Clevidipine is a parenteral dihydropyridine calcium channel blocker that received Food and Drug Administration approval in 2008 for the reduction of blood pressure (BP) when oral therapy is not feasible or not desirable. Soon after approval, our institution incorporated clevidipine into protocols for the management of hypertension among acute stroke patients, based on the drug's rapid onset of action and straightforward titration to goal. A subsequent retrospective review of its use in otherwise alteplase-eligible ischemic stroke patients with BP greater than 185/110 mm Hg (n = 32, in 2014) revealed that clevidipine in that setting demonstrated the shortest median time to BP control, the shortest median door-to-alteplase administration time, and the lowest administered volume of any parenteral antihypertensive used. As a result, clinical protocols in our institution were modified to make clevidipine first-line antihypertensive in both ischemic and hemorrhagic acute stroke. In this study, we report our institution's experience with clevidipine in acute stroke, comprising the largest such report to date. We conducted a retrospective chart review of all acute stroke patients who received clevidipine in the emergency department (ED) or intensive care unit (ICU) (n = 295) for the management of clinically significant hypertension between January 1, 2015, and December 31, 2017. Metrics analyzed included target (goal) BP for thrombolysis eligibility among patients intended for lytic therapy according to stroke management guidelines in effect at the time of care. The median time for initial parenteral antihypertensive dose to goal (DTG) BP for all ischemic stroke patients (both those intended for and those not intended for lytic therapy) with complete data (n = 71 of 204) was 15 minutes; median time for door-to-IV-alteplase administration for ischemic stroke patients with complete data (n = 14 of 34 treated patients) was 59 minutes. The median time for initial parenteral antihypertensive DTG BP for all hemorrhagic stroke patients with complete data (n = 33 of 91 treated patients) was 39 minutes. We conclude that the salutary findings of the initial small study are valid across a larger patient sample of all acute stroke types. Based on these data, clevidipine is shown to be safe, consistent, and effective in the treatment of acute hypertension in ischemic and hemorrhagic stroke events, and is a reasonable first-line treatment option for acute hypertension in this setting.
Dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor is standard of care after percutaneous coronary intervention (PCI) in acute coronary syndrome (ACS). Although aspirin discontinuation after at least 1 month of DAPT reduces bleeding without increasing ischemic events, the safety of aspirin withdrawal before the first 30 days after PCI remains uncertain. Online databases were searched through December 2025 to identify randomized controlled trials (RCTs) comparing aspirin-free P2Y12 inhibitor monotherapy (MAPT) initiated within 30 days after PCI versus standard DAPT in ACS patients. Outcomes were assessed during short-term (0-30 days) and longer-term follow-up (31 days to 12 months). Random-effects models were used to estimate odds ratios (ORs) with 95% confidence intervals (CIs). Three RCTs comprising 10,736 patients were included. Within 30 days after PCI, aspirin discontinuation was associated with a higher risk of myocardial infarction (OR: 2.12; 95% CI: 1.31-3.44), without a reduction in bleeding compared with DAPT. No significant differences were observed in other ischemic, composite or mortality outcomes. During longer-term follow-up, MAPT was associated with significant reductions in bleeding outcomes and net adverse clinical events, without an increase in ischemic outcomes. In ACS patients undergoing PCI with DES, aspirin discontinuation within 30 days did not reduce bleeding and was associated with a higher risk of myocardial infarction. These findings suggest the first 30 days after PCI may represent a period of heightened ischemic vulnerability and routine aspirin withdrawal during this early phase should be interpreted with caution.
Hyperuricemia, characterized by elevated serum uric acid levels, has been linked to cardiovascular diseases such as hypertension, atrial fibrillation, chronic kidney disease, heart failure, metabolic syndrome, and coronary artery disease. This relationship, however, is complex; while some studies indicate a strong association, others suggest that it may be influenced by confounding factors. The rising global prevalence of hyperuricemia underscores the necessity for a deeper understanding of its cardiovascular implications. Hyperuricemia results from an imbalance in uric acid production and excretion, driven by dietary factors, obesity, insulin resistance, and other conditions. Elevated uric acid levels contribute to cardiovascular risk through mechanisms such as inflammation, oxidative stress, endothelial dysfunction, and activation of the renin-angiotensin-aldosterone system. This review highlights the importance of ongoing research to clarify hyperuricemia's role in cardiovascular disease and suggests that urate-lowering therapies, such as xanthine oxidase inhibitors, may confer cardiovascular benefits; however, evidence remains conflicting. The Cardiovascular Safety of Febuxostat and Allopurinol in Patients with Gout and Cardiovascular Morbidities (CARES) trial indicated an increased risk of cardiovascular and all-cause mortality with febuxostat compared with allopurinol, raising safety concerns. In contrast, the Febuxostat versus Allopurinol Streamlined Trial (FAST) demonstrated that febuxostat was noninferior to allopurinol, with even lower all-cause mortality. These opposing findings emphasize the complexity of treatment decisions and the need for individualized management strategies for hyperuricemia. Clinical decisions should consider individual patient risks and characteristics. Ultimately, this comprehensive analysis aims to enhance prevention and management strategies for cardiovascular diseases related to hyperuricemia. The overview includes discussions on major studies such as the Framingham Heart Study, CARES, FAST, PRIZE, and FREED trials, examining their results. It explores whether hyperuricemia is a causal factor versus an associated risk factor and whether it serves as a marker or mediator of disease. Additionally, the review addresses novel biomarkers and predictive models, the management of hyperuricemia in the context of cardiovascular risk, the role of urate-lowering therapies in cardiovascular disease, variability in guidelines and recommendations, and the impact of hyperuricemia in special populations such as those with diabetes and chronic kidney disease. The cardiovascular risk associated with hyperuricemia across various demographics is also discussed. Furthermore, the review suggests that existing risk scores might be modified to include uric acid levels in patients with hyperuricemia.
