Pub Date : 2024-09-01DOI: 10.1016/j.ajpc.2024.100787
Mingma Sherpa DO
Therapeutic Area
Pharmacologic Therapy
Case Presentation
We report the case of a 77-year-old female who presents after a LifeVest defibrillator shock. She had initially presented a month prior with new-onset heart failure and atrial fibrillation with rapid ventricular response. She was diagnosed with tachycardia-mediated cardiomyopathy. After three unsuccessful attempts at cardioversion, she was started on oral amiodarone 400mg twice a day. On discharge, she was prescribed oral amiodarone 200mg daily, along with entresto, metoprolol succinate, and empagliflozin.
She returned a month later after a shock at home. LifeVest interrogation demonstrated polymorphic ventricular tachycardia (VT)/ventricular fibrillation (VF) with prolonged QTc of 712 msec before VT/VF. Laboratory evaluation on admission within normal limits. Initial EKG showed sinus bradycardia with QTc 630 milliseconds (ms). The patient experienced recurrent TdP, requiring defibrillation three additional times while in the emergency department. Cardiac catheterization showed non-obstructive CAD. Amiodarone was held with improvement in her QTc to 398 ms. She was switched to mexiletine 150 mg TID, remained in sinus rhythm, and was discharged with a dual chamber pacemaker and defibrillator for secondary prevention.
Background
Due to age-related electrophysiological and structural changes, elderly individuals face an elevated risk of acquired long-QT syndrome (LQTS). Females are at a higher risk than males, with a 1-3% incidence of amiodarone-induced Torsades de Pointes (TdP). Older women taking amiodarone are especially susceptible to proarrhythmic effects, including QT interval prolongation, which can potentially lead to clinical complications.
Conclusions
Amiodarone is frequently utilized to treat atrial fibrillation refractory to cardioversion. However, current guidelines are based on studies conducted mainly on middle-aged men with minimal inclusion of women, especially older women, with a lack of sex-specific analysis and reporting. Women are prone to adverse drug reactions, and these reactions may be more severe due to doses that do not consider body weight differences. This can result in higher plasma levels and potential overdosage in women compared to men. Personalizing treatment by identifying sex differences in dosing, efficacy, and safety of cardiovascular drugs may help reduce the rate of adverse effects.
{"title":"VENTRICULAR FIBRILLATION ARREST IN AN ELDERLY FEMALE DUE TO AMIODARONE-INDUCED ACQUIRED LONG-QT SYNDROME","authors":"Mingma Sherpa DO","doi":"10.1016/j.ajpc.2024.100787","DOIUrl":"10.1016/j.ajpc.2024.100787","url":null,"abstract":"<div><h3>Therapeutic Area</h3><div>Pharmacologic Therapy</div></div><div><h3>Case Presentation</h3><div>We report the case of a 77-year-old female who presents after a LifeVest defibrillator shock. She had initially presented a month prior with new-onset heart failure and atrial fibrillation with rapid ventricular response. She was diagnosed with tachycardia-mediated cardiomyopathy. After three unsuccessful attempts at cardioversion, she was started on oral amiodarone 400mg twice a day. On discharge, she was prescribed oral amiodarone 200mg daily, along with entresto, metoprolol succinate, and empagliflozin.</div><div>She returned a month later after a shock at home. LifeVest interrogation demonstrated polymorphic ventricular tachycardia (VT)/ventricular fibrillation (VF) with prolonged QTc of 712 msec before VT/VF. Laboratory evaluation on admission within normal limits. Initial EKG showed sinus bradycardia with QTc 630 milliseconds (ms). The patient experienced recurrent TdP, requiring defibrillation three additional times while in the emergency department. Cardiac catheterization showed non-obstructive CAD. Amiodarone was held with improvement in her QTc to 398 ms. She was switched to mexiletine 150 mg TID, remained in sinus rhythm, and was discharged with a dual chamber pacemaker and defibrillator for secondary prevention.