Volume 1 Issue 2

Research Article: Fibroblast Gross Factor - 23 and Arterial Stiffness in Hemodialysis Patients

Hussein S. Hussein*, Lamyaa E. Allam, Amr Mohab, Nadia M. Elbarghouty and Salwa Y. Mohammed

Background: Increased FGF23 levels have been shown to be independently associated with a variety of adverse renal and cardiovascular outcomes in Hemodialysis (HD) patients although the mechanisms are not fully understood. The association between FGF - 23 and arterial stiffness among HD patients remains still controversial with conflicting data.
Methods: In this cross - sectional study, serum FGF - 23 concentrations were measured in 30 HD patients without known CVD, in hemodialysis unit of Ain Shams University. Plasma FGF - 23 concentrations were measured using two -site enzyme - linked immunosorbent assay. Assessment of arterial stiffness was through assessing radial artery Pulse Pressure (PP) using sphygmomanometer, both Carotid Arteries Intima - Media Thickness (CIMT) and presence of Carotid Plaques (CP) measured by B-Mode Doppler ultrasound.
Results: Patients had elevated serum levels of FGF - 23 ranging from 100 up to 700 pg/ml. Duration of arterial Hypertension had a strong positive correlation with serum FGF - 23 (r is 0.754, p value is 0.007). Statistically significant positive correlation was recorded between marked elevations of FGF - 23 and CIMT (r = 0.776, p value < 0.001) as well as presence of CP, while no significant correlation was found between FGF - 23 and PP (r = 0.334, p value 0.071).
Conclusions: Higher serum FGF - 23 is strongly associated with CIMT and presence of CP as markers of arterial stiffness which could possibly explain its role in pathogenesis of atherosclerosis among HD patients without known CVD.

Cite this Article: Hussein HS, Allam LE, Mohab A, Elbarghouty NM, Mohammed SY. Fibroblast Gross Factor - 23 and Arterial Stiffness in Hemodialysis Patients. Int J Clin Cardiol Res. 2017;1(2): 067-071.

Published: 27 November 2017

Review Article: Right Ventricular Systolic Function and Pulmonary Pressure: The Weak Correlation in Stable Patients

Paolo Giovanardi*, Enrico Tincani, Carlo Cappelli, Paolo Magnavacchi, Cristina Leonardi, Fabrizio Turrini, Guglielmo Stefanelli, Giovanni Pinelli and Stefano Tondi

Purpose: Right Ventricular (RV) function and Pulmonary Artery Pressure (PAP) play a role in the morbility and mortality of cardiopulmonary diseases and they are commonly considered strictly related parameters. Not enough attention is given to Pulmonary Vascular Resistances (PVR) even though they play a pivotal role in RV afterload. This cohort study consisted of clinically stable patients and was designed to improve knowledge between echocardiographic indices of RV function, PAP, and PVR.
Methods: 529 consecutive patients underwent a complete echocardiographic examination with the evaluation of Tricuspid Annular Plane Systolic Excursion (TAPSE), RV Systolic Peak (RVSyP) and RV Presystolic Peak (RVPrP). Pulmonary Artery Systolic Pressure (PAPs) and Mean Pulmonary Artery Pressure (mPAP) were measured, thus PVR and RV diastolic function were assessed.
Results: Only TAPSE showed a correlation with PAPs (p < 0.001, correlation coefficient -3.131, r2 0.025), mPAP (p < 0.001, correlation coefficient -1.91, r2 0.025), and PVR (p < 0.001, correlation coefficient -0.21, r2 0.064). In the stepwise multiple linear regressions only PVR entered. RVSyP and RVPrP were not related to PAPs, mPAP, and PVR. RV diastolic function was related to PVR (p < 0.001), PAPs (p 0.001), mPAP (p 0.001), and to TAPSE (p 0.001).
Conclusions: The study showed the capacity only of TAPSE, among the considered indexes of tricuspid annular motion, to reflect PAP and PVR in stable patients. RV function indexes and PAP are not closely related in stable patients.
Keywords: Pulmonary Pressure; Pulmonary Hypertension; Pulmonary Vascular Resistances; Right Ventricular Function, TAPSE

Cite this Article: Giovanardi P, Tincani E, Cappelli C, Magnavacchi P, Leonardi C, et al. Right Ventricular Systolic Function and Pulmonary Pressure: The Weak Correlation in Stable Patients. Int J Clin Cardiol Res. 2017;1(2): 060-066.

