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2.
Clin Infect Dis ; 74(10): 1713-1721, 2022 05 30.
Article in English | MEDLINE | ID: covidwho-1873862

ABSTRACT

BACKGROUND: Patients hospitalized for coronavirus disease 2019 (COVID-19) may experience complications following hospitalization and require readmission. In this analysis, we estimated the rate and risk factors associated with COVID-19-related readmission and inpatient mortality. METHODS: In this retrospective cohort study, we used deidentified chargemaster data from 297 hospitals across 40 US states on patients hospitalized with COVID-19 from 15 February 2020 through 9 June 2020. Demographics, comorbidities, acute conditions, and clinical characteristics of first hospitalization are summarized. Multivariable logistic regression was used to measure risk factor associations with 30-day readmission and in-hospital mortality. RESULTS: Among 29 659 patients, 1070 (3.6%) were readmitted. Readmitted patients were more likely to have diabetes, hypertension, cardiovascular disease (CVD), or chronic kidney disease (CKD) vs those not readmitted (P < .0001) and to present on first admission with acute kidney injury (15.6% vs 9.2%), congestive heart failure (6.4% vs 2.4%), or cardiomyopathy (2.1% vs 0.8%) (P < .0001). Higher odds of readmission were observed in patients aged >60 vs 18-40 years (odds ratio [OR], 1.92; 95% confidence interval [CI], 1.48-2.50) and those admitted in the Northeast vs West (OR, 1.43; 95% CI, 1.14-1.79) or South (OR, 1.28; 95% CI, 1.11-1.49). Comorbidities including diabetes (OR, 1.34; 95% CI, 1.12-1.60), CVD (OR, 1.46; 95% CI, 1.23-1.72), CKD stage 1-5 (OR, 1.51; 95% CI, 1.25-1.81), and CKD stage 5 (OR, 2.27; 95% CI, 1.81-2.86) were associated with higher odds of readmission; 12.3% of readmitted patients died during second hospitalization. CONCLUSIONS: Among this large US population of patients hospitalized with COVID-19, readmission was associated with certain comorbidities and acute conditions during first hospitalization. These findings may inform strategies to mitigate risks of readmission due to COVID-19 complications.


Subject(s)
COVID-19 , Cardiovascular Diseases , Kidney Failure, Chronic , COVID-19/epidemiology , COVID-19/therapy , Cardiovascular Diseases/epidemiology , Hospitalization , Humans , Patient Readmission , Retrospective Studies , Risk Factors , United States/epidemiology
3.
Pharmacol Res ; 169: 105689, 2021 07.
Article in English | MEDLINE | ID: covidwho-1525917

ABSTRACT

Genome wide association, epidemiological, and clinical studies have established high lipoprotein(a) [Lp(a)] as a causal risk factor for atherosclerotic cardiovascular disease (ASCVD). Lp(a) is an apoB100 containing lipoprotein covalently bound to apolipoprotein(a) [apo(a)], a glycoprotein. Plasma Lp(a) levels are to a large extent determined by genetics. Its link to cardiovascular disease (CVD) may be driven by its pro-inflammatory effects, of which its association with oxidized phospholipids (oxPL) bound to Lp(a) is the most studied. Various inflammatory conditions, such as rheumatoid arthritis (RA), systemic lupus erythematosus, acquired immunodeficiency syndrome, and chronic renal failure are associated with high Lp(a) levels. In cases of RA, high Lp(a) levels are reversed by interleukin-6 receptor (IL-6R) blockade by tocilizumab, suggesting a potential role for IL-6 in regulating Lp(a) plasma levels. Elevated levels of IL-6 and IL-6R polymorphisms are associated with CVD. Therapies aimed at lowering apo(a) and thereby reducing plasma Lp(a) levels are in clinical trials. Their results will determine if reductions in apo(a) and Lp(a) decrease cardiovascular outcomes. As we enter this new arena of available treatments, there is a need to improve our understanding of mechanisms. This review will focus on the role of Lp(a) in inflammation and CVD.


Subject(s)
Inflammation/metabolism , Lipoprotein(a)/blood , Animals , Cardiovascular Diseases/blood , Cardiovascular Diseases/etiology , Cardiovascular Diseases/metabolism , Humans , Inflammation/blood , Inflammation/etiology , Lipoprotein(a)/metabolism , Lipoprotein(a)/physiology
4.
J Sci Med Sport ; 23(9): 792-799, 2020 Sep.
Article in English | MEDLINE | ID: covidwho-1454328

