Neuronal damage and abnormal contraction: Is the circle of synchronicity complete?
Received Dec
Neuronal damage and abnormal contraction: Is the circle of synchronicity complete?
Claudio Marcassa 0
0 Reprint requests: Claudio Marcassa, MD, Cardiology Department, Maugeri Clinical and Scientific Institutes, IRCCS, Scientific Institute of Veruno , Via Per Revislate 13, 28010, Veruno, NO , Italy; J Nucl Cardiol 1071-3581/$34.00 Copyright 2018 American Society of Nuclear Cardiology
1 Cardiology Department, Maugeri Clinical and Scientific Institutes, IRCCS, Scientific Institute of Veruno , Veruno, NO , Italy
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Asynchronous cardiac contraction is considered one
of the substrates of heart failure. Myocardial ischemia,
fibrosis, or conduction disturbances are the pieces of a
complex puzzle that lead to a regional delayed
contraction and ultimately to an asynchronous
intraventricular contraction. Since early ‘80s, it is known
that the amount of asynchrony is significantly and
inversely correlated to the global left ventricular (LV)
systolic function.1
Several imaging techniques are currently available
to evaluate and quantify the presence of inter- and
intraventricular asynchronous contraction.
Echocardiography (M-mode, 2D, Tissue Doppler Imaging, strain,
strain rate, tissue tracking, and three-dimensional
imaging) is an imaging modality widely available to
cardiologists for the assessment of asynchrony.
However, most of the proposed methods are limited by the
use of a single imaging plane and the operator
dependency, which affects the reproducibility of the
measurements obtained, particularly those related to the
intraventricular asynchrony. In addition, it is still
unclear which parameters may actually allow the
accurate identification of responders to resynchronization
therapy.2
Concerning the correlation between surface 12-lead
ECG and mechanical asynchrony, it was documented by
radionuclide ventriculography that intra- and
interventricular asynchrony are well correlated with the
amount of QRS widening or the LV ejection fraction
value.3
At the end of the last millennium, it was observed
that a decrease of sympathetic tone to the heart resulted
in an asynchronous wall motion pattern and an impaired
LV relaxation;4 a close correlation between LV
dyssynchrony and impaired myocardial sympathetic
tone has been then hypothesized. In a group of 83
patients undergoing an evaluation of LV perfusion and
sympathetic innervation on
99mTc-tetrofosmin/123Imetaiodobenzylguanidine (123I-MIBG) imaging, it was
documented that patients with LV dyssynchrony showed
an elevated burden of ‘‘innervation/perfusion’’
mismatch that is concentrated at the level of the most
dyssynchronous walls.5 Moreover, the extent of regional
innervation/perfusion mismatch was also an independent
predictor of LV diastolic abnormalities.6
On the other side, in patients with dual-chamber
pacemaker it was observed that stimulation from the
apex of the right ventricle is responsible for regional
alteration of the adrenergic innervation of the left
ventricular myocardium, as assessed by I(123)-MIBG
activity.7
Magnetic resonance imaging (MRI) has also been
used to assess ventricular asynchrony and its response to
pacing therapy.8,9 In patients with non-ischemic heart
failure, spatial dyssynchrony, as assessed by
cross-correlation analysis of time curves of myocardial
circumferential strains delivered from cine-tagging MRI
images, was correlated with an impairment of cardiac
sympathetic activity.10 MRI, however, is affected by
limited availability, the technique is time consuming,
and several patients cannot be studied (i.e., those with
ICD-CRT devices, in particular before and after
implantation).
In this issue of the Journal, Cruz et al., in a group of
81 patients with heart failure and reduced LV ejection
fraction submitted to cardiac resynchronization therapy
(CRT), tested the hypothesis that regional myocardial
contractility is linked to the integrity of local autonomic
innervation; this would allow an indirect estimation of
cardiac autonomic dysfunction.11 They used the
longitudinal strain as determined by speckle tracking in 2D
echocardiography as a surrogate for cardiac autonomic
dysfunction. Cruz et al. documented a statistically
significant correlation between strain and
heart/mediastinum ratio with MIBG both at baseline and
6 months after CRT. Echocardiography, obviously, is
the imaging modality cardiologists are more confident
with, and is easily available. However, the best method
and index for the assessment of LV asynchrony with
echocardiography is still to be defined. Nuclear
cardiology techniques, however, offer the possibility to
quantify LV asynchrony from gated SPECT perfusion or
blood pool images by phase analysis software in an
almost automatic and highly reproducible way.
Moreover, with myocardial perfusion gated SPECT images an
integration of perfusion, function, and asynchrony is
obtained in a single study. Nevertheless, in this
manuscript Cruz et al. reversed the point of view, estimating
the neuronal damag (...truncated)