</div></div><div><h3>Background</h3><div>Due to age-related electrophysiological and structural changes, elderly individuals face an elevated risk of acquired long-QT syndrome (LQTS). Females are at a higher risk than males, with a 1-3% incidence of amiodarone-induced Torsades de Pointes (TdP). Older women taking amiodarone are especially susceptible to proarrhythmic effects, including QT interval prolongation, which can potentially lead to clinical complications.</div></div><div><h3>Conclusions</h3><div>Amiodarone is frequently utilized to treat atrial fibrillation refractory to cardioversion. However, current guidelines are based on studies conducted mainly on middle-aged men with minimal inclusion of women, especially older women, with a lack of sex-specific analysis and reporting. Women are prone to adverse drug reactions, and these reactions may be more severe due to doses that do not consider body weight differences. This can result in higher plasma levels and potential overdosage in women compared to men. Personalizing treatment by identifying sex differences in dosing, efficacy, and safety of cardiovascular drugs may help reduce the rate of adverse effects.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"19 ","pages":"Article 100787"},"PeriodicalIF":4.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142422825","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}
Pub Date : 2024-09-01DOI: 10.1016/j.ajpc.2024.100751
Sophia Navajas MD
Therapeutic Area
CVD Prevention – Primary and Secondary
Case Presentation
A 27-year-old male with a history of presumed viral myopericarditis in 2021 presented with chest pain. He was found to have elevated troponin but coronary angiography was normal. On an echocardiogram, he was found to have a moderately thickened pericardium without effusion and a preserved LV systolic function. He was treated with indomethacin, prednisone, and colchicine however his symptoms recurred in 2023. An electrocardiogram (EKG) showed ST-segment elevation in I and aVL, with mild elevation across septal leads V2-V4. Troponin is 1.86, CPK of 206, and CRP of 5.5. A repeat echocardiogram revealed LVEF 55% Without pericardial effusion and no wall motion abnormalities. The patient clinically improved and was discharged on indomethacin 50 mg q8h to decrease dose by 25 mg per week, colchicine 0.6 mg bid for six weeks, and prednisone 40 mg for weeks with gradual taper.
Background
The United Nations estimated that around 192 million individuals aged 15 to 64 were using cannabis as of 2016(1). Over time, there has been a global trend towards decriminalizing and legalizing recreational cannabis (1). While the immediate impact of cannabis on heart rate is known to occur within 10 to 30 minutes of consumption (2), its long-term effects on cardiovascular health remain less understood due to regulatory constraints (3).
Emerging research suggests a potential connection between prolonged cannabis use and increased risk of cardiovascular diseases, although the precise mechanisms are not fully elucidated (4,5). Conditions like pericarditis and myocarditis, both heart inflammations, share similar symptoms and are diagnosed based on clinical observations, lab tests, and imaging.
Conclusions
Marijuana use has been linked to severe cardiovascular complications, such as myopericarditis. Therefore, healthcare professionals should maintain a high index of suspicion and routinely inquire about marijuana consumption in patients presenting with chest pain. Moreover, there is an apparent demand for further research to ascertain the most efficacious treatment modalities for myopericarditis induced by marijuana usage.
{"title":"\"HIGH AND INFLAMED\" A CURIOUS CASE OF CANNABIS-INDUCED RECURRENT MYOPERICARDITIS","authors":"Sophia Navajas MD","doi":"10.1016/j.ajpc.2024.100751","DOIUrl":"10.1016/j.ajpc.2024.100751","url":null,"abstract":"<div><h3>Therapeutic Area</h3><div>CVD Prevention – Primary and Secondary</div></div><div><h3>Case Presentation</h3><div>A 27-year-old male with a history of presumed viral myopericarditis in 2021 presented with chest pain. He was found to have elevated troponin but coronary angiography was normal. On an echocardiogram, he was found to have a moderately thickened pericardium without effusion and a preserved LV systolic function. He was treated with indomethacin, prednisone, and colchicine however his symptoms recurred in 2023. An electrocardiogram (EKG) showed ST-segment elevation in I and aVL, with mild elevation across septal leads V2-V4. Troponin is 1.86, CPK of 206, and CRP of 5.5. A repeat echocardiogram revealed LVEF 55% Without pericardial effusion and no wall motion abnormalities. The patient clinically improved and was discharged on indomethacin 50 mg q8h to decrease dose by 25 mg per week, colchicine 0.6 mg bid for six weeks, and prednisone 40 mg for weeks with gradual taper.