Jan Jacques Michiels1,3*, Petr Dulicek2, Zwi Berneman1, Alain Gadisseur1, Wilfried Schroyens1

1Departments of Hematology and Coagulation Research, University Hospital Antwerp, Belgium

2Fourth Department of Internal Medicine–Hematology, University Hospital in Hradec Kralove and Charles University Prague, Faculty of Medicine in Hradec Kralove and Prague, Czech Republic on behave of the Central European Vascular Forum: CEVF

3Blood, Coagulation and Cardiovascular Medicine Research Center and International Collaboration and Academic Research on Myeloproliferative Neoplasms: ICAR.MPN, Goodheart Institute & Foundation in Nature Medicine & Health, Rotterdam, The Netherlands

Congenital venous thrombophilia is associated with increased risk of venous thrombosis at adolescent and adult age, with recurrent abortions and fetal loss in females, and less frequently with splanchnic vein thrombosis, but not with arteriolar microvascular circulation disturbances. Based on original observations in view of the literature on thrombocythemia in patients with essential thrombocythemia (ET) and polycythemia vera (PV), both ET and PV are associated with increased risk of platelet-von Willebrand factor (VWF) mediated arteriolar microvascular circulation disturbances at adult age, with recurrent abortions and fetal loss in females, and less frequently with splanchnic vein thrombosis, but not with venous thromboembolism.

The high incidences of congenital venous thrombophilic factors including antithrombin III, protein C and S, factor V Leiden and the prothrombin G20210A mutation, acquired lupus anticoagulant as well as the presence of the JAK2V617F mutation indicative for thrombocythemia in trilinear myeloproliferative disease (MPD) are described as the underlying hypercoagulable states in patients with Budd-Chiari syndrome (BCS) and splanchnic vein thrombosis (SVT). In this editorial we propose the novel concept of coagulation and/or platelet mediated microvascular liver pathology is the primary event for the development of BCS, splanchnic vein thrombosis, and portal hypertension with portal and oesophageal varicosal veins as a serious complication in patients with congenital thrombophilia and/or JAK2V617F mutated sticky platelets in clonal ET and PV. Clinical and liver pathology observations are in line with a two hit hypothesis of coagulation- and/or platelet-mediated thrombosis in the liver microcirculation as the underlying etiology of BCS and splanchnic vein thrombosis in patients with congenital venous thrombophilia and/or an acquired JAK2V617F mutated thrombocythemia in ET and PV patients. Severe ADAMTS13 deficiency in advanced liver cirrhosis is related to the severity of liver cell insufficiency due to the combined ADAMTS13 synthesis defect and autoantibodies against ADAMTS13 thereby explaining the more pronounced ADAMTS13 deficiency as compared to the degree of AT III synthesis deficiency in advanced liver cirrhosis. An imbalance between the severely decreased ADAMTS13:AC level and its substrate may indeed reflect the predisposing state for platelet thrombi in the liver microcirculation in patients with advanced liver cirrhosis similar on op of congenital venous thrombophilia and platelet-VWF mediated arteriolar microvascular thrombosis in JAK2V617F mutated thrombocythemia as etiological risk factors of intrahepatic microvascular obstructive diseases in BCS followed by splanchnic vein thrombosis.

DOI: 10.29245/2578-3025/2018/5.1154 View / Download Pdf

Robert C Bahler*, Neal V Dawson

Case Western Reserve University School of Medicine at MetroHealth Medical Center, Cleveland, Ohio, United States of America

Outcomes in patients with moderate to severe aortic stenosis (AS) from a community hospital cohort are similar those reported from tertiary institutions. Echocardiographic measures of the severity of obstruction are key variables in predicting outcomes. Additional variables that are not direct measures of AS severity are associated with adverse events. A reduced left ventricular (LV) ejection fraction forecasts a less favorable outcome yet most asymptomatic patients have preserved LV ejection fractions. Consequently, other measures of LV systolic function associated with adverse outcomes are important; namely, reduced LV longitudinal shortening and increased LV mass. Diastolic function can be compromised in AS indicated by either elevated E/e´ or left atrial enlargement; both are associated with unfavorable outcomes. Electrocardiographic evidence of LV strain reflects LV mid-wall fibrosis and identifies patients with adverse outcomes. Biomarkers including elevated values of high sensitivity troponin I and BNP contribute to models predicting outcomes. Prediction models help identify asymptomatic patients with quite unfavorable prognoses who may benefit from early aortic valve replacement.