Hypertensionis a leading global health issue associated with high mortality and severe complications. Understanding its molecular mechanisms is essential for identifying novel therapeutic targets. Secreted protein acidic and rich in cysteine (SPARC) is associated with cell migration, disease pathophysiology, and inflammation; however, its role in hypertension remains under investigation. This study investigates the role of SPARC in hypertension, focusing on its impact on endothelial dysfunction.Using the GSE75815 dataset from the GEO database, we identified 71 differentially expressed genes (DEGs) associated with hypertension. Pathway analyses and protein-protein interaction networks constructed through the STRING database highlighted six hub genes, with further evaluation based on Comparative Toxicogenomics Database (CTD) scores. Immune cell profiling via ImmuCellAI revealed an increase in naive B cells, positively correlating with hub gene expression.Experimental validation in human umbilical vein endothelial cells (HUVECs) treated with angiotensin II demonstrated that SPARC downregulation reduced apoptosis and BAX expression. Silencing SPARC enhanced endothelial cell proliferation, migration, and nitric oxide production, counteracting angiotensin II-induced damage. Notably, angiotensin II upregulated SPARC secretion, suggesting its critical role in mediating endothelial dysfunction.These findings establish SPARC as a key contributor to the molecular pathways underlying hypertension. Targeting SPARC may represent a novel therapeutic strategy to mitigate endothelial dysfunction and improve outcomes for hypertensive patients.Our findings highlight SPARC as a key player in the molecular pathways of hypertension. Modulating SPARC expression may offer a promising therapeutic strategy to counteract endothelial dysfunction and improve outcomes in hypertensive patients.
Differentiating type 1 myocardial infarction (T1-MI) from type 2 MI (T2-MI) remains a diagnostic challenge, even with the availability of high-sensitivity cardiac troponin assays. This study explored whether N-Terminal Pro-B-Type Natriuretic Peptide (NT-proBNP), BNP, and their respective ratios to troponin could enhance the ability to distinguish between these MI subtypes. As a High-Sensitivity Cardiac Troponin I Assays in the United States substudy, we examined data from 280 patients diagnosed with non-ST elevation MI (172 with T1-MI and 108 with T2-MI). We assessed NT-proBNP, BNP, high-sensitivity cardiac troponin I, and their ratios as potential discriminative biomarkers. Diagnostic accuracy was evaluated using receiver operating characteristic curves. NT-proBNP levels were markedly elevated in T2-MI patients compared with those with T1-MI (mean: 10,327 ± 12,923 vs. 4675 ± 11,740 ng/L; P = 0.006). Conversely, high-sensitivity cardiac troponin I concentrations were higher in T1-MI (1.4 ± 5.1 vs. 0.5 ± 1.1 ng/L; P = 0.030). Notably, the NT-proBNP-to-troponin ratio was more than 3 times greater in T2-MI cases (94,880 ± 152,648 vs. 24,209 ± 78,727; P = 0.007). NT-proBNP alone demonstrated fair discriminatory capacity [area under the receiver operating characteristic curve (AUC) 0.717, 95% confidence interval (CI): 0.578-0.856], closely matching the NT-proBNP-to-troponin ratio (AUC: 0.720, 95% CI: 0.566-0.873). In contrast, BNP and the BNP-to-troponin ratio offered lower diagnostic values. Mean BNP levels were 505.4 ± 576.6 ng/L for those with T2-MI and 437.1 ± 738.8 ng/L for patients with T1-MI. BNP-to-troponin ratio showed a poor discrimination for the 2 MI types (AUC: 0.660; 95% CI: 0.532-0.789). Both NT-proBNP and its ratio to troponin show potential in differentiating T1-MI from T2-MI, reflecting distinct underlying pathophysiological processes. Given its comparable performance to the ratio, NT-proBNP alone may serve as a practical and cost-effective standalone marker. These findings support the hypothesis that incorporating NT-proBNP testing into routine clinical workflows may better inform the management of patients with suspected MI.
