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1.
European heart journal supplements : journal of the European Society of Cardiology ; 23(Suppl G), 2021.
Article in English | EuropePMC | ID: covidwho-1602422

ABSTRACT

Aims Significant concern has been raised about the effect of pre-existing cardiovascular diseases (CVD), cardiovascular (CV) risk factors and CV therapies on COVID-19 course. On the other hand, COVID-19 could worse pre-existing CVD or trigger the development of new-onset CVD. The aim of this study was to evaluate the relationship between pre-existing CVD, CV risk factors, and CV therapy with the clinical course of hospitalized COVID-19 patients. Methods and results Consecutive hospitalized COVID-19 patients admitted to the Cardiovascular COVID-19 Unit at Policlinico Umberto I of Rome between December 2020 and April 2021 were enrolled. All patients underwent a cardiovascular evaluation including troponin, electrocardiogram (ECG), and echocardiogram. Data on medical history, pre-existing CVD, CV risk factors, and therapy were collected. Admission to the Intensive Care Unit (ICU) or Cardiac Intensive Care Unit (CICU), as well as the development of new-onset CVD, were considered as endpoint of the study. Among n = 229 patients enrolled, 22 (10%) died. Nearly half of patients (112, 49%) were admitted to the ICU/CICU. The presence of prior ischaemic heart disease nearly doubled the probability of hospitalization in the ICU/CICU (HR: 2.09, 95% CI: 1.132–3.866, P 0.018). In regards of therapy, beta blockers reduced the likelihood of admission in the ICU/CICU (HR: −1016, 95% CI: 0.192–10.682, P 0.002). However, neither the use of RAAS blockers, heparin or dexamethasone influenced the risk of ICU/CICU admission (respectively, HR: 0.85, 95% CI: 0.498–1.450, P 0.551;HR: 0.768, 95% CI: 0.435–1.356, P 0.363;HR: 0.861, 95% CI: 0.453–1.635, P 0.647). N = 89 patients (39%) experienced a new onset CVD including arrythmias (18.3%) with nearly half experiencing atrial fibrillation, acute coronary syndrome (10.9%), acute pulmonary embolism (5.3%), heart failure (HF) (3%), and myocarditis and pericarditis (1.3%). A pre-existing diagnosis of HF substantially increased the likelihood of new onset CVD (HR: 2.380, 95% CI: 1.004–5.638, P 0.049). However, treatment with heparin or dexamethasone reduced the risk of new onset CVD (HR: 0.482 95% CI: 0.268–0.867, P 0.015;HR: 0.487, 95% CI: 0.253–0.937, P 0.031, respectively). Conclusions Our study found that hospitalized COVID-19 patients who have at least one CV risk factor or pre-existing CVD had a greater likelihood of being admitted to the ICU/CICU and experiencing new onset CVD.

2.
European heart journal supplements : journal of the European Society of Cardiology ; 23(Suppl G), 2021.
Article in English | EuropePMC | ID: covidwho-1601783

ABSTRACT

Aims Cardiovascular sequelae in COVID-19 survivors remain largely unclear and can potentially go unrecognized. Reports on follow-up focused on cardiovascular evaluation after hospital discharge are currently scarce. Aim of this prospective study was to assess cardiovascular sequelae in previously hospitalized COVID-19 survivors. Methods and results The study was conducted at ‘Sapienza’ University of Rome—Policlinico ‘Umberto I’. After 2 months from discharge, n = 230 COVID-19 survivors underwent a follow-up visit at a dedicated ‘post-COVID Outpatient Clinic’. A cardiovascular evaluation including electrocardiogram (ECG), Troponin and echocardiography was performed. Further tests were requested when clinically indicated. Medical history, symptoms, arterial-blood gas, blood tests, chest computed tomography, and treatment of both in-hospital and follow-up evaluation were recorded. A 1-year telephone follow-up was performed. A total of 36 (16%) COVID-19 survivors showed persistence or delayed onset of cardiovascular disease at 2-months follow-up visit. Persistent condition was recorded in 62% of survivors who experienced an in-hospital cardiovascular disease. Delayed cardiovascular involvement included: myocarditis, pericarditis, ventricular disfunction, new onset of systemic hypertension and arrhythmias. At 1-year telephone follow-up, 105 (45%) survivors reported persistent symptoms, with dyspnoea and fatigue being the most frequent. 60% of survivors showed persistent chest CT abnormalities and among those 28% complained of persistent cardiopulmonary symptoms at long term follow-up. Conclusions Our preliminary data showed persistent or delayed onset of cardiovascular involvement (16%) at short-term follow-up and persistent symptoms (45%) at long-term follow-up. These findings suggest the need for monitoring COVID-19 survivors.

