Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 14 de 14
Filter
1.
Eur J Heart Fail ; 23(11): 1806-1818, 2021 11.
Article in English | MEDLINE | ID: covidwho-1453574

ABSTRACT

Patients with heart failure (HF) who contract SARS-CoV-2 infection are at a higher risk of cardiovascular and non-cardiovascular morbidity and mortality. Regardless of therapeutic attempts in COVID-19, vaccination remains the most promising global approach at present for controlling this disease. There are several concerns and misconceptions regarding the clinical indications, optimal mode of delivery, safety and efficacy of COVID-19 vaccines for patients with HF. This document provides guidance to all healthcare professionals regarding the implementation of a COVID-19 vaccination scheme in patients with HF. COVID-19 vaccination is indicated in all patients with HF, including those who are immunocompromised (e.g. after heart transplantation receiving immunosuppressive therapy) and with frailty syndrome. It is preferable to vaccinate against COVID-19 patients with HF in an optimal clinical state, which would include clinical stability, adequate hydration and nutrition, optimized treatment of HF and other comorbidities (including iron deficiency), but corrective measures should not be allowed to delay vaccination. Patients with HF who have been vaccinated against COVID-19 need to continue precautionary measures, including the use of facemasks, hand hygiene and social distancing. Knowledge on strategies preventing SARS-CoV-2 infection (including the COVID-19 vaccination) should be included in the comprehensive educational programmes delivered to patients with HF.


Subject(s)
COVID-19 , Cardiology , Heart Failure , Aged , COVID-19 Vaccines , Frail Elderly , Humans , SARS-CoV-2 , Vaccination
2.
ESC Heart Fail ; 8(5): 3451-3452, 2021 10.
Article in English | MEDLINE | ID: covidwho-1453572
3.
Eur J Heart Fail ; 23(11): 1891-1902, 2021 11.
Article in English | MEDLINE | ID: covidwho-1209196

ABSTRACT

AIMS: Viral-induced cardiac inflammation can induce heart failure with preserved ejection fraction (HFpEF)-like syndromes. COVID-19 can lead to myocardial damage and vascular injury. We hypothesised that COVID-19 patients frequently develop a HFpEF-like syndrome, and designed this study to explore this. METHODS AND RESULTS: Cardiac function was assessed in 64 consecutive, hospitalized, and clinically stable COVID-19 patients from April-November 2020 with left ventricular ejection fraction (LVEF) ≥50% (age 56 ± 19 years, females: 31%, severe COVID-19 disease: 69%). To investigate likelihood of HFpEF presence, we used the HFA-PEFF score. A low (0-1 points), intermediate (2-4 points), and high (5-6 points) HFA-PEFF score was observed in 42%, 33%, and 25% of patients, respectively. In comparison, 64 subjects of similar age, sex, and comorbidity status without COVID-19 showed these scores in 30%, 66%, and 4%, respectively (between groups: P = 0.0002). High HFA-PEFF scores were more frequent in COVID-19 patients than controls (25% vs. 4%, P = 0.001). In COVID-19 patients, the HFA-PEFF score significantly correlated with age, estimated glomerular filtration rate, high-sensitivity troponin T (hsTnT), haemoglobin, QTc interval, LVEF, mitral E/A ratio, and H2 FPEF score (all P < 0.05). In multivariate, ordinal regression analyses, higher age and hsTnT were significant predictors of increased HFA-PEFF scores. Patients with myocardial injury (hsTnT ≥14 ng/L: 31%) vs. patients without myocardial injury, showed higher HFA-PEFF scores [median 5 (interquartile range 3-6) vs. 1 (0-3), P < 0.001] and more often showed left ventricular diastolic dysfunction (75% vs. 27%, P < 0.001). CONCLUSION: Hospitalized COVID-19 patients frequently show high likelihood of presence of HFpEF that is associated with cardiac structural and functional alterations, and myocardial injury. Detailed cardiac assessments including echocardiographic determination of left ventricular diastolic function and biomarkers should become routine in the care of hospitalized COVID-19 patients.


