Medical Hypotheses 135 (2020) 109484

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Medical Hypotheses
journal homepage: www.elsevier.com/locate/mehy

Spatial velocity of the dynamic vectorcardiographic loop provides crucial T

insight in ventricular dysfunction
⁎
Sukanti Bhattacharyyab, Damodar Prasad Goswamic, Arnab Senguptaa,
a
Dept. of Physiology, ICARE Institute of Medical Sciences and Research, Haldia, 721 645 Haldia, Purba Medinipur, WB, India
b
Dept. of Mathematics, Netaji Subhash Engineering College, Panchpota, Garia, Kolkata 700152, West Bengal, India
c
Dept. of Physiology, Calcutta Medical College, 88, College Street, Calcutta 700073, India

A R T I C LE I N FO A B S T R A C T

Keywords: Vectorcardiogram (VCG) represents the trajectory of the tip of cardiac vectors in three dimensional space with
Vectorcardiogram varying time. It is a recurring, near-periodic pattern of cardiac dynamics that is constructed by drawing the
VCG instantaneous vectors from a zero reference point according to direction, magnitude and polarity in the space.
Spatial velocity Being a three dimensional entity, it is more informative and more sensitive than conventional ECG as an eva-
Spatial velocity ECG
luation tool of the physiology of cardiac dynamics, because of its extra degree of freedom. Accordingly, it is
Ventricular dysfunction
Heart failure
possible to find out even a minute and early electrophysiological alteration in diseases.
Each cardiac cycle primarily consists of three loops in VCG corresponding to P, QRS, and T wave activities.
The morphological assessment of the QRS loop was carried out in three dimensional space in order to analyze the
spatial vectors of the ventricles and their patho-physiological correlation in various cardiac diseases.
Spatial Velocity (SV) is a virtual velocity that represents the rate of movement of the tip of the cardiac vector
through space, coordinated by three orthogonal leads, and can be estimated by using simple mathematical
formula. It is the rate of change in amplitude and the directionality of instantaneous vectors in seriatim in the
three dimensional space to quantify their the temporo-spatial characteristic pattern.
We propose to evaluate this novel VCG descriptor SV, in normal individuals and patients of ventricular
dysfunction. The possible mechanisms consistent with the patho-physiological basis of ventricular dysfunction or
heart failure with altered SV would enrich the current understanding of the disease.
Heart failure is the final common pathway of multitude of cardiac pathologies. Despite etiological hetero-
geneity, there are common mechanisms involved in the complex electrophysiological alteration of the failing
myocardium. The changes observed as a consequence of ventricular dysfunction involve ion channel remodeling,
intercellular uncoupling, myocardial ischemia, alterations in calcium handling, remodeling of the extracellular
matrix, the presence of scars, activation of the sympathetic & the renin–angiotensin–aldosterone system, dila-
tation as well as stretch of viscous etc. The source modulation of the depolarization wave and its propagation in
the heart and body fluid volume conductor also influence the visual pattern of cardiac vectors. In addition,
patients with heart failure receive pharmacological or non-pharmacological therapies that also influence the
electrophysiological changes.
We hypothesize that the spatial velocity of ventricular depolarization and repolarization vectors of the VCG
loop alters with a characteristic pattern in the patients with ventricular dysfunction and can differentiate healthy
individuals from patients with ventricular dysfunction and also differentiate various categories, gradations and
severity stratifications of the patients with ventricular dysfunction.

Introduction
Cardiac electro-mechanical coupling involves interaction of the
electrical wave driving mechanical contraction and the resulting
change in electrical activation caused by the mechanical contraction.
The electrical and mechanical systems are intimately linked by the
anisotropic microstructure of the heart that regulates the spread of the
electrical wave and the resulting deformation. Each system also reg-
ulates the other via a complex web of feedback mechanisms, with the
extent of deformation dependent on the frequency of electrical

⁎
Corresponding author.
E-mail address: arnabseng@gmail.com (A. Sengupta).

https://doi.org/10.1016/j.mehy.2019.109484
Received 25 September 2019; Accepted 8 November 2019
0306-9877/ © 2019 Elsevier Ltd. All rights reserved.
S. Bhattacharyya, et al.
activation and the deformation dependent electrical properties of the
cell.
Detail analysis of this multi-looped feedback system is required for
quantitative understanding of electromechanical coupling for evalu-
ating cardiac function in health and in disease. Cardiac electro-me-
chanical coupling can be evaluated by utilizing descriptive and analy-
tical tools. The echocardiographic evaluation of mechanical
performance of cardiac ventricles may be combined with electro-
physiological evaluation of heart by a novel Vectorcardiography (VCG)
derived descriptor. Ventricular dysfunction may be taken as a candidate
pathological entity and compared with the normal control volunteers.
