Background: The dependence of the acquisition of the coronary artery calcification score (CACS) on computed tomography (CT) has drawbacks, including the ethical concerns of radiation exposure in the care of patients with non-cardiovascular diseases, where CACS has been shown to correlate with its prognosis. Significant heterogeneities exist between patients with and without coronary artery calcification (CAC). Mathematical formulae using medical history and common, non-invasive test results enable cheap, ready assessment of CAC and subsequent research into how it can be used for clinical decision making.Methods: 694 patient records of visits to Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College from 2009 to 2023 were partitioned into a training (visited before 2023) and an independent validation set (visited in 2023). With age, gender, current smoking, diabetes, low-density lipoprotein cholesterol (LDL-C), reduced renal function, usage of statins and aspirin as candidate predictors, five logistic regression models were built under two paradigms. Bootstrap resampling was employed for internal validation, followed by external validation and calibration on the validation set. Models built under each paradigm were compared, followed by head-to-head comparison of the "best" models built under each paradigm with a comprehensive criteria involving both model performance and predictor parsimony.Results: 694 records were used for modeling, with 536 and 158 records in the training and validation set respectively. Model 1 (c statistic upon external validation: 0.77) outperformed other models built under Paradigm 1 while Models 4 (c statistic upon external validation: 0.79) and 5 (c statistic upon external validation: 0.79) built under Paradigm 2 outperformed Model 1. Model 5 was more parsimonious in predictors. All models were well calibrated.Conclusion: With gender, current smoking, LDL-C, age, diabetes and reduced renal function as predictors, Model 5 outperformed other models and was hence recommended for further use. By assessing the presence of CAC with medical history and blood test results instead of CT, our model offers an approach to immediate, radiation-free assessment of CAC, which may further unleash the clinical utility of CAC in clinical practice that may have remained unraveled.

Reliable prognostic markers are essential for optimizing risk stratification and clinical management in patients with cardiovascular disease (CVD). The advanced lung cancer inflammation index (ALI), an integrated measure of systemic inflammatory and nutritional status, has shown promise as a predictor of cardiovascular outcomes. This study aimed to examine the association of ALI with the risk of all-cause and cardiovascular mortality in patients with CVD. In this prospective cohort study, we utilized data from the National Health and Nutrition Examination Survey (NHANES) between 1999 and 2018, linked to mortality records from the National Death Index (NDI). A total of 4,247 adult CVD patients were included. The association of ALI with mortality risk was evaluated using Kaplan–Meier survival analysis with log-rank tests and Cox proportional hazards regression models. To examine the nonlinear association, restricted cubic spline (RCS) analysis was performed. Additionally, Time-dependent receiver operating characteristic (ROC) curve analysis was conducted to evaluate the predictive performance of ALI for survival outcomes. During a median follow-up period of 84 months, 1,795 deaths were recorded, including 741 were cardiovascular-related. Kaplan–Meier survival analysis demonstrated significantly improved survival for participants in the highest ALI tertile compared to those in lower tertiles, for both all-cause and cardiovascular mortality. Weighted Cox proportional hazards models revealed that patients with high ALIs had significantly lower risks of all-cause and cardiovascular mortality than did those with low ALIs. RCS analysis further supported a nonlinear, inverse dose-response relationship between ALI and all-cause and cardiovascular mortality. The ROC demonstrated moderate discriminative performance for short- and long-term mortality risk, with AUCs of 0.727, 0.728 at 1 year and 0.638, 0.639 at 10 years, for all-cause and cardiovascular mortality, respectively. ALI is independently associated with mortality in patients with CVD, and low ALI levels are significantly correlated with an elevated risk of mortality. Therapeutic interventions focused on mitigating inflammation and optimizing nutritional status may have important clinical implications for reducing mortality risk in this patient population, given the observed association between ALI and mortality outcomes.

