Page: ii-vii (6)
Author: Atta-ur-Rahman and M. Iqbal Choudhary
Page: 1-11 (11)
Author: Carlos A. Feldstein
Hypertension is highly prevalent in industrialized countries. Older age is associated with more uncontrolled hypertension New developments to reinforce antihypertensive drug effects include the use of statins. The beneficial effects of statins that are partly independent of their lipid-lowering actions are referred to as pleiotropic effects. These effects include the improvement of vascular endothelial function, inhibition of vascular smooth muscle cell prolife-ration and migration, anti-inflammatory actions, anti-oxidative effects or stabilization of vulnerable plaques, and enhancement of arterial compliance. So far, the available data support only a modest antihypertensive effect of statins that is most prominent in those patients with uncontrolled hypertension. Even though they only produce minor reduction in blood pressure, their effects may be relevant from the point of view of cardiovascular prevention. From trials results it appears consistent that statins may be useful in hypertensive subjects with high serum total cholesterol, in those whose hypertension is not well controlled with antihypertensive agents even without high serum total cholesterol, in hypertensive subjects well controlled with antihypertensives without high serum cholesterol when they have high PCR levels, in those with other concomitant cardiovascular risk factors, or when they require secondary prevention. Future research could further characterize the impact of statin use alone or in combination with antihypertensive agents to prevent the development of stage 1 hypertension in prehypertension.
Page: 12-31 (20)
Author: Luca Puccetti, Maurizio Acampa, Marcello Pastorelli, Vittoria Soldati, Francesca Scarpini and Alberto Auteri
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Cardiovascular disease has become the global leading cause of death worldwide, representing the most frequent cause of morbidity and mortality in the developed world.
Statins, the most widely prescribed cholesterol-lowering drugs, are considered to be first-line therapeutics for the prevention of coronary heart disease and atherosclerosis. Meta-analyses from several primary and secondary intervention studies have clearly shown that cholesterol-lowering medication, significantly reduces cardiovascular events, mortality, and morbidity, but considerable interindividual variation exists in response to statin therapy.
Pharmacogenomics can provide important insights into statins therapy through elucidation of the genetic (or genomic) contribution to variable response for these drugs. The search for genetic polymorphisms may enable us to identify novel determinants of drug responsiveness by means of the study of three candidate genes groups: (1) genes encoding proteins involved in metabolism or drug transport, or both, that influence drug pharmacokinetics; (2) genes encoding proteins involved in mechanism of action and/or metabolic pathways on which drugs operate (that influence pharmacodynamics); (3) genes encoding proteins involved in the underlying disease condition or intermediate phenotype.
This review briefly summarizes the recent pharmacogenomic and pharmacogenetic patents and the potential contributions of genetic variations in candidate genes related to lipid and lipoprotein metabolism and statins efficacy.
Page: 32-60 (29)
Author: Mahesh T. Chhabria, Bhanubhai N. Suhagia and Pathik S. Brahmkshatriya
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High density lipoprotein (HDL) has proven its role in reverse cholesterol transport and cellular cholesterol efflux thus acting as a protective factor against atherogenic cardiovascular diseases. The article focuses primarily on structure and function of genes influencing HDL metabolism. Various novel targets involve liver X receptor, retinoid X receptor and peroxisome proliferators activated receptor agonists and apoA-I mimetics. New molecules targeting these receptors are described. Phospholipid transfer protein and scavenger receptor B1 are also attractive targets in HDL metabolism. ATP-Binding Cassette transporter A1 and several lipases also play a crucial role in HDL metabolism and are very useful target for atherogenic dyslipidemia. Several cholesterol ester transfer protein inhibitors have shown great promise as possible drug candidates of future. Notably, JTT-705 (Japan Tobacco, Roche) is of great interest in spite of withdrawal of torcetrapib. Considering modest effect of currently available therapeutic options on HDL, these novel HDL elevating targets are doubtlessly the target for future atherosclerotic intervention.
