\documentclass[10pt]{article}

\usepackage{fullpage}
\usepackage{setspace}
\usepackage{parskip}
\usepackage{titlesec}
\usepackage[section]{placeins}
\usepackage{xcolor}
\usepackage{breakcites}
\usepackage{lineno}
\usepackage{hyphenat}





\PassOptionsToPackage{hyphens}{url}
\usepackage[colorlinks = true,
            linkcolor = blue,
            urlcolor  = blue,
            citecolor = blue,
            anchorcolor = blue]{hyperref}
\usepackage{etoolbox}
\makeatletter
\patchcmd\@combinedblfloats{\box\@outputbox}{\unvbox\@outputbox}{}{%
  \errmessage{\noexpand\@combinedblfloats could not be patched}%
}%
\makeatother


\usepackage{natbib}




\renewenvironment{abstract}
  {{\bfseries\noindent{\abstractname}\par\nobreak}\footnotesize}
  {\bigskip}

\titlespacing{\section}{0pt}{*3}{*1}
\titlespacing{\subsection}{0pt}{*2}{*0.5}
\titlespacing{\subsubsection}{0pt}{*1.5}{0pt}


\usepackage{authblk}


\usepackage{graphicx}
\usepackage[space]{grffile}
\usepackage{latexsym}
\usepackage{textcomp}
\usepackage{longtable}
\usepackage{tabulary}
\usepackage{booktabs,array,multirow}
\usepackage{amsfonts,amsmath,amssymb}
\providecommand\citet{\cite}
\providecommand\citep{\cite}
\providecommand\citealt{\cite}
% You can conditionalize code for latexml or normal latex using this.
\newif\iflatexml\latexmlfalse
\providecommand{\tightlist}{\setlength{\itemsep}{0pt}\setlength{\parskip}{0pt}}%

\AtBeginDocument{\DeclareGraphicsExtensions{.pdf,.PDF,.eps,.EPS,.png,.PNG,.tif,.TIF,.jpg,.JPG,.jpeg,.JPEG}}

\usepackage[utf8]{inputenc}
\usepackage[T2A]{fontenc}
\usepackage[ngerman,polish,greek,english]{babel}



\usepackage{float}








\begin{document}

\title{Comparing of Peak Longitudinal Strain and Post Systolic Shortening in
Detecting Ischemia at Rest in Stable Coronary Artery Disease: An
Angiography Verified Study}



\author[1]{ahmet barutcu}%
\author[2]{Mehmet Arslan}%
\author[3]{Özge  Özden Tok}%
\author[2]{emine gazi}%
\affil[1]{Çanakkale Onsekiz Mart University Faculty Of Medicine }%
\affil[2]{Affiliation not available}%
\affil[3]{Memorial Bahcelievler Hospital}%


\vspace{-1em}



  
  \date{June 16, 2024}


\begingroup
\let\center\flushleft
\let\endcenter\endflushleft
\maketitle
\endgroup





\selectlanguage{english}
\begin{abstract}
Background: Coronary artery disease is a major public health problem.
Early diagnosis and treatment of coronary artery disease is crucial.
There is a need for a practical, reliable and cost-effective
non-invasive imaging tool. We aimed to evaluate the rest ischemia with
speckle tracking echocardiography (STE) compare to the two methods in
patients who were scheduled coronary angiography according to the stress
tests. Methods: We included fifty patients with stable angina pectoris
who were scheduled for conventional coronary angiography after the
stress tests in our study. Speckle tracking echocardiography was
performed just before coronary angiography. The association of 2
parameters with coronary artery disease was investigated and compared.
Results: Among 50 patients recruited for the study, 38 of them had
severe CAD (\textgreater{}50\%), whereas 12 patients had non-significant
CAD. Post systolic shortening (PSS) was significantly related with CAD
(p\textless{}0.0001). The relationship of PLS with the area at risk was
found to be statistically insignificant but global longitudinal strain
(GLS) was significantly lower in patients with severe CAD (p=0.011)
Conclusion: PSS may detect coronary ischemia in patients with stable
coronary artery disease and it is more sensitive and specific in
patients with stable CAD. PSS is a very useful, practical and easy
applicable non invasive tool for the detection of severe coronary artery
disease at rest.%
\end{abstract}%



\sloppy


\textbf{INTRODUCTION}

Coronary artery disease(CAD) is a major public health problem. It is the
leading cause of all deaths (1,2) and thus early diagnosis and treatment
of CAD is of critical importance. To diagnose the CAD in patients
presenting with chest pain is sometimes costly and time consuming.

