ORIGINAL ARTICLE
Heart Vessels (2003) 18:136–141 © Springer-Verlag 2003
DOI 10.1007/s00380-003-0697-9
Nobuyuki Ohte · Che-Ping Cheng · William C. Little
Tachycardia exacerbates abnormal left ventricular–arterial coupling in
heart failure
Received: October 26, 2002 / Accepted: March 7, 2003
N. Ohte (*)
1
· C.-P. Cheng · W.C. Little
Cardiology Section, Wake Forest University School of Medicine,
Winston-Salem, NC, USA
Present address:
1
Department of Internal Medicine and Pathophysiology, Nagoya City
University Graduate School of Medical Sciences, Mizuho-cho,
Mizuho-ku, Nagoya 467-8601, Japan
Tel. +81-52-853-8221; Fax +81-52-852-3796
e-mail: ohte@med.nagoya-cu.ac.jp
Abstract The purpose of this study was to assess the effect
of heart rate on left ventricular (LV)–arterial coupling and
LV mechanical efficiency before and after heart failure
(CHF). The production of LV stroke work (SW) and me-
chanical efficiency depends on the coupling of the LV and
arterial system. The response of LV–arterial coupling to
tachycardia may be altered in heart failure. We compared
the response of LV–arterial coupling to increased heart rate
(HR) in six conscious, instrumented dogs before and after
pacing-induced CHF. Coupling was quantified as E
ES
/E
A
,
where E
ES
is the slope of end-systolic pressure (P)–volume
(V) relation, and E
A
is arterial elastance. Mechanical
efficiency was determined as the ratio of SW to a total P–V
area (PVA). Before CHF, E
ES
and E
A
increased similarly
with increased heart rate to 180 min
-1
. Thus, E
ES
/E
A
re-
mained unaltered (0.96 0.08 vs 0.94 0.35), and SW/PVA
was unchanged (0.62 0.03 vs 0.59 0.06). Compared with
the results prior to CHF and after CHF the resting E
ES
was
decreased, thus both E
ES
/E
A
(0.58 0.09) and SW/PVA
(0.48 0.06) were less (P 0.05) than baseline. After CHF,
an increase in HR to 180 min
-1
increased E
A
but not E
ES
,
thus E
ES
/E
A
fell to 0.44 0.06 (P 0.05) and SW/PVA fell
to 0.41 0.05 (P 0.05). Under normal conditions, LV–
arterial coupling remains optimal during increases in HR.
After CHF, tachycardia exacerbates the suboptimal
baseline LV–arterial coupling, reducing the efficiency of
producing SW.
Key words Conscious dog · Congestive heart failure ·
Force–frequency relation · Left ventricular–arterial
coupling
Introduction
The performance of the cardiovascular system depends on
the interaction of its components. The left ventricle (LV)
pumps the stroke volume (SV) into the arterial system that
delivers the flow to the tissues. Thus, optimal cardiovascular
function requires appropriate coupling of the LV and the
arterial system. Functional analysis of this interaction
requires that the LV and arterial system be described in
similar terms.
1
Sunagawa et al.
2
and Burkhoff and Sagawa
3
proposed
that LV–arterial coupling could be analyzed in the
pressure–volume (P–V) plane. The intersection of the LV
end-systolic pressure (P
ES
)–volume (V
ES
) relation and the
arterial P
ES
–SV relation determines the SV. The slope of
the P
ES
–V
ES
relation is the end-systolic elastance (E
ES
) of
the LV, whereas the slope of the arterial P
ES
–SV relation
represents the effective arterial end-systolic elastance (E
A
).
If the ejection portion of the LV P–V loop is assumed to be
flat and the end-diastolic pressure is negligible, this analysis
predicts that stroke work (SW) should be maximized
when E
A
equals E
ES
.
2,4,5
The efficiency of producing SW
is predicted to decline as E
ES
/E
A
is reduced. Despite the
limitations of the required simplifying assumptions, these
predictions are correct in conscious animals. Furthermore,
at rest, the LV and arterial system operate close to this
point that produces optimal SW.
6
Furthermore, SW is within 95% of its maximum value
when E
ES
/E
A
is between 0.9 and 1.3. During exercise in
normal animals, the E
ES
/E
A
ratio remains in this range, indi-
cating that the LV and arterial system are nearly optimally
coupled to produce SW, both at rest and during exercise.
6,7
We hypothesized that heart failure (CHF) should ad-
versely alter LV–arterial coupling as E
ES
is reduced and E
A
may be increased, thus reducing E
ES
/E
A
to below 0.9 where
SW rapidly declines with decreasing E
ES
/E
A
. Normally, E
ES
increases with higher heart rates,
8
which would be expected
to match the increase in E
A
. This manifestation of the
force–frequency response is lost in CHF due to changes
in sarcoplasmic reticular calcium handling.
9,10
In addition,