With urbanization, rapid economic development, and an ageing population, cardiovascular diseases (CVDs) have become the leading causes of morbidity and mortality in China, and the burden of these diseases is increasing at an alarming rate [1]. Consequently, a public health policy of primordial prevention has been advocated. CVDs are long-term chronic diseases that develop over decades from risk factors to subclinical impairment and then progress to clinical events [2]. Subclinical impairment, which is the presymptomatic stage of CVDs, is a fundamental precursor that can help identify early subjects who are at high risk for future CVDs and who can benefit the most from early interventions. This approach is also part of primary prevention. Some non-invasive established biomarkers and markers can detect and measure the subclinical stages of CVDs, such as C-reactive protein (CRP), carotid intima-media thickness (CIMT), carotid plaque, left ventricular (LV) hypertrophy, and LV systolic dysfunction.

In 2010, the American Heart Association (AHA) defined a simplified 7-item tool to promote ideal cardiovascular health (CVH), including both modifiable behaviours and objective measures, such as the following CVH metrics: physical activity, diet, body mass index (BMI), smoking, blood pressure, serum glucose and total serum cholesterol [3]. This approach emphasizes primordial prevention in which efforts are focused on preventing the development of risk factors, which is in contrast to primary or secondary prevention in which the focus is on the prevention of the first occurrence or recurrence of CVDs. Achieving a greater number of ideal CVH metrics has been reported to be associated with a lower risk of CVD incidence and mortality [4‐7].

Few studies have investigated the joint effects of the 7 CVH metrics on the subclinical impairments of CVDs [8‐10]. Most of these studies have investigated a single subclinical marker or a few makers (mainly aortic arch plaque, coronary artery calcification or common CIMT), and the studies have been relatively limited to US and European populations [8, 11]. Accordingly, the aim of the present study was to simultaneously investigate both the biomarkers and markers of subclinical impairments of CVDs with ideal CVH metrics in a community-based cohort in a Chinese population.

In this study, we investigated the relationships between subclinical biomarkers and subclinical disease markers of CVDs with ideal CVH metrics in a general urban population from central south China. We found that the CVH score was inversely related to both the biomarker levels (homocysteine, CRP, and microalbuminuria) and the presence of subclinical disease markers (increased CIMT, carotid plaques, LV hypertrophy, LV systolic dysfunction, and peripheral arterial disease). A similar negative correlation was observed in the female and male subgroups, and consistent trends were observed with the 14-point CVH score. To the best of our knowledge, this study is the first to correlate the relatively comprehensive subclinical profile of CVDs with ideal CVH in Chinese adults.

The biomarkers used in the study represent different biological pathways of atherosclerosis. CRP is the most clinically accepted inflammatory biomarker used to predict future cardiovascular events in asymptomatic individuals [21]. Hyperhomocysteinaemia has multiple potentially toxic effects on atherogenesis, including damaging endothelial cells, reducing the flexibility of vessels, and adversely affecting the process of homeostasis [22, 23]. Microalbuminuria is predictive of worsening microvascular disease in the kidney, reflects a generalized abnormality of vascular function, and is associated with a strong risk of increasing CVDs [24]. Notably, the items in the CVH metrics are risk factors associated with the biomarkers. BMI, smoking, and diabetes are associated with CRP [25]. Smoking, lack of exercise, and hypertension are related to hyperhomocysteinaemia [26]. Diabetes, hypertension, smoking, blood lipids, BMI, and dietary protein are correlated with microalbuminuria [27]. The observed associations of the selected biomarkers with the CVH scores suggest that a range of biological pathways can mediate the favourable effects of the CVH score on subclinical atherosclerosis or disease.

The subclinical stage serves as an intermediate endpoint for the risk evaluation and optimal treatment. We used previously validated markers of subclinical disease. An increased CIMT, carotid plaques and reduced ABI were indicators for macrovascular disease (coronary heart disease, myocardial infarction, PAD and stroke), whereas LV hypertrophy and LV systolic dysfunction were indicators of target organ damage. Among the composite of the subclinical disease markers, the majority of the participants (55.5%) had no subclinical disease markers, only 12.7% had at least 2 components, and 1.9% had ≥3 components, which was consistent with a previous study [9]. There may be several reasons for this status. First, the median age in our cohort was relatively young (48.6 years) with regard to CVD risk. Second, the prevalence of hypertension and diabetes was low, implying a lower CVD risk. Third, many CVH metrics (e.g., mean lipid, fasting glucose, and BP values) were inside the normal ranges, suggesting that the subjects were either healthy or well treated.