Numerous clinical studies have been conducted for the early diagnosis of
CAD (3-7). Currently there are various available invasive and
noninvasive tests, however all of them have several limitations. Some
are expensive and difficult to access, while some others have a high
dose of radiation. Due to all these reasons, there is an absolute need
for a reliable and cost effective non-invasive imaging method. Speckle
tracking echocardiography (STE) is a new cardiac ultrasound technique
that allows to assess LV function semi automatically, with a simplified
operational process and high reproducibility. Furthermore, STE has been
demonstrated to be superior to conventional echocardiographic methods to
evaluate cardiac functions and predict cardiovascular outcomes as well
(8,9). Another advantageous feature of STE is it's low intra-and
inter-observer variability. Being independent from angle and index makes
it more useful too and thus, with all those positive aspects it may
become the optimal method for global LV systolic function evaluation
(10). Peak Longitudinal strain (PLS) and post systolic shortening (PSS)
have been shown to detect resting ischemia in the literature (11-15). In
our study, we aimed to evaluate the rest ischemia with STE and compare
it with the two methods in patients who were scheduled coronary
angiography according to the stress tests .

\textbf{METHODS}

\textbf{Study population}

The study was approved by the \selectlanguage{ngerman}Çanakkale Onsekiz Mart University Ethics
Committee and conformed to the principles outlined in the Declaration of
Helsinki. All subjects participating in the study gave informed consent.
The subjects who underwent either myocardial perfusion scintigraphy or
treadmill test for myocardial stress, were included in this prospective
study and the ones who had positive stresss test and scheduled for
coronary angiography were evaluated with STE.

All participants were initially evaluated by a standard
echocardiographic examination. Patients with previous myocardial
infarction, patients with acute coronary syndrome, moderate and severe
valve disease, cardiomyopathy, chronic systemic or inflammatory diseases
or any form of malignancy, and patients with previous thoracic surgery,
were excluded from the study.

Ventricular function was assessed by STE before the angiography and it
was compared with angiography results thereafter (Figure 1)

\textbf{Standard echocardiography}

Echocardiographic examinations were performed using a high-quality
echocardiography machine (Vivid 7, GE, USA) by two cardiologists. Our
echocardiography machine was additionally calibrated for international
studies by an independent organization (certificate no: B14091148).
Measurements of LV and LA dimensions were made in accordance with the
most up to date European Society of Echocardiography recommendations
(16). LVEF was measured using the modified biplane Simpson's rule. The
ratio between peak early (E) and late (A) diastolic LV filling
velocities and E wave deceleration time was determined by standard
Doppler imaging. The timing of mitral and aortic valve opening and
closing were defined by a pulsed-wave Doppler tracing of the mitral
inflow and LV outflow. Lateral wall and septal tissue Doppler parameters
(E\selectlanguage{english}' and A\selectlanguage{english}') were measured as well. E/E\selectlanguage{english}' was calculated manually.
Particular attention was given to limit myocardial tissue and
extracardiac structures, providing sufficient reliable data to obtain a
gray-scale image.

\textbf{Speckle tracking echocardiography}

Apical four and two-chamber, apical long-axis and parasternal short-axis
images were acquired using conventional two-dimensional gray-scale
echocardiography for speckle tracking evaluation on breath hold with a
stable ECG recording and further Speckle tracking evaluation was
performed by the same cardiologist. Three consecutive heartbeats were
recorded and averaged. The frame rate was adjusted to between 90 and 120
frames per second. Automatic function imaging method was used for the
assessment. The region of interest (ROI) was manually outlined by
marking the endocardial borders at the mitral annulus level and at the
apex on each digital loop. The epicardial surface was generated by the
software (EchoPac, version 7.0.1 GE, USA) so that the ROI was created
(Figure 2). The ROI was corrected manually at the end, if needed. After
manual adjustments, ROI was divided into six segments and each segment
was scored automatically by the software according to the image quality.
Whether the tracking quality for each segment could be considered
acceptable was determined by the software. The peak systolic strain
values in a 17-segment LV model were used in the presented study. End-
systole was defined as aortic valve closure in the apical long- axis
view. The results for all three planes were then combined in a single
bulls-eye summary that provided the global longitudinal strain

\textbf{Defining peak longitudinal strain and post systolic shortening}

Peak longitudinal systolic strain (PLS) was measured as the maximum
value of strain in systole, which was defined as the time interval
between the aortic valve opening and closure. Strain values were also
evaluated segmentally according to the area at risk. Values above -18
were considered significant for PLS.

