Pub Date : 2026-03-01Epub Date: 2025-12-11DOI: 10.1016/j.ajpc.2025.101381
Yun-Jiu Cheng , Li-Juan Liu , Su-Hua Wu , Li-Chun Wang , Hai Deng , Hui-Qiang Wei , Wei-Dong Lin , Xian-Hong Fang , Yi-Jian Liao , Shu-Lin Wu , Yu-Mei Xue , Yue-Dong Ma , Yang Wu
Background
Although both genetic susceptibility and air pollution are established risk factors for cardiovascular disease (CVD), evidence for their interaction, particularly on the additive scale, remains limited and inconclusive. We aimed to investigate the individual and joint effects of long-term exposure to air pollutants and polygenic risk on incident CVD.
Methods
In a prospective cohort of 460,572 participants from the UK Biobank, we estimated hazard ratios (HRs) for CVD associated with particulate matter (PM2.5 and PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOX) using Cox models. A polygenic risk score (PRS) for CVD was constructed, and additive and multiplicative interactions between PRS and air pollution were assessed.
Results
Over a median follow-up of 11.92 years, 48,690 incident CVD cases occurred. Both a higher genetic risk and increased air pollution exposure were independently associated with elevated CVD risk. Notably, a significant synergistic effect was observed. Compared to participants with low genetic risk and low pollution exposure, those with high genetic risk and high exposure faced the greatest hazard, with HRs of 1.76 (1.68–1.84) for PM2.5, 1.74 (1.66–1.83) for PM10, 1.82 (1.73–1.91) for NO2, and 1.81 (1.73–1.90) for NOx. These associations persisted at concentrations below WHO air quality guidelines and were robust across a series of sensitivity analyses.
Conclusions
Our findings call for a reevaluation of air quality standards and indicate that genetic profiling could identify subpopulations that would derive the greatest benefit from air pollution mitigation strategies.
{"title":"Synergistic effects of genetic susceptibility and air pollution on cardiovascular disease","authors":"Yun-Jiu Cheng , Li-Juan Liu , Su-Hua Wu , Li-Chun Wang , Hai Deng , Hui-Qiang Wei , Wei-Dong Lin , Xian-Hong Fang , Yi-Jian Liao , Shu-Lin Wu , Yu-Mei Xue , Yue-Dong Ma , Yang Wu","doi":"10.1016/j.ajpc.2025.101381","DOIUrl":"10.1016/j.ajpc.2025.101381","url":null,"abstract":"<div><h3>Background</h3><div>Although both genetic susceptibility and air pollution are established risk factors for cardiovascular disease (CVD), evidence for their interaction, particularly on the additive scale, remains limited and inconclusive. We aimed to investigate the individual and joint effects of long-term exposure to air pollutants and polygenic risk on incident CVD.</div></div><div><h3>Methods</h3><div>In a prospective cohort of 460,572 participants from the UK Biobank, we estimated hazard ratios (HRs) for CVD associated with particulate matter (PM<sub>2.5</sub> and PM<sub>10</sub>), nitrogen dioxide (NO<sub>2</sub>), and nitrogen oxides (NO<em><sub>X</sub></em>) using Cox models. A polygenic risk score (PRS) for CVD was constructed, and additive and multiplicative interactions between PRS and air pollution were assessed.</div></div><div><h3>Results</h3><div>Over a median follow-up of 11.92 years, 48,690 incident CVD cases occurred. Both a higher genetic risk and increased air pollution exposure were independently associated with elevated CVD risk. Notably, a significant synergistic effect was observed. Compared to participants with low genetic risk and low pollution exposure, those with high genetic risk and high exposure faced the greatest hazard, with HRs of 1.76 (1.68–1.84) for PM<sub>2.5</sub>, 1.74 (1.66–1.83) for PM<sub>10</sub>, 1.82 (1.73–1.91) for NO<sub>2</sub>, and 1.81 (1.73–1.90) for NO<em><sub>x</sub></em>. These associations persisted at concentrations below WHO air quality guidelines and were robust across a series of sensitivity analyses.</div></div><div><h3>Conclusions</h3><div>Our findings call for a reevaluation of air quality standards and indicate that genetic profiling could identify subpopulations that would derive the greatest benefit from air pollution mitigation strategies.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"25 ","pages":"Article 101381"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145791086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2025-12-08DOI: 10.1016/j.ajpc.2025.101368
Kazutoshi Hirose , Koki Nakanishi , Masao Daimon , Naoko Sawada , Satoshi Konoma , Satomi Kobayashi , Hikari Seki , Yuriko Yoshida , Megumi Hirokawa , Tomoko Nakao , Hiroyuki Morita , Marco R. Di Tullio , Shunichi Homma , Makoto Kurano , Norihiko Takeda
Background
Recently developed Predicting Risk of cardiovascular disease EVENTs (PREVENT) risk model has shown excellent performance for cardiovascular risk stratification, but its relationship with body fat distribution and left ventricular (LV) mechanics is unknown.
