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Perioperative Echocardiography and Cardiovascular Education: Original Clinical Research Report

Early Left and Right Ventricular Response to Aortic Valve Replacement

Duncan, Andra E. MD, MS*†; Sarwar, Sheryar MD; Kateby Kashy, Babak MD; Sonny, Abraham MD; Sale, Shiva MD§; Alfirevic, Andrej MD§; Yang, Dongsheng MS†‖; Thomas, James D. MD; Gillinov, Marc MD#; Sessler, Daniel I. MD

Author Information
doi: 10.1213/ANE.0000000000001108

Patients with symptomatic aortic stenosis are at high risk of death or heart failure unless aortic valve replacement (AVR) is performed.1 Long-term survival and quality of life are improved with surgical AVR2; however, when myocardial dysfunction occurs early after surgery, unadjusted 30-day mortality is increased approximately 5-fold.3 Furthermore, the presence of perioperative right ventricular (RV) impairment increases the risk for in-hospital mortality or postoperative circulatory failure approximately 25-fold.4 A better understanding of intraoperative left ventricular (LV) and RV response to AVR may help guide anesthetic and hemodynamic management during and after surgery to reduce postoperative myocardial dysfunction and ultimately improve outcomes after AVR.

Myocardial function after surgery is affected by opposing factors that may worsen or improve ventricular function. For example, cardioplegia-induced myocardial arrest and an ischemia-reperfusion sequence adversely affect LV function,5–7 especially when LV hypertrophy is present.8,9 In contrast, removal of a stenotic aortic valve abruptly decreases LV afterload, thus improving LV ejection.10,11 RV function, in contrast, may be more susceptible to injury from cardioplegic arrest than the LV,12 without benefiting from afterload reduction. The net effect of these events on intraoperative RV and LV function in patients undergoing AVR for aortic stenosis has not been fully characterized.

Although load-independent measures of ventricular contractility, such as the slope of the end-systolic pressure-volume relationship13,14 or preload recruitable stroke work,15 are sensitive to changes in inotropy, they are invasive, cumbersome, and thus not suitable for the clinical setting. Ejection phase measures, including LV ejection fraction (LVEF), are dependent on loading conditions; however, they provide clinically meaningful information because an increase in afterload induces physiologic compensatory changes in preload and contractility in an intact cardiovascular system which offsets the increase in afterload.16 Furthermore, echocardiographically measured LVEF is noninvasive, easy to measure, and thus suitable for the clinical setting. LVEF, however, evaluates volumetric changes during systole and diastole rather than the magnitude and speed of myocardial muscle contraction, which are important descriptors of myocardial function.17 LVEF also relies on geometric assumptions that are subject to measurement error. Therefore, a noninvasive echocardiographic measure that provides a reproducible and quantitative assessment of the magnitude and rate of myocardial contraction would be useful.

Myocardial strain and strain rate assess myocardial deformation and provide quantitative measures of myocardial contractility. Strain and strain rate correlate with load-dependent measures, including LVEF18 and the maximal rate of rise of LV pressure.19 Strain rate also correlates with a load-independent measure of LV function, the slope of the end-systolic pressure-volume relationship.20 Strain and strain rate assess the percent and rate of change in ventricular wall dimensions and are measured by tracking displacement of “speckles” from 2D echocardiographic images.21 Longitudinal strain in healthy individuals measured by transthoracic echocardiography varies slightly depending on the analysis technique but is typically between −18% and −21%,21–23 whereas longitudinal strain rate is −1.1 ± 0.2 s−1.21,22 The effect of AVR on postoperative strain 1 week or longer after AVR has been described,24–26 but acute intraoperative changes in myocardial deformation with transesophageal echocardiography (TEE) have not yet been reported.

Using strain and strain rate measured by speckle-tracking echocardiography, our primary objective was to characterize the effect of intraoperative events on LV and RV function after surgical replacement of a stenotic aortic valve. Specifically, we tested the hypothesis that LV function measured by strain and strain rate was improved at the end of surgery. Next, the change in RV function was evaluated during cardiac surgery. Patient characteristics and perioperative variables, which potentially contribute to the change in myocardial deformation, were also assessed.

