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Last Updated: 02 July 2021

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| Coronaviruses form enveloped spherical particle that consists of four structural proteins spike, envelope, membrane and nucleocapsid and a positive - sense, single - strand RNA genome that is 30 kb in length. B | 5 - terminal two - thirds of severe acute respiratory syndrome coronavirus 2 genome encodes polyproteins pp1a and pp1ab, which are cloven into 16 different non - structural proteins. Structural proteins are encoded in 3 - terminals one - third of the genome. The S protein consists of two subunits; S1 subunit contains receptor - binding domain that bind to angiotensin - converting enzyme 2 on the surface of host cells, whereas S2 subunit mediates fusion between membranes of the virus and host cell. Compared with S protein of SARS - CoV, S protein of SARS - CoV - 2 has two notable features. First, within the RBD of S1 subunit, five of six residues that are crucial for binding to human ACE2 are mutate. Second, insertion of four amino acid residues at the boundary between S1 and S2 subunits is present in SARS - CoV - 2 but not in SARS - CoV, which introduces novel furin cleavage site. C | SARS - CoV - 2 infection is triggered by binding of S protein to ACE2 on the surface of host cells, and the viral complex is incorporated into cytoplasm either by direct fusion with cell membrane or via endocytosis with later release into cytoplasm from endocytic vesicle. S protein is cloven at the S1 / S2 boundary and the S2 subunit facilitates membrane fusion. Viral genome RNA is released into cytoplasm, and the first open reading frame is translated into polyproteins pp1a and pp1ab, which are then cloven by viral proteases into small, non - structural proteins such as RNA - dependent RNA polymerase. Viral genomic RNA is replicated by RdRP. Viral nucleocapsids are assembled from genomic RNA and N proteins in the cytoplasm, whereas budding of new particles occurs at the membrane of the endoplasmic reticulum - golgi intermediate compartment. Finally, genomic RNA and structural proteins are assembled into new viral particles, leading to their release via exocytosis. 3cl, 3 - chymotrypsin - like protease. Cardiovascular comorbidities such as hypertension and coronary artery Disease are associated with high mortality in patients with coronavirus Disease 2019. Drugs used to reduce cardiovascular risk such as angiotensin - converting enzyme inhibitors and angiotensin II receptor blockers have numerous effects that might influence susceptibility to or severity of COVID - 19. Furthermore, although the main presentation of COVID - 19 is viral pneumonia, COVID - 19 can also induce cardiovascular manifestations including myocardial injury, myocarditis, arrhythmias, acute coronary syndrome and thromboembolism. Among these cardiovascular manifestations, myocardial injury has been independently associated with high mortality among patients with COVID - 19. Finally, medications that have been proposed as treatments for COVID - 19 such as hydroxychloroquine and azithromycin have pro - arrhythmic effects. Af, atrial fibrillation; VF, ventricular fibrillation; VT, ventricular tachycardia. Angiotensin II, main effector molecule in the renin - angiotensin - aldosterone system, is upregulated in many pathological conditions, for which inhibition of angiotensin II by RAAS inhibitors is a common therapeutic strategy.