</div></div><div><h3>Background</h3><div>The United Nations estimated that around 192 million individuals aged 15 to 64 were using cannabis as of 2016(1). Over time, there has been a global trend towards decriminalizing and legalizing recreational cannabis (1). While the immediate impact of cannabis on heart rate is known to occur within 10 to 30 minutes of consumption (2), its long-term effects on cardiovascular health remain less understood due to regulatory constraints (3).</div><div>Emerging research suggests a potential connection between prolonged cannabis use and increased risk of cardiovascular diseases, although the precise mechanisms are not fully elucidated (4,5). Conditions like pericarditis and myocarditis, both heart inflammations, share similar symptoms and are diagnosed based on clinical observations, lab tests, and imaging.</div></div><div><h3>Conclusions</h3><div>Marijuana use has been linked to severe cardiovascular complications, such as myopericarditis. Therefore, healthcare professionals should maintain a high index of suspicion and routinely inquire about marijuana consumption in patients presenting with chest pain. Moreover, there is an apparent demand for further research to ascertain the most efficacious treatment modalities for myopericarditis induced by marijuana usage.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"19 ","pages":"Article 100751"},"PeriodicalIF":4.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142422908","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}
Pub Date : 2024-09-01DOI: 10.1016/j.ajpc.2024.100725
David Bleich , Mary L. Biggs , Julius M. Gardin , Mary Lyles , David S. Siscovick , Kenneth J. Mukamal
Aims
To determine whether discrete lipid profiles (refer to as lipid phenotyping) can be used to stratify cardiovascular risk in individuals with type 2 diabetes.
Methods and results
Cardiovascular Health Study participants with diabetes and fasting lipid profiles at baseline (n = 866) were categorized separately by level of LDL cholesterol and HDL-C/Triglyceride (Tg) profiles (low Tg/high HDL-C; high Tg/low HDL-C; high Tg only or low HDL-C only). We performed Cox multivariate regression analysis to assess the risk of CVD mortality, incident myocardial infarction (MI), heart failure (HF), stroke, and composite MACE (MI, HF, stroke, and CVD mortality) associated with each lipid category. We also calculated risk estimates for MACE using lipid measures as continuous variables. In the fully adjusted model, the high triglyceride plus low HDL-C cholesterol phenotype demonstrated risk that was at least as high as the highest LDL-C sub-group phenotype for CVD mortality (Hazard ratio {HR} 1.58 vs 1.48), MI (HR 1.53 vs 1.58), HF (HR 1.47 vs 1.20), stroke (HR 2.02 vs 1.43), and MACE (HR 1.58 vs 1.38). When modeled continuously, the HR per SD for MACE was 1.12 (p = 0.03) for LDL-C and 1.19–1.20 (p < 0.001) for triglycerides or remnant cholesterol.
Conclusions
Participants with the high triglyceride/low HDL-C phenotype had equivalent or higher CVD risk than those with the high LDL-C phenotype. Further studies are necessary to determine whether lipid phenotyping accounts for the substantial CVD risk not explained by LDL cholesterol among individuals with type 2 diabetes.
方法和结果心血管健康研究参与者中,有糖尿病且基线时有空腹血脂图谱者(n = 866),按低密度脂蛋白胆固醇和高密度脂蛋白胆固醇/甘油三酯 (Tg) 图谱水平(低 Tg/ 高密度脂蛋白胆固醇;高 Tg/ 低密度脂蛋白胆固醇;仅高 Tg 或仅低密度脂蛋白胆固醇)分别进行分类。我们进行了 Cox 多变量回归分析,以评估与每种血脂类别相关的心血管疾病死亡率、心肌梗死(MI)事件、心力衰竭(HF)、中风和复合 MACE(MI、HF、中风和心血管疾病死亡率)的风险。我们还将血脂指标作为连续变量计算了MACE的风险估计值。在完全调整模型中,在心血管疾病死亡率(危险比{HR} 1.58 vs 1.48)、心肌梗死(HR 1.53 vs 1.58)、高密度脂蛋白胆固醇(HR 1.47 vs 1.20)、中风(HR 2.02 vs 1.43)和 MACE(HR 1.58 vs 1.38)方面,高甘油三酯加低高密度脂蛋白胆固醇表型的风险至少与最高低密度脂蛋白胆固醇亚组表型一样高。结论高甘油三酯/低高密度脂蛋白胆固醇表型的参与者与高低密度脂蛋白胆固醇表型的参与者相比,具有同等或更高的心血管疾病风险。有必要开展进一步研究,以确定血脂表型是否解释了 2 型糖尿病患者中低密度脂蛋白胆固醇无法解释的巨大心血管疾病风险。
