Predictors of Spontaneous Echo Contrast in Left Heart Chambers in Patients with Dilated Cardiomyopathy: Slowing Down Might not Always Mean Enjoying Life.

INTRODUCTION: Spontaneous echo contrast(SEC) is usually detected in heart chambers as a result of reduced flow velocity in the cavity. The clinical importance of SEC lies in its association with embolic events. The aim of our study was to determine the frequency of SEC in left heart chambers in sinus rhythm patients with dilated cardiomyopathy and predictors for its emergence.
MATERIALS AND METHODS: This was a prospective cross-sectional transesophageal echocardiography study conducted in 101 sinus rhythm patients with dilated heart and mild-to-moderate systolic dysfunction.
RESULTS: Moderate-degree SEC was found in the left ventricle(LV) in around 9% of patients, in the left atrium(LA) in 12% and in left atrial appendage(LAA) in 40%. Multiple regression analysis showed that lower heart rate(95% confidence interval[CI]: 0.845-0.978; P = 0.011) and larger LV end-systolic diameter(LVESD)(95% CI: 1.034-1.394; P = 0.017) were independent predictors for LV SEC presence. Lower LV ejection fraction(LVEF) (95% CI: [-0.079]-[-0.037]; P = 0.0001) was the only independent predictor for SEC in the LA. Whereas, independent predictors for SEC in LAA were lower heart rate(95% CI:[-0.030]-[-0.003]; P = 0.018), greater LA indexed diameter (95% CI: 0.016-0.116; P = 0.010), and higher value of C-reactive protein(CRP)(95% CI: 0.0026-0.031; P = 0.027).
CONCLUSIONS: SEC in left heart chambers is a frequent finding in patients with dilated cardiomyopathy in sinus rhythm. Lower heart rate and LVEF, larger LVESD and LA, as well as higher CRP, predict the presence of SEC in left heart chambers. Lower heart rate might be an essential predictor for SEC presence and severity in these patients. Copyright:

INTRODUCTION

Spontaneous echo contrast (SEC) is the swirling “smoke like” echo detected in the heart chambers as a result of reduced flow velocity in the cavity. Most frequent causes of SEC are rheumatic mitral stenosis, mitral valve prosthesis, atrial fibrillation, dilated heart chambers, dyskinetic segments of left ventricle, and impaired myocardial contractility. The clinical importance of SEC lies in its association with embolic events. The prevalence of SEC in patients with cerebral embolic events or peripheral embolic events varies from 16% to 84%.[123]

The purpose of this study was to determine the frequency of SEC in left heart chambers in patients with dilated cardiomyopathy and sinus rhythm, as well as predictors for its emergence.

MATERIALS AND METHODS

This was a prospective cross-sectional transesophageal echocardiography (TEE) study that included 101 patients with dilated cardiomyopathy of mild-to-moderate systolic dysfunction and sinus rhythm, who were not taking anticoagulation medications. Exclusion criteria were patients with atrial fibrillation/flutter, severe left ventricular dysfunction, prosthetic valves, and valvular disease, in whom SEC is expected. Demographic and history data, physical examination, laboratory tests, electrocardiogram (ECG), chest X-ray, transthoracic echocardiography (TTE), and TEE were obtained for each patient. According to symptoms, patients were classified by New York Heart Association (NYHA) class from I (no symptoms after ordinary activities) to IV (symptoms occur at rest).

The study was approved by the Ethical Board of our institution and written informed consent was taken from every patient that entered the study.

Echocardiography

TTE (Phillips iE 33) examinations and measurements were performed according to the recommendations of the American Society of Echocardiography.[4] Left ventricular end diastolic diameter (LVEDD), left ventricular end systolic diameter (LVESD), septal wall and posterior wall thickness were measured from parasternal M-mode view according to standard criteria. Left ventricular ejection fraction (LVEF) was determined from apical views with modified Simpson's rule. LVEF <50% was considered as systolic dysfunction, whereas LVEF under 30% was considered as severe left ventricular dysfunction. Left atrial (LA) diameter was measured in two-dimensional projection at end-ventricular systole in parasternal long axis view. Measurement of LA volume was done with area-length (L) method using apical 4-chamber (A4C) and apical 2-chamber (A2C) views at ventricular end-systole (maximum LA size), whereas L was measured from back wall to line across hinge points of mitral valve. Calculation of LA volume was made by the following formula: 8/3 π [(A1)(A2)/L]. Wall motion score index (WMSI) was evaluated by the 17 segment model and the sum of all scores, acquired from wall kinetics, was divided by the number of segments. Mitral annular plane systolic excursion (MAPSE) was measured in millimeters (mm) by M-mode echocardiography from four different points (septal, lateral, inferior and anterior mitral annuli) by apical four-chamber and apical two-chamber approaches and subsequently the average value was generated. LV sphericity index in end-diastole and end-systole was defined as the ratio of LV width (measured at midpoint of LV length) to LV length (measured from apex to the middle of mitral annular plane) in the four-chamber view.

