a b s t r a c t

Aims: Assessment of right ventricular (RV) function in acute pulmonary embolism (PE) has prognostic signifi- cance. The aim of this study was to evaluate right atrium (RA) and RV myocardial damage with 2-dimensional speckle-tracking in patients with an acute central vs an acute peripheral PE.

Methods and Results: Twenty-six patients with acute PE and 10 controls were retrospectively enrolled. Right atri- um and RV myocardial deformation was analyzed using speckle-tracking imaging echocardiography. Parameters were evaluated to illustrate myocardial damage in patients with a central or a peripherally located PE. Thirteen of the enrolled patients had a massive central PE, and thirteen subjects had a peripheral located PE. Base- line characteristics were not significantly different between the 3 groups besides a more elevated heart rate among patients with a central PE (P = .02) and a tendency of an increased D-dimer in this group. Right ventric- ular dimensions were more affected among patients with a PE. Compared with controls, segmental RV and RA strain/strain rate in the free wall was significantly reduced in patients with PE (P b .05). No difference was shown between the 2 groups of PE.

Conclusion: This pilot study suggests that basal-/mid-segments of RA and RV free wall are more affected in pa- tients with a PE compared with controls. Interestingly, we found no significant difference in myocardial RA and RV damage between patients with a central and a peripheral PE. We advocate that PE no matter central or peripheral is a Serious condition and that a peripheral PE has to be intensively treated similar to a central PE.

(C) 2016

Introduction

The assessment of right ventricular (RV) function in acute pulmonary embolism (PE) is of prognostic significance [1]. The aim of this study was to assess regional changes in RV and right atrial (RA) parameters deter- mined, respectively, by 2-dimensional speckle-tracking (2D-STE) and standard echocardiography (2D-TTE) in patients with acute PE.

Massive acute PE is related to high in-hospital or 30-day mortality rates ranging from 4% to 13%. Extensive PE causes an acute increase in the RV afterload and may result in an RV failure [2]. Echocardiography is normally used to evaluate the RV function and so guide the choice of treatment in PE. Ultrasound is low cost, portable, real-time, and non- invasive, and often useful to detect acute PE in patients both in ward and at the emergency department (ED).

Two-dimensional STE has reformed cardiovascular imaging over the past decade. The methodology is based on standard B-mode images to track the motion of speckles over time and to measure the lengthening

? Funding/Support: None.

?? Institution where work was done: Department of Cardiology, Amager Hospital, Co- penhagen, Denmark. Not presented.

* Corresponding author at: Department of Cardiology, Amager Hospital, Italiensvej 1-3, 2300 Copenhagen S, Denmark. Tel.: +45 32343234.

E-mail address: [email protected] (E. Ramberg).

and shortening relative to the baseline value. This enables angle- independent assessment of myocardial mechanics, from which dis- placement, velocity, strain, and strain rate can be derived [3,4].

Myocardial mechanics have been used to study primarily RV and left ventricle performance. Since 2007, strain has been applied to analyze RV and the left atrium in different clinical settings [5-7].

Methods

Patients and protocol

This single-center, retrospective cohort study was conducted at Amager Hospital between January 1, 2013, to April 30, 2015, and com- prised patients with acute PE who were admitted to ED. Ten age- matched Healthy adults served as controls (NL). We enrolled 45 patients with acute PE. Pulmonary embolism was diagnosed in 26 subjects who presented with a refilling defect in pulmonary arteries, in spiral com- puted tomographic angiography and/or a Perfusion defects in V/Q scin- tigraphy [6]. Nineteen subjects were excluded because of suboptimal images. Patients were divided into 2 groups based on the presence of a central (n = 13) or peripherally (n = 13) located PE. Central PE was defined as saddle embolus or any thrombus in the main pulmonary

http://dx.doi.org/10.1016/j.ajem.2016.09.059

0735-6757/(C) 2016

arteries. Identified patients and NL underwent 2D-STE performed by an experienced cardiologist less than 72 hours after the diagnosis of PE. Controls had no evidence of heart diseases. All 2D-STE images made were retrospectively reviewed by physicians who were blinded to the patients’ clinical data. The echocardiographic focus was on the dimen- sion and function of the RV and RA.