{"title":"Phenotyping lipid profiles in type 2 diabetes: Risk association and outcomes from the Cardiovascular Health Study","authors":"David Bleich , Mary L. Biggs , Julius M. Gardin , Mary Lyles , David S. Siscovick , Kenneth J. Mukamal","doi":"10.1016/j.ajpc.2024.100725","DOIUrl":"10.1016/j.ajpc.2024.100725","url":null,"abstract":"<div><h3>Aims</h3><p>To determine whether discrete lipid profiles (refer to as lipid phenotyping) can be used to stratify cardiovascular risk in individuals with type 2 diabetes.</p></div><div><h3>Methods and results</h3><p>Cardiovascular Health Study participants with diabetes and fasting lipid profiles at baseline (<em>n</em> = 866) were categorized separately by level of LDL cholesterol and HDL-C/Triglyceride (Tg) profiles (low Tg/high HDL-C; high Tg/low HDL-C; high Tg only or low HDL-C only). We performed Cox multivariate regression analysis to assess the risk of CVD mortality, incident myocardial infarction (MI), heart failure (HF), stroke, and composite MACE (MI, HF, stroke, and CVD mortality) associated with each lipid category. We also calculated risk estimates for MACE using lipid measures as continuous variables. In the fully adjusted model, the high triglyceride plus low HDL-C cholesterol phenotype demonstrated risk that was at least as high as the highest LDL-C sub-group phenotype for CVD mortality (Hazard ratio {HR} 1.58 vs 1.48), MI (HR 1.53 vs 1.58), HF (HR 1.47 vs 1.20), stroke (HR 2.02 vs 1.43), and MACE (HR 1.58 vs 1.38). When modeled continuously, the HR per SD for MACE was 1.12 (<em>p</em> = 0.03) for LDL-C and 1.19–1.20 (<em>p</em> < 0.001) for triglycerides or remnant cholesterol.</p></div><div><h3>Conclusions</h3><p>Participants with the high triglyceride/low HDL-C phenotype had equivalent or higher CVD risk than those with the high LDL-C phenotype. Further studies are necessary to determine whether lipid phenotyping accounts for the substantial CVD risk not explained by LDL cholesterol among individuals with type 2 diabetes.</p></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"19 ","pages":"Article 100725"},"PeriodicalIF":4.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266666772400093X/pdfft?md5=34ecc037be6eeb164d07124684c133f3&pid=1-s2.0-S266666772400093X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142094638","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}
Pub Date : 2024-09-01DOI: 10.1016/j.ajpc.2024.100827
Teresa J. Yoon BS
Therapeutic Area
ASCVD/CVD Risk Factors
Background
Early metabolic imbalance (EMI) is a hidden condition characterized by compensated insulin resistance, often accompanied by oxidative stress, subclinical inflammation, and hypoxia. Individuals with EMI have fasting glucose, triglycerides, hemoglobin A1c, and high-density lipoprotein cholesterol (HDL-C) values all within normal limits. Thus, EMI is undetected in routine screening for diabetes and cardiovascular risk. Previously, we reported that EMI is an independent risk factor for type 2 diabetes (T2D) and atherosclerotic cardiovascular disease (CVD). Hypothesis: EMI in young adults increases the 35-year mortality risk compared with healthy, balanced metabolism.
Methods
We conducted a retrospective cohort study using data from the Coronary Artery Risk Development in Young Adults (CARDIA) study. The parent study began in 1985, enrolling 5,113 young adults ages 18-30, with study visits every five years for 35 years. For this retrospective analysis, the baseline exclusion criteria were fasting hyperglycemia, hypertriglyceridemia, low HDL-C, pregnancy, diabetes, or CVD; n=3,292. Cox proportional hazards regression analysis was performed using Stata 18.0 (StataCorp). The primary exposure variable was EMI, measured as the upper and lower halves of baseline homeostatic model assessment of insulin resistance v.2 (HOMA2-IR). The baseline covariates included other known causes of death. The primary outcome was time-to-incident mortality or censor. Mortality risk was measured as a Cox hazard ratio (HR) with 95% confidence interval (CI) and p-value. Each model met the assumption of proportional hazards.