DOI: 10.29245/2578-3025/2018/5.1157 View / Download Pdf

Lindsay A Sobotka*, Khalid Mumtaz#

Department of Gastroenterology, Hepatology and Nutrition, The Ohio State Wexner Medical Center, USA

Decompensated cirrhosis with ascites results in high health care expenditures, 30 day readmission, morbidity, and mortality. Paracentesis is indicated in patients with cirrhosis and ascites to rule out spontaneous bacterial peritonitis and for symptomatic control. Performing at least a diagnostic paracentesis has been proved to reduce inpatient mortality; however, the procedure was also associated with longer length of stay, higher costs during hospitalization and increased risk of 30-day readmission. In summary, diagnostic paracentesis is crucial to rule out infection, but other interventions should be utilized to control ascites, as worse hospital outcomes as likely associated with a large volume paracentesis.

DOI: 10.29245/2578-3025/2018/5.1153 View / Download Pdf

Jason Salsamendi, Yi Shuen Chang*

Department of Vascular and Interventional Radiology, University of Miami Miller School of Medicine/Jackson Memorial Hospital, 1611 NW 12th Ave. WW-279, Miami, FL, 33136, USA

DOI: 10.29245/2578-3025/2018/5.1152 View / Download Pdf

Monica Sacco1*, Stefano Lancellotti1*, Maria Basso1, Raimondo De Cristofaro1,2*

1Servizio Malattie Emorragiche e Trombotiche, Fondazione Policlinico Universitario “A. Gemelli”, IRCCS, Italy

2Istituto di Medicina Interna e Geriatria, Università Cattolica S. Cuore, Roma, Italy

Increasing evidence shows a potential role of ADAMTS13 deficiency as a risk factor for the high prevalence of portal vein thrombosis (PVT) in cirrhotic patients. This deficiency, due to myofibroblastic transformation of hepatic stellate cells (HSCs), the source of ADAMTS13, is responsible for the prevalence of ultra large molecular weight multimers of von Willebrand factor (UL-VWF) in the hepatic microcirculation. This phenomenon would favor the pro-haemostatic function of VWF, which, together with an elevation of coagulation FVIII, which is associated to VWF, could sustain microcirculatory thrombosis in the liver. These phenomena, triggering an increase of the intra-hepatic pressure, would cause a slowdown of the portal flow, favoring the occurrence of PVT. Although this scenario is justified by retrospective observational clinical studies, it will be mandatory to clarify the ADAMTS13 expression in HSCs associated with the activity of plasma ADAMTS13 in different stage of liver diseases. Hence, a prospective clinical trial (ClinicalTrials.gov Identifier: NCT03322696) is ongoing to unravel the linkage between all the actors involved in the complex phenomenon of PVT occurring in cirrhosis.

DOI: 10.29245/2578-3025/2018/5.1150 View / Download Pdf

Yanina Post, Achim Paululat*

University of Osnabrueck, Faculty of Biology & Chemistry, Zoology and Developmental Biology, Barbarastraße 11, 49076 Osnabrueck, Germany

