scholarly journals Cardiovascular predictors associated with poor short-term prognosis in patients diagnosed with SARS-CoV-2 in Spain

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
L Esteban-Lucia ◽  
A Devesa-Arbiol ◽  
M A Zambrano Chacon ◽  
A M Venegas Rodriguez ◽  
M Gonzalez-Rodriguez ◽  
...  

Abstract Background On January 2020, the first patient with coronavirus 2 (SARS-CoV-2) was detected in Spain. Since then, 3 280 000 cases have been confirmed and 75.305 people have died. We aimed to clarify the epidemiological and clinical characteristics related with poor short-term prognosis in patients diagnosed with SARS-CoV-2. Methods Observational, retrospective single-center study including consecutive patients (≥40yo) diagnosed with SARS-CoV-2 through PCR, since March 2nd to 20th 2020 in our center in Spain. The primary endpoint (PE) was the combined of all-cause death or need for orotracheal intubation within the first 30 days of infection symptoms. Results 704 patients were included (table). A follow-up period of thirty-days was fully completed in 692 of 704 patients (98.3%). At the end of this period, 148 patients (21.4%) met the PE; they were older, more frequently male, obese and smokers. Patients who met the PE had a higher prevalence of hypertension, diabetes, dyslipidemia, ischemic heart disease, heart failure, peripheral and cerebrovascular disease, cancer and lung pathologies. They received more frequently therapies with renin-angiotensin system inhibitors, betablockers, calcium channel blockers and statins, as well as antiplatelet and anticoagulant therapies Multivariate analysis showed that age (OR 1.99 for every 10 years, 95% CI [1.637–2.4], p<0.001), female sex (OR 0.49, [0.30–0.80], p=0.004), diabetes (OR 2.09, [1.17–3.71], p=0.012), lung disease (OR 1.99, [1.14–3.44], p=0.014) and body mass index (OR 1.33 for each 5 kg/m2 increased, [1.05–1.68], p=0.017) were predictors of the PE. Hypertension was not significantly related to the PE (OR 1.55, [0.93–2.60], p=0.09) Conclusion In our group of patients with SARS-CoV-2, age, male sex, diabetes, lung disease and obesity were found to be independent predictors of the combined of all case death or need for orotracheal intubation within the first 30 days of infection symptoms. Larger studies are needed to confirm these results. FUNDunding Acknowledgement Type of funding sources: None. Description of studied population Odds-ratio and CI for the combined PE

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Edouard L Fu ◽  
Catherine M Clase ◽  
Marie Evans ◽  
Bengt Lindholm ◽  
Joris Rotmans ◽  
...  

Abstract Background and Aims There is a lack of data that could help to guide the choice of antihypertensive agents in patients with advanced chronic kidney disease (CKD). We evaluated whether initiating treatment with a renin-angiotensin system inhibitor (RASi) is superior to calcium channel blockers (CCB) in preventing mortality, major adverse cardiovascular events (MACE) or kidney replacement therapy (KRT) in patients with advanced CKD. Method Observational study from the Swedish Renal Register, 2007-2017. We identified all nephrologist-referred patients in Sweden who initiated RASi or CCB treatment and had non-dialysis dependent advanced CKD (eGFR <30 ml/min/1.73m2). The associations between RASi vs CCB initiation, mortality, MACE and KRT were assessed by Cox regression. Analyses were adjusted with propensity score weighting for a wide range of confounders, including demographics, blood pressure, laboratory measures, comorbidities and medications. As a positive control we evaluated new use of the same drugs in patients with CKD G3 (N = 2608; eGFR between 30-60 ml/min/1.73m2). Furthermore subgroup, as-treated and competing risk analyses were performed. Results The propensity-score weighted cohort included 2479 RASi and 2327 CCB initiators who were well-matched for baseline confounders (all standardized differences <0.1). Median follow-up was 4.1 years, with a maximum follow-up of over 10 years. Compared to CCB, initiation of RASi was associated with a similar risk of mortality (adjusted HR 0.94; 95% CI 0.85-1.03) and MACE (0.99; 0.87-1.13), but with a lower risk of KRT (0.87; 0.78-0.98). Results were consistent across subgroups, in as-treated analyses and after accounting for the competing risk of death. In the control cohort of patients with CKD G3, initiation of RASi (versus CCB) was associated with lower KRT risk (adjusted HR 0.67; 0.47-0.96), and similar risk of mortality (0.91; 0.76-1.08) and MACE (1.06; 0.82-1.35). Conclusion Compared with CCB, initiation of RASi in patients with advanced CKD was associated with a lower risk of KRT, but no different risk of mortality or MACE.


Perfusion ◽  
2021 ◽  
pp. 026765912199599
Author(s):  
Esther Dreier ◽  
Maximilian Valentin Malfertheiner ◽  
Thomas Dienemann ◽  
Christoph Fisser ◽  
Maik Foltan ◽  
...  