Results
Over the 35-year follow-up period, 280 individuals died for a cumulative incidence of 8.5%. Cox Model 1 incorporated categorical HOMA2-IR (high/low) at baseline. Model 2 included the interaction between HOMA2-IR, sex, and race as a categorical variable (Table 1). Model 3 included the interaction variable from Model 2, along with other causes of death as covariates. As seen in Table 1, the Cox hazard ratios for EMI were modified by sex and race.
Conclusions
For young adults in CARDIA, EMI had a variable impact on 35-year mortality. The risk was modified by sex and race, even after adjusting for known risk factors. Further analysis is warranted.
{"title":"EARLY METABOLIC IMBALANCE IN YOUNG ADULTS HAS VARIABLE IMPACT ON 35-YEAR MORTALITY RISK","authors":"Teresa J. Yoon BS","doi":"10.1016/j.ajpc.2024.100827","DOIUrl":"10.1016/j.ajpc.2024.100827","url":null,"abstract":"<div><h3>Therapeutic Area</h3><div>ASCVD/CVD Risk Factors</div></div><div><h3>Background</h3><div>Early metabolic imbalance (EMI) is a hidden condition characterized by compensated insulin resistance, often accompanied by oxidative stress, subclinical inflammation, and hypoxia. Individuals with EMI have fasting glucose, triglycerides, hemoglobin A1c, and high-density lipoprotein cholesterol (HDL-C) values all within normal limits. Thus, EMI is undetected in routine screening for diabetes and cardiovascular risk. Previously, we reported that EMI is an independent risk factor for type 2 diabetes (T2D) and atherosclerotic cardiovascular disease (CVD). <strong>Hypothesis:</strong> EMI in young adults increases the 35-year mortality risk compared with healthy, balanced metabolism.</div></div><div><h3>Methods</h3><div>We conducted a retrospective cohort study using data from the Coronary Artery Risk Development in Young Adults (CARDIA) study. The parent study began in 1985, enrolling 5,113 young adults ages 18-30, with study visits every five years for 35 years. For this retrospective analysis, the baseline exclusion criteria were fasting hyperglycemia, hypertriglyceridemia, low HDL-C, pregnancy, diabetes, or CVD; n=3,292. Cox proportional hazards regression analysis was performed using Stata 18.0 (StataCorp). The primary exposure variable was EMI, measured as the upper and lower halves of baseline homeostatic model assessment of insulin resistance v.2 (HOMA2-IR). The baseline covariates included other known causes of death. The primary outcome was time-to-incident mortality or censor. Mortality risk was measured as a Cox hazard ratio (HR) with 95% confidence interval (CI) and p-value. Each model met the assumption of proportional hazards.</div></div><div><h3>Results</h3><div>Over the 35-year follow-up period, 280 individuals died for a cumulative incidence of 8.5%. Cox Model 1 incorporated categorical HOMA2-IR (high/low) at baseline. Model 2 included the interaction between HOMA2-IR, sex, and race as a categorical variable (Table 1). Model 3 included the interaction variable from Model 2, along with other causes of death as covariates. As seen in Table 1, the Cox hazard ratios for EMI were modified by sex and race.</div></div><div><h3>Conclusions</h3><div>For young adults in CARDIA, EMI had a variable impact on 35-year mortality. The risk was modified by sex and race, even after adjusting for known risk factors. Further analysis is warranted.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"19 ","pages":"Article 100827"},"PeriodicalIF":4.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142423106","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}
Pub Date : 2024-09-01DOI: 10.1016/j.ajpc.2024.100746
Jonathan Kermanshahchi BA
Therapeutic Area
ASCVD/CVD Risk Assessment
Background
The initial presentation of atherosclerotic cardiovascular disease (ASCVD) may be a severe, sometimes fatal outcome, and there is need for improved understanding and identification of ASCVD in asymptomatic individuals.
Methods
Using data from 6,779 participants the Multi-Ethnic Study of Atherosclerosis (MESA) without known cardiovascular disease, we evaluated the association between traditional risk factors and coronary artery calcium (CAC) with first ASCVD event (angina, stroke, myocardial infarction [MI], or death/resuscitated cardiac arrest [RCA]) in cox proportional hazards models.