It is well known that cardiovascular diseases are becoming the number one cause of mortality in developed countries1. Minimal differences in a wide range of biological pathways can lead to organ malfunction or failure. In addition to the heart itself, its surroundings are also crucial for proper organ integrity and functionality. Changes in extracellular matrix (ECM) composition, such as a higher amount of incorporated collagens, can result in cardiac hypertrophy2 or hypertension-related diastolic dysfunction3 by stiffening the surrounding matrix and constricting the embedded organ. Similar observations have been made while studying the heart of the fruit fly, Drosophila melanogaster. In this model organism, altered amounts of ECM components, including Laminin or Collagen IV (Viking), cause impaired cardiac function4. This demonstrates the notable relevance of an organ-specific ECM composition that provides the correct balance of stiffness and elasticity, both in vertebrates and invertebrates. In our recent study we were able to unravel the function of several protein domains belonging to the ADAMTS-like protein Lonely heart5. Furthermore, we analysed its interaction with the Collagen IV-like protein Pericardin and described new interactions within the extracellular matrix that led to a more detailed model of the whole network. In addition, we investigated the impact of altered Pericardin levels on physiological aspects, including locomotion and heart beating parameters, and strengthened the hypothesis that ECM composition is crucial for proper organ functionality. Here we summarize our approaches and comment on additional observations, possible follow-up analyses and restrictions as well as advantages. Moreover, we discuss possible additional roles of ADAMTS-like proteins within an extracellular matrix.

DOI: 10.29245/2578-3025/2018/5.1143 View / Download Pdf

Ashlee L Culver1, Annika S Silfvast-Kaiser2, Alan Menter1,2*

1Texas A&M Health Science Center College of Medicine, TX

2Division of Dermatology, Baylor University Medical Center, Dallas, TX

Psoriasis is a systemic inflammatory disease which contributes to an increased risk for cardiovascular disease, specifically coronary artery disease. Patients with psoriasis tend to have greater total coronary plaque burden and more high risk plaque than healthy controls. This likely contributes to the higher rate of myocardial infarction and 4-5 year reduction in lifespan observed in our psoriasis population. With biologic therapy and improvement in PASI scores, total plaque burden and noncalcified coronary plaque decreases as well. Specifically, ustekinumab decreases intima-media thickness and reduces vascular inflammation. Likewise, TNF-α inhibitors decrease vascular inflammation and reduce cardiovascular events in both sexes, and reduce coronary plaque formation in men with psoriasis. This may be due to elevation in glycoprotein acetylation, which is associated with cardiovascular events and elevated in psoriasis. This elevation has also been shown to decrease with adalimumab usage. Despite all of the knowledge gained on this topic, the incidence of myocardial infarction in psoriasis patients currently remains unchanged when compared to prior years. Consequently, we emphasize the need for further research on the unique pathogenesis of psoriatic coronary plaque formation as well as the effect biologic agents have on this coronary plaque in order to improve the wellbeing of this patient population.

DOI: 10.29245/2578-3025/2018/5.1149 View / Download Pdf

Mo Chen , Hongqian Wang , Erliang Kong , Jinmin Zhang , Weifeng Yu , Feixiang Wu*

Department of Anesthesiology & Intensive Care, Shanghai Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai 200438, P.R. China

Acute renal failure occurring in patients with obstructive jaundice after surgery is still a serious clinical complication. Renin-angiotensin-aldosterone system (RAAS) plays a key role in the progression of kidney disease. Previous studies have demonstrated that angiotensin-converting-enzyme-2 (ACE2), a component of the RAAS system, acts as a local regulator for renal protection, and has a beneficial effect on renal fibrosis. This review will summarize the role of ACE2 and the protective effects on renal dysfunction in obstructive jaundice.

DOI: 10.29245/2578-3025/2018/5.1146 View / Download Pdf

Karim Saleb*

Department of Internal Medicine, Ascension St. John Hospital, USA

Pulmonary embolism remains one of the major causes of morbidity and mortality in the United States. For patients with an intermediate-risk pulmonary embolism, Ultrasound-Assisted Catheter-Directed Thrombolysis (USAT) is a contemporary treatment modality that has emerged as a potential alternative to systemic thrombolysis and surgical embolectomy. Multiple studies have demonstrated the efficacy of USAT in reducing the thrombus burden and reversing right ventricular dysfunction in patients with an intermediate-risk pulmonary embolism. However, literature addressing the potential impact of an early catheter directed revascularization is lacking. A recent retrospective study carried out by Edla et al suggests that, compared to a delayed intervention, early USAT can improve recovery of pulmonary hemodynamics in patients with submassive pulmonary embolism and also reduce the overall in-hospital length of stay. This commentary provides a thorough analysis of the results of this study and revisits the existing information on ultrasound-assisted thrombolysis for acute pulmonary embolism.

