American journal of preventive cardiology最新文献

{"title":"MASSIVE AORTIC ATHEROMA AS CAUSE OF ISCHEMIC STROKE","authors":"Mitchell Padkins MD","doi":"10.1016/j.ajpc.2024.100753","DOIUrl":"10.1016/j.ajpc.2024.100753","url":null,"abstract":"<div><h3>Therapeutic Area</h3><div>CVD Prevention – Primary and Secondary</div></div><div><h3>Case Presentation</h3><div>A 78-year-old-male was referred for assessment of the etiology of a symptomatic ischemic stroke in the right cerebellum. Vascular imaging including CT angiogram of the head and neck as well as prolonged electrocardiogram monitoring did not reveal a cause of his stroke.</div><div>A transesophageal echocardiogram (TEE) demonstrated no embolic source in the cardiac chambers and no intra-atrial shunt was identified. However, upon inspection of the descending thoracic aorta, a large atheroma was visualized measuring 2 cm in diameter and 0.7 cm thick (Figure). This finding led to a CT to further characterize this lesion. CT demonstrated non-calcified atherosclerotic plaque in the descending thoracic aorta which was determined to be the likely etiology of the stroke.</div><div>The identification of significant atherosclerotic plaque led to aggressive secondary prevention with the addition of aspirin 81 mg and high-intensity statin therapy. The patient's LDL cholesterol decreased from 120 mg/dL prior to the event to 42 mg/dL 12 weeks after initiating high-intensity statin therapy. At 1-year follow-up the patient has had no neurologic events and is tolerating therapy well.</div></div><div><h3>Background</h3><div>After a cerebrovascular accident is diagnosed, testing is warranted to identify the etiology. Unless a known etiology is identified, testing typically includes laboratory studies, prolonged ambulatory cardiac monitoring, imaging of the head and neck vessels, and imaging of the cardiac structures. Cardiac imaging typically begins with a transthoracic echocardiogram (TTE). However, TTE lacks the spatial resolution to identify atheromatous disease in the descending thoracic aorta. Thus, further imaging with TEE is often necessary for imaging the aorta and to rule out an intra-cardiac shunt.</div><div>After the etiology of a stroke is defined, management focuses on aggressive risk factor modification. Recent guidelines recommend initiating high-intensity statin therapy with a goal of reducing LDL to reduce the risk of future sequela related to atherosclerosis. In this case, aggressive antiplatelet and lipid lowering therapy was initiated with a significant reduction in the patient's LDL cholesterol.</div></div><div><h3>Conclusions</h3><div>This case represents a massive descending aortic atheroma, identified on TEE, as the cause of an ischemic stroke that led to aggressive secondary risk factor modification.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"19 ","pages":"Article 100753"},"PeriodicalIF":4.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142422716","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":"BASELINE CHARACTERISTICS OF PARTICIPANTS ENROLLED IN VICTORION-INCEPTION: A RANDOMIZED STUDY OF INCLISIRAN VS. USUAL CARE IN PATIENTS WITH RECENT HOSPITALIZATION FOR AN ACUTE CORONARY SYNDROME","authors":"Kirk U Knowlton MD","doi":"10.1016/j.ajpc.2024.100756","DOIUrl":"10.1016/j.ajpc.2024.100756","url":null,"abstract":"<div><h3>Therapeutic Area</h3><div>CVD Prevention – Primary and Secondary</div></div><div><h3>Background</h3><div>Patients with recent acute coronary syndrome (ACS) are at high risk for recurrent atherosclerotic cardiovascular disease (ASCVD) events. Lowering low-density lipoprotein cholesterol (LDL-C) to &lt;70 mg/mL can reduce this risk; thus, lipid-lowering therapy (LLT), including non-statin therapy, should be intensified within 4–6 weeks of ACS. Despite this recommendation, few patients achieve LDL-C &lt;70 mg/dL after an ACS event. When added to maximally tolerated statin therapy, inclisiran lowered LDL-C by an additional ∼50% in patients with ASCVD in prior trials, but those with ACS within 3 months of screening were excluded.</div></div><div><h3>Methods</h3><div>VICTORION-INCEPTION (NCT04873934) is an ongoing, Phase 3b, US, randomized, parallel-group, open-label, multicenter trial in patients with recent ACS. Eligible patients were screened within 5 weeks of hospital discharge and had LDL¬ C ≥70 mg/mL (or non-high-density lipoprotein cholesterol [HDL-C] ≥100 mg/dL) either on statin therapy or with statin intolerance. Patients were randomized 1:1 to inclisiran 284 mg (equivalent to 300 mg inclisiran sodium) on Days 0, 90, and 270 plus usual care or usual care alone (standard of care per treating physician). This interim analysis describes patient demographics and clinical characteristics.