Methods
We investigated 517 participants free of overt cardiac disease who underwent an extensive cardiovascular health examination. The PREVENT risk score was calculated in each participant, and the study population was categorized into three groups based on the tertiles of the risk score. Body fat distribution was assessed using computed tomography and quantitatively assessed as visceral fat area (VFA) and subcutaneous fat area (SFA) at the level of the umbilicus. All participants also underwent two-dimensional transthoracic echocardiography, and LV global longitudinal strain (LVGLS) was obtained with speckle-tracking analysis. Univariable and multivariable logistic regression models were constructed to investigate the association between the PREVENT risk model and abnormal LVGLS (<17.0 % for male and <18.0 % for female) adjusting for the clinically relevant covariates.
Results
Individuals with high PREVENT score had the largest VFA (160.0 [109.7–194.4] cm2), followed by intermediate and low score groups (138.6 [92.0–176.4] cm2 and 89.4 [50.6–123.9] cm2, p < 0.001), while SFA was comparable among the three groups (p = 0.480). LVGLS was significantly lower with increasing PREVENT risk score (20.4 ± 3.3 % vs. 18.9 ± 2.8 % vs. 18.1 ± 2.7 %, p < 0.001). Multivariable logistic regression analysis showed that the PREVENT risk score carried an independent risk for abnormal LVGLS (adjusted odds ratio per 1 % increase 1.06, p = 0.006).
Conclusion
The PREVENT risk model was associated with abdominal visceral fat accumulation and subclinical LV dysfunction.
最近开发的预测心血管疾病事件风险(prevention)模型在心血管风险分层方面表现优异,但其与体脂分布和左心室(LV)力学的关系尚不清楚。方法我们调查了517名无明显心脏疾病的参与者,他们接受了广泛的心血管健康检查。计算每个参与者的预防风险评分,并根据风险评分的分位数将研究人群分为三组。使用计算机断层扫描评估体脂分布,并定量评估脐水平的内脏脂肪面积(VFA)和皮下脂肪面积(SFA)。所有参与者还接受了二维经胸超声心动图,并通过斑点跟踪分析获得左室整体纵向应变(LVGLS)。构建单变量和多变量logistic回归模型,探讨预防风险模型与LVGLS异常(男性17.0%,女性18.0%)之间的相关性,并对临床相关协变量进行校正。结果预防得分高的个体VFA最大(160.0 [109.7-194.4]cm2),中低分组次之(138.6 [92.0-176.4]cm2和89.4 [50.6-123.9]cm2, p < 0.001),三组间SFA具有可比性(p = 0.480)。LVGLS随着prevention风险评分的增加而显著降低(20.4±3.3% vs. 18.9±2.8% vs. 18.1±2.7%,p < 0.001)。多变量logistic回归分析显示,prevention风险评分存在LVGLS异常的独立风险(校正优势比每增加1%为1.06,p = 0.006)。结论预防风险模型与腹部内脏脂肪堆积和亚临床左室功能障碍有关。
{"title":"Association of PREVENT risk model with body fat distribution and subclinical left ventricular dysfunction","authors":"Kazutoshi Hirose , Koki Nakanishi , Masao Daimon , Naoko Sawada , Satoshi Konoma , Satomi Kobayashi , Hikari Seki , Yuriko Yoshida , Megumi Hirokawa , Tomoko Nakao , Hiroyuki Morita , Marco R. Di Tullio , Shunichi Homma , Makoto Kurano , Norihiko Takeda","doi":"10.1016/j.ajpc.2025.101368","DOIUrl":"10.1016/j.ajpc.2025.101368","url":null,"abstract":"<div><h3>Background</h3><div>Recently developed Predicting Risk of cardiovascular disease EVENTs (PREVENT) risk model has shown excellent performance for cardiovascular risk stratification, but its relationship with body fat distribution and left ventricular (LV) mechanics is unknown.