Frailty is a well-established determinant of adverse outcomes in patients with aortic disease, but its role in incident aortic aneurysm (AA) and aortic dissection (AD) remains unclear. We examined the associations of frailty with long-term risks of AA and AD in a large community-based cohort. We included 474,302 UK Biobank participants free of AA/AD at baseline. Frailty was assessed using physical frailty and the frailty index, categorized as non-frail, prefrail, or frail. The primary outcomes were AA, with secondary outcomes, including abdominal AA (AAA), thoracic AA (TAA) and AD, ascertained through linkage to hospital and death records. During a median follow-up of 15.1 years, 3,675 AA, 2,289 AAA, 1,114 TAA, and 310 AD events occurred. After multivariable adjustment, both prefrailty (physical frailty: HR 1.24, 95

Background: While the association between estimated glomerular filtration rate (eGFR) and cardiovascular disease has been well established in younger populations, the prognostic significance of this marker in older individuals remains less well defined. Thus, this study aimed to evaluate the predictive value of eGFR in patients aged 80 years or older with acute coronary syndrome (ACS). Methods: We enrolled 551 patients aged ≥80 years hospitalized for ACS, who had the eGFR calculated at admission. The participants were further stratified into three groups by eGFR levels: Low-eGFR group (L-eGFR, eGFR < the 20th percentile), Medium-eGFR group (M-eGFR, the 20th percentile ≤ eGFR < the 80th percentile), and High-eGFR group (H-eGFR, eGFR ≥ the 80th percentile). Major adverse cardiovascular events (MACEs) were recorded during the follow-up period. Results: During a median 63-month follow-up, the L-eGFR group exhibited a higher cumulative incidence of MACEs, while the H-eGFR group showed a relatively improved prognosis compared with the M-eGFR group. A multivariate Cox regression analysis revealed that reduced eGFR levels remained independently predictive for long-term MACEs. Compared with the M-eGFR group, the L-eGFR group showed a higher risk (hazard ratio (HR) 1.542, 95% confidence interval (CI): 1.104–2.155). The H-eGFR group exhibited a protective effect (HR 0.643, 95% CI: 0.438–0.943). Conclusions: Reduced eGFR levels were independent predictors for long-term MACEs in older ACS patients. The H-eGFR group had an improved prognosis, suggesting that further exploration of the underlying mechanism linking renal function and prognosis is warranted.

Background: Research results on the association between alcohol consumption and abdominal aortic calcification (AAC) has yielded inconsistent results. There is a paucity of evidence on the association of smoking and alcohol consumption with AAC in the general middle-aged and elderly population, including age subgroups. This study utilizes nationwide survey data to explore these associations. Methods: Data from middle-aged and elderly National Health and Nutrition Examination Survey (NHANES) 2013–2014 participants receiving dual X-ray absorptiometry were analyzed. AAC severity was assessed using a scoring system with a maximum value of 24. Presence of AAC was defined as an AAC score >0, and severe AAC as an AAC score ≥6. Binary logistic regression was employed for analyzing the association of smoking and alcohol consumption-related indices with the presence of AAC, while cumulative odds logistic regression explored their associations with severe AAC. Results: Data of 3135 participants were analyzed. Investigation in the entire population found that smoking history was linked to both AAC and severe AAC. In contrast, alcohol consumption history was not linked to AAC or severe AAC. After adjusting for confounders, the findings confirmed a significant association of smoking history with AAC and severe AAC. No significant associations were found for current alcohol consumption with either AAC or severe AAC. Compared with never smokers, former smokers and current smokers experienced increased AAC risk. Former smokers had a significantly lower AAC risk compared to current smokers. Compared with never alcohol consumers, neither former nor current alcohol consumers experienced a different AAC risk. No difference in AAC risk was found between former and current alcohol consumers. Individuals consuming more than 2 drinks of alcohol per day suffered from a significant increase in risk of AAC. Subgroup analyses found elderly ever and current smokers suffered from a significantly elevated AAC risk, as did middle-aged ever smokers. Elderly ever and current alcohol consumers also experienced increased risk of AAC. Conclusions: Smoking history is significantly associated with both AAC and severe AAC. The cardiovascular benefits associated with smoking cessation primarily manifest as reduction in risk of AAC presence rather than severe AAC. Elderly smokers are exposed to a greater risk of AAC. In contrast, alcohol consumption shows no association with severe AAC. Alcohol consumption is not associated with AAC except in heavy drinking and elderly subpopulations.

