{"title":"A Father's Last Message: The Value of Polygenic Risk Scoring in Familial CAD","authors":"Daniel Soffer MD, Ranvir Bhatia BA","doi":"10.1016/j.jacl.2024.04.029","DOIUrl":"10.1016/j.jacl.2024.04.029","url":null,"abstract":"<div><h3>Background/Synopsis</h3><p>Given the strong familial aggregation of CAD, genetic profiling has the potential to enhance CVD risk assessment. Historically, this approach has been limited to the identification of monogenic variants, which fail to explain most of the heritable CVD risk in the population. Genome wide association studies have identified numerous single nucleotide variants (SNVs) associated with CVD risk. Polygenic risk scoring (PRS) provides a quantitative assessment of CVD risk based on the number of identified SNVs and their respective effect sizes. PRS has been shown to significantly improve event prediction when used in conjunction with the AHA/ACC risk calculator.</p></div><div><h3>Objective/Purpose</h3><p>Here, we describe a family with a significant burden of premature CVD who demonstrate strong correlation between PRS and their clinical phenotypes.</p></div><div><h3>Methods</h3><p>Case presentation: AA is a 24-year-old female with newly diagnosed CAD s/p 2 vessel CABG and hypercholesterolemia with no pathogenic variants associated with monogenic familial hypercholesterolemia. She presented to lipid clinic for new evaluation one week before her wedding. She was found to have combined hyperlipidemia and lipoprotein(a)>2x upper limit of normal (ULN). Within five days, her 54-year-old father (DD) experienced acute myocardial infarction/sudden cardiac death (AMI/SCD). AA's 55-year-old mother, BB, was subsequently found to have combined hyperlipidemia as well, and after a period of grieving and stabilization, underwent cardiac evaluation demonstrating obstructive triple-vessel CAD requiring 2x percutaneous coronary intervention (PCI) with drug-eluting stents (DES). BB has combined hyperlipidemia and Lp(a)>2x ULN. AA's younger sister, CC, age 22, underwent evaluation and was found to have Lp(a)∼1.8x ULN, a normal lipid profile, and unremarkable coronary computed tomography angiogram (CTA).</p></div><div><h3>Results</h3><p>Case Presentation 2/2: All three underwent Allelica Inc. PRS, revealing 99th percentile, 91st percentile, and 64th percentile respective CAD risk. All three family members continue to be treated with pharmacotherapy and are doing well.</p></div><div><h3>Conclusions</h3><p>In this case, no monogenic variant was identified to explain AA's hyperlipidemia. PRS strongly correlated with the clinical phenotypes of the family members, helping to potentially explain the differential atherosclerotic burden between the two sisters. In this context, there is no urgency for intensive pharmacotherapy for the unaffected sister. PRS is a growing part of CV risk stratification, providing valuable insight in families with a substantial premature CAD burden. It represents an important complementary tool in risk stratification and can be used in conjunction with genetic testing for monogenic lipid disorders.</p></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"18 4","pages":"Pages e503-e504"},"PeriodicalIF":3.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141839715","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Leonid Khokhlov MD, Gehna Kishore MD, Godbless Ajenaghughrure MD, Kamal Shemisa MD, Sindhu Kishore MD
