American journal of preventive cardiology最新文献

{"title":"GENETICALLY PREDICTED LIPOPROTEIN(A) IS ASSOCIATED WITH CORONARY ARTERY PLAQUE SEVERITY INDEPENDENT OF LOW-DENSITY LIPOPROTEIN CHOLESTEROL","authors":"Shoa L. Clarke MD, PhD","doi":"10.1016/j.ajpc.2024.100757","DOIUrl":"10.1016/j.ajpc.2024.100757","url":null,"abstract":"<div><h3>Therapeutic Area</h3><div>ASCVD/CVD Risk Factors</div></div><div><h3>Background</h3><div>Elevated Lipoprotein(a) [Lp(a)] is a causal risk factor for atherosclerotic cardiovascular disease, but mechanisms are debated. The role of Lp(a) in atherogenesis has been questioned by prior small studies showing a lack of association with markers of atherosclerosis, including carotid intima media thickness and coronary artery calcification. Some have hypothesized that the association between Lp(a) and atherosclerosis may depend on low-density lipoprotein cholesterol (LDL-C).</div></div><div><h3>Methods</h3><div>We examined participants of the Million Veteran Program who have undergone an invasive angiogram. The primary exposure was genetically predicted Lp(a), estimated by a validated polygenic score consisting of 43 single nucleotide variants at the LPA locus. The primary outcome was coronary artery plaque severity, categorized as normal, non-obstructive disease, 1-vessel disease, 2-vessel disease, and 3-vessel or left main disease. Multivariable multinomial regression was used to assess the association between genetically predicted Lp(a) and coronary plaque severity, independent of age, sex, LDL-C, lipid-lowering therapy, hypertension, diabetes, tobacco use, and genetic principal components. Similar logistic regression models were used to assess the overall risk for obstructive plaque. Odds ratios were calculated per 1 standard deviation increase in predicted Lp(a) and by comparing the top 20% to bottom 80%.</div></div><div><h3>Results</h3><div>Among 18,927 adults of genetically inferred European ancestry (mean age 66 years; 96.8% male), we observed significant associations between genetically predicted Lp(a) and all categories of obstructive plaque. The association was borderline significant for non-obstructive plaque. We observed a consistent pattern of increasing effect sizes for increasingly severe categories of atherosclerosis (Figure [A]). Participants with genetically predicted high Lp(a) were at significantly increased risk for obstructive plaque across LDL-C levels (Figure [B]).</div></div><div><h3>Conclusions</h3><div>Genetically predicted Lp(a) is positively associated with coronary plaque severity independent of LDL-C, consistent with Lp(a) promoting atherogenesis. However, Lp(a) may contribute more to plaque progression towards obstructive disease than to plaque initiation. Our findings suggest that Lp(a) reduction could protect against the development of obstructive coronary plaque beyond what might be achieved by LDL-C reduction alone.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"19 ","pages":"Article 100757"},"PeriodicalIF":4.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142422752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DISCREPANCIES IN AMI MORTALITY IN THE US SOUTHERN BORDER REGION 1999-2020","authors":"Ramon H Guillen MD","doi":"10.1016/j.ajpc.2024.100735","DOIUrl":"10.1016/j.ajpc.2024.100735","url":null,"abstract":"<div><h3>Therapeutic Area</h3><div>ASCVD/CVD in Special Populations</div></div><div><h3>Background</h3><div>The US-Mexican border region (BR) faces distinct demographic and health challenges. Analyzing premature acute myocardial infarction (AMI) mortality disparities can inform targeted health strategies.</div></div><div><h3>Methods</h3><div>Mortality data for premature AMI (&lt;55y men, &lt;65y women) from 1999-2019 were extracted from CDC death certificate data. ANOVA tests were done for race &amp; BR, and for Hispanic origin &amp; BR. Join point regression with tests for parallelism was applied to significant ANOVA subsets to analyze time trends.