DOI: 10.29245/2578-3025/2018/4.1144 View / Download Pdf

Adam R. Holmes1, Francis J. Castellino1,2, Rashna D. Balsara1,2*

1W. M. Keck Center for Transgene Research, University of Notre Dame, Indiana 46556, USA

2Department of Chemistry and Biochemistry, University of Notre Dame, Indiana 46556, USA

Ischemia-mediated glutamate elevation causes activation of the N-methyl-D-aspartate receptor (NMDAR) and consequent excitotoxicity. This triggers a cascade of pathological events, including aberrant NMDAR ion channel kinetics, large neuronal Ca2+ influx, and activation of pro-death signaling pathways. Previous studies have shown that functional outcomes of post-ischemia are influenced by the type of GluN2 subunit assembled in the NMDAR (GluN2A, GluN2B, GluN2C, or GluN2D), as well as its cellular location. GluN2A-containing synaptic NMDAR’s activate pro-survival pathways, whereas, activation of GluN2B-containing extrasynaptic NMDARs results in cell death. However, there is no consensus omnium on the individual role of the GluN2 subunits in ischemia. Published studies suggest that the GluN2A, GluN2B, and GluN2C subunits can promote either neuronal death or survival, depending on the experimental model employed and the CNS region investigated. In this mini-review, we aim to succinctly outline the mechanisms that underlie the dichotomous role of the NMDAR in ischemic stroke and possible NMDAR--directed therapeutic approaches.

DOI: 10.29245/2578-3025/2018/4.1133 View / Download Pdf

Neyla Ben Gdara*, Ikram Khemiri, Amel Belgacem, Safa Mannai, Lotfi Bitri

Department of Biology, University of Tunis El Manar, Faculty of Sciences of Tunis, University campus 2092, El Manar, Tunis, Tunisia

Liver ischemia-reperfusion induced hepatocellular damage that contributes to the morbidity and mortality1,2 associated with shock, thermal injury, re-sectional surgery and liver transplantation. One of the earliest events associated with reperfusion of ischemic liver is the release of Reactive Oxygen Species (ROS) causing oxidative stress. The following review focuses on the antioxidant effects of nitric oxide (NO) and Phycocyanin (Pc) after cold ischemia/reperfusion injury (IRI). In this regard, this review investigates in the first part the effect of the addition of NO to the preservation solution at different concentrations (1000, 500 and 50 nM) and in the second part the effect of the addition of phycocyanin to the conservation solution at two doses (0.2 mg / ml / g of liver and 0.1 mg / ml / g of liver) on liver graft quality. In conclusion, phycocyanin and nitric oxide (at a low dose) are effective in preserving the hepatic graft and protecting it against IRI by acting as a potent antioxidant against the products of oxidative stress.

DOI: 10.29245/2578-3025/2018/4.1141 View / Download Pdf

Natalie Berger1, Charles L. Shapiro2*

1Hematology/Oncology Fellowship Program, Icahn School of Medicine at Mount Sinai, New York, NY

2Division of Hematology and Medical Oncology, Icahn School of Medicine at Mount Sinai, New York, NY

DOI: 10.29245/2578-3025/2018/4.1136 View / Download Pdf

Patrick Dunn1,2*, Scott Conard3

1Walden University, Minneapolis, MN, USA

2American Heart Association, Dallas, TX, USA

3Converging Health, Dallas, TX, USA

DOI: 10.29245/2578-3025/2018/4.1138 View / Download Pdf

Cristina Aurigemma1*, Francesco Burzotta2, Carlo Trani2

1Institute of Cardiology, Fondazione Policlinico Agostino Gemelli IRCCS, Rome, Italy