Chronic kidney disease (CKD) is a global health concern associated with an elevated risk of cardiovascular (CV) and all-cause mortality. The ankle-brachial index (ABI), a noninvasive diagnostic tool, is widely recognized for detecting peripheral arterial disease. This meta-analysis aims to assess whether abnormally low or high ABI values independently predict CV and all-cause mortality in CKD patients, including those on hemodialysis. A systematic review and meta-analysis was conducted following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, using PubMed, Cochrane, and Google Scholar databases through September 2024 to identify studies on abnormal ABI and mortality outcomes in CKD patients with or without hemodialysis. Data was analyzed with random-effects models, and subgroup analyses evaluated variations by patient characteristics, region, sample size, and follow-up duration. The analysis included 10 cohort studies comprising 13,378 participants. ABI values between 0.9 and 1.3 were defined as normal. Individuals with abnormally low ABI (<0.9) demonstrated a significantly higher incidence in CV mortality [hazard ratio (HR) = 2.23; confidence interval (CI), 1.75-2.83) and all-cause mortality (HR = 1.78; CI, 1.55-2.05). Those with high ABI ≥1.3 were associated with a 2.77-fold increase in CV mortality (HR = 2.77; CI, 1.74-4.41) and a 1.49 higher risk of all-cause mortality (HR = 1.49; CI, 1.09-2.02). Overall, abnormal ABI values were linked to a 1.74 higher risk of all-cause mortality (HR = 1.74; CI, 1.54-1.96) and a 2.34-fold increase in CV mortality (HR = 2.34; CI, 1.93-2.85). Subgroup analyses revealed higher mortality risks in hemodialysis patients compared with nondialysis CKD patients and in studies conducted in Asia. Abnormal ABI values show a U-shaped relationship with mortality, serving as strong predictors of CV and all-cause mortality in CKD patients, particularly those on hemodialysis. Since CV and all-cause mortality are high in CKD patients, these findings suggest that ABI measurement is a useful screening technique to assist in prognosticating such patients. Further studies are warranted to validate these findings and to better understand the prognostic utility of ABI across different CKD stages, including both dialysis-dependent and nondialysis CKD patients.
Hyperlipidemia (HLD) is a major contributor to atherosclerotic cardiovascular disease (ASCVD). Nearly 30% of emergency department (ED) patients with chest pain have undiagnosed and/or unmanaged HLD, putting them at an increased risk of ASCVD. Although safe and effective HLD treatments exist, the ED traditionally focuses on acute care and does not offer preventive cardiovascular care services. This represents a large, missed opportunity to improve cardiovascular health for the millions of Americans evaluated in the ED each year who are not receiving appropriate preventive care in the outpatient setting. The goals of this study are to determine the efficacy of novel ED-initiated preventive care on lowering cholesterol while also informing our understanding of patient adherence and implementation determinants of ED-initiated preventive cardiovascular care. We will use a randomized, controlled, parallel-group trial of 130 ED patients being evaluated for acute coronary syndrome at a single site. Participants will be 40-75 years old with prior ASCVD, known diabetes, or 10-year ASCVD risk ≥7.5% who are not already receiving guideline-directed outpatient preventive care. Patients will be randomized with equal probability to EMERALD (Emergency Medicine Cardiovascular Risk Assessment for Lipid Disorders) or usual care. Patients in the EMERALD arm will be started on a statin and referred for a 30-day follow-up with cardiology or primary care, depending on the 10-year ASCVD risk level. Usual care arm patients will not be prescribed a statin in the ED and will be asked to follow up with a primary care provider. The primary outcome will be a percent change in low-density lipoprotein cholesterol at 30 days. Secondary outcomes include percent change in low-density lipoprotein cholesterol at 180 days and nonhigh-density lipoprotein cholesterol at 30- and 180 days, the proportion of EMERALD patients who pick up their statin, and the proportion of patients who attend 30-day outpatient follow-up. We will also use mixed methods and semistructured interviews to identify patient adherence facilitators and barriers and implementation determinants for Emergency Medicine providers. This is the first study to evaluate a novel, protocolized ED-initiated preventive cardiovascular care approach for HLD. If successful, the EMERALD intervention may be able to improve the cardiovascular health for at-risk patients and serve as a use case for other modifiable cardiovascular disease risk factors, such as diabetes, hypertension, tobacco use, and obesity. This single-site study will inform a planned multisite trial.