PSS is described as myocardial contraction that occur after end systole
or aortic valve closure. Criteria for pathologic PSS was, when PSS
exceeds 20\% of ejection time and when it takes more than 90 ms after
AVC (5).

\textbf{Statistical analysis}

Statistical analysis was carried out with the SPPS program (version
21.0, SPSS, Chicago, \selectlanguage{polish}İ\selectlanguage{english}llinois, USA). All measurements were evaluated
with the Kolmogorov-Smirnov test for normality. A comparison of
continuous variables between the groups was performed using the
Mann-Whitney U test. All continuous variables were expressed as mean \selectlanguage{ngerman}±
standartd deviation values. PLS values were compared to according to
presence of more than 50\% stenosis least one vessel. Categorical
variables were analysed using the Chi-square test. Presence of PSS in
each segment were compared according to more than 50\% stenosis in
segment related coronary artery. We also evaluated the relation between
presence of PSS of segments and presence of severe coronary artery
disease of at least one vessel. Correlations between coronary artery
disease severity and peak systolic strain for each coronary artery and
its territory was evaluated by a Pearson correlation test where
two-sided P values \textless{}0.05 were accepted as statistically
significant

\textbf{RESULTS}

50 patients were recruited in our study. The general characteristics of
the study population depicted in table 1. Echocardiographic findings of
the study population were in normal range. Conventional echocardiography
parameters shown in table 2. 38 patients had severe CAD
(\textgreater{}50\%) whilst 12 patients had no significant CAD. PSS was
significantly related with CAD and area at risk in all echo planes.
(p\textless{}0.0001) LV wall analysis of PSS according to the coronary
occlusion was showed in Table 3. In the segmental PSS analysis, the
presence of PSS in the basal anterior and mid anterior segments was
found to be significantly associated with left anterior descending
artery (LAD) stenosis, respectively p\textless{}0.001,
p\textless{}0.001. The presence of PSS in the basal lateral wall was
found to be significantly associated with circumflex (LCX) stenosis,
p=0.032. The presence of PSS in the basal inferior wall was found to be
significantly associated with right coronary artery (RCA) stenosis,
p=0.021. Detailed segmental analysis of PSS according to the coronary
artery stenosis was showed in supplementary table 1. The relationship of
PLS with the area at risk was found to be statistically insignificant
whereas GLS was significantly lower in patients with severe CAD
(p=0.011). LV wall analysis of PSS according to the coronary occlusion
was showed in Table 4. The presence of PSS was not associated with the
coronary stenosis in segmental PLS analysis. Detailed segmental analysis
of PSS according to the coronary artery stenosis was showed in
supplementary table 2.

\textbf{DISCUSSION}

In our study we found that PSS is more sensitive and specific for
coronary arterial lesion than PLS in patients with stable CAD. We also
found that GLS was lower in patients with severe coronary artery disease
but there was no correlation with ischemic risk area. It has been shown
that in different clinical and experimental studies, that PSS is
superior to conventional methods, such as wall thickening and peak
longitudinal systolic strain in detecting acute coronary ischemia and
coronary artery disease (4,17,18). We also tested the capability of PSS
and PLS to predict coronary lesions in patients scheduled for coronary
angiography as a result of a stress test and confirmed the results with
coronary angiography.

It has been proven in a vast number of studies that strain is highly
correlated with severity of coronary artery disease (3-10) and that PLS
and PSS can detect acute coronary ischemia (4,12,15). Additionally, it
is also known that PSS can be seen in around 15\% of normal healthy
people, particularly in basal segments. We applied the criteria from
previous studies for PSS assessment to avoid false positive results (5).
PSS was mostly seen in the basal and mid segments in our study too.
Similarly, it has been shown that PSS is more common in basal segments
(5), and contraction anomalies are seen in apical segments rather than
temporal anomalies (19).

Experimental animal studies have also demonstrated that PLS and PSS are
significantly reduced in coronary artery occlusion (20-22). PSS
continued while systolic strain recovered rapidly after reperfusion.
Even after 2 minutes of occlusion, PSS was persisting (23, 24). These
findings depicted that PSS can be more sensitive and specific in
detecting intermittent mild ischemia. Mechanism of PSS is still
speculative. Some studies claimed that it is due to prolonged
contraction and delayed relaxation (25) while some others suggested that
fatty acid metabolism is responsible fot that, which is suppressed
during ischemia (26,27). This may also be a combination of active and
passive processes (28,29).