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Introduction

Cardiovascular Disease IS leading cause of morbidity and mortality worldwide. In the United States, CVD accounts for ~600 000 deaths each year, and after continuous decline over the last 5 decades, its incidence IS increasing again. Among many risk factors that predispose to CVD development and progression, sedentary lifestyle, characterized by consistently low levels of physical Activity, is now recognized as a leading contributor to poor cardiovascular health. Conversely, regular exercise and physical activity are associated with remarkable widespread health benefits and significantly lower CVD risk. Several long - term studies have shown that increased physical activity is associated with reduction in all - cause mortality and may modestly increase life expectancy, effect which is strongly linked to a decline in Risk of Developing Cardiovascular and Respiratory Diseases. Consistent with this notion, death rates among men and women have been found to be inversely related to cardiorespiratory fitness levels, even in the presence of other predictors of cardiovascular mortality such as smoking, hypertension, and hyperlipidemia. Moreover, better fitness levels in both men and women can partially reverse elevated rates of all - cause mortality as well as CVD mortality associated with high body mass index. Recent work from cardiovascular cohorts shows that sustained Physical Activity IS associated with more favorable inflammatory marker profile, decreases heart failure risk, and improves survival at 30 years follow - up in individuals with coronary artery Disease. Despite the robust beneficial effects of physical activity and exercise on cardiovascular health, processes and mechanisms by which frequent physical activity promotes cardiorespiratory fitness and decreases CVD risk remain unclear. In the past several decades, considerable research effort has aimed at identifying major physiological and biochemical contributors to cardiovascular benefits of exercise, and as a result, significant advances have been made from observational and interventional studies with human participants. In parallel, valuable mechanistic insights have been garnered from experimental studies in animal models. Thus, in this review, we provide a synopsis of major known effects of exercise and physical activity on principal factors associated with risk of poor cardiovascular health, including blood lipids, hypertension, and arterial stiffness. For the purpose of review, we follow the definition of exercise as a subset of Physical Activity that IS plan, structure, and repetitive and has as final or intermediate objective improvement or maintenance of physical fitness. These characteristics distinguish exercise from less structure and Plan Physical Activity, which IS often not solely for the purpose of maintaining or improving physical fitness. Most long - term observational studies report levels of physical activity, whereas more controlled and short - duration studies examine effects of exercise. Throughout the text, we distinguish between these two types of activities to the extent possible. We also discuss means by which a healthy cardiovascular system adapts to exercise conditioning as well as recently proposed mechanisms of adaptation that may work to antagonize Cardiovascular Disease.


Redox Signaling

Inflammaging partly results from increased concentrations of alarmins, which activate pattern recognition receptors. Toll - like and nucleotide - binding oligomerization domain - like receptors are expressed not only on or in innate immunocytes but also on or in cells of the neurovascular unit and blood - brain barrier. Among these PRRs, TLR2, TLR4, NLRP1, and NLRP3 are activated during aging in neurons, astrocytes, microgliocytes, and possibly endotheliocytes and pericytes. Cardiovascular disease is linked to chronic obstructive pulmonary disorder via chronic inflammation and aging with reduced Sirtuin activity and exposure to cigarette smoke. Desmosine and isodesmosine are involved in elastin crosslinking and can serve as indicators of elevated elastin fiber turnover and degradation, such as in COPD and atherosclerosis complications. Sirtuins are NAD + - dependent protein deacetylases implicated in lifespan and health regulation. Sirtuin - 1 regulates endothelial function as it deacetylates NOS3. In addition, it counters senescence, as it deacetylates P53 and STK11, and angiogenesis, as it deacetylates FoxO1 and notch - 1. It also activates the liver X receptor, which is involved in reverse cholesterol transport, hence promoting cholesterol efflux. It has an antioxidant effect. Furthermore, it inhibits NFB. On the other hand, Sirtuin - 1 precludes vascular smooth myocyte proliferation and atherothrombosis, as it downregulates endothelial formation of tissue factor and upregulates that of tissue inhibitor of metallopeptidase TIMP3. Prolonged moderate exercise training enhances FoxO3a expression, reduces redox stress, and raises SIRT1 activity in heart and adipose tissue of aged rats. Sirtuin - 3 hampers cardiac hypertrophy as it controls ROS concentrations. Sirtuin - 6 in endotheliocytes protects against telomere and gene damage, and Sirtuin - 7 interacts with P53 and protects CMCs against apoptosis and redox and genotoxic stresses. Reactive oxygen species participate in aging. However, dietary antioxidants, such as vitamins C and E, do not slow aging. Mitochondria are major ROS sources and thus mediate adverse processes in aging. Supplementation with orally active mitochondrial antioxidant MitoQ, derivative of potent antioxidant ubiquinone conjugate to triphenylphosphonium, which accumulates within mitochondria, prevents mitochondrial redox damage. It thus attenuates production of proliferative, proinflammatory, and profibrogenic mediators by neighboring and infiltrating cells in the liver, and hence redox stress, hepatocyte death, and hepatic inflammation, together with liver fibrosis and cirrhosis in mice. Its administration for 4 weeks limited reduction of elastin content and decreased aortic stiffness in 27 - month - old mice, affected neither young mice nor age - related collagen synthesis and deposition, and increased proinflammatory cytokine formation.

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How Much Exercise Is Enough?

