Journal of clinical lipidology最新文献

{"title":"Double heterozygosity for variants in ABCG8 and ABCG5 and potential association with sitosterolemia","authors":"Mauricio De Castro MD,&nbsp;Sidney Brown BS","doi":"10.1016/j.jacl.2025.04.097","DOIUrl":"10.1016/j.jacl.2025.04.097","url":null,"abstract":"<div><h3>Background/Synopsis</h3><div>Sitosterolemia is a rare autosomal recessive lipid disorder caused by pathogenic variants in the ABCG5 and/or ABCG8 genes. These genes encode ATP-binding cassette transporters responsible for the regulation of sterol absorption and excretion. Sitosterolemia leads to the accumulation of plant sterols in the blood, resulting in hypercholesterolemia, xanthomas, premature atherosclerosis, and other complications. We present the case of an individual with abnormal plant sterol levels and heterozygous variants in both genes. This case supports nascent evidence that double heterozygosity in ABCG5 and ABCG8 could lead to sitosterolemia.</div></div><div><h3>Objective/Purpose</h3><div>Very few cases of double heterozygosity in ABCG5 and ABCG8 leading to sitosterolemia have been reported in the literature. This case adds to the growing body of evidence supporting this association.</div></div><div><h3>Methods</h3><div>Comprehensive cholesterol balance panel including plant sterols was performed through a commercial laboratory (Boston Heart Diagnostics). Genetic testing was performed through a direct-to-consumer (DTC) testing platform and results validated through a CLIA-approved laboratory. The effectiveness of interventions was assessed through biochemical markers and clinical assessment.</div></div><div><h3>Results</h3><div>A 24-year-old female with syncope episodes and gastrointestinal symptoms underwent comprehensive testing including a cholesterol panel that showed elevated low-density lipoprotein (125 mg/dL) and considerably elevated plant sterol levels (Beta-sitosterol 244 µmol x 100/mmol and Campesterol 345 µmol x 100/mmol) suggestive of sitosterolemia. Genetic testing identified a pathogenic heterozygous variant in the ABCG8 gene (rs137852987 G&gt;A), as well as a heterozygous variant of uncertain significance in the ABCG5 gene (rs778605187 G&gt;C). Based on laboratory results and clinical findings, the patient received a presumptive diagnosis of sitosterolemia. Dietary changes and ezetimibe therapy resulted in significant symptom improvement, reduction in LDL levels, and normalization of plant sterol levels.</div></div><div><h3>Conclusions</h3><div>This case underscores the need for further research into the clinical impact of heterozygous and VUS mutations in ABCG5/ABCG8. It highlights the importance of personalized dietary and pharmacologic interventions in managing sitosterolemia-like presentations. The findings have implications for the evaluation and management of patients with rare genetic disorders, particularly those involving sterol metabolism.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Page e69"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144167953","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":"Coronary artery disease in a zero calcium score patient: questioning the reliability of CAC in high-risk individuals","authors":"Nosagie Ohonba MBBS,&nbsp;Tanay Modi MBBS,&nbsp;Paige Seepaulsingh MBBS,&nbsp;Tiffany Haynes MD,&nbsp;Robert Fishberg MD,&nbsp;Marlin Mousa MB ChB","doi":"10.1016/j.jacl.2025.04.048","DOIUrl":"10.1016/j.jacl.2025.04.048","url":null,"abstract":"<div><h3>Background/Synopsis</h3><div>Coronary calcium score (CAC) is a non-invasive test that measures calcified plaque in the coronary arteries. It is often used to improve risk assessment in patients with a borderline 10-year ASCVD risk (5-7.5%) or with a strong family history of ASCVD. A CAC score of 0 has a high negative predictive value (95%-99%) and is reassuring. While CAC detects calcified plaques, it cannot identify non-calcified, potentially unstable plaques, which could contribute to acute coronary syndromes. This limitation is important in patients who are symptomatic despite a zero score.