Goyal, Aman

Importance Elevated low-density lipoprotein cholesterol (LDL-C) is a modifiable risk factor for cardiovascular disease, the leading cause of premature death worldwide. Assessing the LDL-C–related burden is critical for guiding prevention and treatment strategies. Objectives To estimate the global, regional, and national burden of ischemic heart disease and ischemic stroke attributable to elevated LDL-C (relative to 35-54 mg/dL) from 1990 to 2023 and to quantify the contributions of population growth, aging, risk-deleted burden, and exposure changes to burden trends. Design, Setting, and Population This comparative risk assessment, part of the Global Burden of Disease Study 2023, estimated population-level LDL-C exposure and associated health loss in 204 countries and territories. Mean LDL-C levels were estimated using spatiotemporal gaussian process regression based on 806 studies across 161 countries. Relative risks were derived from meta-analyses of 38 randomized clinical trials. Population-attributable fractions for deaths and disability-adjusted life-years (DALYs) were estimated by age and sex for adults aged 25 years or older from 1990 to 2023, with 95% uncertainty intervals. Exposure Population-level LDL-C concentrations. Main Outcomes and Measures Population-attributable fractions, counts, and rates (all ages and age standardized per 100 000) of LDL-C–attributable deaths and DALYs from ischemic heart disease and ischemic stroke, with uncertainty intervals. Results In 2023, elevated LDL-C accounted for 3.6 million deaths (95% uncertainty interval, 2.2-5.4 million; 6.0% of global mortality) and 90.7 million DALYs (95% uncertainty interval, 58.9-123.3 million; 3.2% of DALYs). Although global all-ages rates remained stable, age-standardized death and DALY rates decreased by 45.6% and 39.5%, respectively, since 1990. In 2023, age-standardized LDL-C–attributable DALY rates were highest in Eastern Europe and lowest in high-income Asia-Pacific. One-third of the global LDL-C burden occurred in India and China. Population growth and aging drove the increasing burden, with notable regional disparities in LDL-C exposure and risk-deleted DALY rates shifting toward middle-sociodemographic settings. Conclusions and Relevance Despite declining age-standardized rates, the absolute LDL-C burden has increased since 1990 due to demographic changes and has shifted toward middle-sociodemographic countries. Measurement and surveillance gaps persist. Strengthened prevention, diagnosis, and treatment access strategies are essential to mitigate the health burden of LDL-C.

Summary Frailty is independently associated with significantly higher 1‐year mortality and MACCE following MTEER. Frail patients also demonstrated increased risks of HF exacerbation, major bleeding, and readmission. Incorporating frailty assessment into pre‐procedural evaluation may improve risk stratification and guide personalized management strategies.

Background: Sarcoidosis is a multisystem disorder characterized by non-caseating granulomas in various organs. While cardiac sarcoidosis (CS) is clinically rare, it has significant implications, including heart failure, ventricular arrhythmias, and sudden cardiac death. Speckle-tracking echocardiography has emerged as a promising tool for detecting subclinical myocardial dysfunction, which is cost-efficient and readily available. This meta-analysis aims to evaluate differences in functional echocardiographic parameters between patients with CS and extracardiac sarcoidosis (ECS) to improve early recognition and management. Methods: A comprehensive search of major bibliographic databases was conducted to identify studies up to December 2024. Mean differences (MDs) with 95% CIs were pooled using the inverse-variance random-effect model. Results: Seven studies with 478 patients with sarcoidosis (CS: 159 and ECS: 319) were included. Patients with CS had a significant reduction in left ventricular global longitudinal strain (MD: −2.73; 95% CI: −4.09, −1.38; p < 0.0001) and tricuspid annular plane systolic excursion (MD: −0.59; 95% CI: −1.12, −0.05; p = 0.03) compared to patients with ECS. No significant differences in the LV global circumferential strain, interventricular septum thickness, left ventricular ejection fraction, E/A ratio, E/E’ ratio, LV end-diastolic diameter, and LV end-systolic diameter were noted. Conclusions: LV GLS and TAPSE are promising parameters for the early detection of cardiac involvement in sarcoidosis, with significant prognostic implications. Although STE provides a cost-effective and accessible alternative to CMR and FDG-PET, further research is needed to standardize its use and validate diagnostic cut-offs.