METHODS

With the approval from the Cleveland Clinic IRB and written patient consent, we evaluated 100 patients scheduled for AVR who were enrolled in a randomized controlled investigation entitled, “The effect of the hyperinsulinemic normoglycemic clamp on myocardial function and utilization of glucose” (ClinicalTrials.gov NCT01187329, Andra Duncan, principal investigator, registered on August 19, 2010).27 Briefly, patients who were considered to be at increased risk for myocardial injury induced by cardioplegic arrest (patients with aortic stenosis and LV hypertrophy)28,29 were randomly assigned to intraoperative glucose control using standard glucose control (insulin treatment for blood glucose >150 mg·dL−1) versus hyperinsulinemic normoglycemia. Hyperinsulinemic normoglycemia involves a high-dose insulin infusion at a fixed rate (5 mU·kg−1·min−1) with a concomitant variable glucose (dextrose 20%) infusion supplemented with potassium (40 mEq·L−1) and phosphate (30 mmol·L−1), titrated to a target glucose concentration of 80 to 110 mg·dL−1.27 Because the primary results did not find a meaningful difference in myocardial function between groups (minimal change in LV strain rate, which was statistically significant [−0.16 {−0.30 to −0.03} s−1; P = 0.007], but not clinically meaningful, and no difference in LV strain, RV strain, or RV strain rate),27 the study groups were combined for this supplementary analysis to assess change in LV and RV myocardial deformation during AVR surgery.

Table 1.
Table 1.:
Preoperative Baseline Characteristics of Patients With Aortic Stenosis (n = 97)
Figure 1.
Figure 1.:
Consolidated statement of reporting trials flow diagram. LV indicates left ventricular; RV, right ventricular; TEE, transesophageal echocardiographic examination.

Exclusion criteria included the presence of aortic insufficiency without aortic stenosis, contraindication for TEE, poor-quality echocardiographic images, which were unsatisfactory for speckle-tracking strain analysis (>3 unacceptable myocardial segments as deemed by a blinded investigator), and requirement for intraoperative hypothermic circulatory arrest. Of 100 patients enrolled in the randomized controlled trial, 3 patients with aortic insufficiency as the predominant valvular pathophysiology and 2 patients with contraindications for TEE examinations were excluded. Twenty-three patients had echocardiographic images that were unacceptable for LV strain analysis, 28 were unacceptable for LV strain rate analysis, and 41 were unacceptable for RV strain and strain rate analysis (Figure 1). Thus, echocardiographic images were acceptable in 72 patients for LV strain analysis and 67 for LV strain rate analysis. RV strain and strain rate analyses were adequate for 54 patients. Demographics and patient characteristics for 97 patients with aortic stenosis and a subgroup of 72 patients with LV strain data are shown in Table 1.

Anesthetic and Surgical Management

Routine procedures for anesthesia, surgery, and conduct of cardiopulmonary bypass (CPB) were used, as previously described.27 Epinephrine was administered for low cardiac index (<2.0 L·min−1·m−2), and/or norepinephrine was given for low systemic vascular resistance (<700 dyn·sec·cm−5) after separation from CPB to maintain mean arterial blood pressures higher than 80 mm Hg and cardiac index greater than 2.0 L·min−1·m−2.

Collection of Echocardiographic Data

TEE was performed, as previously described.27 Briefly, Vivid S6 or Vivid E9 Ultrasound systems (GE Healthcare Vingmed Ultrasound AS, Horten, Norway) with a multiplane phased array GE 6Tc-RS 2.9 to 8.0 MHz transducer or an active matrix 4D volume phased array 3.0 to 8.0 MHz transducer were used to collect echocardiographic data for off-line analysis using dedicated analysis software (EchoPAC v.112; GE Healthcare Vingmed Ultrasound AS).