Stable CAD and low-risk unstable angina are most commonly caused by
atheromatous plaques in the coronary arteries that obstruct blood flow
and may lead to the silent ischemia (30). Silent ischaemia is common and
prognostically important entity (31). There is also evidence that silent
myocardial ischemia is seen more frequently than anginal attacks in
patients with coronary artery disease (32). It has been already found
that more than 70\% of patients with stable angina have frequent
episodes of silent ischemia (33). In different studies silent myocardial
ischemia has been indicated to occur frequently even during treatment
with conventional anti-anginal drugs (33, 34). Both an increase in
myocardial oxygen demand and abnormalities of coronary vasomotor tone
appear to play a significant role in the genesis of silent ischemia
(34). For this reasons, we consider that silent ischemia is present in
stable coronary artery patients and we suggest that PSS may detect
serious coronary artery disease without performing stress test.

GLS was lower in patients with severe coronary artery disease, similar
to previous studies (7-10). However, segmental analysis was not
performed in these above mentioned studies. Unlike previous studies, we
performed segmental analysis and also investigated the relationship
between PLS and the area at risk as well. No relation was found between
the area with severe coronary artery disease and PLS in our study.
Although strain values are within normal limits, PSS was seen in
ischemic segments in patients with severe coronary lesion. Similarly, a
recent published study demonstrated that PLS could be a sensitive but
nonspecific imaging method to determine significant CAD at rest (35).
Figure 3

\textbf{STUDY LIMITATIONS}

The major limitation of our study was echo window quality. Good echo
window is \emph{sine qua non for an accurate} speckle tracking imaging.
Despite a high quality echocardiography machine we used and experienced
cardiologists, we couldn't overcome this problem completely when
particularly the problem is patient related. Another limitation was that
we could not exclude microvascular disease in our study. Furthermore,
regrettably in some patients coronary lesion severity was evaluated
visually and FFR technique was not available for all patients.

\textbf{CONCLUSION}

PSS may detect coronary ischemia in patients with stable CAD and it is
more sensitive and specific in patients with stable CAD. STE is a great
help for clinicians as it is a practical, useful, easy applicable cost
effective noninvasive tool for detecting severe coronary artery disease
at rest.

\textbf{Funding} : No funding

\textbf{Conflict of interest} : There is no conflict of interest

\textbf{Author contributions} :

All authors contributed to: substantial contributions to conception and
design, or acquisition of data, or analysis and interpretation of data,
drafting the article or revising it critically for important
intellectual content, and, final approval of the version to be
published.

