Early Left Ventricular Global Longitudinal Strain Deterioration After Aortic Aneurysm Repair: Impact of Aortic Stiffness

Abstract

Purpose

To associate the impact of aortic reconstruction using currently available grafts and endografts on pulse wave velocity in patients with abdominal aortic aneurysm (AAA) and to evaluate its effect on early cardiac systolic function indices.

Materials and Methods

Seventy-three consecutive patients with AAA (mean age 70±8 years; all men) who underwent open (n=12) or endovascular repair (EVAR; n=61) were prospectively enrolled in an observational cohort study. Left ventricular global longitudinal strain (GLS; an important diagnostic and prognostic index of early systolic dysfunction) and carotid-femoral pulse wave velocity (cf-PWV) were estimated 1 week preoperatively, as well as at 1 and 6 months postoperatively.

Results

A significant time effect was found for cf-PWV, which showed an increase at 1 month that remained through 6 months (p=0.007). Additionally, a deterioration in GLS values was revealed, with a significant change at 1 month that persisted 6 months later (p<0.001). No significant group effect was observed between EVAR and open repair (p=0.98), and there was no significant interaction (p=0.96). Notably, the difference in GLS between baseline and 6 months significantly correlated with the corresponding changes in cf-PWV (r=0.494, p<0.001).

Conclusion

AAA repair leads not only to an increase in aortic stiffness, as measured by the increase in pulse wave velocity, but also to reduced cardiac systolic function. Our findings highlight the need for a more intense cardiac surveillance program after aortic reconstruction. Further studies are needed to investigate how this may translate into long-term manifestations of cardiovascular complications and symptomatology.

Keywords

abdominal aortic aneurysm arterial stiffness endograft endovascular aneurysm repair hypertension left ventricular hypertrophy myocardial strain open repair pulse wave velocity stent-graft

Introduction

Although abdominal aortic aneurysm (AAA) repairs, open or endovascular, may have a lifesaving impact on the course of the disease, their overall effects are quite complex, probably due to the adverse interaction between the aortic graft and the myocardium.¹ Endovascular aneurysm repair (EVAR) has become the preferred treatment in most AAAs due to its less invasive nature and the low risk of associated periprocedural complications.² Although the short-term outcomes in these patients are superior to those of open surgery, long-term follow-up has failed to demonstrate that the perioperative survival advantage of EVAR is maintained.^3–5 Furthermore, a significant portion of long-term mortality has been attributed in part to cardiac events, for both open repair and EVAR.⁶ Specifically, Schouten et al⁶ reported a significantly increased combined 30-day endpoint of nonfatal myocardial infarction and all-cause mortality, 17% in the open repair group vs 4% in the EVAR group. In the same study, during a follow-up of 3.3 years, total mortality was 31% and did not differ between the groups (p=0.38).⁶

Aortic grafts have been shown to increase arterial pulse wave velocity (PWV) immediately after the procedure.^7–9 This phenomenon may be associated with the poorer than expected long-term outcomes in these patients since greater arterial stiffness is associated with an increased risk of atherosclerotic heart disease, myocardial infarction, and stroke.¹⁰ In addition, cardiac ejection into a stiffer vascular net induces structural and functional changes in the left ventricle, even at a similar level of mean arterial pressure.¹¹ As a result, negative long-term effects on cardiac remodeling, as shown in experimental animal models, might be expected.^12,13 A small patient series has also shown that aortic grafts may cause alterations in aortic mechanical properties that can directly impact cardiac structure, worsening left ventricular (LV) hypertrophy and inducing diastolic dysfunction.⁹

Although concern has been expressed in the literature about the deterioration of myocardial function after the placement of an aortic graft, detailed evidence about its effect on cardiac structure and function are limited,^7,13,14 and many pieces of the puzzle are still missing. The pathophysiological mechanisms behind the above findings are unclear but may be related to the fact that, although aortic stent-graft technology has evolved, aortic grafts are not designed to reproduce the physiological properties of the aorta and may predispose to long-term complications.

