PNI role in the history
Nutrition assessment results have previously been proven to define the incidence of post-operative complications, mortality, and morbidity in patients with heart failure or malignant cancers(8-13). While many nutritionists suggest using the Controlling Nutritional Status (CONUT) score to assess the nutrition status of acute heart failure, a large retrospective cohort study demonstrated that PNI has the same prognostic impact in patients with decompensated heart failure(14, 15). PNI was an independent predictor for evaluating the correlation between nutritional status and malignancy or vital organ failure mortality by comparing subjects of the high-PNI and low-PNI groups(12, 16, 17). In addition to being used with adult diseases, PNI can also predict the clinical outcome of the pediatric population in the intensive care unit after cardiac operation(18). However, we found PNI could predict CAA risk in acute KD patients in addition to correlating with nutrition status.
Hypoalbuminemia in KD and CAL formation
KD is a form of chronic vasculitis that may last for months to years in regard to pathophysiology. Therefore, all KD patients with or without coronary ectasia are considered at high risk for accelerated atherosclerosis according to the epidemiological evidence and should undergo nutrition counseling and diet education in an effort to reduce their future cardiovascular burden(19). Research has identified that younger than 6 months of age, male, incomplete KD, longer fever duration, higher CRP levels (>100 mg/l), and lower albumin levels (<35 g/L) were all independent risk factors for CAA formation(20), thus indicating that both delayed initiation of KD target therapy and hypoalbuminemia, which indicates a relatively poor nutritional status, result in higher incidence rates of CAA complications in patients with acute KD, despite the administration of IVIG therapy.
PNI predicts KD with CAA & IVIG non-responder
In the current study, we showed that PNI, an albumin based long-term predictor of cancer, was also a significant independent predictor of CAA in any coronary segment during the 6 months after the onset of illness (PNI<55, estimator: 1.999, p=0.030), as well as gender, IVIG non-responder, and platelet count. However, the associations of pre-treatment platelet count and CAA formation were relatively weak in this cohort, with a 95% confidence interval of estimator between 1.002-1.007. To the best of our knowledge, this study is the first to discuss the predictive value of PNI on CAA formation in KD patients before they receive initial IVIG therapy. Kobayashi et al. constructed a seven-variable predictive model to identify IVIG-resistant KD using pretreatment laboratory data. Although previous research has shown that most KD patients with CAA are unresponsive to IVIG, the detailed mechanism between IVIG non-responders and CAA formation has yet to be explained. Our results are in line with Kuo et al.’s previously published studies demonstrating the significant relationship between hypoalbuminemia and IVIG-resistant KD, which often indicates a higher incidence of CAA(6). Of particular interest is the discrepancy conclusion from Japan(21) (Kobayashi et al., 2006) to Taiwan (Kuo et al., 2010) regarding the correlation between IVIG non-responder and hypoalbuminemia using multivariate logistic regression models(6, 21). Assuming that both research methods were appropriately and strictly designed, we may presume that an unknown ongoing process involved nutrition status, in addition to vascular inflammation. However, early validation research on Japan scoring models yield inconsistent result between different races(2, 22-24). It showed multiple ethnicity-exclusive models are required. Our findings revealed that a low pre-treatment PNI level (PNI<55) correlated to a high incidence of CAA complication in KD patients, as well as IVIG non-responder.
PNI practice
Low-PNI alone before initial IVIG therapy have nearly 2-fold (estimator: 1.999, Table4) risk to develop future CAA. In the setting of low-PNI, IVIG non-responder, male gender, and higher platelet count will give rise to at least 8.8-fold higher risk to develop CAA. Therefore, PNI in conjunction with IVIG response, gender, and platelet will have better prediction of developing CAA within 6 months of illness.