Current Vascular Pharmacology (CURR VASC PHARMACOL)

Publications in this journal

• Article: Editorial (sulodexide, an old drug with recent renewed interest).

  Giuseppe Maria Andreozzi
  Current Vascular Pharmacology 05/2013; 11(3):352-3.
• Article: Pleiotropic Effects of PPARγ Agonist on Hemostatic Activation in Type 2 Diabetes Mellitus.

  Patrizia Ferroni, David Della-Morte, Antonello Pileggi, Silvia Riondino, Tatjana Rundek, Camillo Ricordi, Fiorella Guadagni
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  ABSTRACT: Thiazolidinediones (TZDs) represent a class of peroxisome proliferator-activated receptor (PPAR)γ agonists widely used as insulin-sensitizers in the treatment of type 2 diabetes mellitus (T2DM). The beneficial effects of hypoglycemic drugs, including TZDs, on the hemostatic abnormalities associated to T2DM have been formerly related to improved metabolic control, rather than to direct effects. However, in recent years the pleiotropic effects of PPARγ agonists on hemostatic function have become evident. In particular, the role of platelets as a pivotal player in diabetes complications by stimulating and sustaining inflammation has been lately acknowledged. Upon activation platelets synthesize and release many bioactive substances such as thromboxane A2 (TXA2) or pro-inflammatory mediators including CD40 ligand (CD40L) that exert autocrine and paracrine activation processes in vascular inflammation leading to cardiovascular disease (CVD). Although PPARγ is a nuclear hormone receptor, anucleate platelets also highly express this receptor and treatment with synthetic PPARγ ligands dampens the release of soluble(s)CD40L and TXA2 in thrombin-activated platelets. Moreover, PPARγ through Sirtuin1 pathway has been implicated in modulating inflammatory and atherosclerotic processes in patients with T2DM. Therefore, in T2DM, where platelet activation contributes to the pathogenesis of CVD, TZDs may have an enhanced therapeutic role, despite some potentially serious adverse side effects. This review will discuss the pleiotropic effects of PPARγ treatment on the hemostatic abnormalities associated with T2DM, with particular focus on platelet activation.
  Current Vascular Pharmacology 05/2013; 11(3):338-51.
• Article: Angiotensin 1-7 Promotes Cardiac Angiogenesis Following Infarction.

  Wenyuan Zhao, Tieqiang Zhao, Yuanjian Chen, Yao Sun
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  ABSTRACT: Angiogenesis is central to cardiac repair following myocardial infarction (MI). Cardiac angiotensin converting enzyme (ACE)2 is significantly increased postMI, which is coincident with activated angiogenesis. The function of ACE2 is to generate angiotensin (Ang)1-7, an active peptide with cellular actions mediated by Mas receptors. The current study is to determine whether Ang(1-7) is involved in cardiac angiogenesis and facilitates cardiac repair. In the first portion of the study, the temporal expressions of cardiac ACE2 and Mas receptors were detected in rats with MI. In the second portion, MI rats were treated with or without a Mas receptor antagonist, A779 (1mg/kg/day given by minipump) for 7 days. Vascular density and expression of angiogenic mediators in the infarcted myocardium and cardiac function were examined. Compared to controls, ACE2 and Mas receptor levels were significantly increased in the infarcted myocardium for 4 weeks of the observation period. Newly formed vessels were evident in the infarcted myocardium at day 7. Mas receptor blockade significantly reduced vascular density in the infarcted myocardium and impaired ventricular function. In addition, A779 treatment significantly suppressed the cardiac expressions of vascular endothelial growth factor (VEGF)-D and matrix metalloproteinase (MMP)-9 but not expression of other angiogenic mediators, including monocyte chemoattactant protein (MCP-1), VEGF-C, transforming growth factor (TGF)-β1 and integrin β3. These observations indicate that Ang(1-7) promotes angiogenesis via stimulating the expression of cardiac VEGF-D and MMP-9, thus facilitating cardiac repair and ventricular function.
  Current Vascular Pharmacology 04/2013;
• Article: Non Invasive Imaging of Myocardial Infarction with Computed Tomography and Magnetic Resonance.