A standardized TEE examination was performed after anesthetic induction (before surgical incision) and repeated near the end of surgery after sternal closure by 1 of 3 experienced staff cardiothoracic anesthesiologists who are certified in Perioperative Transesophageal Echocardiography by the National Board of Echocardiography. Standard echocardiographic parameters of LV systolic and diastolic function using 2D and Doppler echocardiography were performed, as previously described.27 LV end-systolic meridional wall stress (LVESS) measured in dynes·cm−2 was calculated using the equation:

where ESD represents end-systolic dimension (cm) and h represents the end-systolic posterior wall thickness (cm).30,31 To apply this calculation to patients with aortic stenosis whose echocardiographic measurements were collected with TEE, the equation was modified as follows: LV peak pressure was estimated as the sum of systolic blood pressure and the peak intraoperative aortic transvalvular gradient; ESD was measured as the anterior-inferior end-systolic internal dimension measured from the transgastric midpapillary LV short-axis echocardiographic view (cm); end-systolic inferior wall thickness measured from the transgastric midpapillary LV short-axis was used as h rather than using the measurement of the thickness of the posterior myocardial wall, which is compromised by poor resolution by TEE.

RV systolic function was assessed in the 2D transesophageal 4-chamber view with focus on the RV at 0° by fractional area change (%).32 M-mode measurement of tricuspid annular plane systolic excursion (TAPSE) was not possible because of poor alignment of the tricuspid annular motion with the echocardiographic beam; thus, TAPSE was measured off-line on 2D images by measuring the apical displacement of the lateral tricuspid annulus (cm) between systole and diastole.

Echocardiographic Analysis of Myocardial Deformation Using Speckle-Tracking Echocardiography

Echocardiographic data were digitally collected and stored for off-line analysis of myocardial deformation with speckle-tracking analysis software (EchoPAC v. 112; GE Healthcare Vingmed Ultrasound AS). Two-dimensional strain analysis uses grayscale (B-mode) sector images and is based on frame-by-frame tracking of myocardial movement and deformation using a unique pattern of bright and dark pixels or speckles in echocardiographic images.21 These speckles, which are constructive and destructive interference patterns generated by reflected ultrasound from inhomogeneous myocardial tissue, are tracked from one frame to another throughout the cardiac cycle and are used to assess myocardial deformation. Analysis of echocardiographic views for strain analysis involves tracing the endocardial contour on an end-systolic cavitary frame and defining the thickness of the myocardial region. The software automatically tracks the ventricular wall on subsequent frames and divides it into 6 segments. Manual adjustment of the endocardial contour and thickness of the region is performed when necessary. The software program deems tracking quality acceptable or unacceptable. However, the user can override this designation based on visual confirmation of proper tracking of myocardial motion.

Serial echocardiographic examinations were collected at equally spaced intervals of 60° (ie, 0°, 60°, 120°) of rotation of the transducer in attempts to reproduce images for each echocardiographic examination, while circumferentially describing global LV function. Frame rates between 40 and 90 Hz were used. For LV analysis, 6-segment LV strain and strain rate measurements from 3 views, including the midesophageal 4-chamber, mitral commissural, and long-axis view, were averaged (total of 18 segments). All measurements that included at least 15 “acceptable” segments were included in the LV analysis. Our previous report demonstrated accurate and consistent results with the inclusion of assessments with a minimum of 15 acceptable segments.27

For RV analysis, strain and strain rate measurements from the 4-chamber view centered on the RV were used. At least 5 of 6 acceptable myocardial segments were required for analysis of the RV, although all segments from the RV free wall were required. LV and RV early diastolic strain rates were also assessed. All analyses of myocardial deformation were performed by the same investigator. We adhere to the convention of referring to the absolute value when comparing 2 strain measurements (eg, a change in strain from −18% to −12% reflects a decrease in myocardial shortening and thus a “decrease” in strain).33

Hemodynamic Data Collection

Invasive arterial blood pressures were recorded on all patients using radial or brachial arterial catheters. Patients with normal biventricular function and scheduled for isolated AVR received central venous catheterization. Those with abnormal myocardial function or scheduled for complex cardiac surgery (combined AVR with coronary artery bypass grafting or additional valve procedure) received pulmonary artery catheterization. Data recorded from patients with pulmonary artery catheters included systolic and diastolic pulmonary artery pressures, thermodilution cardiac output, and cardiac index. Cardiac output/index data were only reported from patients with pulmonary artery catheters and measured using the thermodilution technique. Hemodynamic data were recorded during TEE examination, which occurred after anesthesia induction before surgical incision and at the end of surgery after sternal closure.

