Aims
The coronavirus disease‐2019 (COVID‐19) pandemic has changed the landscape of medical care delivery worldwide. We aimed to assess the influence of COVID‐19 pandemic on hospital admissions and in‐hospital mortality rate in patients with acute heart failure (AHF) in a retrospective, multicentre study.
Methods and results
From 1 January 2019 to 31 December 2020, a total of 101 433 patients were hospitalized in 24 Cardiology Departments in Poland. The number of patients admitted due to AHF decreased by 23.4% from 9853 in 2019 to 7546 in 2020 (
P
< 0.001). We noted a significant reduction of self‐referrals in the times of COVID‐19 pandemic accounting 27.8% (
P
< 0.001), with increased number of AHF patients brought by an ambulance by 15.9% (
P
< 0.001). The length of hospital stay was overall similar (7.7 ± 2.8 vs. 8.2 ± 3.7 days;
P
= not significant). The in‐hospital all‐cause mortality in AHF patients was 444 (5.2%) in 2019 vs. 406 (6.5%) in 2020 (
P
< 0.001). A total number of AHF patients with concomitant COVID‐19 was 239 (3.2% of AHF patients hospitalized in 2020). The rate of in‐hospital deaths in AHF patients with COVID‐19 was extremely high accounting 31.4%, reaching up to 44.1% in the peak of the pandemic in November 2020.
Conclusions
Our study indicates that the COVID‐19 pandemic led to (i) reduced hospital admissions for AHF; (ii) decreased number of self‐referred AHF patients and increased number of AHF patients brought by an ambulance; and (iii) increased in‐hospital mortality for AHF with very high mortality rate for concomitant AHF and COVID‐19.
Background:
Observational studies suggested that residual risk of cardiovascular events after LDL (low-density lipoprotein) cholesterol lowering may be linked to remnant cholesterol (RC). We conducted a large-scale Mendelian randomization study to investigate the causal role of RC to predict coronary artery disease (CAD), myocardial infarction (MI), and stroke risk.
Methods:
We extracted single-nucleotide polymorphisms for RC and LDL from large-scale genome-wide association databases. We estimated the genetic association with outcomes from the CARDIoGRAMplusC4D consortium (Coronary Artery Disease Genome-Wide Replication and Meta-Analysis Plus the Coronary Artery Disease Genetics), the Metastroke consortium, as well as the GLGC (Global Lipids Genetics Consortium). Genetic variants were used as instruments, thereby minimizing residual confounding and reverse causation biases of observational studies.
Results:
By leveraging data from a combined sample of 958 434 participants, we found evidence for a significant causal effect of RC on the risk of CAD (odds ratio [OR], 1.51 per SD unit increase in RC [95% CI, 1.42–1.60];
P
=5.3×10
-5
), MI (OR, 1.57 [95% CI, 1.21–2.05];
P
=9.5×10
-4
), and stroke (OR, 1.23 [95% CI, 1.12–1.35];
P
=3.72×10
-6
). There was no evidence of pleiotropy. The effect of RC on CAD and MI remained consistent after accounting for the effects of RC-associated genetic variants on LDL cholesterol: OR, 1.49 (95% CI, 1.37–1.61) for CAD and OR, 1.80 (95% CI, 1.70–19.1) for MI without a meaningful indirect effect exerted on these outcomes via the LDL cholesterol mediator. Lifelong genetic inhibition of RC led to a 40% MI relative risk reduction which is superior to any intensity of pharmacological reduction from clinical trials with an average 3.5 years follow-up.
Conclusions:
This large-scale Mendelian randomization study showed a robust genetic causal association between RC and cardiovascular outcomes. The effect on CAD and MI is independent of LDL cholesterol. Early screening for RC along with long-term inhibition of RC should be the focus of future therapeutic interventions.
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