Current Cardiology Reviews - Volume 14, Issue 4, 2018

Background: Aging is a process that affects all living organisms. The transition through life elicits tissue specific alterations in the functional and structural capabilities of all physiological systems. In particular, the vasculature is vulnerable to aging specific adaptations which induces morphological changes and ultimately increases the risk of pathological states. Matrix metalloproteinases are a group of extremely active enzymes that regulate the age-associated structural changes of the vasculature which has been regarded as the hallmark of arterial aging. Although this process in unavoidable, the structural and functional changes to the vasculature that occur as a result of advancing age can be positively or negatively influenced by our lifestyle choices. Conclusion: Exercise training has profound effects on the age-associated changes of the arteries which have been shown to be beneficial in offsetting the detrimental responses of aging. This review provides a brief synopsis of the matrix metalloproteinase induced alterations of the arteria during aging and highlights the potential of resistance exercise to influence such changes.

Background: The endothelium plays an important role in cardiovascular regulation, from blood flow to platelet aggregation, immune cell infiltration and demargination. A dysfunctional endothelium leads to the onset and progression of Cardiovascular Disease (CVD). The aging endothelium displays significant alterations in function, such as reduced vasomotor functions and reduced angiogenic capabilities. This could be partly due to elevated levels of oxidative stress and reduced endothelial cell turnover. Circulating angiogenic cells, such as Endothelial Progenitor Cells (EPCs) play a significant role in maintaining endothelial health and function, by supporting endothelial cell proliferation, or via incorporation into the vasculature and differentiation into mature endothelial cells. However, these cells are reduced in number and function with age, which may contribute to the elevated CVD risk in this population. However, lifestyle factors, such as exercise, physical activity obesity, and dietary intake of omega-3 polyunsaturated fatty acids, nitrates, and antioxidants, significantly affect the number and function of these circulating angiogenic cells. Conclusion: This review will discuss the effects of advancing age on endothelial health and vascular regenerative capacity, as well as the influence of diet, exercise, and obesity on these cells, the mechanistic links and the subsequent impact on cardiovascular health.

Background: Ageing is associated with an inexorable decline in cardiac and vascular function, resulting in an increased risk of Cardiovascular Disease (CVD). Lifestyle factors such as exercise have emerged as a primary therapeutic target in the prevention of CVD, yet older individuals are frequently reported as being the least active, with few meeting the recommended physical activity guidelines. In contrast, well trained older individuals (Masters athletes) have superior functional capacity than their sedentary peers and are often comparable with young non-athletes. Therefore, the 'masters' athlete may be viewed as a unique non-pharmacological model which may allow researchers to disentangle the inexorable from the preventable and the magnitude of the unavoidable 'true' reduction in cardiac function due to ageing. Conclusion: This review examines evidence from studies which have compared cardiac structure and function in well trained older athletes, with age-matched controls but otherwise healthy.

Background: Cardiovascular Disease (CVD) remains one of the leading causes of morbidity and mortality. Strategies to predict development of CVD are therefore key in preventing and managing CVD. One stratergy in predicting CVD is by examining the role of traditional risk factors for CVD (e.g. age, sex, weight, blood pressure, blood lipids, blood glucose, smoking and physical activity). Although these measures are non-invasive and simple to perform, they provide limited information of CVD prediction. Directly examining functional characteristics of arteries that are involved in the pathophysiological changes that contribute to the development of CVD improve prediction of future CVD. Nevertheless, examining the function of arteries susceptible to atherosclortic changes, such as the coronary arteries, is invasive, expensive, and associated with high risk for complications. More accessible arteries can be used as a surrogate measure of coronary artery function. For example, the carotid artery may be a superior surrogate measure of coronary artery function given that, the carotid artery represents a central vessel that shows similarities in vasomotor function and anatomical structure with coronary arteries. Conclusion: This review summarises the similarities between the carotid and coronary arteries, describes how both arteries respond to specific vasoactive stimuli, and discusses if the easily assessible carotid artery can provide information about vascular function (e.g. vasomotor reactivity to sympathetic stimulation) which is prognostic for future cardiovascular events. Finally, the impact of older age and lifestyle interventions (e.g. exercise training) on carotid artery function will be discussed.