  M Midiri, L La Grutta, E Grassedonio, P Toia, G Guglielmi
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  ABSTRACT: Myocardial infarction is a major cause of death and disability worldwide. Myocardial infarction may represent a major catastrophic event leading to severe hemodynamic failure or sudden death or it may occur repeatedly in patients with established heart disease. In this context, the role of imaging techniques may become useful for the understanding of the determinants in a preclinical setting before acute coronary events, and for an accurate and correct diagnosis of myocardial infarction. Three-dimensional noninvasive imaging techniques, such as Cardiac CT (CCT) and Cardiac MR imaging (CMR) were widely developed in the last two decades. These imaging techniques may provide new insights into understanding, assessment and follow-up of myocardial infarction. CCT is mainly oriented to morphological assessment including applications such as the detection of coronary artery stenoses even in acute settings, the evaluation of coronary atherosclerotic burden, and the follow-up of patients with known coronary artery disease who underwent myocardial revascularization. On the other hand, CMR is the reference standard for the functional assessment of the heart with evaluation of volumes, mass, and contractility of the ventricles. CMR myocardial viability imaging with delayed contrast enhancement has become broadly accepted for the detection and characterization of the extent of acute and chronic myocardial infarction.
  Current Vascular Pharmacology 04/2013;
• Article: The Meaning of Different Forms of Structural Myocardial Injury, Immune Response and Timing of Infarct Necrosis And Cardiac Repair.

  Emanuela Turillazzi, Cristoforo Pomara, Stefania Bello, Margherita Neri, Irene Riezzo, Vittorio Fineschi Emanuela Turillazzi
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  ABSTRACT: Although a decline in the all-cause and cardiac mortality rates following myocardial infarction (MI) during the past 3 decades has been reported, myocardial infarction is a major cause of death and disability worldwide. From a pathological point of view MI consists in a particular myocardial cell death due to prolonged ischemia. After the onset of myocardial ischemia, cell death is not immediate, but takes a finite period of time to develop. Once complete myocytes' necrosis has occurred, a process leading to a healed infarction takes place. In fact, myocardial infarction is a dynamic process that begins with the transition from reversible to irreversible ischemic injury and culminates in the replacement of dead myocardium by a fibrous scar. The pathobiological mechanisms underlying this process are very complex, involving an inflammatory response by several pathways, and pose a major challenge to ability to improve our knowledge. An improved understanding of the pathobiology of cardiac repair after myocardial infarction and further studies of its underlying mechanisms provide avenues for the development of future strategies directed toward the identification of novel therapies. The chronologic dating of MI is of great importance both to clinical and forensic investigation, that is, the ability to create a theoretical timeline upon which either clinicians or forensic pathologist may increase their ability to estimate the time of MI. Aging of MI has very important practical implications in clinical practice since, based on the chronological dating of MI, attractive alternative to solve therapeutic strategies in the various phases of MI are developing.
  Current Vascular Pharmacology 04/2013;
• Article: Confocal Laser Scanning Microscope, Raman Microscopy and Western Blotting to Evaluate Inflammatory Response After Myocardial Infarction.

  Irene Riezzo, Santina Cantatore, Dania De Carlo, Carmela Fiore, Margherita Neri, Emanuela Turillazzi, Vittorio Fineschi
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  ABSTRACT: Cardiac muscle necrosis is associated with inflammatory cascade that clears the infarct from dead cells and matrix debris, and then replaces the damaged tissue with scar, through three overlapping phases: the inflammatory phase, the proliferative phase and the maturation phase. Western Blotting, Laser Confocal Microscopy, Raman Microscopy are valuable tools for studying the inflammatory response following myocardial infarction both humoral and cellular phase, allowing the identification and semiquantitative analysis of proteins produced during the inflammatory cascade activation and the topographical distribution and expression of proteins and cells involved in myocardial inflammation. Confocal laser scanning microscopy (CLSM) is a relatively new technique for microscopic imaging, that allows greater resolution, optical sectioning of the sample and three-dimensional reconstruction of the same sample. Western blotting used to detect the presence of a specific protein with antibody-antigen interaction in the midst of a complex protein mixture extracted from cells, produced semi-quantitative data quite easy to interpret. Confocal Raman Microscopy combines the three-dimensional optical resolution of confocal microscopy and the sensitivity to molecular vibrations, which characterizes Raman spectroscopy. The combined use of western blotting and confocal microscope allows detecting the presence of proteins in the sample and trying to observe the exact location within the tissue, or the topographical distribution of the same. Once demonstrated the presence of proteins (cytokines, chemokines, etc.) is important to know the topographical distribution, obtaining in this way additional information regarding the extension of the inflammatory process in function of the time stayed from the time of myocardial infarction. These methods may be useful to study and define the expression of a wide range of inflammatory mediators at several different timepoints providing a more detailed analysis of the time course the infarct.
  Current Vascular Pharmacology 04/2013;
• Article: Cardiac Oxidative Stress and Inflammatory Cytokines Response After Myocardial Infarction.