</div></div><div><h3>Objective/Purpose</h3><div>To evaluate the predictability of CAC in risk assessment of CAD in patients with high clinical risk.</div></div><div><h3>Methods</h3><div>A 47-year-old female with a history of hypertension, preeclampsia, and antiphospholipid syndrome presented with intermittent chest pain for weeks. Her echocardiogram and Holter monitoring were negative for CAD. She had no history of venous thromboembolism or smoking, but has a family history of SCAD, CABG, MI, and CVA. Initial ECG, troponin, and CAC score (0) were normal. LDL was 81, triglycerides 160, and ASCVD risk 0.8%. No further diagnostic test was pursued. However, she subsequently developed typical chest pain. ECG showed anterolateral STEMI, though troponins remained negative.</div></div><div><h3>Results</h3><div>PCI with left heart catheterization was done and showed non calcified plaque in proximal LAD with an 80% stenosis. A drug eluting stent was inserted, and she was treated with dual antiplatelet therapy and high intensity statins.</div></div><div><h3>Conclusions</h3><div>This case highlights the limitations of over-relying on CAC for risk assessment. While a CAC=0 has a high predictive value (95-99%) for obstructive CAD, the “power of zero” applies to asymptomatic patients and does not reliably exclude CAD risk in symptomatic younger patients.</div><div>Complementary functional tests could have helped make the correct diagnosis such as cardiac stress test, with sensitivity and specificity of 68% and 77% or Sestamibi Scintigraphy with a sensitivity and specificity of 92% and 68%. Coronary Computed Tomography Angiography (CCTA) with a sensitivity of 96% and NPV of 99% for excluding severe (≥ 70%) coronary stenosis could have been considered. This case highlights the importance of applying the correct diagnostic test when evaluating patients with chest pain. This is particularly important in women who are less likely to have coronary calcification and often have a lower calculated ASCVD risk score.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Page e35"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144168311","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":"Lipid-lowering intensification post-ACS in very high-risk patients on high-intensity statins: Insights from a mayo clinic registry","authors":"Danielle Sparenga DNP,&nbsp;Regis Fernandes MD,&nbsp;Winston Wang MD","doi":"10.1016/j.jacl.2025.04.019","DOIUrl":"10.1016/j.jacl.2025.04.019","url":null,"abstract":"<div><h3>Background/Synopsis</h3><div>After experiencing acute coronary syndrome (ACS), particularly in very high-risk (VHR) patients, current guidelines recommend a 50% reduction in low-density lipoprotein (LDL) levels, aiming for an LDL target below 55 mg/dL. We hypothesize that a significant number of VHR patients who present with ACS and are already on high-intensity statins (HIS) do not have their lipid-lowering therapy (LLT) intensified. This leads to an underutilization of non-statin therapies that could help achieve these LDL goals.</div></div><div><h3>Objective/Purpose</h3><div>To quantify the practice gap in intensifying LLT for patients who present with acute coronary syndrome while already on high-intensity statins.</div></div><div><h3>Methods</h3><div>We reviewed all patients from January 2019 to August 2024 who underwent percutaneous coronary intervention (PCI) for ACS at Mayo Clinic Arizona and were already on HIS. Ninety-one patients met these criteria, and of these, 45 were followed at Mayo Clinic and had repeat lipid panels drawn between 2 and 12 months after the ACS event. A one-tailed, two-sample t-test was used to determine statistical significance.</div></div><div><h3>Results</h3><div>Out of the 91 patients presenting with ACS already on HIS, 59 (64.8%) maintained the same LLT. Among these patients, 65 (71.4%) met the American College of Cardiology (ACC) criteria for VHR, but 22 of these (66.2%) did not have their therapy intensified. Notably, 37 patients (45.7%) had already achieved their LDL target upon presentation, with a median LDL of 60 mg/dL (54 mg/dL for VHR). The mean change in LDL for the group that had their LLT increased was -15.1% (standard deviation = 33.3%), while the mean change for the unchanged therapy group was significantly higher at +14.6% (standard deviation = 65.4%) (p = 0.0455).