COMMENTS
Postinfarction VSD was an uncommon but challenging mechanical complication for surgeons. In the reperfusion era, approximately 0.2% of the STEMI patients would be diagnosed as VSR2,13-15. However, the reported postoperative mortality of emergency VSR repairs was no less than 30%1,16-19, which nearly stood for the poorest prognosis in cardiac surgery. Therefore, it is important to identify patients with excessive risk in whom surgical intervention should be cautious.
It has been conventionally believed that the average time between infarction and VSR decreased from 5 days to close to 1 day after the introduction of thrombolytic therapy2,20-22. However, such a change was not supported by our finding, probably because only 13.4% of the patients in this research got thrombolysis, and 26.8% underwent PCI. It is obvious that reperfusion therapy prevents the extensive myocardial necrosis typically associated with mechanical complications2. However, patients who already have VSR would benefit little from reperfusion therapy, because their unstable status was related to left-to-right shunt more than myocardial ischemia. So facing unstable VSR patients, many cardiologists preferred IABP implantation rather than PCI or thrombolysis. Similar results were also reported in previous researches6,7,23, which support our findings.
In this study, a shorter infarction-surgery interval was found to be a significant risk factor for postoperative mortality, with operative mortality rates of 100%, 21.4%, and 4.08% in the acute, healing, and healed phases, respectively. The result was generally consistent with the previous studies6,24. The mortality of emergency VSR surgery kept high due to the hemodynamic instability of patients in the acute phase of AMI, the fragile tissues surrounding the VSR, and hypoperfusion of systemic organs20,24,25. However, as mechanical assist implantation has become increasingly popular over the last decades, quite a few patients can be stabilized by mechanical assistance and safely past the acute phase. According to the STS database, patients who underwent surgery within 7 days of presentation had a 54.1% mortality compared with 18.4% mortality if the repairs was delayed until after 7 days6. With longer infarction-surgery intervals, consequent myocardial fibrosis would significantly reduce the difficulty of surgical procedures, which resulted in good surgical outcomes. For the patients who could be stabilized by mechanical assistance, they would benefit from the delayed surgery. Therefore, the 2017 ESC guidelines for STEMI suggest that delayed surgery could be considered for patients who respond well to aggressive treatment10, which agreed with our opinion.
Moreover, the delayed surgery strategy was adopted in our center, not only because of the substantial impact of short infarction-surgery intervals on the surgical outcomes7, but also only 22 cases (19.6%) were transported to our center within 7 days after infarction. The other 90 cases (80.4%) already missed the acute phase when they came.
Elder age and female gender were predictors of 30-day mortality in our study, which was also supported with other reports2,6,20. Although several reports had different results23, it was undebatable that elder or female patients were more vulnerable especially with a risky disease like VSR. Different results were probably due to varied samples.
This study found that the rupture enlargement rate was not only an independent risk factor, but also a strong predictor for postoperative mortality. Moreover, the results showed that the rupture enlargement was related to the critical preoperative status, as well as prolonged postoperative ventilation time, ICU length of stay, and reoperation. Such results were not reported by other researchers. The rupture enlargement rate was overlooked in previous studies, probably because it was difficult to observe in the immediate surgery strategy. The VSR patients in previous studies received emergency operations early, so there was not enough time for surgeons to observe the change of rupture size preoperatively. In clinical, the abrupt enlargement of rupture was usually associated with reinfarction or reperfusion injury. After the rupture enlargement, significantly increased shunts and delay in fibrosis at defect edges would lead to hemodynamic instability, sooner timing of surgery, and increased difficulty of operation. These factors result in worse surgical outcomes including increased postoperative mortality and morbidity.
Surprisingly, rupture enlargement was regarded as a protective factor by multivariable analysis with an OR value of 0.464, which was against the clinical experience. The unstable patients got surgery sooner than the stable patients, so they got less time for rupture to expand despite their higher rupture enlargement rate. In contrast, the stable patients had more time for adjustment before surgery, so they got larger rupture enlargement although their rupture expanded slowly. As a result, the effect of rupture enlargement was corrected in multivariable analysis. Due to the small sample, our results only generated a research hypothesis that needs to be verified in further studies.
In addition, the results showed a statistical significance in rupture size between the critical and noncritical groups, but similar results were not found between the survivors and non-survivors groups. Univariate regression also did not find an association between rupture size and postoperative mortality, and the ROC curve confirmed the poor predictive power of rupture size for postoperative mortality. The conventional opinion believed that a larger rupture size or larger preoperative shunt can lead to cardiogenic shock7,26, and it was also verified by our data. The reason that rupture size affects the hemodynamic status was probably that rapid rupture enlargement leads to both bigger rupture size and sudden rise of shunts. However, most of the patients in this study with delayed surgery received preoperative mechanical assistance for weeks, so hemodynamic instability caused by large rupture was likely to be corrected before the operations. Therefore, the impact of rupture size on surgical outcome was eliminated by mechanical assistance in the delayed surgery strategy.
Although the ROC curves demonstrated the satisfactory predictive power of rupture enlargement rate on postoperative mortality, the median values of rupture enlargement rate for the non-survivor and survivor groups were 0.07 mm/d and 0.32 mm/d respectively, and the cutoff point of the ROC curve was 0.205 mm/d, which is apparently extremely difficult for transthoracic echocardiography to observe. More accurate examinations and further researches are needed to explain the clinical significance of the rupture enlargement rate.
There are some limitations in this study. The retrospective design of this study makes it more prone to confounding, selection bias, and information bias. The small sample size forced researchers to use Bootstrap in multivariable analysis to correct the result, which led to limited reliability of the results. Multi-center research with large sample size is needed to further confirm the results.