Abdominal aortic calcification (AAC) is closely related to cardiovascular disease. Although its clinical significances have primarily been investigated in patients with chronic kidney disease, its association with cardio-cerebrovascular mortality in the general middle-aged and elderly population has not been sufficiently investigated. To study the association of AAC and cardio-cerebrovascular mortality in both the entire general middle-aged and elderly populations and age subgroups. Data of participants of the National Health and Nutrition Examination Survey (NHANES) 2013–2014 were analyzed. This study included middle-aged and elderly (≥ 40 years old) individuals who underwent dual-energy X-ray absorptiometry. The severity of AAC was assessed by an AAC scoring system (AAC score) with a maximum possible value of 24. Participants were tracked for survival status and major cause of death till 31st December 2019. This study utilized AAC score = 6 as the optimal cut-off according to Harrell’s c statistic. Based on AAC scores, participants were trichotomized (0, 0–6, and ≥ 6). Groupwise survival curves and cumulative incidence functions were plotted to reveal the association of AAC and cardio-cerebrovascular mortality. Given results under trichotomization, combination of participants with AAC scores 0 and 0–6 was conducted to reaffirm the association of AAC and adverse prognosis. Correlation between increased AAC score and poorer survival, higher cumulative incidence of events was revealed. Cox models identified AAC score ≥ 6 as an independent risk factor of cardio-cerebrovascular mortality (AAC score ≥ 6 vs. AAC score = 0: Hazard ratio: 2.38, P = 0.008) after adjusting for cardiovascular risk factors. Results remained significant after regrouping (AAC score ≥ 6 vs. AAC score < 6: Hazard ratio: 2.06, P = 0.016). Subgroup analysis provided no evidence of unparallel change in hazard for the same amount of increase in AAC score among middle-aged (40–65 years old) and elderly (≥ 65 years old) individuals. AAC score ≥ 6 independently indicate increased risk of cardio-cerebrovascular death and would be effective in risk stratification among the general middle-aged and elderly population in clinical practice.

BACKGROUND:There are currently no specialized risk scoring systems for critically ill patients with coronary heart disease (CHD). Arterial stiffness, as measured by estimated pulse wave velocity (ePWV), has emerged as a potential indicator of mortality or adverse cardiovascular events in individuals with CHD. This study aimed to evaluate the association between ePWV and all-cause mortality among critically ill patients with CHD beyond traditional risk scores. METHODS AND RESULTS:This study included 11 001 participants with CHD from the Medical Information Mart for Intensive Care IV, with a 1-year follow-up. The primary endpoint was 1-year all-cause mortality, and the secondary endpoint was in-hospital mortality. Elevated ePWV was significantly associated with higher risks of in-hospital [odds ratio 1.15, 95% confidence interval (CI) 1.12-1.17, P < 0.001] and 1-year (hazard ratio 1.21, 95% CI 1.20-1.23, P < 0.001) mortality. These associations remained consistent when adjusted for traditional risk scores and potential confounders. When ePWV was integrated into traditional risk scoring models (Oxford Acute Severity of Illness Score, Sequential Organ Failure Assessment score, Acute Physiology Score III, Systemic Inflammatory Response Syndrome score, Simplified Acute Physiology Score II, and Logistic Organ Dysfunction System score), the predictive accuracy (area under the curve: 64.55-70.56, 64.32-72.51, 72.35-75.80, 55.58-67.68, 71.27-73.53, and 67.24-73.40, P < 0.001) and reclassification (net reclassification index: 0.230, 0.268, 0.257, 0.255, 0.221, and 0.254; integrated discrimination improvement: 0.049, 0.072, 0.054, 0.068, 0.037, and 0.061, P < 0.001) of these models significantly improved for 1-year mortality. Similar results were also found for in-hospital mortality. CONCLUSIONS:Estimated pulse wave velocity is a strong independent predictor of both short- and long-term mortality in critically ill patients with CHD. Importantly, integrating ePWV into traditional risk scores significantly boosts the predictive accuracy for 1-year and in-hospital all-cause mortality.

Background: Statin therapy is associated with an increased risk of new-onset diabetes (NOD), possibly due to a reduction in coenzyme Q10 (CoQ10) levels as a result of statin use. This study aimed to investigate the relationship between exogenous CoQ10 supplementation and the development of NOD. Methods: This study included 4394 participants from the National Health and Nutrition Examination Survey (NHANES). Baseline characteristics were compared between those with and without NOD and between those with and without CoQ10. Univariate logistic regression was performed to identify factors associated with NOD. Two models were used for confounding factors, including demographics and various covariates. Multifactor logistic regression further assessed the association between CoQ10 supplementation and NOD. Additionally, restricted cubic spline (RCS) analysis was conducted to evaluate the potential nonlinear relationship between daily CoQ10 dose and NOD. Results: Univariate logistic regression showed an association between CoQ10 supplementation and a reduced risk of NOD (odds ratio [OR] = 0.323, 95% confidence interval [CI] 0.157–0.668, p = 0.003), which remained significant after adjustments in model 1 (OR = 0.344, 95% CI 0.160–0.737, p = 0.006) and model 2 (OR = 0.232, 95% CI 0.057–0.942, p = 0.041). There was no evidence of a linear association between daily CoQ10 dose and NOD in logistic regression analysis (OR = 0.999, 95% CI 0.994–1.004, p = 0.720), and no evidence of a nonlinear correlation in the RCS analysis (p > 0.05). Conclusions: CoQ10 supplementation in individuals taking statins was associated with a reduced risk of NOD, and this association was independent of the CoQ10 dose.

