Abstract
Purpose
Previous studies have indicated that right ventricular (RV) function is damaged in diabetes mellitus (DM); however, it is not clear whether in the presence of chronic ischemia, RV function is different between patients with and without DM (DM + and DM − , respectively).
Methods
This cross-sectional study enrolled 90 consecutive candidates for coronary artery bypass graft surgery and allocated them to 3 groups: 24 DM − patients with the absence of stenosis of more than 50% in the proximal and mid parts of the right coronary artery (the DM − RCA − group [control]), 33 DM − patients with the presence of significant stenosis (> 70%) in the proximal part of RCA (the DM − RCA + group), and 33 DM + patients with RCA + (the DM + RCA + group). RV function was evaluated based on longitudinal deformation markers, measured via the 2D speckle-tracking echocardiographic examination of right ventricular free wall (RVFW).
Results
The systolic strain value, systolic strain rate, and late diastolic strain rate of RVFW were not statistically significantly different between the three groups. Our adjusted post hoc analysis showed that the early diastolic strain rate of RVFW in the DM + RCA + group was lower than that in the DM − RCA + and DM − RCA − groups (1.5 s−1 ± 0.4 vs 1.7 s−1 ± 0.5 vs 1.7 s−1 ± 0.4).
Conclusions
Diastolic function in the presence of DM was impaired irrespective of RCA − or RCA + . Additionally, RCA + had no effect on systolic and diastolic RV functions at rest in our DM − patients.
Keywords: Right ventricle, Diabetes, Speckle-tracking echocardiography, Coronary artery disease
Introduction
It is estimated that about one-fifth of patients with diabetes mellitus (DM) are affected by coronary artery disease (CAD) [1]. DM has also been reported in up to one-third of patients following percutaneous coronary interventions and one-fourth of patients after coronary artery bypass graft surgery (CABG) [2]. Right ventricular (RV) function in the preoperative course is predictive of circulatory failure and mortality after cardiac surgery [3]. It is, therefore, crucial to identify the factors that affect RV function.
Previous studies have indicated that DM damages RV function [4, 5], and chronic ischemia is associated with RV dysfunction [6]. Most of the vessels that supply RV originate from the mid-part of the right coronary artery (RCA); they are termed “acute marginal branches.” Stenosis at the proximal portion of RCA (pRCA), before the origination of the branches, is presumed to impact RV function [7]. Nonetheless, RV function in patients with DM (DM +) in the presence of ischemia has yet to be fully investigated. Indeed, it is not clear whether chronic ischemia impacts RV function differently in DM + and DM − patients. In other words, there are no robust data on the comparison between the detrimental effects of ischemia on RV function between DM + patients and their DM − counterparts.
Two-dimensional speckle-tracking echocardiography (2D-STE) is a method widely utilized for the evaluation of RV function [8]. This method measures longitudinal systolic and diastolic deformation indices, which are used for the detection of subtle myocardial systolic and diastolic dysfunction in the presence of various conditions such as DM and ischemia [4–6].
In the present study, we drew upon 2D-STE for the assessment of RV function in DM + and DM − patients candidated for CABG in the presence of chronic ischemia, defined as significant stenosis at pRCA.