In his 2001 summary Report from Hockley Valley Symposium, Kohl Report findings from 8 published studies based on 5 large cohort studies of Association between Physical Activity dose and cardiovascular Disease. 12 With Follow - Up data ranging from 5 to 26 years, majority of studies report graded inverse Association of Physical Activity intensity and / or duration with incidence of CVD. Despite consistent inverse Association observe across studies, it is still not possible to determine the summary minimum dose required to prevent CVD because of the variety of instruments used to quantify physical activity. In 2003, Yu and colleagues tested Association of Activity dose on 10 - year incidence of CVD, CHD and all - cause mortality in 2512 middle - age British men. 13 Physical Activity was measured using Minnesota Leisure Time Physical Activity Questionnaire 14 and used to generate an Activity index. Activities in light tertile had intensity codes of < 4, and moderate Activity had Activity codes of 4. 5 to 5. 5 and heavy activity had intensity codes > 6. 0. In age - adjusted models, relative hazard of CVD and CHD mortality decreased with increasing intensity and duration of total Leisure Time Activity. However, following additional adjustment for blood pressure, body mass index, cigarette smoking, family history of Heart Disease, social class and occupational activity, association between highest level of activity as compared with lowest, attenuated to non - significance. Increasing frequency of heavy activities was associated with a 62% lower likelihood of CVD mortality, and the trend across activity levels was statistically significant even following risk factor adjustment. Neither time spent engaging in job - related Physical Activity nor combination of light and moderate activities, was associated with CVD mortality. The patterns were similar with CHD was studied separately. Findings from the present study underscore the importance of higher intensity activities to lower CVD risk. Base on epidemiologic evidence that overall levels of Physical Activity are lower in men as compared with women and because women engage in different types of activities than men, Oguma and colleagues review literature on Association of Physical Activity With cardiovascular Disease in women. 15 Figure 1 displays meta - analytic results from reviewed studies. When physical activity levels from longitudinal studies were combined into a 5 - level ranking from low - to - high, there was an inverse association of relative physical activity level with incidence of CVD in women. As compared with women in the lowest combined quintile of relative activity, women in the highest quintile were 37% less likely to experience cardiovascular disease events. However, one caution is that one of three studies included in that particular meta - analytic estimate was based on Lipid Research Clinics Study 16, which directly measures cardiorespiratory fitness, objective measure that is commonly more strongly associated with morbidity and mortality than activity. Chd is the leading cause of death in the United States. 1 At the Hockley Symposium, there were 23 observational studies describing the Association of amount of Leisure Time or occupational Activity on CHD.

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Physical Fitness and Mortality

An inverse association between PHYSICAL activity and incidence of chronic diseases and life expectancy has long been establish; 1 However, many large studies linking PHYSICAL activity with long - term health outcomes have relied on self - report data and questionnaires which limit robust associations by recall bias. 2 3 Additionally, some studies of exercise habits and mortality have suggested the possible existence of a U - shape curve, in which extremely active individuals may have increased cardiovascular morbidity and overall mortality compared to those who engage in some, but not extreme, amounts of activity. 4 5 Such findings invite questions about just how much PHYSICAL activity is safe. Recent original investigation by Mandsager et al. Aim to address some of these issues by examining the Association between Cardiorespiratory fitness in participants undergoing routine exercise treadmill testing and long - term mortality. This was a large, retrospective analysis of 122 007 consecutive patients who underwent ETT during a 24 - year period at a tertiary care Center with a median Follow - up of 8. 4 years. The most common reasons for referral for testing include evaluation for coronary artery disease and symptom assessment. Crf was assessed by performance during symptom - limited Exercise stress testing, and was quantified as peak estimated metabolic equivalents using well - established formulas for each sex. Normal distribution of achieved METs was separated by decade of age for each sex. Performance on ETT by age group was stratified as elite, high, above average, below average and low. The primary outcome was all - cause mortality as determined by the Social Security Death Index and supplemented by the institutional Death Index. Authors use a multivariable regression model to adjust for differences in baseline characteristics between groups. The model includes the following variables: age, sex, body mass Index, history of CAD, hyperlipidemia, Hypertension, Diabetes, smoking, end - stage renal Disease and current medication use of aspirin, beta - blockers or Statins. Among 122 007 patients included in the study, mean age was 53. 4 years, and 59. 2% were male. The prevalence of associated comorbidities decreased significantly with increasing performance except for hyperlipidemia, which was present in more elite performers than low performers. In this study, authors find that risk - adjusted all - cause mortality was inversely associated with increasing CRF in dose - effect manner. This finding was also observed when cohort was separated by sex. The increase in mortality associated with incremental reductions in CRF was comparable to or greater than risks observed with traditional Clinical Risk factors, including CAD, smoking, Diabetes and ESRD. Risk - adjusted all - cause mortality was lowest in elite performers as cohort. When analyzed by age group, difference in survival between elite and high performers was seen only among those 70 years or older. In younger age groups, and when stratified by sex, there was no significant difference in survival between elite and high performing groups. Multivariate regression was also performed amongst clinical subgroups with known CAD, Diabetes, Hypertension and hyperlipidemia. In each subgroup, all - cause mortality was inversely associated with CRF when compared to low performers, and mortality was lowest among elite performers.