The current study prospectively monitored a group of AAA patients who underwent EVAR or open repair to evaluate changes in indexes of systolic LV function in the early and midterm postprocedural period. Global longitudinal strain (GLS), which has been used to measure systolic function and has advantages compared with LV ejection fraction (LVEF), was chosen for this study owing to its superiority in assessing subtle and subclinical deterioration of LV function.^15,16 GLS is derived from speckle-tracking echocardiography and expresses longitudinal shortening as a percentage of change in length in proportion to baseline length on apical images of the left ventricle. The differences in peak GLS were related to changes in arterial stiffness in these patients.

Materials and Methods

Study Cohort

This was a single-center, nonrandomized, prospective, observational cohort study enrolling consecutive patients who underwent elective endovascular or open surgical repair of their AAA between January 2017 and June 2018 with maximum follow-up terminating on October 31, 2019. The following inclusion criteria were applied to patient selection: (1) no history of previous open repair or EVAR, (2) no aortic dissection, and (3) LVEF ≥50% as assessed by echocardiography. Exclusion criteria were emergency surgery, rhythm other than sinus or cardiac pacemaker, aortic surgery requiring cardiopulmonary bypass, severe aortic or mitral valve disorders, thoracoabdominal para-anastomotic pseudoaneurysms, and ruptured aneurysms. Also excluded were patients with collagen-related disorders, malignancies, severe hematological diseases, autoimmune diseases, end-stage renal failure, and any inflammatory disease during the past 6 months.

The choice between EVAR and open repair was based on the patient’s anatomical eligibility, operative risk, and comorbidities. Anatomical eligibility for the EVAR group included a proximal neck length ≥13 mm, an inner neck diameter between 16 and 30 mm, a juxtarenal neck angulation ≤60°, and a distal seal zone ≥10 mm long and between 8 and 25 mm in diameter.¹⁷ To avoid any potential graft-related effect, the Ovation Abdominal Stent Graft System (Endologix Inc, Irvine, CA, USA) was used for all endovascular repairs. Aortic grafts in open repair were made of polyester or polytetrafluoroethylene (PTFE).

The study was carried out in accordance with the ethical guidelines of the Declaration of Helsinki, and the study protocol was approved by the Hospital Scientific and Ethics Committee (decision 4667/14-6-2017). All participants signed an informed consent document.

Patient Evaluation and Velocity Measurement

All participants were evaluated for hypertension, renal function, and cardiovascular comorbidities and underwent a full laboratory workup, an echocardiographic study, and computed tomography angiography of the aorta before the intervention and at 1 and 6 months afterward. Carotid-femoral PWV (cf-PWV) was measured at 1 week preoperatively and 1 month and 6 months postoperatively, as previously described.¹⁸ For this test, all subjects were asked to refrain from caffeine, alcohol, and smoking during the preceding 12 hours. The study was carried out between 8:00 and 9:00 AM in a quiet room at 22±1°C. Height and weight were measured. Subjects were allowed a further 15 minutes supine before baseline measurements. Brachial blood pressure was measured over the brachial artery 3 times at 5-minute intervals; the mean of the last 2 measurements was recorded as representative of brachial blood pressure. Carotid-femoral artery waveforms were measured, and PWV (Complior SP; Atech Medical, Cholet cedex, France) was determined. The distance traveled by the pulse waves was assessed in triplicate over the surface of the body with a nonelastic tape measure. Pulse wave transit time was determined from the time delay between the proximal and distal “foot” waveforms.