</div></div><div><h3>Methods</h3><div>We investigated 517 participants free of overt cardiac disease who underwent an extensive cardiovascular health examination. The PREVENT risk score was calculated in each participant, and the study population was categorized into three groups based on the tertiles of the risk score. Body fat distribution was assessed using computed tomography and quantitatively assessed as visceral fat area (VFA) and subcutaneous fat area (SFA) at the level of the umbilicus. All participants also underwent two-dimensional transthoracic echocardiography, and LV global longitudinal strain (LVGLS) was obtained with speckle-tracking analysis. Univariable and multivariable logistic regression models were constructed to investigate the association between the PREVENT risk model and abnormal LVGLS (<17.0 % for male and <18.0 % for female) adjusting for the clinically relevant covariates.</div></div><div><h3>Results</h3><div>Individuals with high PREVENT score had the largest VFA (160.0 [109.7–194.4] cm<sup>2</sup>), followed by intermediate and low score groups (138.6 [92.0–176.4] cm<sup>2</sup> and 89.4 [50.6–123.9] cm<sup>2</sup>, <em>p</em> < 0.001), while SFA was comparable among the three groups (<em>p</em> = 0.480). LVGLS was significantly lower with increasing PREVENT risk score (20.4 ± 3.3 % vs. 18.9 ± 2.8 % vs. 18.1 ± 2.7 %, <em>p</em> < 0.001). Multivariable logistic regression analysis showed that the PREVENT risk score carried an independent risk for abnormal LVGLS (adjusted odds ratio per 1 % increase 1.06, <em>p</em> = 0.006).</div></div><div><h3>Conclusion</h3><div>The PREVENT risk model was associated with abdominal visceral fat accumulation and subclinical LV dysfunction.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"25 ","pages":"Article 101368"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145791034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2025-12-11DOI: 10.1016/j.ajpc.2025.101380
Erin D. Michos , David Cherney , Pam Kushner
Chronic kidney disease (CKD) has a high global prevalence, affecting around 1 in 7 adults in the United States; however, most adults with CKD are unaware that they have the condition. Diagnosis and treatment of CKD is essential due to the associated increased morbidity and mortality, including increased risk of cardiovascular disease (CVD) and heart failure. Importantly, people with CKD are more likely to die from CVD than progress to end-stage kidney disease. Dual evaluation of estimated glomerular filtration rate (eGFR) and urinary albumin-to-creatinine ratio (UACR) is essential to determine the level of risk and to guide appropriate treatment. Although abnormalities in both eGFR and UACR can be modifiable risk factors for CKD progression and adverse CV outcomes, there is evidence of underuse of this dual screening for CKD. However, for patients with diagnosed CKD, striking reductions in cardiorenal risk may be achieved by combining appropriate evidence-based therapies. Current approaches to management of CKD involve the use of multiple therapies that target different pathological pathways to reduce cardiorenal risk. Therefore, we raise a call to action to improve the standard of care for early diagnosis and management of CKD, to minimize the risk of disease progression and complications, reduce CV risk, and ultimately improve patient outcomes. Alongside primary care clinicians, cardiologists can also lead the way for preventive efforts and implementation of guideline-directed therapies that can reduce the risk of both CKD progression and adverse CV outcomes.
