Search Results (465)

Stroke is a significant global health concern characterized by the abrupt disruption of cerebral blood flow, leading to neurological impairment. Accurate and timely diagnosis—enabled by imaging modalities such as computed tomography (CT) and magnetic resonance imaging (MRI)—is essential for differentiating stroke types and initiating interventions like thrombolysis, thrombectomy, or surgical management. In parallel, recent advancements in wearable technology, particularly smart clothing, offer new opportunities for stroke prevention, real-time monitoring, and rehabilitation. These garments integrate various sensors, including electrocardiogram (ECG) electrodes, electroencephalography (EEG) caps, electromyography (EMG) sensors, and motion or pressure sensors, to continuously track physiological and functional parameters. For example, ECG shirts monitor cardiac rhythm to detect atrial fibrillation, smart socks assess gait asymmetry for early mobility decline, and EEG caps provide data on neurocognitive recovery during rehabilitation. These technologies support personalized care across the stroke continuum, from early risk detection and acute event monitoring to long-term recovery. Integration with AI-driven analytics further enhances diagnostic accuracy and therapy optimization. This narrative review explores the application of smart clothing in conjunction with traditional imaging to improve stroke management and patient outcomes through a more proactive, connected, and patient-centered approach. Full article

Background: Clinical outcomes among older adults hospitalized with heart failure with preserved ejection fraction (HFpEF) in the setting of metabolically healthy obesity (MHO) remain insufficiently explored. This study aimed to evaluate whether MHO status is associated with different rates of major adverse cardiac and cerebrovascular events (MACCEs) during HFpEF-related hospitalizations compared to patients without MHO. Methods: Data from the 2019 National Inpatient Sample (NIS) database was analyzed using relevant ICD-10 codes to identify HFpEF admissions in older adults. Propensity score matching (1:1) was applied to generate balanced cohorts of patients with and without MHO. Multivariable adjustments were performed to assess primary outcomes, including MACCEs, all-cause mortality (ACM), acute myocardial infarction (AMI), dysrhythmia, cardiac arrest (CA), and stroke. Statistical significance was set at p < 0.05. Results: Each MHO cohort included 22,405 patients with a median age of 75 years. The MHO+ group demonstrated a significantly higher risk of dysrhythmia (OR 1.32, 95% CI 1.21–1.43, p < 0.001). Interestingly, an “obesity paradox” was observed, as the MHO+ cohort had lower odds of MACCEs (OR 0.70, 95% CI 0.61–0.81, p < 0.001), ACM (OR 0.66, 95% CI 0.54–0.82, p < 0.001), and AMI (OR 0.71, 95% CI 0.59–0.86, p = 0.001) compared to MHO−. No significant differences were found for CA or stroke between the groups. Conclusions: Although the MHO+ group had an elevated risk of dysrhythmia, they exhibited more favorable outcomes in terms of MACCEs, ACM, and AMI—supporting the concept of an “obesity paradox.” Further research is needed to better understand the role of MHO as a comorbid condition in patients with HFpEF. Full article

Spontaneous coronary artery dissection (SCAD) is an increasingly recognized, non-atherosclerotic cause of acute coronary syndrome (ACS), particularly in younger women. This comprehensive review outlines SCAD’s unique pathophysiology, which is linked to underlying arteriopathies like fibromuscular dysplasia, and highlights the critical role of advanced intravascular imaging for accurate diagnosis. A fundamental shift in management is detailed, with evidence favoring a conservative strategy for stable patients due to high rates of spontaneous vessel healing, reserving technically challenging invasive interventions for high-risk cases. Importantly, this review also addresses long-term outcomes, noting significant rates of recurrence and Major Adverse Cardiac Events (MACE), a high prevalence of persistent chest pain, and the central role of beta-blocker therapy in secondary prevention. Ultimately, SCAD requires a departure from standard ACS protocols towards a personalized approach that emphasizes accurate diagnosis, cautious initial management, and vigilant long-term follow-up. Full article