ABSTRACT

OBJECTIVES: To determine the prevalence of cardiovascular disease (CVD) risk factors in current field-based athletes. DESIGN: Meta-analysis. METHODS: This review was conducted and reported in accordance with PRISMA and pre-registered with PROSPERO. Articles were retrieved via online database search engines, with no date or language restriction. Studies investigating current field-based athletes (>18years) for CVD risk factors according to the European Society of Cardiology and American Heart Association were screened. Full texts were screened using Covidence and Cochrane criteria. Eligible articles were critically appraised using the AXIS tool. Individual study estimates were assessed by random-effect meta-analyses to examine the overall effect. RESULTS: This study was ascribed a 1b evidence level, according to the Oxford Centre for Evidence-based Medicine. 41 studies were identified, including 5546 athletes from four sports; American football; soccer; rugby and baseball mean ages: 18-28. Despite participation in sport, increased body mass was associated with increased total cholesterol, low-density lipoprotein, triglycerides, hypertension, systolic blood pressure, and decreased high-density lipoprotein. Linemen had increased prevalence of hypertension compared to non-athletes. Conflicting findings on fasting glucose were prevalent. There were inconsistencies in screening and reporting of CVD risk factors. Sport specific anthropometric demands were associated with elevated prevalence of CVD risk factors, most notably: elevated body mass; dyslipidemia; elevated systolic blood pressure and; glucose. CONCLUSIONS: There are elevated levels of risk for CVD in some athletes, primarily football players. Lifestyle behaviours associated with elite athleticism, particularly football linemen potentially expose players to greater metabolic and CVD risk, which is not completely offset by sport participation.


Subject(s)
Athletes , Cardiovascular Diseases/epidemiology , Sports/statistics & numerical data , Anthropometry , Biomarkers/blood , Blood Pressure , Career Choice , Humans , Prevalence , Risk Factors
5.
Oxid Med Cell Longev ; 2021: 5529256, 2021.
Article in English | MEDLINE | ID: covidwho-1394272

ABSTRACT

Cardiovascular disorders (CVD) are highly prevalent and the leading cause of death worldwide. Atherosclerosis is responsible for most cases of CVD. The plaque formation and subsequent thrombosis in atherosclerosis constitute an ongoing process that is influenced by numerous risk factors such as hypertension, diabetes, dyslipidemia, obesity, smoking, inflammation, and sedentary lifestyle. Among the various risk and protective factors, the role of glucose-6-phosphate dehydrogenase (G6PD) deficiency, the most common inborn enzyme disorder across populations, is still debated. For decades, it has been considered a protective factor against the development of CVD. However, in the recent years, growing scientific evidence has suggested that this inherited condition may act as a CVD risk factor. The role of G6PD deficiency in the atherogenic process has been investigated using in vitro or ex vivo cellular models, animal models, and epidemiological studies in human cohorts of variable size and across different ethnic groups, with conflicting results. In this review, the impact of G6PD deficiency on CVD was critically reconsidered, taking into account the most recent acquisitions on molecular and biochemical mechanisms, namely, antioxidative mechanisms, glutathione recycling, and nitric oxide production, as well as their mutual interactions, which may be impaired by the enzyme defect in the context of the pentose phosphate pathway. Overall, current evidence supports the notion that G6PD downregulation may favor the onset and evolution of atheroma in subjects at risk of CVD. Given the relatively high frequency of this enzyme deficiency in several regions of the world, this finding might be of practical importance to tailor surveillance guidelines and facilitate risk stratification.


Subject(s)
Cardiovascular Diseases/physiopathology , Glucosephosphate Dehydrogenase Deficiency/physiopathology , Humans , Risk Factors
6.
Front Physiol ; 11: 802, 2020.
Article in English | MEDLINE | ID: covidwho-1389234

ABSTRACT

We dissect the mechanism of SARS-CoV-2 in human lung host from the initial phase of receptor binding to viral replication machinery. Two independent lung protein interactome were constructed to reveal the signaling process on receptor activation and host protein hijacking machinery in the pathogenesis of virus. Further, we test the functional role of the hubs derived from the interactome. Most hubs proteins were differentially regulated on SARS-CoV-2 infection. Also, the proteins in viral replication hubs were related with cardiovascular disease, diabetes and hypertension confirming the vulnerability and severity of infection in the risk individual. Additionally, the hub proteins were closely linked with other viral infection, including MERS and HCoVs which suggest similar infection pattern in SARS-CoV-2. We identified five hubs that interconnect both networks that show the preparation of optimal environment in the host for viral replication process upon receptor attachment. Interestingly, we propose that seven potential miRNAs, targeting the intermediate phase that connects receptor and viral replication process a better choice as a drug for SARS-CoV-2.

7.
Curr Diabetes Rev ; 2021 06 01.
Article in English | MEDLINE | ID: covidwho-1367728

ABSTRACT

The article has been withdrawn at the request of the authors and editor of the journal Current Diabetes Reviews, due to incoherent content.Bentham Science apologizes to the readers of the journal for any inconvenience this may have caused.The Bentham Editorial Policy on Article Withdrawal can be found at https://benthamscience.com/editorial-policies-main.php. BENTHAM SCIENCE DISCLAIMER: It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submit-ting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript, the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication.