  Margherita Neri, Vittorio Fineschi, Marco Di Paolo, Cristoforo Pomara, Irene Riezzo, Emanuela Turillazzi, Daniela Cerretani
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  ABSTRACT: Oxidative stress in heart failure or during ischemia/reperfusion occurs as a result of the excessive generation or accumulation of free radicals or their oxidation products. Free radicals formed during oxidative stress can initiate lipid peroxidation, oxidize proteins to inactive states and cause DNA strand breaks. Oxidative stress is a condition in which oxidant metabolites exert toxic effects because of their increased production or an altered cellular mechanism of protection. In the early phase of acute heart ischemia cytokines have the feature to be functional pleiotropy and redundancy, moreover, several cytokines exert similar and overlapping actions on the same cell type and one cytokine shows a wide range of biological effects on various cell types. Activation of cytokine cascades in the infarcted myocardium was established in numerous studies. In experimental models of myocardial infarction, induction and release of the pro-inflammatory cytokines like TNF-α (Tumor Necrosis Factor α), IL-1β (Interleukin-1β) and IL-6 (Interleukin-6) and chemokines is steadily described. The current review examines the role of oxidative stress and pro-inflammatory cytokines response following acute myocardial infarction and explores the inflammatory mechanisms of cardiac injury.
  Current Vascular Pharmacology 04/2013;
• Article: The Prostaglandin Agonist Beraprost Aggravates Doxorubicin-Mediated Apoptosis by Increasing iNOS Expression in Cardiomyocytes.

  Wei-Shiung Lian, Herng-Cheng Chiou, Heng Lin, Jin-Jer Chen, Ching-Feng Cheng
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  ABSTRACT: Doxorubicin (DOX) is widely used as an anti-cancer agent although it causes irreversible cardiomyopathy by increasing oxidative stress and deregulating nitric oxide production. Beraprost (BPS), a stable prostacyclin (PGI2) analog, is a potent vasodilator that has beneficial effects on myocardial ischemia. The objectives of the present study were to delineate the uncertain effects of prostcyclin therapy on DOX induced cardiomyopathy and to explore the mechanisms underlying PGI2 and DOX interaction. For this reason, we stimulated endogenous PGI2 production using bicistronic COX-1/PGIS gene transfer and BPS supplementation, and investigated the effects on DOX-induced cardiomyopathy. Caspase-dependent protein content, lactate dehydrogenase (LDH), DNA fragmentation, and TUNEL positive cells were elevated in DOX-treated cardiomyocytes. These indicators were further elevated by adenovirus-COX-1/PGIS transfection or BPS supplementation. In addition, PGI2 overexpression further increased iNOS expression and superoxide accumulation in cardiomyocytes compared with DOX alone, which may be the reason for aggravated cytotoxicity. Moreover, BPS can induce cAMP response elements (CRE) binding to the iNOS promoter and phospho- cAMP response element binding protein (CREB) expression in a cyclic AMP-dependent manner. Our in vivo studies show that MnTBAP and aminoguanidine treatment of DOX and BPS co-administered mice can attenuate caspase-3 and PARP-1 protein expression, and improve mouse survival, as observed in the iNOS gene-deleted mice. In conclusion, we demonstrated that BPS or adv-COX-1/PGIS increases PGI2 levels through iNOS expression and peroxynitrite production, via CREB protein phosphorylation; thereby aggravating DOX-mediated cardiotoxicity.
  Current Vascular Pharmacology 04/2013;
• Article: Role of Innate Immune System in Inflammation and Cardiac Remodeling After Myocardial Infarction.

  Masafumi Takahashi
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  ABSTRACT: The innate immune system is well recognized as the first line defense of foreign pathogens; however, it can also recognize endogenous signals released from injured tissues and induce sterile inflammation. Toll-like receptors (TLRs) and Nod-like receptors (NLRs) have been identified as its receptors, and they have been shown to play a key role in the disease processes of sterile inflammation, including myocardial infarction (MI). In particular, NLRs are the key components of the caspase-1 activating platform known as the "inflammasome" which produces the potent proinflammatory cytokine interleukin-1β. The current article reviews the role of the innate immune system, especially TLRs and inflammasomes, in the pathophysiology of MI.
  Current Vascular Pharmacology 04/2013;
• Article: Insulin Resistance in Brain and Possible Therapeutic Approaches.

