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Air pollution (PM2.5) has been associated with cardiovascular disease (CVD) globally and with early atherosclerosis surrogate markers in modernized China. A sizeable number of Chinese have migrated overseas, with an increase in their vulnerability to CVD. To evaluate the impact of PM2.5 air pollution on atherogenesis in native vs. overseas Chinese, we recruited 756 asymptomatic native Chinese and 507 age- and gender-matched overseas Chinese from Sydney and San Francisco. Their cardiovascular profiles were evaluated. PM2.5 was derived from remote sensing technology; atherosclerosis surrogate markers, flow-mediated dilation (FMD) and carotid intima-media thickness (IMT) were measured by ultrasound. The native Chinese had a higher proportion of smokers as well as higher blood pressure, glucose, metabolic syndrome and PM2.5 exposure (p < 0.001), but lower lipids and folate than the overseas Chinese (p < 0.0001). Carotid IMT was lower in the native Chinese (p < 0.0001), but the other vascular parameters were similar. A multivariate regression revealed that FMD in the native Chinese was related to the male gender, age and location; in the overseas Chinese, it was related to age, but not to PM2.5. Carotid IMT in the native Chinese was related to PM2.5, independent of atherosclerotic risk factors and location (R2 = 0.384, F = 34.5, p < 0.0001) whereas in the overseas Chinese, IMT was related to the male gender and age, but not to PM2.5 or overseas location (R2 = 0.282, F = 19.7, p < 0.0001). PM2.5 had a greater impact on atherogenesis in the native Chinese, independent of traditional risk factors, with implications for preventive strategies.

In Chinese populations, hypertension is common and is a major risk factor for cerebrovascular and coronary heart disease. The renin-angiotensin-aldosterone system (RAAS) helps maintain blood pressure and salt homeostasis and appears important in the pathogenesis of hypertension and some forms of vascular disease. We investigated three RAAS gene polymorphisms, the angiotensin-converting enzyme (ACE) insertion/deletion, angiotensinogen (AGT) M235T and angiotensin II type 1 receptor A1166C polymorphisms in 232 hypertensive and 178 normotensive Chinese subjects. The hypertensives were generally more obese and dyslipidaemic. No significant differences in genotype or allele frequencies for any of the polymorphisms were identified between the groups, nor was there any interactive contribution to blood pressure by the ACE and AGT polymorphisms. However, there were large differences in genotype and allele frequencies between the healthy Chinese and published data for equivalent Caucasian populations. These findings suggest these polymorphisms are unlikely to be involved in the pathogenesis of hypertension in Chinese.

Atherosclerosis is an important medical problem of the 21st century, but traditional risk factors could only account for 50% of the problem. Hyperhomocysteinemia is emerging as an independent atherosclerosis risk factor, associated with folate deficiency, renal failure, and relative deficiency of MTHFR (C677T polymorphism) or other enzymes depending on gender, age, and smoking status. Hyperhomocysteinemia has been reported to occur in 11-22% of western people, in 3-5% of normal asymptomatic Chinese subjects aged 18-70 years in Hong Kong, Macau, Sydney, and San Francisco, 23-36% of Chinese in Hong Kong with premature coronary artery disease, and 29% of a nonselective series of coronary subjects in Hong Kong. Evidence is accumulating that documents its associations with atherosclerosis disease in both case-control observations and prospective cohort studies, in vitro experiments, and in vivo experimental models in both animals and human subjects, as well as the successful improvement by homocysteine-lowering of endothelial function as surrogate atherosclerosis endpoints in asymptomatic human and coronary patients (secondary prevention). A number of large scale homocysteine-lowering trials are currently underway for stroke and heart attacks prevention. Collectively these trials will include more than 65,000 patients at high-risk for cardiovascular and stroke events, and should provide a reliable evidence-base for prevention.

Despite current interest in the biology and diagnostic application of plasma cell-free DNA (1), there is little knowledge regarding the cellular origin of this DNA. Recently, we have used a sex-mismatched bone marrow transplantation model to study the relative contributions of hematopoietic and nonhematopoietic cells to circulating DNA (2). We have demonstrated that the predominant proportion of plasma DNA originates from the hematopoietic system (2). However, the proportions of cell-free plasma DNA originating from other organs (e.g., heart, liver, and kidneys) remain unknown. We therefore investigated the contribution of the heart, liver, and kidneys to circulating DNA with use of sex-mismatched heart, liver, and renal transplantation models, respectively. Sex-mismatched heart, liver, and renal transplantation patients were recruited for the study. Twenty-one patients who had received heart transplants were recruited from the Grantham Hospital, Hong Kong. Fourteen of these heart transplantation patients were females with male donors, whereas the remaining 7 were males with female donors. Four sex-mismatched liver transplantation patients at the Pediatric Surgical Unit of the Department of Surgery, Prince of Wales Hospital were recruited; two of these patients were females with male donors and the other two were males with female donors. Six sexmismatched renal transplantation patients were recruited from the Department of Medicine and Therapeutics of …

The echocardiographic features of a coronary artery fistula that drains into the left ventricle were described in two patients. The clinical picture mimicked moderate to severe aortic insufficiency; however, M-mode echocardiogram revealed unusual features. Diastolic fluttering of the anterior mitral leaflet and the septum was absent in the first patient, while the second patient had marked diastolic fluttering of the posterior mitral leaflet and the left ventricular wall at the atrioventricular junction. In both, the coronary artery fistula could be visualized by cross-sectional echocardiography. Contrast echocardiography performed during cardiac catheterization in the second patient demonstrated that the diastolic fluttering of the posterior mitral leaflet was related to the jetting of blood from the coronary artery fistula.