Results
Overall, 1037 participants (15.3%) experienced a first ASCVD event over median follow-up of 15.8 years. The most common first presentation was death/RCA (27.7%). Those with CAC>0 were significantly more likely to present with angina than those with CAC=0 (26.% vs 13.0%, overall p<0.001). Black (35.6%) and Chinese (28.7%) individuals were more likely to present with death/RCA than White individuals (24.8%, overall p=0.011) and Black (25.7%) and Hispanic (29.3%) individuals were more likely to present with stroke than White (21.7%, p<0.001 overall) individuals. Women were more likely to present with death/RCA than men (29.8 vs 26.3%, overall p<0.001). Age, systolic blood pressure, diabetes, and smoking were significantly associated with a first presentation of death/RCA, while female sex and HDL-C were inversely associated. CAC (ln-transformed) was also significantly associated with first presentation of death/RCA (HR 1.15, 95% CI 1.10-1.22) and improved risk prediction when added to the Pooled Cohort Equations (continuous NRI 0.6081, 95% CI 0.4971-0.7141).
Conclusions
In previously asymptomatic individuals, the most common initial presentation of ASCVD was death/resuscitated cardiac arrest. In addition to traditional risk factors, CAC was associated with an initial presentation of death/RCA, and improved risk prediction for death/RCA when added to traditional risk factors. These findings suggest CAC scoring may help to identify individuals at risk for death or resuscitated cardiac arrest as a first presentation of ASCVD.
治疗领域ASCVD/心血管疾病风险评估背景初次出现动脉粥样硬化性心血管疾病(ASCVD)可能是一种严重的结果,有时甚至是致命的结果,因此需要更好地了解和识别无症状个体的 ASCVD。方法利用多种族动脉粥样硬化研究(MESA)中 6779 名未患已知心血管疾病的参与者的数据,在 cox 比例危险模型中评估了传统危险因素和冠状动脉钙(CAC)与首次 ASCVD 事件(心绞痛、中风、心肌梗死或死亡/心脏骤停抢救[RCA])之间的关系。结果在15.8年的中位随访期间,共有1037名参与者(15.3%)经历了首次ASCVD事件。最常见的首次事件是死亡/RCA(27.7%)。CAC>0者出现心绞痛的几率明显高于CAC=0者(26.0% vs 13.0%,总P<0.001)。黑人(35.6%)和中国人(28.7%)比白人(24.8%,总体 p=0.011)更容易出现死亡/心绞痛,黑人(25.7%)和西班牙裔(29.3%)比白人(21.7%,总体 p<0.001)更容易出现中风。女性比男性更容易出现死亡/RCA(29.8% vs 26.3%,总体 p<0.001)。年龄、收缩压、糖尿病和吸烟与首次出现死亡/RCA显著相关,而女性性别和高密度脂蛋白胆固醇则成反比。CAC(ln-transformed)也与首次出现死亡/心脏骤停显著相关(HR 1.15,95% CI 1.10-1.22),当加入到集合队列方程中时(连续 NRI 0.6081,95% CI 0.4971-0.7141),其风险预测能力有所提高。除了传统的风险因素外,CAC还与死亡/心脏骤停的初始表现相关,并且在加入传统风险因素后,还能改善死亡/心脏骤停的风险预测。这些研究结果表明,CAC评分可能有助于识别首次出现ASCVD时有死亡或心脏骤停复苏风险的人。
{"title":"FIRST PRESENTATION OF CARDIOVASCULAR DISEASE IN PREVIOUSLY HEALTHY INDIVIDUALS: THE MULTI-ETHNIC STUDY OF ATHEROSCLEROSIS","authors":"Jonathan Kermanshahchi BA","doi":"10.1016/j.ajpc.2024.100746","DOIUrl":"10.1016/j.ajpc.2024.100746","url":null,"abstract":"<div><h3>Therapeutic Area</h3><div>ASCVD/CVD Risk Assessment</div></div><div><h3>Background</h3><div>The initial presentation of atherosclerotic cardiovascular disease (ASCVD) may be a severe, sometimes fatal outcome, and there is need for improved understanding and identification of ASCVD in asymptomatic individuals.</div></div><div><h3>Methods</h3><div>Using data from 6,779 participants the Multi-Ethnic Study of Atherosclerosis (MESA) without known cardiovascular disease, we evaluated the association between traditional risk factors and coronary artery calcium (CAC) with first ASCVD event (angina, stroke, myocardial infarction [MI], or death/resuscitated cardiac arrest [RCA]) in cox proportional hazards models.</div></div><div><h3>Results</h3><div>Overall, 1037 participants (15.3%) experienced a first ASCVD event over median follow-up of 15.8 years. The most common first presentation was death/RCA (27.7%). Those with CAC>0 were significantly more likely to present with angina than those with CAC=0 (26.% vs 13.0%, overall p<0.001). Black (35.6%) and Chinese (28.7%) individuals were more likely to present with death/RCA than White individuals (24.8%, overall p=0.011) and Black (25.7%) and Hispanic (29.3%) individuals were more likely to present with stroke than White (21.7%, p<0.001 overall) individuals. Women were more likely to present with death/RCA than men (29.8 vs 26.3%, overall p<0.001). Age, systolic blood pressure, diabetes, and smoking were significantly associated with a first presentation of death/RCA, while female sex and HDL-C were inversely associated. CAC (ln-transformed) was also significantly associated with first presentation of death/RCA (HR 1.15, 95% CI 1.10-1.22) and improved risk prediction when added to the Pooled Cohort Equations (continuous NRI 0.6081, 95% CI 0.4971-0.7141).