Background: Calcific aortic valve disease is common in an aging population. It is an active atheroinflammatory process that has an initial pathophysiology and similar risk factors as atherosclerosis. However, the ultimate disease phenotypes are markedly different. While coronary heart disease results in rupture-prone plaques, calcific aortic valve disease leads to heavily calcified and ossified valves. Both are initiated by the retention of low-density lipoprotein particles in the subendothelial matrix leading to sterile inflammation. In calcific aortic valve disease, the process towards calcification and ossification is preceded by valvular thickening, which can cause the first clinical symptoms. This is attributable to the accumulation of lipids, inflammatory cells and subsequently disturbances in the valvular extracellular matrix. Fibrosis is also increased but the innermost extracellular matrix layer is simultaneously loosened. Ultimately, the pathological changes in the valve cause massive calcification and bone formation - the main reasons for the loss of valvular function and the subsequent myocardial pathology. Conclusion: Calcification may be irreversible, and no drug treatments have been found to be effective, thus it is imperative to emphasize lifestyle prevention of the disease. Here we review the mechanisms underpinning the early stages of the disease.

Background: Reactive oxygen species and reactive nitrogen species, which are collectively called reactive oxygen-nitrogen species, are inevitable by-products of cellular metabolic redox reactions, such as oxidative phosphorylation in the mitochondrial respiratory chain, phagocytosis, reactions of biotransformation of exogenous and endogenous substrate in endoplasmic reticulum, eicosanoid synthesis, and redox reactions in the presence of metal with variable valence. Among medicinal plants, there is growing interest in Crocus Sativus L. It is a perennial, stemless herb, belonging to Iridaceae family, cultivated in various countries such as Greece, Italy, Spain, Israel, Morocco, Turkey, Iran, India, China, Egypt and Mexico. Objective: The present study aims to address the anti-toxicant role of Crocus Sativus L. in the case of cardiovascular disease and its role towards the cardioprotective role of Crocus Sativus L. Materials and Methods: An electronic literature search was conducted by the two authors from 1993 to August 2017. Original articles and systematic reviews (with or without meta-analysis), as well as case reports were selected. Titles and abstracts of papers were screened by a third reviewer to determine whether they met the eligibility criteria, and full texts of the selected articles were retrieved. Results: Our review has indicated that scientific literature confirms the role of Crocus Sativus L. as a cardiovascular-protective agent. The literature review showed that Saffron is a potent cardiovascular- protective agent with a plethora of applications ranging from ischemia-reperfusion injury, diabetes and hypertension to hyperlipidemia. Conclusion: Literature findings represented in current review herald promising results for using Crocus Sativus L. and/or its active constituents as a cardiovascular-protective agent and in particular, Crocus Sativus L. manifests beneficial results against ischemia-reperfusion injury, hypertension, hyperlipidemia and diabetes.

Background: Redox signaling plays an important role in the lives of cells. This signaling not only becomes apparent in pathologies but is also thought to be involved in maintaining physiological homeostasis. Reactive Oxygen Species (ROS) can activate protein kinases: CaMKII, PKG, PKA, ERK, PI3K, Akt, PKC, PDK, JNK, p38. It is unclear whether it is a direct interaction of ROS with these kinases or whether their activation is a consequence of inhibition of phosphatases. ROS have a biphasic effect on the transport of Ca2+ in the cell: on one hand, they activate the sarcoplasmic reticulum Ca2+-ATPase, which can reduce the level of Ca2+ in the cell, and on the other hand, they can inactivate Ca2+-ATPase of the plasma membrane and open the cation channels TRPM2, which promote Ca2+-loading and subsequent apoptosis. ROS inhibit the enzyme PHD2, which leads to the stabilization of HIF-α and the formation of the active transcription factor HIF. Conclusion: Activation of STAT3 and STAT5, induced by cytokines or growth factors, may include activation of NADPH oxidase and enhancement of ROS production. Normal physiological production of ROS under the action of cytokines activates the JAK/STAT while excessive ROS production leads to their inhibition. ROS cause the activation of the transcription factor NF-ΚB. Physiological levels of ROS control cell proliferation and angiogenesis. ROS signaling is also involved in beneficial adaptations to survive ischemia and hypoxia, while further increases in ROS can trigger programmed cell death by the mechanism of apoptosis or autophagy. ROS formation in the myocardium can be reduced by moderate exercise.