</div></div><div><h3>Results</h3><div>Through February 5, 2024, 788 patients were screened across 40 sites, of whom 400 were eligible and randomized: median age 61 years, 29.3% female, 12.3% Black or African American, and 14.3% Hispanic or Latino. The most common index ACS event (93%) was myocardial infarction (MI); 22% of patients had a prior MI. The median time from discharge to randomization was 34 days (Q1–Q3: 26–43). At baseline, median calculated LDL-C was 84.0 mg/dL (Q1–Q3: 71.0–103.0), non-HDL-C was 107.0 mg/dL (Q1–Q3: 93.0–129.0), and 95.5% of patients were receiving LLT (any statin therapy [alone or combination]: 93.3%; any high-intensity statin therapy: 81.3%; combination therapy [statin plus non-statin LLT]: 9.0%). Demographic and baseline characteristics are comparable between treatment arms (Table).</div></div><div><h3>Conclusions</h3><div>VICTORION-INCEPTION evaluates the LDL-C lowering effect of implementing a systematic LDL-C management pathway including inclisiran in patients with a recent ACS. The enrolled study population is reflective of real-world US clinical practice.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"19 ","pages":"Article 100756"},"PeriodicalIF":4.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142422728","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":"PREDICTORS OF LIPOPROTEIN(A) TESTING ACROSS A NATIONAL COHORT: INSIGHTS FROM THE VETERANS HEALTH ADMINISTRATION","authors":"Tania Chen MBBS, MPH","doi":"10.1016/j.ajpc.2024.100767","DOIUrl":"10.1016/j.ajpc.2024.100767","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 genetically determined, independent, causal risk factor for atherosclerotic cardiovascular diseases (ASCVD). Multiple practice guidelines increasingly recommend Lp(a) testing to refine cardiovascular risk assessment. We aimed to evaluate sociodemographic and clinical factors influencing Lp(a) testing in the Veterans Affairs (VA) healthcare system.</div></div><div><h3>Methods</h3><div>We assembled a retrospective cohort using data from the VA electronic health record, Medicare claims, and community care for Veterans having at least one outpatient visit in the VA between July 1, 2020, and June 30, 2023, and at least one prescription filled in 180 days before the date of the last VA outpatient encounter to ensure adequate healthcare system contact. We evaluated patient-level sociodemographic and clinical predictors of Lp(a) testing. Predictors included self-reported race and ethnicity, social vulnerability, the presence and type of ASCVD, and low-density lipoprotein cholesterol (LDL-C) levels. Neighborhood social vulnerability was defined using the CDC's Social Vulnerability Index (SVI) and categorized by quartiles (higher numbers associated with higher vulnerability). Associations between patient characteristics and Lp(a) testing were estimated using generalized estimating equations.</div></div><div><h3>Results</h3><div>Among 5,331,271 Veterans, the median age was 67 years (IQR 52-76) with 10.3% female; 69.6% identified as White, 18.8% Black, 7.4% Hispanic. Less than 1% of eligible Veterans have received Lp(a) testing. Lp(a) was more likely to be tested among Veterans with older age, White race, non-Hispanic ethnicity, living in urban neighborhoods, and those with low SVI (less vulnerable neighborhoods). After multivariable adjustment, Lp(a) testing was more likely among women, Veterans identified as Black or Asian, and those with established ASCVD (Figure). Across 130 VA facilities, Lp(a) testing ranged from 0.01-3.40%. The median Lp(a) level among those tested at VA facilities was 16 mg/dL (IQR 6-53) with 26% of Veterans with ASCVD and 20% of Veterans without ASCVD having Lp(a) levels &gt;50 mg.</div></div><div><h3>Conclusions</h3><div>Lp(a) testing is infrequent in the VA healthcare system, with disparities in testing by sociodemographic and clinical characteristics. About a quarter of those tested had elevated Lp(a) levels. Developing strategies to improve overall Lp(a) testing and reduce existing gaps in testing by sociodemographic factors is critical as targeted therapeutics become available.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"19 ","pages":"Article 100767"},"PeriodicalIF":4.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142422731","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":"TEMPORAL TRENDS IN LIPOPROTEIN(A) TESTING AMONG UNITED STATES VETERANS FROM 2014-2023","authors":"Sofia E. Gomez MD","doi":"10.1016/j.ajpc.2024.100758","DOIUrl":"10.1016/j.ajpc.2024.100758","url":null,"abstract":"<div><h3>Therapeutic Area</h3><div>Novel Biomarkers</div></div><div><h3>Background</h3><div>Elevated lipoprotein(a) [Lp(a)] is a genetically-determined, independent, causal risk factor for atherosclerotic cardiovascular disease (ASCVD). Multiple contemporary clinical practice guidelines endorse Lp(a) testing to refine risk stratification for ASCVD and guide clinical decision-making among high-risk patients. Changes in rates of testing and detection of elevated Lp(a) over time have not been well described.