Epicardial adipose tissue morphology diversity in Māori, Pacific and New Zealand/European post mortem cases

Abstract

Obesity is a global epidemic, and is the leading risk factor for heart disease and associated morbidities in New Zealand. Furthermore, Māori and Pacific New Zealand populations are up to 8 times more likely to develop both conditions. Obesity is characterised by an increase in fat (adipose tissue) throughout the body, both viscerally (surrounding organs) and subcutaneously (beneath the skin). Epicardial Adipose tissue (EAT) is a form of visceral fat located within the heart’s pericardial cavity, meaning EAT and the myocardium, maintain a unique, intimate relationship. This relationship has highlighted EAT as a possible tool in diagnosing cardiovascular disease. Recent studies found that obesity-induced morphological changes to EAT are dissimilar to those seen in other subcutaneous or visceral adipose tissues. In obesity, while adipocyte size increased in subcutaneous, appendicular and pericardial adipose tissues, EAT adipocyte size remained unchanged. Additionally, the well-established increase in overall EAT thickness in relation to body mass index (BMI), was not observed in Māori nor Pacific New Zealanders. This finding may provide insight into the disproportionate cardiac health outcomes for Māori and Pacific peoples in New Zealand. My study aimed to investigate how obesity effects EAT morphology and cardiac localisation, and how these potential changes in EAT might coincide with cardiac remodelling (myocardial adipocyte infiltration and fibrosis) and cardiovascular disease prevalence in diverse ethnic populations in New Zealand. Additionally, my study aimed to uncover any novel correlations between EAT morphology/localisation, cardiac remodelling and anthropomorphic variables such as age and sex. I hypothesised that in post mortem cases, NZ/European, but not Māori nor Pacific would demonstrate a linear relationship between BMI and mean adipocyte size only in non-epicardial adipose tissues (subcutaneous, appendicular and pericardial). Additionally, I hypothesised that Māori and Pacific cases would present with a greater percentage of myocardial adipocyte infiltration and fibrosis than their NZ/European, age and BMI matched counterparts. Statistical analysis of adipocyte and left ventricular histology from 91 post mortem cases revealed that mean subcutaneous, appendicular and pericardial adipocyte size positively correlated with BMI in NZ/European and Māori populations, while not in Pacific populations. A significant correlation was identified between the percentage of myocardial adipocyte infiltration and mean EAT adipocyte size in Māori/Pacific but not in NZ/European populations. Interestingly the opposite was seen in relation to myocardial fibrosis where subcutaneous and visceral (appendicular, pericardial, epicardial) adipocyte size significantly correlated with myocardial fibrosis in NZ/European, but not Māori/Pacific populations. Lastly, NZ/European cases showed a significant correlation between heart weight and BMI, while Māori/Pacific cases did not. In conclusion, the observed differences in adipocyte morphology/localisation between Māori, Pacific and NZ/European cases, highlight possible physiological differences, which could associate with potential differences in risks factors and disease characteristics between populations. My findings question the efficacy of current methods for diagnosis and treatment of heart disease and obesity, in all New Zealanders. My research illuminates the unconscious bias present in New Zealand healthcare, and highlights the need for more Māori led initiatives in both research and clinical practice, to facilitate the provision of equitable healthcare for all.