Cardiovascular System
Download ===== https://shurll.com/2tE0ab
The cardiovascular system is sometimes called the blood-vascular, or simply the circulatory, system. It consists of the heart, which is a muscular pumping device, and a closed system of vessels called arteries, veins, and capillaries. As the name implies, blood contained in the circulatory system is pumped by the heart around a closed circle or circuit of vessels as it passes again and again through the various \"circulations\" of the body.
As in the adult, survival of the developing embryo depends on the circulation of blood to maintain homeostasis and a favorable cellular environment. In response to this need, the cardiovascular system makes its appearance early in development and reaches a functional state long before any other major organ system. Incredible as it seems, the primitive heart begins to beat regularly early in the fourth week following fertilization.
The vital role of the cardiovascular system in maintaining homeostasis depends on the continuous and controlled movement of blood through the thousands of miles of capillaries that permeate every tissue and reach every cell in the body. It is in the microscopic capillaries that blood performs its ultimate transport function. Nutrients and other essential materials pass from capillary blood into fluids surrounding the cells as waste products are removed.
Numerous control mechanisms help to regulate and integrate the diverse functions and component parts of the cardiovascular system in order to supply blood to specific body areas according to need. These mechanisms ensure a constant internal environment surrounding each body cell regardless of differing demands for nutrients or production of waste products.
Importance: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19) has reached a pandemic level. Coronaviruses are known to affect the cardiovascular system. We review the basics of coronaviruses, with a focus on COVID-19, along with their effects on the cardiovascular system.
Observations: Coronavirus disease 2019 can cause a viral pneumonia with additional extrapulmonary manifestations and complications. A large proportion of patients have underlying cardiovascular disease and/or cardiac risk factors. Factors associated with mortality include male sex, advanced age, and presence of comorbidities including hypertension, diabetes mellitus, cardiovascular diseases, and cerebrovascular diseases. Acute cardiac injury determined by elevated high-sensitivity troponin levels is commonly observed in severe cases and is strongly associated with mortality. Acute respiratory distress syndrome is also strongly associated with mortality.
Conclusions and relevance: Coronavirus disease 2019 is associated with a high inflammatory burden that can induce vascular inflammation, myocarditis, and cardiac arrhythmias. Extensive efforts are underway to find specific vaccines and antivirals against SARS-CoV-2. Meanwhile, cardiovascular risk factors and conditions should be judiciously controlled per evidence-based guidelines.
The coronavirus disease 2019 (COVID-19) pandemic has affected health and economy worldwide on an unprecedented scale. Patients have diverse clinical outcomes, but those with preexisting cardiovascular disease, hypertension, and related conditions incur disproportionately worse outcome. The high infectivity of severe acute respiratory syndrome coronavirus 2 is in part related to new mutations in the receptor binding domain, and acquisition of a furin cleavage site in the S-spike protein. The continued viral shedding in the asymptomatic and presymptomatic individuals enhances its community transmission. The virus uses the angiotensin converting enzyme 2 receptor for internalization, aided by transmembrane protease serine 2 protease. The tissue localization of the receptors correlates with COVID-19 presenting symptoms and organ dysfunction. Virus-induced angiotensin converting enzyme 2 downregulation may attenuate its function, diminish its anti-inflammatory role, and heighten angiotensin II effects in the predisposed patients. Lymphopenia occurs early and is prognostic, potentially associated with reduction of the CD4+ and some CD8+ T cells. This leads to imbalance of the innate/acquired immune response, delayed viral clearance, and hyperstimulated macrophages and neutrophils. Appropriate type I interferon pathway activation is critical for virus attenuation and balanced immune response. Persistent immune activation in predisposed patients, such as elderly adults and those with cardiovascular risk, can lead to hemophagocytosis-like syndrome, with uncontrolled amplification of cytokine production, leading to multiorgan failure and death. In addition to the airways and lungs, the cardiovascular system is often involved in COVID-19 early, reflected in the release of highly sensitive troponin and natriuretic peptides, which are all extremely prognostic, in particular, in those showing continued rise, along with cytokines such as interleukin-6. Inflammation in the vascular system can result in diffuse microangiopathy with thrombosis. Inflammation in the myocardium can result in myocarditis, heart failure, cardiac arrhythmias, acute coronary syndrome, rapid deterioration, and sudden death. Aggressive support based on early prognostic indicators with expectant management can potentially improve recovery. Appropriate treatment for heart failure, arrhythmias, acute coronary syndrome, and thrombosis remain important. Specific evidence-based treatment strategies for COVID-19 will emerge with ongoing global collaboration on multiple approaches being evaluated. To protect the wider population, antibody testing and effective vaccine will be needed to make COVID-19 history.
