Left ventricular hypertrophy in patients with acute type A aortic dissection: a formidable challenge

J Thorac Dis 2022;14(11):4209-4211 | https://dx.doi. org/10.21037/jtd-22-938 Hypertension is the most common risk factor for acute aortic dissection and is a major determinant of left ventricular (LV) remodeling, including LV hypertrophy (LVH) (1). Alterations in LV geometry result in high arterial load and vascular damage, elevated levels of neuroendocrine components, reduced coronary flow reserve, and high risk of LV dysfunction (2,3). The association between LVH and overall mortality is well established; Haider et al. analyzed data from 3,661 Framingham Heart study participants and found that LVH was associated with an increased risk of sudden cardiac death: 2.16-fold for any degree of LVH, and 1.45-fold for every 50 gm of LV mass (4). In their study titled “Prognostic value of left ventricular hypertrophy in postoperative outcomes in Type A acute aortic dissection”, Zuo and colleagues (5) from Wuhan, China analyzed the utility of LVH in predicting postoperative outcomes in patients with acute aortic Type A dissection (ATAAD). This was a retrospective, singlecenter analysis of 193 patients who underwent ATAAD surgical repair over a nearly four-year period. Patients were classified as having or not having LVH according to their echocardiographically measured LV mass index (LVMI) and were propensity-score matched. LVH was noted in 28.5% of the patient cohort. The LVH patients were more likely to be female, to present with cardiac tamponade, and to have lower LV ejection fraction (LVEF). There was no significant difference between groups in the prevalence of hypertension, although the severity of hypertension and number of baseline antihypertensive medications were not known. The incidence of composite major outcomes (CMO), which included operative mortality, stroke, paraplegia, dialysis, and adverse cardiac events, was 30.9% in patients with LVH vs. 15.2% in patients without LVH. The LVH group had higher operative mortality (18.2% vs. 7.2%) and higher incidences of postoperative stroke, low cardiac output syndrome, and ventricular arrhythmias (5). Multivariable logistic regression identified three independent risk factors for postoperative CMO: LVH (OR 2.6, P=0.04), hyperlipidemia (OR 3.0, P=0.01), and emergency surgery (OR 2.8, P=0.02). LVMI (as a continuous variable) predicted postoperative CMO with an OR of 1.2 (P=0.02) for every 10 g/m of LVMI. The need for postoperative dialysis, the need for tracheostomy for respiratory failure, and atrial fibrillation were also associated with greater LVMI. Interestingly, although patients with LVH had higher rates of reduced LVEF, logistic regression analysis found no significant association between lower LVEF and postoperative CMO (OR 2.6, P=0.21). Both the LVH and LVMI models showed good clinical utility and consistency in predicting postoperative CMO and adverse cardiac events. Although LVH is a common echocardiographic finding in patients with aortic dissection, its clinical significance is unclear. In a study by Rocha et al., LVH was unrelated to 1-year mortality in patients with type A aortic dissection (6). Others have found that LVH may be a biomarker for early Editorial