Page: 61-72 (12)
Author: Jose Luis Perez-Castrillon and Antonio Duenas-Laita
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Atherosclerosis is the leading cause of death and disability in the developed world. Although low-density lipoprotein (LDL) cholesterol lowering drugs reduce the mortality and morbidity associated with coronary artery disease, mortality and morbidity remain high. Reverse cholesterol transport mediated by high-density lipoproteins (HDL) may provide an independent pathway for lipid removal from atheroma. The current NCEP ATPIII include HDL-cholesterol ≥1.6 mmol/l as a negative risk factor. Torcetrapib is an inhibitor of cholesteryl estertransfer protein (CETP) that increases HDL-cholesterol levels. Published studies show a favourable lipid profile of torcetrapib but no clinical efficacy, with greater mortality, lack of antiatherosclerotic action and increased blood pressure and aldosterone, leading to its use being abandoned. However, these detrimental effects are related to the molecule itself and not to CETP inhibition.Raising HDLcholesterol by CETP inhibition could be a new approach to atherosclerotic cardiovascular disease, although trials based on hard clinical end points are necessary.
Page: 73-78 (6)
Author: Athanasios Tsatsaris, Efstathios Koukounaris, Theodoros Motsakos and Despina Perrea
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Objective: To investigate the role of infrasound aortic pressure waves (IPW) in atherosclerotic plaque rupture. Methods: Atherosclerotic plaques have been simulated partly, in two dimensions, as being short or long Conical Intersections(CIS) , that is to say elliptic, parabolic or hyperbolic surfaces. Consequently, the course and reflection of the generated aortic pressure wave (infrasound domain-less than 20Hz) has been examined around the simulated plaques. Results: The incidence of IPW on plaque surface results in reflection and “refraction” of the wave. The IPW course within tissue, seems to be enhanced by high Cu-level presence at these areas according to recent evidence (US2003000388213). The “refracted”, derived wave travels through plaque tissue and is eventually accumulated to the foci of the respective CIS-plaque geometry. Conclusions: The foci location within or underneath atheroma declares zones where infrasound energy is mostly absorbed. This process, among other mechanisms may contribute to plaque rupture through the development of local hemorrhage and inflammation in foci areas. In future, detection of foci areas and repair (i.e. via Laser Healing Microtechnique) may attenuate atherosclerotic plaque rupture behavior.
Page: 79-95 (17)
Author: Harish Ramakrishna
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Cardiovascular anesthesiologists have traditionally resorted to using intravenous therapy in the operating room to manipulate hemodynamics and the determinants of cardiac output and systemic vascular resistance during cardiac surgery. General anesthesia involves the administration of both intravenous and inhaled drug therapy to achieve the desired goals, i.e. analgesia, amnesia, muscle relaxation and blockade of autonomic activity. Anesthesiologists are the experts in the use and titration of drugs that are administered through the inhaled route. However, this method of drug delivery presents many challenges, notably timing, dosage accuracy, rapid titratability and consistency of drug delivery. Arguably the most rapid method of treating acute reactive pulmonary vasculature would be by drugs that directly act upon the pulmonary endothelium. In the operating room, pulmonary hypertension and right ventricular failure are high predictors of morbidity and mortality and present significant challenges to the anesthesiologist. In this article, we will focus on advances in inhaled therapy of these conditions, including concerned recent patents. This review will focus on some of the advances in the pharmacology of inhaled drugs that are being used to treat pulmonary hypertension, right and left ventricular failure in the perioperative setting.
The Role of Small, Dense LDL in Cardiovascular Risk: The Contributions of the Universities of Palermo and Zurich
Page: 96-104 (9)
Author: Manfredi Rizzo and Kaspar Berneis
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Low density lipoproteins (LDL) size seems to be an important predictor of cardiovascular events and progression of coronary artery disease and the predominance of small dense LDL has been accepted as an emerging cardiovascular risk factors by the National Cholesterol Education Program Adult Treatment Panel III. We recently showed increased LDL size or higher levels of small and dense LDL in different categories of patients at higher cardiovascular risk, such as those with coronary (including acute myocardial infarction) and non-coronary (including carotid disease, abdominal aortic aneurysm and peripheral arterial disease) forms of atherosclerosis or metabolic diseases (including type-II diabetes, polycystic ovary syndrome, growth hormone deficiency, gestational diabetes and the metabolic syndrome). Screening for the presence of small, dense LDL may potentially identify those with even higher risks and may contribute in directing specific treatments in order to prevent new cardiovascular events. This seems particularly true for statins and fibrates. Promising data are available for rosuvastatin, the latest statin molecule introduced in the market, and ezetimibe, a cholesterol absorption inhibitor.