{"title":"Chronic kidney disease screening to reduce cardiovascular risk: a call to action","authors":"Erin D. Michos , David Cherney , Pam Kushner","doi":"10.1016/j.ajpc.2025.101380","DOIUrl":"10.1016/j.ajpc.2025.101380","url":null,"abstract":"<div><div>Chronic kidney disease (CKD) has a high global prevalence, affecting around 1 in 7 adults in the United States; however, most adults with CKD are unaware that they have the condition. Diagnosis and treatment of CKD is essential due to the associated increased morbidity and mortality, including increased risk of cardiovascular disease (CVD) and heart failure. Importantly, people with CKD are more likely to die from CVD than progress to end-stage kidney disease. Dual evaluation of estimated glomerular filtration rate (eGFR) and urinary albumin-to-creatinine ratio (UACR) is essential to determine the level of risk and to guide appropriate treatment. Although abnormalities in both eGFR and UACR can be modifiable risk factors for CKD progression and adverse CV outcomes, there is evidence of underuse of this dual screening for CKD. However, for patients with diagnosed CKD, striking reductions in cardiorenal risk may be achieved by combining appropriate evidence-based therapies. Current approaches to management of CKD involve the use of multiple therapies that target different pathological pathways to reduce cardiorenal risk. Therefore, we raise a call to action to improve the standard of care for early diagnosis and management of CKD, to minimize the risk of disease progression and complications, reduce CV risk, and ultimately improve patient outcomes. Alongside primary care clinicians, cardiologists can also lead the way for preventive efforts and implementation of guideline-directed therapies that can reduce the risk of both CKD progression and adverse CV outcomes.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"25 ","pages":"Article 101380"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145926018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2025-12-12DOI: 10.1016/j.ajpc.2025.101379
Xiang Li , Tong Xia , Paul Landsbergis , Imelda Wong , Jian Li
Background
Shift work is a known risk factor for cardiometabolic diseases (CMD), including cardiovascular diseases (CVD) and diabetes. However, limited evidence exists on the long-term prognosis of individuals already diagnosed with CMD, particularly regarding mortality outcomes following continued exposure to shift work. This study aimed to investigate the prospective association between shift work and mortality outcomes, including all-cause, CMD, and CVD mortality, among U.S. workers with CMD.
Methods
The data of 2010 and 2015 National Health Interview Survey (NHIS) were linked to mortality records from the National Death Index through December 31, 2019. A total of 9,622 workers with CMD were included. Shift work exposure was self-reported usual work schedules and categorized as shift versus regular daytime work. Cox proportional hazards models were performed, with adjustment for baseline demographic information, socioeconomic status, and occupational characteristics.
Results
At baseline, 25.7 % (2,470) reported shift work. During follow-up period, 308 deaths in the non-shift work group (100 CMD deaths and 90 CVD deaths) and 129 deaths in the shift work group (50 CMD deaths and 43 CVD deaths) were documented. Shift work was associated with a higher risk of all-cause mortality (HR=1.28, 95 % CI=1.02, 1.62), CMD mortality (HR=1.57, 95 % CI=1.01, 2.42), and CVD mortality (HR=1.61, 95 % CI=1.02, 2.53), adjusting for baseline covariates.
Conclusions
Among U.S. workers with CMD, shift work was associated with substantially higher risks of all-cause and cause-specific mortality, highlighting the need to consider occupational exposures in clinical care and workplace policies to support secondary prevention for workers with CMD.
{"title":"Long-term prognosis of cardiometabolic diseases among U.S. workers: The contribution of shift work to mortality","authors":"Xiang Li , Tong Xia , Paul Landsbergis , Imelda Wong , Jian Li","doi":"10.1016/j.ajpc.2025.101379","DOIUrl":"10.1016/j.ajpc.2025.101379","url":null,"abstract":"<div><h3>Background</h3><div>Shift work is a known risk factor for cardiometabolic diseases (CMD), including cardiovascular diseases (CVD) and diabetes. However, limited evidence exists on the long-term prognosis of individuals already diagnosed with CMD, particularly regarding mortality outcomes following continued exposure to shift work. This study aimed to investigate the prospective association between shift work and mortality outcomes, including all-cause, CMD, and CVD mortality, among U.S. workers with CMD.