Field:

  • Cardiology

Location: Ochsner Clinical School

Type of student:

  • PGY1 
  • PGY2 

Type of work:

  • Chart reviews 
  • Clinical work 
  • Qualitative methods 
  • Secondary data analysis

Brief synopsis:

As a busy vascular surgeon, the most effective way I have found to make meaningful and innovative academic contributions is to form solid collaborations. I first met my long-standing collaborator, T Cooper Woods, when we were co-investigators on the LSUHSC NIH CoBRE cardiovascular grant. Since then, we have been studying the molecular changes associated with carotid atherosclerotic plaque vulnerability. We have obtained several competitive grants and have reported our work in StrokeCirculation: Cardiovascular GeneticsProstaglandins, and Leukotrienes and Essential Fatty Acids.  Our work is the basis of a current NIH RO1 grant we are currently preparing.

We utilize a translational model based on a carotid biobank I established in 2010 alongside a clinical collaboration with the Section of Vascular Neurology/Stroke at the Ochsner Clinic. The biobank has to date > 260 samples of carotid plaques and sera from patients undergoing carotid endarterectomy for asymptomatic carotid disease (stable phenotype), as well as from patients with an acute stroke (unstable phenotype; mean time to intervention of 2.4 days). This gives us a unique view into the events occurring shortly after plaque rupture for which there is no reliable animal model. This translational model has allowed us to focus on how non-coding RNAs influence vascular smooth muscle cell volume loss in unstable plaques, and we recently demonstrated that an acute loss of miR-221/miR-222 and an increase in p27Kip1 mRNA expression occurs in the plaque shoulder, suggesting a new venue of plaque instability. Along with a lipidomics expert, we have also shown decreased intraplaque and sera content of the cardioprotective omega-3 fatty acids DHA, EPA, and resolvins, and these findings are the focus of ongoing larger scale lipidomic studies. This work aims to fill major gaps in our understanding of the events leading to intimal disruption (plaque rupture) and atheroemboli, resulting in stroke in the carotid territory and myocardial infarction in the coronary.

The collaboration with stroke/neurology has also allowed us to address important clinical questions about acute stroke management in the patient with carotid disease that are helping to evolve clinical practice. This clinical research has been presented and published (Journal of Vascular Surgery) detailing how a collaboration between vascular surgery and neurology aids in the acute management of patients presenting with acute carotid disease. For example, such patients are at risk of a recurrent stroke after an initial TIA or stroke – up to 14% within 10 days.  By assessing the neurologic outcomes of these patients, using the modified Rankin scale and quantifying stroke severity using the National Institutes of Health Stroke Severity (NIHSS) score, we have been able to identify the safety of an urgent carotid intervention in patient who present with minor to moderate strokes.  We have described 1) the benefits (i.e. lower recurrent stroke risk) and have been able to identify patient-specific factors that are associated with poor outcomes (i.e. large stroke, NIHSS > 10; < 48 hour to intervention, poor ischemic penumbra on brain perfusion imaging), 2) optimal timing to intervene after an acute stroke to prevent post-procedure complications, including cerebral hemorrhage and 3) have demonstrated how use penumbra imaging aids in optimal patient selection. Lastly, our work has also demonstrated the safety of urgent carotid interventions for patients receiving thrombolysis after an acute stroke so that they are no longer definitive carotid treatment. Our work has been corroborated by other groups around the world and, together, this has evolved clinical practice and the approach of the patient presenting with acute carotid disease.  

Supervisor