Author + information
- Allan Stewart, MD∗ ( and )
- Joanna Chikwe, MD
- ↵∗Reprint requests and correspondence:
Dr. Allan Stewart, Mount Sinai Health System, 1190 Fifth Avenue, Box 1028, New York, New York 10029.
Acute type A aortic dissection is a catastrophic disease, with mortality traditionally estimated at 80% in the first 48 h of symptoms and operative mortality approaching 20%. In this issue of the Journal, Czerny et al. (1) analyze one of the largest multicenter registries of aortic dissection patients with the aim of quantifying the effect of pre-operative end-organ malperfusion syndromes on early post-operative mortality and major morbidity.
Malperfusion syndromes were reported in more than one-third of the 2,137 patients in the registry that underwent operative intervention. This probably under-represents the prevalence of malperfusion and ischemia in patients presenting with type A dissections, because such patients are less likely to be considered appropriate candidates for surgical intervention. The mechanism of ischemia is compression or complete occlusion of the true lumen of branch vessels by the dissection flap. Czerny et al. (1) report that cerebral, coronary, renal, and peripheral extremity ischemia were the most common types of pre-operative malperfusion, each of which were seen in slightly more than 10% of patients, whereas mesenteric and spinal ischemia were less common. In most cases, replacement of the ascending aorta corrects malperfusion by restoring the normal pathway of blood flow. Surgery often converts an acute type A to a chronic type B dissection, and between 80% and 90% of these patients will still have flow in the false lumen distal to the ascending aortic replacement after surgical repair. Consequently, the potential still exists for post-operative end-organ malperfusion: the most common malperfusions seen post-operatively in this registry were renal and cerebral ischemia, which each occurred in 6.8% of patients. The authors identify several risk factors for post-operative malperfusion beyond the pre-operative presence of malperfusion, including the extent of the dissection.
Perhaps more importantly, Czerny et al. (1) add to single-center data, quantifying the incremental mortality associated with pre-operative malperfusion syndromes (2,3). In this registry, operative mortality for emergency type A dissection repair was only 12.6% in patients without any malperfusion, increasing by approximately 10% with each additional system affected by malperfusion or ischemia, to more than 40% in patients with 3 or more systems affected. Although this model does not claim to predict the futility of care, it may help frame a discussion with patients and families about the operative risks and likely quality of post-operative life. When 3 or more organ systems are involved, palliation may be more appropriate than surgery. The authors have taken an important step toward creating an individual treatment strategy not only focusing on treatment of the primary tear, but also addressing each malperfused organ. In this setting, a hybrid approach may be most appropriate (4). For instance, patients presenting with malperfusion may benefit from a concurrent peripheral bypass at the time of aortic surgery; simultaneous catheter-based intervention on visceral ischemia at the time of aortic surgery; or even a 2-team approach, where a renal artery stent is placed during the core cooling period for aortic replacement. For patients presenting with a retrograde dissection from a primary tear in the descending aorta, operative therapy should include a total arch replacement and perhaps frozen elephant trunk for complete treatment of the diseased aorta to reduce the increased risk of adverse outcomes seen by these patients in this registry.
The authors elected not to include 2 very different variables that have each been shown to independently predict operative outcomes of aortic dissection. First, the severity of malperfusion syndromes, which can range from an asymptomatic finding on computed tomographic angiography to circulatory collapse, is an obvious risk factor for worse clinical outcomes that was not evaluated in this analysis (2,3). The clinical value of their predictive model is weakened as a result. The second key determinant of outcome is the experience of the surgical team (5). The registry data suggest an average operative volume of only 11 cases/center per year. In a recent comparison of outcomes of type A dissection by specialist versus nonspecialist teams, patients who were operated on by nonspecialist cardiac surgeons were less likely to undergo axillary cannulation (which is associated with a lower stroke risk than aortic cannulation), were less likely to undergo hemiarch replacement (potentially leaving residual ascending aorta dissection), and had worse operative outcomes (6). In this series reported by Czerny et al. (1), the incidence of axillary cannulation was only 42%, and a hemiarch replacement was performed in only 62% of patients. These data may provide further support for the creation of regional centers of excellence where high volume and focused expertise consistently improve surgical outcomes.
In this regard, as well as in their primary aim, the authors should be congratulated for quantifying the well-recognized effect of malperfusion on patient outcomes. Instead of applying an optimism that “it ought to get better” after surgery, end-organ salvage may improve with aggressive strategies by experienced teams to address ischemia pre-operatively, intra-operatively, or with hybrid therapy.
↵∗ Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology.
Both authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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