</div></div><div><h3>Conclusions</h3><div>Our analysis highlights a significant gap between best practices and the actual intensification of LLT in VHR patients on HIS following ACS. Approximately 66% of these patients did not have their LLT adjusted. Additionally, 45% of patients on HIS had already achieved their LDL target upon presentation. Adjunctive therapies such as ezetimibe and PCSK9 inhibitors were underutilized in the acute care setting. There is a pressing need for further initiatives to improve LDL control in this high-risk population. We hope our study will encourage the initiation of non-statin therapies during hospitalization, promote the establishment of educational programs for physicians, and lead to the implementation of automated prompts in electronic medical records when appropriate.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Pages e13-e14"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144168317","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":"Outcomes of percutaneous coronary intervention among patients with metabolic dysfunction-associated steatotic liver disease: A nationwide study","authors":"Derek Ugwendum MD,&nbsp;Aseed Mestarihi MD,&nbsp;Oluwatoyosi Awotorebo MD,&nbsp;Ikponmwosa Ogieuhi MD,&nbsp;Karldon Nwaezeapu MD,&nbsp;Godbless Ajenaghughrure MD,&nbsp;Anuoluwa Oyetoran MD,&nbsp;Kayode Ogunniyi MBBS","doi":"10.1016/j.jacl.2025.04.084","DOIUrl":"10.1016/j.jacl.2025.04.084","url":null,"abstract":"<div><h3>Background/Synopsis</h3><div>Metabolic dysfunction-assoc-iated steatotic liver disease (MASLD) is increasingly recognized as a multisystemic disorder and an independent risk factor for cardiovascular disease. Although MASLD has been implicated in worsened atherosclerosis, its direct impact on percutaneous coronary intervention (PCI) outcomes remains uncertain.</div></div><div><h3>Objective/Purpose</h3><div>To evaluate whether MASLD (in the absence of cirrhosis, alcohol use disorder, or alcoholic fatty liver) affects in-hospital outcomes among patients undergoing PCI.</div></div><div><h3>Methods</h3><div>Using data from the 2021 National Inpatient Sample, we identified patients who underwent PCI and classified them based on MASLD status, as determined by the International Classification of Diseases codes (ICD-10 codes). We excluded patients with co-existing alcohol use disorder, alcoholic fatty liver disease, or cirrhosis. Outcomes of interest were in-hospital mortality, vasopressor requirements, length of hospital stay, and total hospital charges. Multivariate logistic regression models, adjusted for age, sex, and Charlson comorbidity index, were used to assess the association between MASLD and these outcomes.</div></div><div><h3>Results</h3><div>A total of 314,505 patients underwent PCI, of whom 4,320 (1.4%) had MASLD. These patients were younger (median age 61 vs. 66 years; p &lt; 0.001) but had a higher comorbidity burden (Charlson comorbidity index of 3.9 vs. 2.8; p &lt; 0.001), with no significant difference in gender distribution. In unadjusted analyses, there were no differences in in-hospital mortality (p = 0.725) or vasopressor requirement (p = 0.376). Patients with MASLD experienced a slightly longer hospital stay (additional 0.47 days; p = 0.02) and higher total charges (+8,496 USD; p = 0.039). After adjustment for confounders, MASLD was not associated with increased in-hospital mortality (p = 0.634), vasopressor requirement (p = 0.234), length of stay (p = 0.102), or total hospital charges (p = 0.514).