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.