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Low leptin plasma levels are associated with progression of coronary atherosclerosis in patients with stable coronary artery disease from the SMARTool Study

Session Poster Session 7

Speaker Chiara Caselli

Event : ESC Congress 2019

  • Topic : imaging
  • Sub-topic : Computed Tomography: Plaque Imaging
  • Session type : Poster Session

Authors : C Caselli (Pisa,IT), S Rocchiccioli (Pisa,IT), A Rosendael (Leiden,NL), R Buechel (Zurich,CH), A Teresinska (Warsaw,PL), MN Pizzi (Barcelona,ES), JM Smith (Leiden,NL), R Poddighe (Lido Di Camaiore,IT), J Campolo (Milan,IT), F Vozzi (Pisa,IT), J Knuuti (Turku,FI), G Pelosi (Pisa,IT), O Parodi (Pisa,IT), A Scholte (Leiden,NL), D Neglia (Pisa,IT)

Authors:
C Caselli1 , S Rocchiccioli1 , A Rosendael2 , R Buechel3 , A Teresinska4 , MN Pizzi5 , JM Smith2 , R Poddighe6 , J Campolo7 , F Vozzi1 , J Knuuti8 , G Pelosi1 , O Parodi1 , A Scholte2 , D Neglia9 , 1Institute of Clinical Physiology (IFC) - Pisa - Italy , 2Leiden University Medical Centre - Leiden - Netherlands (The) , 3University of Zurich - Zurich - Switzerland , 4Institute of Cardiology - Warsaw - Poland , 5University Hospital Vall d'Hebron - Barcelona - Spain , 6Versilia Hospital - Lido Di Camaiore - Italy , 7CNR Institute of Clinical Physiology - Milan - Italy , 8University of Turku - Turku - Finland , 9Fondazione Toscana Gabriele Monasterio - Pisa - Italy ,

On behalf: SMARTool study

Citation:

Background. Leptin is an adipokine involved in energy homeostasis and has been related with established vascular risk factors. However, studies on the association of leptin plasma levels with coronary artery disease (CAD) have yielded conflicting results.

Purpose. Aim of the present study was to evaluate the association between leptin plasma levels and presence, severity and progression of coronary atherosclerosis in patients with suspected stable CAD.

Methods. In a cohort of 257 patients with symptoms of stable CAD enrolled in the SMARTool study, coronary computed tomography angiography (CTA), plasma leptin levels and clinical and bio-humoral CAD risk profile (including glucose, lipid and inflammation variables) were obtained at enrolment and after 6±1yrs of follow-up. Sixty-four patients were revascularized and the remaining 193 represent the population for the present study. CTA findings were categorised as no-minimal CAD (<30% stenosis), non-obstructive CAD (30%-50% stenosis) and obstructive CAD (=50% stenosis in at least one major coronary vessel).  A CTA risk score (based on plaque extent, severity, composition, and location) was calculated at baseline and at follow-up to assess coronary atherosclerotic burden and its progression (? CTA score=5).

Results. CTA findings showed obstructive CAD in 11% of patients at baseline and in 15% at follow-up (p<0.0001). CTA risk score, was 8.03±7.80 at baseline and increased to 10.33±8.17 at follow-up (p<0.0001) with CAD progression in 20% of patients. Leptin plasma levels were inversely related with CTA findings both at baseline and follow-up (Figure). In a Cox model, baseline plasma leptin was an independent predictor of CAD progression, after adjustment for clinical risk factors, biomarkers, and treatment (HR 0.572, 95%CI 0.393-0.834, P=0.0037).

Conclusion. Plasma leptin is inversely associated with coronary atherosclerotic burden and disease progression in patients with stable CAD. This association is independent of known factors affecting leptin levels. These results could prompt further investigations on the pathophysiological mechanisms of this association.

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