The surgical times and procedures were similar between the two groups (Table 4). Two patients from Group 1 required reinstitution of CPB for biventricular failure and hemodynamic instability. Use of inotropes and IABP are presented in Table 4. All study patients received inotropic therapy. For Group 1 patients, there was a greater need for two or more inotropes and/or an IABP to achieve hemodynamic goals after CPB.
Hemodynamic and echocardiographic measurements are listed in Table 5. In all patients, there was no evidence of valvular stenosis. All patients had less than moderate valvular regurgitation. The ventricular septum was recorded as convex toward the right (normal) during the cardiac cycle in all patients. Five of seven patients from Group 1 had RV free-wall akinesis with or without other akinetic segments of the RV. The other two Group 1 patients had severe hypokinesis of the RV free wall. By contrast, there was no evidence of significant RV free-wall injury for Group 2 patients. The pre-CPB LVEF was similar between the two study groups (15.8% versus 17.8%). Group 1 patients had a smaller increase in LVEF immediately after CPB compared with Group 2 (4.1% versus 12.6%;P = 0.03). Both study groups had similar increases in RVFAC after CPB, although the mean RVFAC for Group 1 was less than that of Group 2.
Before surgery, Group 1 patients had statistically significantly higher mPAP (33.7 versus 27.0 mm Hg;P ≤ 0.05) and lower CI (1.9 versus 2.6 L · min−1 · m−2;P = 0.01). Group 1 had a higher intra-/pre-CPB mPAP (34.4 ± 9.1 versus 24.8 ± 8.7 mm Hg;P = 0.01). Immediately after CPB, Group 1 patients tended to have lower SVI (24.2 versus 30.5 L · min−1 · m−2). There were no significant differences between the pre- and post-CPB RVSWI, nor did either group show a significant change from before to after CPB.
All patients received inotropic support after CPB. More Group 1 patients required two inotropic drugs (4 of 7; 57%) compared with Group 2 (2 of 34; 6%) (P < 0.01). Although a similar percentage of Group 1 and 2 patients had an IABP placed before surgery (2 of 7 [29%] versus 8 of 34 [23%], respectively), more Group 1 patients had an IABP placed in the postoperative period for hemodynamic instability (4 of 5 [80%] versus 2 of 26 [8%];P < 0.01). Patients in Group 1 had a significantly increased incidence of LV diastolic dysfunction (6 of 7 [86%] versus 14 of 34 [41%];P = 0.01). Group 1 patients also had an increased severity of diastolic dysfunction (pseudonormal, restrictive; 6 of 7 [86%] versus 8 of 34 [24%]).
Outcome was significantly better for patients in Group 2 in a univariate analysis (Tables 4 and 5;Fig. 2). After exclusion of two Group 1 patients who died in the OR or within 2 h of arrival to the SICU, the median number of days patients required mechanical ventilation (1 versus 12 days;P < 0.01), the duration of SICU stay (2 versus 14 days;P < 0.01), and the duration of hospital stay (7 versus 14 days;P = 0.02) were significantly less for Group 2 patients. The associations between pre-CPB RVFAC and outcomes continued to be statistically significant (i.e., P ≤ 0.05) after pre- and intraoperative covariables were controlled for in multivariate regression analysis, suggesting that the results were not confounded by or due to other variables that were recorded in the study.
Overall early and late mortalities for the study population were 12% (5 of 41) and 21% (8 of 38; 3 patients were lost to follow-up). During this same study period, the reported 30-day mortality for the same surgical department for all patients (n = 1984) undergoing CABG ranged from 2.1% to 4.8%. Follow-up was unobtainable for three patients from Group 2. Survival was significantly better for patients in Group 2 (P < 0.0001;Fig. 2). All seven Group 1 patients died by the 2-yr follow-up. Of these seven patients, there were two immediate cardiac deaths (one in the OR and one within 3 h in the SICU). Both died of severe biventricular failure. Three other Group 1 patients died during the same hospital admission (postoperative Days 14, 19, and 20). Their postoperative course was complicated by low cardiac output and subsequent multiorgan failure (cardiac, pulmonary, and hepatic failure, with or without renal failure). Two other patients died of cardiac causes at 15 and 18 mo after CABG. These two patients presented with congestive heart failure and biventricular failure. Three patients from Group 2 were lost to follow-up after discharge from the hospital. Ninety-four percent (29 of 31) of Group 2 patients survived beyond the first 2 yr after surgery. One patient died of complications of colon cancer at 18 mo after CABG. A second patient (RVFAC 40%) died of cardiac causes 24 mo 6 days after surgery. A third patient died of cardiac causes 48 mo after surgery. A fourth is awaiting cardiac transplantation 4 yr after surgery. The postoperative course of the last three patients was complicated by recurrent congestive heart failure. Of the remaining 27 patients, all were of New York Heart Association Classification I or II.