Subject(s)
COVID-19 , Heart Failure , Adult , Aged , Echocardiography , Female , Heart Failure/epidemiology , Humans , Middle Aged , SARS-CoV-2 , Stroke Volume , Ventricular Function, Left
4.
J Cachexia Sarcopenia Muscle ; 12(1): 9-13, 2021 02.
Article in English | MEDLINE | ID: covidwho-1001858

ABSTRACT

Patients with COVID-19 disease are prone to develop significant weight loss and clinical cachexia. Three reports with altogether 589 patients that reported on weight loss and cachexia in COVID-19 were identified. Disease severity of patients and the timing of the assessment during the disease course in these patients were variable-65 patients (11%) were intensive care treated at the time of assessment, and 183 (31%) were cared for in sub-intensive or intermediate care structures. The frequency of weight loss ≥5% (that defines cachexia) was 37% (range 29-52%). Correlates of weight loss occurrence were reported to be raised C-reactive protein levels, impaired renal function status, and longer duration of COVID-19 disease. Underweight status by WHO criteria (BMI < 18.5 kg/m2 ) was only observed in 4% of patients analysing data from seven studies with 6661 patients. Cachexia assessment in COVID-19 needs assessment of weight loss. COVID-19 associated cachexia is understood to affect muscle and fat tissue as is also seen in many other chronic illness-associated forms of cachexia. There are many factors that can contribute to body wasting in COVID-19, and they include loss of appetite and taste, fever and inflammation, immobilization, as well as general malnutrition, catabolic-anabolic imbalance, endocrine dysfunction, and organ-specific complications of COVID-19 disease such as cardiac and renal dysfunction. Treatment of COVID-19 patients should include a focus on nutritional support and rehabilitative exercise whenever possible. Specific anti-cachectic therapies for COVID-19 do not exist, but constitute a high medical need to prevent long-term disability due to acute COVID-19 disease.


Subject(s)
COVID-19/complications , Cachexia/etiology , Malnutrition/etiology , SARS-CoV-2/isolation & purification , Weight Loss , COVID-19/transmission , COVID-19/virology , Cachexia/pathology , Humans , Malnutrition/pathology
5.
ESC Heart Failure ; 7(6):3261-3267, 2020.
Article in English | ProQuest Central | ID: covidwho-986033

ABSTRACT

The ultimate primary endpoint of SOLOST‐WHF—which in order to preserve statistical power was changed because of the premature closure of the study due to loss of funding from the sponsor during the onset of the COVID‐19 pandemic—was the composite of total HHF, urgent heart failure visits, or cardiovascular deaths. The HR for the primary outcome was apparently similarly reduced in all groups (0.69, 0.74, and 0.66, respectively). Because the subgroup of patients with ejection fraction above 50% was modest in size, further data of SGLT2 inhibitors in heart failure with preserved ejection fraction (HFpEF) are eagerly anticipated. 2 Figure. DAPA‐HF, Study to Evaluate the Effect of Dapagliflozin on the Incidence of Worsening Heart Failure or Cardiovascular Death in Patients With Chronic Heart Failure;EF, ejection fraction;EMPEROR‐Reduced, EMPagliflozin outcomE tRial in Patients With chrOnic heaRt Failure With Reduced Ejection Fraction;GDMT, guideline‐directed medical therapy;HFrEF, heart failure with a reduced ejection fraction;MRA, mineralocorticoid receptor antagonists;RASi, renin‐angiotensin system inhibitors;WHF, worsening heart failure. The EMPEROR‐Preserved (EMPagliflozin outcomE tRial in Patients With chrOnic heaRt Failure With Preserved Ejection Fraction) 34 and DELIVER (Dapagliflozin Evaluation to Improve the LIVEs of Patients With PReserved Ejection Fraction Heart Failure;ClinicalTrials.gov Identifier: NCT03619213) trials that are ongoing will provide valuable information in those with HFpEF in the ambulatory setting.