Despite advances in percutaneous coronary procedures, in-stent restenosis remains a significant challenge. Although sirolimus- and paclitaxel-coated balloons are promising alternatives, their comparative safety and efficacy remain uncertain. PubMed, Embase, and Cochrane databases were searched using relevant keywords from inception until August 2025. A total of 11 studies (7 randomized controlled trials and 4 observational cohort studies) were included, comprising 3633 participants overall. The primary outcomes assessed were target lesion revascularization and target lesion failure. Meanwhile, the Secondary outcomes included stent thrombosis, all-cause mortality, myocardial infarction, major adverse cardiovascular events, survival, binary restenosis, and angiographic endpoints (acute gain, diameter stenosis, in-segment late lumen loss, in-lesion late lumen loss, and in-segment minimal lumen diameter). Interstudy heterogeneity was assessed using I ² and X ² statistics ( I ²>50% = significant heterogeneity). Interstudy heterogeneity was low for most outcomes, including all primary clinical endpoints, with moderate heterogeneity observed only for select angiographic measures (notably in-segment late lumen loss and diameter stenosis). Statistical analysis was conducted using R software and RStudio (version 4.4.2), with a P value of < 0.05 indicating statistical significance. This meta-analysis examined studies that compared paclitaxel-coated balloon (PCB) versus standard balloon [sirolimus-coated balloon (SCB)] angioplasty. Regarding primary outcomes, there were no notable variations in target lesion failure [risk ratio (RR), 1.08, 95% CI, 0.90-1.29, P = 0.36] or target lesion revascularization (RR, 1.16, 95% CI, 0.98-1.37, P = 0.08). With all aggregated estimates being nonsignificant, secondary outcomes such as stent thrombosis, all-cause mortality, myocardial infarction, major adverse cardiovascular events, and survival were similar between groups. Angiographic endpoints revealed no discernible variations in late lumen loss (in-lesion and in-segment), acute gain, or diameter stenosis. Nonetheless, the SCB group's minimal lumen diameter was significantly smaller than that of the PCB group (MD, -0.08 mm, 95% CI, -0.14 to -0.01, P = 0.02). In treating coronary in-stent restenosis, SCB and PCBs show similar overall safety and effectiveness; lesion-specific angiographic variations indicate that customized selection may improve patient outcomes.
Data on outcomes between unfractionated heparin and bivalirudin anticoagulation during percutaneous coronary intervention (PCI) in acute coronary syndromes remain inconclusive. We aimed to systematically analyze PCI outcomes by comparing unfractionated heparin and bivalirudin. We systematically searched Ovid MEDLINE, Ovid Embase, Ovid Cochrane Database of Systematic Reviews, Scopus, and Web of Science from database inception in 1966 through January 2024 for studies evaluating PCI outcomes comparing unfractionated heparin and bivalirudin. Two investigators independently reviewed the data. Conflicts were resolved through consensus. Random-effects meta-analyses were used. A total of 10 prospective trials were identified that enrolled 42,253 individuals who presented with an acute coronary syndrome. Our analysis found that heparin when compared to bivalirudin was associated with an increased risk of trial-based definition of major bleeding [relative risk (RR): 1.68, 95% confidence interval (CI): 1.29-2.20], nonaccess site complications (RR: 4.6, 95% CI: 1.75-12.09), thrombolysis in myocardial infarction major bleeding (RR: 1.70, 95% CI: 1.20-2.41), major bleeding risks (RR: 1.87, 95% CI: 1.49-2.36), cardiovascular disease death (RR: 1.26, 95% CI: 1.02-1.57), and thrombocytopenia (RR: 1.67, 95% CI: 1.07-2.62). There were no statistically significant differences between heparin and bivalirudin for all-cause mortality, major adverse cardiovascular event, stroke, reinfarction, target vessel revascularization, and acute or stent thrombosis. The present meta-analysis demonstrates bivalirudin reduces major bleeding when used for anticoagulation during PCI in patients with acute coronary syndromes and is not associated with an increased risk of stent thrombosis or major adverse cardiovascular event.
Type 2 myocardial infarction (Type 2 MI) is increasingly recognized among older adults and individuals with multiple comorbidities. We evaluated the association between maximum troponin levels and 30- and 90-day all-cause mortality using both continuous values and clinically meaningful thresholds. We conducted a retrospective cohort study using the Medical Information Mart for Intensive Care IV database. Our analysis focused on patients with Type 2 MI, with maximum troponin level being the primary exposure of interest. We examined troponin's association with both 30-day and 90-day mortality, treating it as a continuous variable and categorizing it into thresholds: 10×, 100×, and 1000× the upper limit of normal (ULN), using 0.04 ng/mL (99th percentile of ULN) as the reference group. 1398 patients met our inclusion criteria. Maximum troponin was an independent predictor of 30-day mortality and 90-day mortality after adjusting for confounders ( P = 0.018, P = 0.016, respectively). Compared with the reference group (<0.04 ng/mL), the relative risks of 30-day mortality were 1.39 [95% confidence intervals (CI), 0.89-2.17] for 10× ULN, 1.72 (95% CI, 1.10-2.71) for 10-100× ULN, 1.85 (95% CI, 1.16-2.95) for 100-1000× ULN, and 2.45 (95% CI, 1.31-4.57) for >1000× ULN. A similar pattern was seen for 90-day mortality, with relative risks of 1.28 (95% CI, 0.89-1.96), 1.76 (95% CI, 1.22-2.69), 1.63 (95% CI, 1.09-2.54), and 2.07 (95% CI, 1.05-3.35), respectively. Higher troponin levels are independently associated with increased short- and intermediate-term mortality in Type 2 MI, supporting the potential use of troponin thresholds for risk stratification in this high-risk population.