Settings for image accession and measurements

Two-dimensional TTE was performed on all patients on GE Vivid S6, USA. The digital stored images were retrieved and analyzed with offline software (GE Healthcare ECHO PAC). The different cardiac measure- ments were calculated according to the recommendations of the American Society of Echocardiography [6].

The general principles that underlie 2D-STE modalities have previ- ously been described [3,4,8].

Myocardial strain is expressed as the relative change from the orig- inal dimension at end-diastole. Myocardial thickening or lengthening was represented by a positive value, and myocardial thinning or short- ening was represented by a negative value.

Myocardial displacement toward the contractile center in the short- axis view or toward the apex in the longitudinal direction was repre- sented by a positive value.

The software automatically divided the short-axis and apical 4- chamber image into 6 standard segments. We divided the myocardium of the RV in 3 different layers (endocardium/midcardium and pericardi- um) and RA in endocardium and pericardium.

Myocardial systolic deformation (S) in longitudinal strain, strain rate, and displacement was obtained from time-strain and time- displacement curves and based on the pulmonary valve closure (PVC). Strain values from the RA were only obtained at PVC because the S value was not accessible.

Strain rate values E and A present early and late events in the cardiac cycle related to the PVC closure.

Statistical analysis

Data were analyzed using standard software. Summary data were expressed as mean values +- SD or as a percentage of the patients. t Test analyses and nonparametric tests were performed to evaluate the relationship between variables. A P value less than .05 was considered statistically significant for all tests.

Results

We evaluated 45 subjects. Our study enrolled 26 patients with com- plete datasets including both echocardiographic and hemodynamic data. We divided the patients into 2 groups; 13 patients diagnosed as having central PE and 13 patients with peripherally PE. We obtained echocardio- graphic data from 10 healthy individuals for comparison. Table 1 summa- rizes baseline characteristics of the patients. There were no significant differences between the groups except for elevated heart rate (P b .02). Eighty-five percent of the patients with central PE had tachycardia com- pared with only 31% among the patients with a peripheral PE. D-dimer level was lower than 1 mg/mL in 15% of the patients with PE. There was a tendency of an increased D-dimer in patients with a central PE.

Right ventricular diameter and volume at end-diastole were signifi- cantly larger in the group of PE in comparison with controls. We found that RVarea, tricuspid annular plane systolic excursion , and RV ejection fraction were significantly reduced in the group of patients with a central PE compared with the measurements in NL (P = .002, P = .02, P = .02). Mean RV ejection fraction was 47% and mean TAPSE was 1.9 cm in the PE group. inferior vena cava diameter was measured as larger in patients with central PE paralleled to patients with a periph- eral PE. Dimensions of the RA did not differ significantly between the groups.

Table 1

Baseline characteristics

	Peripheral PE	Central PE	Control	P
Female (%)	85	62	40	.4
Age (y)	64 (19,5)	66 (20.0)	63 (14.4)	.7
SBP (mm Hg)	133 (19.6)	140 (19.7)	127 (15.1)	.3
DBP (mm Hg)	85 (16.9)	83 (13.3)	72 (10.1)	.1
HR (beats/min)	93 (20.3)	110 (13.6)		.02
SAT-O2 (%)	94 (5.2)	95 (3.3)		.5
D-dimer (mg/L)	9 (11.2)	18 (50)		.3
ECG changes (%)	54	54		.7

Abbreviations: DBP, diastolic blood pressure; ECG, electrocardiogram, changes observed as Q3T3S1/right bundle-block/right-axis deviation or precordial t-segmenT inversion; HR, heart rate, SBP, systolic blood pressure. Data are expressed as mean (SD) or as number/ percentage.

Diastolic relaxation parameters such as isovolumetric relaxation time and the deceleration time were impaired among patients with PE, but the findings were not statistically significant and all measure- ments were within normal range. We found no differences between the groups regarding early filling velocities (E) and the ratio between E and atrial filling velocity (A). Velocity A was observed lower in the group of patients with central PE compared with patients with periph- erally PE (Table 2).

Figs. 1 and 2 show examples of strain imaging and corresponding time-strain/displacement in a healthy subject and in a patient with central PE.