VCG represents the summation of all the instantaneous electrical
vectors generated in the heart by myocardial cells and is designed to
display the multidirectional view of space-time cardiac electrical ac-
tivity [1]. The wave of cardiac electrical depolarization propagates
through the cardiac muscle and represented by time-varying current
dipole – termed as vectors. Movement of the electrically charged par-
ticles that occur during spread of the cardiac action potential generates
such vectors. VCG is the graphical representation of the trajectory of the
tip of these vectors in three dimensional space with varying time [1].
VCG is constructed by drawing the instantaneous vectors from a
zero reference point according to direction, magnitude and polarity in
the space (Fig. 1). It is more informative and more sensitive than con-
ventional ECG because of its one extra degree of freedom as an eva-
luation tool of the physiology of cardiac dynamics. As a result, with the
help of VCG it is possible to correlate even a minute electro-
physiological alteration with the patho-physiological changes in dis-
eases which is essential for early diagnosis [2].
However, the difficulty, inaccuracy & cumbersomeness in con-
structing a VCG loop and lack of standardization of accepted metho-
dology so far prevented the study of VCG to become popular.
In the recent years, the analysis of the vectorcardiogram has de-
veloped with vigour because of growing recognition that spatial ana-
lysis of the cardiac electric phenomena is likely to yield information not
furnished by the conventionally recorded electrocardiogram [3,4].
Moreover, recent development and wide availability of signal acquisi-
tion system, computer based technology, mathematical and computa-
tional tools etc made VCG construction potentially easier, objectively
designable and get standardized. There are a number of methodologies
to construct VCG, where special lead systems are required. In a recent
paper [5], Ray et al. proposed a quasi-orthogonal lead system with I,
aVF and V2 and utilized them to emulate the traditionally used Frank's
orthogonal leads (X, Y, and Z respectively) [6]. They also validated
these leads of conventional ECG as reasonably accurate representatives
of X, Y and Z axes.
It is prudent to undertake the morphological assessment of the
Fig. 1. Vectorcardiogram in normal subject.
2
Medical Hypotheses 135 (2020) 109484
spatial QRS loop of VCG with respect to shape, contour, angularity and
other spatial dimension in health and in disease states in order to ob-
jectively enumerate the normal features of the spatial vectors of the
ventricles and also to understand their patho-physiological correlation
in the state of various cardiac diseases [7].
The spatial VCG loop is constructed as recurring and near-periodic
patterns of cardiac dynamics, to capture beat to beat interrelations, or
plotted as a static attractor in a 3D space that provides the topological
relationships (Fig. 1). Each heart cycle consists of three spatial loops
corresponding to P, QRS, and T wave activities.
Spatial Velocity (SV) [8] refers to the velocity of the moving cursor
of the dynamic vectorcardiographic loop on the monitor of the PC
[video online material: 3d-VCG]. The term is a misnomer in that it is a
virtual velocity that represents the rate of movement of the tip of the
cardiac vector through space i.e. the rate of change in amplitude and
the directionality of instantaneous vectors in seriatim in the three di-
mensional space. SV is basically a mathematical construct based upon
certain information regarding the integrative effect of three orthogonal
inputs.
As the spatial velocity basically quantifies the temporo-spatial
characteristic pattern of the cardiac vectors, it has got great theoretical
potential to be a good parametric expression of cardiac electro-
physiology in health and in disease. However, although this entity was
proposed long back, it has not been much used clinically, except to
some extent in discriminating different diagnostic classifications [9,10].
VCG may be displayed by a simple technique to characterize tem-
poro-spatial patterns of cardiac electrical activity as per Ray et al. [5]
and also be objectively characterized the spatial velocity of the dynamic
QRS and T loops of the VCG. We propose to evaluate this novel VCG
descriptor in normal individuals and patients of ventricular dysfunc-
tion. The possible mechanisms consistent with the patho-physiological
basis of ventricular dysfunction with altered spatial SV would enrich
the current understanding of the disease.
The Spatial Velocity of dynamic QRS loops (SVQRS) and dynamic T
loops (SVT) may be estimated from the concurrently obtained QRS
complex and T wave data from three orthogonal leads as per Ray et al.
[5], using a simple mathematical equation [11].
1
SV = [(Δx )2) + (Δy )2) + (Δz )2)]
Δt
where Δx, Δy and Δz are the change of the vector component in X, Y
and Z axes respectively in the sampling interval Δt.