{"title":"Differences in Clinical outcomes between Non-Obese Hispanic and Asian populations Who have Hyperlipidemia","authors":"Leonid Khokhlov MD, Gehna Kishore MD, Godbless Ajenaghughrure MD, Kamal Shemisa MD, Sindhu Kishore MD","doi":"10.1016/j.jacl.2024.04.097","DOIUrl":"10.1016/j.jacl.2024.04.097","url":null,"abstract":"<div><h3>Background/Synopsis</h3><p>Hyperlipidemia (HLD) is a metabolic disease that is closely linked with ethnicity. There is limited data on its outcomes in different racial groups. Treating HLD will reduce the risk of atherosclerotic cardiovascular disease.</p></div><div><h3>Objective/Purpose</h3><p>The purpose of this study is to compare differences in clinical outcomes in non-obese Hispanic and Asian populations with HLD.</p></div><div><h3>Methods</h3><p>Conducted as an observational study, it utilized data from the National Inpatient Sample from 2017 to 2020 focusing on non-obese adults over 18 years, with a BMI <30 kg/m<sup>2</sup>, and HLD diagnosis, excluding those under 18, obese or without HLD. Primary outcome was in-hospital mortality. Secondary outcomes were cardiogenic shock, cardiac arrest, GIB, mechanical ventilation, LOS, and total cost. Multivariable logistic and Poisson regression analyses determined the clinical outcomes, considering a p-value <0.05 significant.</p></div><div><h3>Results</h3><p>Among 31,300,000 non-obese adults with HLD, 71.4% were Caucasians, 8.2% were Hispanics, 2.9% were Asians, and the remaining population belonged to other ethnicities. This study revealed higher rates in the Asians for conditions like anemia, DKA, HTN, pHTN, Afib, ACS, STEMI, AKI, stroke, and severe sepsis. Hispanics were seen to have a higher incidence of DM, HF, PVD, CKD, PE, and COPD. In terms of the primary outcome, Asians had more in-hospital mortality than the Hispanics but the results were not statistically significant. Asians were higher than the Hispanics in terms of the secondary outcomes in all aspects as seen in Table 1.</p></div><div><h3>Conclusions</h3><p>The findings undermine the importance of racial differences in such conditions and more in-depth studies are needed to extrapolate the gaps in care. Also, Asian population has been seen to have worse outcomes compared to all the major ethnical groups.</p></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"18 4","pages":"Pages e559-e560"},"PeriodicalIF":3.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141846584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Protein Calorie Malnutrition Effect on Clinical Outcomes And Resource Utilization in Patients Admitted with Acute Pancreatitis And Dyslipidemia","authors":"Mohamad Hijazi MD, Mhd Kutaiba Albuni MD, Bassel Bitar MD, Amin Eshghabadi MD, Fayaz Khan MD, Kamal Shemisa MD, Godbless Ajenaghughrure MD, M Kenan Rahima MD","doi":"10.1016/j.jacl.2024.04.058","DOIUrl":"10.1016/j.jacl.2024.04.058","url":null,"abstract":"<div><h3>Background/Synopsis</h3><p>Severe acute pancreatitis can cause a hypermetabolic state, leading to increased energy expenditure and nutrient requirements. This may contribute to protein-calorie malnutrition (PCM). Malnutrition, in turn, can affect lipid metabolism, potentially exacerbating dyslipidemia. Lipid abnormalities, including hypertriglyceridemia, may be observed during the acute phase of pancreatitis. Malnutrition is associated with various adverse effects on the body's ability to recover and respond to illness, and acute pancreatitis can further exacerbate these issues.</p></div><div><h3>Objective/Purpose</h3><p>Nevertheless, there is limited scientific evidence of clinical outcomes of PCM in patients with acute pancreatitis & dyslipidemia. Hence, we sought to investigate this population.</p></div><div><h3>Methods</h3><p>We queried National Inpatient Sample between 2017-2020 for adult patients who were hospitalized with acute pancreatitis & dyslipidemia who had PCM. The primary outcome was inpatient mortality. The secondary outcomes were cardiogenic shock, cardiac arrest, gastrointestinal bleeding (GIB), intubation, length of stay (LOS) and total hospital charge. Multivariable logistic regression analysis was used to estimate clinical outcomes. P-value < 0.05 was significant.