Statistical Analysis

Patient demographics, clinical characteristics, and comorbidities were summarized using standard descriptive statistics. The primary analysis was to assess the change in systolic LV myocardial function (strain and strain rate) between baseline measured after anesthesia induction and the end of surgery measured after chest closure using paired t tests. The change in systolic RV myocardial function (strain and strain rate) was assessed secondarily. Furthermore, the relationship between LV and RV strain and strain rate and 15 potential risk factors were assessed in a multivariable regression model. Because of small sample size and large number of risk factors, univariable analysis with P < 0.05 was used to select initial candidates. A stepwise variable selection procedure with inclusion/exclusion criterion of P < 0.05 was used to select the final variables.

Comparisons on additional prespecified intraoperative echocardiographic and hemodynamic parameters between baseline and the end of surgery were implemented using separate paired t tests. The paired binary myocardial pacing (atrial and ventricular pacing) status between baseline and the end of surgery was compared by the McNemar test.

Intraobserver variability of the speckle-tracking analysis was examined using the Lin concordance correlation,34 Bland-Altman limits of agreement, and the binomial exact method. We conducted a preliminary analysis to assess the change in LV strain and strain rate in the first 45 patients. We used the O’Brien-Fleming alpha-spending method to adjust for this look (efficacy alone). As such, with an overall α of 0.05, the remaining α for the final analysis was 0.048. Using a Bonferroni correction, the significance criterion was 0.048/2 = 0.024 for each of the 2 primary and secondary analyses. SAS statistical software v. 9.4 (SAS Institute, Cary, NC) was used for all analyses.

Sample Size Consideration

With the attained sample size of 72 for change in LV strain and observed standard deviation of 3.1 and a correlation coefficient of 0.73 between pre- and post-CPB measurements, we had 90% power at the overall 0.025 significance level (Bonferroni correction for 2 primary outcomes) to detect a change in mean strain change of 1% or larger. Similarly, with an observed total sample size of 67 and standard deviation of 0.30 and observed correlation coefficient of 0.52 between pre- and post-CPB measurements, we had 90% power to detect mean change of 0.13 s−1 or more in strain rate.

RESULTS

Clinical Characteristics and Events

Table 1 presents the demographics, clinical characteristics, comorbidities, surgical, and anesthesia variables for 97 patients with aortic stenosis. A subgroup of 72 patients who had acceptable echocardiographic images for LV strain is also shown in Table 1. In all patients with aortic stenosis, the mean (± SD) age was 70 ± 10 years, 30 (31%) were women, and cardiac reoperations were performed in 23 (24%) patients. Valve replacement was successful in all patients, as indicated by the absence of significant residual regurgitation or transvalvular stenosis.

Primary and Secondary Outcomes of Myocardial Deformation

Table 2.
Table 2.:
Echocardiographic and Hemodynamic Parameters During Surgery (n = 97)
Figure 2.
Figure 2.:
Boxplot and series plot for left ventricular (LV) systolic strain (A and B) and strain rate (C and D) at the beginning and end of surgery in patients with aortic stenosis. Interquartile range (IQR, box), median (horizontal line), high and low values within 1.5 IQR (whiskers), and mean (diamond) are shown.
Figure 3.
Figure 3.:
Boxplot and series plot for right ventricular (RV) systolic strain (A and B) and strain rate (C and D) at the beginning and end of surgery in patients with aortic stenosis. Interquartile range (IQR, box), median (horizontal line), high and low values within 1.5 IQR (whiskers), and mean (diamond) are shown.

LV strain did not change at the end of surgery compared with baseline measurement (difference: 0.7 [97.6% confidence interval {CI}, −0.2 to 1.5]%; P = 0.071), whereas LV systolic strain rate improved (became more negative) (−0.3 [−0.4 to −0.2] s−1; P < 0.001). In contrast, RV systolic strain worsened (became less negative) at the end of surgery (4.6 [3.1 to 6.0]%; P < 0.001) although RV systolic strain rate was unchanged (0.0 [97.6% CI, −0.1 to 0.1] s−1; P = 0.83; Table 2; Figures 2 and 3).

