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1.
J Cardiovasc Med (Hagerstown) ; 24(Suppl 1): e15-e23, 2023 04 01.
Article in English | MEDLINE | ID: covidwho-2300416

ABSTRACT

The coronavirus disease 19 (COVID-19), due to coronavirus 2 (SARS-CoV-2) infection, presents with an extremely heterogeneous spectrum of symptoms and signs. COVID-19 susceptibility and mortality show a significant sex imbalance, with men being more prone to infection and showing a higher rate of hospitalization and mortality than women. In particular, cardiovascular diseases (preexistent or arising upon infection) play a central role in COVID-19 outcomes, differently in men and women. This review will discuss the potential mechanisms accounting for sex/gender influence in vulnerability to COVID-19. Such variability can be ascribed to both sex-related biological factors and sex-related behavioural traits. Sex differences in cardiovascular disease and COVID-19 involve the endothelial dysfunction, the innate immune system and the renin-angiotensin system (RAS). Furthermore, the angiotensin-converting enzyme 2 (ACE2) is involved in disease pathogenesis in cardiovascular disease and COVID-19 and it shows hormone-dependent actions. The incidence of myocardial injury during COVID-19 is sex-dependent, predominantly in association with a greater degree of inflammation and coagulation disorders among men. Its pathogenesis is not fully elucidated, but the main theories foresee a direct role for the ACE2 receptor, the hyperimmune response and the RAS imbalance, which may also lead to isolated presentation of COVID-19-mediated myopericarditis. Moreover, the latest evidence on cardiovascular diseases and their relationship with COVID-19 during pregnancy will be discussed. Finally, authors will analyse the prevalence of the long-covid syndrome between the two sexes and its impact on the quality of life and cardiovascular health.


Subject(s)
COVID-19 , Cardiology , Cardiovascular Diseases , Female , Humans , Male , COVID-19/complications , Cardiovascular Diseases/diagnosis , Cardiovascular Diseases/epidemiology , Cardiovascular Diseases/complications , SARS-CoV-2/metabolism , Angiotensin-Converting Enzyme 2 , Post-Acute COVID-19 Syndrome , Quality of Life , Peptidyl-Dipeptidase A/metabolism , Renin-Angiotensin System/physiology
3.
Heart Fail Rev ; 27(1): 251-261, 2022 01.
Article in English | MEDLINE | ID: covidwho-1147607

ABSTRACT

Myocardial inflammation in COVID-19 has been documented. Its pathogenesis is not fully elucidated, but the two main theories foresee a direct role of ACE2 receptor and a hyperimmune response, which may also lead to isolated presentation of COVID-19-mediated myocarditis. The frequency and prognostic impact of COVID-19-mediated myocarditis is unknown. This review aims to summarise current evidence on this topic. We performed a systematic review of MEDLINE and Cochrane Library (1/12/19-30/09/20). We also searched clinicaltrials.gov for unpublished studies testing therapies with potential implication for COVID-19-mediated cardiovascular complication. Eligible studies had laboratory confirmed COVID-19 and a clinical and/or histological diagnosis of myocarditis by ESC or WHO/ISFC criteria. Reports of 38 cases were included (26 male patients, 24 aged < 50 years). The first histologically proven case was a virus-negative lymphocytic myocarditis; however, biopsy evidence of myocarditis secondary to SARS-CoV-2 cardiotropism has been recently demonstrated. Histological data was found in 12 cases (8 EMB and 4 autopsies) and CMR was the main imaging modality to confirm a diagnosis of myocarditis (25 patients). There was a substantial variability in biventricular systolic function during the acute episode and in therapeutic regimen used. Five patients died in hospital. Cause-effect relationship between SARS-CoV-2 infection and myocarditis is difficult to demonstrate. However, current evidence demonstrates myocardial inflammation with or without direct cardiomyocyte damage, suggesting different pathophysiology mechanisms responsible of COVID-mediated myocarditis. Established clinical approaches should be pursued until future evidence support different actions. Large multicentre registries are advisable to elucidate further.