We found no significant regional strain variances between the layers of the RV and RA within the group of patients with PE. Values from the RV and RA endocardium were therefore used as a standard (Figs. 3 and 4).

Right ventricular longitudinal regional strain measured at the time of PVC and at the maximal systolic value (S) revealed that RV basal/ mid free wall was significantly reduced in PE subjects compared with NL (P b .05). We found no significant decrease in longitudinal strain of the RV apical free wall or in the RV septal wall among the patients with PE, but our results indicate a tendency of a distinctly reduced lon- gitudinal strain of the entire endocardium of the RV in the group of PE compared with controls. We found no significant differences in RV lon- gitudinal strain between peripheral or central PE (Table 3).

Almost identical changes were perceived regarding regional longitu- dinal strain measurements for RA. The free basal and mid segment of RA measured in PVC had significantly lower longitudinal strain in the group of PE compared with controls (P b .05). No differences were found in the group of subjects with PE (Table 4).

Notably, the patients with PE had smaller dispersions of longitudinal regional time-displacement curves with abnormal motion in the RV, but the findings were not significant. We found a significantly lower strain rate in the free wall of the RV measured at the time S and E among the patients with a central PE compared with controls. No difference was shown between the 2 groups of PE (Table 3).

Displacement in the free wall of the right atrium (RA) was found to be significantly lower in patients with a central PE compared with con- trols. In general but not quite significant, we found a tendency of im- paired RA displacement in the group of PE. Patients with PE showed a diminished RA strain rate in all measured events of the cardiac cycle, but our findings were not statistically significant (Table 4).

Discussion

This pilot study demonstrates regional RA and RV variation in longi- tudinal strain/strain rates and displacement identified by 2D-STE in sub- jects with acute PE in comparison to NL. Two-dimensional STE could ultimately be automated and be useful in risk stratification of patients with PE in the Acute care settings.

Consistent with previous observations, especially central PE, large RV chamber size and reduced RV systolic function were associated with abnormally high peripherally vascular resistance [9,10]. Inferior

Table 2 Standard TTE
	Peripheral PE (P)	Central PE (C)	Control (NL)	C vs P (P value)	P vs NL (P value)	C vs NL (P value)	P
RVID,d (cm)	3.7 (0.8)	4.0 (0.65)	3.1 (0.5)	.47	.03	.003	.01
RAID,d (cm)	3.9 (1.1)	3.7 (0.1)	4.2 (0.7)	.62	.37	.11	.34
RVvol,d (mL)	50.9 (26.4)	59.2 (18.7)	31.6 (11.2)	.37	.03	.001	.009
RAvol,d (mL)	44.5 (23.6)	46.1 (22.4)	46.9 (13.4)	.86	.77	.92	.62
RVareal,d (cm2)	20.8 (6.1)	23.5 (4.8)	16.5 (3.9)	.24	.06	.002	.006
RAareal,d (cm2)	16.5 (5.3)	16.9 (5.3)	17.0 (4.0)	.85	.77	.94	.95
TRVmax (m/s)	3.1 (0.8)	5.2 (7.1)	2.7 (0.5)	.34	.25	.032	.14
TAPSE (cm)	1.9 (0.6)	1.8 (0.5)	2.3 (0.4)	.67	.08	.018	.07
RVEF (%)	47.9 (16.2)	45.2 (13.2)	58.0 (9.2)	.65	.10	.020	.14
RAP (mm Hg)	6.9 (2.4)	10.0 (3.9)	8.4 (2.2)	.27	.52	.57	.52
IVC (cm)	1.4 (0.4)	1.9 (0.4)	1.6 (0.4)	.01	.44	.35	.12
RVSP (mm Hg)	48.9 (16.3)	53.5 (24)	37.1 (11)	.74	.34	.19	.34
LVID (cm)	3.9 (0.9)	4.3 (0.5)	4.5 (0.7)	.22	.10	.41	.31
Mitral E (ms)	0.9 (0.2)	0.7 (0.3)	0.8 (0.2)	.17	.53	.32	.35
Mitral A (ms)	1 (0.3)	0.7 (0.3)	0.8 (0.2)	.03	.05	.56	.07
E/A ratio	0.9 (0.2)	1 (0.5)	1.1 (0.3)	.41	.16	.90	.41
IVRT (ms)	70 (20.3)	66.4 (25.6)	78.8 (20. 9)	.71	.42	.23	.37
Dec.time (ms)	209.1 (51.1)	158.4 (86.5)	243.4 (62.1)	.20	.26	.05	.08