6.
BMC Med ; 18(1): 403, 2020 12 18.
Article in English | MEDLINE | ID: covidwho-979659

ABSTRACT

BACKGROUND: Due to the overlapping clinical features of coronavirus disease 2019 (COVID-19) and influenza, parallels are often drawn between the two diseases. Patients with pre-existing cardiovascular diseases (CVD) are at a higher risk for severe manifestations of both illnesses. Considering the high transmission rate of COVID-19 and with the seasonal influenza approaching in late 2020, the dual epidemics of COVID-19 and influenza pose serious cardiovascular implications. This review highlights the similarities and differences between influenza and COVID-19 and the potential risks associated with coincident pandemics. MAIN BODY: COVID-19 has a higher mortality compared to influenza with case fatality rate almost 15 times more than that of influenza. Additionally, a significantly increased risk of adverse outcomes has been noted in patients with CVD, with ~ 15 to 70% of COVID-19 related deaths having an underlying CVD. The critical care need have ranged from 5 to 79% of patients hospitalized due to COVID-19, a proportion substantially higher than with influenza. Similarly, the frequency of vascular thrombosis including deep venous thrombosis and pulmonary embolism is markedly higher in COVID-19 patients compared with influenza in which vascular complications are rarely seen. Unexpectedly, while peak influenza season is associated with increased cardiovascular hospitalizations, a decrease of ~ 50% in cardiovascular hospitalizations has been observed since the first diagnosed case of COVID-19, owing in part to deferred care. CONCLUSION: In the coming months, increasing efforts towards evaluating new interventions will be vital to curb COVID-19, especially as peak influenza season approaches. Currently, not enough data exist regarding co-infection of COVID-19 with influenza or how it would progress clinically, though it may cause a significant burden on an already struggling health care system. Until an effective COVID-19 vaccination is available, high coverage of influenza vaccination should be of utmost priority.


Subject(s)
COVID-19/epidemiology , Cardiovascular Diseases/epidemiology , Coinfection/epidemiology , Influenza, Human/epidemiology , Adult , COVID-19/complications , Cardiovascular Diseases/complications , Female , Humans , Influenza, Human/complications , Male , Middle Aged , SARS-CoV-2
7.
Lancet ; 396(10266): 1895-1904, 2020 12 12.
Article in English | MEDLINE | ID: covidwho-922171

ABSTRACT

BACKGROUND: Intravenous ferric carboxymaltose has been shown to improve symptoms and quality of life in patients with chronic heart failure and iron deficiency. We aimed to evaluate the effect of ferric carboxymaltose, compared with placebo, on outcomes in patients who were stabilised after an episode of acute heart failure. METHODS: AFFIRM-AHF was a multicentre, double-blind, randomised trial done at 121 sites in Europe, South America, and Singapore. Eligible patients were aged 18 years or older, were hospitalised for acute heart failure with concomitant iron deficiency (defined as ferritin <100 µg/L, or 100-299 µg/L with transferrin saturation <20%), and had a left ventricular ejection fraction of less than 50%. Before hospital discharge, participants were randomly assigned (1:1) to receive intravenous ferric carboxymaltose or placebo for up to 24 weeks, dosed according to the extent of iron deficiency. To maintain masking of patients and study personnel, treatments were administered in black syringes by personnel not involved in any study assessments. The primary outcome was a composite of total hospitalisations for heart failure and cardiovascular death up to 52 weeks after randomisation, analysed in all patients who received at least one dose of study treatment and had at least one post-randomisation data point. Secondary outcomes were the composite of total cardiovascular hospitalisations and cardiovascular death; cardiovascular death; total heart failure hospitalisations; time to first heart failure hospitalisation or cardiovascular death; and days lost due to heart failure hospitalisations or cardiovascular death, all evaluated up to 52 weeks after randomisation. Safety was assessed in all patients for whom study treatment was started. A pre-COVID-19 sensitivity analysis on the primary and secondary outcomes was prespecified. This study is registered with ClinicalTrials.gov, NCT02937454, and has now been completed. FINDINGS: Between March 21, 2017, and July 30, 2019, 1525 patients were screened, of whom 1132 patients were randomly assigned to study groups. Study treatment was started in 1110 patients, and 1108 (558 in the carboxymaltose group and 550 in the placebo group) had at least one post-randomisation value. 293 primary events (57·2 per 100 patient-years) occurred in the ferric carboxymaltose group and 372 (72·5 per 100 patient-years) occurred in the placebo group (rate ratio [RR] 0·79, 95% CI 0·62-1·01, p=0·059). 370 total cardiovascular hospitalisations and cardiovascular deaths occurred in the ferric carboxymaltose group and 451 occurred in the placebo group (RR 0·80, 95% CI 0·64-1·00, p=0·050). There was no difference in cardiovascular death between the two groups (77 [14%] of 558 in the ferric carboxymaltose group vs 78 [14%] in the placebo group; hazard ratio [HR] 0·96, 95% CI 0·70-1·32, p=0·81). 217 total heart failure hospitalisations occurred in the ferric carboxymaltose group and 294 occurred in the placebo group (RR 0·74; 95% CI 0·58-0·94, p=0·013). The composite of first heart failure hospitalisation or cardiovascular death occurred in 181 (32%) patients in the ferric carboxymaltose group and 209 (38%) in the placebo group (HR 0·80, 95% CI 0·66-0·98, p=0·030). Fewer days were lost due to heart failure hospitalisations and cardiovascular death for patients assigned to ferric carboxymaltose compared with placebo (369 days per 100 patient-years vs 548 days per 100 patient-years; RR 0·67, 95% CI 0·47-0·97, p=0·035). Serious adverse events occurred in 250 (45%) of 559 patients in the ferric carboxymaltose group and 282 (51%) of 551 patients in the placebo group. INTERPRETATION: In patients with iron deficiency, a left ventricular ejection fraction of less than 50%, and who were stabilised after an episode of acute heart failure, treatment with ferric carboxymaltose was safe and reduced the risk of heart failure hospitalisations, with no apparent effect on the risk of cardiovascular death. FUNDING: Vifor Pharma.