The data is processed using the point to point temporal gradient of
the vectors of a representative 3D-QRS loop. Before summing up, the
gradient values are transformed to their respective modulus values. The
velocities along the three individual orthogonal axes is summed up to
S. Bhattacharyya, et al.
have the three-dimensional spatial velocity and the summation proce-
dure constitutes squaring, adding and finally taking the positive square
root. The squaring is necessary to make the entities independent of
signs, summation for accumulating them and taking square root to keep
the dimension balanced. The point-to-point spatial velocity is thus re-
presented as a time series data set. This data set can be further pro-
cessed by standard mathematical and statistical tools to extract and
visualize important features of the spatial velocity pattern.
Review of literature
The concept of spatial velocity electrocardiogram (SVECG) was first
introduced by Hellerstein and Hamilin (1960) [12]. They studied the
QRS component of the spatial vectorcardiogram and of the spatial
magnitude and velocity electrocardiograms of the normal dog and de-
scribed the observed patterns [1]. However, this interesting concept of
spatial velocity has not been used much clinically, except to some ex-
tent in discriminating different diagnostic classifications [9,10].
Yano and Pipberger (1964) studied Spatial Magnitude, Orientation,
and Velocity of the QRS Complex of 252 normal and 328 abnormal
orthogonal electrocardiograms from the ECG repository of the V.A.
Eastern Research Support Center, Mouint Alto Hospital, and the
Department of Medicine, Georgetown University School of Medicine,
Washington, D. C. They attempted to evaluate the diagnostic usefulness
of this type of spatial data display. The introduction of time-based
curves of spatial parameters of the electrocardiogram has been a sig-
nificant step in the development of optimal displays of electrocardio-
graphic data that can also be represented by azimuth and elevation
angles if necessary [13].
Draper et al (1964) studied and corroborated spatial velocity of the
QRS complex in the corrected orthogonal electrocardiogram and vec-
torcardiogram (Frank lead system) in 510 normal men [14].
Gamboa et al (1967) studied the velocity of the electrocardiogram
in right bundle-branch block patients [15].
Chorão de Aguiar et al (1976) while studying left axis deviation;
evaluated the correlation between the orientation of the initial forces
and the spatial velocity between the 27.5 and 30 msec vectors before
the end of the QRS [16]. The same group also studied the normal ve-
locity in the second part of QRS during 1979 [17].
Based upon the findings of Draper et al. (1964), Gamboa et al.
(1967) and Chorão de Aguiar et al. (1976, 1979), Lovov (1982) vali-
dated the spatial velocity of the QRS wave as a novel parameter with
the diagnostic capacity of the electrocardiogram [18].
Mori et al (1972) studied the QRS Waves of the Spatial Velocity
Electrocardiogram in Atrial Septal Defect and found that, the velocity
increased markedly after the initiation of the terminal delay. They also
established a positive correlation between SVECG and pulmonary ar-
tery & right ventricular pressures [19].
Sakamoto et al. (1973) investigated the depolarization phase of the
spatial velocity electrocardiogram in normal and ventricular over-
loading. They classified left and right ventricular overloading utilizing
this tool and also differentiated between volume overload and pressure
overload [20].
Takeuchi et al (1978) investigated the relationship between Spatial
Velocity and Magnitude Electrocardiograms in thirty normal human
subjects, 21 patients suffering from hypertension without cardiac in-
volvement and 70 cases of ischemic heart disease (IHD), such as myo-
cardial infarction, angina pectoris, and asymptomatic IHD, in a re-
cumbent position before and after Master's two-step test. The SMECG of
QRS of the hypertensive patients was significantly greater both before
and after exercise than that of the normal group, while that of the IHD
group showed significance only after the exercise. Most of the peaks of
QRS and T of SVECG are significantly elevated in the hypertensive
patients. SV and SM showed good positive correlation, but the corre-
lation coefficient was poor in the IHD group and worsened after ex-
ercise [21].
3
Medical Hypotheses 135 (2020) 109484
Shakhov and Urumov (1990) studied the diagnostic potentials of
spatial velocity ECG in assessing the changes in ventricular depolar-
ization. They found that, the spatial velocity ECG exhibits a greater
sensitivity in classifying the patients with right ventricular load.
Insufficient number of investigations concerning the spatial velocity
ECG cannot give a clear view of its potentials and its place in the
clinical practice but some of its advantages make it very convenient for
preparing a system of automatic analysis of the heart electro-
physiological signal [22].