Background The prognostic value of the triglyceride-glucose (TyG) index across different renal function strata remains unclear. The study explores the association between the TyG index and major adverse cardiovascular events (MACE) in acute coronary syndrome (ACS) patients at different eGFR levels. Methods A total of 1038 patients with ACS were analyzed, and 241 composite events were recorded during the follow-up. Kaplan-Meier survival analysis and the Cox proportional hazard model were used to determine the relationship between TyG index and the incidence of MACE. Results Patients in the highest TyG index tertile (TyG ≥ 9.25) presented a higher median age, male predominance, and greater prevalence of STEMI and UA. The TyG index was an independent predictor of MACE, with a progressively higher MACE incidence observed across ascending TyG tertiles. The restricted cubic spline analysis showed a linear association between the TyG index and MACE risk in the unadjusted model and a J-shaped association after multivariate adjustment. Notably, this association was present in patients with impaired renal function (eGFR < 60 mL/min/1.73m 2 ), where the risk of MACE increased by 43% for every one standard deviation increase in TyG index (HR 1.43, 95% CI: 1.05–1.95, P = 0.025). However, this relationship was not observed in patients with preserved renal function. Conclusion Elevated TyG index is an independent risk factor for MACE, particularly in patients with renal impairment. These findings suggests that the TyG index is a valuable clinical marker for cardiovascular risk stratification, especially in patients with renal insufficiency.

Background: Aortic aneurysm (AA) is a fatal vascular disease that affects life expectancy. Theory predicts that biological processes of aging may better capture vascular aging than chronological age. Early-life tobacco exposure may induce lasting vascular injury and accelerate aging trajectories. However, the independent contributions of accelerated biological aging and early tobacco exposure to AA risk, as well as their potential synergistic interaction, remain fundamentally unknown. Methods: A total of 268,491 participants from the UK Biobank study were included. We measured biological age from clinical traits using the KDM-BA and PhenoAge algorithms. Early-life tobacco exposure was assessed using self-reported questionnaires that included questions on utero tobacco exposure and age of smoking initiation. Cox proportional hazards models were used to analyse the association between biological ageing, early-life tobacco exposure and incident aortic aneurysm. Furthermore, multiplicative and additive interactions between accelerated biological aging and early-life tobacco exposure were formally tested. Disease subtype-specific analyses were conducted separately for incident thoracic aortic aneurysm (TAA) and abdominal aortic aneurysm (AAA). Results: Accelerated biological aging and early-life tobacco exposure were both significantly associated with increased risk of incident AA. Per standard deviation increase, PhenoAge and KDM-BA accelerations were associated with 26-35% and 27-41% higher AA risk, respectively. Participants in the highest quartile of aging acceleration showed markedly higher cumulative incidence of AA (P-trend <0.001). In utero smoke exposure increased AA risk by 21%. Compared to never-smokers, smoking initiation in adulthood, adolescence, and childhood was associated with progressively elevated AA risk (HRs=2.23, 2.26, and 2.57, respectively). Individuals with both highest quartile of biological aging and early-life exposure had markedly elevated AA risk, peaking for childhood smoking combined with high KDM-BA [5.65 (4.52-7.07) or PhenoAge [4.46 (3.61-5.52)]. Effects were stronger for AAA than TAA. Conclusions: Exposure to tobacco smoke in early life markedly heightens the risk of AA when combined with accelerated biological aging. These findings underscore the need for early-life tobacco control policies and interventions targeting biological aging pathways to reduce AA burden across the lifespan.