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Risk factors

Heart Disease kills more Americans each year than any other disease or illness. It is important to understand what makes heart disease so common and how you can reduce your chances of having heart disease. Heart Disease can be silent in some people. They may not be aware of heart disease until they have a heart attack. More than 2600 Americans die every day from Cardiovascular Disease. August 20 2003, issue of JAMA includes several articles about risk factors for Heart Disease. The risk factor is something that makes you more likely to have disease, illness, or medical problem. Some risk factors are modifiable. Other risk factors, such as age and genetics, cannot be change. Smoking or exposure to environmental tobacco smoking, Obesity, Sedentary lifestyle, diabetes, high cholesterol or abnormal blood lipids, hypertension, male sex age older than 50 years, Family history of Heart Disease stop smoking. Eat a low - fat diet rich in vegetables and fruits. Exercise daily for at least 30 minutes. Control diabetes and hypertension if you already have these medical problems. Manage your cholesterol and blood lipid levels if they are elevate. Know your family history, especially about heart attacks or sudden death at an age younger than 50 years. See your doctor regularly to assess heart risks, manage heart disease if it is already present, and reduce your risk of heart attack or sudden death. American Heart Association 888 / 694 - 3278 http: / www. Americanheart. Org National Heart, Lung, and Blood Institute 301 / 592 - 8573 http: / www. Nhlbi. Nih. Gov Centers For Disease Control and Prevention 888 / 246 - 2675 http: / www. Cdc. Gov National Coalition For Women With Heart Disease 202 / 728 - 7199 http: / www. Womenheart. Org to find this and previous JAMA Patient Pages, go to the Patient Page link on JAMA's Web site at http: / www. Jama. Com. Many are available in English and Spanish. Patient Page on Heart Disease and Women was published on December 25 2002, issue; one on Obesity and Weight loss was published on April 9 2003, issue; and one on smoking and heart was published on July 2 2003, issue. Jama Patient Page is Public Service of JAMA. Information and recommendations appearing on this Page are appropriate in most instances, but they are not a substitute for medical diagnosis. For specific information concerning your personal medical condition, JAMA suggests that you consult your physician. This Page may be photocopy noncommercially by physicians and other health care professionals to share with patients. Any other print or online reproduction is subject to AMA approval. To purchase bulk reprints, call 718 / 946 - 7424.

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Biology of SARS-CoV-2

Division of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China, prevalence of coronavirus Disease 2019 has posed a great threat to people's health worldwide, bringing great challenges to public healthcare systems. A recent study has confirmed that severe acute respiratory syndrome coronavirus 2 uses severe acute respiratory syndrome coronavirus receptor Angiotensinconverting enzyme 2 for host cell entry. 1 ACE2 Expression was previously found to correlate with susceptibility to SARSCoV infection in vitro. 2 As with SARSCoV, higher ACE2 Expression might also lead to higher risk of SARSCoV2 infection. According to available clinical data, 15% to 30% of COVID19 patients are with hypertension and 2. 5% to 15% are with coronary heart Disease. 3 4 5 Angiotensinconverting enzyme inhibitors / angiotensin receptor blockers are widely used in the treatment of these cardiovascular diseases. Interestingly, several studies have shown that ACEIs / ARBs exhibit the ability to upregulate ACE2 Expression in addition to their main pharmacological effect of inhibiting Angiotensinconverting enzyme 1 or blocking angiotensin II type 1 receptor. 6 7 8 Considering that ACE2 Expression might correlate with susceptibility to SARSCoV2, intake of ACEIs / ARBs might predispose patients to infection of SARSCoV2. Therefore, some cardiologists suggest that patients should discontinue ACEIs / ARBs to avoid potential increased risk of SARSCoV2 infection. 9 However, there is evidence demonstrating that activation of reninangiotensin system and downregulation of ACE2 Expression are involved in the pathological process of lung injury after SARSCoV infection. 10 Recently, it has been reported that serum level of angiotensin II is significantly elevated in COVID19 patients and exhibits linear positive correlation to viral load and lung injury. 11 Activation of RAS can cause widespread endothelial dysfunction and varying degrees of multiple organ injuries. Thus, intake of ACEIs / ARBs might probably relieve lung injury and absolutely decrease heart and renal damage resulting from RAS Activation. These possibilities pose a dilemma for cardiologists in terms of recommending whether to discontinue ACEIs / ARBs or not. On basis of current literature, viewpoint on potential influence of ACEIs / ARBs on onset and severity of SARSCoV2 infection is proposed in this article.