Background: The role of venovenous extracorporeal membrane oxygenation (VV ECMO) in patients with COVID-19-induced acute respiratory distress syndrome (ARDS) still remains unclear. Our aim was to investigate the clinical course and outcome of those patients and to identify factors associated with the need for prolonged ECMO therapy. Methods: A retrospective single-center study on patients with VV ECMO for COVID-19-associated ARDS was performed. Baseline characteristics, ventilatory and ECMO parameters, and laboratory and virological results were evaluated over time. Six months follow-up was assessed. Results: Eleven of 16 patients (68.8%) survived to 6 months follow-up with four patients requiring short-term (<28 days) and seven requiring prolonged (⩾28 days) ECMO support. Lung compliance before ECMO was higher in the prolonged than in the short-term group (28.1 (28.8–32.1) ml/cmH2O vs 18.7 (17.7–25.0) ml/cmH2O, p = 0.030). Mechanical ventilation before ECMO was longer (19 (16–23) days vs 5 (5–9) days, p = 0.002) and SOFA score was higher (12.0 (10.5–17.0) vs 10.0 (9.0–10.0), p = 0.002) in non-survivors compared to survivors. Low viral load during the first days on ECMO tended to indicate worse outcomes. Seroconversion against SARS-CoV-2 occurred in all patients, but did not affect outcome. Conclusions: VV ECMO support for COVID-19-induced ARDS is justified if initiated early and at an experienced ECMO center. Prolonged ECMO therapy might be required in those patients. Although no relevant predictive factors for the duration of ECMO support were found, the decision to stop therapy should not be made dependent of the length of ECMO treatment.


Molecules ◽  
2021 ◽  
Vol 26 (7) ◽  
pp. 1912
Author(s):  
Kaushik Chakravarty ◽  
Victor G. Antontsev ◽  
Maksim Khotimchenko ◽  
Nilesh Gupta ◽  
Aditya Jagarapu ◽  
...  

The COVID-19 pandemic has reached over 100 million worldwide. Due to the multi-targeted nature of the virus, it is clear that drugs providing anti-COVID-19 effects need to be developed at an accelerated rate, and a combinatorial approach may stand to be more successful than a single drug therapy. Among several targets and pathways that are under investigation, the renin-angiotensin system (RAS) and specifically angiotensin-converting enzyme (ACE), and Ca2+-mediated SARS-CoV-2 cellular entry and replication are noteworthy. A combination of ACE inhibitors and calcium channel blockers (CCBs), a critical line of therapy for pulmonary hypertension, has shown therapeutic relevance in COVID-19 when investigated independently. To that end, we conducted in silico modeling using BIOiSIM, an AI-integrated mechanistic modeling platform by utilizing known preclinical in vitro and in vivo datasets to accurately simulate systemic therapy disposition and site-of-action penetration of the CCBs and ACEi compounds to tissues implicated in COVID-19 pathogenesis.


2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Riya Job ◽  
Mohamed Abdul Qader ◽  
Pedro Torres ◽  
Baher AL Abbasi ◽  
Nakeya Dewaswala ◽  
...  

Lung India ◽  
2015 ◽  
Vol 32 (5) ◽  
pp. 486 ◽  
Author(s):  
Balamugesh Thangakunam ◽  
DevasahayamJesudas Christopher ◽  
Vikram Mathews ◽  
Alok Srivastava

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
L Kuzma ◽  
EJ Dabrowski ◽  
A Kurasz ◽  
M Swieczkowski ◽  
H Bachorzewska-Gajewska ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: None. Background The short-term effect of air pollution on cardiovascular mortality is well-documented but a scarce number of studies focus on cause-specific mortality in low-polluted areas. Purpose We decided to distinguish deaths due to cerebrovascular disease (CbVD) from a region widely known as the Green Lungs of Poland to assess the short-term effect of air pollution on CbVD mortality. Methods The analysis with almost 4,500,000 person-years of follow-up with a time-stratified case-crossover design was performed. Results are reported as odds ratio (OR) associated with an increase in interquartile range (IQR) of air pollution. Results In the overall analysis of the studied region PM2.5 had an impact on increased CbVD mortality at LAG 0 (OR 1.046, 95% CI 1.013 – 1.080, P = 0.006), LAG 0-1 (1.048, 1.002-1.082, P = 0.040), and LAG 0-3 (1.052, 1.015-1.090, P = 0.006). The influence of PM10 was noted at LAG 0 (1.041, 1.002-1.082, P = 0.040). CbVD mortality in Bialystok was increased by exposure to PM10 at LAG 0 (1.05, 1.00-1.09, P = 0.048) and CO at LAG 1 (1.07, 1.00-1.14, P = 0.04). Additionally, an effect of CO was observed in cold season at LAG 1 (1.09, 1.02-1.17, P = 0.02), LAG 0-1 (1.08, 1.00-1.016, P = 0.04), and LAG 0-3 (1.09, 1.01-1.18, P = 0.04). In Suwalki, an impact of PM2.5 was also observed. Conclusions A short-term increase in air pollutants concentrations, especially in PM2.5 and CO, had an influence on CbVD mortality. Mortality rates were significantly increased in cold season. We also found heterogeneity in the influence of major contributors on mortality between analyzed cities.