TEE (Phillips iE 33) was performed in all patients that entered this study, with the main aim at analysing left atrial appendage (LAA). TEE images were analysed by two experienced cardiologists, separately. In case there were discrepancies in judgment, then a third independent cardiologist, blinded with the results, was asked to solve the dilemma. The LAA was visualized from the two-chamber longitudinal view of the left cavities. Maximum and minimum LAA area was measured by planimetry method, by tracing the LAA starting from the top of the limbus of the upper pulmonary vein along the entire appendage endocardial border. The maximal area of the LAA was measured during LAA diastole at the onset of ECG P wave, while the LAA minimal area was measured at systole during the ECG R wave. The LAA ejection fraction (LAAEF) was calculated from the following equation: LAAEF (%) = 100 × (LAAmax − LAAmin)/LAAmax.

SEC was identified if dynamic “smoke-like” echos with swirling motion in the cavity were seen. SEC was classified according to Fatkin into five categories, from 0 to 4+. Level 0 indicating absence of echogenicity; level 1 showing mild SEC (minimal echogenicity only transiently detectable with optimal gain settings during the cardiac cycle); level 2 with mild-to-moderate SEC (transient SEC without increased gain settings and more dense pattern than 1+); level 3 with moderate SEC (dense swirling pattern throughout the cardiac cycle); and level 4 defined as severe SEC (intense echodensity and very slow swirling patterns).[5]

LAA flow velocities were obtained with pulsed-wave Doppler interrogation, by placing the sample volume at the orifice of the LAA. Four waves were identified: “e” wave, which represents the early diastolic emptying flow; “a” wave, which corresponds to the LAA intrinsic late diastolic contraction; early systolic negative wave, which is the LAA filling; the systolic reflection waves, which appear if the heart rate is slow enough and if the LAA function is normal. Peak “a” wave and peak systolic wave were measured.

Patients with LAA peak emptying velocity <40 cm/s and/or SEC and/or thrombus in LAA were considered as having LAA dysfunction.

Statistical analysis

The data were expressed as mean ± standard deviation (SD) and percentages. Comparison between two groups of continuous variables was performed using two-tailed unpaired t-test and for categorical variables using Pearson's Chi-square test. Correlation of selected variables was estimated using Spearman's correlation coefficient, as we assumed nonlinear correlation existence. Multiple regression analysis was used as a prediction model and the data were expressed with 95% confidence intervals (CIs) and probability value adjusted for all other measured risk factors. Variables with a value of P < 0.05 were considered significant. Statistical software SPSS 22.0 (IBM SPSS, Inc., Chicago, Illinois, USA) packet for statistical analysis was used.

RESULTS

Basic clinical and echocardiography features are presented in Tables 1-3. In regard to patient symptoms, 15.8% of our patients belonged to NYHA class I, 68.3% were in NYHA class II, and 15.8% were classified in NYHA class III. None of our patients had severe symptoms that would classify them in NYHA class IV. One-third of the patients were diagnosed for the first time with dilated cardiomyopathy. Concerning cardiac therapy that they were taking prior to entering the study, 75% of patients were taking aspirin, 71% angiotensin-converting enzyme inhibitors, 67% beta blockers, 57% diuretics, 42% statins, 3% digoxin, and 3% angiotensin II receptor blockers.