\textbf{REFERENCES}

\begin{enumerate}
\tightlist
\item
  Writing Group Members, Lloyd-Jones D, Adams RJ, \emph{et al.} Heart
  disease and stroke statistics-2010 update: A report from the American
  Heart Association. Circulation 2010;121:e46-215.
\item
  Celermajer DS, Chow CK, Marijon E, Anstey NM, \emph{et
  al.}Cardiovascular disease in the developing world: Prevalences,
  patterns, and the potential of early disease detection. J Am Coll
  Cardiol 2012;60:1207-16.
\item
  Bruce RA, DeRouen TA, Hossack KF, \emph{et al.} Value of maximal
  exercise tests in risk assessment of primary coronary heart disease
  events in men. Am J Cardiol 1980;46:371-8.
\item
  Brown MA, Norris RM, Takayama M, \emph{et al.} Post-systolic
  shortening a marker of potential for early recovery of acutely
  ischaemic myocardium in the dog. \emph{Cardiovasc Res} .
  1987;21:703--716.
\item
  Voigt JU, Lindenmeier G, Exner B, \emph{et al.} Incidence and
  characteristics of segmental postsystolic longitudinal shortening in
  normal, acutely ischemic, and scarred myocardium. \emph{J Am Soc
  Echocardiogr} . 2003;16:415--423.
\item
  Choi JO, Cho SW, Song YB, et al. Longitudinal 2D strain at rest
  predicts the presence of left main and three vessel coronary artery
  disease in patients without regional wall motion abnormality. Eur J
  Echocardi- ogr 2009; 10(5): 695-701. Doi: 10.1093
\item
  Singh J, Kannan A, Saleh A, \emph{et al.} Diagnostic accuracy of
  2D-speckle echocardiography for detection of obstructive coronary
  artery disease: a meta-analysis. J Am Coll Cardiol 2013; 61(10\_S):
  Doi: 10.1016/S0735-1097(13)6100
\item
  Monodeep B, Selvin S, Navin CN, et al. Two- and Three-Dimensional
  Speckle Tracking Echocardiography: Clinical Applications and Future
  Directions. Echocardiography 2013; 30(1): 88-105. DOI:
  10.1111/echo.12079
\item
  Geyer H, Caracciolo G, Abe H, Wilansky S, et al. Assessment of
  myocardial mechanics using speckle tracking echocardiography:
  fundamentals and clinical applications. J Am Soc Echocardiogr 2010;
  23: 351-69. Doi: 10.1016
\item
  Montgomery DE, Puthumana JJ, Fox JM, \emph{et al.} Global longitudinal
  strain aids the detection of non- obstructive coronary artery disease
  in the resting echocardiogram. European Heart Journal - Cardiovascular
  Imaging 2012; 13: 579-87.
\item
  Singh J, Kannan A, Saleh A, \emph{et al.} Diagnostic accuracy of
  2D-speckle echocardiography for detection of obstructive coronary
  artery disease: a meta-analysis. J Am Coll Cardiol 2013; 61(10\_S):
  Doi: 10.1016/S0735-1097(13)6100
\item
  Asanuma T, Uranishi A, Masuda K, \emph{et al.} Assessment of
  myocardial ischemic memory using persistence of post- systolic
  thickening after recovery from ischemia. \emph{JACC Cardiovasc
  Imaging} . 2009;2:1253--1261.
\item
  Singh J, Kannan A, Saleh A, \emph{et al.} Diagnostic accuracy of
  2D-speckle tracking echocardiography for detection of obstructive
  coronary artery disease. J Am Coll Cardiol 2013;61 Suppl 10:E1008.
\item
  Biering-Sørensen T, Hoffmann S, Mogelvang R, \emph{et al.} Myocardial
  strain analysis by 2-dimensional speckle tracking echocardiography
  improves diagnostics of coronary artery stenosis in stable angina
  pectoris. \emph{Circ Cardiovasc Imaging} . 2014;7:58--65.
\item
  Ozawa K, Funabashi N, Nishi T, \emph{et al.} Differentiation of
  infarcted, ischemic, and non-ischemic LV myocardium using
  post-systolic strain index assessed by resting two- dimensional
  speckle tracking transthoracic echocardiography. \emph{Int J Cardiol}
  . 2016;219:308--311.
\item
  Lang RM, Badano LP, Mor-Avi V, \emph{et al.} Recommendations for
  cardiac chamber quanti\selectlanguage{english}fication by echocardiography in adults: an update
  from the American Society of Echocardiography and the European
  Association of Cardiovascular Imaging. \emph{J Am Soc Echocardiogr} .
  2015;28:1--39.e14.
\item
  Rambaldi R, Bax JJ, Rizzello V, \emph{et al.} Post-systolic shortening
  during dobutamine stress echocardiography predicts cardiac survival in
  patients with severe left ventricular dysfunction. \emph{Coron Artery
  Dis} . 2005;16:141--145.
\item
  Kukulski T, Jamal F, Herbots L, \emph{et al.} Sutherland GR.
  Identi\selectlanguage{english}fication of acutely ischemic myocardium using ultrasonic strain
  measurements: a clinical study in patients undergoing coronary
  angioplasty. \emph{J Am Coll Cardiol} . 2003;41:810--819.
\item