Introduction

Coronavirus disease 2019 was first reported in Wuhan, China, in late December 2019. Since then, COVID - 19 has spread rapidly worldwide and has become a global pandemic affecting over 200 countries and territories, with unprecedented effects not only on public health, but also social and economic activities. The exponential increase in the number of patients with COVID - 19 in the past 6 months has overwhelmed health - care systems in numerous countries across the world. At present, preventive vaccines and prophylactic therapies for COVID - 19 are not available. Covid - 19 is caused by severe acute respiratory syndrome coronavirus 2, which is member of the genus Betacoronavirus like two other coronaviruses that have caused pandemic diseases severe acute respiratory syndrome coronavirus and Middle East respiratory syndrome coronavirus 1 - 4. As with SARS - CoV and MERS - CoV, SARS - CoV - 2 causes respiratory infection, which leads to viral pneumonia and acute respiratory distress syndrome in some patients 1. However, in addition to respiratory symptoms, uncontrolled SARS - CoV - 2 infection can trigger cytokine storm, whereby pro - inflammatory cytokines and chemokines such as tumour necrosis factor -, IL - 1 and IL - 6 are overproduced by the immune system, resulting in multiorgan damage 5. Furthermore, COVID - 19 causes coagulation abnormalities in a substantial proportion of patients, which can lead to thromboembolic events 6 7. Genomic sequence 1 - 3 8 and viral protein structure 9 - 11 of SARS - CoV - 2 have been studied intensively since its emergence. To date, research shows that SARS - CoV - 2 shares many biological features with SARS - CoV owing to 79. 6% genomic sequence identity 1 2. In particular, both SARS - CoV and SARS - CoV - 2 use the same system of cell entry, which is triggered by binding of viral spike protein to angiotensin - converting enzyme 2 on the surface of host cell 4. Understanding biological features of viruses will contribute to development of diagnostic tests, vaccines and pharmacological therapies and can further our knowledge of tissue tropism. Early clinical data indicate that both susceptibility to and outcomes of COVID - 19 are strongly associated with cardiovascular disease 12 - 16. A high prevalence of pre - existing CVD has been observed among patients with COVID - 19, and these comorbidities are associated with increased mortality 17 - 22. Furthermore, COVID - 19 seems to promote development of cardiovascular disorders, such as myocardial injury, arrhythmias, acute coronary syndrome and venous thromboembolism 23 - 25. Children with COVID - 19 have also been reported to develop hyperinflammatory shock with features akin to Kawasaki disease, including cardiac dysfunction and coronary vessel abnormalities 26. Together, these data indicate the presence of bidirectional interaction between COVID - 19 and the cardiovascular system, but mechanisms underlying this interaction remain elusive. The high burden of systemic inflammation associated with COVID - 19 has been proposed to accelerate development of subclinical disorders or cause de novo cardiovascular damage 5 12 - 14. Ace2, which is a key surface protein for virus entry and part of the renin - angiotensin - aldosterone system, is also thought to be involved in this interaction on the basis of findings from animal models 12 - 15.