Abbreviations: d, diastole; IVC, vena cava inferior; IVRT, isovolumic relaxation time; LVID, left ventricular internal diameter; RAP, RA pressure; RVEF, right ventricle ejection fraction; RVID/ RVvol/RVareal, right ventricle diastolic diameter/volume/areal; RVSP, right ventricle systolic pressure; TRV, tricuspid regurgitation velocity.

vena cava was found significantly larger, but still a maximum of 1.9 cm in subjects with a central PE indicated a greater affection of the RA pres- sure in this group of patients. Right ventricular pressure overload affects left ventricular performance via ventricular interdepence, and it has a potential to contribute to further deterioration of left ventricular perfor- mance [9,11]. We found that patients with a central PE presented with an increased tricuspid regurgitation velocity max compared with con- trols. In the presence of this moderate tricuspid regurgitation, static

RA values did surprisingly not increase indicating the acute onset of the pressure overload.

Our results suggest that there may be a distinct regional strain pat- tern in patients with acute PE. Subjects with acute PE have impaired lon- gitudinal strain and strain rate in the basal and mid free wall of RV compared with healthy controls. These findings were independent of age and sex. Previous studies have described almost identical results re- garding the behavior of RV strain/strain rate in patients with acute PE

Fig. 1. Speckle-tracking echocardiography in a healthy subject.

Fig. 2. Speckle-tracking echocardiography in subject with a central PE.

[12,13]. Our findings suggest that 2D-STE should be performed in the ED with special focus on the free wall of RA and RV to evaluate the conse- quences of an acute PE.

We found no statistical significant differences in 2D-STE between the layers of the RA/RV, although there was a general tendency of a bet- ter contraction in endocardial and midcardiale layers in all groups among subjects with PE.

Based on Sugiura’s findings, the initial extent of RV strain/strain rate reduction diminishes over time from PE diagnosis. Other suggests that the changes may persist during short-term and long-term follow-up and correlate with unfavorable outcomes [2].

Records of inadequate reference values of RA 2D-STE are also obtain- able in the literature [14-17]. We describe for the first time myocardial RA deformation in subjects with acute PE. A decreased RA reservoir strain/strain rate in principle means a reduced compliance and could be associated with reduced cardiac output [17]. Overall RA mechanics revealed by 2D-STE can be useful to detect conditions that may lead to pulmonary Arterial hypertension and increased PVR. We found no dif- ference in the volume or area of the RA comparing PE with controls but a clear difference in the myocardial atrial function by strain. This might be due to the early pathophysiologic process leading to RV dia- stolic and systolic failure in acute PE.

Because impaired longitudinal function has been known to be a sen- sitive marker for identifying early myocardial damage and a reliable predictor of a negative prognosis in patients with heart diseases, nonin- vasive assessment of segmental wall motion can provide useful insight into the pathophysiology of ventricular and atrial interdependence in patients with acute PE.

Previous studies demonstrate that a central PE generates a greater degree of mechanical dyssynchrony compared with a subsegmental lo- cated PE. We could not confirm these results. Our findings may suggest a different approach to the intensity of the acute treatment of a periph- eral PE.

The assessment of STE provides valuable information on quantita- tive assessment of RV and RA function in patients with acute PE. Two- dimensional STE might be a valuable noninvasive diagnostic tool to de- tect PE and may allow for a better prediction of unfavorable outcomes compared with conventional methods. Our study reveal that basal-/ mid-segments of RA and RV free wall are more affected in patients with a PE compared with NL. Interestingly, we found no significant dif- ference in myocardial RA and RV damage between patients with a cen- tral and a peripheral PE. We recommend a greater focus on intensive treatment for patients with a peripheral PE.

Future software improvements are anticipated to improve the track- ing ability of the speckle-tracking echocardiographic and 3-dimensional systems. The refinement of methods and the availability of a greater number of patients with follow-up data will improve the understanding of global and regional RV and RA dysfunction in PE and subsequent management of these patients.