8.
Pharmacol Res ; 161: 105250, 2020 11.
Article in English | MEDLINE | ID: covidwho-1318947

ABSTRACT

Drug-drug interactions (DDI) potentially occurring between medications used in the course of COVID-19 infection and medications prescribed for the management of underlying comorbidities may cause adverse drug reactions (ADRs) contributing to worsening of the clinical outcome in affected patients. First, we conducted a meta-analysis to determine comorbidities observed in the course of COVID-19 disease associated with an increased risk of worsened clinical outcome from 24 published studies. In addition, the potential risk of DDI between medications used in the course of COVID-19 treatment in these studies and those for the management of observed comorbidities was evaluated for possible worsening of the clinical outcome. Our meta-analysis revealed an implication cardiometabolic syndrome (e.g. cardiovascular disease, cerebrovascular disease, hypertension, and diabetes), chronic kidney disease and chronic obstructive pulmonary disease as main co-morbidities associated with worsen the clinical outcomes including mortality (risk difference RD 0.12, 95 %-CI 0.05-0.19, p = 0.001), admission to ICU (RD 0.10, 95 %-CI 0.04-0.16, p = 0.001) and severe infection (RD 0.05, 95 %-CI 0.01-0.09, p = 0.01) in COVID-19 patients. Potential DDI on pharmacokinetic level were identified between the antiviral agents atazanavir and lopinavir/ritonavir and some drugs, used in the treatment of cardiovascular diseases such as antiarrhythmics and anti-coagulants possibly affecting the clinical outcome including cardiac injury or arrest because of QTc-time prolongation or bleeding. Concluding, DDI occurring in the course of anti-Covid-19 treatment and co-morbidities could lead to ADRs, increasing the risk of hospitalization, prolonged time to recovery or death on extreme cases. COVID-19 patients with cardiometabolic diseases, chronic kidney disease and chronic obstructive pulmonary disease should be subjected to particular carefully clinical monitoring of adverse events with a possibility of dose adjustment when necessary.


Subject(s)
COVID-19/complications , COVID-19/therapy , Drug Interactions , Comorbidity , Drug-Related Side Effects and Adverse Reactions , Humans , Treatment Outcome
9.
Biochimie ; 187: 94-109, 2021 Aug.
Article in English | MEDLINE | ID: covidwho-1252495

ABSTRACT

Despite the development of a number of vaccines for COVID-19, there remains a need for prevention and treatment of the virus SARS-CoV-2 and the ensuing disease COVID-19. This report discusses the key elements of SARS-CoV-2 and COVID-19 that can be readily treated: viral entry, the immune system and inflammation, and the cytokine storm. It is shown that the essential nutrients zinc, ω-3 polyunsaturated fatty acids (PUFAs), vitamin D and magnesium provide the ideal combination for prevention and treatment of COVID-19: prevention of SARS-CoV-2 entry to host cells, prevention of proliferation of SARS-CoV-2, inhibition of excessive inflammation, improved control of the regulation of the immune system, inhibition of the cytokine storm, and reduction in the effects of acute respiratory distress syndrome (ARDS) and associated non-communicable diseases. It is emphasized that the non-communicable diseases associated with COVID-19 are inherently more prevalent in the elderly than the young, and that the maintenance of sufficiency of zinc, ω-3 PUFAs, vitamin D and magnesium is essential for the elderly to prevent the occurrence of non-communicable diseases such as diabetes, cardiovascular diseases, lung diseases and cancer. Annual checking of levels of these essential nutrients is recommended for those over 65 years of age, together with appropriate adjustments in their intake, with these services and supplies being at government cost. The cost:benefit ratio would be huge as the cost of the nutrients and the testing of their levels would be very small compared with the cost savings of specialists and hospitalization.


Subject(s)
COVID-19/prevention & control , Fatty Acids, Omega-3/therapeutic use , Magnesium/therapeutic use , Noncommunicable Diseases/prevention & control , Vitamin D/therapeutic use , Zinc/therapeutic use , Aged , COVID-19/therapy , Cardiovascular Diseases/prevention & control , Cardiovascular Diseases/therapy , Cytokine Release Syndrome/therapy , Diabetes Mellitus/prevention & control , Diabetes Mellitus/therapy , Humans , Inflammation/therapy , Lung Diseases/prevention & control , Lung Diseases/therapy , Neoplasms/prevention & control , Neoplasms/therapy , Noncommunicable Diseases/therapy , Nutritional Status , SARS-CoV-2 , Vitamins/therapeutic use
10.
Microcirculation ; 28(7): e12718, 2021 10.
Article in English | MEDLINE | ID: covidwho-1236400