</div></div><div><h3>Results</h3><div>ANOVA revealed significantly higher mortality rates for Hispanics in the BR. Join point regression indicated parallel downtrends in mortality for non-Hispanics in both areas with an average annual percentage change (AAPC) of –2.4916 (p&lt;0.05). Hispanic mortality trended up in the BR (AAPC = +1.2886, p&lt;0.05) and down in the non-BR (AAPC = -1.1370, p&lt;0.05). The parallelism test was refuted for Hispanic groups, with two observed trends in the non-BR: significant downtrend with an annual percentage change (APC) of -2.7949 (p&lt;0.05) from 1999-2009 and no significant change post-2009.</div></div><div><h3>Conclusions</h3><div>Hispanic groups in the US-Mexican border region face higher premature AMI mortality rates. AMI mortality trended down improved for non-Hispanic groups and Hispanic groups in the non-BNR, while Hispanic border region rates are consistently rising worsening despite improvements in myocardial infarction treatment standards. This highlights the need to further investigate specific challenges and methods to improve in cardiovascular health post myocardial infarction care faced by Latinx communities in the US-Mexican border region.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"19 ","pages":"Article 100735"},"PeriodicalIF":4.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142422819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DEMYSTIFYING BAG3 CARDIOMYOPATHY","authors":"Yulith Roca Alvarez MD","doi":"10.1016/j.ajpc.2024.100789","DOIUrl":"10.1016/j.ajpc.2024.100789","url":null,"abstract":"<div><h3>Therapeutic Area</h3><div>Heart Failure</div></div><div><h3>Case Presentation</h3><div>A 56-year-old male with progressive exertional dyspnea and ankle edema was evaluated in the cardiology office. The patient had no overt traditional cardiac risk factors. ECG showed sinus rhythm and a right bundle branch block. The echocardiogram showed an LVEF of 45-50% and a severely dilated LV measuring 7.2 cm at end-diastole, with an abnormal global longitudinal strain (GLS) (11.6%) and apical and mid-wall sparing. Ischemic workup was negative. Genetic testing revealed a pathogenic variant in BAG3 (p.Glu471Argfs*95). His father and two siblings were also carriers of the same variant. He was treated with beta-blockers, angiotensin-neprilysin inhibitor, mineralocorticoid receptor antagonist, and an SGLT2 inhibitor. Frequent runs of non-sustained ventricular tachycardia prompted primary prevention implantable cardioverter defibrillator placement. Close follow-up was arranged, given the high risk for deterioration and progressive heart failure.</div></div><div><h3>Background</h3><div>The cause of dilated cardiomyopathy (DCM) can be determined in approximately 40% of cases due to genetic testing now being widely available. BAG3 mutations account for 2-5% of DCM cases; BAG 3 gene encodes a protein crucial for maintaining the structure and function of cardiomyocytes. Mutations in BAG3 disrupt its normal function, leading to myofibrillar disarray and systolic dysfunction.</div></div><div><h3>Conclusions</h3><div>The BAG3 mutation, in this case, resulted in a premature translational stop of the BAG3 gene, disrupting the last 105 amino acids of the BAG3 protein. Inheritance follows an autosomal dominant pattern, and penetrance is 40%. Left ventricular global longitudinal strain (GLS) may inform outcomes beyond LVEF in patients with heart failure and reduced ejection fraction. Currently, preliminary research involving gene therapy in animal models shows that replenishing normal levels of BAG3 may have salutary effects. However, essential questions remain on how it can be implemented effectively in human subjects.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"19 ","pages":"Article 100789"},"PeriodicalIF":4.