</div></div><div><h3>Conclusions</h3><div>In this nationwide cohort, MASLD was not independently associated with adverse in-hospital outcomes following PCI. Despite having a higher comorbidity burden, patients with MASLD did not experience increased in-hospital mortality or need for vasopressors. Further research is warranted to explore the long-term implications of MASLD on PCI outcomes</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Pages e61-e62"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144168319","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":"Attrition of adipose: Type 2 familial partial lipodystrophy manifesting in severe premature CAD","authors":"Ranvir Bhatia MD,&nbsp;Daniel Soffer MD,&nbsp;Michael Karamardian BS","doi":"10.1016/j.jacl.2025.04.050","DOIUrl":"10.1016/j.jacl.2025.04.050","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background/Synopsis&lt;/h3&gt;&lt;div&gt;Lipodystrophy constitutes a heterogeneous group of rare acquired or inherited conditions characterized by adipose tissue deficiency, typically manifesting in hypertriglyceridemia, insulin resistance, hyperglycemia, and fatty liver. Type 2 Familial Partial Lipodystrophy (FPLD2), also known as Dunnigan variant, is an autosomal dominant disorder with onset around puberty characterized by absence of adiposity in limbs and trunk with increased face and neck fat deposition, sometimes associated with skeletal muscle hypertrophy and phlebomegaly. Here, we describe a patient with history of severe hypertriglyceridemia (HTG) and type 1 diabetes (T1DM) who developed premature multivessel coronary artery disease (CAD) and ischemic cardiomyopathy, ultimately diagnosed with FPLD2.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Objective/Purpose&lt;/h3&gt;&lt;div&gt;Not applicable to this case study abstract submission.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;Case study.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;LD is a 41-year-old female with newly diagnosed ischemic cardiomyopathy (EF 38%), triple-vessel CAD status-post drug-eluting stent to mid-LAD, severe HTG complicated by recurrent acute pancreatitis, and T1DM. Since childhood, LD reported insatiable appetite despite a thin, muscular frame disproportionate to normal activity. At 19, she was diagnosed simultaneously with T1DM, acute pancreatitis, and severe HTG. Family history was notable for a maternal aunt with similar body morphology and metabolic disease. At evaluation, her only complaint was persistent hunger, though less intense than during early adulthood. Hgb A1C was 7.0% on a continuous insulin pump at 1U/hr requiring minimal bolus dosing for meals. Physical exam was notable for absence of abdominal adiposity below the upper chest with sparing of the head and neck, muscular calf muscles, and prominent peripheral veins, consistent with FPLD2. Figure 1 reports lipid panel on high-intensity statin. She had normal serum creatinine, transaminase levels, thyroid stimulating hormone, and urine albumin-creatinine ratio. She was prescribed icosapent ethyl and introduced to a lipodystrophy patient advocacy group. Fasting leptin and genetic testing were ordered, but not completed.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;Lipodystrophy is a clinical diagnosis based on physical exam, family and personal history, and metabolic features of insulin resistance and may be supported by genetic testing. Based on LD's adipose distribution, dyslipidemia, and family history, FPLD2 was diagnosed. Initial management involves targeting insulin resistance and treatment of comorbid sequelae. Metreleptin (recombinant leptin analog) is approved for severe generalized lipodystrophy and under investigation for partial lipodystrophy, while a similar leptin receptor agonist trial was terminated. LD expressed gratitude that knowing her diagnosis and connecting with others made her feel less alone and more supported. This case highlights the","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Pages e36-e37"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144168730","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":"Hypercholesterolemia management in a patient with mitochondrial encephalomyopathy lactic acidosis, and stroke-like episodes","authors":"Susan Halli Demeter APRN,&nbsp;Karen Drechsel APRN,&nbsp;Gretchen Anderson APRN","doi":"10.1016/j.jacl.2025.04.056","DOIUrl":"10.1016/j.jacl.2025.04.056","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background/Synopsis&lt;/h3&gt;&lt;div&gt;Mitochondrial encephalomyopathy lactic acidosis and stroke-like episodes (MELAS) is a rare, genetic neurodegenerative disorder caused by mutations in mitochondrial DNA (mtDNA) or nuclear DNA (nDNA) Belal et al. (2022), Chakrabarty et al. (2021), and Cheng et al. (2022). MELAS can present with a wide range of symptoms, including stroke-like episodes, lactic acidosis, and multi-organ involvement. Statins are contraindicated in MELAS due to potentially exacerbating mitochondrial dysfunction via Coenzyme Q10 (CoQ10) depletion. Non-statin lipid lowering therapies in MELAS patients have appeared favorable.