JACC: HEART FAILURE
VOL. 3, NO. 9, 2015
ª 2015 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION
ISSN 2213-1779/$36.00
PUBLISHED BY ELSEVIER INC.
http://dx.doi.org/10.1016/j.jchf.2015.07.001
EDITORIAL COMMENT
Changing the Carburetor Without Changing the Plugs The Intersection of Stock Car Racing With Mechanically Assisted Circulation* Joseph G. Rogers, MD
T
his Editorial Comment is dedicated to those
survival and symptoms in Stage D heart failure
“who think the last four words of the national
with reduced ejection fraction (HFrEF) coupled
anthem are ‘Gentlemen, start your engines’”
with a shortage of suitable donors and a growing
(Jeff Foxworthy) (1).
heart failure population has fueled exponential
Summer in the South is filled with sweltering
growth in left ventricular assist device (LVAD) im-
heat, the sweet smell of magnolias, lazy summer
plantation (2). Registry and clinical trial data have
weekends, and afternoons at the racetrack watching
demonstrated
well-tuned automobiles run at breakneck speeds in
support live longer, with better quality of life and
such proximity that a driver with an extended arm
submaximal exercise performance, when treated
could easily touch an adjacent car. Although many
with LVAD than would be predicted with ongoing
that
patients
requiring
inotropic
view stock car racing as a testosterone-infused,
medical therapy (2,3). Contemporary LVADs have
estrogen-tolerated
of
a rotary design that moves blood continuously
men who attempt to relive youthful aspiration, I
through the pump and typically empty the left
have developed a deep appreciation for the complex
ventricle
man–machine interplay that results in winning a
opening. As a result, pulse pressure is minimized
race.
The
sport
competitive
composed
advantage
primarily
in
stock
sufficiently
to
minimize
aortic
valve
car
and often undetectable using noninvasive tech-
racing goes to the team that most effectively in-
niques. However, despite near normalization of
tegrates a skilled driver, the best car setup, fuel
central hemodynamics with LVAD, exercise perfor-
strategy, teamwork in the pits, and subtle engine
mance does not return to the level of healthy,
nuances that provide a little more speed than
age-matched controls, and continuous flow (CF)
the competition. It is only in the optimization of
LVAD patients have a persistent risk of vascular
these components that the car achieves maximal
adverse events, including mucosal bleeding and
performance.
stroke, suggesting lingering abnormalities in vas-
Over the past decade, mechanically assisted cir-
cular regulation.
culation has earned an accepted position in the
SEE PAGE 703
treatment of advanced heart failure. The limitations of medical and electrical therapies to improve
In this issue of JACC: Heart Failure, Witman et al. (4) provide important insights into the importance of reduced pulse pressure and potential mechanisms that explain the disconnect among improved cen-
*Editorials published in JACC: Heart Failure reflect the views of the authors and do not necessarily represent the views of JACC: Heart Failure or the American College of Cardiology. From the Division of Cardiology, Duke University School of Medicine,
tral
hemodynamics,
suboptimal
functional
im-
provements, and vascular complications in CFLVAD patients. The authors used flow-mediated vasodi-
Durham, North Carolina. Dr. Rogers has reported that he has no re-
lation to evaluate peripheral vascular function in
lationships relevant to the contents of this paper to disclose.
68 subjects distributed across 4 distinct cohorts:
Rogers
JACC: HEART FAILURE VOL. 3, NO. 9, 2015 SEPTEMBER 2015:712–4
Peripheral Vascular Changes in Continuous Flow LVADs
normal controls, New York Heart Association func-
complication
tional class II HFrEF, New York Heart Association
that has been linked to systemic hypertension with
associated
with
CFLVAD
support
functional class III to IV HFrEF, and patients on a
mean arterial blood pressure >90 mm Hg, a level
CFLVAD. They hypothesize that pulsatility would
that would not typically be concerning in non-VAD
decreases across the heart failure continuum with
patients (5). Loss of appropriate cerebral vaso-
the lowest detectable pulsatility in the CFLVAD
regulation may also be implicated in hemorrhagic
cohort and that pulsatility reduction would be
stroke.
correlated with progressively abnormal vascular
This study has a few noteworthy limitations.
physiology. This interesting model addresses the role
First, study patients had a burden of comorbid
of pulse pressure in vascular health and has the
conditions, including hypertension, hyperglycemia,
potential to provide insights about residual func-
and hyperlipidemia, that predispose to atheroscle-
tional limitations and vascular complications asso-
rosis and abnormal vasoregulation. Second, and
ciated with current LVAD technology.
perhaps more important, patients were maintained
The control group was selected to have no
on prescribed medications at the time of the study,
known cardiovascular disease and was not taking
including
prescription medications. The majority of HFrEF
the vasoregulated response. Third, there is an
patients had underlying ischemic heart disease,
assumption
severe ventricular dysfunction, and were more likely
normal central hemodynamics at the time of this
to have abnormal glycemic control. The patient
study, although this was not proven in the con-
groups had lower mean cholesterol values, although
text of this trial. Finally, there is no definitive
nearly 70% were taking a statin at the time of the
linkage of altered vascular response to clinical
flow
events or exercise performance in this patient
velocity, and shear rates were similar across the
cohort, leaving only inference about the clinical
study cohorts. A progressive decline in pulsatility
implications.
study.