Background: Peripheral endovascular intervention (PEVI) is routinely performed using standard-dose radiation (SDR), which is associated with elevated levels of radiation. No study has evaluated the outcomes of minimal-dose radiation (MDR) in PEVI. Methods: We performed a prospective observational study of 184 patients (65 ± 12 years) at an academic medical center from January 2019 to March 2020 (mean follow-up of 3.9 ± 3.6 months) and compared the outcomes of MDR (n = 24, 13.0%) and SDR (n = 160, 87.0%) in PEVI. Primary endpoints included air kerma, dose area product (DAP), fluoroscopy time, and contrast use. Secondary endpoints included all-cause mortality, cardiac mortality, acute myocardial infarction, acute kidney injury, stroke, repeat revascularization, vessel dissection/perforation, major adverse limb event, access site complications, and composite of complications. Results: For MDR (68 ± 10 years, mean follow-up of 4.3 ± 5.2 months), the primary endpoints were significantly less than SDR (65 ± 12 years, mean follow-up of 3.8 ± 3.2 months; p < 0.001). Regarding the secondary endpoints, one vessel dissection occurred using MDR, while 36 total complications occurred with SDR (p = 0.037). Conclusions: PEVI using MDR was safe and efficacious. MDR showed a significant decrement in radiation parameters and fluoroscopy time. Therefore, MDR can serve as an effective alternative for PEVI in acute or critical limb ischemia. Full article

Background/Objectives: The incidence of cardiac morbimortality in patients with relapsed/refractory (R/R) acute myeloid leukemia (AML) is unknown. Methods: We analyze the characteristics, incidence, risk factors, and outcomes of cardiac events in AML patients treated for second-line (2L) or third-line (3L) episodes. Results: Among 327 2L AML patients (median age 62 years old), 135 experienced cardiac events, with an incidence of 38.6% non-fatal and 1.3% fatal events at 6 months. The grade 1–2 incidence was 16.8%, and the grade 3–4 incidence was 23.5% at 6 months. Overall, 207 cardiac events occurred in the 2L cohort, the most frequent being hypertension (n = 45), bradycardia (n = 39), QTc prolongation (n = 35), heart failure (n = 33), syncope/presyncope (n = 22), arrhythmia (n = 18), and myocardial ischemia (n = 8). Median OS in the 2L cohort was 9.4 months, 21.4 months in patients with grade 1–2, 8.8 months in patients without a cardiac event, 7.6 months in grade 3–4 patients, and 2.1 months with in 5 patients (p = 0.0035). The multivariate analysis showed prior cardiologic antecedents (p = 0.013), intensive 2L chemotherapy (p = 0.01), and inclusion in a 2L clinical trial (p < 0.001) as independent risk factors for non-fatal cardiac events. Among 189 patients of the 3L cohort, the incidence of non-fatal and fatal cardiac events was 49.2% and 0% at 6 months, respectively. Non-fatal cardiac events were more frequent in patients with prior cardiac antecedents (p = 0.004). Conclusions: In summary, cardiotoxicity is a frequent and challenging complication in R/R AML patients. We identified the risk factors that could be relevant to implementing risk-adapted management guidelines, aiming to reduce morbi-mortality in this difficult-to-treat setting. Full article

Coronary plaque vulnerability, more than luminal stenosis, drives acute coronary syndromes. Optical coherence tomography (OCT), intravascular ultrasound (IVUS), and coronary computed tomography angiography (CCTA) visualize plaque morphology in vivo, but manual interpretation is time-consuming and operator-dependent. We performed a narrative literature survey of artificial intelligence (AI) applications—focusing on machine learning (ML) architectures—for automated coronary plaque segmentation and risk characterization across OCT, IVUS, and CCTA. Recent ML models achieve expert-level lumen and plaque segmentation, reliably detecting features linked to vulnerability such as a lipid-rich necrotic core, calcification, positive remodelling, and a napkin-ring sign. Integrative radiomic and multimodal frameworks further improve prognostic stratification for major adverse cardiac events. Nonetheless, progress is constrained by small, single-centre datasets, heterogeneous validation metrics, and limited model interpretability. AI-enhanced plaque assessment offers rapid, reproducible, and comprehensive coronary imaging analysis. Future work should prioritize large multicentre repositories, explainable architectures, and prospective outcome-oriented validation to enable routine clinical adoption. Full article