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The cardiovascular system and COVID-19

As the Coronavirus Disease 2019 pandemic has spread around the globe, there has been growing recognition that people with underlying increased cardiovascular risk may be disproportionately affect. 1 - 3 Several studies of case series have noted cardiac arrhythmias, cardiomyopathy, and cardiac arrest as terminal events in patients with COVID - 19. 1 - 4 Higher incidences of cardiac arrhythmias, acute coronary syndromes, and Heart Failure - related events have also been reported during seasonal influenza outbreaks, which suggest that acute respiratory infections may result in activation of coagulation pathways, proinflammatory effects, and endothelial cell dysfunction. 5 in addition, however, concern has been expressed that medical therapy for Cardiovascular Disease might specifically contribute to severity of illness in patients with COVID - 19. 6 7 severe acute respiratory syndrome Coronavirus 2, causative agent of COVID - 19, has been shown to establish itself in the host through use of angiotensin - converting enzyme 2 as its cellular receptor. 8 ACE2 is a membrane - bound monocarboxypeptidase found ubiquitously in humans and expressed predominantly in heart, intestine, kidney, and pulmonary alveolar cells. 7 9 Entry of SARS - CoV - 2 into human cells is facilitated by interaction of receptor - binding domain in its viral spike glycoprotein ectodomain with the ACE2 receptor. 10 ACE2 is counterregulatory to activity of angiotensin II generated through ACE1 and is protective against detrimental activation of renin - angiotensin - aldosterone System. Angiotensin II is catalyzed by ACE2 to angiotensin -, which exerts vasodilatory, antiinflammatory, antifibrotic, and antigrowth effects. 11 It has been suggested that ACE inhibitors and angiotensin - receptor blockers may increase expression of ACE2, which has been shown in heart in rats, 12 and thereby may confer predisposition to more severe infection and adverse outcomes during COVID - 19. 6 7 Others have suggested that ACE inhibitors may counter the antiinflammatory effects of ACE2. However, in vitro studies have not shown direct inhibitory activity of ACE inhibitors against ACE2 function. 9 13 despite these uncertainties, some have recommended cessation of treatment with ACE inhibitors and ARBs in patients with COVID - 19. 6 However, several scientific societies, including the American Heart Association, American College of Cardiology, Heart Failure Society of America, and the Council on Hypertension of the European Society of Cardiology, have urged that these important medications should not be discontinued in the absence of clear clinical evidence of harm. 14 15 We therefore undertook study to investigate the relationship between underlying Cardiovascular Disease and COVID - 19 outcomes and to evaluate the association between Cardiovascular drug therapy and mortality in this illness. Our investigation confirms previous reports of an independent relationship between older age, underlying Cardiovascular Disease, current smoking, and COPD with death in COVID - 19. Our results also suggest that women are proportionately more likely than men to survive infection. Neither harmful nor beneficial associations were noted for antiplatelet therapy, beta - blockers, or hypoglycemic therapy. It is important to note that we were not able to confirm previous concerns regarding potential harmful association of either ACE inhibitors or ARBs with in - Hospital mortality in this clinical context. In viral infections such as influenza, older age is associated with increased risk of cardiovascular events and death.


Patients

With respect to cardiovascular risk factors, 30. 5% of patients had hyperlipidemia, 26. 3% had hypertension, 14. 3% had diabetes mellitus, 16. 8% were former smokers, and 5. 5% were current smokers. Preexisting cardiovascular disease in this sample includes coronary artery disease, history of congestive heart failure, and a history of cardiac arrhythmia. Other coexisting conditions include COPD and underlying immunosuppressed condition. Medical therapy includes ACE inhibitors, ARBs, statins, beta - blockers, and antiplatelet agents. Insulin was used in 3. 4% of patients, and other hypoglycemic agents were used in 9. 6%. The mean length of hospital stay was 10. 72. 7 days, with an overall in - hospital mortality of 5. 8% of this population of patients with complete outcomes. Of patients who had been admitted to the intensive Care unit at any time during their hospitalization, 24. 7% die, as compared with 4. 0% of patients who had not been admitted to the ICU.

