This review focuses on lipoprotein abnormalities in South Asians (SA) and addresses risk stratification and management strategies to lower atherosclerotic cardiovascular disease (ASCVD) in this high-risk population. South Asians (SAs) are the fastest growing ethnic group in the United States (U.S) and have an increased risk of premature coronary artery disease (CAD). While the etiology may be multifactorial, lipoprotein abnormalities play a key role. SAs have lower low-density lipoprotein cholesterol (LDL-C) compared with Whites and at any given LDL-C level, SA ethnicity poses a higher risk of myocardial infarction (MI) and coronary artery disease (CAD) compared with other non-Asian groups. SAs have lower high-density lipoprotein cholesterol (HDL-C) with smaller particle sizes of HDL-C compared with Whites. SAs also have higher triglycerides than Whites which is strongly related to the high prevalence of metabolic syndrome in SAs. Lipoprotein a (Lp(a)) levels are also higher in SAs compared with many other ethnic groups. This unique lipoprotein profile plays a vital role in the elevated ASCVD risk in SAs. Studies evaluating dietary patterns of SAs in the U.S show high consumption of carbohydrates and saturated fats. SAs have a high-risk lipoprotein profile compared with other ethnicities. Lipid abnormalities play a central role in the pathogenesis of CAD in SAs. More studies are needed to understand the true impact of the various lipoproteins and their contribution to increasing ASCVD in SAs. Aggressive lowering of LDL-C in high-risk groups using medications, such as statins, and lifestyle modification including dietary changes is essential in overall CAD risk reduction.

Severe maternal morbidity (SMM) refers to any unexpected outcome directly related to pregnancy and childbirth that results in both short-term delivery complications and long-term consequences to a womens health. This affects about 60,000 women annually in the United States. Cardiovascular contributions to SMM including cardiac arrest, arrhythmia, and acute myocardial infarction are on the rise, probably driven by changing demographics of the pregnant population including more women of extreme maternal age and an increased prevalence of cardiometabolic and structural heart disease. The utilization of SMM prediction tools and risk scores specific to cardiovascular disease in pregnancy has helped with risk stratification. Furthermore, health system data monitoring and reporting to identify and assess etiologies of cardiovascular complications has led to improvement in outcomes and greater standardization of care for mothers with cardiovascular disease. Improving cardiovascular disease-related SMM relies on a multipronged approach comprised of patient-level identification of risk factors, individualized review of SMM cases, and validation of risk stratification tools and system-wide improvements in quality of care. In this article, we review the epidemiology and cardiac causes of SMM, we provide a framework of risk prediction clinical tools, and we highlight need for organization of care to improve outcomes.

Background and aims

South Asians are at increased risk for cardiovascular disease (CVD). Aortic valve calcium (AVC) is associated with CVD risk and aortic stenosis. Elevated Lp(a) is a heritable risk factor for CVD and AVC. AVC prevalence and its association with Lp(a) have not been studied in South Asians.

Methods

Among participants in the Mediators of Atherosclerosis in South Asians Living in America (MASALA) study (n = 695), AVC prevalence and extent were compared to four race/ethnic groups in the Multi-Ethnic Study of Atherosclerosis (MESA) (n = 4671). Multivariable regression was performed to evaluate associations between Lp(a) and AVC stratified by race/ethnic groups, adjusting for cardiovascular risk factors.

Results

After age and sex adjustment, South Asians had higher median Lp(a) (17.0 mg/dL) compared to Whites (12.9 mg/dL), Hispanics (13.1 mg/dL) and Chinese Americans (12.9 mg/dL), and Blacks had highest Lp(a) levels (35.1 mg/dL). There were no differences in the odds of AVC in South Asians compared with Whites or Hispanics, after age and sex adjustment (p = 0.64 and 0.63, respectively). Odds of AVC was lower in Chinese (OR 0.35; 95%CI 0.23-0.54) and somewhat lower in Blacks compared with South Asians (OR 0.76; 0.56-1.04). There were no associations between Lp(a) and AVC presence or extent in South Asians. Lp(a) was associated with AVC only among Blacks and Whites.

Conclusions

Although present in Whites and Blacks, there were no associations between Lp(a) and AVC in South Asians. These differences may be due to statistic power or race specific modifying factors that influences the effect of Lp(a) particles on AVC pathogenesis.