William M. Feinberg Award for Excellence in Clinical Stroke

■ PAST RECIPIENTS
2012 Jeffrey L. Saver
2011 Stephen Davis
2010 Markku Kaste
2009 Larry B. Goldstein
2008 S. Claiborne Johnston
2007 Geoffrey Donnan
2006 Ralph L. Sacco
2005 John R. Marler
2004 Philip B. Gorelick
2003 Joseph P. Broderick
2002 Julien Bogousslavsky
2001 J. Donald Easton
2000 Anthony J. Furlan
1999 James C. Grotta
1998 Werner Hacke
1997 Thomas Brott
1996 J. P. Mohr
1995 Not Awarded
1994 David G. Sherman
1993 Harold P. Adams Jr.
1992 Philip A. Wolf
© 2013 American Heart Association.
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Dallas, Texas 75231-4596
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William M. Feinberg
Award for Excellence
in Clinical Stroke
Marc I. Chimowitz, MBChB
Medical University of South Carolina
Charleston, SC

■ WILLIAM M. FEINBERG AWARD FOR
EXCELLENCE IN CLINICAL STROKE
Marc I. Chimowitz, MBChB
Dr. Chimowitz grew up in Zimbabwe and
went to medical school at the University of
Cape Town in South Africa. After moving
to the United States, he completed a
Neurology residency at Tufts — New
England Medical Center and a Stroke
fellowship at the Cleveland Clinic. He has
had faculty positions at the University
of Michigan and Emory University, and
is currently Professor of Neurology and Associate Dean of Faculty
Development at the Medical University of South Carolina in Charleston.
His main career interests are in improving treatments for patients with
intracranial arterial atherosclerotic stenosis and helping to mentor the
next generation of clinical and translational scientists. He has led three
large consecutive NIH / NINDS funded multicenter clinical studies over
the past 15 years (the WASID trial, the NIH Wingspan Stent registry,
and the Stenting and Aggressive Medical Management for Preventing
Recurrent stroke in Intracranial Stenosis [SAMMPRIS] trial), which
have led to new standards of care for the treatment of atherosclerotic
intracranial arterial stenosis. Additionally, he has extensive experience
with mentoring trainees and junior faculty and has been the recipient of
a NIH K24 award for this purpose. He is on the editorial boards for the
journals Stroke and Neurosurgery.
■ TREATMENT OF INTRACRANIAL ATHEROSCLEROSIS:
LEARNING FROM THE PAST AND PLANNING FOR
THE FUTURE
Intracranial atherosclerosis is one of the most common causes of
stroke world-wide and is associated with a particularly high risk of
recurrent stroke. Over the past decade, new therapeutic strategies
have emerged for treating this high-risk disease. These include dual
antiplatelet treatment, intensive management of risk factors, and
endovascular therapy.
The early results of the SAMMPRIS trial showed that aggressive
medical management (aspirin and clopidogrel for 90 days followed
by aspirin alone, intensive management of risk factors, and a
lifestyle program) is superior to angioplasty and stenting with the
Wingspan stent system because of the high risk of early stroke
after stenting and lower than expected risk of stroke on aggressive
medical therapy. While the current SAMMPRIS results suggest a
much lower rate of the primary endpoint (any stroke or death within
30 days of enrollment or stroke in the territory beyond 30 days) in
patients treated with aggressive medical management compared
with similar patients treated with usual medical management in the
WASID trial (12.2% at 1 year in SAMMPRIS vs. 25% at 1 year in
WASID), the 1-year stroke rate in SAMMPRIS suggests that there
are still subgroups of patients who are at very high risk of stroke
despite aggressive medical therapy.
To improve the treatment and outcome for these high-risk patients,
further research is needed to identify these patients reliably and to
develop more effective treatments. The mechanisms of stroke in
these high-risk patients include hypoperfusion, distal embolism,
and local branch or perforator occlusive disease. Non-invasive
vascular imaging that could identify patients with impaired distal
perfusion include fractional flow on MRA, quantitative MRA,
and MR and CT perfusion, whereas high resolution MRI could
identify patients with atherosclerotic plaque features (intraplaque
hemorrhage, large lipid core, ruptured fibrous cap) that may
increase the risk of distal embolism or local branch and perforator
occlusion. Depending on the targeted mechanism of stroke,
preventive therapies that may be considered for future clinical trials
include angioplasty alone, indirect revascularization techniques,
such as encephaloduroarteriosynangiosis, upper limb ischemic
preconditioning, PCSK9 inhibitors, and direct thrombin or Xa
inhibitors.