Critical Pathways in Cardiology最新文献

Sustained ventricular tachycardia (VT) and fibrillation-related sudden cardiac death (SCD) account for nearly 450,000 deaths annually in the United States. Catheter ablation (CA) and antiarrhythmic drugs (AADs) are commonly used to manage VT recurrence; however, their comparative efficacy and safety remain uncertain. We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) comparing CA and AADs in patients with ischemic cardiomyopathy and implantable cardioverter-defibrillators (ICDs). PubMed, Embase, and Cochrane CENTRAL Library were searched up to February 15, 2025. Primary outcomes included all-cause mortality, cardiovascular mortality, VT storm, and appropriate ICD shock. Secondary outcomes included inappropriate ICD shock, appropriate antitachycardia pacing (ATP), heart failure hospitalization, stroke/transient ischemic attack (TIA), and myocardial infarction (MI). Risk ratios (RRs) with 95% confidence intervals (CIs) were pooled using a random-effects model. Three RCTs encompassing 587 patients (287 CA, 300 AADs) were included. No significant differences were found between CA and AADs in all-cause mortality (RR 0.88, 95% CI: 0.63-1.22; p=0.43), cardiovascular mortality (RR 1.23, 95% CI: 0.77-1.98; p=0.39), VT storm (RR 0.76, 95% CI: 0.39-1.46; p=0.41), or appropriate ICD shock (RR 0.87, 95% CI: 0.69-1.10; p=0.24). Secondary outcomes, including inappropriate ICD shock, ATP, heart failure hospitalization, stroke/TIA, and MI, were also comparable between the two groups. In this meta-analysis of RCTs, CA and AADs demonstrated comparable efficacy and safety in patients with VT. Larger high-quality trials are warranted to confirm these findings and further define the role of CA as a potential first-line therapy.

Background: Despite the clinical guidelines favoring medical therapy for stable angina, the optimal management of these patients remains unclear. Here, we compare medical management (MM) versus PCI in patients with stable angina.

Methods: An extensive literature search was conducted using PubMed and Embase to identify randomized controlled trials (RCTs) of interest. Data were extracted and analyzed using a random-effects model to calculate pooled odds ratios (OR).

Results: Our meta-analysis of 28 RCTs included 9,346 PCI patients and 9,503 medically managed patients. The mean age was 62.5 ± 7.6 years in the PCI group and 62.8 ± 7.4 years in the other group. Men comprised 68% and 70% of PCI and MM groups, respectively.Over a mean follow-up of 2.64 years, PCI was associated with a significantly lower incidence of myocardial infarction (MI) compared to medical management (OR 0.84, 95% CI 0.74-0.96, p = 0.01). Although PCI showed trends toward lower odds of unplanned revascularizations and major adverse cardiovascular events, these differences were not statistically significant. There were no differences in outcomes of freedom from angina, unstable angina, nonfatal MI, stroke, all-cause mortality, or CV death.

Conclusion: Advances in cardiovascular imaging and catheterization techniques have improved risk stratification and outcomes of PCI in stable angina. Further research is needed to identify clinical subgroups that benefit most from each treatment modality.

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.

Chest discomfort before severe chest pain represents a clinical ischemia marker and indicates live myocardium in jeopardy and often precedes cardiac arrest or acute myocardial infarction (MI). The intermittent or stuttering symptoms that precede MI are referred to as "prodromal symptoms." These symptoms have been shown to correlate with cyclic ST changes and repeated episodes of spontaneous reperfusion and occlusion, occurring during a period of hours or days before the acute ischemia precedes to death or heart damage. These symptoms of premonitory angina have been associated with improved outcomes due to ischemic preconditioning or opening of collateral vascular channels around the area of ischemia. Acute prevention of an MI through prodromal symptoms recognition represents the opportunity for significantly reducing heart attack deaths. The early heart attack care program puts emphasis on prodromal symptom recognition and allows a shift in time backward to prevent the ischemic process from proceeding to MI. This strategy has been shown to pick up 15% of the patients with ischemia in the low probability group and to reduce inappropriate admissions to the hospital, as well as to reduce the number of patients with missed MIs being sent home from the emergency department.

Background: 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.

Methods: 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.

Discussion: 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.

Background: Myocardial infarction with nonobstructive coronary arteries (MINOCA) is defined as myocardial infarction with <50% stenosis of coronary arteries. Atrial fibrillation (AF) is a common arrhythmia that may influence MINOCA outcomes.

Methods: We performed a retrospective analysis of the National Inpatient Sample (2016-2021), identifying MINOCA patients with and without AF using the International Classification of Diseases, Tenth Revision, Clinical Modification codes. Multivariable mixed-effects logistic regression and propensity score matching were applied to control for confounders and assess outcomes.

Results: Of 94,840 MINOCA patients, 28,270 (30%) had AF. AF was associated with higher in-hospital mortality (3.74% vs. 2.75%; P = 0.004), acute heart failure (38.33% vs. 34.97%; P < 0.001), sudden cardiac arrest (2.54% vs. 1.73%; P < 0.050), and cardiogenic shock (3.11% vs. 1.56%; P < 0.001). AF independently predicted in-hospital mortality [adjusted odds ratio (aOR), 1.3; 95% confidence interval (CI), 1.07-1.58; P < 0.001], heart failure (aOR, 1.48; 95% CI, 1.38-1.59; P < 0.001), cardiogenic shock (aOR, 1.85; 95% CI, 1.48-2.30; P < 0.001), and acute kidney injury (aOR, 1.15; 95% CI, 1.07-1.24; P < 0.001). There were no significant differences in percutaneous coronary intervention, mechanical circulatory support, or defibrillator use ( P > 0.050).

Conclusions: AF in MINOCA is associated with worse in-hospital outcomes, including mortality, sheart failure, acute kidney injury, and cardiogenic shock. AF may be a key prognostic marker in this population, warranting further research.

Background: Thirty-day performance of the high-sensitivity troponin T (hs-cTnT) European Society of Cardiology 0/1-hour (ESC 0/1-h) and "one-and-done" (hs-cTnT

Methods: A preplanned secondary analysis of a prospective multisite US cohort was conducted. Adults with chest pain were enrolled from 8 emergency departments (January 2017-September 2018). hs-cTnT measures (0- and 1-h) were used to classify patients by the ESC 0/1-h algorithm into rule-out, observation, and rule-in zones. Patients with 0-h measures

Results: Among 1462 patients with a mean age of 57.6 ± 12.9 years, 46.4% (678/1462) were female, and 14.0% (205/1462) had cardiac death or MI at 90 days. One-and-done strategy efficacy was 32.8% (479/1462), and NPV was 99.0% [95% confidence interval (CI), 97.6-99.7]. Adding the HEART score decreased efficacy to 20.1% (293/1462) and increased NPV to 99.7% (95% CI, 98.1-100). ESC 0/1-h efficacy was 57.8% (826/1430) and NPV was 98.3% (95% CI, 97.2-99.1). Combined with a HEART score, NPV increased to 99.3% (95% CI, 98.0-99.9), but efficacy decreased to 30.8% (95% CI, 28.3-33.2).

Conclusions: The one-and-done strategy and ESC 0/1-hour algorithm had modest rates of missed 90-day cardiac death or MI. Adding a HEART score improved safety but decreased efficacy.

Background: 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.

Methods: 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.

Results: 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.

Conclusions: 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.

Background: 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.

Methods: 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.

Results: 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].

Conclusions: 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.