  Sevki Cetinkalp, Ilgin Yildirim Simsir, Sibel Ertek
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  ABSTRACT: Although the brain has long been considered an insulin-independent organ, recent research has shown that insulin has significant effects on the brain, where it plays a role in maintaining glucose and energy homeostasis. To avoid peripheral insulin resistance, the brain may act via hypoinsulinemic responses, maintaining glucose metabolism and insulin sensitivity within its own confines; however, brain insulin resistance may develop due to environmental factors. Insulin has two important functions in the brain: controlling food intake and regulating cognitive functions, particularly memory. Notably, defects in insulin signaling in the brain may contribute to neurodegenerative disorders. Insulin resistance may damage the cognitive system and lead to dementia states. Furthermore, inflammatory processes in the hypothalamus, where insulin receptors are expressed at high density, impair local signaling systems and cause glucose and energy metabolism disorders. Excessive caloric intake and high-fat diets initiate insulin and leptin resistance by inducing mitochondrial dysfunction and endoplasmic reticulum stress in the hypothalamus. This may lead to obesity and diabetes mellitus (DM). Exercise can enhance brain and hypothalamic insulin sensitivity, but it is the option least preferred and/or continuously practiced by the general population. Pharmacological treatments that increase brain and hypothalamic insulin sensitivity may provide new insights into the prevention of dementia disorders, obesity, and type 2 DM in the future.
  Current Vascular Pharmacology 04/2013;
• Article: Uric Acid Metabolism in Pre-Hypertension and The Metabolic Syndrome.

  Manfredi Rizzo, Milan Obradovic, Milica Labudovic-Borovic, Dragana Nikolic, Giuseppe Montalto, Ali A Rizvi, Dimitri P Mikhailidis, Esma R Isenovic
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  ABSTRACT: In humans uric acid (UA) is the end product of degradation of purines. The handling of UA by the renal system is a complex process which is not fully understood. To date, several urate transporters in the renal proximal tubule have been identified. Among them, urate transporter 1 (URAT1) and a glucose transporter 9 (GLUT9) are considered of greater importance, as potential targets for treatment of hyperuricemia and the potential associated cardio-metabolic risk. Therefore, the recognition of the metabolic pathway of UA and elucidation of occurrence of hyperuricemia may provide important insights about the relationship between UA, pre-hypertension (preHT) and the metabolic syndrome (MetS). We also review the available clinical studies in this field, including experimental studies dealing with the mechanisms of UA transport via different transporters, as well as current treatment options for hyperuricemia in patients with MetS, preHT or cardiovascular risk factors.
  Current Vascular Pharmacology 04/2013;
• Article: Prediabetes, Prehypertension- Do We Need Pre-ckd?

  Jolanta Malyszko, Maciej Banach
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  ABSTRACT: Screening is the systematic use of a test for a health problem or risk factor when no recognized signs or symptoms would indicate the presence of that problem or risk factor. Abnormal glucose metabolism can be documented years before the onset of overt diabetes. Nowadays, prediabetes can be subdivided into impaired fasting glucose or impaired glucose tolerance. Substantial number of subjects with either will progress to overt diabetes within years. Prediabetes bears also the increased risk of cardiovascular complications. Prehypertension is much newer term introduced by the seventh report of the Joint National Committee (JNC 7) published in 2003 as systolic blood pressure from 120 to 139 mmHg or diastolic blood pressure from 80 to 89 mmHg in adults (not receiving blood pressure-lowering treatment). Similarly prehypertension also increased the risk of cardiovascular complications and progression to hypertension. Chronic kidney disease is also highly prevalent mainly in the elderly. It is associated with important adverse outcomes such as cardiovascular mortality and morbidity. Factors associated with higher risk of chronic kidney disease include mainly hypertension, diabetes, obesity and older age. Early detection and diagnosis of chronic kidney disease may prevent the full blown disease and its end-stage requiring renal replacement therapy. The review focus on the problem of high risk population for development of diabetes, hypertension and whether time has come to focus also on the conditions predisposing to the development of chronic kidney disease.
  Current Vascular Pharmacology 04/2013;
• Article: Recommendations for Severe Hypertriglyceridemia Treatment, are There New Strategies?