Cardiovascular diseases (CVDs) are the principal cause of worldwide mortality, with 17.9 million deaths reported in 2019. In Saudi Arabia, CVDs account for 42% of all deaths, occurring on average 10 years earlier than in Western populations. Medical students are particularly susceptible to Cardiovascular disease CVD risk factors due to demanding academic schedules and lifestyle changes. This study aims to identify cardiovascular risk factors (CVRF) among medical students at King Faisal University, highlighting the need for preventive measures and curriculum modifications. This prospective cross-sectional study was conducted from February to April 2024 at King Faisal University, focusing on undergraduate medical students. Participants not enrolled in the College of Medicine, those who declined to complete the survey, or those who submitted incomplete responses were excluded. A total of 313 students participated in the study. Data collection involved physical evaluations and a validated questionnaire covering demographics, medical history, lifestyle, and diet. Measurements included waist circumference, weight, height, blood pressure, and pulse. Data was analyzed using IBM SPSS Statistics version 19. Among participants, 52.4% had a normal body mass index BMI, while 19.5% were overweight and 11.2% obese. Blood pressure measurements showed 45.7% had normal BP, but 44.4% were prehypertensive. A family history of CVDs was reported by 55.6% of students, with hypertension (HTN) and diabetes being the most common. Smoking was infrequent, with only 5.1% reporting regular habits. Dietary analysis showed moderate consumption of unhealthy foods, with 80% maintaining a moderately healthy diet. Physical activity assessment indicated significant portions engaged in light or moderate activities, but only a minority met recommended levels for vigorous activities. Significant associations were found between physical activity levels and academic year, personal history of diseases, and smoking behavior. Most students had normal body weight, but many were overweight or pre-hypertensive. Family histories of CVDs, particularly (HTN) and diabetes, were common. Smoking was rare, but diets included frequent unhealthy foods. These findings underscore the need for targeted health programs to reduce cardiovascular risks in this population.
Pericardial disease represents a diverse clinical spectrum, including acute pericarditis, pericardial effusion, cardiac tamponade, effusive-constrictive pericarditis, and constrictive pericarditis, which vary significantly in presentation, urgency, and management. Recent consensus guidelines from the European Society of Cardiology and the American College of Cardiology have enhanced clinical phenotyping, multimodal imaging techniques, and targeted immunomodulatory therapies; however, their implementation in clinical practice remains variable. We introduce our updated pathway-based framework that structures diagnosis and treatment around five key clinical scenarios: chest pain, hemodynamic collapse, dyspnea, incidental pericardial effusion, and right-sided heart failure. Each scenario guides a systematic process of risk stratification, tiered diagnostic evaluation, and phenotype-specific therapy. In cases of acute pericarditis, management employs a three-tier escalation approach, with interleukin-1 inhibitors (rilonacept, anakinra) as the preferred escalation for inflammatory phenotypes unresponsive to NSAIDs and colchicine. Cardiac magnetic resonance imaging is integral to phenotyping, utilizing late gadolinium enhancement and T2-STIR sequences to inform treatment escalation. Management of pericardial effusion is standardized through a validated drainage scoring system that considers etiology, size, and echocardiographic hemodynamics. Constrictive pericarditis is classified into three subtypes: transient/inflammatory, effusive-constrictive, and chronic/fixed, each with a distinct management pathway, reserving surgical pericardiectomy at specialized centers for fibrotic or medically refractory cases. This pathway consolidates current evidence into a reproducible clinical framework designed to standardize care, enhance diagnostic precision, and facilitate shared decision-making among multidisciplinary pericardial disease teams.
Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiomyopathy and a leading cause of sudden cardiac death in young individuals and athletes. Historically, exercise restrictions were advised because of concerns about arrhythmias, left ventricular outflow tract (LVOT) obstruction, and adverse remodeling; however, emerging evidence challenges these recommendations. To systematically evaluate the effects of structured and habitual exercise on cardiac structure, function, biomarkers, functional capacity, and safety in individuals with HCM. We performed a systematic review and meta-analysis in accordance with PRISMA 2020 guidelines. Randomized and observational studies including patients ≥12 years with confirmed HCM participating in structured exercise or habitual physical activity were eligible. Comparators included usual care, lower-intensity exercise, or sedentary controls. Outcomes included cardiac remodeling parameters (wall thickness, chamber volumes, LVOT gradient, diastolic function), left ventricular ejection fraction (LVEF), B-type natriuretic peptide (BNP), peak oxygen consumption (VO₂ peak), body mass index (BMI), and major adverse clinical events. Random-effects models were used for pooled analyses. Eleven studies (1,457 participants) were included. Exercise was not associated with adverse changes in wall thickness, chamber volumes, LVEF, LVOT gradient, diastolic indices, BNP, or BMI. VO₂ peak changes were heterogeneous, with some trials demonstrating individualized functional improvement. No study reported excess adverse events, including sudden cardiac death, ventricular arrhythmias, syncope, or appropriate ICD therapy. Structured and habitual exercise appear safe in HCM, without evidence of adverse remodeling or increased arrhythmic risk. Functional benefits vary, supporting individualized, supervised exercise prescriptions and more patient-centered counseling.
Heart failure is an increasingly common comorbidity among people with HIV infection, complicating care and heightening the vulnerability of this population to social adversity (SA). However, the impact of different SA domains on outcomes in this population remains poorly understood. We analyzed data on people with HIV infection and heart failure from the NYC 4H (NYC Health + Hospitals HIV-Heart Failure) cohort. Baseline multidimensional SA was assessed by licensed clinical social workers using standardized evaluations and grouped into 5 domains: economic hardship, health care access barriers, neighborhood or built environment instability, social support challenge, and psychobehavioral instability. We used multivariable adjusted Cox models to estimate hazard ratios (HRs) of all-cause, cardiovascular, and infection-related mortality and logistic regression to estimate odds ratios of 6-month rehospitalization risk. Among 1044 participants (62.9% male; mean age, 61.6 years), 601 (58%) reported at least 1 SA: economic hardship (n=130), limited health care access (n=155), unstable housing (n=129), social support challenge (n=179), or psychobehavioral instability (n=438). Over a mean follow-up of 3.8 years, exposure to any SA was associated with higher all-cause mortality (HR, 4.32 [95% CI, 3.03-6.14]), cardiovascular mortality (HR, 4.05 [95% CI, 2.17-6.83]), and infection-related mortality (HR, 2.37 [95% CI, 1.23-4.56]). Social support challenge (HR, 2.19 [95% CI, 1.35-3.55]) and psychobehavioral instability (HR, 1.96 [95% CI, 1.24-3.11]) were associated with higher cardiovascular mortality. Economic hardship (HR, 2.40 [95% CI, 1.22-4.70]) and social support challenge (HR, 3.09 [95% CI, 1.75-5.48]) were associated with higher infection-related mortality. Compared with patients without SA, those with environmental instability, psychobehavioral instability, or social support challenges had a 73% (adjusted odds ratio, 1.73 [95% CI, 1.15-2.06]), 75% (adjusted odds ratio, 1.75 [95% CI, 1.31-2.35]), and 44% (adjusted odds ratio, 1.44 [95% CI, 1.00-2.06]) higher risk of rehospitalization within 6 months, respectively. SA was significantly associated with mortality and rehospitalization among people with HIV infection and heart failure, with domain-specific pathways influencing specific outcomes. Multidimensional assessment of SA may offer a framework for domain-specific risk stratification in people with HIV infection and heart failure.
The pathophysiology of renal dysfunction requires population-based study. It is debatable in the literature whether cardiovascular metrics have an impact on cystatin C levels. Using public-use biomarkers data of The National Longitudinal Study of Adolescent to Adult Health (Add Health) Wave 5 data, we tested, after adjusting for age (range: 32-42), anthropometrics (body mass index, waist circumference, and arm circumference), hemoglobin A1C, low-density lipoprotein, triglyceride, smoking, and sex, the association of 5 clinical cardiovascular measures (systolic blood pressure, diastolic blood pressure, mean arterial pressure, pulse pressure, and pulse rate) with cystatin C levels. Multiple linear regression analysis with a design-based approach was employed for data analysis after log-transformation of cystatin C levels. Our findings showed that there was no significant association between cystatin C levels and any of the previously mentioned cardiovascular parameters in this age group (P > 0.05). However, there was a significant association between cystatin C levels and age [exponentiated estimate (EE) (percent increase per unit) = 1.21; 95% confidence interval (CI) = 0.97-1.103, P < 0.0001], body mass index and waist circumference (EE = 0.702; 95% CI = 0.7-0.705, P < 0.0001), triglycerides level (EE = 0.02; 95% CI = 0.0199-0.0201, P = 0.01), smoking status [EE (compared with nonsmokers) = 8.98, 95% CI = 8.95-9.01, P < 0.0001], and female sex [EE (compared with males) = -5.92; 95% CI = -5.94 to -5.89, P < 0.0001]. Our findings clarify the impact of confounding factors, particularly age, on cystatin C levels. They also demonstrate how the significant correlation between cardiovascular parameters and cystatin C levels that were seen in earlier studies is largely affected by the age. Anthropometrics, age, lipid indices, and smoking should all be considered in clinical practice as possible reasons for increased cystatin C levels in otherwise healthy middle-aged individuals.
