The Heart and Circulation - An Integrative Model

Abstract

This extensively revised second edition traces the development of the basic concepts in cardiovascular physiology in light of the accumulated experimental and clinical evidence. It considers the early embryonic circulation, where blood circulation suggests the existence of a motive force, tightly coupled to the metabolic demands of the tissues. It proposes that rather than being an organ of propulsion, the heart, serves as an organ of control, generating pressure by rhythmically impeding blood flow. New and expanded chapters cover the arterial pulse, circulation in the upright posture, microcirculation and functional heart morphology.

Heart and Circulation offers a new perspective for deeper understanding of the human cardiovascular system. It is therefore a thought-provoking resource for cardiologists, cardiac surgeons and trainees interested in models of human circulation.

Full text

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TITLE LIST
FULL TITLE: Novel patterns of left ventricular mechanical activity during experimental cardiac arrest
in pigs
SHORT TITLE: Ventricular mechanical activity in cardiac arrest
AUTHORS: Roman Skulec, MD, PhD1,2,3; David Astapenko, MD1; Renata Cerna Parizkova, MD, PhD1;
Prof. Branko Furst, MD, FFARCSI4; Marcela Bilska, MD2; Tomas Parizek, MD2; Tomas Hovanec5;
Nikola Pinterova6; Jiri Knor, MD, PhD3,7; Jaroslava Dudakova3; Anatolij Truhlar, MD, PhD1,8; Vera
Radochova, DVM9; Prof. Zdenek Zadak, MD, PhD10,11 and Prof. Vladimir Cerny, MD, PhD,
FCCM1,2,10,12
AFFILIATIONS:
1Department of Anesthesiology and Intensive Care, Charles University in Prague, Faculty of Medicine in
Hradec Kralove, University Hospital Hradec Kralove, Hradec Kralove Czech Republic
2Department of Anesthesiology, Perioperative Medicine and Intensive Care, J.E. Purkinje University,
Masaryk Hospital Usti nad Labem, Usti nad Labem, Czech Republic
3Emergency Medical Service of the Central Bohemian Region, Kladno, Czech Republic
4Department of Anesthesiology, Albany Medical College, NY, United States of America
5Faculty of Medicine in Hradec Kralove, Charles University in Prague, Hradec Kralove, Czech Republic
6Faculty of Science, Charles University in Prague, Prague, Czech Republic
73rd Medical Faculty, Charles University in Prague, Prague, Czech republic
8Hradec Kralove Region Emergency Medical Services, Hradec Kralove, Czech Republic
9Faculty of Military Health Sciences, University of Defence, Brno, Czech Republic
10Department of Research and Development, Charles University in Prague, Faculty of Medicine in
Hradec Kralove, University Hospital Hradec Kralove, Hradec Kralove, Czech Republic
113rd Department of Internal Medicine – Metabolic Care and Gerontology, Charles University in Prague,
Faculty of Medicine in Hradec Kralove, University Hospital Hradec Kralove, Hradec Kralove, Czech
Republic
12Department of Anesthesia, Pain Management and Perioperative Medicine, Dalhousie University,
Halifax, Nova Scotia, Canada
FIRST AND CORRESPONDING AUTHOR: Roman Skulec
Corresponding address: Roman Skulec, Department of Anesthesiology, Perioperative Medicine
and Intensive Care, Masaryk Hospital Usti nad Labem, Socialni pece 3316 /12A, Usti nad Labem 401 13,
Czech Republic
Email: skulec@email.cz Phone: 00420 777 577 497 Fax: 00420 477 115 020

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SUMMARY
We conducted an experimental study to evaluate the presence of coordinated left ventricular mechanical
myocardial activity (LVMA) in two types of experimentally induced cardiac arrest: ventricular fibrillation
(VF) and pulseless electrical activity (PEA). Twenty anesthetized domestic pigs were randomized 1:1
either to induction of VF or PEA. They were left in nonresuscitated cardiac arrest until the cessation of
LVMA and microcirculation. Surface ECG, presence of LVMA by transthoracic echocardiography and
sublingual microcirculation were recorded. One minute after induction of cardiac arrest, LVMA was
identified in all experimental animals. In the PEA group, rate of LVMA was of 106±12/min. In the VF
group, we identified two patterns of LVMA. Six animals exhibited contractions of high frequency (VFhigh
group), four of low frequency (VFlow group) (334±12 vs. 125±32/min., p<0.001). A time from cardiac
arrest induction to asystole (19.2±7.2 vs. 7.3±2.2 vs. 8.3±5.5 min, p=0,003), cessation of LVMA
(11.3±5.6 vs. 4.4±0.4 vs. 7.4±2.9 min, p=0.027) and cessation of microcirculation (25.3±12.6 vs.
13.4±2.4 vs. 23.2±8.7 min, p=0.050) was significantly longer in VFlow group than in VFhigh and PEA
group, respectively. Thus, LVMA is present in both VF and PEA type of induced cardiac arrest and
moreover, VF may exhibit various patterns of LVMA.
Key words: experimental cardiac arrest, left ventricular mechanical activity