Echocardiography Study

A standard M-mode and 2-dimensional (2D) echocardiographic study was performed in all participants, according to the recommendations of the American Society of Echocardiography and the European Association of Echocardiography^19,20 before the aortic repair and at 1 and 6 months postoperatively. Pulsed- and continuous-wave Doppler tracings were obtained and ventricular volumes and LVEF were calculated by the modified Simpson method using apical 4- and 2-chamber views. The early transmitral velocity (E wave) was obtained by pulse wave Doppler from the apical 4-chamber view, with the sample volume positioned at the tip of the mitral leaflet. Peak LV velocity (e′) was measured from the lateral and septal mitral annulus and was averaged. The E/e′ ratio was calculated as the E wave divided by the e′ velocity. Left ventricular mass index was calculated using the Devereux formula.²⁰

The 2D speckle-tracking strain analyses were performed on grayscale images of the left ventricle using EchoPAC (version BT13; GE Healthcare, Waukesha, WI, USA), and peak GLS was measured. For this, loops of 3 cardiac cycles were stored digitally and analyzed offline. The optimal images for speckle tracking were selected. If any segment was not clearly visible, the image was excluded. For each platform, a region of interest (ROI) was outlined by user-defined markers to incorporate the entire myocardial wall. Repeat adjustments of the ROI were done if tracking quality was insufficient. The frame rate for speckle-tracking strain assessment was 50 to 90 frames per second. During strain analysis, the endocardial border was manually traced at end-systole and the width of the region of interest was manually adjusted to include the entire myocardial wall thickness. The EchoPAC software then automatically tracked and accepted segments with good tracking quality and rejected poorly tracked segments. However, the operator could manually override computer-generated tracking and accept or reject individual segments based on visual assessments of the tracking quality. Measurements were made throughout the cardiac cycle in the apical 4-chamber, 2-chamber, and long-axis views. GLS was obtained by averaging peak values of segmental strain in the apical views. All measurements were performed by 2 experienced operators blinded to previous measurements. Interobserver variability was <3%.²¹

Follow-up and Outcomes

Clinical follow-up visits were performed periodically according to the physician’s judgment. The clinical outcomes were event-free survival and cardiovascular event–free survival. Events included death from any cause or cardiovascular cause, stroke, myocardial infarction, acute coronary syndrome, any reintervention, or the presence of an endoleak.²²

Patient Sample

The study recruited 73 men (mean age 70±8 years) who underwent a scheduled AAA repair procedure (61 EVAR and 12 open repair). Half of the grafts in open repair were Dacron and half PTFE. In addition, half of the grafts were bifurcated and half were straight. The patients’ clinical and demographic characteristics are shown in Table 1. The patients who underwent EVAR were older than those who had an open repair, and their maximum aortic diameter showed a trend to be smaller compared with the latter group. All patients had hypertension, and a striking majority were smokers [55 (90%) EVAR and 10 (83%) open repair], while 28 (45%) in the EVAR group and 4 (35%) in the open repair group had type 2 diabetes. Coronary artery disease was present in a third of both groups (20 EVAR and 4 open repair), but chronic obstructive pulmonary disease was more prevalent in EVAR patients (28, 46%) vs open repair patients (2, 16%).

Table 1.

Baseline Clinical Characteristics of the Enrolled Patients.^a

	EVAR (n=61)	OR (n=12)	p
Age, y	71±7	66±8	0.01
Body mass index, kg/m²	28.2±4.9	28±4	0.9
Systolic blood pressure, mm Hg	131±12	132±14	0.6
Diastolic blood pressure, mm Hg	79±8	85±11	0.04
Heart rate, bpm	72±9	69±6	0.2
Hematocrit, %	42.4±3.8	41.1±3.2	0.3
Creatinine, mg/dL	1.4±1.1	1.1±1.2	0.04
Maximum sac diameter, mm	6.02±0.98	6.6±1.47	0.08
Left ventricular ejection fraction, %	59.9±4	59.4±4.4	0.6
Stroke volume index, mL/m²/beat	38.3±5.4	37.9±4.8	0.7
Aortic root diameter, mm	38.1±3	38.7±5	0.6
Left atrial volume index, mL/m²	36.2±5.1	36.4±2.7	0.9
Left ventricular mass index, g/m²	99.5±21.6	105.5±21.7	0.4
E/e′	10.9±2.6	10.8±2.4	0.8
Carotid-femoral pulse wave velocity, m/s	10.1±3.3	10.8±2.1	0.4
Global longitudinal strain, %	−17.4±3	−17.3±2.1	0.9

Abbreviations: bpm, beats per minute; E, peak early diastolic flow velocity of transmitral flow velocity curve; e′, peak early diastolic velocity of the tissue Doppler imaging of the mitral annulus movement at the septal position; EVAR, endovascular aneurysm repair; OR, open repair.