We have been pacing the right ventricular apex, creating an artificial left bundle branch block (LBBB) for more than 4 decades. We learned that some patients would develop dys-synchronization and hence heart failure due to QRS widening. If the lead is implanted in the left bundle area and a narrow QRS is achieved, those patients with LBBB will improve after implant, but those with non-LBBB morphologies might not benefit from QRS narrowing. However, there is not enough information regarding patients with narrow or wide QRS with different types of atrioventricular block that could also benefit from QRS narrowing. Demonstrate that a narrow-paced QRS is a significant determinant of mortality in patients receiving a permanent pacemaker despite the previous QRS morphology. We analyzed 204 patients from our pacemaker database. We attempted to implant the lead in the septal area. In our lab, we utilized standard lead electrodes. The criteria for appropriate implant were an electrogram with injury potential, an acceptable lead positioning in the right anterior oblique and left anterior oblique, and a ventricular bipolar threshold less or equal to 1.0 V @ 0.5 ms. QRS duration was assessed according to the global QRS method (from the earliest onset of the QRS in any of the 12 simultaneously recorded standard leads). A QRS interval of 135 ms was determined as a cutoff point using a receiver operator curve (mortality). The first implants were performed in March 2008 and ended in March 2024. A narrow QRS (<135 ms) was observed in 140 subjects (140/204, 68%). The primary endpoint (death from cardiovascular cause) was met in 10 (4.9%) patients. LBBB was present before implant in 29 patients and a QRS <135 ms was measured in 12/29 (41%). We did not observe more complications compared with the conventional technique. The survival curve using Kaplan-Meier analysis comparing the 2 groups was significantly different with a significant mortality reduction in the narrow QRS group. A narrow-paced QRS is an independent variable associated with increased survival rates.
During the COVID-19 pandemic, a temporary policy change required emergency medical services (EMS)-identified ST-segment elevation myocardial infarction (STEMI) patients to undergo COVID testing in the emergency department (ED) before percutaneous coronary intervention, suspending the standard ED bypass to the catheterization lab. We compared system performance metrics during this COVID-era routing to pre- and postpandemic periods in a large rural health system. This was a retrospective single-center cohort study of consecutive EMS-identified STEMI activations across 3 periods: pre-COVID (May 27, 2018-March 26, 2020), COVID-era ED routing (March 27, 2020-January 25, 2022), and post-COVID with resumed ED bypass (January 26, 2022-November 26, 2023). Primary outcomes were standard STEMI system performance metrics; the secondary outcome was in-hospital mortality. A total of 373 patients were included (pre-COVID: 132; COVID: 104; post-COVID: 137). Compared to pre-COVID, the median time from EMS first medical contact to device time increased by 13 minutes ( P = 0.017). The median time from symptom onset to device time increased by 30 minutes ( P = 0.0013). The median time of first EMS electrocardiogram to device placement was increased by 14 minutes ( P = 0.013). The median door-to-device time was increased by 6 minutes ( P = 0.0007). There was a nonsignificant trend toward higher in-hospital mortality during the COVID era. In a rural STEMI system, pandemic-era routing of EMS-identified patients through the ED was associated with significant delays in key reperfusion metrics. While in-hospital mortality did not differ significantly, likely due to limited statistical power, these findings underscore the importance of preserving streamlined STEMI pathways. Larger multicenter studies to assess outcomes are warranted.
Complete revascularization improves outcomes in patients with ST-segment elevation myocardial infarction (STEMI) and multivessel coronary artery disease (MVD); however, the optimal timing of noninfarct-related artery intervention during the index procedure, immediate revascularization (IR) versus a staged approach (SR), remains uncertain. We conducted a systematic review and meta-analysis of randomized controlled trials comparing SR and IR in patients with STEMI and MVD. The primary outcome was major adverse cardiovascular events. Secondary outcomes included all-cause and cardiovascular mortality, recurrent myocardial infarction, unplanned ischemia-driven revascularization, stent thrombosis, stroke, major bleeding, acute kidney injury, and heart failure hospitalization. Random-effects models with Hartung-Knapp adjustment were used. Trial sequential analysis assessed evidence conclusiveness, and the certainty of evidence was evaluated using the Grading of Recommendations Assessment, Development, and Evaluation. Eight randomized trials, including 5077 patients (2556 SR; 2521 IR), were analyzed. No significant differences were observed between SR and IR for major adverse cardiovascular events [odds ratios (ORs), 1.07; 95% confidence intervals (CI), 0.76-1.49], recurrent myocardial infarction (OR, 1.30; 95% CI, 0.80-2.14), cardiovascular mortality (OR, 0.76; 95% CI, 0.51-1.13), or all-cause mortality (OR, 0.75; 95% CI, 0.54-1.06). Rates of stent thrombosis, stroke, unplanned ischemia-driven revascularization, major bleeding, acute kidney injury, and heart failure hospitalization were also comparable. Trial sequential analysis indicated insufficient information size to draw definitive conclusions, and the certainty of evidence ranged from very low to low. In patients with STEMI and MVD, staged and immediate complete revascularization provide comparable ischemic, safety, and mortality outcomes. Current evidence supports clinical equipoise, and revascularization timing should be individualized pending results from adequately powered trials.