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Objective/Purpose&lt;/h3&gt;&lt;div&gt;To highlight the challenges in hypercholesterolemia management with existing mitochondrial disorders and the potential of non-statin options.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;Statins inhibit CoA reductase activity, which also affects the synthetic pathway of CoQ10 (Argov, 2024). CoQ10 is a component of normal mitochondrial function, and low levels of CoQ10 in muscle tissue have been found in statin associated myopathy (Lamperti et al., 2005). Two reported case studies describe a MELAS-like clinical syndrome that occurred after several months of statin therapy (Chariot et al., 1993; Tsivgoulis et al., 2006). Both developed rhabdomyolysis with elevated CK (20,000 U/L and 45,000-48,000 U/L, respectively). No mitochondrial DNA mutation was identified, yet the statin unmasked a subclinical mitochondrial muscle disease.&lt;/div&gt;&lt;div&gt;Research on use of non-statin therapies (ezetimibe and PCSK9 inhibitors) in patients with MELAS or mitochondrial disorders is limited. However, one case study in a patient with mitochondrial myopathy due to heteroplasmic mitochondrial DNA missence mutation in MTCO1 gene (m.7671T&gt;A) demonstrated stable CK levels without recurrence of myalgia while taking alirocumab 75 mg every 2 weeks, ezetimibe 10 mg daily, marine omega 3 fatty acids daily, and 145 mg of micronized fenofibrate every 2 days (Cicero et al., 2020).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;A 48-year-old male presented with MELAS due to a mitochondrial mutation. He had a history of hypercholesterolemia with debilitating myalgias on simvastatin, atorvastatin and rosuvastatin prior to MELAS diagnosis. His baseline total cholesterol was 248 mg/dL, HDL 38 mg/dL, LDL-C 254 mg/dL, triglycerides 278 mg/dL, and non-HDL 310 mg/dL. Ezetimibe 10 mg daily and icosapent ethyl 4 g daily was initiated and well tolerated. His total cholesterol improved to 221 mg/dL, HDL 37 mg/dL, LDL-C 155 mg/dL, triglycerides 146 mg/dL, non-HDL 184 mg/dL. Evolocumab 140 mg subcutaneous every 14 days was prescribed and tolerated without side effects. His cholesterol further improved to 108 mg/dL, HDL 38 mg/dL, LDL-C 43 mg/dL, triglycerides 162 mg/dL, and non-HDL 70 mg/dL. AST and ALT remained normal throughout treatment.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;This case highlights consideration for MELAS in young ","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Pages e41-e42"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144168784","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":"Comparative cardiovascular outcomes of statin monotherapy versus statin plus ezetimibe combination therapy in patients with atherosclerotic cardiovasc","authors":"M Kenan Rahima MD,&nbsp;Fernando Faxas MD,&nbsp;Kayode Oguniyi MD,&nbsp;Muayad Alzamara MD,&nbsp;Godbless Ajenaghughrure MD","doi":"10.1016/j.jacl.2025.04.024","DOIUrl":"10.1016/j.jacl.2025.04.024","url":null,"abstract":"<div><h3>Background/Synopsis</h3><div>The optimal lipid-lowering strategy for patients with atherosclerotic cardiovascular disease (ASCVD) remains debated. While statins are the cornerstone of therapy, the additional benefit of ezetimibe in real-world settings needs further investigation.</div></div><div><h3>Objective/Purpose</h3><div>To compare the clinical outcomes of patients with atherosclerotic cardiovascular disease (ASCVD) who were treated with statin monotherapy versus those treated with statin plus ezetimibe combination therapy in a real-world setting.