Pub Date : 2026-01-01DOI: 10.1016/j.ahjo.2025.100692
Christelle Lteif , Paula Wachs , Ravindra K. Sharma , Julio D. Duarte
Objective
To investigate the role of Id genes in the development of pulmonary hypertension (PH) in heart failure (HF) and evaluate genetic variants of the ID genes associated with HF-PH.
Design
Experimental study using an AKR/J mouse model of HF-PH and a genetic association study using the UK Biobank cohort.
Setting
Laboratory animal study and population-based cohort study.
Participants
AKR/J mice with HF-PH and participants with HF from the UK Biobank cohort.
Interventions
Administration of tacrolimus (Id signaling inducer) in the mouse model.
Main outcome measures
Tissue-specific gene expression of Id1, Id2, and Id3 in HF-PH mice; severity of HF-PH after tacrolimus treatment; associations of single nucleotide polymorphisms of ID1, ID2, and ID3 with PH development and mortality in participants with HF.
Results
Id1 was upregulated in the left ventricle (Fold Change (FC) = 1.65; P = 3.0 × 10−4) of HF-PH mice. In adipose tissue, Id1 and Id3 were downregulated (FC = 0.33; P = 5.2 × 10−3 and FC = 0.50; P = 0.01, respectively), while Id2 was upregulated (FC = 1.78; P = 7 × 10−4). Tacrolimus worsened PH and diastolic dysfunction, upregulating only Id2 in adipose tissue. In the clinical cohort, rs7425561 and rs10174593 (expression quantitative loci for ID2) trended toward reduced risk of PH in HF and all-cause mortality in participants with HF-PH.
Conclusion
The results suggest ID1, ID2, and ID3 are involved in HF-PH pathogenesis, but more research is needed to characterize their exact role.
{"title":"The role of Id genes on pulmonary hypertension development in left heart failure","authors":"Christelle Lteif , Paula Wachs , Ravindra K. Sharma , Julio D. Duarte","doi":"10.1016/j.ahjo.2025.100692","DOIUrl":"10.1016/j.ahjo.2025.100692","url":null,"abstract":"<div><h3>Objective</h3><div>To investigate the role of <em>Id</em> genes in the development of pulmonary hypertension (PH) in heart failure (HF) and evaluate genetic variants of the <em>ID</em> genes associated with HF-PH.</div></div><div><h3>Design</h3><div>Experimental study using an AKR/J mouse model of HF-PH and a genetic association study using the UK Biobank cohort.</div></div><div><h3>Setting</h3><div>Laboratory animal study and population-based cohort study.</div></div><div><h3>Participants</h3><div>AKR/J mice with HF-PH and participants with HF from the UK Biobank cohort.</div></div><div><h3>Interventions</h3><div>Administration of tacrolimus (Id signaling inducer) in the mouse model.</div></div><div><h3>Main outcome measures</h3><div>Tissue-specific gene expression of <em>Id1</em>, <em>Id2</em>, and <em>Id3</em> in HF-PH mice; severity of HF-PH after tacrolimus treatment; associations of single nucleotide polymorphisms of <em>ID1</em>, <em>ID2</em>, and <em>ID3</em> with PH development and mortality in participants with HF.</div></div><div><h3>Results</h3><div><em>Id1</em> was upregulated in the left ventricle (Fold Change (FC) = 1.65; <em>P</em> = 3.0 × 10<sup>−4</sup>) of HF-PH mice. In adipose tissue, <em>Id1</em> and <em>Id3</em> were downregulated (FC = 0.33; <em>P</em> = 5.2 × 10<sup>−3</sup> and FC = 0.50; <em>P</em> = 0.01, respectively), while <em>Id2</em> was upregulated (FC = 1.78; <em>P</em> = 7 × 10<sup>−4</sup>). Tacrolimus worsened PH and diastolic dysfunction, upregulating only <em>Id2</em> in adipose tissue. In the clinical cohort, rs7425561 and rs10174593 (expression quantitative loci for <em>ID2</em>) trended toward reduced risk of PH in HF and all-cause mortality in participants with HF-PH.</div></div><div><h3>Conclusion</h3><div>The results suggest <em>ID1</em>, <em>ID2</em>, and <em>ID3</em> are involved in HF-PH pathogenesis, but more research is needed to characterize their exact role.</div></div>","PeriodicalId":72158,"journal":{"name":"American heart journal plus : cardiology research and practice","volume":"61 ","pages":"Article 100692"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145924663","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 : 2026-01-01DOI: 10.1016/j.ahjo.2025.100699
Hafsah Alim Ur Rahman , Nimrah Iqbal , Muhammad Ahmed Ali Fahim , Fayza Salman , Syed Hassan Ahmed , Omama Asim , Taha Mansoor , Muhammad Zain Farooq , Muhammad Sohaib Asghar
Background
Heart failure (HF) and colorectal cancer (CRC) are major public health concerns among the aging population in the United States. This study aimed to investigate temporal, regional, urbanization and racial trends in mortality among adults with HF and CRC aged ≥65 years.