  Natarajan, A, and A A Bove. ``Comparison of shortening with timing of
  wall motion in detecting regional abnormalities of the left ventricle
  in coronary disease.''~~\emph{Cathet Cardiovasc Diagn} .
  1993;28(2):106-113.
\item
  Pislaru C, Belohlavek M, Bae RY, \emph{et al} . Regional asynchrony
  during acute myocardial ischemia quanti\selectlanguage{english}fied by ultrasound strain rate
  imaging.\emph{J Am Coll Cardiol} 2001;37:1141--8.
\item
  Belohlavek M, Pislaru C, Bae RY, \emph{et al} . Real-time strain rate
  echocardiographic imaging: temporal and spatial analysis of
  postsystolic compression in acutely ischemic myocardium.\emph{J Am Soc
  Echocardiogr} 2001;14:360--9.
\item
  Masuda K, Asanuma T, Taniguchi A, \emph{et al} . Assessment of
  dyssynchronous wall motion during acute myocardial ischemia using
  velocity vector imaging.\emph{J Am CollCardiol Img} 2008;1:210--20.
\item
  Asanuma T, Fukuta Y, Masuda K, \emph{et al} . Assessment of myocardial
  ischemic memory using speckle tracking echocardiography.\emph{J Am
  Coll Cardiol Img} 2012;5:1--11.
\item
  Asanuma T, Uranishi A, Masuda K, \emph{et al} . Assessment of
  myocardial ischemic memory using persistence of post-systolic
  thickening after recovery from ischemia.\emph{J Am Coll Cardiol Img}
  2009;2:1253--61.
\item
  Akaishi M, Schneider RM, Seelaus PA, \emph{et al} . A non-linear
  elastic model of contraction of ischaemic segments.\emph{Cardiovasc
  Res} 1988;22:889--99.
\item
  Kawai Y, Tsukamoto E, Nozaki Y, \emph{et al} . Signi\selectlanguage{english}ficance of reduced
  uptake of iodinated fatty acid analogue for the evaluation of patients
  with acute chest pain.\emph{J Am Coll} \emph{Cardiol}
  2001;38:1888--94.
\item
  Dilsizian V, Bateman TM, Bergmann SR, \emph{et al} . Metabolic imaging
  wit \selectlanguage{greek}β-\selectlanguage{english}methyl-\emph{p}
  -{[}\textsuperscript{123}I{]}-iodophenyl-pentadecanoic acid identifies
  ischemic memory after demand
  ischemia.\emph{Circulation}2005;112:2169--74
\item
  Claus P, Weidemann F, Dommke C, \emph{et al} . Mechanisms of
  postsystolic thickening in ischemic myocardium: mathematical modelling
  and comparison with experimental ischemic substrates.\emph{Ultrasound
  Med Biol} 2007;33;1963--70.
\item
  Sengupta PP. Exploring left ventricular isovolumic shortening and
  stretch mechanics: ``The heart has its reasons\ldots{}''.\emph{J Am
  Coll Cardiol Img} 2009;2:212--15.
\item
  Berry C. Stable coronary syndromes: the case for consolidating the
  nomenclature of stable ischemic heart
  disease.\emph{Circulation}2017;136:437 9.
\item
  Yeung AC, Barry J, Orav J, et al. Effects of asymptomatic ischemia on
  long-term prognosis in chronic stable coronary disease. Circulation
  1991; 83:1598.
\item
  Deedwania PC, Carbajal EV. Prevalence and patterns of silent
  myocardial ischemia during daily life in stable angina patients
  receiving conventional antianginal drug therapy. Am J Cardiol 1990;
  65:1090.
\item
  Deanfield JE, Maseri A, Selwyn AP, \emph{et al.} Myocardial ischaemia
  during daily life in patients with stable angina: Its relation to
  symptoms and heart rate changes. Lancet 1983;2:753-758
\item
  Deedwania PC, Carbajal E, Nelson J, \emph{et al.} Antianginal therapy
  directed towards symptom control does not abolish silent ischemic
  events (abstract). JAm Coll Cardiol 1988;2:47A.
\item
  Mahjoob MP, Alipour Parsa S, Mazarei A, \emph{et al.} Rest 2D speckle
  tracking echocardiography may be a sensitive but nonspecific test for
  detection of significant coronary artery disease. Acta Biomed. 2018
  Jan 16;88(4):457-461.
\end{enumerate}

\textbf{Figure Legends}Figure 1. Study protocol Figure 2. Contouring of
left ventricle by speckle tracking echocardiography. LV=left Ventricle,
LA=Left Atrium, RV=Right Ventricle,RA= Right Atrium Figure 3. A: Normal
strain values and no PSS in 4ch view. B and C: Strain analysis indicates
significant PSS in basal inferior and basal posterior wall. D: Normal
strain values in bulls eye image. E: Coronary angiography showed that
diffuse atherosclerosis and severe occlusion before the bifurcation in
the RCA, RCA=Right Coronary Artery\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Figure-1/Figure-1}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Figure-2/Figure-2}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Figure-3/Figure-3}

\end{center}
\end{figure}

\selectlanguage{english}
\FloatBarrier
\end{document}