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142422835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LIPOPROTEIN(A) AND CARDIOVASCULAR RISK. A RETROSPECTIVE COHORT STUDY FROM NYC/HHC+ PUBLIC HOSPITAL IN NEW YORK CITY","authors":"Natalia Nazarenko MD","doi":"10.1016/j.ajpc.2024.100759","DOIUrl":"10.1016/j.ajpc.2024.100759","url":null,"abstract":"<div><h3>Therapeutic Area</h3><div>ASCVD/CVD Risk Factors</div></div><div><h3>Background</h3><div>Lipoprotein(a) [Lp(a)] is a independent genetic risk factor for cardiovascular disease with heritability rates ranging from 70% to 90%. Our study aimed to compare demographic and clinical characteristics in patients with normal vs. abnormal Lp(a).</div></div><div><h3>Methods</h3><div>We conducted a retrospective chart review at Jacobi Medical Center from August 2020 to September 2023 and we identified 78 patients with available Lp(a) measurement.</div></div><div><h3>Results</h3><div>Among 78 patients, 32 (41.03%) were female, and 46 (58.97%) were male. 32 patients had abnormal Lp(a) (&gt;75 nmol/L) with a mean of 143.35 nmol/L, mean BMI of 30.34 and median age of 53.5 years. Abnormal Lp(a) correlated with higher LDL levels (111.01 vs. 91.23 mg/dL; p=0.044). Increased Lp(a) was more prevalent among African Americans. No significant association was found between abnormal Lp(a) and aortic or mitral valve calcifications. In the cohort with abnormal Lp(a) levels, the prevalence of heart failure with preserved ejection fraction (HFpEF) was 100%, while the presence of heart failure with reduced ejection was notably lower at 24% (p=0.008). The demographic and clinical characteristics are presented in Table 1.</div></div><div><h3>Conclusions</h3><div>Our study found no significant difference in comorbidities between both groups but did show a correlation with elevated LDL. HFpEF was more prevalent among patients with abnormal Lp(a).</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"19 ","pages":"Article 100759"},"PeriodicalIF":4.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142422906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EVALUATING MISINFORMATION REGARDING CARDIOVASCULAR DISEASE PREVENTION OBTAINED ON A POPULAR, PUBLICLY ACCESSIBLE ARTIFICIAL INTELLIGENCE MODEL (GPT-4)","authors":"Ashish Sarraju MD","doi":"10.1016/j.ajpc.2024.100806","DOIUrl":"10.1016/j.ajpc.2024.100806","url":null,"abstract":"<div><h3>Therapeutic Area</h3><div>Other: Artificial intelligence; Misinformation</div></div><div><h3>Background</h3><div>Misinformation regarding CVD prevention is prevalent on the internet and on social media. Chat-based artificial intelligence (AI) models such as ChatGPT have gained over 100 million users, are publicly accessible, and may provide appropriate information for simple CVD prevention topics. Whether these public AI models may propagate misinformation regarding CVD prevention is uncertain.</div></div><div><h3>Methods</h3><div>This study was performed in March 2024 using the subscription-based version of GPT-4 (OpenAI, USA). Prompts regarding six CVD prevention topics (statin therapy and muscle-side effects, dementia, and liver disease; fish oil; supplements; and low-density lipoprotein-cholesterol and heart disease) were posed. Prompts were framed in two tones: a neutral tone and a misinformation-prompting tone. The misinformation-prompting tone requested specific arguments and scientific references to support misinformation. Each tone and topic was prompted in a different chatbot instance. Each response was reviewed by a board-certified cardiologist specializing in preventive cardiology at a tertiary care center. If a response had multiple bullet-points with individual scientific references, each bullet-point was graded separately. Responses were graded as appropriate (accurate content and references), borderline (minor inaccuracies or references published &gt;20 years ago), or inappropriate (inaccurate content and/or references, including non-existent references).</div></div><div><h3>Results</h3><div>For the six prompts posed with a neutral tone, all responses lacked scientific references and were graded as appropriate (100%). For all six prompts posed with a misinformation-prompting tone, each response consisted of multiple discrete bullet-points with a scientific reference for each individual point. Of 31 bullet-points across the six topics obtained using a misinformation-prompting tone, 32.2% (10/31) were graded as appropriate, 19.4% (6/31) were graded as borderline, and 48.4% (15/31) were graded as inappropriate.