</div></div><div><h3>Methods</h3><div>Using the TriNetX global federated health research network comprising 104 healthcare organizations, we conducted a retrospective cohort study comparing patients on statin monotherapy (n=119,338) versus statin plus ezetimibe (n=119,338) after propensity score matching. All patients had established ASCVD and LDL-C ≥ 70 mg/dL. The primary outcomes included death, cardiovascular events, and neurological outcomes over a 5-year follow-up period.</div></div><div><h3>Results</h3><div>After propensity score matching, baseline characteristics including hypertension (85.4% vs 85.3%), diabetes (46.3% vs 46.3%), and prior myocardial infarction (29.8% vs 29.6%) were well-balanced between groups. The statin plus ezetimibe group showed significantly lower risk across multiple outcomes compared to statin monotherapy: all-cause mortality (HR 1.445, 95% CI 1.412-1.480), dementia (HR 1.498, 95% CI 1.447-1.550), cardiac arrest (HR 1.332, 95% CI 1.263-1.404), and stroke (HR 1.253, 95% CI 1.202-1.306). More modest risk reductions were observed for atrial fibrillation (HR 1.132, 95% CI 1.110-1.154) and heart failure (HR 1.075, 95% CI 1.059-1.091), while ventricular tachycardia showed no significant difference between groups (HR 1.035, 95% CI 0.999-1.072).</div></div><div><h3>Conclusions</h3><div>In this large real-world study of ASCVD patients, combination therapy with statin plus ezetimibe was associated with significantly lower risks of mortality and major cardiovascular outcomes compared to statin monotherapy. These findings support the increased use of combination therapy in high-risk patients with ASCVD</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Page e17"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144166976","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":"Physician-reported reasons for not intensifying lipid-lowering therapy in patients with recent myocardial infarction","authors":"Benjamin Richter MD,&nbsp;Scott Hessen MD,&nbsp;Laney Jones PharmD,&nbsp;Dean Karalis MD","doi":"10.1016/j.jacl.2025.04.005","DOIUrl":"10.1016/j.jacl.2025.04.005","url":null,"abstract":"<div><h3>Funding</h3><div>This study was funded by Amgen.</div></div><div><h3>Background/Synopsis</h3><div>Clinical practice evidence indicates that patients with high risk of a secondary event after a recent myocardial infarction (MI) often do not receive guideline-recommended lipid-lowering therapy (LLT), leaving them at unnecessary cardiovascular risk. We implemented a quality initiative to evaluate and improve LLT prescribing according to the 2018 AHA/ACC/Multisociety guidelines that recommend LDL-C lower than 70 mg/dL for patients with very high ASCVD risk.</div></div><div><h3>Objective/Purpose</h3><div>This study assessed the reasons cardiologists selected for not following AHA/ACC/Multisociety LLT guidelines for patients with recent MI when alerted to best practice recommendations at the point of care.</div></div><div><h3>Methods</h3><div>From August 2020 to February 2021, our practice group (96 cardiologists, 35 locations) implemented a ‘hard stop’ best practice alert in the electronic health records (EHR) of patients with MI history within 12 months and elevated LDL-C (70 mg/dL or greater) or no LDL-C values within 6 months of the index visit. If the patient had no LDL-C within 6 months, clinicians were prompted to order an LDL-C test and schedule a follow-up visit. If LDL-C was current and elevated, clinicians received stepwise prompts to prescribe guideline-recommended LLT (high-intensity statin, ezetimibe, and PCSK9i) or provide a reason for not doing so. Reasons for not intensifying LLT were summarized by the type of intensification recommended.</div></div><div><h3>Results</h3><div>In 42% (244/587) of patients for whom the best practice alert was triggered, treatment was not intensified. In 53/244 (22%) of these patients, treatment was not intensified because the LDL-C was not current, and the physician was prompted to order an LDL-C test. LLT intensification was not followed in 86 patients when high-intensity statin was recommended, 16 patients when ezetimibe was recommended, and 142 patients when PCSK9i was recommended. The most common reasons physicians gave (Figure) for not adding high-intensity statins were intolerance (n=62/86, 72%) and patient refusal (n=14/86, 16%); the most common reasons for not adding ezetimibe were past intolerance (n=8/16, 50%) and no current LDL-C available (n=5/16, 31%); and the most common reasons for not adding PCSK9i were no current LDL-C available (n=42/142, 30%) and patient refusal (n=31/142, 22%).