ABSTRACT

Recently, accumulating evidence has highlighted the role of endothelial dysfunction in COVID-19 progression. Coronary microvascular dysfunction (CMD) plays a pivotal role in cardiovascular disease (CVD) and CVD-related risk factors (eg, age, gender, hypertension, diabetes mellitus, and obesity). Equally, these are also risk factors for COVID-19. The purpose of this review was to explore CMD pathophysiology in COVID-19, based on recent evidence. COVID-19 mechanisms were reviewed in terms of imbalanced renin-angiotensin-aldosterone-systems (RAAS), systemic inflammation and immune responses, endothelial dysfunction, and coagulatory disorders. Based on these mechanisms, we addressed CMD pathophysiology within the context of COVID-19, from five perspectives. The first was the disarrangement of local RAAS and Kallikrein-kinin-systems attributable to SARS-Cov-2 entry, and the concomitant decrease in coronary microvascular endothelial angiotensin I converting enzyme 2 (ACE2) levels. The second was related to coronary microvascular obstruction, induced by COVID-19-associated systemic hyper-inflammation and pro-thrombotic state. The third was focused on how pneumonia/acute respiratory distress syndrome (ARDS)-related systemic hypoxia elicited oxidative stress in coronary microvessels and cardiac sympathetic nerve activation. Fourthly, we discussed how autonomic nerve dysfunction mediated by COVID-19-associated mental, physical, or physiological factors could elicit changes in coronary blood flow, resulting in CMD in COVID-19 patients. Finally, we analyzed reciprocity between the coronary microvascular endothelium and perivascular cellular structures due to viremia, SARS-CoV-2 dissemination, and systemic inflammation. These mechanisms may function either consecutively or intermittently, finally culminating in CMD-mediated cardiovascular symptoms in COVID-19 patients. However, the underlying molecular pathogenesis remains to be clarified.


Subject(s)
COVID-19/physiopathology , Coronary Vessels/physiopathology , SARS-CoV-2 , COVID-19/complications , COVID-19/immunology , Cardiovascular Diseases/etiology , Cardiovascular Diseases/physiopathology , Disease Progression , Endothelium, Vascular/physiopathology , Female , Humans , Inflammation/physiopathology , Male , Microcirculation/physiology , Models, Cardiovascular , Renin-Angiotensin System/physiology , Risk Factors , Thrombosis/etiology , Thrombosis/physiopathology
11.
J Am Heart Assoc ; 10(11): e020997, 2021 06.
Article in English | MEDLINE | ID: covidwho-1234323

ABSTRACT

The COVID-19 pandemic is a public health crisis, having killed more than 514 000 US adults as of March 2, 2021. COVID-19 mitigation strategies have unintended consequences on managing chronic conditions such as hypertension, a leading cause of cardiovascular disease and health disparities in the United States. During the first wave of the pandemic in the United States, the combination of observed racial/ethnic inequities in COVID-19 deaths and social unrest reinvigorated a national conversation about systemic racism in health care and society. The 4th Annual University of Utah Translational Hypertension Symposium gathered frontline clinicians, researchers, and leaders from diverse backgrounds to discuss the intersection of these 2 critical social and public health phenomena and to highlight preexisting disparities in hypertension treatment and control exacerbated by COVID-19. The discussion underscored environmental and socioeconomic factors that are deeply embedded in US health care and research that impact inequities in hypertension. Structural racism plays a central role at both the health system and individual levels. At the same time, virtual healthcare platforms are being accelerated into widespread use by COVID-19, which may widen the divide in healthcare access across levels of wealth, geography, and education. Blood pressure control rates are declining, especially among communities of color and those without health insurance or access to health care. Hypertension awareness, therapeutic lifestyle changes, and evidence-based pharmacotherapy are essential. There is a need to improve the implementation of community-based interventions and blood pressure self-monitoring, which can help build patient trust and increase healthcare engagement.


Subject(s)
Blood Pressure Monitoring, Ambulatory , COVID-19/epidemiology , Health Services Accessibility , Healthcare Disparities/standards , Hypertension , Racism/prevention & control , Social Determinants of Health/ethnology , Blood Pressure Monitoring, Ambulatory/methods , Blood Pressure Monitoring, Ambulatory/statistics & numerical data , Health Services Accessibility/organization & administration , Health Services Accessibility/standards , Health Status Disparities , Humans , Hypertension/ethnology , Hypertension/therapy , Needs Assessment , SARS-CoV-2 , Socioeconomic Factors , United States/epidemiology
12.
Int J Mol Sci ; 22(9)2021 Apr 21.
Article in English | MEDLINE | ID: covidwho-1231490