</p></div><div><h3>Results</h3><p>There were 574,269 hospitalizations with acute pancreatitis & dyslipidemia where 31,955 (5.6%) had PCM. PCM and non-PCM cohorts were with mean age of 64 vs. 60 yrs; males 54.4% vs. 56%; Caucasians 66.8% vs. 64.6%; HTN 49% vs. 56%; HF 17.4% vs. 12%; severe sepsis 12.5% vs. 4.2%; PE 3.7% vs. 2.5%; DKA 3.9% vs. 4.9%; AF 16.6% vs. 11.3%; AKI 37.2% vs. 21.8%; acute respiratory failure 17.4% vs. 6.3%; ACS 4.4% vs. 3%; metabolic syndrome 3.7% vs. 9%; history of stroke 1.0% vs. 0.4%, COPD 18.7% vs. 13.3%; alcohol use 19.9% vs. 18.5%, respectively. NAFLD cohort had significantly higher mortality and worse clinical outcomes (Table 1).</p></div><div><h3>Conclusions</h3><p>PCM group demonstrated significantly higher mortality, worse clinical outcomes and resource utilization, however cardiac arrest and cardiogenic outcomes were not statistically significant. Patients were older, more female population and Caucasians, with more frequent HF, severe sepsis, AF, ACS and AKI. NAFLD is associated with greater risk for cardiovascular events, renal failure, GIB, and ICU care. PCM is an important predictor of adverse outcomes in population. Further research is necessary to describe long-term outcomes.</p></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"18 4","pages":"Pages e533-e534"},"PeriodicalIF":3.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141847200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chad Brands MD, Abuoma Ekpendu DO, Lanson Colaco MD, Muhammad Sohaib Asghar MBBS
{"title":"Trends in Age-Adjusted Cardiovascular Mortality Rates with Hyperlipidemia among the United States Population, from 1999–2023: A CDC Wonder Database Study","authors":"Chad Brands MD, Abuoma Ekpendu DO, Lanson Colaco MD, Muhammad Sohaib Asghar MBBS","doi":"10.1016/j.jacl.2024.04.055","DOIUrl":"10.1016/j.jacl.2024.04.055","url":null,"abstract":"<div><h3>Background/Synopsis</h3><p>Despite the progress made in managing hyperlipidemia in recent years, the mortality trends among the general population in the United States remain understudied. The lack of evidence in the demographic variations hampers the ability to implement evidence-based interventions on community-based levels. Our synthesis is to analyze the trends in hyperlipidemia-related mortality among United States residents by demographic characteristics such as age, gender, race or ethnicity, urbanization, and census region. Furthermore, state-wise age-adjusted mortality rates (AAMR) and county-wise data for highly prevalent states were subsequently analyzed.</p></div><div><h3>Objective/Purpose</h3><p>Prior studies have reported cardiovascular mortality rates in general, but they lack sufficiently updated data and trends among variable demographic groups suffering from hyperlipidemia. Furthermore, there haven't been any prior studies conducted to show specific correlations between mortality rates and certain geographically vulnerable areas.</p></div><div><h3>Methods</h3><p>We abstracted national mortality data from the multiple cause of death/underlying case of death files in the CDC WONDER database retrieved from death certificates nationwide. The ICD-10 codes (E78.0-E78.9) were used to identify any type of hyperlipidemia-related deaths (including familial hypercholesterolemia) among the United States population from 1999 to 2023 in the multiple causes of death section. While ICD codes for cardiovascular (circulatory) system were identified by using I00–I99 for the underlying cause of death as a sensitivity analysis to only measure cardiovascular-related mortality in the hyperlipidemic population. Trends in age-adjusted mortality rate (AAMR) were assessed using joinpoint regression analysis (version 5.0.2) and the data was reported per 100,000 population. For 10-year increment age groups, only crude mortality rates were reported. Results were expressed as annual percentage changes (APC), average annual percentage changes (AAPC), and 95% confidence intervals (CI). For urbanization, the 2013 NCHS Urban-Rural Classification Scheme for Counties was used.