</div></div><div><h3>Conclusions</h3><div>In this exploratory study, GPT-4 – a popular and publicly accessible chat-based AI model – was easily prompted to support CVD prevention misinformation. Misinformation-supporting arguments and scientific references were inappropriate due to inaccurate content and/or references nearly 50% of the time. Robust research efforts and policies are needed to study and prevent AI-enabled propagation of misinformation regarding CVD prevention.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"19 ","pages":"Article 100806"},"PeriodicalIF":4.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142422911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LONG-TERM EFFICACY OF EVINACUMAB IN PATIENTS WITH HOMOZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA: RESULTS FROM SUBGROUP ANALYSES","authors":"Daniel Gaudet MD, PhD","doi":"10.1016/j.ajpc.2024.100801","DOIUrl":"10.1016/j.ajpc.2024.100801","url":null,"abstract":"<div><h3>Therapeutic Area</h3><div>Pharmacologic Therapy</div></div><div><h3>Background</h3><div>Homozygous familial hypercholesterolemia (HoFH) is a rare genetic disorder characterized by severely elevated low-density lipoprotein cholesterol (LDL-C) and increased risk of early-onset atherosclerotic cardiovascular disease. Despite treatment with multiple lipid-lowering therapies (LLTs), most patients with HoFH do not attain guideline-recommended LDL-C treatment goals. In a phase 3 trial (NCT03409744), evinacumab, an angiopoietin-like 3 inhibitor, substantially reduced mean LDL-C by 43.6% from baseline to Week 24. Here, we report on the long-term LDL-C lowering efficacy of evinacumab analyzed by patient subgroups from the open-label treatment period (OLTP) of this phase 3 trial.</div></div><div><h3>Methods</h3><div>This single-arm, open-label, phase 3 study (NCT03409744) comprised patients with HoFH aged ≥12 years who were evinacumab-naïve or had previously received evinacumab in other trials. The study included a run-in period (≤10 weeks), a screening period (2 weeks), an OLTP (≤192 weeks), and a follow-up period (24 weeks). In the OLTP, all patients received intravenous evinacumab 15 mg/kg every 4 weeks alongside optimized LLT.</div></div><div><h3>Results</h3><div>Overall, 116 patients were enrolled with a mean (standard deviation [SD]) age of 38.8 (15.9) years. The proportion of male and female patients was similar (50.9% vs 49.1%, respectively). Most patients were White (69.0%) or Asian (10.3%). At baseline, mean (SD) LDL-C was 261.0 (160.1) mg/dL. Evinacumab reduced mean (SD) LDL-C from baseline to Week 96 by 57.6% (16.7%), 36.4% (54.6%), and 38.0% (52.9%) in patients &lt;18 years of age, patients ≥18 years of age, and overall, respectively. Among female and male patients, mean (SD) LDL-C reduction from baseline to Week 96 was 48.8% (32.3%) and 30.5% (62.6%), respectively. Mean (SD) LDL-C reduction from baseline to Week 96 was 43.1% (36.9%) in patients with null-null variants in either the low-density lipoprotein receptor (LDLR) gene or the low-density lipoprotein receptor adapter protein 1 (LDLRAP1) gene; mean (SD) LDL-C reduction was 35.1% (62.4%) in patients with non-null variants in LDLR or LDLRAP1. From baseline to Week 96, reductions in LDL-C with evinacumab were observed irrespective of background LLT (Figure).</div></div><div><h3>Conclusions</h3><div>In patients with HoFH, evinacumab showed substantial and sustained LDL-C reduction irrespective of age, sex, LDLR genotype, and background LLT.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"19 ","pages":"Article 100801"},"PeriodicalIF":4.