ABSTRACT

Obesity is globally a serious public health concern and is associated with a high risk of cardiovascular disease (CVD) and various types of cancers. It is important to evaluate various types of obesity, such as visceral and sarcopenic obesity. The evidence on the associated risk of CVD, cancer and sarcopenic obesity, including pathophysiological aspects, occurrence, clinical implications and survival, needs further investigation. Sarcopenic obesity is a relatively new term. It is a clinical condition that primarily affects older adults. There are several endocrine-hormonal, metabolic and lifestyle aspects involved in the occurrence of sarcopenic obesity that affect pathophysiological aspects that, in turn, contribute to CVD and neoplasms. However, there is no available evidence on the role of sarcopenic obesity in the occurrence of CVD and cancer and its pathophysiological interplay. Therefore, this review aims to describe the pathophysiological aspects and the clinical and epidemiological evidence on the role of sarcopenic obesity related to the occurrence and mortality risk of various types of cancer and cardiovascular disease. This literature review highlights the need for further research on sarcopenic obesity to demonstrate the interrelation of these various associations.


Subject(s)
Cardiovascular Diseases/physiopathology , Neoplasms/physiopathology , Obesity/complications , Sarcopenia/complications , Animals , Cardiovascular Diseases/etiology , Humans , Neoplasms/etiology
13.
Molecules ; 26(10)2021 May 11.
Article in English | MEDLINE | ID: covidwho-1224076

ABSTRACT

Resveratrol is a phytoalexin produced by many plants as a defense mechanism against stress-inducing conditions. The richest dietary sources of resveratrol are berries and grapes, their juices and wines. Good bioavailability of resveratrol is not reflected in its high biological activity in vivo because of resveratrol isomerization and its poor solubility in aqueous solutions. Proteins, cyclodextrins and nanomaterials have been explored as innovative delivery vehicles for resveratrol to overcome this limitation. Numerous in vitro and in vivo studies demonstrated beneficial effects of resveratrol in cardiovascular diseases (CVD). Main beneficial effects of resveratrol intake are cardioprotective, anti-hypertensive, vasodilatory, anti-diabetic, and improvement of lipid status. As resveratrol can alleviate the numerous factors associated with CVD, it has potential as a functional supplement to reduce COVID-19 illness severity in patients displaying poor prognosis due to cardio-vascular complications. Resveratrol was shown to mitigate the major pathways involved in the pathogenesis of SARS-CoV-2 including regulation of the renin-angiotensin system and expression of angiotensin-converting enzyme 2, stimulation of immune system and downregulation of pro-inflammatory cytokine release. Therefore, several studies already have anticipated potential implementation of resveratrol in COVID-19 treatment. Regular intake of a resveratrol rich diet, or resveratrol-based complementary medicaments, may contribute to a healthier cardio-vascular system, prevention and control of CVD, including COVID-19 disease related complications of CVD.


Subject(s)
COVID-19/drug therapy , Cardiovascular Diseases , Resveratrol , SARS-CoV-2/metabolism , Biological Availability , COVID-19/complications , COVID-19/metabolism , Cardiovascular Diseases/drug therapy , Cardiovascular Diseases/etiology , Cardiovascular Diseases/metabolism , Humans , Resveratrol/pharmacokinetics , Resveratrol/therapeutic use
14.
Nat Rev Cardiol ; 18(9): 666-682, 2021 09.
Article in English | MEDLINE | ID: covidwho-1220034

ABSTRACT

Thrombosis is the most feared complication of cardiovascular diseases and a main cause of death worldwide, making it a major health-care challenge. Platelets and the coagulation cascade are effectively targeted by antithrombotic approaches, which carry an inherent risk of bleeding. Moreover, antithrombotics cannot completely prevent thrombotic events, implicating a therapeutic gap due to a third, not yet adequately addressed mechanism, namely inflammation. In this Review, we discuss how the synergy between inflammation and thrombosis drives thrombotic diseases. We focus on the huge potential of anti-inflammatory strategies to target cardiovascular pathologies. Findings in the past decade have uncovered a sophisticated connection between innate immunity, platelet activation and coagulation, termed immunothrombosis. Immunothrombosis is an important host defence mechanism to limit systemic spreading of pathogens through the bloodstream. However, the aberrant activation of immunothrombosis in cardiovascular diseases causes myocardial infarction, stroke and venous thromboembolism. The clinical relevance of aberrant immunothrombosis, referred to as thromboinflammation, is supported by the increased risk of cardiovascular events in patients with inflammatory diseases but also during infections, including in COVID-19. Clinical trials in the past 4 years have confirmed the anti-ischaemic effects of anti-inflammatory strategies, backing the concept of a prothrombotic function of inflammation. Targeting inflammation to prevent thrombosis leaves haemostasis mainly unaffected, circumventing the risk of bleeding associated with current approaches. Considering the growing number of anti-inflammatory therapies, it is crucial to appreciate their potential in covering therapeutic gaps in cardiovascular diseases.