</p></div><div><h3>Results</h3><p>Between 1999 and 2023, a total of 639,786 hyperlipidemia patients died secondary to cardiovascular causes within the United States (AAMR = 7.1 per 100,000; 95% CI: 7.0–7.2). Overall mortality trends increased at an annual rate of 6.21% (95% CI: 5.41–7.01) and were much higher in females from 1999–2006 and then 2018–2023; however, in the male population, APC was evidently higher in 1999–2006 and 2018–2021, respectively. Specifically, the trends in crude mortality rate would increase with each age group in 10-year increments, with the most steep rises from 1999–2004 and then 2018 onwards (P<0.001). Hispanic race is least affected amongst all subgroups; however, both non-Hispanic whites and more recently non-Hispanic blacks were increasingly highly af","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"18 4","pages":"Pages e530-e532"},"PeriodicalIF":3.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141851404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tiffany Haynes MD, Nosagie Ohonba MBBS, Robert Fishberg MD, Matthew Proute MBBS
{"title":"Negative LDL-C levels with Detectable Apolipoprotein B: Surrogate Markers of Atherosclerotic Disease and Cardiac Event Risk","authors":"Tiffany Haynes MD, Nosagie Ohonba MBBS, Robert Fishberg MD, Matthew Proute MBBS","doi":"10.1016/j.jacl.2024.04.026","DOIUrl":"10.1016/j.jacl.2024.04.026","url":null,"abstract":"<div><h3>Background/Synopsis</h3><p>Serial LDL-C measurements remain the mainstay of targeted therapy for patients on lipid lowering therapy including statins, ezetimibe as well as PCSK9 inhibitors. However, Apolipoprotein (apo) B is the primary lipoprotein that serves as the transport medium for all atherogenic lipid particles: chylomicrons, VLDL, LDL, IDL and also lipoprotein(a). LDL-C is generally measured by way of calculation, however in settings of significantly elevated triglyceride levels or very low LDL-C levels, calculations become inaccurate thereby necessitating direct measurement in those instances.</p></div><div><h3>Objective/Purpose</h3><p>To demonstrate the importance of apo B levels in determining the risk of future cardiac events compared to LDL-C.</p></div><div><h3>Methods</h3><p>A 58-year-old male with severe mixed hyperlipidemia presented on fenofibrate and simvastatin. He had initial triglyceride (TG) levels >2000 mg/L, total cholesterol (TC) 300mg/dL, HDL 13 mg/dL with uncalculatable LDL levels. He had an elevated coronary artery calcium score (CAC) of 1600, with predominant disease in the LAD and RCA. Evolocumab was added to his medication regimen, along with icosapent ethyl. He underwent stress testing which subsequently led to cardiac catheterization revealing significant occlusions of the PLA and LCx requiring stent placement, as well as diseased right PDA and mid LAD.</p></div><div><h3>Results</h3><p>Four months after starting evolocumab and icosapent ethyl therapy, there was a significant decrease in TG levels to 1050, TC 139 mg/dL, LDL-C 28 mg/dL, apo B 47 mg/dL and Lp (a) <10nmol/L. Repeat testing five months later, showed continued improvements in his lipid levels with TG 305 mg/dL, TC 65 mg/dL, LDL-C 23 mg/dL and apo B 30 mg/dL.</p></div><div><h3>Conclusions</h3><p>Aggressive therapy with PCSK9 inhibitors and statins may lead to significant decreases in LDL-C, to undetectable or calculated negative levels. It is important to note however, that at elevated triglyceride levels usually exceeding 300 mg/dL, calculated LDL levels are grossly inaccurate, and will not serve as a reliable marker of atherosclerotic cardiovascular disease (ASCVD) risk. Sniderman et al. found apo B to be a more reliable marker of the risk of angiographic coronary lesions at any given level of LDL-C and thereby a greater indicator of the risk of future cardiac events. However, at levels less than 40 mg/dL, the risk of a cardiac event should be minimal.</p></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"18 4","pages":"Pages e501-e502"},"PeriodicalIF":3.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141853237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Serge Korjian MD, Yazan Daaboul MD, Gerald Chi MD, Ginger Jiang MD, Peter Libby MD, Deepak Bhatt MD, Matthew Reynolds MD, Roxana Mehran MD, Paul Ridker MD, Suzanne Baron MD, Frank Sacks MD, Paul Nara MD, Alka Shaunik MD, C. Michael Gibson MD, M. Cecilia Bahit MD