Table 1

Basic characteristics of all patients in the study (n=101)

Parameter	Mean±SD or n (%)
Age	58.13±12.66
Gender male/female (%)	70/31 (69.3/30.7)
BMI (kg/m2)	28.39±4.04
Smoking (%)	30 (29.7)
Alcohol (%)	10 (9.9)
HT (%)	52 (51.5)
DM (%)	30 (29.7)
Duration of DM (years)	6.83±6.23
Dyslipidemia (%)	25 (24.8)
History of CAD	57 (56.4)
History of vascular disease	6 (5.9)
Heart rate (beats/min)	75.25±11.19
PT (%)	101.14±12.62
PTT (s)	25.54±4.22
TT (s)	11.23±0.89
RBC (×1012/L)	4.16±0.54
PCV (g/L)	88.41±7.09
Plt (×109/L)	218.24±58.19
WBC (×109/L)	8.51±2.88
Glucose (mmol/L)	6.71±3.02
Creatinine (µmol/L)	96.80±39.57
CRP (mg/L)	5.63±10.63
ALT (IU/L)	22.59±12.67

BMI=Body mass index, HT=Hypertension, DM=Diabetes mellitus, CAD=Coronary artery disease, PT=Prothrombin time, PTT=Partial thromboplastin time, TT=Thrombin time, RCB=Red blood cells, PCV=Packed cell volume, Plt=Platelets, WBC=White blood cell, CRP=C-reactive protein, ALT=Alanine transaminase

Table 3

Characteristics of left atrial appendage size and function assessed by transesophageal echocardiography in all patients (n=101)

Parameter	Mean±SD or n (%)
LAA maximum area (cm2)	4.73±1.59
LAA minimum area (cm2)	2.55±1.41
LAA EF (%)	47.50±20.92
a’ wave (cm/s)	54.11±24.44
Filling wave (cm/s)	44.86±20.97
LAA dysfunction (%)	87 (86.1)

LAA=Left atrial appendage, EF=Ejection fraction

SEC in all left heart chambers was a frequent finding in our patients, as shown in Table 4 and Figure 1. We found predominantly mild and moderate degree of SEC. Severe SEC was found in only two patients and it was present in the LAA.

Table 4

Presence of spontaneous echo contrast assessed by transesophageal echocardiography in all patients (n=101)

Parameter	n (%)
SEC LV
0	7 (6.9)
1+	43 (42.6)
2+	42 (41.6)
3+	9 (8.9)
4+	0 (0)
SEC LA
0	5 (5.0)
1+	51 (50.5)
2+	33 (32.7)
3+	12 (11.9)
4+	0 (0)
SEC LAA
0	2 (2.0)
1+	17 (16.8)
2+	40 (39.6)
3+	40 (39.6)
4+	2 (2.0)

SEC=Spontaneous echo contrast, LV=Left ventricle, LA=Left atrium, LAA=Left atrial appendage

Figure 1

(a and b) Transthoracic echocardiography and transesophageal echocardiography figures of a 75-year-old male patient at sinus rhythm with dilated cardiomyopathy and history of diabetes mellitus, coronary artery disease and peripheral artery disease. Left ventricle spontaneous echo contrast grade 2, left atrium spontaneous echo contrast grade 2, and left atrial appendage spontaneous echo contrast grade 3 were registered. Left ventricular end diastolic diameter was 67 mm, left atrium diameter 52 mm, and left ventricular ejection fraction was 30%. In (a), an apical left ventricle mural thrombus of 25 mm × 2 mm is depicted by transthoracic echocardiography. In (b) in a transesophageal echocardiography image of the same patient, a spherical mobile thrombus of 4 mm × 5 mm dimension is seen in left atrial appendage

SEC in left heart chambers was significantly related to several parameters, as shown in Table 5. However, multiple regression analysis showed that only lower heart rate (95% CI: 0.845–0.978; P = 0.011) and larger LVESD (95% CI: 1.034–1.394; P = 0.017) were independent factors for LV SEC presence. Whereas, lower LVEF (95% CI: [−0.079]–[−0.037]); P = 0.0001) was the only independent predictor for SEC in the LA. While, independent predictors for SEC presence in LAA were lower heart rate (95% CI: [−0.030]–[−0.003]; P = 0.018), greater LA d/BSA (95% CI: 0.016–0.116; P = 0.010), and higher value of C-reactive protein (CRP) (95% CI: 0.0026–0.031; P = 0.027). Lower heart rate was an independent predictor for SEC, both in LV and in LAA. Lower heart rate was responsible for 23.8% severity of SEC in left heart chambers (R2 = 0.238), meaning that for every one beat decrease of heart rate, the severity of SEC in left heart cavities increases by 0.018 units (95% CI: [−0.032]–[−0.003]) (P = 0.016).