Subject(s)
Anemia, Iron-Deficiency/drug therapy , Ferric Compounds/therapeutic use , Heart Failure/drug therapy , Maltose/analogs & derivatives , Administration, Intravenous , Aged , Aged, 80 and over , Double-Blind Method , Female , Ferric Compounds/administration & dosage , Heart Failure/complications , Heart Failure/mortality , Hospitalization/statistics & numerical data , Humans , Male , Maltose/administration & dosage , Maltose/therapeutic use , Middle Aged , Patient Discharge , Treatment Outcome , Ventricular Function, Left
8.
J Am Coll Cardiol ; 76(20): 2368-2378, 2020 11 17.
Article in English | MEDLINE | ID: covidwho-912306

ABSTRACT

The coronavirus disease-2019 (COVID-19) pandemic has profoundly changed clinical care and research, including the conduct of clinical trials, and the clinical research ecosystem will need to adapt to this transformed environment. The Heart Failure Academic Research Consortium is a partnership between the Heart Failure Collaboratory and the Academic Research Consortium, composed of academic investigators from the United States and Europe, patients, the U.S. Food and Drug Administration, the National Institutes of Health, and industry members. A series of meetings were convened to address the challenges caused by the COVID-19 pandemic, review options for maintaining or altering best practices, and establish key recommendations for the conduct and analysis of clinical trials for cardiovascular disease and heart failure. This paper summarizes the discussions and expert consensus recommendations.


Subject(s)
Clinical Trials as Topic , Coronavirus Infections , Pandemics , Pneumonia, Viral , COVID-19 , Endpoint Determination , Humans , Socioeconomic Factors , Statistics as Topic
9.
SSRN; 2020.
Preprint | SSRN | ID: ppcovidwho-826

ABSTRACT

Background: Understanding cardiovascular risk factors and complications in coronavirus disease 2019 (COVID-19) patients may be important to effectively manage t