Additional Echocardiographic and Hemodynamic Outcomes

Pairwise comparisons (end of surgery minus beginning of surgery) in echocardiographic and hemodynamic parameters are shown in Table 2. Pairwise comparisons limited to the subgroup of patients with acceptable images for LV strain analysis are shown in the Supplemental Digital Content, Supplemental Table A (http://links.lww.com/AA/B322). Ten patients with RV strain data did not have acceptable images for LV strain analysis; thus, only 44 patients with RV strain data are included in Supplemental Table A. Considering that TEE measurement of LV chamber size may be foreshortened and result in volume measurements smaller than those measured by 3D echocardiography (although LVEF estimates remain accurate),35,36 end-diastolic LV volumes (82 ± 44 [beginning] versus 69 ± 38 mL [end of surgery]; change [95% CI] −13 [−20 to −7] mL; P < 0.001, or −9% [95% CI, −23% to 6%]) and end-systolic volumes (39 ± 35 [beginning] versus 27 ± 32 mL [end of surgery]; change −10 [−13 to −7] mL; P < 0.001, or −25% [−34% to −17%]) were lower at the end of surgery in all patients with aortic stenosis. Measures of LV systolic function, including LVEF and peak systolic myocardial velocity, improved at the end of surgery, but LV diastolic function was not different at the end of surgery. As expected, LV afterload measured by LVESS and aortic transvalvular gradient were lower at the end of surgery (Table 2). RV function, measured by conventional echocardiographic measures (TAPSE, fractional area change), was reduced at the end of surgery.

Assessment of intraobserver agreements between the first and the secondary readings of LV strain and strain rate was excellent, with the Lin concordance correlation (95% CI) of 0.94 (0.87 to 0.98) for strain and 0.93 (0.85 to 0.97) for strain rate. Bland-Altman limits of agreement and the binomial exact method demonstrated good to excellent intraobserver agreement, as previously described.27

Heart rate was more rapid and arterial blood pressure lower at the end of surgery (Table 2; all P < 0.001). More patients had atrial pacing at the end of surgery (2 [2%] beginning versus 11 [11%] at the end of surgery, McNemar test; P < 0.001), but ventricular pacing at the beginning (1 [1%]) compared with end of surgery 6 (6%) was not different (P = 0.06). Cardiac output and cardiac index increased at the end of surgery. Of all 97 patients with aortic stenosis, 11 (11%) required IV infusion of epinephrine only; 23 (24%) required IV infusion of norepinephrine only; 6 (6%) required both epinephrine and norepinephrine, and 1 (1%) required epinephrine, norepinephrine, and milrinone. In the subgroup of 72 patients with images for LV strain analysis, 9 (13%) required epinephrine, 22 (31%) required norepinephrine, 2 (3%) required both, and 1 (1%) required epinephrine, norepinephrine, and milrinone.

Relationship Between Baseline and Intraoperative Factors and LV/RV Strain and Strain Rate

Table 3.
Table 3.:
Univariable Relationships Between the Change in Left (LV) and Right (RV) Ventricular Strain and Strain Rate and Risk Factors
Table 4.
Table 4.:
Multivariable Relationships Between the Change in Left (LV) and Right (RV) Ventricular Strain and Strain Rate and Risk Factorsa

Results of the univariable and multivariable relationship examining the change in LV and RV strain and strain rate with patient characteristics and intraoperative variables are listed in Tables 3 and 4. In the multivariable model, aortic cross-clamp time and previous cardiac procedure were associated with change in LV strain. For every 10-minute increase in aortic cross-clamp time, mean LV strain worsened by 0.6% (P = 0.001), and those who had previous cardiac surgery had a mean change in LV strain of 1.8% (worsening) compared with those having a primary surgery (P = 0.018). Use of the hyperinsulinemic normoglycemic clamp (P = 0.005) and epinephrine use (P = 0.04) were significantly associated with the change in LV strain rate. Patients who received the hyperinsulinemic normoglycemic clamp had a −0.2 s−1 mean improvement in LV strain rate compared with those who did not receive this treatment. Patients who received epinephrine had a 0.2 s−1 worse LV strain rate compared with patients who did not receive epinephrine (P = 0.04). Women had a worse RV strain (less negative) at the end of surgery (P = 0.04), and patients with a history of hypertension had improved RV strain rate (more negative) at the end of surgery (P = 0.02).

