into three groups. To evaluate the risk variables of CAD, multivariate logistic analysis was employed. RESULTS: The PIV (odds ratio: 1.003; 95% CI: 1.001-1.005; p = 0.005) was found to be an independent predictor of a high SxS in the multivariate logistic regression analysis. Additionally, there was a positive association between the PIV and SxS (r: 0.68; p < 0.001). The PIV predicted the severe coronary lesion in the receiver-operating characteristic curve analysis with a sensitivity of 91% and specificity of 81.1%, using an appropriate cutoff value of 568.2. CONCLUSIONS: In patients with non-STEMI, the PIV, a cheap and easily measured laboratory variable, was substantially correlated with a high SxS and the severity of CAD.

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.

The Role of Pan-Immune-Inflammation Value in Predicting Contrast-Induced Nephropathy Development in Patients Undergoing Percutaneous Coronary Intervention Due to NSTEMI.

Contrast-induced nephropathy (CIN), which can develop after procedures involving contrast agents, is a significant cause of patient morbidity and mortality. This study aims to investigate the role of pre-procedural pan-immune-inflammation value (PIV) in predicting CIN development in patients undergoing percutaneous coronary intervention (PCI) due to non-ST segment elevation myocardial infarction (NSTEMI). A total of 1006 NSTEMI patients were included in the study. CIN was defined as an increase of at least 0.5 mg/dl or 25% in serum baseline creatinine level 72 h after the procedure. Patients were divided into two groups: those with and without CIN. NSTEMI patients who developed CIN, glucose level (P = .01), platelet count (P < .01), monocyte count (P < .001), neutrophil-to-lymphocyte ratio (NLR) (P < .001), systemic immune inflammation index (SII) score (P < .001), and PIV (P < .001) were higher compared with those without CIN. In the multivariate analysis of all these parameters, the Odds ratios of PIV and SII were similar and slightly lower than NLR. Receiver operating characteristic curve analysis (ROC) showed a PIV cut-off value of 448.43 with a sensitivity of 83.1% and a specificity of 72.8% in patients with CIN. Our study demonstrated an independent relationship between PIV at admission and CIN development in NSTEMI patients.

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.

Endothelial Progenitor Cells and NADPH Oxidase Enzyme Activity in the Development of an Aortic Aneurysm

Abstract Introduction: Endothelial progenitor cells (EPCs) and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase enzyme activity may affect the vessel wall and have a role in development of aortic aneurysms. EPCs originate from hematopoietic stem cells and can be enumerated from peripheral blood samples by flow cytometry. In this study, we aimed to evaluate the relation of EPC number and NADPH oxidase enzyme activity in the development of thoracic aortic aneurysm (TAA). Methods: Patients with TAA (n=30) and healthy individuals without TAA (control, n=10) were included in our study. Characterization and enumeration of EPC from peripheral blood samples were performed by flow cytometry with panels including markers of EPCs (CD34/CD133/CD309/CD146/CD144). Additionally, NADPH oxidase enzyme activity (capacity) was also measured by the dihydrorhodamine 123 (DHR 123) test. Results: The enumeration of EPC with CD34+/CD146+ marker showed that the number of mean EPC/106 cells was increased in the patient group (41.5/106 cells), but not in the control group (20.50/105 cells) (P<0.01). Additionally, patients with TAA presented significantly lower NADPH oxidase activity by DHR assay than healthy controls (mean stimulation index: 60.40± 7.86 and 75.10±5.21, respectively) (P<0.01). Conclusion: Our results showed that the number of EPCs is significantly higher in aortic aneurysm patients and may have a role in disease progression. The crosstalk between NADPH oxidase enzyme capacity and EPC number may be useful as a parameter to explain the clinical progression of TAA.

Endothelial Progenitor Cells and NADPH Oxidase Enzyme Activity in the Development of an Aortic Aneurysm.