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Introduction
Implementation of point-of-care echocardiography in clinical and experimental resuscitation medicine has
brought new knowledge about the cardiac arrest (Soar et al. 2015). It has been documented that the
clinical syndrome of cardiac arrest is not always accompanied by the presence of mechanical cardiac
standstill (Bocka et al. 1988, Breitkreutz et al. 2010). Conversely, in most cases of pulseless electrical
activity (PEA) and in some patients presenting with asystole, a preserved coordinated left ventricular
mechanical myocardial activity (LVMA) can be observed (Breitkreutz et al. 2010, Cohn et al. 2013). It
has been shown that the presence or absence of LVMA exhibits a strong predictive prognostic value for
achieving return of spontaneous circulation (ROSC) (Blyth et al. 2012, Blaivas et al. 2001). The absence
of LVMA during cardiopulmonary resuscitation (CPR) of patients with non-shockable rhythm indicates a
significantly reduced chance of ROSC and vice versa. Intra-arrest ultrasonographic examination may help
in the decision-making process regarding the termination of cardiopulmonary resuscitation. In addition to
confirming its absence, the presence of LVMA can reinforce enthusiasm of the rescuers to continue
providing high-quality CPR. However, many questions remain unanswered, such as the presence of the
pathophysiological mechanism of LVMA in patients presenting with asystole. It is further unknown
whether myocardial viability depends on the presence of residual cardiac output resulting from LVMA, or
on autonomous blood movement at the level of the microcirculation as observed in our previous study
and documented in several reports (Thompson 1948, Manteuffel-Szoege et al. 1966, Furst 2014). Finally,
it is also necessary to identify whether the phenomenon of LVMA is related only to non-shockable
rhythms, or may also occur in cardiac arrest induced by ventricular fibrillation (VF).
We conducted an experimental study to evaluate the presence of coordinated LVMA in two types of
experimentally induced cardiac arrest: VF and PEA. We hypothesized that LVMA will be detected in the
majority of animals with induced PEA and VF and that its presence will be associated with a longer time
to asystole than in animals without LVMA.
Methods

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We performed a prospective randomized controlled experimental study on 20 healthy female domestic
experimental pigs (Sus scrofa f. domestica) with weight of 33±2 kg. The experiment was carried out at the
Animal Research Laboratory of the University of Defence, Faculty of Military Health Sciences. The
study protocol was approved by the Animal Investigation Committee of the University of Defence Brno,
Faculty of Military Health Sciences Hradec Kralove, Czech Republic and the Departmental Commission
for the Protection of Animals of the Ministry of Defence, Prague, Czech Republic (approved 14.3.2015,
No. 010-2015). All experimental animals received humane care in compliance with the institutional
guidelines and with the International Association of Veterinary Editors’ Consensus Author Guidelines on
Animal Ethics and Welfare.
Animal preparation
The animals were premedicated by intramuscular injection of azaperone (2.0 mg/kg), atropine (0.2
mg/kg) and ketamine (20.0 mg/kg) 30 minutes before surgery. After the animals were brought into the
operating room, peripheral intravenous access was secured and in a supine position, animals were
intubated and mechanically ventilated 19 breaths/min, FiO2 of 0.4. Tidal volumes were adjusted to
maintain end tidal CO2 of 35-45 mm Hg. Anaesthesia was maintained with a continuous infusion of
fentanyl (5–20 μg/kg/h) and isoflurane inhalation and all animals were given a continuous infusion of
normal saline at room temperature (50 ml/h). Vital signs including ECG were continuously monitored.
The thoracic aorta was cannulated via the carotid artery with a 7F 200 mm catheter Certofix Duo (B.
Braun Melsungen AG, Melsungen, Germany) for monitoring of the aortic blood pressure. An 8.5F
percutaneous sheath introducer (Intro-Flex, Edwards Lifesciences LLC, Irvine, CA, USA) was inserted
via the internal jugular vein into the superior vena cava to facilitate insertion of the bipolar pacing lead
and continual monitoring of right atrial pressure. A 5-mm diameter burr-hole craniotomy at the upper part
of the frontal bone was created on the left side to insert an intracranial pressure-monitoring probe 20 mm
into the frontal lobe (Codman, Johnson & Johnson, Raynham, MA, USA). Coronary perfusion pressure
(CoPP) was calculated as the pressure difference between diastolic aortic pressure and right atrial