{"title":"†High Rates of Cardiovascular Events in Patients with Multivessel Disease in the First Year Post-Myocardial Infarction: A Systematic Literature Review","authors":"Serge Korjian MD, Yazan Daaboul MD, Gerald Chi MD, Ginger Jiang MD, Peter Libby MD, Deepak Bhatt MD, Matthew Reynolds MD, Roxana Mehran MD, Paul Ridker MD, Suzanne Baron MD, Frank Sacks MD, Paul Nara MD, Alka Shaunik MD, C. Michael Gibson MD, M. Cecilia Bahit MD","doi":"10.1016/j.jacl.2024.04.047","DOIUrl":"10.1016/j.jacl.2024.04.047","url":null,"abstract":"<div><h3>Study Funding</h3><p>This study was sponsored by CSL Behring and performed in collaboration with the Baim Institute.</p></div><div><h3>Background/Synopsis</h3><p>Patients who survive an acute myocardial infarction (AMI) are at a heightened risk of further major adverse cardiovascular events (MACE), particularly in the first few months following an AMI. Multivessel disease (MVD) is known to further exacerbate the risk of MACE. The elevated risk in this early post-AMI period is not addressed by current secondary preventative therapies.</p></div><div><h3>Objective/Purpose</h3><p>To evaluate the impact of MVD on clinical and patient-centered outcomes in the first year post-AMI, in the context of the current treatment landscape.</p></div><div><h3>Methods</h3><p>In this systematic literature review, relevant articles published between March 2019 and July 2022 were identified from MEDLINE, Embase, Cochrane databases, and cardiovascular (CV) and health outcomes conferences. Articles reporting on pre-specified clinical or patient-centered outcomes in post-AMI patients with MVD at timepoints within 1 year were eligible for inclusion. Studies that included patients with AMI and cardiogenic shock were excluded from this review.</p></div><div><h3>Results</h3><p>Clinical outcomes were reported in five randomized-controlled trials (RCTs) and 25 observational studies across 32 articles. Patient-centered outcomes were reported in one RCT across two articles. The definition of MVD varied across the studies; however, it was typically characterized by ≥50% stenosis in ≥1 non-infarct-related coronary artery. Of the individual MACE endpoints extracted for this review (all-cause mortality, CV mortality, AMI, stroke), all-cause mortality and AMI were most frequently reported. Although rates of individual MACE endpoints were variable (Table), likely due to heterogeneity in study populations and interventions, a trend was identified; MACE rates at 1-year post-AMI were typically not substantially higher than those reported at earlier timepoints. EQ-5D scores, indicative of quality of life (QoL), increased marginally from baseline to 1 year following treatment, indicating minimal improvements in QoL. Nevertheless, EQ-5D was only reported in one RCT.</p></div><div><h3>Conclusions</h3><p>MVD is associated with high rates of MACE early after AMI that persist at 1 year. Novel therapies that address CV risk in the early period post-AMI may support improved CV outcomes among patients with MVD. Further data on patient-centered outcomes are warranted to determine the impact of post-AMI treatment options on QoL.</p></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"18 4","pages":"Page e518"},"PeriodicalIF":3.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141853631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stephen Eason MBA, Frances Compton MD, Merlyn Sayers MB ChB, Amit Khera MD, Zahid Ahmad MD, Caroline Abe MD
