Academic Editors: Zhonghua Sun and Yung-Liang Wan
Background: In patients with inferior myocardial infarction (MI),
involvement of the right chambers has a prognostic impact. The objective of this
study was to evaluate the influence of left ventricular (LV) inferior wall MI in
the right atrial (RA), and right ventricular (RV) longitudinal strain (LS) by 2D
speckle tracking echocardiography (STE). Methods: 60 consecutive
patients who underwent myocardial perfusion (MP) gated SPECT for chest pain were
included. We studied 30 patients with LV inferior MI and 30 control subjects with
normal MP. RV ejection fraction was measured by 3D transthoracic
echocardiography, RV-free wall LS and RA reservoir, contraction, and conduit
phases strain were analyzed by 2D speckle tracking echocardiography
(STE). Results: The median age in the LV inferior MI was 65 (54–70)
years, 27% had a transmural myocardial infarction and 47% had residual
myocardial ischemia, most of them, mild (36.7%). RV-free wall LS (–26.1 vs
–30.3, p
The prevalence of right ventricular (RV) involvement in acute myocardial infarction (MI) of the left ventricle (LV) ranges from 50 to 80% in postmortem studies [1]. Diagnosis is based on physical examination, electrocardiogram (ECG) with ST-segment elevation in the right precordial leads, and RV dilatation with functional impairment on echocardiogram [2]. Due to the diagnostic limitations of the ECG and conventional 2D echocardiography, smaller RV infarcts and RV involvement are often not detected in the clinical setting [3]. RV involvement in the LV inferior MI is a strong predictor of major complications and in-hospital mortality, as well as long-term morbidity [4].
The right atrium (RA) modulates cardiac output. Rigid ventricles are highly dependent on the atrial contribution for adequate diastolic filling and maintenance of cardiac output. In RV MI, the dilated and rigid ventricle increases the intracavitary pressure against which the RA must empty, therefore it increases its contractility and diastolic filling as a compensatory mechanism [5]. RA ischemia is a strong prognostic marker in the follow-up of patients with RV MI that signifies a greater extension of RV ischemic injury and, consequently the development of a subgroup with significantly high-risk RV dysfunction [6].
Two-dimensional speckle tracking echocardiography (2D-STE) is a useful technique in monitoring, independent of the angle of myocardial deformation that allows a quantitative evaluation of global or regional myocardial function. This method allows the exploration of the RV-free wall deformation and the RA LS during the phases of the cardiac cycle [7].
The strain rate performance improved the diagnostic accuracy for detecting MI. A
study showed that RV-free wall strain
The objective of this study was to assess the LS of the RV-free wall, and the RA LS using 2D-STE of patients with LV inferior MI. It was hypothesized that subclinical extension to RV in LV inferior MI and the role of RA LS could be evaluated using 2D-STE.
Between January and December 2018, we prospectively included 60 consecutive patients who had myocardial perfusion (MP) Gated-Single Photon Emission Computed Tomography (SPECT) due to chest pain and suspicion of coronary artery disease (CAD). We found 30 patients with LV inferior MI and 30 control subjects, who had normal MP Gated-SPECT. The echocardiographic study was performed in all patients using an ACUSON SC2000 System (Siemens, Germany) with a 4V1c transducer (for 2D measurements) and a 4Z1c (for 3D measurements). All echocardiographic measurements were assessed according to the guidelines of the American Society of Echocardiography [11].
A Symbia Siemens, cardiocentric, smartzoom gamma chamber was used (photopeak
20% in 120 keV, matrix 128
Comprehensive two-dimensional (2D) and color Doppler evaluations were performed. The transmitral E/A ratio was determined in the apical four-chamber plane using pulsed-wave Doppler. Peak mitral annular velocity (e’) was measured with tissue Doppler by placing the volume sample in the basal portion of the interventricular septum in the apical four-chamber view. The E/e’ ratio reflects the LV filling pressure. Diagnosis of diastolic dysfunction was made according to the guidelines of the American Society of Echocardiography [12].
RV dimension was measured in the apical four-chamber view at the level of the RV
basal cavity at end-diastole; dilatation was considered with a RV basal diameter
The RV Tei index was determined as the sum of the isovolumetric contraction time
and isovolumetric relaxation time divided by the ejection time, by pulsed-wave
Doppler tissue imaging (DTI) in an apical four-chamber view. The S wave was
defined as peak systolic velocity of the tricuspid annulus by DTI (cm/sec), in a
four-chamber apical view. The criteria for RV systolic dysfunction were: FAC
The systolic pulmonary artery pressure (SPAP) was evaluated as the sum of the
maximal pressure difference between the right cavities, using color and
continuous-wave Doppler, and the mean right atrial pressure was calculated
measuring the diameter of the inferior vena cava and its respiratory variation.