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   Fig. 3. Right ventricular 2D-STE in PE; central/peripheral and controls in 6 segments of the endocardium.

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    Fig. 4. Right atrium 2D-STE in PE; central/peripheral and controls in 6 segments of the endocardium.

    Table 3 Right ventricular 2D-STE
    	Central	Peripheral PE (P)	Control	P value	P value	P value
    	PE (C)		(NL)	(C vs P)	(P vs NL)	(C vs NL)
    Longitudinal strain, S (%)
    - Segment 1	-14.8992	-18.8315	-30.116	.312	.001	.025
    - Segment 2	-14.1662	-18.7423	-29.202	.269	.001	.033
    - Segment 3	-16.2023	-20.5446	-27.142	.400	.029	.149
    - Segment 4	-17.3292	-17.4969	-22.559	.972	.227	.156
    - Segment 5	-15.3862	-14.8877	-18.685	.832	.088	.049
    - Segment 6	-13.7431	-14.0908	-17.115	.868	.037	.091
    Longitudinal strain, pvc (%) - Segment 1	-12.6662	-16.5492	-29.166	.348	.001	.019
    - Segment 2	-12.8538	-16.9838	-28.204	.317	.002	.028
    - Segment 3	-14.8869	-18.5662	-24.825	.474	.082	.230
    - Segment 4	-16.2362	-16.04	-16.829	.967	.924	.887
    - Segment 5	-14.9569	-14.1269	-17.967	.721	.111	.048
    - Segment 6	-13.3085	-11.13	-16.156	.501	.092	.092
    Longitudinal strain rate, S (1/s) - Segment 1	-1.20308	-1.5	-1963	.188	.001	.051
    - Segment 2	-1.05538	-1.27231	-1655	.398	.008	.146
    - Segment 3	-1.28	-1.12154	-1288	.618	.977	.474
    - Segment 4	-1.29769	-1.02385	-1118	.326	.484	.640
    - Segment 5	-0.91231	-1.07385	-0.85	.364	.556	.169
    - Segment 6	-0.47385	-1.16154	-1.06	.142	.186	.554
    Longitudinal strain rate, E (1/s) - Segment 1	1.156154	1.282308	2073	.726	.006	.056
    - Segment 2	0.885385	1.141538	1893	.381	.002	.027
    - Segment 3	1.238462	1.163846	1.84	.854	.112	.077
    - Segment 4	1.582308	0.981538	1549	.124	.928	.077
    - Segment 5	1.199231	0.707692	1094	.015	.527	.019
    - Segment 6	0.586923	0.89	1102	.540	.285	.339
    Longitudinal strain rate, A (1/s) - Segment 1	1.153077	1.196154	1482	.916	.255	.493
    - Segment 2	1.022308	1.204615	1458	.651	.135	.516
    - Segment 3	1.120769	1 288462	1703	.676	.089	.319
    - Segment 4	1.032308	0.958462	1577	.816	.063	.053
    - Segment 5	0.94	0.923077	1264	.924	.095	.089
    - Segment 6	1.029231	1.053846	1211	.903	.307	.373
    Longitudinal strain rate, pvc (1/s) - Segment 1	-0.04615	-0.21769	-0.025	.527	.937	.527
    - Segment 2	-0.03077	-0.08231	0.036	.833	.135	.646
    - Segment 3	-0.10308	0.190769	0.122	.169	.089	.825
    - Segment 4	-0.11692	0.320769	0.029	.082	.063	.350
    - Segment 5	-0.16846	0.123077	-9.71E-18	.038	.095	.541
    - Segment 6	-0.20538	0.019231	0.169	.098	.307	.453
    Longitudinal displacement, S (mm) - Segment 1	11.86462	15.23154	19.209	.275	.050	.274
    - Segment 2	7.972308	10.36462	10.101	.329	.487	.921
    - Segment 3	4.189231	4.843077	2637	.609	.340	.123
    - Segment 4	-0.87154	-1.23308	1006	.796	.173	.098
    - Segment 5	1.896154	1.843077	4487	.979	.173	.086
    - Segment 6	5.111538	5.705385	8989	.791	.076	.043
    Longitudinal displacement, pvc (mm)
    - Segment 1	11.86462	14.51	18.278	.382	.382	.324
    - Segment 2	7.972308	9.813846	9846	.446	.446	.990
    - Segment 3	4.189231	3.710769	3196	.745	.745	.701
    - Segment 4	-0.87154	-1.06615	0.897	.888	.888	.105
    - Segment 5	1.896154	2.125385	4244	.905	.905	.114
    - Segment 6	5.111538	5.291538	8173	.933	.933	.045