Table 5

Correlation of spontaneous echo contrast with different parameters

	SEC LV	SEC LA	SEC LAA
Age	r=0.2; P=0.045	/	/
Male gender	/	r=0.211; P=0.034	/
History of CAD	r=0.2; P=0.045	/	r=0.284; P=0.004
Duration of DM	/	/	r=0.404; P=0.030
NYHA class	r=0.289; P=0.003	r=0.276; P=0.005	/
HR	r=0.289; P=0.003	r=−0.200; P=0.045	r=−0.238; P=0.016
Packed cell volume	/	r=0.332; P=0.001	/
Red blood cells	/	r=0.268; P=0.007	/
CRP	/	/	r=0.200; P=0.044
LVEDD	r=0.324; P=0.001	r=0.398; P=0.0001	/
LVESD	r=0.440; P=0.0001	r=0.425; P=0.0001	/
LVEF	r=−0.443; P=0.0001	r=−0.494; P=0.0001	/
WMSI	r=0.295; P=0.02	r=0.468; P=0.0001	/
LV width diastole	r=0.221; P=0.026	/	/
LV width systole	r=0.270; P=0.006	r=0.339; P=0.001	/
LV length diastole	r=0.208; P=0.037	/	r=0.238; P=0.016
LV width systole	/	/	/
MAPSE average	r=−0.330; P=0.001	r=−0.305; P=0.002	/
LA diameter	/	r=0.258; P=0.009	r=0.252; P=0.011
LAd/BSA	/	r=0.256; P=0.01	r=0.284; P=0.004
LA area	/	r=0.255; P=0.01	/
LAV/BSA	/	r=0.210; P=0.035	/
LAA area	/	/	r=0.196; P=0.049
LAA dysfunction	/	/	r=0.354; P=0.0001

SEC=Spontaneous echo contrast, CAD=Coronary artery disease, DM=Diabetes mellitus, NYHA=New York Heart Association, HR=Heart rate, CRP=C-reactive protein, LVEDD=Left ventricular end diastolic diameter, LVESD=Left ventricular end systolic diameter, LVEF=Left ventricular ejection fraction, WMSI=Wall motion score index, LV=Left ventricle, MAPSE=Mitral annular plane systolic excursion, LA=Left atrium, Lad/BSA=Left atrial diameter/body surface area, LAA=Left atrial appendage

Comparison of patients' basic echocardiography features according to severity of SEC, those with lower grade SEC to patients with higher grade SEC, is shown in Table 6. As shown in this Table 6, patients with high grade SEC in the LV and LA (51 and 45 patients, respectively) had significantly larger LVEDD, lower LV EF, and average MAPSE, whereas WMSI was higher. On the other hand, the 42 patients with grade 3 and 4 sec in the LAA had significantly larger LA diameter and LAA area compared to patients with lower grade SEC.

Table 6

Differences in main echocardiographic findings in patients with lower grade spontaneous echo contrast compared to higher grade spontaneous echo contrast in left heart chambers

LV SEC
Echocardiographic parameter	LV SEC Grade 0-1 (n=50)	LV SEC Grade 2-3 (n=51)	P
LVEDD (mm)	64.8±5.8	68.6±6.2	0.02
LVEF (%)	41.8±6.5	36.1±5.2	<0.0001
MAPSE av (mm)	9.9±2.1	8.7±2.1	0.004
WMSI	1.5±0.4	1.65±0.3	0.04
Diastolic dysfunction (n)	34	32	0.8
LA SEC
Echocardiographic parameter	LA SEC Grade 0-1 (n=56)	LA SEC Grade 2-3 (n=45)	P
LVEDD (mm)	64.9±5.4	69.02±6.2	0.0005
LVEF (%)	41.5±6.2	35.9±5.2	<0.0001
MAPSE av (mm)	9.8±2.2	8.7±2.01	0.01
WMSI	1.4±0.4	1.8±0.3	<0.0001
Diastolic dysfunction (n)	39	26	0.5
LA (mm)	45.1±4.4	47±5.5	0.05
LAA SEC
Echocardiographic parameter	LAA SEC Grade 0-2 (n=59)	LAA SEC Grade 3-4 (n=42)	P
LVEDD (mm)	66.6±6.4	66.7±5.6	0.9
LVEF (%)	39.3±6.04	38.6±6.9	0.6
MAPSE av (mm)	9.4±2.3	9.1±1.96	0.5
WMSI	1.58±0.4	1.6±0.38	0.8
Diastolic dysfunction (n)	37	26	0.9
LA (mm)	45.1±4.8	47.1±4.9	0.048
LAA area (mm2)	4.4±1.5	5.1±1.7	0.04
LAA dysfunction (n)	47	40	0.5