Methods
Study population
Between May 2019 and May 2020, the current study consecutively recruited patients admitted to our hospital for CABG. The inclusion criterion was sinus rhythm, while the exclusion criteria consisted of history of inferior myocardial infarction, percutaneous coronary intervention on RCA, previous cardiac surgery, emergency CABG, permanent pacemaker implantation, cardiomyopathy, congenital heart disease, valvular stenosis, more-than-mild valvular regurgitation, estimated systolic pulmonary artery pressure exceeding 34 mm Hg, left ventricular (LV) ejection fraction below 45%, history of myocardial infarction in the recent 4 weeks, bundle branch block, history of cancer, autoimmune disease, thyroid disease, hepatic failure, creatinine level of more than 1.5 mg/dL, and poor echocardiography window. Hospital admission was followed by history taking, medical file reviewing, and electrocardiographic examinations. The morning after admission, venous samples were obtained for biochemistry analyses and cell blood counts after an overnight fast. DM was defined as the consumption of antidiabetic agents or insulin or a fasting blood glucose level of 126 mg/dL or more in two isolated samples. The distal part of RCA was regarded as the portion after the last marginal branches, pRCA was considered the portion of RCA before the first marginal branch, and the mid-part of RCA was considered the portion between the first and last marginal branches. The patients were divided into three groups based on RCA and DM criteria: DM − patients with the absence of stenosis of more than 50% in the proximal and mid parts of RCA (RCA −) were allocated to the DM − RCA − group (the control group), DM − patients with the presence of significant stenosis (> 70%) in the proximal and mid parts of RCA (RCA +) comprised the DM − RCA + group, and DM + patients with RCA + formed the DM + RCA + group. Those who did not fulfill this second inclusion criterion were excluded from the study. Ultimately, the study population was comprised of 24 patients in the DM − RCA − group, 33 patients in the DM − RCA + group, and 33 patients in the DM + RCA + group. The study proposal was approved by the institutional review board, and informed written consent was obtained from the entire study population on admission.
Echocardiography
Standard echocardiography
Transthoracic echocardiography was performed by a cardiologist highly experienced in advanced echocardiography using a commercial setting (Philips, Affinity 70C, Andover, MA, USA) with an S5-1 probe for imaging before CABG. The patients lay in the left lateral decubitus position while one lead of electrocardiography appeared on the screen page of the echocardiography machine. LV end-diastolic and end-systolic volumes in the apical 4- and 2-chamber views were measured, and LV ejection fraction was calculated according to the modified biplane Simpson method. RV end-diastolic and end-systolic areas and RV diameter in the mid-part in the apical 4-chamber view were measured; additionally, RV fractional shortening was calculated. Tricuspid annular plane systolic excursion was obtained via M-mode and measured. The maximal right atrial volume was measured via the single-plane area-length method in the apical 4-chamber view. Pulsed-wave tissue Doppler imaging was employed to obtain lateral tricuspid annulus velocities in systole, early diastole, and late diastole (s′, e′, and a′, respectively), and peak velocities were measured in three consecutive cardiac cycles (Fig. 1). In the modified apical 4-chamber view, the tricuspid blood flow velocity was obtained by pulsed-wave Doppler, and peak velocities in early diastole and late diastole (E and A, respectively) and the deceleration of the E wave were measured (Fig. 2). The RV E/e′ ratio was computed. All these measurements were done according to the recommendations of the American Society of Echocardiography [10, 11]. The tricuspid regurgitation gradient was obtained by continuous-wave Doppler, and systolic pulmonary artery pressure was estimated based on the recommendations of the American Society of Echocardiography [10].
Fig. 1.
The image illustrates the patterns of lateral tricuspid annulus velocities obtained by pulsed-wave tissue Doppler imaging. s′: peak velocity of the systolic wave, e′: peak velocity of the early diastolic wave, a′: peak velocity of the late diastolic wave
Fig. 2.
