Prognostic Value of Measuring Body Surface Area in Patients with Acute Coronary Syndrome

The relation between obesity and outcomes after acute coronary syndrome (ACS) is controversial. Some large prospective studies suggested that the latter relation is mediated by the comorbidities whereas other studies indicated that relation is independent of comorbidities [1]. Obesity has been shown to be associated with more favorable short-term but not long-term outcomes after ACS. In addition, a U-shaped relationship – termed the “obesity paradox” has been suggested, where overweight and obese patients exhibit a more favorable prognosis than patients with recommended normal body weight and underweight in the secondary care of patients with cardiovascular disease and in patients undergoing percutaneous coronary intervention [2, 3]. In common medical practice, obesity is defined by body mass index (BMI) which is calculated using weight and height. A prior study of ≥65-year patients with ST-segment elevation myocardial infarction (STEMI) from the United States reported lower in-hospital mortality, bleeding, and adverse cardiac events in patients with mild obesity compared to worse outcomes in patients with normal weight and extreme obesity [4]. Due to this paradoxical relationship, BMI as a surrogate to define obesity and its relation to prognosis in the secondary care has been widely debated [2].Body surface area (BSA, another measure of body size) has been suggested as a better indicator of weight related risk than BMI. While BMI is an aggregate of body fat and varying amounts of fat free mass, BSA is reflective of body and organ sizes, and is less affected by abnormal adipose mass [5]. BSA is commonly used as a biometric unit to adjust for mass and volume, and to index physiological parameters related to circulation. In an earlier study of 2,197 patients with STEMI, significant reductions in post-PCI complications such as coronary dissection, cardiogenic shock, acute renal failure, bleeding, vascular complications, and in-hospital death were observed in the highest quartile of BSA (>2.2 m2) as compared to the lowest (<1.8 m2). Moreover, BSA remained a strong predictor of 1-year mortality (odds ratio 0.4 per m2 of BSA, 95% confidence interval 0.15–0.9) in the multivariate analysis indicating its better predictive power than BMI [6].In this line, in an article published in the Cardiology journal, Kobayashi et al. [7] retrospectively studied outcomes in 1,829 patients with ACS, most of which were STEMI, based on BSA and optical coherence tomography (OCT) findings. The patients were separated into groups of small-BSA (<1.65 m2), medium-BSA (1.65–1.80 m2) and large-BSA (>1.8 m2). During the 2-year follow up, the BSA groups exhibited a linear relationship with outcomes. The small-BSA group compared with medium-BSA and large-BSA groups had significantly higher incidences of CV death (11.2% vs. 3.3% vs. 5.7%, p < 0.001) and rehospitalization for heart failure (6.1% vs. 3.8% vs. 2.8%, p = 0.033%). In addition, the small-BSA group was associated with a higher frequency of in-hospital left ventricular rupture (p < 0.001), presence of calcified plaques (p = 0.008), and smaller distal and proximal reference lumen areas (p = 0.003 and p < 0.001 respectively). The authors suggest that patients with small-BSA had smaller vessels with more advanced atherosclerosis that correlated with worse 2-year outcomes [7]. Since the study was conducted exclusively in East Asian population, its relevance in other ethnic groups need to be explored.What is the take home message from this latest observation? Is the BSA superior to BMI as a prognostic marker in ACS patients for secondary care? Recently, a large-scale study showed that indexing measures of cardiac and aortic size by BSA was associated with improved prognostic performance regardless of BMI [8]. In addition, a direct correlation between coronary artery diameter and BSA has been shown in patients with and without established coronary artery disease [9]. In a cardiac magnetic resonance imaging study of STEMI patients by Lechner et al. [10], culprit lesion vessel size was significantly associated with BSA in both univariate (p < 0.001) and multivariate analysis (p = 0.01). The current study results support the earlier observations of correlation between BSA and coronary artery diameter, cardiac size and blood volume and their relation to post-PCI outcomes [7]. Unlike BMI, BSA is associated with continuous inverse correlation with post-PCI outcomes that may be attributable to smaller vessels and a higher frequency of calcified plaque. These observations are relevant to South Asian patients who exhibit smaller vessels, and higher calcium scores and reportedly worse CVD outcomes compared to other ethnic groups [11].Since the proportion of the worldwide aged population is increasing significantly, understanding the relation between body weight/obesity is critical for the precise secondary prevention strategy in very high-risk patients like those presenting with STEMI. BSA may provide a better assessment of prognosis than BMI [2]. However, more research is needed to strongly establish the relationship between BMI and BSA while assessing its prognostic value for post-PCI risk; supporting evidence from investigations of pathophysiology (i.e., coronary flow reserve, microvascular function assessment) are needed to bolster the mechanistic link between BSA and worse outcomes. The classic Du Bois formula for BSA (0.007184 × height0.725 × weight0.425) was developed in 1916 and has been considered the gold standard. However, this formula derived BSA has been shown to overestimate by more than 15% as compared with the direct BSA measurements, particularly in obese patients [12]. Finally, a measurement of the fat surrounding the blood vessel wall may provide and assessment of risk by serving as a surrogate indicator of vessel wall inflammation. The latter can be determined by computed tomography [13]. Inclusion of easily available methods, such as an assessment of BSA, may enhance our assessment of future CVD risk in the highest risk population.Dr. Paul A. Gurbel has received consulting fees and/or honoraria from Baron and Budd, Bayer Healthcare, Cleveland Clinic foundation, Medtronic, Vectura/Otitopic, Wolters Kluwer Pharma; institutional research grants from Accriva Diagnostics, Bayer Healthcare, Covance, Cronos, Haemonetics, Hikari Dx, Idorisa, Instrumentation laboratories, Janssen Pharmaceuticals, Medtronic, Novartis, Precision Biology Prolocor, Recor Medical, Vectura Limited in addition, has two patents, detection of restenosis risk in patients issued and Assessment of cardiac health and thrombotic risk in a patient, and was an expert witness in a lawsuit associated with Plavix. Other authors report no conflict of interest.This study was not funded.Paul A. Gurbel: substantial contributions to the conception or design of the work, interpretation of data for the work. Sahib Singh: drafting and reviewing. Udaya S. Tantry: drafting, reviewing, conception or design of the work, and interpretation of data for the work.