Estimated SPAP was considered abnormal when the peak tricuspid regurgitation
velocity
Three-dimensional (3D) left and right ventricular volumes and ejection fraction (EF) were evaluated in the apical four-chamber view focused on the right ventricle for RV analysis (Fig. 1).
Right ventricular 3D ejection fraction. Normal right ventricular EF (64%) in a control subject.
Full volume acquisition was performed by ECG activation in three consecutive
cardiac cycles during a single apnea. The 3D digital data set was analyzed with
commercial software. LVEF was calculated from end-diastolic and end-systolic
volumes, LV systolic function was considered abnormal when LVEF
The global myocardial strain of the LV, the RV-free wall LS, and the RA LS were
measured using the 2D STE analysis. The LV LS was performed in the apical views
of four, two, and three chambers and the abnormal value was
Free wall longitudinal strain of the right ventricle. Normal RV-free wall LS (–28.6%). Abbreviations: LV, left ventricle.
RA LS reservoir (peak strain), contraction and conduit phases were assessed in the apical four-chamber view, the QRS-wave was considered as a reference for calculation. The endocardial border was traced manually, delineating a region of interest (ROI), then, from the quality analysis of the segmental tracking and the eventual manual adjustment of the ROI, the software generated the RA LS curves (Fig. 3).
Right atrial global longitudinal strain. Normal RA LS with its three phases in a control subject. Abbreviations: LV, left ventricle; LA, left atrium; RV, right ventricle.
At present, there is no consensus about the reference value for RA peak strain,
in 2011, Padeletti et al. [15] proposed a mean of 49
Follow-up was made by telephone and patient visits and the primary endpoint was all-cause death.
Data were analyzed with STATA/IC v13 (Stata Corp, College Station, TX, USA). The study was double-blinded, both for echocardiographic analysis and to the SPECT results.
For the descriptive analysis, binary variables were described as frequencies and
proportions, and they were analyzed with Pearson’s independence text (X
The median age in LV inferior MI group was 65 (54–70) years, 83% were male, 60% of cases had systemic hypertension, and 43% diabetes. 27% had a transmural myocardial infarction and 47% had residual myocardial ischemia, most of them, mild (36.7%). Table 1 demonstrates the clinical findings of the studied groups.
LV inferior wall MI patients (n = 30) | Control subjects (n = 30) | p value | |
Age in years (median, IQR) | 65 (54–70) | 54 (29–58) | 0.01 |
Males (n, %) | 25 (83.3) | 14 (46.7) | 0.03 |
Females (n, %) | 5 (16.7) | 16 (53.3) | |
Risk Factors | |||
Diabetes mellitus (n, %) | 13 (43.4) | 2 (6.6) | |
Hypertension (n, %) | 18 (60) | 8 (26.7) | |
Dyslipidemia (n, %) | 9 (30) | 2 (6.7) | 0.02 |
Paroxysmal AF (n,%) | 3 (10) | 0 | 0.11 |
Smoking (n, %) | 11 (36.7) | 1 (3.3) | |
CKD (n, %) | 2 (6.7) | 0 | 0.24 |
Infarction characteristics | |||
RV extension (clinical) (n, %) | 1 (3.3) | 0 | 0.5 |
Transitory AV block (n, %) | 3 (10) | 0 | 0.11 |
Mechanical complication (n, %) | 2 (6.7) | 0 | 0.24 |
SPECT characteristics | |||
Transmural infarction (n, %) | 8 (26.7) | 0 | |
Residual ischemia | |||
Mild (n, %) | 11 (36.7) | 0 | |
Moderate (n, %) | 2 (6.7) | 0 | 0.24 |
Severe (n, %) | 1 (3.3) | 0 | 0.5 |
LV, left ventricle; MI, myocardial infarction; IQR, interquartile range; AF, atrial fibrillation; CKD, chronic kidney disease; RV, right ventricle; AV, atrioventricular; SPECT, single photon emission computed tomography. |
Table 2 describes the echocardiographic measurement of the studied population.