Published: 05 September 2017

Review Article: Endogenous Endothelial Repair System in Heart Failure: Focus on Progenitor Endothelial Cell Dysfunction

Alexander E. Berezin*

Heart Failure (HF) a leading cause of premature death in patients with established Cardio Vascular (CV) disease. Although the global burden of HF is increasing, there is no evidence regarding promising results that improves long-term clinical outcomes especially for HF with preserved and mid-regional pump function. In this context, determination of the vulnerable populations at higher risk of HF development and progression is very promising. Endothelial Dysfunction (ED) plays a central role in the manifestation of HF regardless its phenotypes. There is a large body of evidence regarding that the Endothelial Progenitor Cells (EPCs) as a component of endogenous vascular repair system could be modified by several stimuli including epigenetic factors and thereby they are involved in the pathogenesis of ED. However, there is unclear whether EPC dysfunction is only whiteness of HF or it could be a factor of HF manifestation in vulnerable population. The short communication is depicted the uncertain role of EPC dysfunction in pathogenesis of HF.
Keywords: Heart failure; Biomarkers; Endothelial Progenitor Cells; Prediction.

Cite this Article: Berezin AE. Endogenous Endothelial Repair System in Heart Failure: Focus on Progenitor Endothelial Cell Dysfunction. Int J Clin Cardiol Res. 2017;1(2): 057-059.

Published: 31 August 2017

Review Article: Response of Left Ventricular Volumes and Ejection Fraction during Different Modes of Exercise in Health and CAD Patients

Moran Saghiv* and Michael Sagiv

Different studies support the notion that chronic aerobic, anaerobic and resistive exercise bouts can influence Left Ventricular (LV) function contractility state and volumes. Exercise training in health and disease brings about an improvement in quality of life; alleviate the negative impact of age and pathological state on the maximal work capacity. This review provides an overview of the latest findings in this research field on humans. The aim of this review is to elaborate on what is known about the physiological mechanisms affecting LV volumes following single bout of exercise and exercise training. The different modes of exercise and their impact on LV in young adult, athletes, untrained young adults, trained, untrained healthy older adults and coronary artery disease patients, are reviewed and discussed. Together these findings suggest that long lasting aerobic exercise training, is probably one factor that encounter the aging and coronary artery disease process' by enhancement LV volumes. However, this is not the case during anaerobic and resistive and following training in which the opposite might be true. The purpose of this review was to provide a current clarification for the role of different exercise intensities, and modes on human health.

Cite this Article: Saghiv M, Sagiv M. Response of Left Ventricular Volumes and Ejection Fraction during Different Modes of Exercise in Health and CAD Patients. Int J Clin Cardiol Res. 2017;1(1): 051-056.

Published: 25 July 2017

Case Report: Anomalous Origin of Right Coronary Artery Complicated with Unstable Angina: A Challenging Case for Interventional Treatment

Ahmet Karabulut*

Anomalous origin of coronary artery is a rare congenital malformation which possesses risk of various cardiac events including sudden cardiac death. Although surgery is a usual indication for anomalous origin of left coronary artery, there is not definitive management consensus for anomalous origin of right coronary artery due to relatively benign prognosis. Herein, we presented a case of anomalous high take-off origin of right coronary artery with inter arterial course and discussed the treatment strategies.

Cite this Article: Karabulut A, Anomalous Origin of Right Coronary Artery Complicated with Unstable Angina: A Challenging Case for Interventional Treatment. Int J Clin Cardiol Res. 2017;1(1): 048-050.

Published: 25 July 2017

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