DISCUSSION

Our investigation evaluated the percent and rate of myocardial longitudinal shortening with strain and strain rate and found that RV and LV function demonstrate acute and divergent changes immediately after AVR. Despite intraoperative cardioplegic arrest, an ischemia-reperfusion sequence, and possible myocardial stunning, LV function improved as documented by an approximately 40% increase in LV strain rate. However, LV strain, which measures the amount of LV longitudinal systolic shortening, was unchanged. In contrast, RV strain decreased while RV strain rate was unchanged, demonstrating a reduction in the amount of RV systolic shortening without affecting the rate of contraction.

LV strain rate, a robust noninvasive measure of contractility representing the rate of myocardial shortening,18–20,37 was greatly increased after AVR, consistent with improved LV function. Strain rate correlates with the rate of LV pressure rise, a well-established measure of LV contractility, which is based on evidence that the greater the contractile force exerted, the greater the rate of increase in LV pressure.38 LV strain, in contrast, did not improve. The lack of improvement in LV strain was unexpected because strain detects subtle changes in myocardial function that are not apparent with conventional echocardiography.39–41 Decreased LV preload, documented by smaller intraventricular volumes at the end of surgery, reduces strain by the Frank-Starling mechanism42 and may have contributed to the lack of improvement in LV strain.

Other clinical settings have similarly documented improved contractility by an improvement in strain rate without corresponding changes in LV strain. β-Adrenergic stimulation with dobutamine infusion in normally perfused myocardium increases strain rate with a minimal effect on strain,43 and patients with low flow-low gradient aortic stenosis increase peak strain rate, but not strain, at peak stress during dobutamine stress echocardiography.44 Strain rate is less sensitive to changes in preload and heart rate than strain,18,45,46 and thus served as a more robust measure of LV function in our patients.

Whether the increase in LV strain rate was related to an improvement in intrinsic myocardial contractility, the myocardial response to an acute decrease in afterload or a mild increase in heart rate cannot be determined from our results because strain and strain rate are load-dependent measures.42,47 However, there certainly was a substantial decrease in afterload as demonstrated by an approximately 5-fold reduction in the mean transvalvular gradient and 40% decrease in LVESS. Several techniques adjust myocardial deformation measures for changes in load, although each method has limitations. Some investigations “normalize” LV strain for changes in preload by adjusting for end-diastolic volume,48 although this modifies strain from a dimensionless quantity (it has the same value regardless of units) to a measure restricted to end-diastolic volume. In addition, normalizing strain for end-diastolic volume may result in a measurement that reflects LV size more than myocardial contraction. One investigation, for example, adjusted strain for end-diastolic volume in patients with aortic regurgitation48 and reported that absolute (actual) values of strain were not improved by corrective surgery, while normalized (strain/end-diastolic volume) strain values were improved. However, the improvement in normalized strain was driven by a reduction in LV size, not a change in strain, and thus could be interpreted that LV volume decreases after AVR rather than strain improves.48 Another important point is that loading conditions do not change in isolation and adjustment for a single factor ignores the effects of other important variables. Indeed, changes in preload also affect contractility and afterload and invoke baroreceptor responses and reflex changes that further alter the inotropic state.16,49 Another method of adjustment uses a multivariable model to adjust for loading conditions,50 but this method assumes a linear relationship between strain or strain rate and other variables, which may not be accurate.

Because of limitations associated with the above methods to adjust for loading changes, we chose to report the actual strain values without adjustment in our primary results. Our secondary analysis, however, explored the association between myocardial deformation and afterload using LVESS49 and preload assessed by LV end-diastolic dimension. Neither the change in preload nor afterload was associated with the change in measures of myocardial deformation, suggesting that other factors may have contributed to an improvement in strain rate such as activation of autonomic reflexes or increases in endogenous and exogenous circulating catecholamines at the end of surgery. Heart rate is also increased by these factors that may further improve myocardial contractility. Harpole and colleagues51 reported that intrinsic myocardial contractility assessed by a load-independent measure, the stroke work-end-diastolic volume relationship, was unchanged after replacement of a stenotic aortic valve. This differed from our results likely because of the use of load-dependent versus load-independent measures.