The image depicts the tricuspid flow pattern obtained by pulsed-wave Doppler. E: peak velocity of the early diastolic wave, A: peak velocity of the late diastolic wave, DT: Deceleration time of the early diastolic wave
Two-dimensional speckle-tracking echocardiography
Three expiratory consecutive cardiac cycles of the RV-focused apical 4-chamber view were obtained at a rate of 47 ± 4 frames per second. Thereafter, via the use of the aCMQ option of QLAB 11.0 software (Philips, Andover, MA, USA), the longitudinal deformation markers of right ventricular free wall (RVFW) were measured. Next, via the 3-click method, the septal and lateral tricuspid annuli and RV apex were determined in the end-diastolic frame, with the software automatically tracing the endocardial and epicedial borders of RV. Each RV wall (ie, the interventricular septum and the free wall) was then divided into three segments by the software. At this point, the edit option enabled the adjustment of the traced borders with the corresponding real borders. After confirmation, the strain and strain rate curves of each segment were visualized. The edit option once again allowed the adjustment of the traced borders at end-systole. The end-systolic time was set as the smallest RV frame after a frame-by-frame checking of the saved movies. Subsequently, the endocardial layer was selected for measurement. This stage was repeated for the other two saved movies. The strain curve had a negative peak. Afterward, the peak value of the strain curve during systole was measured for three RVFW segments; the average value of the three segments was computed. The strain rate curves had one negative systolic peak and two positive peaks at early and late diastolic times. These peaks were measured for each segment, and the average values of the three RVFW segments were calculated (Fig. 3). These measurements were repeated for the other two movies. Finally, the mean values of the peak systolic strain of RVFW and the peak systolic strain rate of RVFW as markers of RV systolic function, the peak early diastolic strain rate of RVFW as an index of RV early diastolic function, and the peak late diastolic strain rate of RVFW as a parameter of late diastolic RV function were recorded. All the steps were done in accordance with the American Society of Echocardiography consensus [9]. The absolute value of the longitudinal deformation markers was presented. The 2D-STE analyses were conducted after May 2020 gradually by another cardiologist highly experienced in 2D-STE. One month after the completion of the study, the first and second cardiologists independently evaluated 14 patients (15%) randomly selected for interobserver and intraobserver variabilities. The cardiologists were blinded to the original measurements and the presence or absence of DM and RCA stenosis.
Fig. 3.
Speckle-tracking echocardiography of the right ventricle in the apical 4-chamber view shows a strain curves and b strain rate curves
Statistical analysis
Categorical data were presented as frequencies and percentages and compared by using the χ2 test or the Fisher exact test, whichever was indicated. Continuous data with normal distributions were presented as the mean and the standard deviation and those with non-normal distributions as the median and the interquartile range; thereafter, the data were compared via generalized linear regression models. This method was also applied for adjustments regarding variables with a P value of less than 0.10 if they were physiologically meaningful as confounding factors such as the heart rate after the assumptions of the analysis were checked. Based on the results of these analyses, the differences between two groups with a P value of less than 0.05 were presented as (parameter estimates) B and 95% Wald confidence intervals. Interobserver and intraobserver variabilities were assessed using intraclass correlation coefficients and 95% levels of agreement. The statistical analyses were carried out using IBM SPSS Statistics for Windows, version 24 (Armonk, NY: IBM Corp). A P value of less than 0.05 was regarded as statistically significant.
Results
The study population’s demographic, clinical, and laboratory data are presented in Table 1. The 3 study groups were not statistically significantly different vis-à-vis these variables, except for fasting blood sugar and triglycerides, which were elevated in the DM + patients. The standard and 2D-STE-related variables are demonstrated in Table 2. The standard echocardiography variables were not significantly different between the three groups, except for RV diameter, which was within the normal range in all three study groups. The differences between the three groups were not statistically significant concerning the systolic strain value of RVFW (24.0% ± 3.0 vs 22.8% ± 3.6 vs 22.4% ± 3.4; P = 0.181), the systolic strain rate of RVFW (2.2 s−1 ± 0.4 vs 2.0 s−1 ± 0.4 vs 2.2 s−1 ± 0.5; P = 0.131), and the late diastolic strain rate of RVFW (2.5 s−1 ± 0.6 vs 2.5 s−1 ± 0.6 vs 2.7 s−1 ± 0.5; P = 0.436). Apropos the early diastolic strain rate of RVFW, the difference was significant in the unadjusted model (1.7 s−1 ± 0.4 vs 1.7 s−1 ± 0.5 vs 1.5 s−1 ± 0.4; P = 0.026). The post hoc analysis showed that the early diastolic strain rate of RVFW in the DM + RCA + group was lower than that in the DM − RCA + group (B = − 0.24 [− 0.43 to − 0.04]; P = 0.020) and the DM − RCA − group (B = − 0.26 [− 0.47 to − 0.04]; P = 0.021). The difference between the DM − RCA + and DM − RCA − groups was nonsignificant (B = − 0.02 [− 0.24 to 0.20]; P = 0.856). After adjustments for the heart rate, the early diastolic strain rate of RVFW in the DM + RCA + group was lower than that in the DM − RCA + group (B = − 0.23 [− 0.43 to − 0.22]; P = 0.030) and the DM − RCA − group (B = − 0.25 [− 0.47 to − 0.03]; P = 0.027). The difference between the DM − RCA + and DM − RCA − groups did not constitute statistical significance (B = − 0.02 [− 0.24 to 0.19]; P = 0.843). The results concerning the interobserver and intraobserver variabilities are presented in Table 3.