Data are presented as the mean ± standard deviation.

Statistical Analysis

Summary descriptive statistics are given as mean ± standard deviation or frequency (percentage) as appropriate. Confidence intervals (CI) were calculated as appropriate. Repeated-measures analysis of variance with one between-group factor (EVAR, open repair) was used to assess (1) the time course from preoperative to 1 and 6 months, (2) any group effect, and (3) group or time interaction effects for GLS and cf-PWV. Pearson correlation coefficients were used to evaluate the relationship between changes in GLS, PWV, and E/e′. Kaplan-Meier product-limit survival curves were constructed to estimate the outcomes. Log-rank tests were used to compare curves. All tests were performed at the 2-sided α=5% level of significance using IBM-SPSS software (version 25; IBM Corporation, Armonk, NY, USA).

Results

Impact of Intervention on PWV and Cardiac Function

Six months after the procedure, a trend toward reduction in LVEF was seen (Table 2), while there was a significant increase in left atrial volume, with a concomitant deterioration in indexes of diastolic dysfunction (E/e′ from 10.9±2.6 to 13.5±3.8, p<0.001) and GLS-based systolic dysfunction (from −17.4%±2.9% to −15.3%±3.3%, p<0.01). A significant time effect on cf-PWV was seen, which showed an increase after 1 month that remained stable thereafter (p=0.007). The effect of AAA repair on PWV regardless of the type of surgery was evaluated, but there was no significant group or interaction effect between EVAR and open repair (p=0.91 and p=0.53, respectively).

Table 2.

Clinical and Echocardiographic Characteristics of All Participants Before and After Abdominal Aortic Aneurysm Repair.^a,b

	Baseline	1 Month	6 Months	Mean Differences	p
Hematocrit, %	42.2±3.7	37.2±5.8	34.8±3.8	−6.3±4	<0.001
Body mass index, kg/m²	28.2±4.8	28.1±3.9	28.8±4.9	0.6±0.7	0.4
Systolic blood pressure, mm Hg	131±13	130±11	136±12	3.7±14	0.09
Diastolic blood pressure, mm Hg	80±10	77±12	79±12	0.5±11	0.7
Pulse pressure, mm Hg	52.3±14.4	53.5±15	56.5±15	4.2±18.4	0.09
Heart rate, bpm	72±8	71±8	70±9	−1±7	0.4
Left ventricular ejection fraction, %	59.8±4.1	59.5±3.9	58.5±4.6	2.5±4.8	0.07
Stroke volume index, mL/m²/beat	38.8±5.3	37.5±4.0	37.1±6.3	2.1±5.1	0.3
Left atrial volume index, mL/m²	36.2±4.8	37.5±5.8	37.9±4.5	2.3±3.5	0.03
Aortic root diameter, mm	38.1±3	38.3±3.2	38.5±2.8	0.5±1	0.4
Left ventricular mass index, g/m²	100.4±21.7	100.2±19.4	101.2±21.4	1.5±2.8	0.8
E/e′	10.9±2.6	12.2±3.4	13.5±3.8	2.6±2.7	<0.01
Global longitudinal strain, %	−17.4±2.9	−17.3±3.8	−15.3±3.3	2.1±2.3	<0.01
Carotid-femoral pulse wave velocity, m/s	10.2±3.1	11.1±4.9	11.8±3.9	1.8±3.3	0.05

Data are presented as the mean ± standard deviation.

Comparison of all time points and mean differences between values at baseline and 6 months.