Less is known about RV function during cardiac surgery because the complex geometry and crescent-like shape complicates echocardiographic assessment.52 Using myocardial deformation analysis, our investigation demonstrated that, in distinct contrast to the beneficial effects of AVR on the LV, RV function did not improve after surgery. In fact, reduced longitudinal strain suggests worse RV function. Other echocardiographic measures of RV function including fractional area change and TAPSE similarly decreased at the end of surgery. This is consistent with worsening of RV function, although RV strain rate was unchanged. These results are consistent with the divergent effects of AVR on perioperative RV and LV function.

Why RV strain and other measures of RV function worsened at the end of surgery is unclear. One study similarly reports a decline in RV function after cardiac surgery and suggests that inadequate myocardial protection and subsequent interventricular septal dysfunction contribute to this finding.53 Another report suggests that pericardiotomy caused a decline in RV function.54 Others described a change in the pattern of RV contraction after surgery where longitudinal shortening was reduced, whereas transverse shortening increased, thus maintaining low normal RV function.55 Hemodynamic variables may also affect RV function: the LV benefits from an acute reduction in afterload while RV afterload is maintained, demonstrated by preserved pulmonary artery pressures. RV preload, however, was reduced as indicated by a decrease in RV end-diastolic area. Other contributing factors may include interventricular dependence, where the size, shape, and compliance of one ventricle affect the other through direct mechanical interaction. Whether this change in RV function has clinical implications is unclear. Our study population was small with few adverse events and thus could not assess whether there was an association with adverse postoperative complications. However, because the overall mortality after AVR is widely reported to be <2%,56,57 this reduction in RV strain does not appear to profoundly impact postoperative outcomes.

In addition to the expected hemodynamic effects of removal of a stenotic aortic valve, our secondary analysis examined other contributors to the change in myocardial deformation at the end of surgery. As reported previously, patients who received the hyperinsulinemic normoglycemic clamp demonstrated increased LV strain rate27 but not other measures of myocardial deformation. Prolonged aortic cross-clamp time decreased LV strain, although LV strain rate and RV deformation parameters were unaffected. Interestingly, patients who did not receive epinephrine had a greater improvement in strain rate compared with those who received epinephrine, providing evidence that an increase in strain rate after surgery was not related to the use of epinephrine. Alternatively, epinephrine use likely identified patients who experienced post-CPB myocardial dysfunction and thus required inotropic support. Epinephrine and norepinephrine use was not related to the change in other myocardial deformation measures.

Strain and strain rate assessments are uncommon in the operating room because of a lack of availability and experience with these techniques. Furthermore, strain rate measurements are characterized by significant noise and require substantial experience for interpretation. However, future improvements in image acquisition, analysis programs, real-time availability of strain and strain rate, and use of 3D assessment may increase the use of strain and strain rate in the operating room. As demonstrated by our investigation, strain and strain rate may be used to detect subtle improvements or decrements in myocardial performance that cannot be appreciated by simple visual assessment of LV or RV motion by echocardiography. Importantly, there is currently no 2D echocardiographic method available for the assessment of rate of systolic contraction comparable with strain rate.

Although strain can be measured in longitudinal, radial, and circumferential dimensions, we focused on longitudinal strain because it provides a more reliable and reproducible measure of systolic function.58,59 Importantly, longitudinal function plays an important role in patients with aortic stenosis.39,60 Furthermore, longitudinal strain predicts outcomes in patients with aortic stenosis61 and other clinical scenarios, including ischemic cardiomyopathy,62 heart failure,63 acute myocardial infarction,64 and mitral valve repair.65 In patients with heart failure, longitudinal strain best discriminates between patients who will require rehospitalization or die of cardiac causes.66 Importantly, longitudinal strain is easily calculated from routinely collected echocardiographic views that are acquired during the intraoperative period. Because the RV is more dependent on longitudinal shortening during ejection than the LV,67 the use of longitudinal strain and strain rate measurements are especially well-suited for assessment of RV function.