</div></div><div><h3>Conclusions</h3><div>For patients with an MI in the last 12 months, opportunities to intensify LLT and monitor LDL-C were frequently missed. In addition to a ‘hard-stop’ best practice alert in the EHR, additional strategies need to be explored to overcome common reasons for not intensifying LLT, including addressing adverse events/intolerance and better routine monitoring of LDL-C.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Pages e2-e3"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144167917","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":"Lipoprotein apheresis to address residual risk in recurrent atherosclerotic events","authors":"Anish Adhikari MB ChB,&nbsp;Eugenia Gianos MD,&nbsp;Caleb Wutawunashe MD,&nbsp;Guy Mintz MD,&nbsp;Mahima Mangla DO","doi":"10.1016/j.jacl.2025.04.052","DOIUrl":"10.1016/j.jacl.2025.04.052","url":null,"abstract":"<div><h3>Background/Synopsis</h3><div>Optimal medical therapy may be insufficient in attenuating cardiovascular risk in individuals with elevated Lipoprotein(a) (Lp(a)). Lipoprotein apheresis can play a role in such cases.</div></div><div><h3>Objective/Purpose</h3><div>To describe a unique case of accelerated atherosclerosis refractory to aggressive LDL-C lowering.</div></div><div><h3>Methods</h3><div>Medical record review.</div></div><div><h3>Results</h3><div>A 66-year-old male, non-smoker, with controlled type 2 diabetes mellitus, familial hypercholesterolemia (FH), peripheral vascular disease, and recurrent acute coronary syndrome (ACS) presented to our lipid clinic. His mother had severe hyperlipidemia. Baseline lipid panel from 40 years prior showed a total cholesterol of 330 mg/dL and LDL-C of 220 mg/dL. He took rosuvastatin and ezetimibe for over 20 years. His first ACS event five years prior required a left anterior descending artery (LAD) stent. At this time, icosapent ethyl was added and his lipid profile was controlled with apolipoprotein B of 60 mg/dL. However, months later, he required carotid endarterectomy for severe carotid stenosis. Two years later, another LAD stent was placed for new disease in the setting of an LDL-C of 54 mg/dL. After this event, PCSK9 inhibitor was prescribed but denied by insurance. One year later, repeat lipid panel showed: LDL-C 37 mg/dL, apolipoprotein B 66 mg/dL, Lp(a) 297 nmol/L, and hs-CRP 2.6mg/L. PCSK9 inhibitor was denied again so bempedoic acid was added. Lipid apheresis was recommended but denied by insurance. The following year, he had severe two-vessel coronary disease including in-stent restenosis of a prior LAD stent, necessitating coronary artery bypass graft. Two days after surgery, evolocumab was approved and initiated. However, one month later, he required a stent to his bypass graft. Eventually he received insurance approval for lipoprotein apheresis and had significant LDL-C and Lp(a) reduction.</div><div>This case demonstrates that despite optimal lipid and anti-platelet therapy, risk factor control, and invasive treatment, recurrent ACS and plaque progression ensued. This was likely mediated by high Lp(a). Lipoprotein apheresis is the only FDA approved treatment for elevated Lp(a), now with an approved FDA indication for Lp(a) ≥ 60 mg/dL or ≥ 130 nmol/L with coronary or peripheral artery disease, noting a cardiovascular event reduction greater than 75% in such patients. Phase 3 trials are ongoing for Lp(a) lowering agents which will inform future treatment.</div></div><div><h3>Conclusions</h3><div>Patients with FH, elevated Lp(a) and hs-CRP represent an ultra high-risk profile for aggressive atherosclerosis. For our patient, delays in PCSK9 inhibitor and apheresis initiation likely influenced disease progression. Lipoprotein apheresis has demonstrated a reduction in cardiovascular events.