In this study, early (30 days) and late (2 years) cardiac mortalities for the entire study group were 12% (5 of 41) and 21% (8 of 38), respectively, which was more than the mortality for all nonemergent CABG patients at this institution but similar to previous reports for patients with severe LVSD (8%–11% operative mortality) (7–10,13,14). An RVFAC ≤35% (Group 1) before CPB was associated with prolonged mechanical ventilation, SICU stay, and hospital stay and increased early and late mortality. Patients in Group 1 had a more frequent incidence and severity of LV diastolic dysfunction, no significant change in LVEF, and an increased incidence of RV free-wall injury. Before and after CPB, Group 1 patients tended to have higher central pressures and lower cardiac output and stroke volumes. After CPB, Group 1 patients had a faster HR. Comparatively, patients with RVFAC >35% (Group 2) had a relatively uncomplicated perioperative course (0% 30-day mortality), a larger increase in LVEF immediately after CPB, improvement in functional status, and excellent long-term survival (94% [29 of 31] overall survival; 96% [29 of 30] cardiac survival).
Hemodynamic differences between the two groups were a lower CI before surgery and higher CVP and mPAP before surgery and before CPB, respectively. After CPB, patients from Group 2 had a higher SVI despite less inotropic and mechanical support. Although there were no statistically significant differences in areas of LV infarct (persistent akinesis), there were significant differences in RV segment injuries. Patients from Group 1 had a significantly more frequent incidence of injury of all RV walls except the apical segment.
Previous risk-assessment analyses have identified increasing age (>70 years), female sex, decreased LVEF (<25%–30%), reoperation, preoperative IABP, extent of coronary artery disease, complex surgery, coexisting organ dysfunction, and emergency surgery to be associated with increased morbidity and mortality after CABG (1–5). Coexisting diseases found to be significant risk factors include diabetes, renal failure requiring dialysis, and chronic obstructive lung disease (1–5). In this study, Group 1 patients had an increased incidence of diabetes and renal failure (serum creatinine >1.5 mg/dL), but none required dialysis before surgery. These differences did not affect the significance of RV function and outcome, nor were they associated with outcome.
There are increasing data demonstrating an association between RV function and patient outcome. Although isolated RV infarct is uncommon (5%), the incidence increases with LV anterior wall infarction (5%–15%) and even more with LV inferior wall infarction (30%–85%) (26,27). Combined morbidity and mortality are as much as 47% in patients when RV injury is documented by echocardiography, electrocardiography, or both (26–32). Data from surgical and nonsurgical patients demonstrate worse outcome with RVFAC or RVEF <35%(17–19,28). In nonsurgical patients with LVSD, multivariate analyses showed RVEF to be associated with exercise capacity, oxygen consumption, and a morbid cardiac end-point (pharmacological or mechanical support, heart transplantation, or death) (28,33). Two-year mortality for patients with severely reduced (<25%), moderately reduced (25%–35%), and mildly reduced or normal (>35%) RVEF was 93%, 77%, and 59%, respectively (28). In a study of 52 postoperative surgical or nonsurgical patients with hypotension despite receiving inotropic therapy, the hospital mortality was 86% when severe RV dysfunction was present (19). Mortality was 30%–40% for patients with severe LVSD and moderately impaired or normal RV function (19). For patients with normal RV and LV systolic function, the mortality was only 15% (2 of 13; both died of hemorrhage) (19). For patients undergoing CABG, a trend was reported (P = 0.07) between preoperative RV function and outcome for 42 patients with a preoperative LVEF <20%(20). The majority of these patients (34) underwent emergent or urgent CABG, defined as within 48 hours of presentation, and 10 patients underwent additional surgical procedures (20). Despite these data, current risk assessments do not list RVSD as a significant risk factor (1–5). One explanation relates to previous issues in measuring RV systolic function with echocardiography. However, data have demonstrated the accuracy of RV systolic function measurements with echocardiography (22,23). They also demonstrate the superiority of a midesophageal four-chamber view over other single-plane assessments (22,23). On the basis of these previous outcome data, we used an RVFAC of ≤35% as our cutoff between the two groups. All patients in Group 1 had an RVFAC of <35% (25%–34%), and the RVFAC for Group 2 patients ranged from 40% to 85%.