</div></div><div><h3>Methods</h3><div>We performed a retrospective cohort study using Veterans Affairs electronic health record data to evaluate temporal trends in Lp(a) testing from January 1, 2014 to December 31, 2023 among United States Veterans. We identified Veterans in each year who had a primary care or cardiology visit, an active medication filled, and no prior Lp(a) testing. We stratified testing rates based on demographic and clinical factors: age, sex, race and ethnicity, history of ASCVD, and neighborhood social vulnerability index (SVI) scores as defined by the Centers for Disease Control. The SVI incorporates variables such as employment, income, crowding, and education, with higher scores suggesting greater vulnerability. We classified elevated Lp(a) levels using three clinically meaningful thresholds: 50 mg/dL, 70 mg/dL and 90 mg/dL.</div></div><div><h3>Results</h3><div>Lp(a) testing increased nationally from 1 test per 10,000 eligible Veterans (558 tests) in 2014 to 9 tests per 10,000 (4,440 tests) in 2023. While testing increased across all groups, prevalent ASCVD was strongly associated with an increase in Lp(a) testing over time (Figure). Rates of testing increased less among those residing in neighborhoods with high social vulnerability compared with low social vulnerability. Rates of testing increased most among Asian Veterans but similarly across other racial and ethnic groups. The percent of elevated tests across clinically meaningful thresholds has remained stable over time.</div></div><div><h3>Conclusions</h3><div>We found a 9-fold increase in Lp(a) testing among US Veterans over the last decade, particularly among those with ASCVD, but the overall rate remains extremely low. The proportion of Veterans with elevated Lp(a) has remained steady, supporting the clinical utility of testing expansion. Efforts to increase testing among Veterans living in neighborhoods with high social vulnerability will be important to reduce emerging disparities as novel therapeutics to target Lp(a) become available.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"19 ","pages":"Article 100758"},"PeriodicalIF":4.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142422753","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":"PERFORMANCE OF PREVENT AND POOLED COHORT EQUATIONS FOR PREDICTING 10 YEAR ASCVD RISK IN THE UK BIOBANK","authors":"Matthew Ambrosio MS","doi":"10.1016/j.ajpc.2024.100782","DOIUrl":"10.1016/j.ajpc.2024.100782","url":null,"abstract":"<div><h3>Therapeutic Area</h3><div>ASCVD/CVD Risk Assessment</div></div><div><h3>Background</h3><div>The Pooled Cohort Equations (PCE) were created in 2013 to assess ASCVD risk in primary prevention. In 2023 the American Heart Association published the PREVENT equations to assess the risk of cardiovascular disease, including ASCVD and heart failure, in primary prevention. The comparative performance of PCE and PREVENT for predicting 10-year ASCVD risk has not been evaluated in an external large-scale epidemiologic cohort.</div></div><div><h3>Methods</h3><div>The study population includes participants of the UK Biobank who were free of clinical cardiovascular disease. 10-year ASCVD risk was calculated using the PCE and PREVENT equations, respectively.</div><div>Individuals who died from non-ASCVD events, or were lost to follow-up before 10 years without developing ASCVD were excluded. C-statistics (AUCs) were calculated separately for men and women to evaluate risk discrimination, and correlated delta AUCs were calculated using DeLong's method. Predicted 10-year risks were divided into deciles for each equation and stratified by gender to compare predicted risk versus observed risk within each decile, with a Hosmer-Lemeshow test performed for goodness of fit.</div></div><div><h3>Results</h3><div>The final cohort was 370,885 individuals (mean age 56, 55.3% women, 94.0% white), after excluding 14,604 individuals lost to follow-up before 10 years without developing ASCVD. The observed 10-year ASCVD (95% CI) was 2.4% (2.31%-2.44%) for women and 5.5% (5.45%-5.56%) for men; the median (IQR) PCE predicted 10-year ASCVD risk was 3.6% (1.53%-7.12%) for women and 10.6% (5.33%-17.03%) for men. The median PREVENT predicted 10-year ASCVD risk was 2.9% (1.47%-4.95%) for women and 5.2% (3.02%-7.93%) for men. The C-statistics for PCE were 0.732 (0.7253-0.7389) for women and 0.695 (0.6893-0.7000) for men. In comparison, the C-statistics for PREVENT were 0.732 (0.7249-0.7382) for women and 0.695 (0.6894-0.6998) for men. Delta AUC was -0.0009 (p=0.36) for women and -0.0009 (p=0.21) for men. Figure 1 displays the mean PCE and PREVENT predicted 10-year ASCVD risks compared to observed risks for each decile. The PREVENT equations appear to be better calibrated than the PCE.