INTRODUCTION: Endothelial progenitor cells (EPCs) and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase enzyme activity may affect the vessel wall and have a role in development of aortic aneurysms. EPCs originate from hematopoietic stem cells and can be enumerated from peripheral blood samples by flow cytometry. In this study, we aimed to evaluate the relation of EPC number and NADPH oxidase enzyme activity in the development of thoracic aortic aneurysm (TAA). METHODS: Patients with TAA (n=30) and healthy individuals without TAA (control, n=10) were included in our study. Characterization and enumeration of EPC from peripheral blood samples were performed by flow cytometry with panels including markers of EPCs (CD34/CD133/CD309/CD146/CD144). Additionally, NADPH oxidase enzyme activity (capacity) was also measured by the dihydrorhodamine 123 (DHR 123) test. RESULTS: The enumeration of EPC with CD34+/CD146+ marker showed that the number of mean EPC/106 cells was increased in the patient group (41.5/106 cells), but not in the control group (20.50/105 cells) (P<0.01). Additionally, patients with TAA presented significantly lower NADPH oxidase activity by DHR assay than healthy controls (mean stimulation index: 60.40± 7.86 and 75.10±5.21, respectively) (P<0.01). CONCLUSION: Our results showed that the number of EPCs is significantly higher in aortic aneurysm patients and may have a role in disease progression. The crosstalk between NADPH oxidase enzyme capacity and EPC number may be useful as a parameter to explain the clinical progression of TAA.

Predictive power of diastolic parameters on medical cardioversion success in acute atrial fibrillation.

BACKGROUND: Diastolic function assessment has been reported to provide valuable data in patients with atrial fibrillation (AF). The purpose of this study was to evaluate the effects of diastolic parameters on predicting the effectiveness of medical cardioversion in restoring sinus rhythm among patients with acute AF. METHODS: 40 non-valvular, new onset AF patients were included. All participants received an intravenous infusion of amiodarone. In patients whom sinus rhythm could not be restored with amiodarone, an electrical cardioversion was performed. Two groups, patients who achieved sinus rhythm with amiodarone (Group-1) and who failed to achieve sinus rhythm with amiodarone (Group-2) were compared with respect to initial echocardiographic measurements. RESULTS: Group-1 patients were younger comparing with Group-2 (mean age; 54.4 ± 13.9 years vs 63.3 ± 10.3 years, p = 0.028). Comparing with Group-1, Group-2 patients had; a higher left atrium volume index (17.1 ± 4.8 cm3 / m2 vs 22.6 ± 6.6 cm3 / m2 , p = 0.03); a shorter pulmonary vein S (49.6 ± 3.8 cm/sec vs 41.1 ± 3.0 cm/sec, p < 0.001); and a shorter pulmonary vein D peak velocity (55.9 ± 2.4 cm/sec vs 52.3 ± 1.8 cm/sec, p < 0.001). Moreover, both IVRT and DT were significantly shorter in Group-2, comparing with Group-1 (45.1 ± 2.1 msec vs 51.1 ± 2.5 msec, p < 0.001 and 51.3 ± 2.4 msec vs 56.5± 3.2 msec, p < 0.001, respectively). CONCLUSION: The present study revealed that admission pulmonary vein S and D wave peak velocities, IVRT, DT, and Pro-BNP levels could be predictors of failure of medical cardioversion among AF patients.

Systemic Immune Inflammation Index: A Novel Predictor of Contrast-Induced Nephropathy in Patients With Non-ST Segment Elevation Myocardial Infarction.

We investigated whether the systemic immune inflammation index (SII) on admission is an independent risk factor that predicts the development of contrast-induced nephropathy (CIN) in patients with non-ST segment elevation myocardial infarction (NSTEMI) who underwent percutaneous coronary intervention (PCI). A total of 429 patients with NSTEMI were enrolled in the study. Contrast-induced nephropathy was defined as an increase in serum creatinine level of ≥0.5 mg/dL or ≥25% above baseline within 72 hour after the procedure. Patients were divided into 2 groups: with and without CIN. Demographics, clinical risk factors, angiographic and laboratory parameters, CIN incidence, and SII score were compared between the 2 groups. Non-ST segment elevation myocardial infarction patients, who developed CIN, had higher glucose levels (P = .009), neutrophil counts (P < .001), platelet counts (P < .001), neutrophil-lymphocyte ratios (P < .001), high sensitivity C-reactive protein levels (P = .009), and SII levels (P < .001) than those who did not develop CIN. The receiver operating characteristic curve analysis showed that at a cutoff of 933.2, the value of SII exhibited 77.6% sensitivity and 69.2% specificity for detecting CIN. Our study showed that the SII levels on admission were independently associated with CIN development after PCI in patients with NSTEMI.