3.
European heart journal supplements : journal of the European Society of Cardiology ; 23(Suppl G), 2021.
Article in English | EuropePMC | ID: covidwho-1601782

ABSTRACT

Aims A possible interference between ACE-i or ARBs with ACE-2 receptor and SARS-CoV-2 pathway has been raised. Despite data have shown no clinical impact of therapy with ACE-I or ARBs on COVID-19, these drugs are often discontinued upon hospitalization or diagnosis. To evaluate the effects of cardiovascular risk factors (CVRF) and prior outpatient therapy with RAAS inhibitors on the chest CT severity score performed within 24 h of diagnosis of SARS-CoV-2 infection (before stopping medications or starting specific therapy for COVID-19) and on 1-year survival. Methods and results This is a multicentre, prospective, observational study. All admitted patients diagnosed with SARS-CoV-2 infection who performed chest CT within 24 h of arrival were consecutively enrolled from 1 March to 1 June 2020. A severity score was attributed to Chest CT by two radiologists in blind to the patient’s clinical information and a cut-off value of 19.5 was considered to define severe radiological pneumonia. A 1-year telephone follow-up was performed in order to evaluate the determinants of 1-year survival. 590 patients with a mean age of 63 ± 14 years were included. Seventy-three (12.4%) patients were treated with ACE-I, 85 (14.4%) with ARBs and 62 (10.5%) with CCB. Cox regression analysis showed that male gender (OR: 1.4;95% CI: from 1.02 to 2.07;P = 0.035), diabetes (OR: 1.6;95% CI: from 1.03 to 2.7;P = 0.037), age (OR: 1.02;95% CI: from 1.008 to 1.033;P = 0.001), and obesity (OR: 3.04;95% CI: from 1.3 to 6.7;P < 0.001) were independently associated with a severe CT score. Of note, while prior outpatient therapy with ACE-I and ARBs was not independently associated with severe CT score, therapy with CCB was independently associated with a severe CT score (OR: 1.9, 95% CI: from 1.05 to 3.4, P = 0.033). Severe chest CT severity score (OR: 1.05;95% CI: from 1.02 to 1.08;P < 0.001), P/F ratio (OR: 0.998;95% CI: from 0.994 to 0.998;P < 0.001), and older age (OR: 1.06;95% CI: from 1.03 to 1.1;P < 0.001) were independently associated with mortality at 1-year follow-up. Neither ACE-I, ARBs, and CCB were associated with mortality at 1 year follow-up. Conclusions ACE-I and ARBs do not influence the chest CT presentation of COVID-19 patients at the time of diagnosis. Furthermore, ACE-I and ARBs do not influence 1-year survival of COVID-19 survivors.

4.
J Sports Med Phys Fitness ; 61(8): 1137-1143, 2021 Aug.
Article in English | MEDLINE | ID: covidwho-1310334

ABSTRACT

Recent reports based on cardiovascular magnetic resonance (CMR) showed a wide range of prevalence of inflammatory heart diseases in COVID-19 convalescent athletes ranging from 0.4 up to 15%. These observations had an important impact in the field of sport cardiology opening an intense debate around the best possible screening strategy before the return-to-play. The diagnostic yield of CMR for detecting acute inflammatory disease is undebatable. However, the opportunity to use it in the screening protocol after COVID-19 has been questioned. Current evidence does not seem to support the routine use of CMR and the prescription of CMR should be based upon clinical indication.


Subject(s)
COVID-19 , Athletes , Humans , Magnetic Resonance Imaging , Magnetic Resonance Spectroscopy , Medical Futility , Return to Sport , SARS-CoV-2
5.
Int J Cardiol ; 339: 235-242, 2021 09 15.
Article in English | MEDLINE | ID: covidwho-1293831

ABSTRACT

BACKGROUND: Cardiovascular disease (CVD) can occur in COVID-19 and has impact on clinical course. Data on CVD prevalence in hospitalized COVID-19 patients and sequelae in survivors is limited. Aim of this prospective study carried out on consecutive unselected COVID-19 population, was to assess: 1) CVD occurrence among hospitalized COVID-19 patients, 2) persistence or new onset of CVD at one-month and one-year follow-up. METHODS: Over 30 days n = 152 COVID-19 patients underwent cardiovascular evaluation. Standard electrocardiogram (ECG), Troponin and echocardiography were integrated by further tests when indicated. Medical history, arterial blood gas, blood tests, chest computed tomography and treatment were recorded. CVD was defined as the occurrence of a new condition during the hospitalization for COVID-19. Survivors attended a one-month follow-up visit and a one-year telephone follow-up. RESULTS: Forty-two patients (28%) experienced a wide spectrum of CVD with acute myocarditis being the most frequent. Death occurred in 32 patients (21%) and more frequently in patients who developed CVD (p = 0.032). After adjustment for confounders, CVD was independently associated with death occurrence. At one-month follow-up visit, 7 patients (9%) presented persistent or delayed CVD. At one-year telephone follow-up, 57 patients (48%) reported persistent symptoms. CONCLUSION: Cardiovascular evaluation in COVID-19 patients is crucial since the occurrence of CVD in hospitalized COVID-19 patients is common (28%), requires specific treatment and increases the risk of in-hospital mortality. Persistence or delayed presentation of CVD at 1-month (9%) and persistent symptoms at 1-year follow-up (48%) suggest the need for monitoring COVID-19 survivors.