  T D Filippatos, M S Elisaf
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  ABSTRACT: This review considers drug combinations and newer treatment strategies for patients with severe hypertriglyceridemia. Hypertriglyceridemia is associated with an atherogenic metabolic profile and in most studies with increased CVD risk. Patients with severe hypertriglyceridemia also have increased incidence of pancreatitis. All types of severe hypertriglyceridemia are associated with a reduction in lipoprotein lipase activity. Patients with severe hypertriglyceridemia and abdominal pain or pancreatitis should be hospitalized and treated with hypolipidemic drugs and, if needed, with insulin/dextrose infusion or therapeutic apheresis. Fibrates are the first-line treatment in patients with severe hypertriglyceridemia. Omega-3 fatty acids and niacin are very useful drugs for patients with hypertriglyceridemia. Statins in high doses exhibit a significant hypotriglyceridemic activity. Drugs that interfere with chylomicron production such as orlistat are also useful for hypertriglyceridemic patients. In most patients with severe hypertriglyceridemia drug combinations are needed to maintain an acceptable TG concentration. Gene therapy is under development for patients with known genetic abnormalities of TG metabolism. Clinicians should be vigilant for the recognition and prompt treatment of patients with severe hypertriglyceridemia aimed to avoid the serious complication of pancreatitis and to reduce their cardiovascular risk.
  Current Vascular Pharmacology 04/2013;
• Article: Nutraceuticals for Metabolic Syndrome Management: from Laboratory to Benchside.

  A Fg Cicero, E Tartagni, S Ertek
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  ABSTRACT: Metabolic syndrome (MetS) is a world-wide epidemic disease associated with increased morbidity and mortality. Treatment strategies include pharmacologic and non-pharmacologic methods, with varying degrees of success rate all over the world. Pharmaceutical interest in this field is growing, together with patients requests' for supplementary (or "alternative") treatments. The knowledge of nutraceuticals beneficial effects in subjects with the MetS could help us to better define the appropriate treatment for these subjects, in particular those with contraindications for commonly used drugs, or to achieve guidelines suggested targets. On the other side, it could be not convenient to use a nutraceutical to treat each metabolic syndrome component (i.e.: from 3 to 5) in each affected subjects. Thus, this review tries to focus on widely marketed nutraceuticals with clinically demonstrated effects on more than one component of the MetS, namely omega-3 fatty acids, berberine, psyllium and other soluble fibers, cinnamon, chromium picolinate, banaba, and bitter gourd.
  Current Vascular Pharmacology 04/2013;
• Article: Is There U Turn From Insulin Back to Pills in Diabetes?

  S Ertek, S Cetinkalp
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  ABSTRACT: Type 2 diabetes is characterized by insulin resistance together with progressive loss of beta-cell function. After recognition of gluco- and lipo-toxicity, attention was focused on the preservation and/or restoration of beta cell function, especially at the early stages of the diabetes, with better beta-cell reserve and in the absence of complications. Early treatment of glucotoxicity with insulin was searched by early insulin treatment studies, and these studies have some promising results, pointing the possibility of ''remission'' of diabetes in some patients. According to the results of these studies, patients with early diagnosis of diabetes, the ones with better beta cell reserve, patients with low tendency for ''insulin-abuse'' could make ''U' -turn from insulin to pills or even drug-free life. Criteria to turn back to pills could be listed as disappearance of diabetic symptoms, daily insulin need < 0.25 unit/kg, euglycemia in both fasting and postprandial state, and better beta cell function. The main problems in early insulin treatment are the ''insulin resistance'' of both patients and doctors, hypoglycemia, weight gain and increased appetite. Meanwhile, hyperinsulinemia desensitizes receptors and causes worsening of situation in a vicious cycle of insulin resistance and hyperglycemia. Therefore, patients should be selected properly and U-turn could be performed in relevant conditions explained in the text. It could be possible to see early insulin treatment and U-turn strategies in future guidelines for type 2 diabetes.
  Current Vascular Pharmacology 04/2013;
• Article: Insulin Resistance, Small LDL Particles, and Risk for Atherosclerotic Disease.