Introduction: Thoracic aortic aneurysms (TAA) are a significant health concern, with the true prevalence likely underestimated due to undiagnosed cases. Outcomes in TAA are influenced by factors like age, sex, and comorbidities such as hypertension. This study examines mortality trends and disparities associated with TAA in US adults. Methodology: This study analyzed death certificates from 1999 to 2020 using the CDC WONDER Database to identify TAA-related deaths in individuals aged 25 and older using ICD-10 codes I71.1 and I71.2. Age-adjusted mortality rates (AAMRs) per 1 000 000 and annual percent changes (APCs) were calculated and stratified by year, sex, age group, race/ethnicity, region, and urbanization status. Results: Between 1999 and 2020, 47 136 TAA-related deaths were reported among US adults. The AAMR decreased from 16.2 to 8.2 per 1 000 000, with a significant decline from 1999 to 2013 (APC: −5.00; 95% CI: −5.54 to −4.54; P<0.001). Older adults had the highest AAMRs at 44.6 per 1 000 000. Men had higher AAMRs than women (11.2 vs. 9). AAMRs were highest among non-Hispanic (NH) Black (11), followed by NH White (10.3), NH Asian or Pacific Islander (9.5), NH American Indian or Alaska Native (7.8), and Hispanic (5.2) populations. Nonmetropolitan areas had higher AAMRs than metropolitan areas (11 vs. 9.8). Conclusions: The analysis showed a significant decline in TAA mortality since 1999, with recent stabilization. However, disparities persist, with higher AAMRs among men, older adults, NH Black adults, and nonmetropolitan residents, highlighting the need for targeted and equitable interventions.

Background: Hypertensive heart disease (HHD) poses a growing public health concern. Global data reveal a concerning rise in HHD prevalence, deaths, and disability-adjusted life years (DALYs) between 1990 and 2019. The Framingham Study highlights that hypertension is linked to approximately one-quarter of heart failure cases. This association is even stronger among older adults, in whom hypertension is responsible for up to 68% of heart failure cases. Methods: This study analyzed death certificates within the CDC WONDER database for patients in the United States from 1999 to 2020. We identified deaths among individuals aged 25 years and older caused by HHD and CHF using the International Classification of Diseases, Tenth Revision (ICD-10) code I11.0. Age-adjusted mortality rates (AAMRs) per 1,000,000 individuals and annual percent change (APC) were computed and categorized based on year, gender, race/ethnicity, and urbanization status. Results: Between 1999 and 2020, a total of 302,270 deaths were reported in patients due to HHD with CHF. Overall, AAMR increased from 37.3 to 134.9 per 1,000,000 population between 1999 and 2020, with a significant decrease from 1999 to 2004 (APC: -7.91; 95% CI: -20.16 to -1.04), followed by a significant increase from 2004 to 2007 (APC: 42.47; 95% CI: 21.27 to 55.62), a slight decrease from 2007 to 2014 (APC: -0.9; 95% CI: -9.38 to 2.39), and finally a steep increase from 2014 to 2020 (APC: 14.22; 95% CI: 10.87 to 20.84). Gender-based analysis revealed that men had slightly higher AAMRs than women (Men: 63.1; 95% CI: 62.8 to 63.5 vs. Women: 60.7; 95% CI: 60.5 to 61). Moreover, AAMRs were highest among non-Hispanic African Americans (109.6; 95% CI: 108.6 to 110.6), followed by non-Hispanic American Indian or Alaska Natives (66.6; 95% CI: 63.1 to 70.1), non-Hispanic Whites (58.5; 95% CI: 58.2 to 58.7), Hispanics (53.7; 95% CI: 52.9 to 54.5), and non-Hispanic Asian or Pacific Islanders (39; 95% CI: 38–39.9). In addition, non-metropolitan areas had higher AAMRs than metropolitan areas (non-metropolitan: 65.7; 95% CI: 65.2 to 66.3 vs. metropolitan: 62.1; 95% CI: 61.8 to 62.3) (Figure 1). Conclusions: Despite an initial decline, mortality from combined HHD and CHF has risen significantly since 1999. Notably, mortality was most pronounced among men, non-Hispanic African Americans, and individuals residing in non-metropolitan areas.

Background: According to the American Cancer Society, there are currently over 18 million adult cancer survivors in the US, and by 2030, that figure is estimated to rise to over 22 million. While this is positive, more and more survivors are now at risk for cardiovascular disease (CVD). Hypothesis: This meta-analysis aims to evaluate the association between cancer survivors and cardiovascular event. Methods: A systematic search was conducted in electronic databases from inception until March 2024 using appropriate Mesh terms for ‘Cancer’, and ‘cardiovascular risk’. Pooled risk ratios (RR) with their corresponding 95% confidence intervals (CI) were calculated using random effects models. A p-value of <0.05 was considered statistically significant. Results: A total of nine studies with 1,209,168 people (Cancer survivor: 140697 and non-cancer: 1068471) were included in our study. The mean follow-up duration was 12.4 years. The risk of cardiovascular events was seen in all cancer survivors (RR: 1.69, 95%CI: 1.31-2.08, P <0.05). The cardiovascular risk was statistically significant in patients with leukemia (RR: 1.71, 95%CI: 1.54-1.88), lung cancer (RR: 1.99, 95%CI: 1.38-2.6) and lymphoma (RR: 1.65, 95%CI: 1.29-2.01), and comparable in breast cancer (RR: 1.22, 95%CI: 0.98-1.46), colorectal cancer (RR: 1.13, 95%CI: 0.89-1.37), prostate cancer (RR: 1.08, 95%CI: 0.99-1.17) and thyroid cancer (RR: 0.96, 95%CI: 0.57-1.35). Conclusion: Our study showed that overall cancer survivors had significant risk for cardiovascular events; mainly leukemia, lung cancer, and lymphoma patients had a significant result. Early identification, continuous monitoring, and proactive management strategies are essential to mitigate the long-term cardiovascular effects of cancer treatments.