Population-based studies of cardiovascular disease markers, such as high-sensitivity C-reactive protein (hs-CRP), are crucial. However, studies exploring the effect of metabolic indices on hs-CRP while controlling for confounding variables adequately in middle-aged adults are limited. Using Wave 5 public-use biomarkers data from the National Longitudinal Study of Adolescent to Adult Health (Add Health), we examined the impact of various metabolic indices on hs-CRP in adults aged 32-42, controlling for eight allergic and infectious factors that may elevate hs-CRP levels. We used multiple linear regression analysis to determine which factors predict hs-CRP levels after the log transformation of the dependent variable. The total number of participants was N = 1839 (weighted N = 1,390,763), with a mean age of 38.1 (SD = 2.0) and 46.4% having obesity. Among the controlled variables, recent surgery was the only confounder to significantly predict increased hs-CRP levels [ P = 0.029; exponentiated estimate (EE) = 1.61; 95% confidence interval (Cl), 1.31-1.91]. Notably, current smoking and altered low-density lipoprotein levels did not show a significant association with hs-CRP levels ( P > 0.05). However, a significant increase in hs-CRP levels was observed in females compared with males ( P < 0.001; EE = 1.43; 95% Cl, 1.35-1.51). Similar findings were noted for diabetic HbA1c levels ( P = 0.001; EE = 1.6; 95% CI, 1.42-1.78), high waist circumference ( P = 0.015; EE = 1.25; 95% CI, 1.15-1.35), and stage 3 obesity ( P = 0.006; EE = 7.62; 95% CI, 2.86-12.38). Although not statistically significant, hs-CRP levels exhibited a gradual increase with rising body mass index after controlling for other variables. These findings will improve the clinical application of hs-CRP in predicting coronary artery disease, especially in younger adults.
The ABCD2 score is a validated risk stratification tool used to quantify the risk of stroke within 48 hours among patients presenting with suspected transient ischemic attack (TIA). Limited data exist regarding its performance among patients in an emergency department observation unit (EDOU). The objective of this study was to determine the safety and efficacy of the ABCD2 score in a US EDOU cohort. We conducted an observational cohort study using the Wake Forest Emergency Medicine TIA Registry. Patients ≥18 years old who were evaluated for possible TIA in the EDOU of Atrium Health Wake Forest Baptist from July 1, 2021 to December 1, 2023 were accrued. This analysis included patients without a persistent neurologic deficit, except for amaurosis fugax, vertigo, or paresthesias, as determined by the consulting neurologist and attending emergency physician. Patients were risk-stratified using the ABCD2 score as low- (0-3), moderate- (4-5), and high- (≥6) risk for short-term stroke. The primary safety outcome was index encounter stroke, as determined by the consulting neurologist and imaging. Efficacy was defined as the proportion of patients classified to the low-risk group. Negative predictive values and positive predictive values, and negative likelihood ratios and positive likelihood ratios for the ABCD2 score were calculated for index stroke and reported with 95% confidence intervals (CI). Of the 340 EDOU TIA patients, 55.9% (190/340) were female, 27.9% (95/340) were nonwhite, and the mean age was 67.1 ± 13.6 years. During the index visit, 21.8% (74/340) were diagnosed with acute stroke. The ABCD2 score classified 45.0% (153/340) as low-, 45.6% (155/340) as moderate-, and 9.4% (32/340) as high-risk. Of those identified as low-risk, 17.7% (27/153) had an index acute stroke. Negative predictive values and negative likelihood ratios of the ABCD2 score for index stroke were 63.5% (95% CI, 53.3-72.6) and 0.7 (95% CI, 0.5-1.1). Among patients classified as high-risk, 34.4% (11/32) had an index stroke, corresponding to a positive predictive value of 34.4% (95% CI, 20.9-50.9) and a positive likelihood ratio of 1.9 (95% CI, 1.0-3.7). Although the ABCD2 score classified approximately half of patients as low-risk, nearly 20% of this group were diagnosed with an acute stroke during EDOU evaluation. These findings suggest that the ABCD2 score is not appropriate for ruling-out acute stroke among EDOU patients as it would lead to a high rate of missed strokes.