{"title":"†A Pilot Study of Triglyceride Screening in Blood Donors","authors":"Stephen Eason MBA, Frances Compton MD, Merlyn Sayers MB ChB, Amit Khera MD, Zahid Ahmad MD, Caroline Abe MD","doi":"10.1016/j.jacl.2024.04.056","DOIUrl":"10.1016/j.jacl.2024.04.056","url":null,"abstract":"<div><h3>Study Funding</h3><p>Ionis Young Investigators Award.</p></div><div><h3>Background/Synopsis</h3><p>Few attempts at community-based screening have been made for triglyceride levels, which has the potential to identify individuals at risk for cardiovascular disease as well as acute hypertriglyceridemic pancreatitis. One opportunity for such screening is among blood donors.</p></div><div><h3>Objective/Purpose</h3><p>Demonstrate feasibility of measuring non-fasting triglyceride level in blood donors.</p></div><div><h3>Methods</h3><p>We prospectively measured non-fasting triglyceride levels (Beckman Coulter assay, California) among volunteer blood donors at Carter BloodCare North Texas over 3 weeks from December 2023 to January 2024. Donor self-reported demographic data included age, gender, ethnicity/race and BMI. Blood pressure and total cholesterol level were checked per routine protocol at Carter BloodCare. Per the 2021 ACC expert consensus on management of hypertriglyceridemia, non-fasting triglyceride levels were stratified into normal <175 mg/dL, moderate 175-499 mg/dL, and severe >500 mg/dL hypertriglyceridemia. Results reported as median (IQR).</p></div><div><h3>Results</h3><p>10,175 unique blood donors had a triglyceride level measured [35.2% female, age 53 years (42-62), BMI 29.4 (26-33), 71.6% White]. Additionally, 98 individuals donated multiple times [first triglyceride 141 mg/dL (99-198), second triglyceride 142 mg/dL (103-205), interpersonal absolute change in triglyceride +/- 39.5 mg/dL (17-86)]. Among unique donors, triglyceride levels ranged from 23-2342 mg/dL (median 154 mg/dL, mean 185 mg/dL). Of note, 7 donors had triglycerides >1000 mg/dL (min 1051- max 2342). Overall, 58.4% had normal triglycerides [triglyceride 111 mg/dL (84-140), 41.6% female, age 52 years (40-62), BMI 28.4 (25-32), 71.7% White; 16.9% elevated blood pressure, total cholesterol 169 mg/dL (146-193)]; 39.2% had moderate hypertriglyceridemia [triglyceride 243 mg/dL (204-309), 26.8% female, age 53 years (43-61), BMI 30.5 (27.4-34.2), 71.8% White, 21.9% elevated blood pressure, total cholesterol 181 mg/dL (156-206)]; 2.4% severe hypertriglyceridemia [triglyceride 582 (539-705), 17% female, age 52 years (44-59), BMI 30.9 (28-35), 67.5% White, 27.6% elevated blood pressure, total cholesterol 209 mg/dL (178-235)]. Triglyceride levels were associated with male gender (p < 0.001), high blood pressure (p < 0.001), high cholesterol (p < 0.001), and Hispanic ethnicity (p<0.001).</p></div><div><h3>Conclusions</h3><p>Our pilot study demonstrates the feasibility of non-fasting community-based screening for hypertriglyceridemia among volunteer blood donors. Such efforts can rapidly screen triglycerides in many individuals. Furthermore, such screening has the potential to identify individuals at risk for cardiovascular disease (moderate hypertriglyceridemia) and acute pancreatitis (severe hypertriglyceridemia). Future efforts will explore donors’ u","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"18 4","pages":"Page e532"},"PeriodicalIF":3.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141853643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effect of statin use on liver enzymes and lipid profile in patients with non-alcoholic fatty liver disease (NAFLD)","authors":"","doi":"10.1016/j.jacl.2024.03.003","DOIUrl":"10.1016/j.jacl.2024.03.003","url":null,"abstract":"<div><h3>BACKGROUND</h3><p>Non-alcoholic fatty liver disease (NAFLD) is an independent risk factor for cardiovascular disease (CVD). Statins are recommended for treatment of dyslipidemia to reduce the overall cardiovascular risk in patients with NAFLD. However, statin treatment was underutilized and the effect of statins on liver enzymes remained unclear in this patient population.