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142422967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HOW CAN WE UTILIZE DIGITAL MEDIA FOR ASCVD PREVENTION? A RANDOMIZED CONTROLLED TRIAL","authors":"Brandon Rafison DO, MPH","doi":"10.1016/j.ajpc.2024.100803","DOIUrl":"10.1016/j.ajpc.2024.100803","url":null,"abstract":"<div><h3>Therapeutic Area</h3><div>CVD Prevention – Primary and Secondary</div></div><div><h3>Background</h3><div>The growing complexity of cardiology, higher patient volumes, and increasing administrative/charting demands pose challenges for providers to spend valuable clinic time on educating patients sufficiently about Atherosclerotic Cardiovascular Disease (ASCVD). We performed a prospective randomized controlled trial to determine if using an animated video in the clinical setting to educate patients about cardiac anatomy and pathophysiology is an effective method of ASCVD prevention.</div></div><div><h3>Methods</h3><div>This study took place in a busy cardiology clinic within a teaching hospital in New York City. Patients with traditional risk factors for ASCVD were asked to participate if they were &gt;18 years, and understood English or Spanish. Willing participants were randomized to either the intervention or control, “usual-care”, cohort. Both cohorts were asked to complete a pre-visit questionnaire regarding coronary artery disease (CAD), physical activity, and patient satisfaction before their scheduled clinical encounter. Only the intervention cohort was then shown a novel, 3.5-minute animated video via tablet that illustrates anatomy and pathophysiology of CAD. Next, all participants completed their clinical encounter with their cardiologist, and finally were asked to complete a post-visit questionnaire which was identical to the pre-visit version.</div></div><div><h3>Results</h3><div>A total of 48 participants were enrolled in this study, 23 in the control (usual care) cohort and 25 in the intervention cohort. Baseline demographic characteristics are summarized in Table 1. The average score on the 5-point Likert scale of the pre-visit questionnaire for the intervention cohort was 3.81, and post-visit improved to 4.64 (average change of 0.96 points, p=0.003). The average score of the pre-visit questionnaire for the control cohort was 3.68, and post-visit score was 3.73 (average change of 0.05 points, p=0.19).</div><div>Results:</div></div><div><h3>Conclusions</h3><div>This pilot study demonstrates that digital media, in conjunction with the clinical encounter, is more effective in bolstering peoples’ knowledge of ASCVD risk, improving attitudes towards their provider and increasing patient satisfaction, compared to usual care. The positive results suggest the need for more prospective studies to evaluate the efficacy of utilizing digital media to deliver patient education and prevent cardiovascular disease.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"19 ","pages":"Article 100803"},"PeriodicalIF":4.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142422969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PERSISTENT ATRIAL FIBRILLATION AFTER CATHETER ABLATION IN HUMAN IMMUNODEFICIENCY VIRUS TYPE‐1 POSITIVE PATIENTS","authors":"Sophia Navajas MD","doi":"10.1016/j.ajpc.2024.100805","DOIUrl":"10.1016/j.ajpc.2024.100805","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Therapeutic Area&lt;/h3&gt;&lt;div&gt;Other: Electrophysiology&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Case Presentation&lt;/h3&gt;&lt;div&gt;A 35-year-old African-American male with medical history of HIV-1 infection on 800 mg Darunavir, 150 mg Cobicistat, 200 mg Emtricitabine, and 10 mg Tenofovir Alafenamide presented with the complain of palpitations and sweating. He reported resting tachycardia, 120-140 beats per minute, from his smartwatch. Upon arrival, 12-lead electrocardiogram showed atrial flutter with variable A-V block. Patient's troponin I was &lt;0.01 ng/ml. Subsequently, he underwent transesophageal echocardiogram and was successfully cardioverted to sinus rhythm with one dose of 200 joules of synchronized cardioversion. After multidisciplinary management, patient was discharged on Sotalol 80 mg twice a day and Dabigatran 150 mg twice a day. 45 days after initial presentation, patient underwent successful outpatient atrial flutter ablation. 