SEC=Spontaneous echo contrast, LVEDD=Left ventricular end diastolic diameter, LVEF=Left ventricular ejection fraction, WMSI=Wall motion score index, LV=Left ventricle, MAPSE av=Mitral annular plane systolic excursion average, LA=Left atrium, LAA=Left atrial appendage

DISCUSSION

SEC was a frequent finding in the left heart cavities in our patients. However, most frequently we found SEC of mild or mild-to-moderate degree, whereas moderate and severe SEC were encountered to a much lesser rate. Therefore, moderate degree of SEC in LV was found in 9 (8.9%) patients, in LA in 12 (11.9%) patients, and in LAA in 40 (39.6%) patients, which is within the range observed by other authors. Severe form of SEC was seen in only 2 (2%) patients, located in LAA.

Findings by other authors in regard to SEC frequency in heart chambers are presented below. In random population undergoing TEE, the prevalence of SEC ranges from 3% to 20%.[67] In smaller series of patients, we reported a high frequency of SEC in left heart chambers in patients with dilated cardiomyopathy at sinus rhythm.[8] Siostrzonek et al. reported that 33% of patients with idiopathic dilated cardiomyopathy had LA SEC, whereas Shen et al. observed SEC in 42% of their 86 patients with dilated cardiomyopathy.[910] Bilge et al. have seen LA SEC in 43% of hypertensive patients with LV systolic dysfunction and sinus rhythm.[11] Furthermore, Kozdag et al. found that silent cerebral infarction is a frequent finding in patients with dilated cardiomyopathy and moderate-to-severe LA SEC is an important factor contributing to this condition.[12] In a large trial, SEC was discovered in 21% of patients with stroke who were in sinus rhythm and had reduced left ventricular function.[13] Chou andWang demonstrated that SEC in LAA is associated with dilated LAA and its impaired contractile function, as well as it presents a sign of increased tromboembolic risk.[14] Handke et al. in a cerebral ischemic patient population reported that 31% of patients with detected LA SEC were in sinus rhythm, and additional 9% were in sinus rhythm but had episodes of paroxysmal atrial fibrillation.[15] We believe that a higher rate of SEC reported in our patients is due to the fact that we have registered even mild degrees of SEC, while we suppose that the above-mentioned authors took into account only more pronounced forms of SEC, as SEC grading was not stated in these papers. Thus, if we compare moderate and severe degree of SEC in left chamber heart cavities in our patients, we conclude that SEC frequency detected in our patients is within the range reported by other authors.

In our study, independent factors for SEC appearance in left heart chambers in patients with dilated cardiomyopathy and sinus rhythm were lower heart rate and larger LVESD for SEC in LV; lower LV EF for SEC in LA; and lower heart rate, larger LAd/BSA, and higher CRP levels for SEC in LAA. Handke et al. in their study identified the following independent predictors of LA SEC and/or thrombus in stroke patients with sinus rhythm and LV systolic dysfunction: LAA flow velocity less than 55 cm/s and LV EF less or equal to 35%.[13] This is in agreement with our results, as LV EF resulted to be an independent predictor for LA SEC in our patient population, also. Sadanandan and Sherrid also found decreased LAA emptying velocity as an independent predictor of LA SEC in patients with sinus rhythm, but in addition to this parameter, they also recognized LA size and history of cerebrovascular event as independent predictors.[16] Earlier Black et al. identified atrial fibrillation, mitral stenosis, left atrial dimension, history of embolism, and mitral regurgitation as independent predictors for LA SEC appearance among the 400 patients that underwent TEE for different indications.[17] Vincelj et al. found that LA SEC was significantly associated with atrial fibrillation, mitral stenosis, absence of mitral regurgitation, and left atrial dimension among the 290 evaluated patients undergoing TEE.[18] Left atrial volume index, in conjunction with LA fractional shortening and acceleration slope of mitral A wave, showed to be independent TTE predictors for LA SEC in a study conducted in stroke patients with sinus rhythm.[19] Ozer et al. described that decreased LAA flow velocity and increased LAA size are significantly associated with LAA SEC in patients with nonvalvular atrial fibrillation and history of stroke.[20] CRP has proved to be related to LA SEC and thrombi by other authors, as well. Thus, Sahin et al. found that high sensitive CRP was significantly related to the presence of mild-moderate SEC and thrombi, mainly in mitral stenosis patients. In addition to this, hs-CRP was the most important determinant of RAA thrombus formation. They concluded that higher hs-CRP level in AF patients may be a predictor for the presence of SEC and thrombi in the atria.[21] Moreover, Ederhy et al. concluded that the combination of clinical risk markers and normal level CRP can help exclude the presence of LA/LAA SEC or LA/LAA thrombus, particularly in patients classified at low or moderate risk of stroke.[22]

