PMID- 37705370
OWN - NLM
STAT- Publisher
LR  - 20230914
IS  - 2724-5772 (Electronic)
IS  - 2724-5683 (Linking)
DP  - 2023 Sep 13
TI  - IL-1 blockade in cardiovascular disease: an appraisal of the evidence across 
      different inflammatory paradigms.
LID - 10.23736/S2724-5683.23.06390-1 [doi]
AB  - Pre-clinical and clinical studies suggest a role for inflammation in the 
      pathophysiology of cardiovascular (CV) diseases. The NLRP3 (NACHT, leucine-rich 
      repeat, and pyrin domain-containing protein 3) inflammasome is activated during 
      tissue injury and releases interleukin-1beta (IL-1beta). We describe three paradigms in 
      which the NLRP3 inflammasome and IL-1beta contribute to CV diseases. During acute 
      myocardial infarction (AMI), necrotic cell debris, including IL-1alpha, induce NLRP3 
      inflammasome activation and further damage the myocardium contributing to heart 
      failure (HF) (acute injury paradigm). In chronic HF, IL-1beta is induced by 
      persistent myocardial overload and injury, neurohumoral activation and systemic 
      comorbidities favoring infiltration and activation of immune cells into the 
      myocardium, microvascular inflammation, and a pro-fibrotic response (chronic 
      inflammation paradigm). In recurrent pericarditis, an autoinflammatory response 
      triggered by cell injury and maintained by the NLRP3 inflammasome/IL-1beta axis is 
      present (autoinflammatory disease paradigm). Anakinra, recombinant IL-1 receptor 
      antagonist, inhibits the acute inflammatory response in patients with ST 
      elevation myocardial infarction (STEMI) and acute HF. Canakinumab, IL-1beta 
      antibody, blunts systemic inflammation and prevents complications of 
      atherosclerosis in stable patients with prior AMI. In chronic HF, anakinra 
      reduces systemic inflammation and improves cardiorespiratory fitness. In 
      recurrent pericarditis, anakinra and rilonacept, a soluble IL-1 receptor chimeric 
      fusion protein blocking IL-1alpha and IL-1beta, treat and prevent acute flares. In 
      conclusion, the NLRP3 inflammasome and IL-1 contribute to the pathophysiology of 
      CV diseases, and IL-1 blockade is beneficial with different roles in the acute 
      injury, chronic inflammation and autoinflammatory disease paradigms. Further 
      research is needed to guide the optimal use of IL-1 blockers in clinical 
      practice.
FAU - Bonaventura, Aldo
AU  - Bonaventura A
AD  - Division of Internal Medicine, Medical Center, Ospedale di Circolo & 
      Fondazione Macchi, ASST Sette Laghi, Varese, Italy - 
      aldo.bonaventura@asst-settelaghi.it.
FAU - Moroni, Francesco
AU  - Moroni F
AD  - Heart and Vascular Center, Division of Cardiology, Berne Cardiovascular Research 
      Center, School of Medicine, University of Virginia, Charlottesville, VA, USA.
FAU - Golino, Michele
AU  - Golino M
AD  - Department of Medicine and Surgery, University of Insubria, Varese, Italy.
AD  - VCU Health Pauley Heart Center, Virginia Commonwealth University, Richmond, VA, 
      USA.
FAU - Del Buono, Marco G
AU  - Del Buono MG
AD  - Department of Cardiovascular and Thoracic Sciences, IRCCS A. Gemelli University 
      Polyclinic Foundation, Sacred Heart Catholic University, Rome, Italy.
FAU - Vecchie, Alessandra
AU  - Vecchie A
AD  - Division of Internal Medicine, Medical Center, Ospedale di Circolo & 
      Fondazione Macchi, ASST Sette Laghi, Varese, Italy.
FAU - Potere, Nicola
AU  - Potere N
AD  - Department of Medicine and Ageing Sciences, "G. D'Annunzio" University, 
      Chieti, Italy.
FAU - Abbate, Antonio
AU  - Abbate A
AD  - Heart and Vascular Center, Division of Cardiology, Berne Cardiovascular Research 
      Center, School of Medicine, University of Virginia, Charlottesville, VA, USA.
LA  - eng
PT  - Journal Article
DEP - 20230913
PL  - Italy
TA  - Minerva Cardiol Angiol
JT  - Minerva cardiology and angiology
JID - 101776555
SB  - IM
EDAT- 2023/09/14 06:43
MHDA- 2023/09/14 06:43
CRDT- 2023/09/14 02:47
PHST- 2023/09/14 06:43 [medline]
PHST- 2023/09/14 06:43 [pubmed]
PHST- 2023/09/14 02:47 [entrez]
AID - S2724-5683.23.06390-1 [pii]
AID - 10.23736/S2724-5683.23.06390-1 [doi]
PST - aheadofprint
SO  - Minerva Cardiol Angiol. 2023 Sep 13. doi: 10.23736/S2724-5683.23.06390-1.