Although there are data for surgical and nonsurgical patients associating outcome with LV diastolic function, it, too, is not included in risk assessment tables for cardiac surgical patients (1–5). The incidence of diastolic dysfunction after myocardial infarction may be as frequent as 60% within 24 hours and 60%–70% one year later (34). Diastolic dysfunction has been correlated with reduced exercise capacity, congestive heart failure, and death (34–38). Congestive heart failure and death are most frequent for patients with a pseudonormal or restrictive Doppler pattern during echocardiographic examination (34–37). The mortality for patients with restrictive pattern may be as much as 60% within one year after myocardial infarction (34,35). In this study, 85% (6 of 7) of patients with RVFAC ≤35% had an LV restrictive pattern compared with 24% (8 of 34) for Group 2.
RVSD and LV diastolic dysfunction have been reported in patients after heart surgery with CPB (39–45). RV dysfunction may not peak for four hours after CPB and may not begin to recover until eight hours after CPB (40,41). During this time, the RV has a decreased ability to tolerate fluid challenges, increases in afterload, and changes in Pco2(40,42–44). LV diastolic dysfunction after CPB alters the pressure-volume relation and may be manifested by increased pulmonary vascular pressures and an increased need for inotropic therapy to facilitate weaning from CPB (45–47). Although most patients with enough functional reserve are able to tolerate small decreases in RV and LV function, those with significant baseline dysfunction may not be able to tolerate further deterioration.
Because RV and LV functions are related, it is difficult to determine whether RV dysfunction was a primary event (i.e., myocardial infarction) or was secondary to LV dysfunction. Ventricular interdependence occurs at several levels, including the pericardium, septum, and pulmonary vessels (27,29,48). The intact pericardium imposes a mechanical constraint to outward expansion. Because both ventricles exist within the same pericardial space, an increase in volume or pressure in one ventricle may limit the ability to expand or even cause a reduction in volume of the other ventricle. In the case of LV failure and dilation, filling of the RV may be impaired. Although removing the pericardial constraint may improve RV filling, the increased preload may unmask significant underlying RV dysfunction. Ventricular interdependence also occurs at the interventricular septum. An intact pericardium, which limits outward expansion, enhances interdependence at the ventricular septum. Normally, the septum bulges toward the RV during the cardiac cycle. This rightward shift is more prominent with a failing LV. With primary RV failure or when RV failure is more than LV failure, the ventricular septum shifts to the left. Changes in septal shift are related to relative changes in pressures and volumes between the two ventricles. As a result, diastolic filling of the more functional ventricle may be impaired. Changes in end-diastolic septal position also affect the systolic function of the less dysfunctional chamber (i.e., the one that the septum shifts toward). Finally, interventricular communication occurs through the pulmonary vascular system, which normally offers little resistance to RV ejection. Increasing left-sided pressures can be transmitted via the pulmonary vasculature, which may increase RV afterload and dysfunction. RV dysfunction may be due to severe LV diastolic and systolic function, which may transmit increased intracavitary pressures to the right heart via the septum, the pericardium (if intact), or the pulmonary vasculature. In this study, the ventricular septal position was toward the right, suggesting that RV dysfunction, if present, was not significantly worse than LV dysfunction. Hemodynamic measurements after CPB showed that Group 1 patients had significantly lower SVI after CPB. Although both groups showed increases in RVFAC, only Group 2 showed a significant increase in LVEF. These post-CPB differences occurred despite revascularization and the more frequent use of inotropes and IABP in Group 1. These data are consistent with the greater degree of LV dysfunction and perhaps less reserve function for Group 1, suggesting that a significant component of RV dysfunction was due to increased severity of LV dysfunction in these patients. Nevertheless, there was a significantly more frequent incidence of RV segment dysfunction for patients in Group 1 (except the apex), suggesting that the cause of RV dysfunction was likely due to both greater LV dysfunction and primary RV injury.