Page: 105-120 (16)
Author: GianLuca Colussi, Cristiana Catena, Elisa Nadalini, Alessandra Chiuch, Alessandro Di Fabio, Marica Valeri and Leonardo A. Sechi
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ω-3 and ω-6 Polyunsaturated fatty acids (PUFA) are the major families of PUFA that can be found as components of the human diet. After ingestion, both ω-3 and ω-6 PUFA are distributed to every cell in the body where they are involved in a myriad of physiological processes, including regulation of cardiovascular, immune, hormonal, metabolic, neuronal, and visual functions. At the cell level, these effects are mediated by changes in membrane phospholipids structure, interference with eicosanoid intracellular signaling, and regulation of gene expression. Two long-chain ω-3 PUFAs, the docosahexaenoic (DHA) and eicosapentaenoic (EPA) acid, are found in fatty fish and other marine sources and might be the putative dietary components thought to modify the cardiovascular risk in subjects consuming high amounts of such food. Evidence of an inverse relationship between fatty fish intake and cardiovascular risk has, in fact, emerged in studies performed more than twenty years ago in Eskimos and has been subsequently confirmed in other ethnic groups. The benefits of ω-3 PUFA might relate principally to prevention of coronary heart disease, coronary artery restenosis after angioplasty, and sudden arrhythmic death. In this brief review, we will cover the general biochemical aspects of ω-3 PUFA, summarize the evidence relating these fatty acids with control of cardiovascular risk factors and prevention of cardiovascular events, and overview the most recent and relevant patents that are related to these issues. More specifically, we will deal with the possibility to use PUFA in association with other molecules that can potentiate their antiinflammatory and antiatherogenic effects
Page: 121-137 (17)
Author: Zia A. Khan and Subrata Chakrabarti
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We are approaching the 100-year anniversary of Dr. Frederick Banting ’ s discovery of insulin for the treatment of diabetes. The population of patients with diabetes is ever-increasing. However, with the availability of insulin, the cause of mortality has shifted from diabetic coma and ketoacidosis to chronic secondary complications. Dysfunction and failure of selected organs is now the most prominent cause of morbidity and mortality. These ‘target’ organs include the eyes, kidneys, heart, lower limbs, and the nervous system. A common feature of these complications is the aberration in the vasculature of the target organs. Studies over the past few decades have shown that dysfunction of the vascular endothelial cells may be the key to the development and progression of the chronic diabetic complications. We present the hypothesis and supporting evidence that preservation and restoration of the endothelial cell function may potentially be the most efficient means of targeting the adverse effects of diabetes.
Page: 138-153 (16)
Author: Reiko Inagi
Oxidative stress is a common denominator in many aspects of the pathogenesis of atherosclerosis and cardiovascular diseases. Some drugs, such as vitamin C, vitamin E, and a free radical scavenger, edaravone, are prescribed with oxidative stress as their main target. Furthermore, the drugs in current clinical use, such as anti-hypertension reagents including angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB), and antihyperlipidemic reagents like statins, protect various organs, e.g., vessel, brain, heart, and kidney, via anti-oxidative stress effects in addition to their original pharmacological properties. While results of clinical trials of anti-oxidative stress reagents in patients with cardiovascular disease are contradictory to date, this may be explained by a variety of reasons such as an inadequate study design. More competent anti-oxidative reagents are awaited, and superoxide dismutase mimetics, thiols, xanthine oxidase and NAD(P)H oxidase inhibitors, which regulate intracellular redox reaction and subsequently inhibit oxidative stress, are among promising candidates of future drug developments currently receiving much interest. In this review, the current advances will be highlighted in development of novel anti-oxidative therapeutic approaches against cardiovascular diseases.