In the year 2012, Yang, Bukkapatnam & Komanduri [23] developed
an automated spatiotemporal representation protocol of cardiac Vec-
torcardiogram, which was used to characterize various spatiotemporal
pathological patterns for healthy control, myocardial infarction, atrial
fibrillation and bundle branch block. They proposed a classifier of those
pathological conditions, and attempted to characterize the space-time
cardiac pathological patterns and enhance the automatic assessment of
cardiovascular diseases.
Recently, Bystricky et al (2019) studied T vector velocity and pro-
posed it as a new ECG biomarker for identifying drug effects on cardiac
ventricular repolarization. They showed that, TVV analysis sub-
stantially improves assessment of drug effects on cardiac repolarization,
providing a plausible and improved mechanistic link between drug
effects on ionic currents and overall ventricular repolarization reflected
in the body surface ECG [24].
Discussion and hypothesis
Instead of the regular and smooth movement of the propagating
dipole in the healthy myocardium, the left ventricular dysfunction
might lead to irregular, disorganized or criss-cross propagation of the
excitation and recovery waves through the ailing myocardium. This
could have led to loss of the time-space interrelations of the in-
stantaneous vectors.
The spatial velocity of the T wave may undergo measurable al-
teration due to repolarization disorders of the failing heart.
Certain basic patho-physiological aspects of ventricular dysfunction
which might have relevance to the phenomenon of spatial velocity of
the dynamic VCG loop are reviewed.
Heart failure is the final common pathway of a multitude of cardiac
pathologies. Despite etiological heterogeneity, there are common me-
chanisms involved in the complex electrophysiological alteration of the
failing myocardium. There are different categories of left ventricular
dysfunction based upon the nature of the functional derangement of the
ventricle. While systolic dysfunction denotes the pumping function
deficiency of the ventricle; diastolic dysfunction signifies the disorder of
filling of the relatively inexpansile ventricle. Also these various cate-
gories of ventricular dysfunction can be classified with respect to their
gradation or severity stratification; e.g mild-moderate-severe or grades
I-II-III [25]. There are clear-cut objective criteria based upon a number
of echocardiographic features to define and differentiate these cate-
gories, gradations and severity stratifications [26,27,28].
The multiple and complex electrophysiological changes observed as
a consequence of ventricular dysfunction, involve ion channel re-
modeling, intercellular uncoupling, myocardial ischemia, alterations in
calcium handling, remodeling of the extracellular matrix, the presence
of scars, activation of the sympathetic & the re-
nin–angiotensin–aldosterone system, and dilatation as well as stretch of
viscous etc [29]. The source modulation of the depolarization wave and
its propagation in the heart and volume conductor also influence the
propagation pattern of cardiac vectors. In addition, patients with heart
failure receive pharmacological or non-pharmacological therapy that
also influences the electrophysiological changes [29].
Action potential prolongation is commonly seen in patients with
heart failure, which occurs due to the relative dominance of repolar-
ization [29]. There is a reduction of the outward repolarizing currents
as a result of down-regulation of potassium currents Ito and IKs. The
S. Bhattacharyya, et al.
action potential reflects a delicate balance between the activity of
several depolarizing and repolarizing ionic currents, transporters, and
exchangers, which are not uniformly expressed throughout the ven-
tricular wall. The prolongation of APD in heart failure is heterogeneous,
exaggerating the physiological inhomogeneity of electrical properties in
the failing heart. [30,31].
The function and expression of K+ channels differ widely across the
heart, mainly reflecting heterogeneity in the type and/or expression
pattern of the K+ channels in the genesis of the cardiac action poten-
tial. Moreover, the expression and properties of K+ channels are not
static but are influenced by heart rate, neurohumoral state, pharma-
cological agents, cardiovascular diseases (cardiac hypertrophy and
failure, myocardial infarction, atrial fibrillation etc) [32–35]. Ito is
present in the epicardium, but largely absent in the endocardium,
which contributes to dynamic (rate-dependent) variation in action po-
tential duration and refractoriness in the epicardium and endocardium.
This differential distribution explains how electrical activity is de-
pressed earlier in the ventricular epicardium leading to greater short-
ening of action potential duration there than in the endocardium. This
faster depression of electrical activity in the epicardium [36] con-
tributes to the reversal of transmural repolarization sequence in ven-
tricular dysfunction.
The broad activation front propagating through the Purkinje net-
work arrives at the epicardium, and breaks throughout the surface in a
dynamic fashion during ventricular depolarization. In contrast epi-
cardial potential patterns of normal repolarization which propagate
from epicardium to endocardium are static, reflecting the relatively
slow process of repolarization [37].