This investigation has limitations. As discussed earlier, strain and strain rate are both affected by loading conditions. Strain and strain rate naturally vary among individuals. For example, strain ranged between −5.5% and −27.5% and strain rate between −0.3 and −1.8 s−1 in our study population, but by using a paired analysis with patients serving as their own controls, we were able to isolate the specific effects of surgical events. Midesophageal echocardiographic images used for myocardial deformation analysis may have been subject to foreshortening; however, our analysis assessed the within-patient change from baseline, thus reducing bias from foreshortened images. Although this investigation was limited to patients with aortic stenosis having AVR, there was variability in the surgical procedure, surgical approach, and myocardial protection strategy; however, our supplemental analysis found that the effect of these variables on myocardial deformation was not significant, and this heterogeneity enhances the generalizability of our results. Strain and strain rate measurements may vary somewhat among operators; we thus restricted all echocardiographic measurements and analyses to a single experienced investigator who used a software analysis program from a single vendor. Intraobserver variability demonstrated excellent agreement between measurements, although the use of a single observer may result in a consistent bias. Because measurements of strain rate using speckle tracking are limited by a lower frame rate (typically 50–90 frames per second) compared with tissue Doppler measurements (>100 frames per second), undersampling resulting in reduced peak strain rate may have occurred,68 although all patients would be similarly affected. Finally, we present a subanalysis of a larger study in which patients were randomized to a hyperinsulinemic normoglycemic clamp or routine glucose management. However, the hyperinsulinemic normoglycemic clamp had minimal clinical effect,27 and the contribution of this treatment was evaluated in the secondary analysis.

In conclusion, surgical removal of a stenotic aortic valve improves LV function, as measured intraoperatively by myocardial strain rate. LV strain, in contrast, did not improve, possibly because loading conditions also changed considerably after valve replacement. RV strain, however, was reduced, although the clinical implications of this finding require further exploration.

DISCLOSURES

Name: Andra E. Duncan, MD, MS.

Contribution: This author was responsible for the study design, conduct of the study, data collection, data analysis, data interpretation, and manuscript preparation. This author is the archival author.

Conflicts of Interest: None.

Name: Sheryar Sarwar, MD.

Contribution: This author was responsible for data collection and manuscript preparation.

Conflicts of Interest: None.

Current Affiliation:Sheryar Sarwar, MD, is currently affiliated with Department of Family Medicine, Case Medical Center, University Hospitals of Cleveland, Cleveland, Ohio.

Name: Babak Kateby Kashy, MD.

Contribution: This author was responsible for data collection and manuscript preparation.

Conflicts of Interest: None.

Current Affiliation:Babak Kateby Kashy, MD, is currently affiliated with Department of Anesthesiology, Northwestern University, Chicago, Illinois.

Name: Abraham Sonny, MD.

Contribution: This author was responsible for data collection and manuscript preparation.

Conflicts of Interest: None.

Current Affiliation:Abraham Sonny, MD, is currently affiliated with Department of Anesthesia, Critical care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts.

Name: Shiva Sale, MD.

Contribution: This author was responsible for data collection and manuscript preparation.

Conflicts of Interest: None.

Name: Andrej Alfirevic, MD.

Contribution: This author was responsible for data collection and manuscript preparation.

Conflicts of Interest: None.

Name: Dongsheng Yang, MS.

Contribution: This author was responsible for data analysis and interpretation.

Conflicts of Interest: None.

Name: James D. Thomas, MD.

Contribution: This author was responsible for study design, conduct of study, data interpretation, and manuscript preparation.

Conflicts of Interest: None.

Current Affiliation:James D. Thomas, MD, is currently affiliated with Center for Heart Valve Disease, Bluhm Cardiovascular Institute, Northwestern University, Chicago, Illinois.

Name: Marc Gillinov, MD.

Contribution: This author was responsible for conduct of study, data interpretation, and manuscript preparation.

Conflicts of Interest: Marc Gillinov serves as a consultant for Edwards Lifesciences, Medtronic, Tendyne, Abbott, On-X, and PleuraFlow. Dr. Gillinov has served as a speaker and/or received honoraria from Edward Lifesciences, Medtronic, and Intuitive Surgical and receives research support from St. Jude Medical.

Name: Daniel I. Sessler, MD.

Contribution: This author was responsible for study design, conduct of study, data interpretation, and manuscript preparation.

nal data and analysis and approved the final manuscript.

Conflicts of Interest: None.

This manuscript was handled by: Martin J. London, MD.

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