Patients who underwent AAA repair showed a steady worsening of their GLS values during the 6 months of echocardiographic follow-up (Table 2). In particular, GLS showed a clear time effect (p<0.001), with a significant increase at 1 month that persisted 6 months later (Figure 1). No significant group effect was observed between EVAR and open repair (p=0.98) and no significant interaction (p=0.96).

The change in GLS at 6 months after the intervention was moderately correlated (Figure 2) with the corresponding changes in cf-PWV (r=0.494, p<0.001) and E/e′ (r=0.468, p<0.001).

Clinical Outcome

Median follow-up time was 18 months. The cardiovascular event–free rates were 93.2% at 6 months, 83.3% at 12 months, and 80.3% at 24 months. Mean time to events was 23 months (95% CI 21 to 25). Five patients died, 1 due to a cardiovascular event and 4 from non-cardiovascular causes. One patient presented a dissection of the ascending aorta, 3 had a stroke, 4 experienced acute pulmonary edema, and 4 had acute coronary syndromes. Eight AAA patients presented an endoleak: 4 type Ia and 4 type II. Two of the type Ia endoleaks spontaneously resolved during follow-up as has been previously shown to occur.²² A central cuff was inserted in the other 2 patients to resolve the type Ia endoleaks. None of the type II endoleaks needed any further intervention. The adverse events, however, were too few to show any statistically significant correlation with the echocardiographic changes or the changes in aortic stiffness.

Discussion

Our study attempted to delineate the precise influence of AAA repair on early indices of myocardial systolic function. The investigation found that patients who underwent AAA repair, either endovascular or open, showed a stable deterioration in LV systolic function, as expressed by GLS, appearing very soon after the procedure and persisting over 6 months of echocardiographic follow-up. Notably, this deterioration may have some association with the detrimental effect of the aortic graft on arterial stiffness, since there was a moderate but statistically significant relationship between the changes in GLS and cf-PWV.

Strain analysis, particularly GLS, has been reported as a more sensitive predictor of overall cardiovascular mortality compared with LVEF.²³ GLS measures the maximal shortening of myocardial longitudinal length during systole; reduced GLS reflects abnormal systolic function before the loss of LVEF becomes apparent. GLS has emerged as a fine-tuned, highly reproducible method for quantification of LV function and a prognostic tool in a wide spectrum of cardiac diseases.²⁴

Our results are not surprising and mirror the existing clinical skepticism on this issue. Previous studies have shown that replacing the aorta with a noncompliant vascular prosthesis or introducing an aortic endograft may change the elastic properties of the arterial system, compromise the arterial distensibility, and thereby interfere with the ventriculo-arterial coupling.^{12,13,25–27}

Patients who undergo aortic aneurysm surgery are a population with a very high risk of cardiovascular complications and often poor clinical outcomes.^7,28,29 Patients with AAA may present with significantly elevated PWV values compared with controls.⁷ Notably, this finding is not consistent, and there are studies indicating that postrepair cf-PWV may be normal or decreased, probably due to the disruption of the smooth continuity of the aorta.³⁰ According to the reference values of PWV,³¹ our study did not disclose significantly high cf-PWV values related to age or gender, which indicates that PWV may be influenced not only by hypertension and age but also by aortic structure.

Stent-graft repair is often associated with a significant increase in PWV after 6 months.^7,30 There is evidence in the literature from previous experimental and clinical studies that aortic endografting results in increased arterial stiffness and a further deterioration in the mechanical properties of the aorta.^5,7,8 Alterations in these aortic mechanical properties can have a direct impact on heart function and can provide explanations for the poor outcomes in these patients. However, there are contradictory data in the literature: Studies either do not show a postprocedural increase in PWV^32,33 or indicate a higher PWV elevation in the open repair group.³⁴ Obviously, there is a need for a more adequate investigation of this impact.