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pressure during the decompression phase. Continuous echocardiographic monitoring was performed by
Vivid i ultrasound device (GE Healthcare, Little Chalfont, United Kingdom).
Left ventricular end-diastolic dimension (LVEDD, mm), left ventricular end-systolic dimension (LVESD,
mm), interventricular septal thickness at end-diastole (IVSd, mm) and posterior wall thickness at end-
diastole (PWd, mm) were recorded every minute and fractional shortening (FS, %) was calculated
following the formula FS = ((LVEDD-LVESD) / LVEDD) · 100. LVMA was defined as the presence of
visible thickening of the interventricular septum and/or left ventricular posterior wall, calculated as FS >0
% and related to opening of the valve.
Experimental protocol
After animal preparation and stabilization, 20 pigs were randomly assigned by envelope method into two
groups to induce either ventricular fibrillation (VF group, 10 animals) or pulseless electrical activity (PEA
group, 10 animals). Ventricular fibrillation (VF) was induced with an alternating current of 5–10 V using
intra-cardiac bipolar pacing lead introduced into the right ventricle. Pulseless electrical activity (PEA)
was initiated by intravenous administration of T61 agent. Cardiac arrest was confirmed as the time point
at which both the carotid and femoral pulse was no longer palpable. The animals were left in the state of
non-resuscitated cardiac arrest until the cessation of LVMA and sublingual microcirculation. During this
period, the animals were monitored for all variables. Thereafter, the animals were autopsied.
Sublingual microcirculation was recorded in each animal by Sidestream dark-field imaging videocamera
(MicroVision Medical, Amsterdam, Netherlands). All records at baseline were analysed off-line by
specialized software AVA 3.0 (MicroVision Medical, Amsterdam, Netherland) and selected parameters
of the microcirculation were evaluated, namely, perfused vessel density (PVD) and microvascular flow
index (MFI). After initiation of cardiac arrest, the microcirculation was monitored continuously by an
experienced observer. Microcirculatory arrest was defined as cessation of red blood cell movement in the
visual field.

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Major outcomes were the time from cardiac arrest induction to asystole, the time from cardiac arrest
induction to cessation of LVMA and the time from cardiac arrest induction to cessation of sublingual
microcirculation.
Statistical analysis
For the statistical analysis, measurements were taken at the baseline and each minute until the end of the
experimental protocol. Mean values ± SD or percentages were calculated as necessary. Differences
between groups were compared using the χ2 test, and statistical significance was calculated by the Fischer
exact test for alternative variables. Statistical significance for continuous variables was determined by the
paired Student t test. Data were analysed using Microsoft Excel 2010 (Microsoft, Redmond, WA, USA)
and JMP 3.2 statistical software (SAS Institute, Cary, NC, USA). A p value of <0.05 was considered
statistically significant.
Results
The protocol was completed in all experimental animals. One minute after induction of cardiac arrest,
LVMA was identified in all experimental animals. In the PEA group, it was tightly coupled with the
frequency of QRS complexes on the surface ECG with the heart rate of 106±12/min. In the VF group, we
identified two different patterns of LVMA, regardless of the uniform origin of VF. Six animals exhibited
mechanical contractions of high frequency (subsequently assigned as VFhigh group) and four developed
low frequency contractions (subsequently assigned as VFlow group) (334±12 vs. 125±32/min, p<0.001).
Therefore, we compared three groups in further analysis.
During untreated cardiac arrest, asystole developed in all experimental animals before protocol
termination, first in VFhigh group, followed by PEA and VFlow groups (figure 1). The time to cessation of
LVMA was shortest in VFhigh group, followed by PEA and VFlow groups, respectively (figure 2).
Analysis of the sublingual microcirculation showed normal and comparable values in experimental
groups at the baseline for PVD (24.1±1.1 mm/mm2) and MFI score (2.9±0.1).