  Peter P Toth
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  ABSTRACT: There is a global epidemic of obesity, metabolic syndrome, and diabetes mellitus. Insulin resistance (IR) is etiologic for both metabolic syndrome and diabetes mellitus. IR induces a broad range of toxic systemic effects, including dyslipidemia, hypertension, hyperglycemia, increased production of advanced glycosylation end products, increased inflammatory tone, as well as a prothrombotic and pro-oxidative state. Patients with IR are highly vulnerable to the development of accelerated atherosclerosis as well its clinical sequelae, including coronary artery disease and myocardial infarction, carotid artery disease and ischemic stroke, peripheral arterial disease and claudication/lower extremity amputation, and coronary mortality. Among the most important risk factors patients afflicted with IR develop is the so-called atherogenic lipid triad: large numbers of small, dense low-density lipoprotein (sdLDL) particles, hypertriglyceridemia, and low serum concentrations of high-density lipoprotein cholesterol. Though controversial, much recent evidence suggests that the formation of sdLDL particles in the setting of IR is an important metabolic transition. Some studies suggest that these smaller particles are more atherogenic than their larger, more buoyant counterparts. At least part of the explanation for the apparent augmented atherogenicity of small LDL particles is their reduced systemic clearance by the LDL receptor, increased vulnerability to oxidation rendering them more apt for scavenging by macrophages, and possible increased flux into the subendothelial space of arterial walls. Numerous small studies suggest that sdLDL is highly correlated with cardiovascular events. Cardiovascular medicine is in need of a large prospective, randomized study that would more definitively investigate the impact of small, dense LDL (sdLDL) on risk for cardiovascular disease and whether therapeutic interventions designed to specifically reduce the burden of sdLDL are associated with reductions in cardiovascular events over and above that seen with LDL-C reduction per se.
  Current Vascular Pharmacology 04/2013;
• Article: Patients with Prehypertension-Do We Have Enough Evidence to Treat Them?

  Michalska Marta, Alberto Zanchetti, Nathan D Wong, Jolanta Malyszko, Jacek Rysz, Maciej Banach
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  ABSTRACT: In 2003, the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure established a definition of a new category of BP levels called 'prehypertension'(preHT) that included individuals with a systolic BP of 120-139 mm Hg or a diastolic BP of 80-89 mm Hg. Patients with preHT were considered to be at increased risk for progression to hypertension and in individuals with BP in the range 130/80 to 139/89 mmHg the risk of developing hypertension was twice as high as in subjects with lower values. Still then there has been a large debate whether the introduction of preHT was based on evidence and as a consequence, it was fully justified. It has been suggested that the term prehypertension may in many subjects create anxiety and a need for unnecessary medical visits and examinations. This group of patients is also very heterogeneous and it has been pointed out that subdividing preHT group into individuals with normal BP and high normal BP would much better correspond to the continuum of BP risk for CV disease. Finally, despite some data suggesting the potential benefits of antihypertensive therapy in patients with preHT (high normal BP), there are still no hard evidences on the outcome reduction by giving antihypertensive drugs in these individuals.
  Current Vascular Pharmacology 04/2013;
• Article: Controversies on HDL: Should it Be a Target Biomarker in Patients With Lipid Disorders?

  Stephen Nicholls
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  ABSTRACT: LDL cholesterol lowering with statins have had a profound impact on cardiovascular (CV) event rates and accordingly have become an integral component of strategies designed to reduce CV risk. The finding of a residual clinical risk, despite LDL cholesterol lowering, supports the need to develop additional therapeutic strategies for CV prevention. Numerous lines of evidence suggest that targeting the protective properties of HDL may be beneficial. Disappointing results from recent reports of HDL genetics and raising agents and clinical events has fueled considerable debate as towhether attempts to target HDL will be of clinical benefit or futility.
  Current Vascular Pharmacology 04/2013;
• Article: Characteristics Other Than the Diagnostic Criteria Associated with Metabolic Syndrome: an Overview.

  Niki Katsiki, Vasilios G Athyros, Asterios Karagiannis, Dimitri P Mikhailidis
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  ABSTRACT: Metabolic syndrome (MetS), a cluster of dyslipidaemia, central obesity, hypertension and/or insulin resistance, is associated with increased cardiovascular disease (CVD) type 2 diabetes risk. Different diagnostic criteria for MetS have been proposed but in 2009 a joint statement by several scientific societies was released. Apart from the diagnostic criteria, MetS has also been associated with other risk factors including waist to hip ratio, high density lipoprotein dysfunction, small dense low density lipoprotein, postprandial hypertriglyceridaemia, lipoprotein (a), uric acid, liver function tests, prothrombotic factors, cytokines, adipokines, vitamin D, arterial stiffness, renal dysfunction, nephrolithiasis, polycystic ovary syndrome, obstructive sleep apnea. We discuss the extensive list of MetS-associated factors that may influence vascular risk. Furthermore, we discuss the impact of frequently prescribed drugs (e.g. hypolipidaemic agents) on these variables. These effects may need to be taken into consideration when treating MetS patients.
  Current Vascular Pharmacology 04/2013;