10.
ESC Heart Fail ; 7(5): 2838-2852, 2020 10.
Article in English | MEDLINE | ID: covidwho-643370

ABSTRACT

AIMS: Left ventricular (LV) dysfunction in viral myocarditis is attributed to myocardial inflammation and fibrosis, inducing acute and long-time cardiac damage. Interventions are not established. On the basis of the link between inflammation, fibrosis, aldosterone, and extracellular matrix regulation, we aimed to investigate the effect of an early intervention with the mineralocorticoid receptor antagonist (MRA) eplerenone on cardiac remodelling in a murine model of persistent coxsackievirus B3 (CVB3)-induced myocarditis. METHODS AND RESULTS: SWR/J mice were infected with 5 × 104 plaque-forming units of CVB3 (Nancy strain) and daily treated either with eplerenone (200 mg/kg body weight) or with placebo starting from Day 1. At Day 8 or 28 post infection, mice were haemodynamically characterized and subsequently sacrificed for immunohistological and molecular biology analyses. Eplerenone did not influence CVB3 load. Already at Day 8, 1.8-fold (P < 0.05), 1.4-fold (P < 0.05), 3.2-fold (P < 0.01), and 2.1-fold (P < 0.001) reduction in LV intercellular adhesion molecule 1 expression, presence of monocytes/macrophages, oxidative stress, and apoptosis, respectively, was observed in eplerenone-treated vs. untreated CVB3-infected mice. In vitro, eplerenone led to 1.4-fold (P < 0.01) and 1.2-fold (P < 0.01) less CVB3-induced cardiomyocyte oxidative stress and apoptosis. Furthermore, collagen production was 1.1-fold (P < 0.05) decreased in cardiac fibroblasts cultured with medium of eplerenone-treated vs. untreated CVB3-infected HL-1 cardiomyocytes. These ameliorations were in vivo translated into prevention of cardiac fibrosis, as shown by 1.4-fold (P < 0.01) and 2.1-fold (P < 0.001) lower collagen content in the LV of eplerenone-treated vs. untreated CVB3-infected mice at Days 8 and 28, respectively. This resulted in an early and long-lasting improvement of LV dimension and function, as indicated by reduced LV end-systolic volume and end-diastolic volume, and an increase in LV contractility (dP/dtmax ) and LV relaxation (dP/dtmin ), respectively (P < 0.05). CONCLUSIONS: Early intervention with the MRA eplerenone modulates the acute host and defence reaction and prevents cardiac disease progression in experimental CVB3-induced myocarditis without aggravation of viral load. The findings advocate for an initiation of therapy of viral myocarditis as early as possible, even before the onset of inflammation-induced myocardial dysfunction. This may also have implications for coronavirus disease-19 therapy.


Subject(s)
Endomyocardial Fibrosis/prevention & control , Enterovirus B, Human/pathogenicity , Eplerenone/pharmacology , Myocarditis/drug therapy , Myocarditis/virology , Ventricular Dysfunction, Left/virology , Analysis of Variance , Animals , Biopsy, Needle , Disease Models, Animal , Disease Progression , Endomyocardial Fibrosis/pathology , Immunohistochemistry , Male , Matrix Metalloproteinases/drug effects , Matrix Metalloproteinases/metabolism , Mice , Mice, Transgenic , Myocarditis/prevention & control , Random Allocation , Reference Values , Treatment Outcome , Ventricular Dysfunction, Left/pathology , Ventricular Dysfunction, Left/physiopathology
11.
Eur Heart J ; 41(19): 1810-1817, 2020 05 14.
Article in English | MEDLINE | ID: covidwho-629506

ABSTRACT

AIMS: The current pandemic coronavirus SARS-CoV-2 infects a wide age group but predominantly elderly individuals, especially men and those with cardiovascular disease. Recent reports suggest an association with use of renin-angiotensin-aldosterone system (RAAS) inhibitors. Angiotensin-converting enzyme 2 (ACE2) is a functional receptor for coronaviruses. Higher ACE2 concentrations might lead to increased vulnerability to SARS-CoV-2 in patients on RAAS inhibitors. METHODS AND RESULTS: We measured ACE2 concentrations in 1485 men and 537 women with heart failure (index cohort). Results were validated in 1123 men and 575 women (validation cohort).The median age was 69 years for men and 75 years for women. The strongest predictor of elevated concentrations of ACE2 in both cohorts was male sex (estimate = 0.26, P < 0.001; and 0.19, P < 0.001, respectively). In the index cohort, use of ACE inhibitors, angiotensin receptor blockers (ARBs), or mineralocorticoid receptor antagonists (MRAs) was not an independent predictor of plasma ACE2. In the validation cohort, ACE inhibitor (estimate = -0.17, P = 0.002) and ARB use (estimate = -0.15, P = 0.03) were independent predictors of lower plasma ACE2, while use of an MRA (estimate = 0.11, P = 0.04) was an independent predictor of higher plasma ACE2 concentrations. CONCLUSION: In two independent cohorts of patients with heart failure, plasma concentrations of ACE2 were higher in men than in women, but use of neither an ACE inhibitor nor an ARB was associated with higher plasma ACE2 concentrations. These data might explain the higher incidence and fatality rate of COVID-19 in men, but do not support previous reports suggesting that ACE inhibitors or ARBs increase the vulnerability for COVID-19 through increased plasma ACE2 concentrations.