</p></div><div><h3>OBJECTIVES</h3><p>This study aimed to provide real-world evidence of the safety and effect of statin use in patients with NAFLD.</p></div><div><h3>METHODS</h3><p>We conducted a cross-sectional survey study of adults with NAFLD using pooled data from the US NHANES database 2009–2018. NAFLD was defined by Fatty Liver Index (FLI) ≥ 60 and United States Fatty Liver Index (USFLI) ≥ 30. Multivariate regression analyses adjusted for baseline clinical and demographic characteristics were performed to compare the liver enzymes and lipid profile between statin and non-statin users.</p></div><div><h3>RESULTS</h3><p>The study included 2,533 adults with NAFLD, representing 22.6 million individuals in the US, with 27% receiving statin treatment between 2009 and 2018. The mean differences of liver enzymes for AST, ALT, ALP, and GGT between statin and non-statin users were -0.86 (p=0.539), -3.49 (p=0.042), -0.25 (p=0.913), and 0.57 (p=0.901), respectively. In individuals with NAFLD and dyslipidemia, total cholesterol and LDL levels were significantly lower in statin users compared to non-statin users (mean difference, -28.9; p<0.001 and -27.7; p<0.001).</p></div><div><h3>CONCLUSION</h3><p>The use of statins was not associated with elevated liver enzymes in patients with NAFLD. Significantly lower levels of ALT, total cholesterol, and LDL were observed in statin users compared to non-statin users.</p></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"18 4","pages":"Pages e501-e508"},"PeriodicalIF":3.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1933287424000357/pdfft?md5=58c0893f7293309aa8318154d95f1087&pid=1-s2.0-S1933287424000357-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140203459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The role of genetically-influenced phospholipid transfer protein activity in lipoprotein metabolism and coronary artery disease","authors":"","doi":"10.1016/j.jacl.2024.03.007","DOIUrl":"10.1016/j.jacl.2024.03.007","url":null,"abstract":"<div><h3>BACKGROUND</h3><p>Phospholipid transfer protein (PLTP) transfers surface phospholipids between lipoproteins and as such plays a role in lipoprotein metabolism, but with unclear effects on coronary artery disease (CAD) risk. We aimed to investigate the associations of genetically-influenced PLTP activity with 1-H nuclear magnetic resonance (<sup>1</sup>H-NMR) metabolomic measures and with CAD. Furthermore, using factorial Mendelian randomization (MR), we examined the potential additional effect of genetically-influenced PLTP activity on CAD risk on top of genetically-influenced low-density lipoprotein-cholesterol (LDL-C) lowering.</p></div><div><h3>METHODS</h3><p>Using data from UK Biobank, genetic scores for PLTP activity and LDL-C were calculated and dichotomised based on the median, generating four groups with combinations of high/low PLTP activity and high/low LDL-C levels for the factorial MR. Linear and logistic regressions were performed on 168 metabolomic measures (<em>N</em> = 58,514) and CAD (<em>N</em> = 318,734, N-cases=37,552), respectively, with results expressed as <em>β</em> coefficients (in standard deviation units) or odds ratios (ORs) and 95% confidence interval (CI).</p></div><div><h3>RESULTS</h3><p>Irrespective of the genetically-influenced LDL-C, genetically-influenced low PLTP activity was associated with a higher high-density lipoprotein (HDL) particle concentration (<em>β</em> [95% CI]: 0.03 [0.01, 0.05]), smaller HDL size (-0.14 [-0.15, -0.12]) and higher triglyceride (TG) concentration (0.04 [0.02, 0.05]), but not with CAD (OR 0.99 [0.97, 1.02]). In factorial MR analyses, genetically-influenced low PLTP activity and genetically-influenced low LDL-C had independent associations with metabolomic measures, and genetically-influenced low PLTP activity did not show an additional effect on CAD risk.