Background Arterial stiffness is recognized as a new risk factor for stroke. However, the association between estimated pulse wave velocity (ePWV), a well‐established indirect measure of arterial stiffness and stroke among older adults, remains incompletely investigated. Methods This study utilized data from 3 prospective, nationally representative cohorts: the Health and Retirement Study in the United States, the English Longitudinal Study of Aging in the United Kingdom, and the China Health and Retirement Longitudinal Study in China. ePWV was calculated based on age and mean arterial pressure. Cox proportional hazard models were used to compute hazard ratios and 95% CIs. Results The final analysis included 6458 participants from the Health and Retirement Study (mean age: 66.99 years; 40.4% men), 6458 from the English Longitudinal Study of Aging (mean age: 66.32; 44.4% men), and 12 415 from the China Health and Retirement Longitudinal Study (mean age: 58.60; 46.2% men). Over follow‐up periods of 10.28 years in the Health and Retirement Study, 9.95 years in the English Longitudinal Study of Aging, and 6.30 years in the China Health and Retirement Longitudinal Study, 624 (9.7%), 374 (5.8%), and 656 (5.3%) participants developed stroke, respectively. Fully adjusted Cox regression analysis revealed a significant association between ePWV and incident stroke across all cohorts (Health and Retirement Study: hazard ratio, 1.29 [95% CI, 1.24–1.35]; English Longitudinal Study of Aging: hazard ratio, 1.37 [95% CI, 1.28–1.46]; China Health and Retirement Longitudinal Study: hazard ratio, 1.20 [95% CI, 1.15–1.25]). Conclusions This study demonstrated that higher levels of ePWV were associated with increased risks of incident stroke among middle‐aged and older populations. Arterial stiffness assessment through ePWV could potentially improve primary prevention and treatment strategies for stroke.

BACKGROUND AND AIMS:The relationship between baseline frailty status, changes in frailty status, and the risk of diabetes onset among older adults remains unclear. METHODS AND RESULTS:This study used data from the China Health and Retirement Longitudinal Study, a prospective and nationally representative cohort. Baseline frailty status was measured by the frailty index (FI) and classified as robust, pre-frail, or frail. Changes in frailty status were assessed by the transitions between non-frailty and frailty at baseline and the second survey within 2-year interval. A total of 11,044 participants were included in the baseline analysis (57.61 years, 49.5 % men), and 7005 participants (56.81 years; 50.3 % men) were included in the analysis of changes in frailty status. Compared with the robust group, the hazard ratio (HR) for diabetes was 1.40 [95 % confidence interval (CI) 1.19-1.64] for the pre-frail group and 2.07 (95 % CI 1.67-2.57) for the frail group. Each 0.1 increase in FI was independently associated with a 30 % higher risk of diabetes. Compared to the stable non-frail group, participants who progressed to frail status had an elevated risk of diabetes (HR 1.72, 95 % CI 1.26-2.35). Conversely, participants who recovered to non-frail status had a decreased risk of diabetes compared to those in the stable frail group (HR 0.46, 95 % CI 0.25-0.83). CONCLUSION:Pre-frail and frail participants showed elevated risks of diabetes among middle-aged and older adults. Progression of frailty status correlated with increased diabetes risk, while recovery of frailty status was associated with reduced risk.

To investigate the association of coronary plaque burden variables derived from coronary computed tomography angiography (CCTA) before patients underwent their first percutaneous coronary intervention (PCI) procedure and major adverse cardiovascular events (MACEs) after PCI. Patients who underwent CCTA before their first PCI were included retrospectively. A radiologist and a cardiologist analyzed CCTA images on a dedicated workstation. The coronary plaque burden variables included total plaque volume, total percent atheroma volume, volumes and fractions of total low-attenuation plaque, total fibrous plaque, and total calcified plaque. The primary outcomes were MACEs, a composite of all-cause death, nonfatal myocardial infarction, nonfatal stroke, and unscheduled coronary revascularization. A total of 230 patients were included in the final analysis. During a median follow-up of 4.8 years, 67 MACEs occurred. Total plaque volume, total percent atheroma volume, volumes of total low-attenuation plaque and total fibrous plaque but not their fractions were independent predictors for MACEs. Compared with the first tertiles, the hazard ratio of the third tertile of total plaque volume, total percent atheroma volume, total low-attenuation plaque volume, and total fibrous plaque volume were 2.06 (95