Subject(s)
Angiotensin Receptor Antagonists/therapeutic use , Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Heart Failure/blood , Mineralocorticoid Receptor Antagonists/therapeutic use , Peptidyl-Dipeptidase A/blood , Renin-Angiotensin System/drug effects , Aged , Angiotensin-Converting Enzyme 2 , Betacoronavirus , COVID-19 , Coronavirus Infections , Europe , Female , Humans , Male , Middle Aged , Pandemics , Pneumonia, Viral , SARS-CoV-2 , Sex Factors
13.
Eur Heart J ; 41(22): 2109-2117, 2020 06 07.
Article in English | MEDLINE | ID: covidwho-526858

ABSTRACT

The coronavirus disease 2019 (COVID-19) pandemic, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has important implications for the safety of participants in clinical trials and the research staff caring for them and, consequently, for the trials themselves. Patients with heart failure may be at greater risk of infection with COVID-19 and the consequences might also be more serious, but they are also at risk of adverse outcomes if their clinical care is compromised. As physicians and clinical trialists, it is our responsibility to ensure safe and effective care is delivered to trial participants without affecting the integrity of the trial. The social contract with our patients demands no less. Many regulatory authorities from different world regions have issued guidance statements regarding the conduct of clinical trials during this COVID-19 crisis. However, international trials may benefit from expert guidance from a global panel of experts to supplement local advice and regulations, thereby enhancing the safety of participants and the integrity of the trial. Accordingly, the Heart Failure Association of the European Society of Cardiology on 21 and 22 March 2020 conducted web-based meetings with expert clinical trialists in Europe, North America, South America, Australia, and Asia. The main objectives of this Expert Position Paper are to highlight the challenges that this pandemic poses for the conduct of clinical trials in heart failure and to offer advice on how they might be overcome, with some practical examples. While this panel of experts are focused on heart failure clinical trials, these discussions and recommendations may apply to clinical trials in other therapeutic areas.


Subject(s)
Betacoronavirus , Clinical Trials as Topic/methods , Coronavirus Infections , Heart Failure , Pandemics , Pneumonia, Viral , Research Design/standards , COVID-19 , Clinical Trials as Topic/ethics , Clinical Trials as Topic/standards , Europe , Heart Failure/complications , Heart Failure/therapy , Humans , Informed Consent/ethics , Informed Consent/standards , Patient Safety , Patient Selection/ethics , SARS-CoV-2
14.
Eur J Heart Fail ; 22(6): 941-956, 2020 Jun.
Article in English | MEDLINE | ID: covidwho-401833

ABSTRACT

The coronavirus disease 2019 (COVID-19) pandemic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is causing considerable morbidity and mortality worldwide. Multiple reports have suggested that patients with heart failure (HF) are at a higher risk of severe disease and mortality with COVID-19. Moreover, evaluating and treating HF patients with comorbid COVID-19 represents a formidable clinical challenge as symptoms of both conditions may overlap and they may potentiate each other. Limited data exist regarding comprehensive management of HF patients with concomitant COVID-19. Since these issues pose serious new challenges for clinicians worldwide, HF specialists must develop a structured approach to the care of patients with COVID-19 and be included early in the care of these patients. Therefore, the Heart Failure Association of the European Society of Cardiology and the Chinese Heart Failure Association & National Heart Failure Committee conducted web-based meetings to discuss these unique clinical challenges and reach a consensus opinion to help providers worldwide deliver better patient care. The main objective of this position paper is to outline the management of HF patients with concomitant COVID-19 based on the available data and personal experiences of physicians from Asia, Europe and the United States.


Subject(s)
Betacoronavirus , Cardiology , Coronavirus Infections/epidemiology , Disease Management , Heart Failure/therapy , Pandemics , Pneumonia, Viral/epidemiology , Societies, Medical , COVID-19 , China , Comorbidity , Coronavirus Infections/therapy , Europe , Heart Failure/epidemiology , Humans , Pneumonia, Viral/therapy , SARS-CoV-2
SELECTION OF CITATIONS
SEARCH DETAIL