We demonstrated that patients with concurrent elevation of PWV and E/e’ carried a higher risk of POAKI, POAF, and POSD in addition to the need for longer ventilator support and hospital stay compared with patients without high PWV and E/e’. Furthermore, the significant long-term survival difference was observed even after adjustment for potential risk factors between the patient groups with and without concurrent elevation.
Due to the absence of early mortality in this study, how arterial stiffness and diastolic filling pressure affect early mortality could not be analyzed. However, POAKI, POAF, and POSD were all significantly affected by the concurrent elevation in PWV and E/e’. Whether these complications are related to early cardiovascular mortality in this kind of population needs to be further investigated [11.12]. Consistent with earlier studies  and our report , isolated high PWV was an independent risk factor associated with POAKI (OR, 4.8; p = 0.016). However, the combination of elevated E/e’ and high PWV led to a substantial increase in the odds ratio of POAKI (OR, 22.6; p < 0.001) even though the isolated high E/e’ was not associated with POAKI. Recently, a retrospective observational study revealed that an E/e’ > 15 was an independent predictor of POAKI occurring after OPCAB . There has been some explanations of the association between high E/e’ and POAKI. First, the high E/e’ indicates elevated LV filling pressure and may contribute to increased intra-abdominal venous pressure and subsequent reduction in renal blood flow and GFR . Second, increased LV filling pressure aggravates hemodynamic instability, which is frequently triggered by lifting the heart during OPCAB, which in turn causes renal ischemia. Third, fluid overload during and after operation can induce capillary dysfunction at the glomerulus and may also trigger POAKI. In fact, high PWV is linked to elevated E/e’, which affects postoperative renal function. Increased arterial stiffness triggers premature return of reflected pulse waves, which facilitates diastolic coronary artery filing during late systole . This premature return decreases diastolic pressure and compromises coronary blood flow, which can aggravate the ventricular relaxation disturbance and elevate LV filling pressure .
Our data also emphasized the combined impact of elevated arterial stiffness and LV filling pressure on POAF. The isolated high-PWV-only and high-E/e’-only group failed to show statistical significance in predicting POAF, whereas high PWV-and-E/e’ group did demonstrate significance. In fact, some reports showed the association only between AF and PWV or between AF and E/e’. PWV has been significantly correlated with left atrial dimension independent of usual determinants such as age, gender, body mass index, ventricular remodeling and filling pressure, and thus associated with the risk of AF . The broad association of diastolic dysfunction and AF has been investigated . Current reviews suggest that left atrial and pulmonary vein pressure overload caused by non-compliant LV lead to atrial myocardial remodeling electrically and structurally, which increases the risk of AF . However, these reports did not investigate either combined effect or isolated effect of PWV and E/e’ on AF.
High PWV can elicit elevated pulse pressures, which are correlated with stroke . The carotid-femoral PWV exhibited poor neurocognitive dysfunction after aortic valve replacement . However, this study showed that the risk of POSD was not significantly higher in the high-PWV-only group although it was significantly elevated in the high-PWV-and-E/e’ group. In fact, POSD was associated with high baPWV even in our previous study . However, patients with high baPWV in the previous study involved both the high-PWV-only and high-PWV-and-E/e’ groups, suggesting the role of both elevated PWV and E/e’ and not from a single elevation. Thus, the combination of high PWV and E/e’ has a synergistic effect on POSD.
Elevated E/e’ in the two groups with high-E/e’-only and high-PWV-and-E/e’ had an impact on long-term overall survival in our study, while isolated elevation of PWV did not. This negative impact is in line with a recent study of 222 patients undergoing transcatheter aortic valve replacement. Advanced and indeterminate diastolic dysfunction was associated with increased mortality during follow-up (median 385 days) . In a cohort of 577 patients undergoing CABG, aortic valve replacement (AVR), or CABG with AVR, the higher LV filling pressure was associated with higher risk of mortality . The prognostic implications of E/e' have been investigated mainly in non-surgical patients with various heart diseases. A retrospective review of 2018 hospitalized patients with heart failure, the all-cause mortality over more than 6 years increased in proportion to the severity of diastolic dysfunction, and in patients with EF < 40%, severe diastolic dysfunction was independently associated with increased all-cause mortality . In a study enrolling 230 patients with non-valvular AF, the cumulative survival during follow-up (average 245 days) was significantly lower in subjects with E/e’ > 15 than in those with E/e’ ≤ 15, and the high E/e’ was an independent predictor of mortality .
Results of multiple Cox regression analysis revealed that the elevation in both PWV and E/e’, compared with the elevation in neither parameters, were independent prognostic predictors after adjustment of multiple clinical covariates (Table 4), which suggests that long-term survival is affected by the combination of E/e' and PWV but not by either parameter alone. These findings are supported by the results of our pairwise group comparison (Table 5) suggesting a statistical trend of higher hazard ratios in the high-PWV-and-E/e’ group compared with the high-E/e’-only and high-PWV-only groups.
This study has some limitations that must be addressed. First, the study did not evaluate PWV as well as E/e’ consecutively. A number of parameters were not measured in patients undergoing urgent operation, which contributed to selection bias. Second, the study did not consider the potential effect of antihypertensive drugs or hemodynamic alteration on E/e’ and PWV. Third, no perioperative hemodynamic status or transfusion volume affecting postoperative renal function was analyzed. Fourth, we could not determine the overall cause of late mortality and thus a comprehensive survival analysis related to cardiovascular outcome is needed. Lastly, because PWV was not a routinely measured parameter, the data was relatively small and the study was retrospective, suggesting the need for a larger, prospective study to corroborate or further investigate the findings reported here.