Although the overall mortality of all patients with severe LVSD is frequent, we have shown that there is a subset of lower-risk patients. Identification of this subset of patients is possible by assessing heart function beyond the LVEF. Initially, this may include assessments of RV systolic and LV diastolic function. We speculate that, for patients with severe LVSD, the absence of significant RV dysfunction may indicate a greater amount of LV reserve or viability, which may be seen, clinically, by an increase in LVEF after revascularization and the use of inotropic therapy. This association is supported by Gudjonsson and Rahko (49), who studied the change in oxygen consumption and ventricular ejection fraction during exercise in 35 nonsurgical patients with dilated cardiomyopathy (49). Increases in oxygen consumption during exercise were correlated with both LV inotropic reserve and resting RV function. Significant LV inotropic reserve was correlated with normal or mildly impaired baseline RV function, whereas poor LV inotropic reserve had greater impairment of baseline RV dysfunction (49). In another study of 16 patients with severe biventricular failure (LVEF, 20% ± 5%; RVEF, 22% ± 6%), the ability to augment right-sided function (RVEF, 22% to 35%) with dobutamine was associated with improved short-term outcome (16). From the data presented in this study and reported elsewhere, accurate assessment of heart function and prediction of outcome should include measures beyond the LVEF. These assessments would and, we suggest, should be used to guide the decision for and timing of therapeutic options, which may include surgical revascularization.
Conclusions regarding the predictive ability of RV function cannot be made, because the data were obtained retrospectively. Furthermore, the small number of patients studied would weaken the argument. This, however, does not detract from the significantly different outcomes associated with RV function.
Our conclusions are based on retrospective data obtained in the OR after the induction of anesthesia. Although several anesthetics may cause cardiac depression, there may be an improvement in loading (decreased preload and afterload) conditions, which may improve function. Ideally, statements regarding preoperative assessment should be based on preoperative data; however, the preoperative evaluation of the RV was incomplete. Fewer than 50% of patients were assessed with echocardiography before coming to the OR, and all assessments were qualitative. As a result, we are unable to make meaningful comparisons between preoperative RV assessment and intraoperative assessment. Because all patients were stable in the pre-CPB period, we suspect that ventricular function had not changed significantly from preinduction.
In this study, calculations of LVEF and RVFAC were accomplished with single-plane echocardiography. Ideally, these data should be obtained on the basis of measurements from two or more planes to obtain a three-dimensional assessment and take into account the effect of multiple wall-motion abnormalities that were clearly present in these patients. However, during the review of echocardiographic studies, the midesophageal four-chamber view was the only view consistently obtained in all patients with adequate visualization of the endocardium necessary for tracing.
Statements regarding an association between reserve RV function and LV viability are speculative. Conclusive statements can be made only by comparing baseline RV function with an accepted viability analysis.
Another limitation to our study is the lack of documentation (i.e., coronary angiography) that all coronary bypass grafts were patent during the early and late postoperative periods. Our results may have been due to failure to achieve and/or maintain adequate coronary arterial flow. Our data are pertinent to patients undergoing CABG using total CPB and cardioplegic arrest and may or may not apply to CABG without CPB.
Pre-CPB RV function is associated with outcome after CABG in patients with severe LVSD. In the presence of severe LVSD, evaluation of RV systolic function and, perhaps, LV diastolic function may further define risk. For patients with normal RV function, one could expect a good outcome after CABG. For patients with significant biventricular systolic dysfunction (RVFAC ≤35% and LVEF ≤25%), further assessment of both LV and RV viability may be useful for predicting the benefits of CABG.
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