Background: Despite the majority of studies have identified smoking as a risk factor for coronary artery calcification (CAC), some studies have not identified this relationship. Differences on results reached by studies on the association of alcohol consumption with CAC exist. Moreover, studies have almost exclusively investigated the association between smoking and alcohol consumption independently. Whether an interaction effect of alcohol on the association of smoking and CAC exists has hardly been investigated. Methods: The data of 2431 adult patients who visited Fuwai Hospital, Chinese Academy of Medical Sciences from September, 2001 to December, 2023 and had Agaston coronary artery calcification score (CACS) reported were utilized. Patients who (1) underwent percutaneous coronary intervention, coronary bypass graft and heart transplantation, or (2) were complicated by acute medical conditions, chronic kidney disease or malignant neoplasms were excluded. Data from 1528 patients were eventually analyzed. Logistic regression was employed to investigate the association of smoking and alcohol consumption with presence of CAC and severe CAC. Interaction effects of alcohol consumption history on the association of current smoking and both presence of and severe CAC were examined. Results: Smoking history was significantly associated with presence of CAC and severe CAC. Current alcohol consumption was also significantly associated with presence of CAC and severe CAC. After adjusting for confounders, alcohol consumption history demonstrated an interaction effect on the association of current smoking with both presence of and severe CAC. Using non-alcohol consumers not smoking at the time of the study as reference, current smokers with an alcohol consumption history suffered from an increased risk of presence of CAC and severe CAC. Conclusions: Both smoking history and current alcohol consumption were associated with presence of and severe CAC. Alcohol consumption history demonstrated an interaction effect on the association of current smoking with both presence of and severe CAC.

Serum lycopene exhibits distinct associations with all-cause and cardiovascular mortality in populations with or without obesity.

BACKGROUND:Uric acid (UA) plays an important role in cardiovascular diseases, yet its implications in elderly patients remains incompletely understood. This study aimed to explore the impact of UA on the prognosis in advanced-age patients with acute coronary syndrome (ACS). METHODS:We included 526 patients aged 80 and older who were diagnosed with ACS. The UA levels were measured at admission, and patients were divided into four groups based on quartiles of UA levels. Major adverse cardiovascular events (MACE) during follow-up were recorded. RESULTS:The median UA level was 344.09 μmol/L, while the median follow-up duration was 64 months. Kaplan-Meier curves demonstrated a higher cumulative incidence of MACE during long-term follow-up in the Q4 group (Log-rank p < 0.05). Cox regression analysis revealed an independent correlation between UA levels and an increased risk of MACE (HR 1.002, 95%CI 1.000-1.003, p = 0.021). The ROC curve indicated that the optimal UA value for predicting MACE was 324.25 μmol/L. After matching through PSM, the MACE-free survival rate was lower in both hyperuricemia group (UA> 420.00 μmol/L) and high UA group (324.25 μmol/L < UA≤ 420.00 μmol/L) compared to the control group. Both hyperuricemia and high UA levels were independent risk factors for long-term MACE in advanced-age ACS patients, with HR values of 1.546 (1.049-2.280, p = 0.028) and 1.491 (1.011-2.198, p = 0.044), respectively. CONCLUSION:Elevated UA levels were identified as independent risk factors for MACE in elderly patients with ACS. The optimal predictive value of UA for poor cardiovascular prognosis was significantly lower than the traditional definition of hyperuricemia.

The coronary plaque burden represents an essential tool for evaluating coronary blood flow and cardiovascular outcomes. However, the concept of “coronary plaque burden” does not accurately reflect the complex pathological progression of coronary artery disease. In this review, various aspects of the total coronary atherosclerosis burden are present, including its mechanics, geometrical characteristics, plaque morphology, coronary artery calcium deposition, and coronary inflammation, to provide a complete view. Different tools used to evaluate the coronary atherosclerosis burden are also assessed according to the most recent studies. Compelling evidence is provided by our findings to advocate for a comprehensive use of the term “coronary atherosclerosis burden”.

医学的发展进步从来都不是孤立于其他学科的,在医学发展进程中充分吸收其他学科的知识,形成了相应的交叉学科,进一步推动了医学发展.不过,现代医学发展到今天,仍有许多问题悬而未决.

我国正面临人口老龄化和心血管疾病危险因素持续流行的双重压力 [1-2],传统的医疗模式难以有效应对持续增长的心血管疾病风险及负担,严峻的心血管疾病流行形势对我国心血管疾病的防治策略和医疗资源的配置提出了更高的要求.