Methods
Mortality data were sourced from the Centers for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research (CDC WONDER) database, utilizing ICD-10 codes to identify deaths related to colon cancer and heart failure from 1999 to 2020. Age-adjusted mortality rates (AAMRs) per 100,000 individuals were calculated, along with Annual Percentage Changes (APCs) and their respective 95 % confidence intervals (CIs).
Results
The AAMRs remained relatively stable between 1999 (8.5) and 2004 (7.3) (APC: −2.61; 95 % CI: −3.86, 0.09). From 2004 to 2009, a significant decline to 5.0 was observed (APC: −7.08; 95 % CI: −9.28, −3.58). Subsequently, the rates stabilized by 2015 (3.8) (APC: −4.84; 95 % CI: −6.58 to 2.04) but demonstrated a modest increase to 4.4 by 2020 (APC: 2.55; 95 % CI: 0.08 to 8.19). Mortality rates were consistently higher among males (6.7 vs. 4.5 for females) and varied across racial/ethnic groups, with Non-Hispanic (NH) Whites (5.7) and NH Black/African Americans (5.4) exhibiting the highest rates, while Hispanics (2.8) and NH Asians/Pacific Islanders (2.3) had the lowest. Regional disparities showed that the Midwest had the highest AAMRs (6.5) followed by the Northeast (5.4), West (5.2), and South (4.8). Additionally, non-metropolitan areas exhibited significantly higher rates than metropolitan areas (7.1 vs. 5.0, respectively). The states in the 90th percentile for AAMRs were West Virginia, Mississippi, South Dakota, Nebraska, and North Dakota.
Conclusion
Although there was an overall decline in mortality rates during the study period, disparities remained evident, with higher mortality observed among males, non-Hispanic Whites, residents of the Midwest, and individuals in non-metropolitan areas. This highlights the need for targeted public health intervention.
{"title":"Mortality trends in heart failure and colon cancer: Insights into gender, ethnic, and regional disparities in the United States (1999–2020)","authors":"Hafsah Alim Ur Rahman , Nimrah Iqbal , Muhammad Ahmed Ali Fahim , Fayza Salman , Syed Hassan Ahmed , Omama Asim , Taha Mansoor , Muhammad Zain Farooq , Muhammad Sohaib Asghar","doi":"10.1016/j.ahjo.2025.100699","DOIUrl":"10.1016/j.ahjo.2025.100699","url":null,"abstract":"<div><h3>Background</h3><div>Heart failure (HF) and colorectal cancer (CRC) are major public health concerns among the aging population in the United States. This study aimed to investigate temporal, regional, urbanization and racial trends in mortality among adults with HF and CRC aged ≥65 years.</div></div><div><h3>Methods</h3><div>Mortality data were sourced from the Centers for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research (CDC WONDER) database, utilizing ICD-10 codes to identify deaths related to colon cancer and heart failure from 1999 to 2020. Age-adjusted mortality rates (AAMRs) per 100,000 individuals were calculated, along with Annual Percentage Changes (APCs) and their respective 95 % confidence intervals (CIs).</div></div><div><h3>Results</h3><div>The AAMRs remained relatively stable between 1999 (8.5) and 2004 (7.3) (APC: −2.61; 95 % CI: −3.86, 0.09). From 2004 to 2009, a significant decline to 5.0 was observed (APC: −7.08; 95 % CI: −9.28, −3.58). Subsequently, the rates stabilized by 2015 (3.8) (APC: −4.84; 95 % CI: −6.58 to 2.04) but demonstrated a modest increase to 4.4 by 2020 (APC: 2.55; 95 % CI: 0.08 to 8.19). Mortality rates were consistently higher among males (6.7 vs. 4.5 for females) and varied across racial/ethnic groups, with Non-Hispanic (NH) Whites (5.7) and NH Black/African Americans (5.4) exhibiting the highest rates, while Hispanics (2.8) and NH Asians/Pacific Islanders (2.3) had the lowest. Regional disparities showed that the Midwest had the highest AAMRs (6.5) followed by the Northeast (5.4), West (5.2), and South (4.8). Additionally, non-metropolitan areas exhibited significantly higher rates than metropolitan areas (7.1 vs. 5.0, respectively). The states in the 90th percentile for AAMRs were West Virginia, Mississippi, South Dakota, Nebraska, and North Dakota.