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Conclusions

Give that numerous studies have demonstrated that SARS - CoV - 2 shares many biological features with SARS - CoV, our knowledge of pathophysiological mechanisms underlying SARS can be used to understand disease processes involved in COVID - 19. Mechanistically, interaction between S protein and ACE2 is likely to have a central role in disease pathogenesis, especially in cardiovascular manifestations of this disease, and this interaction is a potential target for prevention and treatment of COVID - 19. Several hurdles need to be overcome in study of mechanisms underlying COVID - 19. First, biological experiments using SARS - CoV - 2 can be performed only in laboratories with a biosafety level 3 rating of 161 162. Second, use of animal models to mimic disease process is associated with numerous challenges 163 164 165. Give that cellular or tissue tropism is likely to be an important factor contributing to diverse phenotypes of COVID - 19, mouse or rat models are not ideal for studying host tropism because they are not as susceptible to SARS - CoV - 2 as humans owing to differences in amino acid sequence of ACE2. To use mice or rats, human ACE2 needs to be introduced artificially. Transgenic mice expressing ACE2 infected with SARS - CoV - 2 have been reported to show signs of pneumonia, but overall symptoms experienced by these mice are much milder than those in humans 163. Therefore, alternative platforms might involve genome - edit mouse or rat models in which ACE2 is replaced by human ACE2, other animal species that are naturally susceptible to SARS - CoV - 2 infection 164 165 167 168 169 170 or in vitro models such as induced pluripotent stem cells 171 172 173 and organoids 114 174 175. The COVID - 19 pandemic is changing our lives in unprecedented ways. Give lack of safe and effective vaccines or proven treatments for COVID - 19, our main strategy to combat pandemic is social distancing. The capacity of health - care systems globally has been severely test, and the effect of this pandemic on social interactions, health - care delivery and the global economy continues to mount. Reduced physical activity owing to lockdown measures might also contribute to poor control of cardiovascular risk factors. Vaccine development is expected to take 12 - 18 months 34. To meet the urgent need for effective treatment and preventative strategies, concerted effort must be made by researchers globally to investigate and integrate biological and clinical findings relate to COVID - 19.

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Heart Disease

Heart beat about 2. 5 billion times over average lifetime, pushing millions of gallons of blood to every part of the body. This steady flow carries with it oxygen, fuel, hormones, other compounds, and a host of essential cells. It also whisks away waste products of metabolism. When the heart stop, essential functions fail, some almost instantly. Give heart's never - ending workload, it's wonder it perform so well, for so long, for so many people. But it can also fail, brought down by poor diet and lack of exercise, smoking, infection, unlucky genes, and more. The key problem is atherosclerosis. This is accumulation of pockets of cholesterol - rich gunk inside arteries. These pockets, called plaque, can limit blood flow through arteries that nourish heart coronary arteries and other arteries throughout the body. When plaque breaks apart, it can cause heart attack or stroke. Although many people develop some form of cardiovascular disease as they get older, it isn't inevitable. A healthy lifestyle, especially when started at a young age, goes a long way to preventing cardiovascular disease. Lifestyle changes and medications can nip heart - harming trends, like high blood pressure or high cholesterol, in bud before they cause damage. And variety of medications, operations, and devices can help support the heart if damage occur. Coronary artery disease: accumulation of cholesterol - fill plaque in arteries that nourish heart muscle heart attack: sudden stopping of blood flow to part of heart muscle heart failure: inability of the heart to pump as forcefully or efficiently as needed to supply the body with oxygenated blood heart rhythm disorders: heartbeats that are too fast, too slow, or irregular heart valve disorders: problems with valves that control blood flow from one part of heart to another part of heart or to body. Sudden cardiac arrest: sudden cessation of heartbeat cardiomyopathy: disease of heart muscle that causes the heart to become abnormally enlarged, thicken, and / or stiffen pericarditis: inflammation of pericardium, thin sac that surrounds heart myocarditis: inflammation of myocardium, middle layer of heart wall congenital heart disease: heart diseases or abnormalities in heart's structure that occur before birth

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Cardiovascular Disorders

Cardiovascular diseases are a group of disorders of heart and blood vessels and they include: Coronary heart Disease - Disease of blood vessels supplying heart muscle; cerebrovascular Disease - Disease of blood vessels supplying brain; Peripheral arterial Disease - Disease of blood vessels supplying arms and legs; rheumatic heart Disease - damage to heart muscle and heart valves from rheumatic fever, cause by streptococcal bacteria; congenital heart Disease - malformations of heart structure existing at birth; deep vein thrombosis and pulmonary embolism - blood clots in leg veins, which can dislodge and move to heart and lungs. Heart attacks and strokes are usually acute events and are mainly caused by blockage that prevents blood from flowing to the heart or brain. The most common reason for this is the build - up of fatty deposits on the inner walls of blood vessels that supply the heart or brain. Strokes can also be caused by bleeding from blood vessels in the brain or from blood clots. The causes of heart attacks and strokes are usually the presence of a combination of risk factors, such as tobacco use, unhealthy diet and obesity, physical inactivity and harmful use of alcohol, hypertension, diabetes and hyperlipidaemia.