Subject(s)
COVID-19 , Myocarditis , Humans , Male , Myocarditis/diagnosis , Myocytes, Cardiac , Registries , SARS-CoV-2
4.
Eur J Clin Invest ; 50(10): e13362, 2020 Oct.
Article in English | MEDLINE | ID: covidwho-684327

ABSTRACT

BACKGROUND: Identification of reliable outcome predictors in coronavirus disease 2019 (COVID-19) is of paramount importance for improving patient's management. METHODS: A systematic review of literature was conducted until 24 April 2020. From 6843 articles, 49 studies were selected for a pooled assessment; cumulative statistics for age and sex were retrieved in 587 790 and 602 234 cases. Two endpoints were defined: (a) a composite outcome including death, severe presentation, hospitalization in the intensive care unit (ICU) and/or mechanical ventilation; and (b) in-hospital mortality. We extracted numeric data on patients' characteristics and cases with adverse outcomes and employed inverse variance random-effects models to derive pooled estimates. RESULTS: We identified 18 and 12 factors associated with the composite endpoint and death, respectively. Among those, a history of CVD (odds ratio (OR) = 3.15, 95% confidence intervals (CIs) 2.26-4.41), acute cardiac (OR = 10.58, 5.00-22.40) or kidney (OR = 5.13, 1.78-14.83) injury, increased procalcitonin (OR = 4.8, 2.034-11.31) or D-dimer (OR = 3.7, 1.74-7.89), and thrombocytopenia (OR = 6.23, 1.031-37.67) conveyed the highest odds for the adverse composite endpoint. Advanced age, male sex, cardiovascular comorbidities, acute cardiac or kidney injury, lymphocytopenia and D-dimer conferred an increased risk of in-hospital death. With respect to the treatment of the acute phase, therapy with steroids was associated with the adverse composite endpoint (OR = 3.61, 95% CI 1.934-6.73), but not with mortality. CONCLUSIONS: Advanced age, comorbidities, abnormal inflammatory and organ injury circulating biomarkers captured patients with an adverse clinical outcome. Clinical history and laboratory profile may then help identify patients with a higher risk of in-hospital mortality.


Subject(s)
Acute Kidney Injury/epidemiology , Cardiovascular Diseases/epidemiology , Coronavirus Infections/therapy , Fibrin Fibrinogen Degradation Products/metabolism , Pneumonia, Viral/therapy , Procalcitonin/metabolism , Smoking/epidemiology , Thrombocytopenia/epidemiology , Acute Disease , Adrenal Cortex Hormones/therapeutic use , Adult , Age Factors , Aged , Aged, 80 and over , Betacoronavirus , C-Reactive Protein/metabolism , COVID-19 , Cerebrovascular Disorders/epidemiology , Coronavirus Infections/epidemiology , Coronavirus Infections/metabolism , Coronavirus Infections/mortality , Diabetes Mellitus/epidemiology , Female , Ferritins/metabolism , Heart Diseases , Hospital Mortality , Hospitalization , Humans , Hypertension/epidemiology , Intensive Care Units , Interleukin-6/metabolism , Liver Diseases/epidemiology , Lymphopenia/epidemiology , Male , Middle Aged , Neoplasms/epidemiology , Obesity/epidemiology , Pandemics , Pneumonia, Viral/epidemiology , Pneumonia, Viral/metabolism , Pneumonia, Viral/mortality , Prognosis , Pulmonary Disease, Chronic Obstructive/epidemiology , Respiration, Artificial , SARS-CoV-2 , Severity of Illness Index , Sex Factors , Young Adult
6.
JACC Case Rep ; 2(9): 1307-1310, 2020 Jul 15.
Article in English | MEDLINE | ID: covidwho-437296

ABSTRACT

There is an urgent need for effective treatments for coronavirus disease-2019 (COVID-19). Amiodarone, like hydroxychloroquine, exerts antiviral actions by interfering with endocytosis and viral replication. Here, to our knowledge, we report the first case of a patient affected by respiratory failure related to COVID-19 who recovered after only supportive measures and a short amiodarone course. (Level of Difficulty: Beginner.).

7.
Eur J Prev Cardiol ; 27(10): 1017-1025, 2020 Jul.
Article in English | MEDLINE | ID: covidwho-232751

ABSTRACT

Patients with cardiovascular risk factors or established cardiovascular disease have an increased risk of developing coronavirus disease 19 and have a worse outcome when infected, but translating this notion into effective action is challenging. At present it is unclear whether cardiovascular therapies may reduce the likelihood of infection, or improve the survival of infected patients. Given the crucial importance of this issue for clinical cardiologists and all specialists dealing with coronavirus disease 19, we tried to recapitulate the current evidence and provide some practical recommendations.


Subject(s)
Cardiovascular Agents/administration & dosage , Cardiovascular Diseases/drug therapy , Cardiovascular Diseases/epidemiology , Cause of Death , Coronavirus Infections/epidemiology , Pandemics/statistics & numerical data , Pneumonia, Viral/epidemiology , COVID-19 , Cardiovascular Agents/pharmacology , Cardiovascular Diseases/diagnosis , Comorbidity , Coronavirus Infections/prevention & control , Europe/epidemiology , Female , Humans , Male , Pandemics/prevention & control , Pneumonia, Viral/prevention & control , Prevalence , Risk Assessment , Survival Analysis
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