</div></div><div><h3>Conclusions</h3><div>In previously asymptomatic individuals, the most common initial presentation of ASCVD was death/resuscitated cardiac arrest. In addition to traditional risk factors, CAC was associated with an initial presentation of death/RCA, and improved risk prediction for death/RCA when added to traditional risk factors. These findings suggest CAC scoring may help to identify individuals at risk for death or resuscitated cardiac arrest as a first presentation of ASCVD.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"19 ","pages":"Article 100746"},"PeriodicalIF":4.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142422718","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}
Pub Date : 2024-09-01DOI: 10.1016/j.ajpc.2024.100757
Shoa L. Clarke MD, PhD
Therapeutic Area
ASCVD/CVD Risk Factors
Background
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).
Methods
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%.
Results
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]).
Conclusions
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.
{"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}
Pub Date : 2024-09-01DOI: 10.1016/j.ajpc.2024.100735
Ramon H Guillen MD
Therapeutic Area
ASCVD/CVD in Special Populations
Background
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.
Methods
Mortality data for premature AMI (<55y men, <65y women) from 1999-2019 were extracted from CDC death certificate data. ANOVA tests were done for race & BR, and for Hispanic origin & BR. Join point regression with tests for parallelism was applied to significant ANOVA subsets to analyze time trends.
Results
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<0.05). Hispanic mortality trended up in the BR (AAPC = +1.2886, p<0.05) and down in the non-BR (AAPC = -1.1370, p<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<0.05) from 1999-2009 and no significant change post-2009.
Conclusions
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.
{"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 (<55y men, <65y women) from 1999-2019 were extracted from CDC death certificate data. ANOVA tests were done for race & BR, and for Hispanic origin & 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<0.05). Hispanic mortality trended up in the BR (AAPC = +1.2886, p<0.05) and down in the non-BR (AAPC = -1.1370, p<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<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}
Pub Date : 2024-09-01DOI: 10.1016/j.ajpc.2024.100789
Yulith Roca Alvarez MD
Therapeutic Area
Heart Failure
Case Presentation
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.
Background
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.
Conclusions
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.
{"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}
Pub Date : 2024-09-01DOI: 10.1016/j.ajpc.2024.100759
Natalia Nazarenko MD
Therapeutic Area
ASCVD/CVD Risk Factors
Background
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).
Methods
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.
Results
Among 78 patients, 32 (41.03%) were female, and 46 (58.97%) were male. 32 patients had abnormal Lp(a) (>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.
Conclusions
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).
{"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) (>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}
Pub Date : 2024-09-01DOI: 10.1016/j.ajpc.2024.100806
Ashish Sarraju MD
Therapeutic Area
Other: Artificial intelligence; Misinformation
Background
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.
Methods
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 >20 years ago), or inappropriate (inaccurate content and/or references, including non-existent references).
Results
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.
Conclusions
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.
{"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 >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}