</div></div><div><h3>Conclusions</h3><div>There is no significant difference in 10-year ASCVD risk discrimination between PCE and PREVENT equations. However, the PREVENT equations appear to be better calibrated at predicting risk compared to the PCE.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"19 ","pages":"Article 100782"},"PeriodicalIF":4.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142422820","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":"IMPACT OF CARDIOMETABOLIC DISORDERS ON THE DIAGNOSIS OF METABOLIC ASSOCIATED FATTY LIVER DISEASE (MAFLD) AMONG HOSPITALIZED PATIENTS: A 5-YEAR RETROSPECTIVE STUDY OF NIS DATABASE BETWEEN 2016-2020.","authors":"Adedeji Adenusi MD, MPH","doi":"10.1016/j.ajpc.2024.100785","DOIUrl":"10.1016/j.ajpc.2024.100785","url":null,"abstract":"<div><h3>Therapeutic Area</h3><div>ASCVD/CVD Risk Factors</div></div><div><h3>Background</h3><div>Cardiometabolic disorders are health conditions that are associated with increased risk for cardiovascular events and sudden cardiac death in the US. However, only a few studies explored these health conditions on the increasing trend of MAFLD. This study aims to explore the impact of cardiometabolic disorders among patients diagnosed with MAFLD in US hospitals.</div></div><div><h3>Methods</h3><div>We used the NIS data of 2016-2020 period for this cross-sectional study. Our main outcome was MAFLD while predictors were cardiometabolic syndrome (hypertension, diabetes, CKD, dyslipidemia, obesity) with co-variates (race, age, sex). We did descriptive analysis, bivariate and multivariate logistic regressions to identify potential predictors associated with MAFLD.</div></div><div><h3>Results</h3><div>A total of 252,254,979 hospitalized patients were analyzed of which 112,375 patients were hospitalized with principal diagnosis of MAFLD/NAFLD. MAFLD were predominantly diagnosed in females (61.3%), individuals over 45 years (89.4%), white (78.4%), those with obesity (66.2%), without dyslipidemia (55.1%), with metabolic syndrome (98.8%), hypertension (66.2%), diabetes (80.4%) and chronic kidney disease (67.7%). Patients with obesity were two-fold likely to be diagnosed with MAFLD compared to patients with normal BMI. (aOR= 2.319 [95%CI 2.223-2.419], p&lt;.0001). Conversely patients with dyslipidemia were less likely to be diagnosed with MAFLD than those without dyslipidemia. (0.903 [0.870-0.936], p&lt;.0001). Patients with metabolic syndrome were four-fold likely to be diagnosed with MAFLD compared with non-metabolic syndrome patients. (4.353 [3.583-5.289], p&lt;.0001). Patients with hypertension had a marginal likelihood to be diagnosed with MAFLD compared to non-hypertensive patients. (1.044 [1.003-1.086], p=0.0348). Patients with diabetes or CKD were two-fold likely to be diagnosed with MAFLD compared with non-diabetic and non-CKD patients respectively. (2.439 [2.345-2.536], p&lt;.0001), (2.305 [2.206-2.409], p&lt;.0001). Patient of Hispanic descent were more likely to have MAFLD compared with patients of white descents. (1.169 [1.082-1.264], p&lt;.0001), while patients from black and Asian descent were less likely to have MAFLD respectively. (0.235 [0.219-0.251], p&lt;.0001), (0.651 [0.585-0.724], p&lt;.0001)</div></div><div><h3>Conclusions</h3><div>The results of this study contribute to the body of knowledge on the risk and pattern of MAFLD among patients with cardiometabolic disorders, emphasizing the complex interplay between sociodemographic and clinical factors. This further informs lifestyle modification, early detection and treatment of cardiometabolic disorders as preventive strategy for MAFLD.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"19 ","pages":"Article 100785"},"PeriodicalIF":4.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142422823","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":"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}

{"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}

{"title":"Phenotyping lipid profiles in type 2 diabetes: Risk association and outcomes from the Cardiovascular Health Study","authors":"David Bleich ,&nbsp;Mary L. Biggs ,&nbsp;Julius M. Gardin ,&nbsp;Mary Lyles ,&nbsp;David S. Siscovick ,&nbsp;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> &lt; 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}

{"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}