The Clinical Impact of Hyperphosphatemia in Chronic Kidney Disease Patients: The Role of Lanthanum Carbonate
Page: 154-164 (11)
Author: Mario Cozzolino and Diego Brancaccio
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Vascular calcification is a very common event in patients affected by diabetes and chronic kidney disease (CKD). Recently, it has been well documented that abnormalities in mineral and bone metabolism in CKD patients associate with increased morbidity and mortality. Elevated serum phosphate and calciumphosphate product levels play an important role in the pathogenesis of vascular mineralization in uremic patients and also appear to be associated with increased cardiovascular mortality. Together with classical passive precipitation of calciumphosphate in soft tissues, during the last decade it has been demonstrated that inorganic phosphate may cause extraskeletal calcification directly through a real “ossification” of the tunica media in the vasculature of CKD patients. Therefore, control of phosphate retention is now an even more crucial target of treatment in patients affected by chronic kidney disease. The “classical” treatment of secondary hyperparathyroidism and hyperphosphatemia in CKD patients consists of either calcium or aluminium based phosphate-binders and calcitriol administration. Unfortunately, this “old generation” therapy is not free of complications. Lanthanum carbonate represents a novel phosphate binder used for the treatment of hyperphosphataemia in patients with renal failure. This new calcium- and aluminium-free phosphate binder can be used to treat hyperphosphatemia and secondary hyperparathyroidism, reduce atherosclerotic process, and prevent vascular calcification in CKD.
Myocardial Protection Against Ischemia-Reperfusion Injury: Novel Approaches in Maintaining Homeostatic Stability in Blood
Page: 165-191 (27)
Author: Maqsood M. Elahi and Bashir M. Matata
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Homeostatic vascular response to complement activation in cardiac surgery patients requiring cardiopulmonary bypass results in mechanisms leading to ischemia-reperfusion injury and myocardial cell death. Various pro-inflammatory cytokines, released by the inflamed tissue, play an essential role in the activation of the complement system and co-localize with activated complement proteins within the circulating blood and the myocardium.
Throughout the past decade, much effort has thus been spent on deciphering the molecular signaling pathways mediating this pathophysiology. Basic and clinical investigations into many of the diverse aspects of cardiovascular drugs discovery employ varied approaches aimed at determining physiologic and pathophysiological efficiency of candidate agents for therapeutic utility. Identification of novel molecules regulating homeostatic dysfunction has offered the basis, with ultimate hope of identifying agents capable of exerting salutary influence upon cardiac and vascular tissue.
This review will provide detailed synopses on recent insights into the ischemiareperfusion signaling and associated myocardial injury. In addition, we will consider current and emerging novel approaches in attenuating cardiopulmonary bypass mediated injury with ultimate goal to prevent or delay the onset of post pump modulated heart failure and sudden deaths in such patients. Careful examination of the literature on recent patented and non-patented publications has identified several agents shown to be effective and specific in modulating and abrogating ischemia-reperfusion injury with some suggestions of potential clinical use.
The Role of Angiotensin Type 1 Receptor in Inflammation and Endothelial Dysfunction: Clinical Application
Page: 192-200 (9)
Author: Dana Skultetyova, Adriena Sakalova, Pavol Chnupa and Slavomira Filipova
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Endothelial dysfunction plays an important role in all stages of atherosclerosis, and is characterized by an increased activity of vasoconstricting factors, proinflammatory and prothrombotic mediators. The aim of the review is to evaluate the role of angiotensin II (Ang II) and especially of angiotensin type 1 (AT1) receptor in inflammation and endothelial dysfunction.