There is a strong correlation between transmural repolarization and
relaxation sequences. The normal ventricular repolarization sequence is
from the epicardium to the subendocardium/endocardium that is op-
posite to that of the ventricular activation sequence, which normally
starts with the subendocardium (or endocardium) and spreads across
the ventricular wall to the epicardium. A positive T wave that denotes
transmural repolarization sequence from epicardium to endocardium is
essential for normal diastolic function of the ventricle and hence the
alteration of such a sequence is associated with ventricular diastolic
dysfunction [38]. Any abnormal morphology of the T wave (i.e. a ne-
gative or inverted T wave or biphasic or notched T wave) indicates an
abnormal ventricular repolarization sequence. Abnormalities in the
ventricular repolarization, detected as changes in the T wave
morphologies are frequently observed in various categories of ven-
tricular dysfunction [38].
A decreased expression of the major gap junctional protein con-
nexin43 (Cx43) is also a general feature of heart failure [39,40], that
may lead to inter-cellular structural disintegrity and functional un-
coupling of the failing myocytes. The failing myocardium also under-
goes fibrosis [41–43]. Altered extracellular matrix along with the col-
lagenous septae separating the myocardial fibres disrupt the
intercellular coupling, with resulting anisotropy; and thus impede
propagation of the cardiac impulse, especially across (i.e. transverse to
the direction of) the fibres. This culminates in a decrease in the diastolic
function of the heart. Activation in the fibrotic muscle propagates in a
zig-zag fashion along the electrically isolated fibers [44]. Along with all
these there is altered intracellular and transmembrane calcium hand-
ling [45,46], as well as stretch-induced mechanisms due to altered
ventricular loading conditions [47–49] while changes in myocyte
electrical properties [50–52] have also been implicated in the altered
electro-mechanical coupling of the failing heart.
As described earlier, the spatial velocity of the dynamic VCG loop is
the rate of change of magnitude and direction of the serial in-
stantaneous ventricular vectors. In ventricular dysfunction due to var-
ious pathophysiological reasons as described in the previous sections,
the zig-zag nature of the spatio-temporal characteristics of in-
stantaneous ventricular vectors alter the rate of change of subsequent
depolarization vectors, that may lead to alteration of the SVQRS in
4
Medical Hypotheses 135 (2020) 109484
ventricular dysfunction.
The prolongation of ventricular repolarization occurs due to de-
creased outward potassium current as a result of down-regulation of Kto
and Krs. This may contribute to rate-dependent changes in
action potential duration leading to the ventricles
having a longer period of repolarization. Accordingly,
the rate of change of magnitude of the serial instantaneous ventricular
repolarization vectors undergo alteration, that may lead to certain
characteristics alteration of SVT.
Hypotheses.
1. The spatial velocity of ventricular depolarization and repolarization
vectors of the VCG loop alters with a characteristic pattern in the patients
with ventricular dysfunction and can differentiate healthy individuals
from patients with ventricular dysfunction.
2. The spatial velocity of ventricular depolarization and repolarization
vectors of the VCG loop can differentiate healthy individuals from pa-
tients with ventricular dysfunction.
3. The spatial velocity of ventricular depolarization and repolarization
vectors of the VCG loop can differentiate various categories, gradations
and severity stratifications of the patients with ventricular dysfunction.
These hypotheses are compatible with our basic understanding of
the electrophysiology of the human heart in ventricular dysfunction.
Understanding the pattern and characteristics of propagation of
normal cardiac excitation provides a necessary baseline for under-
standing abnormal cardiac electrical activity. So far, knowledge of
normal human cardiac excitation has been obtained mostly through
extrapolation from animal studies, including canine, and chimpanzee
etc. In addition, human data have been obtained from intraoperative
epicardial mapping and isolated human hearts [16]. Extrapolation of
animal studies to humans has an inherent limitation by interspecies
differences in structure and electrophysiology. Also, the animal and
human studies were conducted under various manipulative conditions
like anesthesia, intra-operative heart exposure, isolation, absence of
neural inputs, mechanical loading, perfusion etc. Accordingly, the study
of spatial velocity of the dynamic VCG may be validated as a sensitive
diagnostic, prognostic and research approach to acquire valuable in-
sight in understanding intrinsic ventricular electromotive forces in
health and in disease.
Declaration of Competing Interest
The authors declare that they have no known competing financial
interests or personal relationships that could have appeared to influ-
ence the work reported in this paper.
Appendix A. Supplementary data
Supplementary data to this article can be found online at https://
doi.org/10.1016/j.mehy.2019.109484.
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