</div></div><div><h3>Conclusion</h3><div>Although there was an overall decline in mortality rates during the study period, disparities remained evident, with higher mortality observed among males, non-Hispanic Whites, residents of the Midwest, and individuals in non-metropolitan areas. This highlights the need for targeted public health intervention.</div></div>","PeriodicalId":72158,"journal":{"name":"American heart journal plus : cardiology research and practice","volume":"61 ","pages":"Article 100699"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145924710","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}
{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":72158,"journal":{"name":"American heart journal plus : cardiology research and practice","volume":"62 ","pages":"Article 100709"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146647067","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}
{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":72158,"journal":{"name":"American heart journal plus : cardiology research and practice","volume":"62 ","pages":"Article 100710"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146647072","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}
{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":72158,"journal":{"name":"American heart journal plus : cardiology research and practice","volume":"63 ","pages":"Article 100734"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146495129","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}
{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":72158,"journal":{"name":"American heart journal plus : cardiology research and practice","volume":"61 ","pages":"Article 100699"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146429123","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}
{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":72158,"journal":{"name":"American heart journal plus : cardiology research and practice","volume":"61 ","pages":"Article 100683"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146429131","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}
{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":72158,"journal":{"name":"American heart journal plus : cardiology research and practice","volume":"61 ","pages":"Article 100694"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146429135","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 : 2025-12-31DOI: 10.1016/j.ahjo.2025.100710
Bahaa El Deen Wehbeh , Moied Al Sakan , Jamil Francis , Rachad Ghazal , Samir Alam , Fadi Sawaya
Coronary artery disease (CAD) coexists frequently with aortic stenosis (AS), and the optimal management of CAD in patients undergoing transcatheter aortic valve replacement (TAVR) remains incompletely defined due to limited and heterogeneous evidence. This review aims to integrate the current evidence on the epidemiology and shared pathophysiology of CAD and AS, summarize the diagnostic algorithms for CAD in the TAVR population, and evaluates revascularization strategies with a focus on the timing of percutaneous coronary intervention relative to valve replacement. Current evidence suggests that while routine PCI in TAVR candidates for stable CAD may offer limited benefit, revascularization in patients with complex CAD or high anatomical burden may improve outcomes. This review further characterizes the incidence, proposed mechanisms, and prognostic significance of post-TAVR coronary events and outlines emerging strategies to optimize ischemic and procedural outcomes in this high-risk cohort.