65 days status post ablation, he again presented and was admitted due to atrial fibrillation with premature ventricular complexes. Currently, patient remains on rate control with anticoagulation treatment and frequent outpatient surveillance. Since the last incidence, no inpatient hospitalizations have been reported.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Atrial fibrillation (AF) is the most common type of cardiac arrhythmia. It is due to abnormal electrical activity within the atria of the heart, causing them to fibrillate. This arrhythmia may be paroxysmal (less than seven days) or persistent (more than seven days) (1). Researcher studies have found that Human Immunodeficiency Virus (HIV)-positive patients had an incidence of 18.2 AF diagnoses per thousand person-years, compared to 8.9 in patients without HIV (2). Non-pulmonary vein triggers are highly prevalent in HIV-positive AF patients and the mid- and long-term arrhythmia recurrence was observed to be mostly driven by those triggers (3). We present a patient who represents part of the growing study population of young HIV-1 positive male associated with arrhythmia recurrence.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;The prothrombotic nature of HIV infection is well-documented (4). It is believed that HIV-1 infection elevates stroke risk via systemic mechanisms such as low-grade inflammation and heightened oxidative stress, or through direct cardiac toxicity potentially leading to AF (5). A key consideration in the treatment of atrial fibrillation in patients with HIV‐1 who are in combination antiretroviral therapy (ART), is the significant impact these drugs have on liver enzymes like CYP2C9 and CYP3A4 (6). These enzymes are crucial for metabolizing numerous medications, including various oral anticoagulants (6). Given this, there is a strong likelihood of interactions between vitamin K antagonists and ART, particularly with protease inhibitors (PIs) or non‐nucleoside reverse transcriptase inhibitors (NNRTIs) (7).&lt;/div&gt;&lt;div&gt;Additionally, ART regimens containing PIs with or","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"19 ","pages":"Article 100805"},"PeriodicalIF":4.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142422971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LIPOPROTEIN(A) AND APOLIPOPROTEIN B ARE RELATED TO AORTIC STENOSIS: RESULTS FROM THE HISPANIC COMMUNITY HEALTH STUDY/STUDY OF LATINOS (HCHS/SOL) AND ECHOCARDIOGRAPHIC STUDY OF LATINOS (ECHO-SOL)","authors":"Akhil Avunoori Chandra MD","doi":"10.1016/j.ajpc.2024.100823","DOIUrl":"10.1016/j.ajpc.2024.100823","url":null,"abstract":"<div><h3>Therapeutic Area</h3><div>Heart Failure</div></div><div><h3>Background</h3><div>Lipoprotein(a) [Lp(a)] and Apolipoprotein B [apoB] have been previously studied as risk factors of calcific aortic valve disease primarily among non-Hispanic/Latino populations. However, the association between apoB and calcific aortic stenosis (AS) is not as well known.</div></div><div><h3>Methods</h3><div>Data from 8,564 community-dwelling Hispanics/Latinos with echocardiograms performed at Visit 2 (HCHS/SOL, 2014-2017 and Echo-SOL, 2015-2018) were analyzed. These participants had Lp(a) levels (nmol/L) and apoB levels (mg/dL) measured at HCHS/SOL Visit 1 (2008 to 2011). Pearson correlation coefficient (r), linear and logistic regression models were used to study the association of Lp(a) and apoB with the following outcomes: 1. Aortic valve peak velocity (AVPV), cm/s; 2. Aortic valve peak pressure gradient (AVPPG), mmHg, and 3. Aortic stenosis, defined as AVPV ≥ 300 cm/s for moderate or severe AS. AVPV ≤ 100 cm/s was considered normal and used as a reference value for AS. Lp(a) and apoB were modeled as continuous variables. Sampling weights and surveys methods were used to account for HCHS/SOL complex design.