</p></div><div><h3>CONCLUSIONS</h3><p>Low PLTP activity associates with higher HDL particle concentration, smaller HDL particle size and higher TG concentration, but no association with CAD risk was observed.</p></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"18 4","pages":"Pages e579-e587"},"PeriodicalIF":3.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1933287424000436/pdfft?md5=b171e8f09e2e29fe1ddb0b0aec5ec584&pid=1-s2.0-S1933287424000436-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140404578","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Coronary Artery Disease in Familial Hypoalphalipoproteinemia: A Case Report","authors":"Sumer Moussa MD","doi":"10.1016/j.jacl.2024.04.030","DOIUrl":"10.1016/j.jacl.2024.04.030","url":null,"abstract":"<div><h3>Background/Synopsis</h3><p>A 37-year-old Caucasian female was referred for cardiology evaluation of dyslipidemia. Her past medical history included mitral valve prolapse, Gilbert syndrome, hypertension, and aortic atherosclerosis. The patient was physically active with no history of smoking, diabetes, or other cardiovascular risk factors. Family history was notable for low HDL-C levels in the patient's father and sister, with no known premature CAD. Physical examination revealed BMI of 21, well controlled blood pressure, and normal cardiovascular exam.</p><p>Initial lipid panel revealed total cholesterol (TC) 47 mg/dL, HDL-C 5 mg/dL, LDL-C 24 mg/dL, triglycerides 80 mg/dL, and VLDL 18 mg/dL. Further laboratory testing showed apolipoprotein B of 52 mg/dL, normal lipoprotein (a), and normal high-sensitivity CRP. Liver function tests, complete blood count, thyroid function tests, total serum protein, and basic metabolic profile were also normal. Genetic testing showed 2 variants of undetermined significance to the ABCA1 gene [ABCA1 c.2879T>C (p.Leu960Pro); ABCA1 c.3626C>T (p.Pro1209Leu)].</p></div><div><h3>Objective/Purpose</h3><p>N/A</p></div><div><h3>Methods</h3><p>N/A</p></div><div><h3>Results</h3><p>A coronary artery computed tomography (CTCA) demonstrated borderline obstructive areas of eccentric calcified plaque in the mid to distal left anterior descending (LAD) artery with 40-50% luminal diameter narrowing, nonobstructive eccentric calcified plaque in the proximal left circumflex (LCX) artery with less than 40% luminal diameter narrowing, and obstructive plaque in the mid right coronary artery (RCA) with greater than 50% luminal diameter narrowing, with whole-heart Agatston score of 981. A CT coronary angiography scan with fractional flow reserve (FFR) revealed a modeled stenosis in the mid RCA that demonstrated normal FFR measurement of 0.81, although was significant for abrupt relative change (.18) across the lesion. Invasive coronary angiography revealed nonobstructive coronary artery disease, demonstrating mid RCA 50% stenosis, mid LAD 40% stenosis, and ostial LCX 30% stenosis. The patient was initiated on statin and aspirin therapy. A fasting lipid profile at 2-month interval showed TC 26 mg/dL, LDL-C 5 mg/dL, and HDL-C remaining at 5 mg/dL.</p></div><div><h3>Conclusions</h3><p>Given ABCA1 gene variants, with absence of phenotypic findings of Tangier disease, the patient was presumed to have familial hypoalphalipoproteinemia. The inverse relationship between low HDL-C levels and cardiovascular risk has been well documented in population based observational studies. However, clinical trials have failed to show clinical benefit of therapy targeting increasing HDL-C levels. Further studies are needed to determine optimal medical therapy aimed at prevention of CAD in this population which may be genetically predisposed to higher risk of early coronary disease.</p></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"18 4","pages":"Page e504"},"PeriodicalIF":3.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141841351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}