{"title":"Coronary artery disease in patients undergoing transcatheter aortic valve replacement: Current evidence and future directions","authors":"Bahaa El Deen Wehbeh , Moied Al Sakan , Jamil Francis , Rachad Ghazal , Samir Alam , Fadi Sawaya","doi":"10.1016/j.ahjo.2025.100710","DOIUrl":"10.1016/j.ahjo.2025.100710","url":null,"abstract":"<div><div>Coronary artery disease (CAD) coexists frequently with aortic stenosis (AS), and the optimal management of CAD in patients undergoing transcatheter aortic valve replacement (TAVR) remains incompletely defined due to limited and heterogeneous evidence. This review aims to integrate the current evidence on the epidemiology and shared pathophysiology of CAD and AS, summarize the diagnostic algorithms for CAD in the TAVR population, and evaluates revascularization strategies with a focus on the timing of percutaneous coronary intervention relative to valve replacement. Current evidence suggests that while routine PCI in TAVR candidates for stable CAD may offer limited benefit, revascularization in patients with complex CAD or high anatomical burden may improve outcomes. This review further characterizes the incidence, proposed mechanisms, and prognostic significance of post-TAVR coronary events and outlines emerging strategies to optimize ischemic and procedural outcomes in this high-risk cohort.</div></div>","PeriodicalId":72158,"journal":{"name":"American heart journal plus : cardiology research and practice","volume":"62 ","pages":"Article 100710"},"PeriodicalIF":1.8,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145898133","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 : 2025-12-29DOI: 10.1016/j.ahjo.2025.100707
O. Smettei , R.M. Abazid , J.G. Romsa , C. Akincioglu , J.C. Warrington , T.B. Alshaar , P.J. Teefy , S. De , N. Tzemos , R. Zareardalan , M. Badreddine , Y. Bureau , W.C. Vezina
Purpose
Young adults are more likely to have non-calcified coronary plaques. Purpose to assess the predictive value of a zero-coronary artery calcium (CAC) score in young adults and to determine which clinical characteristics are associated with obstructive coronary heart disease.
Methods
6775 patients were prospectively entered a registry. They all had a CAC. Mean age 63 +/− 18 years. 56.2 % males. 3525 patients underwent coronary CT angiography (CCTA). 3250 patients underwent single photon emission tomography (SPECT). SPECT patients were mainly outpatients. CCTA patients also were almost exclusively outpatients. Thus, the population was generally a low-risk population.
Results
Among the CCTA patients, 1888 had a 0 CAC score. 175/1888 (9 %) had less than 70 % stenosis, while 41/1888 (2.2 %) had ≥70 % stenosis. Patients with ≥70 % stenosis: were younger 45 ± 12 yr versus 59 ± 11 yr, p <0.001, predominantly males (51.2% versus 38.8% p< 0.001), had a slightly greater prevalence of family history of CAD (58.5 % vs 57.9 % p = 0.04), smoking history (68.3 % VS.44.6 % p < 0.001), hypertension (61 % versus 39.2 % p = 0.004), dyslipidemia (56.1 % versus 36.2 % p < 0.001), and obesity (70.7 % VS 11.7 % p < 0.001). 3250 patients had CAC and SPECT. Of these, 1161 had a zero CAC score. Of these 42 patients had significant ischemia >10 % of LV, Patients with ischemia >10 % of LV mass, and they were younger 44 ± 10 yr versus 60 ± 12 yr, p < 0.001, had a slightly greater prevalence of family history of CAD 61 % versus 57 % p = 0.07, smoking history (64.3 % versus 48.5 % p = 0.045), hypertension (69 % versus 45.5 % p = 0.003), obesity 19 % versus 11.7 %, and diabetes (35.7 % versus 14.5 % p < 0.001).
Conclusions
A zero CAC does not rule out significant CAD in young adults with chest pain with CAD risk factors. These patients may need further investigations.
