Coronary collateral vessels supply blood to areas of myocardium at risk after arterial occlusion. Flow through these channels is driven by a pressure gradient between the donor and the occluded artery. Concomitant with increased collateral flow is an increase in shear force, a potent stimulus for collateral development (arteriogenesis). Arteriogenesis is self-limiting, often ceasing prematurely when the pressure gradient is reduced by the expanding lumen of the collateral vessel. After the collateral has reached its self-limited maximal conductance, the only way to drive further increases is to re-establish the pressure gradient.During exercise, the myocardial oxygen demand is increased, subsequently increasing coronary flow. Therefore, exercise may represent a means of driving augmented arteriogenesis in patients with stable coronary artery disease. Studies investigating the ability of exercise to drive collateral development in humans are inconsistent. However, these inconsistencies may be due to the heterogeneity of assessment methods used to quantify change. This article summarises current evidence pertaining to the role of exercise in the development of coronary collaterals, highlighting areas of future research.

Depressive symptoms are highly prevalent in patients with cardiac diseases. Co-morbid Depression in cardiac patients causes a significant reduction in health-related quality of life for the patients and inflicts an economic burden on the society. Two types of mechanisms that may explain the link between depression and cardiac diseases are the psychosocial and physiopathological mechanisms. Physiopathological mechanisms are direct biological mechanisms, which include hyperactivity of non-adrenergic and Hypothalamic Pituitary Adrenal Axis (HPA), abnormal platelet activation, endothelial dysfunction, and inflammatory process. Psychosocial factors include behavioral or lifestyle factors like smoking alcoholism and physical inactivity. Pharmacologic and therapeutic interventions are effective at reducing symptoms of depression in patients with cardiac disorders. Among pharmacological treatment, SSRIs seems to be effective for the reduction of depressive symptoms among patients with cardiac disorders because of their good efficacy and minimal cardiovascular side effects. Mechanisms of action of SSRI’s in depressive patients with cardiac disorders are associated with their ability to reduce inflammation, platelet, and endothelial dysfunction. This review focuses on the potential pathophysiological and psychosocial links between cardiac diseases and depression, the treatment options, and the importance of routine screening of depressive symptoms in cardiac settings.

The association between thyroid disease and cardiovascular manifestations is significant and undeniable. Previous studies have explained several aspects of the effects of thyroid hormone on the heart and cardiovascular system. Accordingly, both hyper and hypothyroidism can cause important alterations in cardiac rhythm, output and contractility as well as vascular resistance and blood pressure. Since treating the thyroid abnormality, especially in its initial stages, could lead to a significant improvement in most of its resultant cardiovascular disturbances, early suspicion and recognition of thyroid dysfunction, is necessary in patients with cardiovascular manifestations. In this in-depth review, we discuss the physiological roles as well as the effects of abnormal levels of thyroid hormones on the cardiovascular system. We also review the effects of the medications used for the treatment of hyper and hypothyroidism on cardiac function. In the end, we discuss the association between thyroid function and amiodarone, an effective and frequently-used antiarrhythmic drug, because of its well-known effects on the thyroid.

Background:Cardiovascular diseases are the leading cause of death among dialysis pa-tients, accounting for about 40% of all their mortalities. Sudden cardiac death (SCD) is culpable for 37.5% of all deaths among patients with end-stage renal disease (ESRD). Implantable cardioverter-defibrillators (ICDs) should be considered in dialysis patients for the primary or secondary preven-tion of SCD. Recent studies on the implementation of ICD/cardiac resynchronization therapy do not exclude patients with ESRD; however, individualized decisions should be made in this group of pa-tients. A thorough evaluation of the benefits of ICD implementation in patients with ESRD requires several large-scale mortality studies to compare and follow up patients with ESRD with and without ICDs. In the present study, we sought to determine and clarify the complications associated with ICD implementation and management thereof in patients suffering from ESRD.Methods:To assess the complications allied to the implementation of ICDs and their management in patients with ESRD, we reviewed available related articles in the literature.Results and Conclusions:ICD implementation in dialysis patients has several complications, which has limited its usage. Based on our literature review, the complications of ICD implementation can be categorized as follows: (1) Related to implantation procedures, hematoma, and pneumothorax; (2) Re-lated to the device/lead such as lead fracture and lead dislodgment; (3) Infection; and (4) Central vein thrombosis. Hence, the management of the complications of ICDs in this specific group of patients is of vital importance.

In patients with atrial fibrillation undergoing percutaneous coronary intervention with the placement of stents, a triple antithrombotic therapy is empirically established, which consists of a combination of dual antithrombotic therapy (aspirin plus a P2Y12 inhibitor) and an oral anticoagulant agent. This choice is guided by the desirable result of reducing cerebrovascular and coronary ischemic events. However, there is an unwelcome outcome: an increased incidence of bleeding. On this matter, in 2018, a North American Perspective Update was published, about a year later it was followed by the publication of the European focus update on the dual antiplatelet therapy. After analysing the main differences between these two consensus documents, this review aims at examining the major studies on which they are based on, as a starting point to define the foundation of new trials that can help shed light on this prominent topic.

The management of patients with shock is extremely challenging because of the myriad of possible clinical presentations in cardiogenic shock, septic shock and hypovolemic shock and the limitations of contemporary therapeutic options. The treatment of shock includes the administration of endogenous catecholamines (epinephrine, norepinephrine, and dopamine) as well as various vaso-pressor agents that have shown efficacy in the treatment of the various types of shock. In addition to the endogenous catecholamines, dobutamine, isoproterenol, phenylephrine, and milrinone have served as the mainstays of shock therapy for several decades. Recently, experimental studies have suggested that newer agents such as vasopressin, selepressin, calcium-sensitizing agents like levosimendan, car-diac-specific myosin activators like omecamtiv mecarbil (OM), istaroxime, and natriuretic peptides like nesiritide can enhance shock therapy, especially when shock presents a more complex clinical picture than normal. However, their ability to improve clinical outcomes remains to be proven. It is the purpose of this review to describe the mechanism of action, dosage requirements, advantages and disadvantages, and specific indications and contraindications for the use of each of these catechola-mines and vasopressors, as well as to elucidate the most important clinical trials that serve as the basis of contemporary shock therapy.

Background: Ageing is associated with an inexorable decline in cardiac and vascular func-tion, resulting in an increased risk of Cardiovascular Disease (CVD). Lifestyle factors such as exer-cise 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 ca-pacity 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' reduc-tion 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