</div></div><div><h3>Methods</h3><div>The data of 2010 and 2015 National Health Interview Survey (NHIS) were linked to mortality records from the National Death Index through December 31, 2019. A total of 9,622 workers with CMD were included. Shift work exposure was self-reported usual work schedules and categorized as shift versus regular daytime work. Cox proportional hazards models were performed, with adjustment for baseline demographic information, socioeconomic status, and occupational characteristics.</div></div><div><h3>Results</h3><div>At baseline, 25.7 % (2,470) reported shift work. During follow-up period, 308 deaths in the non-shift work group (100 CMD deaths and 90 CVD deaths) and 129 deaths in the shift work group (50 CMD deaths and 43 CVD deaths) were documented. Shift work was associated with a higher risk of all-cause mortality (HR=1.28, 95 % CI=1.02, 1.62), CMD mortality (HR=1.57, 95 % CI=1.01, 2.42), and CVD mortality (HR=1.61, 95 % CI=1.02, 2.53), adjusting for baseline covariates.</div></div><div><h3>Conclusions</h3><div>Among U.S. workers with CMD, shift work was associated with substantially higher risks of all-cause and cause-specific mortality, highlighting the need to consider occupational exposures in clinical care and workplace policies to support secondary prevention for workers with CMD.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"25 ","pages":"Article 101379"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145791035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2026-01-03DOI: 10.1016/j.ajpc.2026.101410
Aaron L. Troy , Timothy S. Anderson , Alexander C. Razavi , Stacey L. Schott , Jared A. Spitz , Roger S. Blumenthal
{"title":"Personalizing prevention for healthy cardiovascular aging: Geriatric cardiology in the 2024-2025 hypertension and dyslipidemia guidelines","authors":"Aaron L. Troy , Timothy S. Anderson , Alexander C. Razavi , Stacey L. Schott , Jared A. Spitz , Roger S. Blumenthal","doi":"10.1016/j.ajpc.2026.101410","DOIUrl":"10.1016/j.ajpc.2026.101410","url":null,"abstract":"","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"25 ","pages":"Article 101410"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145925940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2026-01-19DOI: 10.1016/j.ajpc.2025.101395
Diane Brisson , Albert Wiegman , Alpana Waldron , Pinay Kainth , Frederick J Raal , Daniel Gaudet
Aim
Evinacumab is an ANGPTL-3 inhibitor developed for the treatment of homozygous familial hypercholesterolemia (HoFH), a rare condition characterized by extremely elevated LDL-cholesterol (LDL-C) levels and premature atherosclerotic cardiovascular disease. Despite important sex-related disparities in lipid metabolism, females are still underrepresented in trials, limiting the generalizability of results. With 116 patients, of which 49 % were females, the ELIPSE-OLE study has the largest cohort of HoFH females involved in a clinical trial. The aim of this analysis was to compare response to evinacumab in females and males in the ELIPSE OLE study.
Methods
This study is a post hoc exploratory analysis of data on 57 females and 59 males, aged ≥12 years and on stable background lipid-lowering therapy (LLT) from ELIPSE OLE. Patients received evinacumab 15 mg/kg intravenously every 4 weeks. The primary efficacy endpoint was the reduction in LDL-C concentration from baseline to week-24.
Results
Baseline LDL-C [mean (SD)] tended to be higher in females aged 18 to <50 than males: 8.4(5.4) vs 6.4(3.5) mmol/L. Following treatment with evinacumab, the percent decrease in LDL-C reached at week-24 was 44 % in the overall cohort and was sustained over time. Evinacumab significantly decreased LDL-C in both sexes, regardless of age and background LLT. There was a trend, although not significant, toward higher relative precent decrease of LDL-C among females.
Conclusion
In a study where half of the participants were females, evinacumab led to substantial LDL-C reduction in HoFH patients of both sexes, regardless of genotype or background LLT.
{"title":"Baseline characteristics and response to evinacumab in females and males with homozygous familial hypercholesterolemia in the ELIPSE OLE study","authors":"Diane Brisson , Albert Wiegman , Alpana Waldron , Pinay Kainth , Frederick J Raal , Daniel Gaudet","doi":"10.1016/j.ajpc.2025.101395","DOIUrl":"10.1016/j.ajpc.2025.101395","url":null,"abstract":"<div><h3>Aim</h3><div>Evinacumab is an ANGPTL-3 inhibitor developed for the treatment of homozygous familial hypercholesterolemia (HoFH), a rare condition characterized by extremely elevated LDL-cholesterol (LDL-C) levels and premature atherosclerotic cardiovascular disease. Despite important sex-related disparities in lipid metabolism, females are still underrepresented in trials, limiting the generalizability of results. With 116 patients, of which 49 % were females, the ELIPSE-OLE study has the largest cohort of HoFH females involved in a clinical trial. The aim of this analysis was to compare response to evinacumab in females and males in the ELIPSE OLE study.