    Table 4 Right atrium 2D-STE
    	Central	Peripheral	Controls	P value	P	P
    	PE (C)	PE (P)	(NL)	(C vs	value	value
    				P)	(P vs	(C vs
    					NL)	NL)
    Longitudinal
    strain, pvc (%) - Segment 1	28.957	36.038	104.12	.616	.018	.010
    - Segment 2	24.032	33.055	62.207	.454	.048	.010
    - Segment 3	18.6	29.1	28.9	.297	.367	.341
    - Segment 4	21.4	28.5	26	.614	.848	.766
    - Segment 5	21.9	25.1	27.5	.693	.770	.482
    - Segment 6	23.1	23.9	26.3	.894	.595	.145
    Longitudinal
    strain rate, S (1/s) - Segment 1	1784	2782	3392	.301	.494	.010
    - Segment 2	1544	2505	2654	.172	.812	.010
    - Segment 3	1.4	1.7	1.9	.358	.717	.341
    - Segment 4	1.6	1.8	1.7	.718	.803	.766
    - Segment 5	1.7	1.5	1.6	.693	.866	.482
    - Segment 6	1.8	1.7	1.6	.894	.891	.658
    Longitudinal
    strain rate, E (1/s) - Segment 1	-1776	-1953	-2771	.837	.331	.068
    - Segment 2	-1.57	-1761	-1.99	.798	.689	.444
    - Segment 3	-1.3	-1.3	-1.5	.674	.885	.706
    - Segment 4	-1.7	-1.2	-1.1	.235	.860	.179
    - Segment 5	-1.7	-0.9	-1.3	.046	.134	.374
    - Segment 6	-1	-1.4	-1.4	.837	.190	.833
    Longitudinal
    strain rate, A (1/s) - Segment 1	-2.6	-2.6	-4.7	.914	.09	.086
    - Segment 2	-2.2	-2.2	-3.5	.934	.06	.036
    - Segment 3	-1.5	-1.4	-2.3	.915	.164	.121
    - Segment 4	-1.7	-1.7	-2	.987	.533	.559
    - Segment 5	-1.8	-1.9	-1.7	.783	.706	.937
    - Segment 6	-2	-2	-1.8	.843	.511	.399
    Longitudinal
    strain rate, pvc (1/s) - Segment 1	-0.4	0.3	0.5	.100	.695	.086
    - Segment 2	0.01	0.4	0.6	.226	.438	.072
    - Segment 3	0.2	0.5	0.8	.284	.253	.059
    - Segment 4	0.2	0.3	0.7	.566	.097	.087
    - Segment 5	0.1	0.1	0.3	.840	.489	.445
    - Segment 6	0.06	-0.9	0.3	.263	.191	.526
    Longitudinal
    displacement, S (mm)
    - Segment 1	-8.1	-11.5	-19.1	.349	.030	.001
    - Segment 2	-4	-6.7	-8.7	.287	.449	.010
    - Segment 3	-0.1	-1.1	-22	.521	.527	.156
    - Segment 4	-3.6	-4.3	-3.1	.634	.459	.773
    - Segment 5	-6.3	-7.1	-6.6	.674	.776	.909
    - Segment 6	-8.4	-13.4	-8.5	.147	.185	.965
    Longitudinal
    displacement, pvc (mm)
    - Segment 1	-6.5	-10.2	-15.8	.163	.695	.01
    - Segment 2	-2.3	-5.2	-6.1	.089	.438	.045
    - Segment 3	0.2	-1.1	-1.2	.315	.253	.284
    - Segment 4	-3.1	-2.8	-2.4	.380	.100	.582
    - Segment 5	-5.8	-6	-4.9	.429	.489	.557
    - Segment 6	-8.7	-9.4	-7.9	.145	.191	.656