Table 1.
Clinical and biochemical characteristics of the study groups
| Groups | DM − RCA − (n = 24) |
DM − RCA + (n = 33) |
DM + RCA + (n = 33) |
P value |
|---|---|---|---|---|
| Variables | ||||
| Age (y) | 63 ± 9 | 63 ± 7 | 63 ± 9 | 0.991 |
| Sex (male, %) | 17 (71) | 28 (85) | 23 (70) | 0.294 |
| Obesity (%) | 5 (21) | 7 (21) | 6 (18) | 0.947 |
| Body mass index (kg/m2) | 26.7 ± 4.0 | 27.2 ± 4.3 | 27.2 ± 3.2 | 0.845 |
| Body surface area (m2) | 1.5 ± 0.1 | 1.5 ± 0.1 | 1.5 ± 0.1 | 0.903 |
| Hypertension (%) | 11 (46) | 21 (64) | 24 (73) | 0.115 |
| Cigarette smoker (%) | 8 (33) | 10 (30) | 8 (24) | 0.737 |
| History of myocardial infarction (%) | 1 (4) | 0 (0) | 2 (6) | 0.388 |
| Antiplatelet (%) | 20 (83) | 29 (88) | 33 (100) | 0.093 |
| Nitrate (%) | 14 (58) | 23 (70) | 20 (61) | 0.625 |
| Calcium channel blockers (%) | 5 (21) | 6 (18) | 8 (24) | 0.833 |
| Beta-blockers (%) | 16 (67) | 23 (70) | 23 (70) | 0.963 |
| ACEI/ARB (%) | 15 (63) | 17 (52) | 19 (58) | 0.705 |
| Diuretics (%) | 1 (4) | 1 (3) | 4 (12) | 0.334 |
| Statins (%) | 20 (83) | 29 (88) | 30 (91) | 0.689 |
| Oral antidiabetic agent (%) | – | – | 26 (79) | – |
| Insulin (%) | – | – | 9 (27) | – |
| Single-vessel disease (%) | 5 (21) | 0(0) | 0(0) | 0.001 |
| Double-vessel disease (%) | 11 (46) | 3 (9) | 4 (12) | 0.001 |
| Triple-vessel disease (%) | 8 (33) | 30 (91) | 29 (88) | < 0.001 |
| Fasting blood sugar (mg/dL) | 96 (87–103) | 93 (90–103) | 138 (94–171) | < 0.001 |
| Triglyceride (mg/dL) | 136 (98–166) | 135 (106–175) | 151 (118–242) | 0.023 |
| Cholesterol (mg/dL) | 141 ± 29 | 148 ± 42 | 143 ± 31 | 0.672 |
| Low-density lipoprotein (mg/dL) | 81 ± 23 | 85 ± 28 | 82 ± 23 | 0.794 |
| High-density lipoprotein (mg/dL) | 39 ± 9 | 37 ± 7 | 37 ± 9 | 0.721 |
| Hemoglobin (g/dL) | 14.0 ± 1.2 | 14.4 ± 1.3 | 14.1 ± 1.5 | 0.386 |
| Creatinine (mg/dL) | 1.1 ± 0.2 | 1.1 ± 0.2 | 1.1 ± 0.2 | 0.870 |
| Heart rate at echocardiography time (bpm) | 66 ± 14 | 67 ± 11 | 72 ± 10 | 0.066 |
| Systolic blood pressure at echocardiography time (mm Hg) | 132 ± 18 | 128 ± 17 | 133 ± 15 | 0.457 |
| Diastolic blood pressure at echocardiography time (mm Hg) | 79 ± 11 | 76 ± 10 | 78 ± 11 | 0.595 |
ACEI/ARB angiotensin-converting enzyme inhibitor/angiotensin receptor blocker, DM − RCA − : the absence of diabetes mellitus and the absence of stenosis more than 50% in the proximal and mid parts of the right coronary artery, DM − RCA + : the absence of diabetes mellitus and the presence of significant stenosis (> 70%) in the proximal part of the right coronary artery, DM + RCA + : the presence of diabetes mellitus and the presence of significant stenosis (> 70%) in the proximal part of the right coronary artery
Table 2.