Baseline
brachial
artery
diameter,
medications that
that
may
device-supported
have
altered
patients
had
Winning at the race track is in many ways similar
was observed in the heart failure patients (control > HFrEF II > HFrEF III-IV > CFLVAD). The proto-
to
typical vasodilatory response to transient arterial
assisted circulation. Success is a highly dependent
occlusion was progressively attenuated as heart
on a complex interplay of factors, some of which
failure advanced and was most abnormal in the
can be controlled and others that cannot. It requires
CFLVAD cohort. The investigators also demonstrate
integration of man and machine, a constant reas-
that the extent of normal vasodilatory response to
sessment of components, and new approaches to
arterial occlusion was dependent on the degree
old challenges. We have reached a point in me-
of pulsatility.
chanically
achieving
clinical
assisted
benefit
circulation
with
mechanically
where
the
new
This study has several intriguing implications.
devices reliably pump blood for prolonged periods
Peripheral vascular adaptations to heart failure may
of time. We are left with the onerous task of un-
plausibly
exercise
derstanding the impact of minimally pulsatile flow
response, muscle metabolism, and end-organ func-
on long-term outcomes, particularly those affecting
tion. Leveraging the novel circulatory characteris-
the vasculature. Junior Johnson, one of the more
be
implicated
in
abnormal
tics of CFLVADs and creating a human model
famous stock car racers in history, once said, “If
of progressive pulse pressure reduction, the in-
you ain’t cheatin,’ you ain’t tryin’ ” (6). In fact,
vestigators of this study have identified pulse
Mr. Johnson was notorious for making minor illegal
pressure as an important mediator of vascular
alterations in his car so the inspectors would stop
dysfunction in chronic heart failure. In addition,
looking and not find the more egregious changes.
perhaps a portion of the observed vascular adverse
Similarly, we need to search for subtle and overt
events that occur in CFLVAD patients are related
biological and physiological changes associated with
to alterations in normal vasoregulation. For ex-
CFLVAD that might serve as targets to minimize
ample, mucosal arteriovenous malformations are
risk
a common cause of post-operative bleeding in
performance.
and
assist
supported
patients
reach
peak
CFLVAD patients, and it has been postulated that chronic mucosal ischemia plays a role. It is plau-
REPRINT REQUESTS AND CORRESPONDENCE: Dr.
sible that abnormal vasoregulation of splanchnic
Joseph G. Rogers, Duke University School of Medi-
resistance arterioles plays a role in that phenome-
cine, Box 3034 DUMC, Durham, North Carolina 27710.
non. Hemorrhagic stroke is a devastating vascular
E-mail:
[email protected].
713
714
Rogers
JACC: HEART FAILURE VOL. 3, NO. 9, 2015 SEPTEMBER 2015:712–4
Peripheral Vascular Changes in Continuous Flow LVADs
REFERENCES 1. Foxworthy J. Available at: www.jefffoxworthy. com. Accessed July 2015.
advanced heart failure patients. J Am Coll Cardiol 2010;55:1826–34.
2. Kirklin JK, Naftel DC, Pagani FD, et al. Sixth INTERMACS annual report: a 10,000-patient database. J Heart Lung Transplant 2014;33: 555–64.
4. Witman MAH, Garten RS, Gifford JR, et al. Further peripheral vascular dysfunction in heart failure patients with a continuous-flow left ventricular assist device: the role of pulsatility. J Am Coll Cardiol HF 2015;3:703–11.
3. Rogers JG, Aaronson KD, Boyle AJ, et al. Continuous flow left ventricular assist device improves functional capacity and quality of life of
5. Teuteberg JJ, Slaughter MS, Rogers JG, et al. The HVAD left ventricular assist device: risk
factors for neurologic events and preventative mitigation strategies. J Am Coll Cardiol HF 2015. in press. 6. Johnson J. Bleacher Report. Available at: www. bleacherreport.com. Accessed July 2015.
KEY WORDS endothelial function, heart failure, mechanically assisted circulation