Subject(s)
Anti-Inflammatory Agents/therapeutic use , Blood Coagulation/drug effects , Fibrinolytic Agents/therapeutic use , Immune System/drug effects , Inflammation Mediators/antagonists & inhibitors , Inflammation/drug therapy , Thrombosis/prevention & control , Anti-Inflammatory Agents/adverse effects , COVID-19/blood , COVID-19/immunology , Fibrinolytic Agents/adverse effects , Humans , Immune System/immunology , Immune System/metabolism , Inflammation/blood , Inflammation/immunology , Inflammation Mediators/metabolism , Risk Assessment , Risk Factors , Signal Transduction , Thrombosis/blood , Thrombosis/immunology
15.
G Ital Cardiol (Rome) ; 22(5): 363-375, 2021 May.
Article in Italian | MEDLINE | ID: covidwho-1219383

ABSTRACT

In over a year, the COVID-19 pandemic caused 2.69 million deaths and 122 million infections. Social isolation and distancing measures have been the only prevention available for months. Scientific research has done a great deal of work, developing in a few months safe and effective vaccines against COVID-19. In the European Union, nowadays, four vaccines have been authorized for use: Pfizer-BioNTech, Moderna, ChAdOx1 (AstraZeneca/Oxford), Janssen (Johnson & Johnson), and three others are currently under rolling review.Vaccine allocation policy is crucial to optimize the advantage of treatment preferring people with the highest risk of contagion. These days the priority in the vaccination program is of particular importance since it has become clear that the number of vaccines is not sufficient for the entire Italian population in the short term. Cardiovascular diseases are frequently associated with severe COVID-19 infections, leading to the worst prognosis. The elderly population suffering from cardiovascular diseases is, therefore, to be considered a particularly vulnerable population. However, age cannot be considered the only discriminating factor because in the young-adult population suffering from severe forms of heart disease, the prognosis, if affected by COVID-19, is particularly ominous and these patients should have priority access to the vaccination program. The aim of this position paper is to establish a consensus on a priority in the vaccination of COVID-19 among subjects suffering from different cardiovascular diseases.


Subject(s)
COVID-19 Vaccines/administration & dosage , COVID-19/prevention & control , Cardiovascular Diseases/complications , Consensus , Age Factors , Animals , COVID-19/epidemiology , COVID-19/mortality , Cardiology , Coronary Disease/complications , Disease Vectors , Heart Failure/complications , Heart Transplantation , Heart Valve Diseases/complications , Humans , Hypertension, Pulmonary/complications , Italy/epidemiology , Prognosis , Renal Insufficiency/complications , SARS-CoV-2/immunology , Societies, Medical , Vaccines, Synthetic/administration & dosage
16.
Ann Palliat Med ; 10(5): 5069-5083, 2021 May.
Article in English | MEDLINE | ID: covidwho-1200423

ABSTRACT

BACKGROUND: Identification of risk factors for poor prognosis of patients with coronavirus disease 2019 (COVID-19) is necessary to enable the risk stratification and modify the patient's management. Thus, we performed a systematic review and meta-analysis to evaluate the in-hospital mortality and risk factors of death in COVID-19 patients. METHODS: All studies were searched via the PubMed, Embase, Cochrane Library, China National Knowledge Infrastructure (CNKI), VIP, and Wanfang databases. The in-hospital mortality of COVID-19 patients was pooled. Odds ratios (ORs) or mean difference (MD) with 95% confidence intervals (CIs) were calculated for evaluation of risk factors. RESULTS: A total of 80 studies were included with a pooled in-hospital mortality of 14% (95% CI: 12.2-15.9%). Older age (MD =13.32, 95% CI: 10.87-15.77; P<0.00001), male (OR =1.66, 95% CI: 1.37-2.01; P<0.00001), hypertension (OR =2.67, 95% CI: 2.08-3.43; P<0.00001), diabetes (OR =2.14, 95% CI: 1.76-2.6; P<0.00001), chronic respiratory disease (OR =3.55, 95% CI: 2.65-4.76; P<0.00001), chronic heart disease/cardiovascular disease (OR =3.15, 95% CI: 2.43-4.09; P<0.00001), elevated levels of high-sensitive cardiac troponin I (MD =66.65, 95% CI: 16.94-116.36; P=0.009), D-dimer (MD =4.33, 95% CI: 2.97-5.68; P<0.00001), C-reactive protein (MD =48.03, 95% CI: 27.79-68.27; P<0.00001), and a decreased level of albumin at admission (MD =-3.98, 95% CI: -5.75 to -2.22; P<0.0001) are associated with higher risk of death. Patients who developed acute respiratory distress syndrome (OR =62.85, 95% CI: 29.45-134.15; P<0.00001), acute cardiac injury (OR =25.16, 95% CI: 6.56-96.44; P<0.00001), acute kidney injury (OR =22.86, 95% CI: 4.60-113.66; P=0.0001), and septic shock (OR =24.09, 95% CI: 4.26-136.35; P=0.0003) might have a higher in-hospital mortality. CONCLUSIONS: Advanced age, male, comorbidities, increased levels of acute inflammation or organ damage indicators, and complications are associated with the risk of mortality in COVID-19 patients, and should be integrated into the risk stratification system.