Echocardiographic profile of the study groups
| Groups | DM − RCA − (n = 24) |
DM − RCA + (n = 33) |
DM + RCA + (n = 33) |
P value |
|---|---|---|---|---|
| Variables | ||||
| LVEDVi (mL/m2) | 57.6 ± 11.7 | 56.5 ± 12.2 | 54.5 ± 12.8 | 0.600 |
| LVESVi (mL/m2) | 24.7 ± 5.8 | 25.0 ± 6.4 | 24.2 ± 5.5 | 0.856 |
| LVEF (%) | 58.1 ± 5.9 | 55.8 ± 5.9 | 57.4 ± 4.7 | 0.492 |
| RVD (mm) | 29 ± 3 | 30 ± 3 | 29 ± 3 | 0.033 |
| TAPSE (mm) | 21 ± 3 | 21 ± 3 | 20 ± 3 | 0.268 |
| RVEDA (cm2) | 18.5 ± 3.2 | 18.6 ± 3.4 | 17.3 ± 3.4 | 0.207 |
| RVESA (cm2) | 9.9 ± 2.4 | 9.6 ± 2.4 | 9.1 ± 2.2 | 0.364 |
| RVFAC (%) | 46.6 ± 8.2 | 48.3 ± 7.1 | 47.3 ± 9.1 | 0.731 |
| E (cm/s) | 46 ± 14 | 47 ± 9 | 47 ± 11 | 0.891 |
| A (cm/s) | 41 ± 12 | 38 ± 10 | 41 ± 12 | 0.200 |
| E/A ratio | 1.0 (1.0–1.3) | 1.2 (1.0–1.4) | 1.1 (1.0–1.4) | 0.694 |
| DT (ms) | 219 ± 56 | 221 ± 61 | 223 ± 57 | 0.781 |
| SPAP (mm Hg) | 26 ± 4 | 25 ± 4 | 26 ± 4 | 0.572 |
| s′ (cm/s) | 12.1 ± 2.4 | 11.4 ± 2.2 | 11.9 ± 1.9 | 0.478 |
| e′ (cm/s) | 8.4 ± 2.4 | 8.1 ± 2.0 | 7.5 ± 2.2 | 0.244 |
| a′ (cm/s) | 13.4 ± 4.0 | 12.2 ± 2.6 | 13.4 ± 2.7 | 0.192 |
| E/e′ ratio | 5.8 ± 1.9 | 6.0 ± 1.9 | 6.7 ± 1.9 | 0.137 |
| e′/a′ ratio | 0.6 (0.5–0.7) | 0.7 (0.5–0.8) | 0.5 (0.4–0.7) | 0.338 |
| RVFW systolic strain (%) | 24.0 ± 3.0 | 22.8 ± 3.6 | 22.4 ± 3.4 | 0.181 |
| RVFW systolic strain rate (s−1) | 2.2 ± 0.4 | 2.0 ± 0.4 | 2.2 ± 0.5 | 0.132 |
| RVFW early diastolic strain rate (s−1) | 1.7 ± 0.4 | 1.7 ± 0.5 | 1.5 ± 0.4 | 0.026 |
| RVFW late diastolic strain rate (s−1) | 2.5 ± 0.6 | 2.5 ± 0.6 | 2.7 ± 0.5 | 0.436 |
A: peak velocity of the tricuspid flow in late diastole, a′: peak velocity of late diastolic motion, DT: deceleration time, E: peak velocity of the tricuspid flow in early diastole, e′: peak velocity of the early diastolic motion, LVEF: left ventricular ejection fraction, LVEDVi: left ventricular end-diastolic volume index, LVESVi: left ventricular end-systolic volume index, RVEDA: right ventricular end-diastolic area, RVESA: right ventricular end-systolic area, RVFAC: right ventricular fraction area change, RVFW: right ventricular free wall, RVD: right ventricular diameter, s′: peak velocity of the systolic motion, SPAP: systolic pulmonary artery pressure, TAPSE: tricuspid annular plane systolic excursion
Table 3.