Ang II with AT1 receptor are involved through several mechanisms in the progression of atherosclerosis. Stimulation of AT1 receptor increases oxidative stress especially through activation of NADH/NADPH oxidase in the vascular cells. Oxidative stress is associated with activation of the inflammatory processes. Ang II via AT1 receptor increases expression of adhesion molecules and stimulates the induction of monocyte chemoattractant protein-1 (MCP-1). AT1 receptor enhances the activation of nuclear factor NF-κB, which stimulates the production of proinflammatory cytokines. Proinflammatory cytokines on the other side may induce acute-phase response in the liver. Activation of AT1 receptor via inducible cyclooxygenase (COX)-2 promotes biosynthesis of matrix metalloproteinases (MMPs). Stimulation of proinflammatory cytokines activates profibrogenic transforming growth factor-beta 1 (TGF-β1). Ang II via NF-κB may regulate peroxisome proliferator activated receptors (PPARs) and the metabolism of glucose and lipids. Ang II is implicated in the process of angiogenesis. AT1 receptor takes part in the regulation of vascular endothelial growth factor (VEGF), which is one of the most angiogenic factors and stimulates the activity of endothelial progenitor cells (EPC).
Recently some patents that were reported discussing the role of different compounds for the treatment of cardiovascular disease, renovascular disease nephropathy, peripheral vascular disease, portal hypertension and ophthalmic disorders, are cyclooxygenase-2 inhibitors. AT1 receptor blockers are widely used in the treatment of cardiovascular, cerebral and renal diseases.
Page: 201-211 (11)
Author: Marek Jankowski
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Brain natriuretic peptide (BNP) plays an important role in cardiovascular homeostasis. Plasma BNP increases markedly in left ventricular dysfunction from several causes, and its levels in heart failure (HF) correlate with symptoms severity. BNP has recently emerged as a potentially important clinical marker for the diagnosis of HF in patients with unexplained dyspnea. Other clinical applications of BNP, such as screening for asymptomatic ventricular dysfunction, establishing the prognosis or guiding the titration of drug therapy, are under investigation and have not yet been sufficiently validated for widespread clinical use. Laboratory-based and point-of-care analyses are available for BNP and N-terminal proBNP as fully-automated immunoassays. Several patented inventions and reagents for the diagnosis of various heart pathologies provide helpful information, particularly in conjunction with other clinical tests. They also have prognostic value for future cardiovascular events. Patents owned by Scios Inc. recommended recombinant BNP for managing acute decompensated HF. However, this treatment apparently has safety problems and no proven clinical advantage over existing treatments in terms of improved survival and prevention of subsequent hospitalizations.
Page: 212-235 (24)
Author: Adinarayana Kunamneni, Bhavani D. Ravuri, Vinjamuri Saisha, Poluri Ellaiah and Taadimalla Prabhakhar
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Urokinase (UK) [EC 126.96.36.199] is a serine protease that activates plasminogen to plasmin, which in turn degrades fibrin clots. Plasmin has diverse physiological roles apart from its fibrinolytic role in the regulation of blood clotting. It has been implicated in complement activation, cell migration, wound healing, and generation of localized extracellular proteolysis during tissue remodelling, pro-hormone conversion, carcinogenesis and neoplasia. Among the plasminogen activators, UK provides a superior alternative for the simple reasons of its being more potent as compared to tissue-plasminogen activator and nonantigenic by virtue of its human origin unlike streptokinase. Based on these observations, UK is an important anti-thromboembolic drug. Hence, UK, as one of the most potent plasminogen activators is attracting a great deal of attention. In this chapter, we will summarize recent patents related to the occurrence, mechanism of action, structure and function, physico-chemical properties, in vitro production, cloning and expression, purification and applications of UK.