Subject(s)
COVID-19 , Aged , China , Disease Outbreaks , Humans , Male , Risk Factors , SARS-CoV-2
17.
Chin Med Sci J ; 36(1): 17-26, 2021 Mar 31.
Article in English | MEDLINE | ID: covidwho-1187236

ABSTRACT

Objective This study aimed to determine the association of hyperlipidemia with clinical endpoints among hospitalized patients with COVID-19, especially those with pre-existing cardiovascular diseases (CVDs) and diabetes. Methods This multicenter retrospective cohort study included all patients who were hospitalized due to COVID-19 from 21 hospitals in Hubei province, China between December 31, 2019 and April 21, 2020. Patients who were aged < 18 or ≥ 85 years old, in pregnancy, with acute lethal organ injury (e.g., acute myocardial infarction, severe acute pancreatitis, acute stroke), hypothyroidism, malignant diseases, severe malnutrition, and those with normal lipid profile under lipid-lowering medicines (e.g., statin, niacin, fenofibrate, gemfibrozil, and ezetimibe) were excluded. Propensity score matching (PSM) analysis at 1:1 ratio was performed to minimize baseline differences between patient groups of hyperlipidemia and non-hyperlipidemia. PSM analyses with the same strategies were further conducted for the parameters of hyperlipidemia in patients with increased triglyceride (TG), increased low-density lipoprotein cholesterol (LDL-C), and decreased high-density lipoprotein cholesterol (HDL-C). Mixed-effect Cox model analysis was performed to investigate the associations of the 28-days all-cause deaths of COVID-19 patients with hyperlipidemia and the abnormalities of lipid parameters. The results were verified in male, female patients, and in patients with pre-existing CVDs and type 2 diabetes. Results Of 10 945 inpatients confirmed as COVID-19, there were 9822 inpatients included in the study, comprising 3513 (35.8%) cases without hyperlipidemia and 6309 (64.2%) cases with hyperlipidemia. Based on a mixed-effect Cox model after PSM at 1:1 ratio, hyperlipidemia was not associated with increased or decreased 28-day all-cause death [adjusted hazard ratio (HR), 1.17 (95% CI, 0.95-1.44), P =0.151]. We found that the parameters of hyperlipidemia were not associated with the risk of 28-day all-cause mortality [adjusted HR, 1.23 (95% CI, 0.98-1.55), P = 0.075 in TG increase group; 0.78 (95% CI, 0.57-1.07), P = 0.123 in LDL-C increase group; and 1.12 (95% CI, 0.9-1.39), P = 0.299 in HDL-C decrease group, respectively]. Hyperlipidemia was also not significantly associated with the increased mortality of COVID-19 in patients accompanied with CVDs or type 2 diabetes, and in both male and female cohorts. Conclusion Our study support that the imbalanced lipid profile is not significantly associated with the 28-day all-cause mortality of COVID-19 patients, even in those accompanied with CVDs or diabetes. Similar results were also obtained in subgroup analyses of abnormal lipid parameters. Therefore, hyperlipidemia might be not a major causative factor for poor outcome of COVID-19, which provides guidance for the intervention of inpatients during the epidemic of COVID-19.


Subject(s)
COVID-19/mortality , Hyperlipidemias/complications , Adult , Aged , Aged, 80 and over , COVID-19/complications , COVID-19/therapy , Cardiovascular Diseases/complications , Case-Control Studies , Cause of Death , China/epidemiology , Diabetes Mellitus, Type 2/complications , Female , Hospitalization , Humans , Male , Middle Aged , Propensity Score , Proportional Hazards Models , Retrospective Studies , Risk Factors
18.
Curr Opin Support Palliat Care ; 15(2): 147-153, 2021 06 01.
Article in English | MEDLINE | ID: covidwho-1177359

ABSTRACT

PURPOSE OF REVIEW: COVID-19 has permeated the very essence of human existence and society and disrupted healthcare systems. The attrition stemming from this highly contagious disease particularly affects those rendered vulnerable by age and infirmity, including those with underlying cardiovascular disease. This article critically reviews how best to integrate supportive care into the management of those affected. RECENT FINDINGS: Numerous studies have described the pathophysiology of COVID-19, including that specifically arising in those with cardiovascular disease. Potential treatment strategies have emerged but there is limited guidance on the provision of palliative care. A framework for implementation of this service needs to be developed, perhaps involving the training of non-specialists to deliver primary palliative care in the community, bolstered by the use of telemedicine. The appropriate use of limited clinical resources has engendered many challenging discussions and complex ethical decisions. Prospective implementation of future policies requires the incorporation of measures to assuage moral distress, burnout and compassion fatigue in healthcare staff who are psychologically and physically exhausted. SUMMARY: Further research based on patient-centred decision making and advance care planning is required to ensure the supportive needs of COVID-19 patients with cardiovascular disease are adequately met. This research should focus on interventions applicable to daily healthcare practice and include strategies to safeguard staff well-being.