Intra- and interobserver variabilities for the 2D speckle-tracking echocardiography-derived parameters of right ventricular longitudinal deformation
| Variable | Intraobserver | Interobserver | ||
|---|---|---|---|---|
| ICC | 95% limit of agreement | ICC | 95% limit of agreement | |
| RVFW systolic strain (%) | 0.911 | (0.684–0.973) | 0.879 | (0.625–0.961) |
| RVFW systolic strain rate (s−1) | 0.935 | (0.806–0.979) | 0.889 | (0.643–0.965) |
| RVFW early diastolic strain rate (s−1) | 0.901 | (0.699–0.968) | 0.909 | (0.718–0.971) |
| RVFW late diastolic strain rate (s−1) | 0.986 | (0.957–0.996) | 0.912 | (0.735–0.972) |
ICC intraclass correlation coefficient, RVFW right ventricular free wall
Discussion
We evaluated RV function by 2D-STE in DM + and DM − patients with pRCA stenosis so as to assess whether RV systolic and diastolic functions differed between these two groups of patients in the presence of chronic ischemia. The main finding of our study was that the early diastolic strain rate of RVFW was different between the RCA + DM + group and the other two DM − groups (ie, DM − RCA + and DM − RCA −), which implied that diastolic function in the presence of DM was impaired irrespective of the presence or absence of pRCA stenosis. The other deformation indices were not statistically significantly different between our three groups, indicating that the presence of pRCA stenosis had no effect on the deformation markers of RV function in our DM − patients.
To the best of our knowledge, we are the first to evaluate RV function in the presence or absence of DM in patients with pRCA stenosis. RV function in the presence of DM type 2 has been previously assessed in several studies via 2D-STE. Tadic et al. (2015), who ruled out CAD only by symptoms, found that all the deformation markers of RVFW were reduced in their DM + patients [12]. Kowsari et al., in an investigation whose study population comprised patients for whom significant CAD was ruled out by elective coronary angiography, reported a decrease in all the deformation parameters of RVFW, except the late diastolic strain rate of RVFW, in their DM + patients [13]. Vukomanovic et al. (2020) demonstrated reduced RVFW systolic strain values in the endocardial layer in DM + patients without hypertension [5]. Scintillatingly, while Tadic et al. detected no such reduction in one of their studies [14], they observed it in another investigation [4]. CAD was excluded in two of the three aforementioned studies by history and in the other by the exercise test. A new study via cardiac magnetic resonance feature tracking demonstrated declined longitudinal RV global strain values in DM + patients; still, not only did the researchers fail to measure RVFW systolic strain value and other longitudinal deformation markers but also they did not exclude CAD by history [15]. To sum up, the existing studies have included either subjects without CAD or those for whom CAD was excluded weakly. We, however, employed selective coronary angiography to confirm the presence or absence of CAD. Our study demonstrated that DM exerted an impact on RV diastolic function irrespective of the presence or absence of a chronic ischemic milieu. Also in regard to RV systolic function, we found that the presence of a chronic ischemic milieu might lessen the difference between DM + and DM − patients. A previous investigation also showed the effect of the chronic ischemic milieu in alleviating the difference between DM + and DM − patients candidated for CABG in terms of left atrial function [16]. DM triggers some metabolic cascades in sugar and fat metabolism that finally result in fibrosis, death of cardiomyocytes, and microvascular dysfunction [17]. An important point to bear in mind in this context is that diastolic function is more sensitive to injuries than is systolic function [18]. Hence, the earliest changes in the presence of DM and chronic ischemia occur in RV function; we measured these changes as reflected by the early diastolic strain rate of RVFW in the current study.