The study of metabolic abnormalities regarding mitochondrial respiration and energy production has significantly advanced our understanding of cell biology and molecular mechanisms underlying cardiovascular diseases (CVDs). Mitochondria provide 90% of the energy required for maintaining normal cardiac function and are central to heart bioenergetics. During the initial phase of heart failure, mitochondrial number and function progressively decline, causing a decrease in oxidative metabolism and increased glucose uptake and glycolysis, leading to ATP depletion and bioenergetic starvation, finally contributing to overt heart failure. Compromised mitochondrial bioenergetics is associated with vascular damage in hypertension, vascular remodeling in pulmonary hypertension and acute cardiovascular events. Thus, mitochondrial dysfunction, leading to impaired ATP production, excessive ROS generation, the opening of mitochondrial permeability transition pores and the activation of apoptotic and necrotic pathways, is revealed as a typical feature of common CVDs. Molecules able to positively modulate cellular metabolism by improving mitochondrial bioenergetics and energy metabolism and inhibiting oxidative stress production are expected to exert beneficial protective effects in the heart and vasculature. This review discusses recent advances in cardiovascular research through the study of cellular bioenergetics in both chronic and acute CVDs. Emerging therapeutic strategies, specifically targeting metabolic modulators, mitochondrial function and quality control, are discussed. Full article

Background and Objectives: Alcoholic hepatitis (AH) is a growing public health concern with its rising incidence and its contribution to nearly half of all cirrhosis-related deaths in the United States. In this systematic review, we aimed to comprehensively evaluate the current evidence and trials on the use of anti-interleukin-1 (anti-IL-1) drugs in patients with AH, assessing their efficacy and adverse events compared to routinely prescribed drugs like corticosteroids. Materials and Methods: A comprehensive literature search was conducted across five databases to identify randomized controlled trials (RCTs) evaluating the role of anti-IL-1 agents like canakinumab and anakinra among patients diagnosed with AH. Data was extracted and pooled in the form of mean and standard deviation for continuous variables and event and total for dichotomous variables. Results: Three RCTs were included for quantitative synthesis, encompassing 307 patients. Using canakinumab, 58% of patients showed improvement in histology. Prednisolone was associated with higher 90-day survival (90% vs. 70%; hazard ratio for death = 0.34, 95% CI 0.14–0.83, p = 0.018) and transplant-free survival. Overall, a higher incidence of acute kidney injury and new-onset cardiac disorders was noted in the anti-IL-1 arm when compared to placebo. Conclusions: This study concludes the lack of efficacy of anti-IL-1 agents in causing improvement in patient outcomes when compared to standard therapies. A higher incidence of adverse events was also noted in the anti-IL-1 arm. These results emphasize the need for future clinical trials to evaluate the use of anti-IL-1 agents in AH objectively. Full article