2Institute of Cardiology, Fondazione Policlinico Agostino Gemelli IRCCS, Università Cattolica del Sacro Cuore, Rome, Italy

Despite 20 years of investigation the Completeness of Revascularization in patients with multivessel coronary artery disease (CAD) remains an unanswered question. The lack of universal definition and the multiplicity of confounding variables that in general favor patients who receive a complete revascularization (CR) are the reason of studies’ conflicting results.

The CR is achieved more commonly with coronary artery by-pass (CABG) than with percutaneous coronary intervention (PCI). In this regard, the possibility of achieving CR is one of variable that should be factored when deciding the optimal strategy of revascularization between PCI and CABG in patients with multivessel coronary artery disease. However clinical features, such as patient’s age, life expectancy, symptoms at presentation, comorbidities and left ventricular function may increase the morbidity or mortality risk of CABG intervention and a “reasonable” incomplete revascularization (IR) achieved with PCI may be a better choice in particular clinical subset.

DOI: 10.29245/2578-3025/2018/4.1137 View / Download Pdf

Penuelas, J1,2* & Sardans, J1,2*

1 CSIC, Global Ecology Unit CREAF-CEAB-UAB, Cerdanyola del Vallès, 08193 Catalonia, Spain

2 CREAF, Cerdanyola del Vallès, 08193 Catalonia, Spain

Rich countries have higher per capita food N and P intake than poor countries. This difference translates into higher human height. The differences among countries provide additional evidence on geopolitical disequilibrium in human wellness distribution but it also may have consequences on the incidence of hearth health. More N and P fertilizer sources are necessary, and they have to be adequately used in poor-countries to solve this additional gap between rich and poor countries.

DOI: 10.29245/2578-3025/2018/3.1129 View / Download Pdf

Clement Kleinstreuer 1,2*, Sriram Vasudevan Chari 1, Shantanu Vachhani 1

1Department of Mechanical and Aerospace Engineering, North Carolina State University, Raleigh, NC 27695, United States

2Joint UNC-NCSU Department of Biomedical Engineering, Raleigh, NC 27695, United States

DOI: 10.29245/2578-3025/2018/3.1134 View / Download Pdf

Barth U1, Wasseroth K1, Meyer F2*

1Center of Vascular medicine, Aschersleben / Schönebeck (certified by the “German Society for Vascular Surgery and Vascular Medicine“), AMEOS Hospital, Schönebeck, Germany

2Dept. of General, Abdominal, Vascular and Transplant Surgery, University Hospital at Magdeburg, Magdeburg, Germany

Introduction: A material-associated non-anastomotic aneurysm after previous use of a vascular prosthesis for arterial reconstruction mostly in peripheral arterial occlusion disease (PAOD) is considered a rare but serious complication.

Aim & method: The aim of the compact short review was – based on selected topic-related references from the medical literature as – to describe the rare finding of prosthetic non-anastomotic aneurysm and its diagnosis-specific care.

Results (complex patient- & clinical finding-associated corner points): Twenty articles were finally evaluated out of initially 321 references found in the literature search, which had been published since 1995. Most frequently, pseudoaneurysms of knitted polyester prostheses at the femoro-popliteal segment occurred after approximately 12.9 years in average. In one third of cases, two or more non-anastomotic aneurysms of Dacron prostheses were described. Histological and electron-microscopic investigations revealed mainly breakings of filaments and foreign body reactions. In more than half of the patients, the non-anastomotic aneurysm was resected and for reconstruction, a novel vascular prosthesis used as inter-positioned vascular segment was implanted. Complete removal of the prosthesis and endovascular therapy were only 2nd choice.