Background: Acute Kidney Injury (AKI) is a multifactorial complication following repair of Stanford Type A aortic dissection (TAAD) with an alarmingly high incidence, varying from 20 to 77%. Postoperative AKI following life-threatening disease tends to be much more complex. However, the exact role of postprocedural AKI in the prognosis of patients undergoing TAAD repair has not been elucidated. Aims: This meta-analysis aimed to evaluate the prognostic significance of postprocedural AKI in patients undergoing TAAD repair. Methods: A literature search was conducted using PubMed, EMBASE, and SCOPUS databases. The primary endpoint was 30-day mortality with several secondary endpoints. Risk ratios (RR) with 95% confidence intervals (CIs) were pooled using Review Manager software. Statistical significance was set at p <0.05. Random-effects meta-analyses were performed for all outcomes. Results: Our analysis included 21 studies comprising 10396 patients. Patients with AKI exhibited a significantly higher risk of 30-day mortality (RR=3.98; 95% CI: 3.04-5.22; p<0.00001; I 2 =57%), stroke (RR= 2.05; 95% CI: 1.68-2.50; p<0.00001; I 2 =32%), dialysis requirement (RR= 32.9; 95% CI: 10.39-104.24; p<0.00001; I 2 =90%) (Figure 1), cardiovascular complications (RR= 2.85; 95% CI: 1.65-4.92; p<0.0002; I 2 =85%), sepsis (RR= 4.92; 95% CI: 2.62-9.24; p<0.00001; I 2 =64%), and re-exploration for bleeding (RR=2.46; 95%CI: 1.79-3.39; p<0.00001; I 2 =58%) compared to those without AKI (Figure 2). Conclusion: Patients with AKI demonstrated a significantly increased risk of mortality, stroke, need for dialysis, sepsis, postoperative cardiovascular complications, and re-exploration for bleeding. Further prospective studies are required to better understand the prevention strategies and long-term effects on prognosis of AKI post-repair for TAAD.

Acute kidney injury (AKI) frequently complicates the repair of Stanford type A aortic dissection (TAAD). This systematic review, meta-analysis, and meta-regression analysis aimed to elucidate the prognostic impact of AKI in these patients. A literature search in PubMed, EMBASE, and Google Scholar identified relevant studies on the predictors and outcomes of AKI following TAAD repair. The primary endpoint was 30-day mortality; secondary endpoints included stroke, dialysis/continuous renal replacement therapy (CRRT), and other complications. Random-effects meta-analyses were used, with significance set at P < 0.05. Twenty-one studies (10 396 patients) were analyzed. AKI was associated with higher risks of 30-day mortality (risk ratio = 3.98), stroke (risk ratio = 2.05), dialysis/CRRT (risk ratio = 32.91), cardiovascular (risk ratio = 2.85) and respiratory complications (risk ratio = 2.13), sepsis (risk ratio = 4.92), and re-exploration for bleeding (risk ratio = 2.46). No significant differences were noted in sternal wound infection, tracheostomy, paraplegia, or hepatic failure. AKI significantly increases mortality, morbidity, hospital, and ICU stay duration in TAAD repair patients.

AbstractStatins are the first line of treatment for both primary and secondary prevention of atherosclerotic cardiovascular disease. Despite the positive effects of statins on cardiovascular events, not all patients can use them at an optimized dose. The reason for this is the skeletal muscle side effects, termed statin‐associated muscle symptoms (SAMS). Despite extensive research, the precise pathophysiology of SAMS remains unclear and multiple mechanisms may contribute to this phenomenon. Various therapeutic options are available for the management of SAMS, ranging from rechallenging with the same or a different statin to utilizing non‐statin therapeutic alternatives in patients intolerant to statins. However, the lack of consensus on the definition of SAMS, the absence of a definitive diagnostic test, and lack of a universally accepted management algorithm pose a great challenge in dealing with this entity. This review aims to explore the various pathophysiological mechanisms involved in SAMS and understand the difference between self‐limited toxic myopathy and immune‐mediated myopathy requiring immunomodulatory therapy. The conundrum of statin withdrawal, tapering, and rechallenge in SAMS will also be explored in detail along with the newer non‐statin therapies that are available.