Although EVAR in the treatment of AAA significantly reduces short-term morbidity and mortality, the rates of late complications and reinterventions remain considerably high. Moreover, EVAR does not independently reduce long-term mortality compared with open repair,^4,5,28,35 revealing a need for comparative studies with long-term follow-up.³⁶

Previous studies have also shown that EVAR increases vascular stiffness, induces LV diastolic dysfunction, and can decrease exercise tolerance, especially in patients with low LV distensibility,^9,37 triggering adverse hemodynamic consequences.^12,13,27

Our observations can be explained by the pathophysiology and clinical findings from other patient categories. The notion of ventricular-arterial interaction, in which the stiffness of both the heart and arteries interacts to limit LV performance, has been well established in the literature.³⁷ The total hydraulic power developed by the LV to propel the blood through the systemic circulation depends not only on the ability of the LV to do external work but also on the properties of the arterial tree into which the blood is ejected.³⁸ The LV is generally thought to adapt to sustained arterial hypertension by developing concentric hypertrophy.³⁸

The behavior of PWV is quite diverse during the follow-up period. This may reflect the reason why the 6-month median increase of PWV was not striking and lacked a strong correlation among the postinterventional changes. It should always be kept in mind that PWV represents the average stiffness of the arterial tree between the measurement sites, but it has many drawbacks. Mainly, PWV measures properties of heterogeneous arterial segments with different wall composition.

Ventricular systolic and diastolic performance is linked to the interaction between the heart and vascular loads and is significantly affected by changes in these parameters,³⁹ and a chronic increase in arterial stiffness is coupled with an increase in ventricular end-systolic stiffness.^40,41 Our patients demonstrated a parallel reduction in diastolic and systolic function, but it is known that GLS is associated with LV diastolic function, independent of afterload changes and the degree of LV hypertrophy.⁴² However, the clinical significance of our findings and their effect on the long-term outcomes of these patients have yet to be elucidated. For this, further prospective longitudinal studies are needed.

Limitations

Unfortunately, our study included no women because none was among the consecutive patients enrolled during the recruitment period. In general, few women with aneurysmal disease have been treated in our department, much fewer than those reported in the literature. This may be attributed to the very low smoking rate of women older than 50 years in our geographical area.

Our patients were not compared with a control group. However, the baseline cf-PWV values in patients with AAA may be paradoxically low in relation to their overall profile because of the anatomy and distension of the aorta and may not represent the true degree of arterial stiffness or the true vascular aging.⁴³ It is feasible that comorbidities, such as hypertension or diabetes, which are very common in AAA patients, could have had an impact on the deterioration of GLS. However, compared to the patients’ preoperative values, our findings appeared immediately after the procedure (within 1 month), suggesting that they were associated predominantly with the AAA repair. In addition, only one type of endograft was used, which might have different properties than endografts implanted in previous studies; therefore, it may not be able possible to extrapolate our findings to other types of grafts.

This was a consecutive observational cohort study. For this reason, a power analysis was not applicable in the initial design. A major limitation of our study is the lack of clinical correlation, and negative results for clinical events may be due to lack of power and the short follow-up. Future trials with clinical endpoints involving the deterioration of echocardiographic systolic and diastolic parameters will enlighten this issue.

The number of patients included in the study was not particularly large, especially in the open repair group. This may have obscured other important statistical differences. However, our results were clear, while previous studies of the effects of AAA repair on cardiovascular parameters had much smaller patient populations.

Finally, our results are based on echocardiography, which is highly operator dependent. In our study, echocardiography was performed by 2 highly experienced senior cardiologists, which should have ensured good-quality data.

Conclusion

Both EVAR and open AAA repair are followed by an immediate deterioration of LV GLS that is related to an increase in aortic stiffness. Future device manufacturers should attempt to develop more compliant devices with biomechanical properties that mimic the elasticity of the native aorta. This may mitigate the detrimental effects of AAA repair on the cardiovascular system. Perhaps a more intensive cardiac surveillance program and optimal medication management may help improve the long-term clinical outcome in these patients.

Footnotes

Declaration of Conflicting Interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

ORCID iDs

George Papadopoulos

Eleni Nakou

Emmanouel Tavlas

Christos V. Ioannou

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