</div></div><div><h3>Methods</h3><div>This study is a post hoc exploratory analysis of data on 57 females and 59 males, aged ≥12 years and on stable background lipid-lowering therapy (LLT) from ELIPSE OLE. Patients received evinacumab 15 mg/kg intravenously every 4 weeks. The primary efficacy endpoint was the reduction in LDL-C concentration from baseline to week-24.</div></div><div><h3>Results</h3><div>Baseline LDL-C [mean (SD)] tended to be higher in females aged 18 to <50 than males: 8.4(5.4) vs 6.4(3.5) mmol/L. Following treatment with evinacumab, the percent decrease in LDL-C reached at week-24 was 44 % in the overall cohort and was sustained over time. Evinacumab significantly decreased LDL-C in both sexes, regardless of age and background LLT. There was a trend, although not significant, toward higher relative precent decrease of LDL-C among females.</div></div><div><h3>Conclusion</h3><div>In a study where half of the participants were females, evinacumab led to substantial LDL-C reduction in HoFH patients of both sexes, regardless of genotype or background LLT.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"25 ","pages":"Article 101395"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147328256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2026-01-24DOI: 10.1016/j.ajpc.2026.101450
Khurram Nasir
{"title":"Lowering barriers Not the bar: Redefining the role of American Journal of Preventive Cardiology in the next era","authors":"Khurram Nasir","doi":"10.1016/j.ajpc.2026.101450","DOIUrl":"10.1016/j.ajpc.2026.101450","url":null,"abstract":"","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"25 ","pages":"Article 101450"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147328296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2026-02-23DOI: 10.1016/j.ajpc.2026.101440
Martha Gulati , Danielle Belardo , Robert J. Ostfeld , American Society for Preventive Cardiology Nutrition Committee
{"title":"The new Dietary Guidelines for Americans: When national nutritional policy outpaces the evidence","authors":"Martha Gulati , Danielle Belardo , Robert J. Ostfeld , American Society for Preventive Cardiology Nutrition Committee","doi":"10.1016/j.ajpc.2026.101440","DOIUrl":"10.1016/j.ajpc.2026.101440","url":null,"abstract":"","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"25 ","pages":"Article 101440"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147328295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2026-01-23DOI: 10.1016/j.ajpc.2026.101416
Mateo Iwanowski , Sonia Ruiz-Bustillo , Joan Vime-Jubany , Flavio Zuccarino , Diego Álvaro Perez Zerpa , Laura Jimenez-Mayorga , Sara Rodriguez , Nuria Rodriguez , Paula Cabero , Consol Ivern , Badosa Marce Neus , Beatriz Vaquerizo-Montilla , Miguel Cainzos-Achirica
Introduction
Lipoprotein(a) (Lp[a]) is an independent risk factor for atherosclerotic cardiovascular events and aortic stenosis. In Spain, the prevalence of elevated Lp(a) and its clinical impact remain poorly defined.
Methods
We conducted a cross-sectional study including two cohorts: patients discharged after a non-fatal acute coronary syndrome (secondary prevention), and asymptomatic patients with subclinical atherosclerosis (“1.5 prevention”). The prevalence of elevated Lp(a) levels was assessed in both groups. Associations with multivessel coronary artery disease (secondary prevention) and with a coronary artery calcium (CAC) score ≥300 AU (1.5 prevention) were analyzed.
Results
A total of 1043 patients were included (788 secondary prevention). Median Lp(a) levels were 61 nmol/L in secondary prevention and 29 nmol/L in the 1.5 prevention cohort. In secondary prevention, 36.8%, 33.6%, 29.2%, and 24.5% had Lp(a) ≥125, ≥150, ≥175, and ≥ 200nmol/L, respectively; in the 1.5 prevention cohort the corresponding proportions were 27.5%, 24.3%, 17.6%, and 14.1%. In secondary prevention, Lp(a) ≥175 nmol/L was associated with multivessel disease after multivariable adjustment for age, sex, LDLc, and statin treatment (OR 1.45, 95% CI: 1.04–2.01; p = 0.027). In 1.5 prevention, Lp(a) ≥175 nmol/L showed a prevalence of CAC ≥300 AU of 86%. Elevated Lp(a) (≥175 nmol/L) was associated with CAC ≥300 AU (OR 4.47, 95% CI 1.39–20.07; p = 0.023), although this association lost significance after multivariable adjustment.
Conclusions
Elevated Lp(a) levels are common in both populations and correlate with greater atherosclerotic burden. These findings support the systematic assessment of Lp(a) to guide preventive strategies across both patient populations.