2017 ◽  
Vol 37 (3) ◽  
pp. 283-289 ◽  
Author(s):  
Htay Htay ◽  
Yeoungjee Cho ◽  
Elaine M. Pascoe ◽  
Darsy Darssan ◽  
Carmel Hawley ◽  
...  

ObjectivePreservation of residual renal function (RRF) is associated with improved survival. The aim of the present study was to identify independent predictors of RRF and urine volume (UV) in incident peritoneal dialysis (PD) patients.MethodsThe study included incident PD patients who were balANZ trial participants. The primary and secondary outcomes were RRF and UV, respectively. Both outcomes were analyzed using mixed effects linear regression with demographic data in the first model and PD-related parameters included in a second model.ResultsThe study included 161 patients (mean age 57.9 ± 14.1 years, 44% female, 33% diabetic, mean follow-up 19.5 ± 6.6 months). Residual renal function declined from 7.5 ± 2.9 mL/min/1.73 m2at baseline to 3.3 ± 2.8 mL/min/1.73 m2at 24 months. Better preservation of RRF was independently predicted by male gender, higher baseline RRF, higher time-varying systolic blood pressure (SBP), biocompatible (neutral pH, low glucose degradation product) PD solution, lower peritoneal ultrafiltration (UF) and lower dialysate glucose exposure. In particular, biocompatible solution resulted in 27% better RRF preservation. Each 1 L/day increase in UF was associated with 8% worse RRF preservation ( p = 0.007) and each 10 g/day increase in dialysate glucose exposure was associated with 4% worse RRF preservation ( p < 0.001). Residual renal function was not independently predicted by body mass index, diabetes mellitus, renin angiotensin system inhibitors, peritoneal solute transport rate, or PD modality. Similar results were observed for UV.ConclusionsCommon modifiable risk factors which were consistently associated with preserved RRF and residual UV were use of biocompatible PD solutions and achievement of higher SBP, lower peritoneal UF, and lower dialysate glucose exposure over time.


2018 ◽  
Vol 45 (5) ◽  
pp. 655-662 ◽  
Author(s):  
Cai Yue ◽  
Guanhong Li ◽  
Yubing Wen ◽  
Xuemei Li ◽  
Ruitong Gao

Objective.To investigate the renal protective effects of early renin-angiotensin-aldosterone system (RAAS) blockade with renin-angiotensin system inhibitors (RASI) in systemic lupus erythematosus (SLE) patients with antiphospholipid-associated nephropathy (aPLN).Methods.Medical data of 57 SLE patients with biopsy-proven aPLN were analyzed. Early RAAS blockade was defined as administration of RASI within 3 months after kidney biopsy and continued for ≥ 12 months.Results.There was no significant difference in demographic data, laboratory findings, and renal histology by the time of kidney biopsy, except that the RASI group had higher proteinuria levels vs the non-RASI group [5.2 (2.8–8.8) vs 1.9 (0.6–2.8) g/d, p = 0.005, respectively] and higher prevalence of hypertension (75% vs 29%, p = 0.001, respectively). No significant difference between the 2 groups was observed in estimated glomerular filtration rate (eGFR), mean arterial pressure, and proteinuria level at 12 months after kidney biopsy. The improvement ratio of eGFR at 12 months was significantly higher in the RASI group versus the non-RASI group [26% (−5 to 86) vs −2% (−20 to 20), p = 0.028, respectively], and the rate of change in eGFR beyond 12 months was similar between the 2 groups. During a mean followup of 80 months, 4 (23%) patients in the non-RASI group and 3 (8%) patients in the RASI group developed kidney disease progression. Early RAAS blockade significantly decreased the risk of kidney disease progression [HR = 0.11 (0.02–0.59); p = 0.010]. Proteinuria and hypertension controls were similar between the 2 groups.Conclusion.Early RAAS blockade improved the short-term and longterm renal outcomes in SLE patients with aPLN. The renal protective effect of RASI was independent of its antihypertensive and antiproteinuric effects.


2020 ◽  
Vol 217 (8) ◽  
Author(s):  
Betty Diamond

The renin–angiotensin system (RAS) has long been appreciated as a major regulator of blood pressure, but has more recently been recognized as a mechanism for modulating inflammation as well. While there has been concern in COVID-19 patients over the use of drugs that target this system, the RAS has not been explored fully as a druggable target. The abbreviated description of the RAS suggests that its dysregulation may be at the center of COVID-19.


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