Subject(s)
COVID-19/epidemiology , Cardiovascular Diseases/epidemiology , Communication , Palliative Care/organization & administration , Advance Care Planning/organization & administration , Burnout, Professional/prevention & control , Burnout, Professional/psychology , Compassion Fatigue/prevention & control , Compassion Fatigue/psychology , Cultural Competency , Decision Making , Humans , Pandemics , Patient Participation/methods , Patient Participation/psychology , SARS-CoV-2 , Telemedicine/organization & administration
19.
Med Hypotheses ; 151: 110590, 2021 Jun.
Article in English | MEDLINE | ID: covidwho-1157616

ABSTRACT

Coronavirus disease 2019 (COVID-19) is an inflammatory process with complex pathophysiology and by affecting the cardiovascular system directly or indirectly that causes life threatening cardiac injuries. Therefore, clarifying the effects of this infection on the cardiovascular system is of importance in terms of the clinical course of the disease. The increases in cardiac and inflammatory biomarkers in COVID-19 have been associated with poor prognosis and mortality. However, there are no specific laboratory markers yet to assess the severity of the disease. In this context, the combination of available biomarkers is needed to better define the clinical course of this disease. Carbohydrate antigen 125 (CA-125) has become a remarkable marker in recent years as a result of the correlation of increasing levels in cardiovascular diseases with clinical, hemodynamic, echocardiographic parameters and its relation with mortality or re-hospitalization due to heart failure. These findings suggest that CA-125 might be useful biomarker to identify the damage mechanisms of COVID-19, monitoring the prognosis of the disease and the course of the treatment.


Subject(s)
COVID-19 , Biomarkers , CA-125 Antigen , Carbohydrates , Humans , Prognosis , SARS-CoV-2
20.
Cureus ; 13(2): e13420, 2021 Feb 18.
Article in English | MEDLINE | ID: covidwho-1143806

ABSTRACT

INTRODUCTION:  Coronavirus disease 2019 (COVID-19) has multiorgan involvement and its severity varies with the presence of pre-existing risk factors like cardiovascular disease (CVD) and hypertension (HTN). Therefore, it is important to evaluate their effect on outcomes of COVID-19 patients. The objective of this meta-analysis and meta-regression is to evaluate outcomes of COVID-19 amongst patients with CVD and HTN. METHODS: English full-text observational studies having data on epidemiological characteristics of patients with COVID-19 were identified searching PubMed from December 1, 2019, to July 31, 2020, following Meta-analysis Of Observational Studies in Epidemiology (MOOSE) protocol. Studies having pre-existing CVD and HTN data that described outcomes including mortality and invasive mechanical ventilation (IMV) utilization were selected. Using random-effects models, risk of composite poor outcomes (meta-analysis) and isolated mortality and IMV utilization (meta-regression) were evaluated. Pooled prevalence of CVD and HTN, correlation coefficient (r) and odds ratio (OR) were estimated. The forest plots and correlation plots were created using random-effects models. RESULTS: Out of 29 studies (n=27,950) that met the criteria, 28 and 27 studies had data on CVD and HTN, respectively. Pooled prevalence of CVD was 18.2% and HTN was 32.7%. In meta-analysis, CVD (OR: 3.36; 95% CI: 2.29-4.94) and HTN (OR: 1.94; 95% CI: 1.57-2.40) were associated with composite poor outcome. In age-adjusted meta-regression, pre-existing CVD was having significantly higher correlation of IMV utilization (r: 0.28; OR: 1.3; 95% CI: 1.1-1.6) without having any association with mortality (r: -0.01; OR: 0.9; 95% CI: 0.9-1.1) among COVID-19 hospitalizations. HTN was neither correlated with higher IMV utilization (r: 0.01; OR: 1.0; 95% CI: 0.9-1.1) nor correlated with higher mortality (r: 0.001; OR: 1.0; 95% CI: 0.9-1.1). CONCLUSION: In age-adjusted analysis, though we identified pre-existing CVD as a risk factor for higher utilization of mechanical ventilation, pre-existing CVD and HTN had no independent role in increasing mortality.

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