In our DM − patients, significant pRCA stenosis did not lead to RV dysfunction as assessed by 2D-STE. Unfortunately, data on the effects of pRCA stenosis on RV function are scarce. Chang et al. (2014) evaluated RVFW systolic strain value and RVFW systolic strain rate in the presence and absence of pRCA stenosis and found diminished RVFW systolic strain value in those with pRCA stenosis. Nevertheless, their study had some shortcomings inasmuch as DM + patients constituted most of the subjects with pRCA stenosis, women comprised the majority of the study population, and there were no adjustments of the results according to several existing confounding variables [6]. Research on LV function is indicative of reduced systolic deformation markers in the presence of significant stable CAD [19–21]. Be that as it may, RV is different from LV in that not only does it supply diastolic and systolic coronary flows and receive collaterals from the left coronary artery system but also it is a low-pressure chamber with less thickness [22, 23].
Our study results demonstrated that the RV E/e′ ratio was increased from the DM − RCA − group to the DM − RCA + and DM + RCA + groups, but it failed to reach statistical significance. This finding might be explained by the detrimental effects of ischemia and/or DM on RV diastolic function. The RV E/e′ ratio is a marker of RV filling pressure, which is related to RV diastolic function [10]. It is calculated with the aid of two markers: E and e′, which are obtained by pulsed-wave Doppler and pulsed-wave tissue Doppler imaging, respectively. Notably, both of these methods are angle-dependent and are, thus, susceptible to measurement error. The early diastolic strain rate of RVFW is a marker of diastolic RV function obtained by 2D-STE, which is an angle-independent method. In addition, 2D-STE can measure myocardial longitudinal deformation in the early diastolic period directly [24].
The rate of CABG in the United States is about 0.1% per adult [25]. During the post-CABG period, RV may encounter increased pulmonary artery pressure and ischemia; accordingly, impaired function in RV renders it more susceptible to failure [26], which underscores the significance of the identification of the factors that can induce RV dysfunction.
In light of the findings of the present study, it can be concluded that DM + patients with pRCA stenosis require more surveillance regarding their RV than do DM − patients with or without pRCA stenosis.
Study limitations
Our study is a cross-sectional, single-center study with a small sample size. The fact that financial constraints precluded us from evaluating RV function by 3D echocardiography or cardiac magnetic resonance imaging is another weak point. It is also worthy of note that the occurrence of myocardial infarction in RCA territory in the presence of DM might be ruled out because of the loss of pain sensation in some DM + patients. Another salient drawback to our study is that its results may be generalizable only to post-CABG patients.
Conclusions
RV diastolic function was impaired in our DM + RCA + group compared with our DM − RCA + and DM − RCA − groups. The systolic function of RV was, however, not different between the DM + RCA + patients, on the one hand, and the DM − RCA + and DM − RCA − groups, on the other. Further, pRCA stenosis was not associated with RV systolic and diastolic functions in our DM − patients.
Funding
This study was funded by X (grant number X). XY has received.
Compliance with ethical standards
Conflict of interest
The authors declare that they have no conflict of interest.
Ethical approval
If human beings have participated in the research (**). All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards. If human beings have NOT participated in the research. This article does not contain any studies with human participants or animals performed by any of the authors.
Informed consent
Informed consent was obtained from all individual participants included in the study.
Footnotes
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Contributor Information
Somayye Norouzi, Email: snorouzimd@gmail.com.
Ali Hosseinsabet, Email: ali_hosseinsabet@yahoo.com.
Reza Mohseni-Badalabadi, Email: mohsenihr@yahoo.com.
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