</div></div><div><h3>Results</h3><div>Overall, the mean (SE) age was 58.4 (0.2) years, and 53.6% were female. Their baseline median IQR (Q1-Q3) Lp(a) and apoB levels were 22.5 (8.1-66.6) nmol/L and 105.1 (88.7-122.9) mg/dL, respectively. HCHS/SOL overall baseline median IQR (Q1-Q3) Lp(a) was 19.7 (7.3-60.6) nmol/L and apoB was 96.7 (79.4-116.0) mg/dL, respectively. Table 1: Higher baseline Lp(a) levels were significantly associated with worsened AVPV and AVPPG at Visit 2. Higher apoB levels were associated with worsened AVPV and AVPPG. Compared to normal AVPV values, using 10-unit increments, increasing Lp(a) levels were associated with increased risk of moderate or severe AS (ORLp(a) 1.10 (95% CI, 1.06-1.14), p&lt;0.0001); and increasing apoB levels were associated with mild AS or Aortic Sclerosis (ORapoB1.032 (95% CI, 1.002-1.063), p&lt;0.04).</div></div><div><h3>Conclusions</h3><div>Lp(a) and apoB are significantly associated with AVPV and AVPPG and are significant predictors of AS; suggesting these markers may be potentially modifiable risk factors for calcific aortic valvular disease among Hispanic/Latinos.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"19 ","pages":"Article 100823"},"PeriodicalIF":4.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142422708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"UNEXPLAINED LOW VOLTAGE PRECORDIAL QRS ON ECG IN ASYMPTOMATIC SUBJECTS SHOULD NOT BE DISMISSED WITHOUT FURTHER INVESTIGATION FOR ABNORMAL CARDIOVASCULAR RISK BIOMARKERS SUCH AS BNP, CRP, MICROALBUMIN AND/OR EPICARDIAL FAT VOLUME","authors":"Mahfouz El Shahawy MD, MS","doi":"10.1016/j.ajpc.2024.100773","DOIUrl":"10.1016/j.ajpc.2024.100773","url":null,"abstract":"<div><h3>Therapeutic Area</h3><div>Novel Biomarkers</div></div><div><h3>Background</h3><div>Low voltage QRS in precordial leads in asymptomatic subjects has been reported to be associated with increased epicardial fat volume which is a novel cardiovascular risk marker.</div><div>Purpose of this study is to examine the prevalence of abnormal cardiovascular risk biomarkers such as BNP, CRP and/or microalbumin in asymptomatic subjects with low voltage QRS complexes in precordial leads on ECG and elevated epicardial fat volume.</div></div><div><h3>Methods</h3><div>330 asymptomatic obese subjects were screened for cardiovascular risk assessment using the Early Cardiovascular Disease Risk Scoring System (ESCVDRS) known as Rasmussen Risk Score (RRS), previously reported. The ESCVDRS includes 7 vascular and 3 cardiac tests. Among the additional test, CRP, proBNP, microalbumin were also measured. Coronary calcium score and epicardial fat volume was measured utilizing cardiac CT Siemens Somatom Definition Dual source CT scanner 64x2. Out of the 330 subjects, 55 subjects with average age 68, also underwent measurement of epicardial fat volume on CT utilizing same and similar forms definition 64 x 2. Waist circumference was also measured. The 55 subjects were divided in 2 groups: Group A, 33 subject with cardio-obesity and low precordial QRS voltage on ECG; Group B, 22 subjects with normal epicardial fat volume and normal ECG.</div></div><div><h3>Results</h3><div>Results are shown in the table below. As seen, Group A had a significant abnormal biomarker, including BNP, CRP and microalbumin as compared with Group B.</div></div><div><h3>Conclusions</h3><div><ul><li><span>(1)</span><span><div>Unexplained low voltage QRS in precordial leads in asymptomatic subjects should not be dismissed as normal without further evaluation for cardiovascular biomarkers to rule out significant early subclinical cardiovascular disease risk.</div></span></li><li><span>(2)</span><span><div>Low Precordial QRS voltage on ECG in the absence of other known causes may be indicative of excess epicardial fat volume which is significant CV disease risk marker and must be treated.</div></span></li></ul></div><div>1 ounce of early cardiovascular disease prevention is better than pounds of late treatment.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"19 ","pages":"Article 100773"},"PeriodicalIF":4.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142423102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}