简介:脂蛋白(a) (Lp[a])是动脉粥样硬化性心血管事件和主动脉狭窄的独立危险因素。在西班牙,Lp(a)升高的患病率及其临床影响仍不明确。方法:我们进行了一项横断面研究,包括两个队列:非致死性急性冠状动脉综合征(二级预防)后出院的患者,以及无症状的亚临床动脉粥样硬化(“1.5预防”)患者。评估两组患者Lp(a)水平升高的发生率。分析与多支冠状动脉疾病(二级预防)和冠状动脉钙(CAC)评分≥300 AU(1.5预防)的相关性。结果:共纳入1043例患者,其中二级预防788例。中位Lp(a)水平在二级预防组为61 nmol/L,在1.5预防组为29 nmol/L。在二级预防中,Lp(a)≥125、≥150、≥175和≥200nmol/L分别为36.8%、33.6%、29.2%和24.5%;在1.5预防组中,相应比例分别为27.5%、24.3%、17.6%和14.1%。在二级预防中,经年龄、性别、低密度脂蛋白和他汀类药物治疗等多变量调整后,Lp(a)≥175 nmol/L与多血管疾病相关(OR 1.45, 95% CI: 1.04-2.01; p = 0.027)。在1.5预防中,Lp(a)≥175 nmol/L表明CAC≥300 AU的患病率为86%。升高的Lp(a)(≥175 nmol/L)与CAC≥300 AU相关(OR 4.47, 95% CI 1.39-20.07; p = 0.023),尽管在多变量调整后这种关联失去了显著性。结论:Lp(a)水平升高在两种人群中都很常见,并且与更大的动脉粥样硬化负担相关。这些发现支持对Lp(a)进行系统评估,以指导两种患者群体的预防策略。
{"title":"Lipoprotein(a) epidemiology and role in secondary and primary-and-a-half cardiovascular prevention: From subclinical atherosclerosis to coronary events","authors":"Mateo Iwanowski , Sonia Ruiz-Bustillo , Joan Vime-Jubany , Flavio Zuccarino , Diego Álvaro Perez Zerpa , Laura Jimenez-Mayorga , Sara Rodriguez , Nuria Rodriguez , Paula Cabero , Consol Ivern , Badosa Marce Neus , Beatriz Vaquerizo-Montilla , Miguel Cainzos-Achirica","doi":"10.1016/j.ajpc.2026.101416","DOIUrl":"10.1016/j.ajpc.2026.101416","url":null,"abstract":"<div><h3>Introduction</h3><div>Lipoprotein(a) (Lp[a]) is an independent risk factor for atherosclerotic cardiovascular events and aortic stenosis. In Spain, the prevalence of elevated Lp(a) and its clinical impact remain poorly defined.</div></div><div><h3>Methods</h3><div>We conducted a cross-sectional study including two cohorts: patients discharged after a non-fatal acute coronary syndrome (secondary prevention), and asymptomatic patients with subclinical atherosclerosis (“1.5 prevention”). The prevalence of elevated Lp(a) levels was assessed in both groups. Associations with multivessel coronary artery disease (secondary prevention) and with a coronary artery calcium (CAC) score ≥300 AU (1.5 prevention) were analyzed.</div></div><div><h3>Results</h3><div>A total of 1043 patients were included (788 secondary prevention). Median Lp(a) levels were 61 nmol/L in secondary prevention and 29 nmol/L in the 1.5 prevention cohort. In secondary prevention, 36.8%, 33.6%, 29.2%, and 24.5% had Lp(a) ≥125, ≥150, ≥175, and ≥ 200nmol/L, respectively; in the 1.5 prevention cohort the corresponding proportions were 27.5%, 24.3%, 17.6%, and 14.1%. In secondary prevention, Lp(a) ≥175 nmol/L was associated with multivessel disease after multivariable adjustment for age, sex, LDLc, and statin treatment (OR 1.45, 95% CI: 1.04–2.01; <em>p</em> = 0.027). In 1.5 prevention, Lp(a) ≥175 nmol/L showed a prevalence of CAC ≥300 AU of 86%. Elevated Lp(a) (≥175 nmol/L) was associated with CAC ≥300 AU (OR 4.47, 95% CI 1.39–20.07; <em>p</em> = 0.023), although this association lost significance after multivariable adjustment.</div></div><div><h3>Conclusions</h3><div>Elevated Lp(a) levels are common in both populations and correlate with greater atherosclerotic burden. These findings support the systematic assessment of Lp(a) to guide preventive strategies across both patient populations.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"25 ","pages":"Article 101416"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147328282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}