Conclusion: Development of prosthetic non-anastomotic aneurysms has not been satisfyingly clarified yet. It belongs to the late complication profile - even it occurs rarely - and should be controlled after a postoperative interval of approximately one decade if the arterial recanalization/reconstruction was performed using prosthetic material after previously – in the sequential approach – endovascular intervention and venous bypass could not be used.

DOI: 10.29245/2578-3025/2018/3.1132 View / Download Pdf

Gundu H. R. Rao1,2*

1Emeritus Professor, Department of Laboratory Medicine and Pathology, Minneapolis, MN, USA

2Director Thrombosis Research, Lillehei Heart Institute, University of Minnesota, Minneapolis, MN, USA

DOI: 10.29245/2578-3025/2018/3.1130 View / Download Pdf

Allen PF Chen1,2*, Rachel Kéry1,2, and Shaoyu Ge1

1Medical Scientist Training Program, Stony Brook, New York, USA

2Department of Neurobiology & Behavior, SUNY Stony Brook, Stony Brook, NY 11794, USA

The acute nature of neurological stroke disorders highlights the massive dependence of the brain on oxygen and energy supplies. The mechanisms of neural blood flow regulation have been intensely studied but are still unclear. Astrocytes are glial cells that communicate with both neurons and blood vessels, making them a cellular candidate for mediating neuronal blood flow. Evidence suggests that perivascular astrocytes of the brain do in part mediate blood flow corresponding to neuronal activity. However, the role of astrocytes in this respect is still to be defined and characterized. Fortunately, many recent technologies have emerged that allow us to investigate how astrocytes may accomplish this task. Gene expression strategies with rodent lines and viral transduction have allowed us to investigate astrocytes in a more targeted manner. Additionally, a variety of tools used previously to study neurons are now being applied to astrocytes. Studying how astrocytes may orchestrate brain blood flow is important for our ability to understand and treat neurovascular disease. We review current methods used to experimentally target, monitor, and manipulate astrocytes in the context of mediating neuronal blood flow.

DOI: 10.29245/2578-3025/2018/3.1128 View / Download Pdf

Adrian Wells1,2,* & Cintia Faija1,2

1The University of Manchester, School of Psychological Sciences, Faculty of Biology, Medicine and Health, Oxford Road, Manchester, M13 9PL, United Kingdom

2Greater Manchester Mental Health NHS Foundation Trust, Rawnsley Building, Manchester Royal Infirmary, Hathersage Road, Manchester, M13 9WL, United Kingdom

Anxiety and depression are common amongst cardiac patients undergoing cardiac rehabilitation and are associated with poorer health, poor quality of life and higher economic costs. There is a paucity of effective psychological treatments and their provision in this care pathway. A new treatment that is proving highly effective in mental health settings, named metacognitive therapy (MCT), could offer a way forward. This commentary delineates the problem of psychological distress (defined by anxiety and depression symptoms) in cardiac rehabilitation, highlights the limitations of current treatment and describes the PATHWAY research programme funded by the UK National Institute of Health Research (NIHR) to translate and test the metacognitive therapy in this population.

DOI: 10.29245/2578-3025/2018/3.1131 View / Download Pdf

Dongmei Gao1 & Wenhua Li1,2*

1Institute of Cardiovascular Disease Research, Xuzhou Medical University, Xuzhou, Jiangsu, 221002, China

2Department of Cardiology, The Affiliated Hospital Of Xuzhou Medical University, Xuzhou, Jiangsu, 221002, China

Contrast agent induced acute kidney injury (CI-AKI) is a leading cause of hospital-acquired acute kidney injury as a result of more and more iodinated contrast-media use for diagnostic purposes. Previous studies have demonstrated that oxidative stress and apoptosis are established processes contributing to contrast agent induced acute kidney injury. Astaxanthin (ATX), a carotenoid found in microalgae, fungi, complex plants, seafood, flamingos and quail has been confirmed have anti-oxidant, and anti-apoptosis effects. Experimental investigations in a range of species using a contrast agent induced acute kidney injury model demonstrated kidney preservation when ATX is administered prior to the induction of contrast agent. ATX?as an natural antioxidant?is capable to prevent CI-AKI effectively?and the mechanism is possibly related to anti-oxidant and anti-apoptosis. In this mini review, we brie?y summarize the potential for ATX as a protector against CI-AKI pathologies.