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Pages e37-e38"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144168308","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":"Association of serum lipoprotein(a) and progression of structural heart disease: Insights from CARDIA study","authors":"Rishi Parikh MPH,&nbsp;Donald Jones MD,&nbsp;John Wilkins MD,&nbsp;Alan Go MD,&nbsp;Norrina Allen PhD,&nbsp;Catherine Shields BS,&nbsp;Mirasol Apostol-Largeteau MPH,&nbsp;Sascha Goonewardena MD,&nbsp;Venkatesh Murthy MD,&nbsp;David Jacobs PhD,&nbsp;Daniel Duprez MD,&nbsp;So Yi PhD,&nbsp;Joao Lima MD,&nbsp;Ankeet Bhatt MD,&nbsp;Zara Butte MD","doi":"10.1016/j.jacl.2025.04.029","DOIUrl":"10.1016/j.jacl.2025.04.029","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background/Synopsis&lt;/h3&gt;&lt;div&gt;Lipoprotein (a) [Lp(a)] is an atherothrombotic and inflammatory lipoprotein associated with atherosclerosis and arterial stiffness, which may contribute to heart failure (HF). Few studies have focused on its role in HF progression.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Objective/Purpose&lt;/h3&gt;&lt;div&gt;This study assessed the association between Lp(a) measured in young adulthood and HF stages over 25 years in the Coronary Artery Risk Development in Young Adults Study (CARDIA) study.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;We identified CARDIA study participants with Lp(a) measurements at Year 7 (ages 25-37). Lp(a) was categorized as normal (&lt; 75 nmol/L), intermediately elevated (75-124 nmol/L), or significantly elevated (&gt; 124 nmol/L), aligned with NLA guidelines. HF stages at Year 5 and Year 30 were defined according to the 2013 AHA/ACC guidelines: stage 0, without risk factors; stage A, HF risk factors; stage B, asymptomatic cardiac structural or functional abnormalities; and stage C/D, symptomatic or end-stage HF. Among those with available data to classify HF stage at Year 5, we evaluated the cross-sectional association between Lp(a) and HF stage. Among those with available HF stages at both Year 5 and Year 30, we evaluated the association between Lp(a) and the change in HF stage from Year 5 to Year 30 (&lt;em&gt;i.e.,&lt;/em&gt; no increase, increase by 1 stage, increase by 2 or more stages) using ordinal logistic regression. All models were stratified by race (Black vs White). Base models adjusted for age and sex, with additional adjustment for HF risk factors (SBP, diabetes, smoking status, total &amp; LDL cholesterol, lipid-lowering medication use).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;We identified 3501 CARDIA participants with both Lp(a) at Year 7 and HF stage at Year 5. 2275 (65%) had normal Lp(a), 584 (16.7%) had intermediately elevated, and 642 (18.3%) had significantly elevated Lp(a) (Figure). At Y5, intermediately elevated Lpa was not associated with higher HF stage in Black (odds ratio [OR]: 1.14, 95% confidence interval [CI]: 0.9, 1.45) or White (OR: 1.10, 95% CI: 0.77, 1.58) participants (interaction p=0.58). Significantly elevated Lp(a) was also not associated with HF stage, and point estimates were slightly but not significantly stronger in White (OR: 1.27, 95% CI: 0.91, 1.78) than in Black (OR: 1.03, 95% CI: 0.82, 1.31) participants. Point estimates for White participants were attenuated after further adjustment for cardiovascular risk factors. Among 2140 participants with available HF stages at both Y5 and Y30, intermediate and significantly elevated serum Lp(a) were not associated with progression of HF stages from Y5 to Y30 in Black (intermediately elevated: 1.02, 95% CI: 0.76, 1.37, significantly elevated: 1.07, 95% CI: 0.81, 1.42) or White (intermediately elevated: 0.96, 95% CI: 0.68, 1.37, significantly elevated: 0.86, 95% CI: 0.6, 1.22) participants (interaction p=0.23).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;Lp(","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Page e22"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144168569","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}