Background/Objectives: Randomized studies of patients with unprotected left main coronary artery (ULMCA) disease involve highly selected populations. Therefore, we sought to investigate the 60-month event-free survival of consecutive patients undergoing ULMCA percutaneous coronary intervention (PCI) and determine the best risk score system and independent predictors of event-free survival. Methods: All patients who underwent ULMCA PCI at our center between 1 January 2007 and 31 December 2014 were included. The primary endpoint was the time to cardiac death, target lesion myocardial infarction, or target lesion revascularization (whichever came first) with a follow-up of 60 months. Results: A total of 513 patients (mean age 68 ± 12 years, 64% male, 157 elective, 356 acute) underwent ULMCA PCI. The 60-month incidence of events was 16.8% and 38.0% in elective and acute patients, respectively. There were significantly more events in the acute group during the first 6.5 months. Of the risk scores, the ACEF (AUC = 0.786) and SYNTAX II (AUC = 0.716) scores had the best predictive power in elective and acute patients, respectively. The SYNTAX score proved to be the least predictive in both groups (AUC = 0.638 and 0.614 in the elective and acute groups, respectively). Left ventricular function (hazard ratio (HR) for +10% 0.53 [95% CI, 0.38–0.75] and 0.81 [95% CI, 0.71–0.92] in elective and acute patients, respectively) and, in acute patients, access site (femoral vs. radial HR 1.76 [95% CI, 1.11–2.80]), hyperlipidemia (HR 0.58 [95% CI, 0.39–0.86]), and renal function (HR for +10 mL/min/1.73 m² higher GFR: 0.87 [95% CI, 0.78–0.97]) were independent predictors of event-free survival. Conclusions: Acute ULMCA PCI patients have worse prognosis than elective patients, having more events during the first 6.5 months. Besides anatomical complexity, clinical and procedural parameters determine the prognosis. Full article

Acute heart failure (AHF) is a clinical syndrome characterized by the sudden onset or rapid worsening of heart failure signs and symptoms, frequently triggered by myocardial ischemia, pressure overload, or cardiotoxic injury. A central component of its pathophysiology is the activation of intracellular signal transduction cascades that translate extracellular stress into cellular responses. Among these, the mitogen-activated protein kinase (MAPK) pathways have received considerable attention due to their roles in mediating inflammation, apoptosis, hypertrophy, and adverse cardiac remodeling. The canonical MAPK cascades—including extracellular signal-regulated kinases (ERK1/2), p38 MAPK, and c-Jun N-terminal kinases (JNK)—are activated by upstream stimuli such as angiotensin II (Ang II), aldosterone, endothelin-1 (ET-1), and sustained catecholamine release. Additionally, emerging evidence highlights the role of receptor-mediated signaling, cellular stress, and myeloid cell-driven coagulation events in linking MAPK activation to fibrotic remodeling following myocardial infarction. The phosphatidylinositol 3-kinase (PI3K)/Akt signaling cascade plays a central role in regulating cardiomyocyte survival, hypertrophy, energy metabolism, and inflammation. Activation of the PI3K/Akt pathway has been shown to confer cardioprotective effects by enhancing anti-apoptotic and pro-survival signaling; however, aberrant or sustained activation may contribute to maladaptive remodeling and progressive cardiac dysfunction. In the context of AHF, understanding the dual role of this pathway is crucial, as it functions both as a marker of compensatory adaptation and as a potential therapeutic target. Recent reviews and preclinical studies have linked PI3K/Akt activation with reduced myocardial apoptosis and attenuation of pro-inflammatory cascades that exacerbate heart failure. Among the multiple signaling pathways involved, glycogen synthase kinase-3β (GSK-3β) has emerged as a key regulator of apoptosis, inflammation, metabolic homeostasis, and cardiac remodeling. Recent studies underscore its dual function as both a negative regulator of pathological hypertrophy and a modulator of cell survival, making it a compelling therapeutic candidate in acute cardiac settings. While earlier investigations focused primarily on chronic heart failure and long-term remodeling, growing evidence now supports a critical role for GSK-3β dysregulation in acute myocardial stress and injury. This comprehensive review discusses recent advances in our understanding of the MAPK signaling pathway, the PI3K/Akt cascade, and GSK-3β activity in AHF, with a particular emphasis on mechanistic insights, preclinical models, and emerging therapeutic targets. Full article