目的年轻人更容易出现非钙化的冠状动脉斑块。目的评估零冠状动脉钙（CAC）评分在年轻人中的预测价值，并确定哪些临床特征与阻塞性冠心病相关。方法对6775例患者进行前瞻性登记。他们都有CAC。平均年龄63±18岁。56.2%为男性。3525例患者行冠状动脉CT血管造影（CCTA）。3250例患者行单光子发射断层扫描（SPECT）。SPECT患者以门诊为主。CCTA患者也几乎完全是门诊患者。因此，该人群总体上属于低风险人群。结果CCTA患者中，1888例患者的CAC评分为0。175/1888（9%）狭窄小于70%，41/1888（2.2%）狭窄≥70%。年轻患者狭窄≥70%:45±12年和59±11年,p & lt; 0.001,主要是男性(51.2%比38.8% p & lt; 0.001),有一个稍微更流行的家族史的CAD (58.5% vs 57.9%, p = 0.04),吸烟史(68.3% VS.44.6 % p & lt; 0.001)、高血压(61%比39.2%,p = 0.004),血脂异常(56.1%比36.2% p & lt; 0.001),和肥胖(70.7% vs 11.7% p & lt; 0.001)。3250例患者行CAC和SPECT检查。其中，1161人的CAC得分为零。42岁的患者明显缺血祝辞LV的10%,缺血患者在LV质量的10%,他们年轻44±60±10年和12年,p & lt; 0.001中,有一个略大的流行CAD家族史的61%比57%,p = 0.07吸烟史(64.3%比48.5%,p = 0.045),高血压(69%比45.5%,p = 0.003),肥胖19%和11.7%,和糖尿病(35.7%比14.5% p & lt; 0.001)。结论：无CAC不能排除有冠心病危险因素胸痛的年轻成人存在明显冠心病的可能性。这些患者可能需要进一步调查。
{"title":"Coronary artery calcium score of zero does not rule out obstructive CAD in young adults","authors":"O. Smettei , R.M. Abazid , J.G. Romsa , C. Akincioglu , J.C. Warrington , T.B. Alshaar , P.J. Teefy , S. De , N. Tzemos , R. Zareardalan , M. Badreddine , Y. Bureau , W.C. Vezina","doi":"10.1016/j.ahjo.2025.100707","DOIUrl":"10.1016/j.ahjo.2025.100707","url":null,"abstract":"<div><h3>Purpose</h3><div>Young adults are more likely to have non-calcified coronary plaques. Purpose to assess the predictive value of a zero-coronary artery calcium (CAC) score in young adults and to determine which clinical characteristics are associated with obstructive coronary heart disease.</div></div><div><h3>Methods</h3><div>6775 patients were prospectively entered a registry. They all had a CAC. Mean age 63 +/− 18 years. 56.2 % males. 3525 patients underwent coronary CT angiography (CCTA). 3250 patients underwent single photon emission tomography (SPECT). SPECT patients were mainly outpatients. CCTA patients also were almost exclusively outpatients. Thus, the population was generally a low-risk population.</div></div><div><h3>Results</h3><div>Among the CCTA patients, 1888 had a 0 CAC score. 175/1888 (9 %) had less than 70 % stenosis, while 41/1888 (2.2 %) had ≥70 % stenosis. Patients with ≥70 % stenosis: were younger 45 ± 12 yr versus 59 ± 11 yr, <em>p <</em> <em>0.001,</em> predominantly males <em>(51.2</em> <em>%</em> versus <em>38.8</em> <em>% p</em> <em>< 0.001),</em> had a slightly greater prevalence of family history of CAD (58.5 % vs 57.9 % <em>p</em> = 0.04), smoking history (68.3 % VS.44.6 % <em>p</em> < 0.001), hypertension (61 % versus 39.2 % <em>p</em> = 0.004), dyslipidemia (56.1 % versus 36.2 % p < 0.001), and obesity (70.7 % VS 11.7 % p < 0.001). 3250 patients had CAC and SPECT. Of these, 1161 had a zero CAC score. Of these 42 patients had significant ischemia >10 % of LV, Patients with ischemia >10 % of LV mass, and they were younger 44 ± 10 yr versus 60 ± 12 yr, <em>p < 0.001,</em> had a slightly greater prevalence of family history of CAD 61 % versus 57 % <em>p</em> = 0.07, smoking history (64.3 % versus 48.5 % <em>p</em> = 0.045), hypertension (69 % versus 45.5 % <em>p</em> = 0.003), obesity 19 % versus 11.7 %, and diabetes (35.7 % versus 14.5 % <em>p</em> < 0.001).</div></div><div><h3>Conclusions</h3><div>A zero CAC does not rule out significant CAD in young adults with chest pain with CAD risk factors. These patients may need further investigations.</div></div>","PeriodicalId":72158,"journal":{"name":"American heart journal plus : cardiology research and practice","volume":"62 ","pages":"Article 100707"},"PeriodicalIF":1.8,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145929170","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}
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