Lower heart rate was an independent predictor of SEC presence in LV and LAA in our study population. In this context, Patel et al. demonstrated that by increasing heart rate in heart failure patients, with acute interventions, decreases the tendency towards stasis, thus SEC disappears or its intensity decreases.[23] On the other hand, Bilge et al. demonstrated that acute phase beta blockade (metoprolol 5 mg bolus plus 50 mg orally twice daily for 1 week) in patients with atrial fibrillation and normal LV systolic function may have harmful effect on LAA function, it may also increase SEC (at 1 week) and cause new thrombi.[24]

Clinical implication of this study

It is well known that beta blockers are indicated in heart failure patients, with the purpose of neurohormonal modification, LVEF improvement, arrhythmia prevention, and ventricular rate control. Therefore, beta blocker benefits are manifold, including reduction in mortality rates, hospitalizations and the risk of sudden death; improvement of LV function and exercise tolerance; and decrease of heart failure functional class. Accordingly, high proportion of heart failure patients take beta blocker therapy; similarly, 67% of our patients were taking beta blockers prior to entering our study. However, besides their many beneficial effects, beta blockers may have an unsafe role regarding SEC presence and severity in left heart chambers. In addition to beta-blockers, other medications that are indicated in heart failure patients, that can lower heart rate, such as digoxin and ivabradine, should be given watchfully. Our statistical analysis demonstrated that reduced heart rate increases severity of SEC. Consequently, medications with negative chronotrope effect should be administered cautiously in order to maintain adequate heart rate. Further studies are needed to elucidate the role that lower heart rate in heart failure patients might have in thromboembolic events. Moreover, in the future clinical practice, this might set new bottom target for heart rate in patients with heart failure.

CONCLUSIONS

SEC in left heart chambers is a frequent finding in patients with dilated cardiomyopathy in sinus rhythm. Lower heart rate and LVEF, larger LVESD and LA, as well as higher CRP predict presence of SEC in left heart chambers. Lower heart rate might be an important predictor for SEC presence and severity, thus inquiring increased awareness with negative chronotrope medication dosage.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

Table 2

Basic left ventricle and left atrium features assessed by transthoracic echocardiography in all patients in the study (n=101)

Parameter	Mean±SD
LVEDD (mm)	66.62±6.07
LVESD (mm)	53.62±7.39
IVSd (mm)	9.90±1.99
LVPWd (mm)	9.75±1.43
LVEF (%)	39.02±6.39
LA (mm)	45.96±4.95
LA/BSA (mm/m2)	23.48±3.06
LA volume (ml)	88.06±37.98
LA volume/BSA (ml/m2)	44.87±18.75
WMSI	1.58±0.38
LV width in diastole (cm)	6.29±0.94
LV length in diastole (cm)	7.77±0.93
LVSId	0.81±0.12
LV width in systole (cm)	5.22±0.98
LV length in systole (cm)	7.28±1.04
LVSIs	0.72±0.12
MAPSE average (mm)	9.28±2.17

LV=Left ventricle, LVEDD=Left ventricular end diastolic diameter, LVESD=Left ventricular end systolic diameter, IVSd=Innterventricular septum in diastole, LVPWd=Left ventricular posterior wall in diastole, LVEF=Left ventricular ejection fraction, LA=Left atrium, BSA=Body surface area, LVSId=LV sphericity index in diastole, LVSIs=LV sphericity index in systole, WMSI=Wall motion score index, MAPSE=Mitral annular plane systolic excursion