Subject(s)
COVID-19 , Myocarditis , Follow-Up Studies , Hospitals , Humans , Prospective Studies , SARS-CoV-2
6.
J Cardiovasc Magn Reson ; 23(1): 68, 2021 06 10.
Article in English | MEDLINE | ID: covidwho-1262508

ABSTRACT

BACKGROUND: Early detection of myocardial involvement can be relevant in coronavirus disease 2019 (COVID-19) patients to timely target symptomatic treatment and decrease the occurrence of the cardiac sequelae of the infection. The aim of the present study was to assess the clinical value of cardiovascular magnetic resonance (CMR) in characterizing myocardial damage in active COVID-19 patients, through the correlation between qualitative and quantitative imaging biomarkers with clinical and laboratory evidence of myocardial injury. METHODS: In this retrospective observational cohort study, we enrolled 27 patients with diagnosis of active COVID-19 and suspected cardiac involvement, referred to our institution for CMR between March 2020 and January 2021. Clinical and laboratory characteristics, including high sensitivity troponin T (hs-cTnT), and CMR imaging data were obtained. Relationships between CMR parameters, clinical and laboratory findings were explored. Comparisons were made with age-, sex- and risk factor-matched control group of 27 individuals, including healthy controls and patients without other signs or history of myocardial disease, who underwent CMR examination between January 2020 and January 2021. RESULTS: The median (IQR) time interval between COVID-19 diagnosis and CMR examination was 20 (13.5-31.5) days. Hs-cTnT values were collected within 24 h prior to CMR and resulted abnormally increased in 18 patients (66.6%). A total of 20 cases (74%) presented tissue signal abnormalities, including increased myocardial native T1 (n = 11), myocardial T2 (n = 14) and extracellular volume fraction (ECV) (n = 10), late gadolinium enhancement (LGE) (n = 12) or pericardial enhancement (n = 2). A CMR diagnosis of myocarditis was established in 9 (33.3%), pericarditis in 2 (7.4%) and myocardial infarction with non-obstructive coronary arteries in 3 (11.11%) patients. T2 mapping values showed a moderate positive linear correlation with Hs-cTnT (r = 0.58; p = 0.002). A high degree positive linear correlation between ECV and Hs-cTnT was also found (r 0.77; p < 0.001). CONCLUSIONS: CMR allows in vivo recognition and characterization of myocardial damage in a cohort of selected COVID-19 individuals by means of a multiparametric scanning protocol including conventional imaging and T1-T2 mapping sequences. Abnormal T2 mapping was the most commonly abnormality observed in our cohort and positively correlated with hs-cTnT values, reflecting the predominant edematous changes characterizing the active phase of disease.


Subject(s)
COVID-19/complications , Cardiomyopathies/complications , Cardiomyopathies/diagnostic imaging , Magnetic Resonance Imaging/methods , Adult , Age Factors , Cohort Studies , Heart/diagnostic imaging , Humans , Male , Middle Aged , Retrospective Studies , Risk Factors , SARS-CoV-2 , Sex Factors
9.
Eur Heart J Cardiovasc Imaging ; 22(7): 728-731, 2021 06 22.
Article in English | MEDLINE | ID: covidwho-978588

ABSTRACT

We proposed a combined cardiothoracic-MRI (CaTh-MRI) protocol for the comprehensive assessment of cardiovascular structures, lung parenchyma, and pulmonary arterial tree, in COVID-19 patients with progressive worsening of clinical conditions and/or suspicion of acute-onset myocardial inflammation. A 25-minutes fast protocol was also conceived for unstable or uncooperative patients by restricting the number of sequences to those necessary to rule out myocardial and to assess pulmonary involvement. In patients requiring CMR characterization of myocardial damage, the addition of lung and thoracic vessel evaluation is of clinical benefit at a minimal time expense.


Subject(s)
COVID-19 , Humans , Lung/diagnostic imaging , Magnetic Resonance Imaging , Pulmonary Artery/diagnostic imaging , SARS-CoV-2
10.
International Journal of Molecular Sciences ; 21(21):8118, 2020.
Article in English | MDPI | ID: covidwho-896522

ABSTRACT

Ischemic heart disease still represents a large burden on individuals and health care resources worldwide. By conventions, it is equated with atherosclerotic plaque due to flow-limiting obstruction in large–medium sized coronary arteries. However, clinical, angiographic and autoptic findings suggest a multifaceted pathophysiology for ischemic heart disease and just some cases are caused by severe or complicated atherosclerotic plaques. Currently there is no well-defined assessment of ischemic heart disease pathophysiology that satisfies all the observations and sometimes the underlying mechanism to everyday ischemic heart disease ward cases is misleading. In order to better examine this complicated disease and to provide future perspectives, it is important to know and analyze the pathophysiological mechanisms that underline it, because ischemic heart disease is not always determined by atherosclerotic plaque complication. Therefore, in order to have a more complete comprehension of ischemic heart disease we propose an overview of the available pathophysiological paradigms, from plaque activation to microvascular dysfunction.

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