Anti-Inflammatory Effects of Endothelin Receptor Antagonists and their Importance for Treating Human Disease
Page: 236-258 (23)
Author: Matthias Barton, Philipp C. Nett, Kerstin Amann and Mauro M. Teixeira
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Endothelin-1 (ET-1) is the main effector peptide of the endothelin family. Aside from being a potent endogenous vasoconstrictor and mitogen acting through its ETA receptors, it contributes to the regulation of immune mechanisms, inflammatory cell activation, and release of cytokines. Thereby, endothelin promotes the developement of a number of chronic disease conditions characterized by inflammtory activation, including atherosclerosis and chronic renal failure. Studies using orally active endothelin receptor antogonists have shown that the ETA receptor is mainly responsible for the immunomodulatory actions of endothelin. This review highlights recent findings in the field showing that the ET system, apart from being a marker and mediator of vascular injury, is directly involved in pathophysiology of these disease processes as an immunomodulatory factor. In this review, we summarize the current understanding of the mechanisms and signal transduction pathways triggered by ET-1 in inflammatory and immunomodulatory processes and discuss the findings of studies evaluating the use of selective and non-selective endothelin receptor antagonists in diseases associated with acute or chronic inflammatory activation, also discussing including the most recent clinical studies in the field using endothelin receptor antagonists.
Page: 259-269 (11)
Author: Charalambos Antoniades, Michael Demosthenous, Dimitris Tousoulis, Costantinos Bakogiannis, Nikolaos Koumallos and Christodoulos Ste
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Heart failure is characterised by decreased cardiac output, which results in the development of both peripheral hypoperfusion and pulmonary congestion and can lead to the development of acute pulmonary edema. The primary objective in treating a patient with decompensated heart failure is hemodynamic stabilization, which is usually achieved by inotropic support. Classic inotropic agents provide short-term hemodynamic improvement, but their use has been correlated with poor prognosis. Levosimendan, a new calcium sensitizer, offers hemodynamic and symptomatic improvement without increasing cAMP and intracellular calcium concentrations. This agent improves contractility without increasing the risk of cardiac events such as arrhythmias. By combining a positive inotropic action mediated via calcium sensitization and a vasodilatory effect via ATP-dependent potassium channels, it appears to be superior than classic positive inotropic agents. Furthermore, it seems to have prolonged benefit in heart failure patients, and it also has anti-inflammatory and antiapoptotic properties. In conclusion, levosimendan seems to be a particularly promising agent for the treatment of decompensated heart failure, as in addition to improving cardiac output, it has a more favorable side-effect profile than classic inotropic agents, and it affects multiple pathways with key role in the pathophysiology of heart failure.
Page: 270-287 (18)
Author: Alessandro Pingitore and Giorgio Iervasi
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Interest in the role of thyroid hormones (TH) in heart failure is steadily increasing due to evidence for a physiological, homeostatic role of TH and the effects of altered TH metabolism on the cardiovascular system, particularly in presence of heart failure.
Experimental studies have shown that altered TH metabolism modifies cardiovascular homeostasis by inducing alterations of cardiac histology, cardiomyocyte morphology and gene expression and consequently, of diastolic and systolic myocardial function. Clinical studies have shown that mild forms of thyroid dysfunction, both primary (subclinical hypothyroidism and subclinical hyperthyroidism) and secondary (low T3 syndrome) have negative prognostic impacts on patients with heart failure. In these patients, the administration of synthetic triiodothyronine (T3) was well tolerated and induced significant improvement in cardiac function without increased heart rate and metabolic demand. Large multicenter, placebo-controlled prospective studies are necessary to evaluate the safety and prognostic effects of chronic treatment with TH replacement therapy in patients with heart failure. The article also discusses recent patents in this field.
Page: 288-306 (19)
Author: Husnain K. Haider, Lei Ye and Muhammad Ashraf
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Treatment of patients with heart failure secondary to myocardial infarction remains a therapeutic challenge. Extensive myocyte death in the heart and post-ischemic remodeling accentuate progressive expansion of the scar area and compromise left ventricular contractile function. The scarcity of resident stem cells in the heart and limited proliferative capacity of adult cardiomyocytes warrant novel strategies of outside intervention to supplement the inept intrinsic repair mechanism. Heart cell therapy using patient's own skeletal muscle derived myoblasts (SkMs) provides a relatively simple and inexpensive therapeutic option. Phase-I and II clinical trials supported by plethora of pre-clinical studies have shown the safety and effectiveness of SkM engraftment in the treatment of infarcted heart. However, before widespread application of this approach in the clinical settings, there remain some fundamental issues including extensive donor cell death during acute phase after SkMs engraftment, failure of SkMs to adopt cardiac phenotype and transient ventricular arrhythmias subsequent to SkMs transplantation which require serious considerations. This review will provide profound analysis of merits and limitations of SkMs as the choice cells for heart cell therapy and will summarize the potential of genetic and pharmacological manipulation SkMs to enhance their therapeutic efficacy for myocardial repair.