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The time from induction of cardiac arrest to the cessation of microcirculatory flow was shortest in the
group VFhigh, and in comparison, significantly prolonged in the PEA and VFlow groups (figure 3).
Table 1 shows the values of hemodynamic parameters and left ventricular fraction shortening. In the PEA
group, we observed significantly higher maximal values of pulse pressure (PP), CoPP and FS as defined
in the study protocol, and higher values of PP, CoPP and FS in the first three minutes after the induction
of cardiac arrest. Maximal post-arrest values of PP and CoPP were observed in the PEA group
significantly later than in the VFhigh and VFlow groups. There were no significant differences in the DAP
values among the groups during the protocol. However, significant differences in FS during the first three
minutes and at the maximal value were identified between VFhigh and VFlow groups.
Discussion
The main findings of the present study are that LVMA was found to be preserved for a certain period
after induction of CA in all experimental animals regardless of the induced electrical activity, two
patterns of LVMA were identified in VF group animals and the pattern with LVMA of low frequency
contractions (VFlow group) was associated with the longest time from CA induction to asystole to
cessation of LVMA and microcirculation among the groups.
It has been known for some time that the clinical syndrome of cardiac arrest is not always accompanied
by a mechanical cardiac standstill. Bocka et al. performed echocardiography in a group of patients
presenting with electromechanical dissociation and demonstrated synchronous myocardial wall motion in
19 out of 22 patients (Bocka et al. 1988). Paradise et al. measured aortic pressure in 94 patients with PEA
and found that 39 have measurable pulse pressure (6.3 ± 3.5 mm Hg) (Paradis et al. 1992). The
phenomenon of preserved LVMA in patients presenting with PEA is known as pseudo-PEA. Studies have
confirmed that pseudo-PEA is a common finding occurring in 58 % of patients with out-of-hospital, and
in up to 55 % of patients with in-hospital cardiac arrest (Breitkreutz et al. 2010, Flato et al. 2015).
Moreover, LVMA has been identified in up to 35 % cardiac arrest patients with asystole (Breitkreutz et
al. 2010). Blyth et al. performed a meta-analysis of 12 clinical studies and showed that intra-arrest

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echocardiography had sensitivity of 91.6 % and specificity of 80.0 % as predictors of ROSC. The absence
of LMVA predicts a very low likelihood of ROSC and vice versa (Blyth et al. 2012).
The observed phenomenon of the presence of LVMA in all animals of the PEA group is consistent with
clinical studies published previously (Breitkreutz et al. 2010, Flato et al. 2015).
Surprisingly, we observed the occurrence of LVMA also in animals with induced VF. Unlike in the case
of PEA, there has been no published observations of coordinated LVMA in VF. Moreover, we identified
two patterns of LVMA. In six animals, subsequently assigned to VFhigh group, LVMA was present at the
limit of measurability and at the rate of anticipated frequency of ventricular fibrillation. LVMA at low
frequency was observed in four experimental animals. We now discuss the possible pathophysiological
sequence of events in the VF groups.
In spite of voluminous literature on the causes of electrical myocardial activity during VF, the nature of
its origin, maintenance and hemodynamic impact are not understood. Several experimental and clinical
observations support the hypothesis of an “organization pattern” in persistent VF. Wiggers et al.
identified in electrically stimulated canine hearts 4 phases in the genesis of VF. At the onset, a well-
organized type of arrhythmia was observed consisting of one or two rotors with re-entrant electrical
activity, called the mother-rotor. This was followed by less-well organized wavefronts which may
constitute the basis for further rotors (Wiggers et al. 2003). This activity was further defined by Huang et
al. who quantitated the VF and showed that its organization does not invariably decrease, but can
fluctuate (Huang et al. 2004). A controversy continues over the issue whether the dominant cause of VF
is a single re-entrant mother-rotor, or the genesis of newly emerging, wandering wavelets. Experimental
findings shows that, depending on the experimental model, duration and stage of VF and drug therapy,
both mechanisms can be present (Chen et al. 2003, Tabereaux et al. 2009, Fenton et al. 2002, Huang et
al. 1998, Bourgeois et al. 2012, Rogers et al. 2007, Li et al. 2008, Pak et al. 2006, Cheng et al. 2012,
Nielsen et al. 2009, Lin et al. 2014). The heterogeneity in VF maintenance and the complexity of its
electrical activity confirms the importance of visual assessment of LVMA by means of point-of-care
ultrasonography.