Our study found that subclinical impairments were independently associated with low CVH scores. Low CVH scores may primarily contribute to chronic subclinical damage, leading to CVDs via subclinical impairments. Previous studies have largely focused on the association of subclinical stages with each individual behaviour or health factor [28]. However, many of these factors coexist or occur in aggregation and thus may be interwoven into multiple biologically related pathways. The association in the present study reflected the combined and cumulative effects of exposure to risk factors on subclinical lesions and thus provided more accurate information compared to exploring each factor individually.

Previous studies also uncovered associations between CVH and subclinical impairments. In the Paris Prospective Study III, more ideal CVH metrics were positively associated with a lower presence of subclinical disease markers of carotid structure and function (common CIMT, carotid plaques, lower Young’s elastic modulus, and carotid dispensability coefficient) among community subjects aged 50 to 75 years [10]. In the Young Finns Study, Laitinen et al. reported that a greater number of average lifetime CVH metrics and favourable changes in the CVH status in childhood or young adulthood were associated with a reduced risk of coronary artery calcification, carotid dispensability, and increased CIMT in middle age [8]. In the Framingham study, higher ideal CVH scores were inversely related to a composite measure of subclinical CVDs (including higher carotid artery IMT or stenosis, LV systolic dysfunction, LV hypertrophy, microalbuminuria, or reduced ABI) [9]. The Special Turku Coronary Risk Factor Intervention Project for Children [STRIP] study reported that healthy CVH scores were directly associated with a lower aortic intima-media thickness and greater elasticity in adolescents [29]. Another study indicated that improvements in ideal cardiovascular health through midlife to late life were associated with a lower CVD prevalence and better cardiac structure and vascular functions, including carotid-femoral and brachial-ankle PWV (baPWV), in the elderly [30]. Similar results were obtained by Yan et al. in a Chinese population after assessing the association between the CVH score and baPWV [31]. Our study findings have confirmed and extended these results in Asian populations.

A global ideal CVH was rare (0.2%) in our study, which was consistent with other studies with more representative samples (values of approximately 0.1 to 0.2% were reported in American and Chinese urban populations) [32‐34]. Females had better CVH profiles and a lower prevalence of most subclinical disease markers than males, and the relationship between the CVH score and markers tended to be stronger among females than that among males, which was also in line with prior reports [35]. The exact mechanism underlying this observed gender difference warrants further investigation. Generally, females may be less exposed to cardiovascular risk factors, such as smoking, alcohol use and overweight, and they may receive more protective effects from endogenous oestrogens prior to reaching the premenopausal age [36, 37]. Considering the above findings, we should attach great concerns to the primary care of CVDs, especially for males. In our study, women were more likely to be classified with a reduced ABI, which was consistent with previous epidemiological evidence showing that women had lower ABI values than men [38, 39]. Gender differences in the ABI value may occur because men on average are taller than women, and men have a greater tendency to experience medial arterial calcinosis, which may avoid an ABI decline [40]. Although the gender differences in PAD must be explored, the intrinsic differences in the ABI criterion and measurements may confound the results [41].

The major strengths of this study include the large population-based sample, the use of a wide range of biomarkers and markers of subclinical data, and the performance of sensitivity analyses. However, some limitations to the present study should also be acknowledged. First, the cross-sectional design of our study only allowed the documentation of one-time sampling data that did not take the time-associated changes in the CVH scores into consideration, which might have improved the accuracy of our findings. Similarly, we did not explore the association between the CVH score and CVD incidence through prospective analyses. Second, some potential biomarkers, such as aldosterone, B-type natriuretic peptide (BNP), and growth differentiation factor-15 (GDF-15), and markers such as coronary artery calcium and lipoprotein-associated phospholipase A2 (Lp–PLA2) were not involved in these observed associations. Third, socioeconomic factors, such as family incomes, paying for medical expenses, frequency of health care visits, and the duration of treatment (antihypertensive, lipid-lowering diabetes and medication), might contribute to the relationship between CVH metrics and subclinical impairments, but we did not have this information. Finally, we used modified definitions of physical activity and diet that varied from the exact AHA definition to compute the scores for the CVH metrics.

In summary, the prevalence of ideal CVH was low in the adult population in central south China. The CVH score was associated with a favourable profile of subclinical biomarkers or markers of CVDs, thereby supporting the use of the CVH score as a reasonable and useful tool for assessing and preventing subclinical impairments, thus reducing the burden of CVDs. These findings may deepen our understanding of the biological mechanisms and processes underlying CVH and CVDs.