Obesity-induced vena cava compression syndrome: a case report of a rare precipitant of a type 2 myocardial infarction in a patient with critical aortic stenosis.

Background: Obesity is a global health problem of increasing prevalence with a broad range of multisystem complications. An under-recognized complication of severe obesity is the potential haemodynamic compromise that may arise due to pathological external compression of the inferior vena cava whilst lying in the supine position, a phenomenon known as obesity-induced vena cava compression syndrome. Case summary: A 56-year-old independent woman presented to a rural Australian hospital for routine dressing care for bilateral lymphoedema on a background of class III morbid obesity (weight 197 kg, body mass index 68.55 kg/m3) and aortic stenosis. Whilst laid in the supine position with both legs elevated to aid lower limb venous return, the patient developed angina with associated troponin rise (15 to 75 to 332 ng/L) and inferolateral territory ischaemic changes on electrocardiogram. The pain then resolved shortly after restoring the patient to the upright position. A transthoracic echocardiogram showed critical bicuspid aortic stenosis. Computerized tomography coronary angiogram showed no significant coronary artery disease. Following multidisciplinary discussions, a transcatheter aortic valve insertion was performed via a transfemoral approach. Post-procedure, she went into atrial fibrillation, she was cardioverted into a sinus rhythm with new left bundle branch block. There were no complications otherwise, and the patient was discharged home following a brief period of convalescence. Discussion: We describe a case of suspected obesity-induced vena cava compression syndrome precipitating a type 2 myocardial infarction in a pre-load dependent patient with critical bicuspid valve aortic stenosis. This case highlights a potential haemodynamic consequence of morbid obesity in the supine position.

Epidemiological transition: a historical analysis of immigration patterns by country of origin (1861-1986) related to circulatory system diseases and all-cause mortality in twentieth-century Australia.

BACKGROUND AND OBJECTIVES: Circulatory system disease (CSD) patterns vary over time and between countries, related to lifestyle risk factors, associated in turn with socioeconomic circumstances. Current global CSD epidemics in developing economies are similar in scale to those observed previously in the USA and Australasia. Australia exhibits an important macroeconomic phenomenon as a rapidly transitioning economy with high immigration throughout the nineteenth and twentieth centuries. We wished to examine how that historical immigration related to CSD patterns subsequently. METHODS AND SETTING: We provide a novel empirical analysis employing census-derived place of birth by age bracket and sex from 1891 to 1986, in order to map patterns of immigration against CSD mortality rates from 1907 onwards. Age-specific generalised additive models for both CSD mortality in the general population, and all-cause mortality for the foreign-born (FB) only, from 1910 to 1980 were also devised for both males and females. RESULTS: The percentage of FB fell from 32% in 1891 to 9.8% in 1947. Rates of CSD rose consistently, particularly from the 1940s onwards, peaked in the 1960s, then declined sharply in the 1980s and showed a strong period effect across age groups and genders. The main effects of age and census year and their interaction were highly statistically significant for CSD mortality for males (p<0.001, each term) and for females (p<0.001, each term). The main effect of age and year were statistically significant for all-cause mortality minus net migration rates for the FB females (each p<0.001), and for FB males, age (p<0.001) was significant. CONCLUSIONS: We argue our empirical calculations, supported by historical and socioepidemiological evidence, employing immigration patterns as a proxy for epidemiological transition, affirm the life course hypothesis that both early life circumstances and later life lifestyle drive CSD patterns.