C-reactive protein (CRP) has emerged as a valuable biomarker in acute myocardial infarction (AMI), offering multiple insights into diagnosis, prognosis, and therapeutic strategies. In the diagnostic domain, elevated CRP levels serve as an early indicator of AMI, aiding in prompt identification and initiation of treatment. Prognostically, CRP is a strong predictor of adverse outcomes post-AMI, correlating with increased mortality and cardiovascular events. Beyond its diagnostic and prognostic roles, CRP also exposes therapeutic avenues in AMI management. Targeting CRP through pharmacological interventions has shown promise in reducing inflammatory responses, thereby mitigating myocardial damage and improving clinical outcomes. However, CRP’s low specificity, influenced by elevation in non-cardiac conditions, remains a clinical limitation that warrants consideration. This review comprehensively examines the evolving role of CRP in AMI, exploring its diagnostic accuracy, prognostic significance, and potential as a therapeutic target. The understanding of the complex role of CRP in AMI provides clinicians with valuable tools for risk stratification, treatment optimization, and personalized patient care in the acute setting. Full article

Background/Objectives: Patients with chronic kidney disease (CKD) are associated with a significantly elevated cardiovascular risk. The incidence and prevalence of mediated cardiac disorders and major adverse cardiac events (MACEs), such as heart failure, arrhythmias, acute coronary syndrome (ACS) based on coronary artery disease (CAD), stroke, venous thromboembolism, and peripheral artery disease, are significantly higher in CKD patients as compared with the general population. Methods: This narrative review summarizes the current clinical understanding, the pathophysiological mechanisms, and the clinical consequences in the context of cardiovascular risk and disease in CKD. Results: The impact of CKD on mediated cardiovascular disorders and elevated MACE prevalence is complex and multifactorial. The underlying mechanisms involve various traditional cardiovascular risk factors, such as arterial hypertension, smoking, dyslipidemia, and diabetes. Furthermore, CKD-specific molecular and pathophysiological factors, such as chronic inflammation and associated oxidative stress and endothelial cell dysfunction, pro-coagulatory status, uremic toxins and uremic lipids, progressive vascular calcification, and alterations in the regulation of the renin–angiotensin–aldosterone system (RAAS) and sympathetic activation cause an increased cardiovascular risk. Conclusions: Understanding the complex disease mechanisms between CKD and elevated cardiovascular risk might contribute to optimizing individual patients’ risk stratification and result in individualized diagnostic and treatment strategies via appropriate clinical biomarker application and individualized anti-inflammatory approaches. Full article

Background: Obstructive sleep apnea (OSA) is a prevalent but frequently underdiagnosed comorbidity in patients undergoing cardiac surgery, including coronary artery bypass grafting (CABG), aortic valve replacement (AVR), and mitral valve repair or replacement (MVR). This systematic review and meta-analytic synthesis investigates the relationship between OSA and postoperative morbidity and mortality, with particular attention to the predictive utility of established screening instruments. Methods: A systematic search of the PubMed database was conducted (April 2025), identifying 724 articles published in the last ten years. Seventeen primary studies met the inclusion criteria for qualitative synthesis, and four additional studies were included in the meta-analyses. Outcomes assessed included atrial fibrillation, major adverse cardiac and cerebrovascular events (MACCE), acute kidney injury (AKI), respiratory complications, pneumonia, hospital length of stay (LOS), and mortality. Risk of bias was assessed qualitatively based on study design and reporting limitations. This review was registered in the PROSPERO database under registration number CRD420251049574. Results: Meta-analyses demonstrated significantly elevated odds of atrial fibrillation (OR = 2.44, 95% CI: 1.46–4.07), major adverse cardiac and cerebrovascular events (OR = 2.06, 95% CI: 1.61–2.63), acute kidney injury (OR = 2.24, 95% CI: 1.67–3.01), and respiratory complications (OR = 1.15, 95% CI: 1.05–1.25) among patients with OSA. Additionally, OSA was associated with a significantly prolonged hospital length of stay (standardized mean difference [SMD] = 0.62, 95% CI: 0.46–0.78) and a marginal increase in pneumonia risk (OR = 1.07, 95% CI: 1.00–1.15). Evidence regarding stroke, intensive care unit (ICU) stay, and mortality was inconsistent or underpowered. Conclusions: Across core outcomes, findings were consistent across multiple studies involving a large patient population. Obstructive sleep apnea is a clinically consequential risk factor in cardiac surgery, associated with increased perioperative complications and prolonged hospitalization. These findings support the integration of routine OSA screening into preoperative risk assessment protocols. Further prospective, multicenter trials are warranted to assess the efficacy of perioperative management strategies, including continuous positive airway pressure (CPAP) therapy, in improving surgical outcomes. Full article