Several functions of the cardiovascular system can control blood pressure. Certain hormones along with autonomic nerve signals from the brain affect the rate and strength of heart contractions. Greater contractile force and heart rate lead to an increase in blood pressure. Blood vessels can also affect blood pressure. Vasoconstriction decreases the diameter of an artery by contracting the smooth muscle in the arterial wall. The sympathetic (fight or flight) division of the autonomic nervous system causes vasoconstriction, which leads to increases in blood pressure and decreases in blood flow in the constricted region. Vasodilation is the expansion of an artery as the smooth muscle in the arterial wall relaxes after the fight-or-flight response wears off or under the effect of certain hormones or chemicals in the blood. The volume of blood in the body also affects blood pressure. A higher volume of blood in the body raises blood pressure by increasing the amount of blood pumped by each heartbeat. Thicker, more viscous blood from clotting disorders can also raise blood pressure.
Cardiovascular disease (CVD) presents a great burden for elderly patients, their caregivers, and health systems. Structural and functional alterations of vessels accumulate throughout life, culminating in increased risk of developing CVD. The growing elderly population worldwide highlights the need to understand how aging promotes CVD in order to develop new strategies to confront this challenge. This review provides examples of some major unresolved clinical problems encountered in daily cardiovascular practice as we care for elderly patients. Next, the authors summarize the current understanding of the mechanisms implicated in cardiovascular aging, and the potential for targeting novel pathways implicated in endothelial dysfunction, mitochondrial oxidative stress, chromatin remodeling, and genomic instability. Lastly, the authors consider critical aspects of vascular repair, including autologous transplantation of bone marrow-derived stem cells in elderly patients.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infects host cells through ACE2 receptors, leading to coronavirus disease (COVID-19)-related pneumonia, while also causing acute myocardial injury and chronic damage to the cardiovascular system. Therefore, particular attention should be given to cardiovascular protection during treatment for COVID-19.
In December 2019, an outbreak of pneumonia caused by a novel coronavirus occurred in Wuhan, Hubei province, and has spread rapidly throughout China, with an ongoing risk of a pandemic1. After virus identification and isolation, the pathogen for this pneumonia was originally called 2019 novel coronavirus (2019-nCoV)2 but has subsequently been officially named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) by the WHO. On 30 January 2020, the WHO declared the outbreak of SARS-CoV-2 a Public Health Emergency of International Concern. Compared with the SARS-CoV that caused an outbreak of SARS in 2003, SARS-CoV-2 has a stronger transmission capacity. The rapid increase in confirmed cases makes the prevention and control of COVID-19 extremely serious. Although the clinical manifestations of COVID-19 are dominated by respiratory symptoms, some patients have severe cardiovascular damage3. In addition, some patients with underlying cardiovascular diseases (CVDs) might have an increased risk of death3. Therefore, understanding the damage caused by SARS-CoV-2 to the cardiovascular system and the underlying mechanisms is of the greatest importance, so that treatment of these patients can be timely and effective and mortality reduced.
The mechanism of acute myocardial injury caused by SARS-CoV-2 infection might be related to ACE2. ACE2 is widely expressed not only in the lungs but also in the cardiovascular system and, therefore, ACE2-related signalling pathways might also have a role in heart injury. Other proposed mechanisms of myocardial injury include a cytokine storm triggered by an imbalanced response by type 1 and type 2 T helper cells3,6, and respiratory dysfunction and hypoxaemia caused by COVID-19, resulting in damage to myocardi