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.

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.

Evaluation of the relationship between pseudo-hypertension and the parameters of subclinical atherosclerosis.

BACKGROUND: Methods using for determining the subclinical atherosclerosis have gained growing interest in the recent years. However, the effects of pseudo-hypertension on the parameters of subclinical atherosclerosis are uncertain. We aimed to evaluate the relationship between pseudo-hypertension and subclinical atherosclerosis in individuals diagnosed with pseudo-hypertension. METHODS: A total of 122 patients who underwent radial elective coronary angiography were included in the present study. These patients were divided into two groups based on the difference between invasive and noninvasive blood pressure (BP) measurements: pseudo-hypertension group who had a difference ≥15 mmHg in SBP or ≥10 mmHg in DBP levels between invasive and noninvasive measurements (n = 28), and the other group who did not have any difference as described on these levels (n = 94). In order to evaluate the subclinical atherosclerosis; flow-mediated dilatation (FMD), carotid intima-media thickness (IMT), pulse wave velocity (PWV), and augmentation index were recorded in all patients. Two groups were compared with respect to these parameters. RESULTS: The median age of the pseudo-hypertension group was 76 years, while the median age of the other group was 63.5 years (P < 0.0001). The incidence of concomitant hypertension was higher in the pseudo-hypertension group as compared to the other group (P < 0.001). There was a significant difference in augmentation index, cardiac output, PWV, FMD, and IMT values between two groups (P = 0.016, P = 0.023, P <0.001, P < 0.001, P < 0.001, respectively). CONCLUSIONS: The present results demonstrated that there was a strong correlation between pseudo-hypertension and the parameters of subclinical atherosclerosis; augmentation index, PWV, FMD, and carotids IMT.

The presence of underlying asthma should be investigated in patients diagnosed with ACE inhibitor induced cough.

INTRODUCTION: Why do only some of patients who are prescribed angiotensin converting enzyme inhibitors (ACE-I) develop cough? The pathogenesis of ACE-I-induced cough remains controversial and requires further studies. OBJECTIVE: We aim to investigate whether asthma is a contributing cause of ACE-I-induced cough. METHODS: Patients attending a cardiology clinic between March 2016 and March 2017 who were diagnosed with ACE-I induced cough were included in this study. ACE-I-induced cough was defined as cough which developed within 4 weeks after initiation of ACE-I therapy and which improved within 4 weeks after discontinuation of the ACE-I. Patients who had received ACE-I treatment for at least 6 months without side effects were included in the study as a control group. Face-to-face questionnaires, pulmonary function tests (PFT) and skin prick tests were applied to all the patients. If there was discordance between asthma history and PFT results, a methacholine bronchial provocation test (BPT) was performed. RESULTS: A total of 43 patients with ACE-I induce cough were compared with 50 controls. Bronchial hyperreactivity (BHR), rhinitis, atopy and family history of asthma were more frequent in patients with ACE-I induced cough (P < .001). Patients with ACE-I-induced cough had significantly higher incidence of diagnosed asthma [OR = 8.28 (95%CI: 3.26-21.03) P < .001]. CONCLUSIONS: Asthma and an atopic background constitute a substantial risk factor for ACE-I induced cough. The presence of underlying asthma should be investigated in patients diagnosed with ACE inhibitor induced cough. However, the fact that most asthma patients tolerate ACE-I therapy, indicates that other cofactors are likely involved.