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Another potential mechanism that may explain our observation of different LVMA rate in VFhigh and
VFlow groups is based on the possible role of atrial activity on mechanical left ventricular performance
during VF. In spite of the fact that atrial activity cannot be assessed from the surface ECG during VF,
effective atrial ejection can be present (Addison et al. 2002). In our experiments, VF was induced in
healthy animals with normal sinus rhythm without structural myocardial abnormality. In such
experimental setting, the loss of sinus rhythm after VF induction requires the presence of retrograde
conduction. However, this is not an ubiquitous feature of the conduction system in humans and
experimental animals (Molina et al. 1989, Goldreyer et al. 1970, Bowman et al. 1984, Pickoff et al.
1984). It is possible that the pattern of ongoing, sustained VF presenting with fully organized atrial
activity, i.e., atrial systole, may have been present in some of our experimental animals, giving rise to
pulsatile volume-loading of the left ventricle and directly, or indirectly inducing the echocardiographic
phenomenon of low-frequency LVMA.
It is also possible that in VFlow group the effective atrial activity was preserved and LVMA phenomenon
was predominantly a passive process. In the VFhigh group, on the other hand, the LVMA may reflect high
frequency contractions with minimal FS directly related to VF activity.
It is questionable, however, whether the presence of LVMA characterizes even a minimal degree of
effective cardiac output. What is essential is that various modes of LVMA during VF can be related to
different electrical patterns of VF maintenance and thus to myocardial viability and resistance to
ischemia. We hypothesize that these factors could influence not only defibrillation thresholds but also the
time window for efficient defibrillation.
Is is noteworthy that in the early phase of induced cardiac arrest, LVMA was observed in all experimental
animals. This suggests that LVMA is a regular occurrence in the early phases of
VF and PEA and supports the idea that cardiac arrest is not a static condition but a dynamic process
which, left untreated, inevitable leads to irreversible cardiac standstill.
Finally, we observed flow of blood at the level of the microcirculation well beyond the timing of the
cardiac arrest in all 3 experimental groups (fig 3). The phenomenon of circulation persisting at the organ
and tissue level after the recordable LVMA supports the concept that blood possesses its own kinetic

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energy determined by the metabolic demands of the tissues and calls for a revision of the conventional,
pressure-propulsion circulation model (Furst 2015, Alexander 2017, Forouhar et al. 2006). Intravital
microscopy of early embryonic circulations has confirmed that a low-pressure circulation already exists
before the functional integrity of the heart (Forouhar et al. 2006). It has further been shown that the
valveless embryo heart functions as an impedance pump which rhythmically interrupts the already
existing flow of blood (Furst 2014). Irrespective of structural differences, the function of the mature heart
is essentially the same as that of the embryonic heart. In addition to rhythmic interruption of the flow, the
ventricles eject the blood into the pulmonary/systemic arterial compartments at higher pressures. Thus,
above the blood’s primary streaming at the level of the microcirculation which is subject to local control,
i.e., organ and tissue autoregulation, the secondary, or macrocirculatory flow is subject to complex
control at the systemic level. According to the ontogenic circulation model the syndrome of cardiac arrest
primarily manifests as the collapse of arterial pressure due to the heart’s inability to rhythmically interrupt
the flow of blood. Even though the resuscitation efforts are primarily directed at restoring a rhythm that
will sustain the macrocirculation, experimental CPR protocols which in addition enhance the
microcirculatory flow have shown favorable outcomes (Yannopoulos et al. 2012). The proposed
circulation model is moreover consistent with recent advances in the understanding of critical illness.
Collectively, they demonstrate uncoupling or incoherence between observed microvascular parameters,
such as functional capillary density and red blood cell velocity, and routinely measured macrovascular
parameters, such as arterial blood pressure, cardiac output, ejection fraction, and mixed venous oxygen
saturation (Ince 2015). The loss of hemodynamic coherence has thus been identified as the common
denominator of various states of shock. Left uncorrected, such incongruence inevitably leads to a
complete dissociation between the two circulatory components and to cardiac arrest. The phenomenon of
persistenting microcirculation after cardiac arrest thus offers a new insight into the pathogenesis and
possible treatment of this insidious condition.
There are a few study limitations. Firstly, this is an experimental study and the results should be
interpreted with caution when related to clinical medicine. Cardiac arrest was induced in healthy young
animals, without any myocardial or pulmonary disease. Since we did not directly measure the intracardiac