In LV inferior MI, a larger LV end-diastolic volume (121 vs 89.5 mL, p
LV inferior wall MI patients (n = 30) | Control subjects (n = 30) | p value | |
3D LV EDV (mL) (median, IQR) | 121 (99.7–150) | 89.5 (73–99) | |
3D LV EF (%) (median, IQR) | 46 (37–53) | 60 (58–63) | |
Mitral E/A (median, IQR) | 0.82 (0.7–1.2) | 1.21 (0.97–1.44) | |
Medial E/e’ (median, IQR) | 9.59 (7.9–13) | 7.7 (6.9–10.5) | 0.01 |
RV EDD (mm) (mean, SD) | 37.6 |
34.7 |
0.12 |
TAPSE (mm) (mean, SD) | 18.6 |
21.7 |
|
RV FAC (%) (mean, SD) | 37.01 |
46.86 |
|
RV S’ (mean, SD) | 9.92 |
11.78 |
|
3D RV EF (%) (median, IQR) | 47.5 (42–52) | 54 (49–57) | |
RIMP (mean, SD) | 0.49 |
0.46 |
0.60 |
SPAP (mmHg) (median, IQR) | 31.5 (27.37) | 29.5 (26.33) | 0.07 |
Speckle tracking analysis | |||
Peak global LV LS (%) (median, IQR) | –13.35 (–17.6, –9.3) | –22 (–23.2, –20.4) | |
Peak free wall RV LS (%) (median, IQR) | –26.1 (–32.1, –17.8) | –30.3 (–36.6, –27.5) | |
RA peak strain (reservoir phase) (%) (median, IQR) | 31.5 (25.2–43) | 56.2 (47–66.4) | |
RA contraction phase strain (%) (Mean, SD) | 20.17 |
24.4 |
0.07 |
RA conduit phase strain (%) (Median, IQR) | 12.5 (5.9–15.6) | 35 (21–47.6) | 0.01 |
LV, left ventricle; MI, myocardial infarction; 3D, three dimensional; EDV, end-diastolic volume; ml, milliliters; IQR, interquartile range; EF, ejection fraction; RV, right ventricle; EDD, end-diastolic diameter; mm, millimeters; SD, standard deviation; TAPSE, tricuspid annular systolic plane excursion; FAC, fractional area change; S’, tissue Doppler imaging of peak systolic tricuspid annulus; RIMP, right ventricle index of myocardial performance; SPAP, systolic pulmonary artery pressure (estimated); LS, longitudinal strain; RA, right atrium. |
LV inferior MI [Odds ratio (OR) 4.3, 95% CI 1.05–17.85, p = 0.04],
reduced 3D LV EF (OR 4.53, 95% CI 1.23–16.58, p = 0.02), and mitral
regurgitation (OR 5.1, 95% CI 1.3–19.5, p = 0.01) were significantly
associated with reduced RV free wall LS (
OR | 95% CI | p value | |
LV inferior wall MI | 4.3 | 1.05–17.9 | 0.04 |
Decreased 3D LV EF | 4.5 | 1.2–16.6 | 0.02 |
Mitral regurgitation | 5.1 | 1.35–19.5 | 0.01 |
RV dilatation (basal diameter |
7.02 | 1.7–29.4 | |
Decreased TAPSE ( |
9 | 2.01–40.2 | |
Decreased 3D RV EF ( |
4.8 | 1.2–18.5 | 0.02 |
Elevated SPAP ( |
16.8 | 3.7–76.6 | |
OR, odds ratio; CI, confidence interval; LV, left ventricle; MI, myocardial infarction; 3D, three dimensional; EF, ejection fraction; RV, right ventricle; TAPSE, tricuspid annular systolic plane excursion; SPAP, systolic pulmonary artery pressure (estimated). |
When patients were divided according to RA peak strain (reservoir phase) cut-off
value of 36%, LV inferior wall MI was significantly associated with reduced RA
peak strain (OR 10.8, 95% CI 2.97–39.2, p
OR | 95% CI | p value | |
LV inferior wall MI | 10.8 | 2.97–39.2 | |
Smoking | 4.3 | 0.36–5.21 | 0.03 |
Decreased 3D LV EF | 7.8 | 2.3–26.1 | |
Mitral regurgitation | 9.5 | 2.8–31.8 | |
Abnormal S’ ( |
4.76 | 1.4–16.7 | 0.01 |
Decreased 3D RV EF ( |
15.6 | 3.01–80.6 | |
Elevated SPAP ( |
4.3 | 1.1–16.4 | 0.03 |
OR, odds ratio; CI, confidence interval; LV, left ventricle; MI, myocardial infarction; 3D, three dimensional; EF, ejection fraction; S’, tissue doppler imaging of peak systolic tricuspid annulus; RV, right ventricle; SPAP, systolic pulmonary artery pressure (estimated). |
A 4-year follow-up was performed, with special attention to survival, subsequent surgical procedures (stent or bypass), NYHA functional class, and deaths. We found that in the group of cases, three patients suffered a reinfarction and one of them died. In these patients, the mean values of the RA peak reservoir strain and LV LS in the baseline echocardiogram were reduced to 30% and –11.09%, respectively. In the patient who died after myocardial reinfarction, RV-free wall LS (–13.6%) was decreased. In the control group, one patient had an inferior MI, despite normal biventricular LS values.