A Practical Approach to Diagnosis and Treatment of Symptomatic Thromboembolic Events in Children with Acute Lymphoblastic Leukem
Page: 307-323 (17)
Author: Paola Giordano, Giovanni Carlo Del Vecchio, Paola Saracco, Marco Zecca, Angelo Claudio Molinari and Domenico De Mattia
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Intensified treatments with multi-drug regimens are responsible for the continuously increasing survival of children with acute lymphoblastic leukaemia. However, together with the widespread use of central venous lines, they are also considered the main risk factors for the growing number of thromboembolic complications in this population.
The rate of thrombosis that was observed in 17 prospective studies was 5.2%. Due to the high survival rate, it is relevant to apply strategies to the long term survivors who overcome the disease but who experience thromboembolic complications. Specific treatment includes anticoagulants, especially unfractionated heparin and low molecular weight heparins, and thrombolytic drugs in few cases.
Guidelines for the treatment of thrombosis in childhood only became available recently, but they do not include specific clinical subsets such as children with acute lymphoblastic leukaemia. The problems involved in scheduling thrombosis treatment in children with malignancy have recently been discussed, however the paper does not provide practical diagnostic schemes or treatment schedules. Some important questions regarding optimal prevention and treatment are still unanswered. Moreover, antithrombotic therapy in these patients is quite challenging owing to the higher risk of bleeding. We believe it would be possible to propose reasoned appropriate recommendations for treating thrombosis in children with acute lymphoblastic leukaemia, looking forward for the effects of recent patents. This paper is an attempt to provide a practical guide to the diagnosis and treatment of thrombotic events in children with acute lymphoblastic leukaemia, and it is aimed at physicians who have no specific knowledge of the diagnosis and management of thrombosis and haemostasis alterations in children.
Recent Progress in Pharmacological Research of Antioxidants in Pathological Conditions: Cardiovascular Health
Page: 324-346 (23)
Author: Milagros Rocha, Remedios Garcia-Bou, Raul Herance, Antonio Hernandez-Mijares and Victor M. Victor
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Antioxidants are essential, and are involved in several important biological processes such as immunity, protection against tissue damage, reproduction, growth and development. Antioxidants preserve adequate function of cells against homeostatic disturbances such as those caused by septic shock, aging and, in general, processes involving oxidative stress. Each year, many scientific articles are published describing the pharmacological and biological properties of antioxidants. This review article compiles recent findings on these properties, focusing mainly on the anti-inflammatory properties of antioxidants in different pathological areas, such as cardiovascular damage and sepsis. In relation to this process, this review focuses on the involvement of reactive oxygen and nitrogen species. Finally, the protective role of antioxidants against homeostatic disturbances such as those caused by endotoxin toxicity and cardiovascular damage, their potential clinical use, and the effects on the redox state of immune cells are discussed.
Page: 347-348 (2)
Author: Atta-ur-Rahman and M. Iqbal Choudhary
&ldquo;Frontiers in Cardiovascular Drug Discovery&rdquo; is an eBook series devoted to publishing the latest and the most important advances in Cardiovascular drug design and discovery. Eminent scientists write contributions on all areas of rational drug design and drug discovery including medicinal chemistry, in-silico drug design, combinatorial chemistry, high-throughput screening, drug targets, recent important patents, and structure-activity relationships. The eBook series should prove to be of interest to all pharmaceutical scientists involved in research in cardiovascular drug design and discovery. Each volume is devoted to the major advances in cardiovascular drug design and discovery. The eBook series is essential reading to all scientists involved in drug design and discovery who wish to keep abreast of rapid and important developments in the field.