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Scope & Mission

Over the past several decades, considerable amount has been learnt about determinants OF CVD as well as how to reduce CVD incidence and mortality. Building on this knowledge and emerging evidence of the growing burden OF CVD in Developing Countries, there has been a steady escalation of International Reports, declarations, and resolutions calling attention to the growing threat of the Global CVD Epidemic. These are summarized in Figure 1. 1 and Box 1. 1 later in this chapter, where they are discussed in more detail to set historical CONTEXT for this Report. These declarations, reports, and resolutions have resulted in growing recognition that CVD, and chronic Noncommunicable Diseases more broadly, are a worldwide problem whose burden is increasingly felt by low and middle income countries. In the past several years, this recognition has begun to translate into guidance for action. However, despite examples from the developed world that demonstrate promise and hope for reduction of disease burden on national level, burden OF CVD has continued to grow and concrete steps toward scaling up CVD treatment and prevention efforts in Developing Countries have been slow to materialize. Recognizing the need to help catalyze progress from guidance and strategies to actions, National Heart, Lung, and Blood Institute sponsored this Study by the Institute OF Medicine, and an ad hoc Committee was convened to study the evolving Global Epidemic OF CVD and offer conclusions and recommendations pertinent to its Control. The Full Statement OF Task for Committee on Preventing Global Epidemic OF Cardiovascular Disease: Meeting Challenges in Developing Countries can be found in Appendix. In summary, committee was charged with synthesizing and expanding relevant evidence and knowledge based on research findings, with emphasis on developing concepts of global partnership and collaborations, and on recommending actions targeted at global governmental organizations, nongovernmental organizations, policy and decision makers, funding agencies, academic and research institutions, and General public. In response to its charge, Committee undertook an analysis OF CURRENT State OF efforts to reduce Global Epidemic OF CVD based on review OF available literature and OF information gathered from various stakeholders in CVD and Global Health. In this analysis, committee evaluates why there has not been more action to address CVD; assesses available evidence on intervention approaches to prevent and manage CVD, including knowledge and strategies pertinent to their implementation in low and middle income countries; and draws conclusions about necessary next steps to move forward. Prior Reports have identified General Priorities and recommended a wide range OF possible actions for a multitude OF stakeholders; indeed, findings and conclusions of this Report reinforce many OF those messages and priorities. In these Reports recommendations, however, Committee has emphasized advancing field beyond messages about broad conceptual solutions and has identified a limited set of specific actions targeted to specific stakeholders.


Aims and Scope

Jhh commits to publishing results of research and clinical practice in Cardiovascular disease, stressing out syndromes like valve disease, aortic dissection, and inheriting Cardiovascular conditions as well as Cardiovascular Pathology, Epidemiology, Genomics, Cardiovascular Pharmacology, and Translational Cardiology. Likewise, journal is attentive to medical diagnosis and treatment of arrhythmias, coronary artery disease, cardiovascular risk, and valvular heart disease interesting to an international audience of professionals, scholars, internists, residents and researchers, avid for the most updated and substantial medical progress in clinical, Translational heart and Cardiovascular knowledge. Core areas of interest of JHH include arrhythmia and electrophysiology, myocardial fibrosis, Cardiovascular nursing, myocardial infarction, Cardiovascular surgery, myocardial ischemia, resuscitation science, congenital heart disease, myocardial perfusion, and coronary heart disease. Moreover, JHH focuses on acute cardiac care, Exercise Physiology, Vascular Biology, Health Services and outcomes research, Cardiovascular Pathology, Pediatric Cardiology, Cardiovascular interventions, peripheral Vascular disease, and preventive Cardiology. Journal delves into distinctive papers which prioritise merit, uniqueness, applicability, clarity and appeal to readership. Internists specialise in Cardiology, electrophysiologists, heart failure specialists, interventional cardiologists, pharmacologists, paediatric cardiologists, medical geneticists, Cardiovascular surgeons, clinical researchers and basic scientists are contributors of articles to JHH. Jhh is peer - review to ascertain the scientific worth and clinical significance of its varied content.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Sources

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

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