Our study found that RV-free wall and RA LS were significantly reduced in patients with LV inferior MI compared with control individuals. Previously published studies have demonstrated that RV LS measured by STE may be a valid method for the evaluation of the RV function in multiple clinical scenarios [16, 17, 18], including right coronary artery disease [18], first inferior wall MI [19], and right ventricular MI [20]. It also has prognostic information that is superior to conventional echocardiographic measures [21, 22].
STE also has been used to perform LV strain rate and its value is being applied with favorable results in the diagnosis and prognosis of clinical outcome, LV remodeling, and cardiotoxicity. In addition, speckle tracking has already proven to be a useful prognostic tool for predicting major cardiovascular events in patients with CAD; however, the use of RV-free wall strain and RA LS to predict major cardiovascular events after an inferior MI is still unknown [23, 24, 25].
The mechanism of RV dysfunction after left ventricular MI is not well established, but it is often presumed that failure of the LV provokes pulmonary hypertension and increment of the RV afterload, which leads to RV remodeling and dysfunction. In 2013, Konoshi K et al. [26], found that RV LS depends on LV systolic function in patients with old inferior wall MI; we found a significant association between decreased 3D LVEF and elevated SPAP, with reduction of RV free wall LS. We also found a significant association between RV dilatation and systolic dysfunction (measured by 3D RV EF and TAPSE) with reduced RV free wall LS. The involvement of RV and/or septum by myocardial infarction or ischemia are common in patients with LV MI, and it is a possible mechanism leading to RV systolic dysfunction and dilatation [27].
RA has an important role in RV filling (1) it acts as a reservoir for venous return, (2) as a passive conduit in early diastole, and (3) as reinforcement in end-diastole during atrial contraction [28]. A significant reduction in RA maximum deformation, as a function of RA reservoir phase, was also found in the inferior LV MI group. Furthermore, RA conduit function was lower in this group of patients. These data demonstrate that in patients with left ventricular inferior wall MI, the reservoir and conduit function of the RA was impaired.
Previously Nourian S et al. [29], found reduced RA reservoir values (mean value of 26.6%) and conduit phase strain in patients with inferior MI and right ventricular involvement compared with those without right ventricular extension. Our study group was compared with control subjects, the median strain value for the RA reservoir phase and the conduit phase was reduced, but the booster function was preserved (atrial contraction was found to increase in the presence of ventricular systolic dysfunction) [30].
Ventricular function is an important determinant of atrial function. RA reservoir function during early ventricular systolic time is related to RV systolic function, due to longitudinal contraction of the ventricle and downward pull of the base of the ventricle [31]. Our study found a significant association between reduced 3D RVEF and S’ with abnormal RA peak strain (reservoir phase). We also found an association between smoking and reduced RA peak strain, it is known that smoking can induce atrial fibrosis through nicotine [32], and acute consumption can increase afterload due to transitory diastolic dysfunction and increased systolic pulmonary artery pressure [33].
At follow-up, we found that in the patients who developed reinfarction and death, the mean values of the RA peak reservoir strain, LV LS, and RV-free wall LS were reduced at baseline echocardiogram. However, we need a longer follow-up and a larger sample to determine a significant prognostic value.
The data presented here were obtained from a small group of patients, at a single center, referred for clinically indicated myocardial perfusion SPECT. The global strain was measured only in the longitudinal direction, the radial strain may provide more evidence. Strain in LV inferior wall MI and in RV infarction needs extensive validation studies. We use some not well standardized cutoff values in the RA strain parameters.
RV free wall LS, RA peak strain (reservoir phase), and RA conduit phase strain were significantly lower in patients with LV inferior MI than in control individuals.
The subclinical extension to the RV in LV inferior MI and its role in the longitudinal strain of RA could be determined using speckle tracking echocardiography.
NEZ, EAR—Research idea and study design; PJGV, GCC—data acquisition; NEZ, JB, JIAM ESP, RGN—data analysis/interpretation; RGN, VFB—statistical analysis; NEZ, PJGV, JB, JIAM, VFB, ESP—manuscript drafting; NEZ—supervision or mentorship.
All subjects gave their written informed consent before they participated in the study. The study was conducted in accordance with the Declaration of Helsinki and the protocol was approved by the Ethics Committee of the National Institute of Cardiology, Mexico. Reference number: PT-17-087.
We would like to thanks to all the peer reviewers for their opinions and suggestions.
This research received no external funding.
The authors declare no conflict of interest.