DOI: 10.29245/2578-3025/2018/3.1123 View / Download Pdf

Debjit Chatterjee*

Consultant Cardiologist, Queens Hospital, Burton on Trent, UK

This is a rare coronary angiogram showing myocardial bridge affecting more than one coronary artery.

DOI: 10.29245/2578-3025/2018/3.1126 View / Download Pdf

Paul M. Starker1*, Bertram Chinn2

1Overlook Medical Center, Columbia University College of Physicians and Surgeons, New York, NY, USA

2Division of Colon and Rectal Surgery, Overlook Medical Center, Robert Wood Johnson Medical School, New Brunswick, NJ, USA

DOI: 10.29245/2578-3025/2018/3.1127 View / Download Pdf

Huaqing Chen1*, Dali Li1, Mingyao Liu1,2*

1Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences, School of Life Sciences, East China Normal University, Shanghai, China

2Institute of Biosciences and Technology, Department of Molecular and Cellular Medicine, Texas A&M University Health Science Center, Houston, Texas, USA

Mouse models have been widely used in atherosclerosis research and related therapy development. However, data suggested that it was difficult to translate discovery in mice to human. Thanks to the fast development and optimization in gene editing technology, atherosclerotic models in rats generated recently provide more options for different studies and could make a difference to the situation which is exclusively dependent on mouse. Here we reviewed novel rat models for atherosclerosis generated through genetic approaches in recent years, including Ldl receptor (Ldlr) and apolipoprotein e (Apoe) knockout rats. The phenotypes in hyperlipidemia, atherosclerosis, as well as related inflammatory responses, were compared. These models developed typical atherosclerosis. More importantly, some of them present certain advantages over mouse models. These not only provide novel options for animal models of atherosclerosis, but also will benefit future investigations of atherosclerotic pathology and anti-atherosclerotic therapeutics.

DOI: 10.29245/2578-3025/2018/2.1124 View / Download Pdf

Ozaifa Kareem1, Masood Tanvir2, Amreen Naqash1, and G. N. Bader1*

1Department of Pharmaceutical Sciences, University of Kashmir, Hazratbal Srinagar, Kashmir, India

2Department of General Medicine, Government Medical College Srinagar, India

Obstructive Sleep Apnoea (OSA) is the most prevalent condition among sleep disordered breathing that leads to increased risk of cardiovascular (CV) and cerebrovascular morbidity and mortality. The most common comorbidity associated with OSA is systemic hypertension (HTN). Various epidemiological studies suggest a link between OSA and hypertension that involves complex interactions between various pathophysiological mechanisms and metabolic risk factors. OSA causes changes in normal physiological functions during nocturnal apneic episodes which in-turn lead to daytime hypertension. The widely accepted mechanisms by which the OSA contributes to the development of hypertension include sympathetic activation, inflammation, oxidative stress, and endothelial dysfunction. OSA and hypertension coexist in millions of people and both have been associated with heart disease, stroke, and premature death. Worldwide the prevalence of hypertension in OSA is estimated between 30 and 70%, thus setting it off as a major public health problem. Furthermore, not only has OSA been implicated in causing new hypertension but also it is said to promote resistant hypertension in already existent hypertensive patients, which may further grim the clinical and therapeutic outcomes. It is necessary to recognize the underlying OSA in-order to decrease the overall healthcare burden in terms of rigorous anti-hypertensive therapy instituted to OSA subjects. The review summarizes an up-to-date scenario of obstructive sleep apnoea as a cause of systemic hypertension and the overall cardiovascular risks.

DOI: 10.29245/2578-3025/2018/2.1122 View / Download Pdf