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pressures and ECG’s, only a hypothetical explanation regarding electrical events and intracardiac blood
flows can be given. Secondly, with regard to LVMA patterns, we can not completely rule out effect of
anaesthetics agents on the obtained results in experimental groups. Several authors show that inhaled and
intravenous anaesthetic may have differential, direct or indirect, effect on myocardial functions (Süzer et
al. 1998, De Hert SG 1991, Stowe DF et al. 1992) Addition of fentanyl and sevoflurane was associated
with inhibiting ventricular fibrillation in one clinical report (Yamagishi A et al. 2003). On the other hand,
the same type of anesthesia was used in all experimental animals in comparable doses.
In conclusion, we observed that LVMA was found to be preserved for a certain period of induced cardiac
arrest in all animals in our experiment. In the VF group, two patterns of LVMA were identified, one with
low and one with very high frequency. We hypothesize the underlying mechanism of different LVMA
pattern in animals with induced VF. Anyhow, presentation of LVMA with low frequency contractions was
associated with increased resistance to cessation of LVMA and microcirculation. We also observed the
persistence of microcirculatory blood flow after cardiac standstill. This phenomenon supports the concept
that blood possesses its own kinetic energy determined by the metabolic demands of the tissues and
support a revision of the conventional circulation model. Further research is needed to explain the
pathophysiological explanation of our observations and potential consequences for clinical medicine.
Conflict of interest
We declare no conflict of interest.
Acknowledgments
Supported by the programme PROGRES Q40/2 and by MH CZ - DRO (UHHK, 00179906).
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Figure 1. Time from induction of cardiac arrest to development of asystole in experimental groups.
Figure 2. Time from induction of cardiac arrest to cessation of LVMA in experimental groups.
LVMA…left ventricular mechanical activity

17
Figure 3. Time from induction of cardiac arrest to cessation of microcirculation.
Table 1. PP, DAP, CoPP and FS values during the protocol and comparison among the groups in different
time points. PP…pulse pressure, DAP…diastolic arterial pressure, CoPP…coronary perfusion pressure,
Tmax…time from cardiac arrest induction to the maximal value during the protocol. * indicates p<0.05
between PEA group and VFhigh and VFlow groups, ● indicates p<0.05 between VFhigh group and VFlow
group
Baseline
1 min
2 min
3. min
maximal
Tmax
PP
(mm Hg)
PEA group
45.3±13.5
7.8±2.6*
14.0±8.7*
10.8±6.6*
15.8±5.0*
2.9±0.6*
VFlow group
46.2±12.2
4.3±1.0
4.1±3.1
5.0±5.4
7.1±5.0
2.2±0.6
VFhigh group
47.0±13.9
4.5±3.1
3.2±1.2
1.5±3.7
5.2±3.8
1.7±1.0
DAP
(mm Hg)
PEA group
62.3±8.6
19.6±4.5
20.5±6.8
19.6±7.9
22.5±5.6
2.4±0.8
VFlow group
62.7±13.4
17.3±3.0
16.5±4.0
16.7±3.7
18.8±2.6
2.0±0.6
VFhigh group
64.2±7.5
17.7±2.9
16.5±0.7
15.7±0.5
18.5±1.9
2.0±1.4
CoPP
(mm Hg)
PEA group
55.4±8.5
8.6±4.1*
8.2±7.0*
6.9±8.6
10.8±6.5*
2.6±0.8*
VFlow group
56.8±14.8
2.8±1.2
1.3±2.4
2.5±2.9
4.0±2.3
1.7±0.8
VFhigh group
57.7±5.8
2.7±1.7
2.2±2.7
1.5±2.4
3.5±1.7
1.5±0.6
FS (%)
PEA group
49.2±6.0
30.9±11.4*
44.1±21.4*
35.3±19.7*
41.9±12.2*
2.1±0.8
VFlow group
51.2±6.2
14.9±8.8●
11.4±4.7●
9.8±6.4●
15.5±8.3●
1.3±0.5
VFhigh group
52.1±1.4
4.4±3.5
5.8±2.4
2.7±0.9
7.0±2.9
1.7±0,5