Background: Sleep-disordered breathing (SDB), particularly Cheyne–Stokes respiration (CSR), is highly prevalent among patients hospitalized with acute decompensated heart failure (ADHF) and is associated with worse clinical outcomes. Sodium-glucose cotransporter-2 inhibitors (SGLT2i) have demonstrated cardiorenal benefits in heart failure, but their effects on nocturnal respiratory parameters remain underexplored. Objectives: This study aims to evaluate the impact of SGLT2i therapy on key respiratory and cardiac indices including CSR burden, oxygenation, and right heart function in patients with ADHF and reduced left ventricular ejection fraction. Methods: In this single-center prospective cohort study, 60 patients with ADHF, LVEF < 40%, and a baseline apnea–hypopnea index (AHI) > 5 were assessed before and three months after the initiation of SGLT2i therapy. Sleep respiratory parameters were measured using home polygraphy (ApneaLink^TM), while cardiac and renal indices were evaluated by echocardiography, NT-proBNP, and the estimated glomerular filtration rate (eGFR). Structural and functional echocardiographic changes were analyzed both at baseline and following the 3-month treatment period. Patient-reported outcomes were assessed using the Epworth Sleepiness Scale (ESS) and Kansas City Cardiomyopathy Questionnaire (KCCQ). Results: After 3 months of SGLT2i therapy, significant improvements were observed in daytime sleepiness (ESS: −2.68 points; p < 0.001), CSR index (−5.63 events/h; p < 0.001), AHI (−3.07 events/h; p < 0.001), ODI (−6.11 events/h; p < 0.001), and mean nocturnal SpO₂ (+1.95%; p < 0.001). KCCQ scores increased by 9.16 points (p < 0.001), indicating improved quality of life. Cardiac assessments revealed reductions in NT-proBNP (−329.6 pg/mL; p < 0.001) and E/e′ ratio (−1.08; p < 0.001), with no significant change in LVEF or chamber dimensions. Right ventricular function improved, as evidenced by the increased TAPSE/sPAP ratio (+0.018; p < 0.001). Renal function remained stable, with a non-significant upward trend in eGFR. Conclusions: This exploratory study suggests that SGLT2 inhibitors may be associated with the attenuation of Cheyne–Stokes respiration and an improvement in right heart function in patients with ADHF, warranting further investigation in controlled trials. These findings highlight the potential of SGLT2is to address overlapping cardio-respiratory dysfunction in this high-risk population. Full article

Background/Objectives: Cardiovascular disease remains the leading global cause of death, with atherosclerotic plaque vulnerability, rather than stenosis severity, playing a central role in acute coronary events. Epicardial adipose tissue (EAT) has emerged as a key contributor to coronary atherosclerosis and myocardial ischemia. This study aimed to investigate the relationship between EAT thickness and the development and severity of atherosclerotic plaques in these coronary arteries, and to evaluate the influence of demographic factors on EAT thickness and plaque vulnerability. Methods: A retrospective analysis was conducted on autopsy data from 245 sudden cardiac death (SCD) cases (2021–2023). EAT thickness was measured at the left anterior descending artery (LAD) and left circumflex coronary artery (LCx) levels. From each artery, one segment that showed evidence of an atherosclerotic plaque was collected and sent for histological examination. Additionally, we documented demographic data, including age, sex, and body mass index (BMI) for each case. Results: In the present study, we enrolled 245 subjects with SCD, among whom 175 (71.42%) were male, and 70 (28.58%) were female. The mean age was 62.31 ± 12.69 years, and the mean BMI was 26.12 ± 4.16. We observed a mean EAT thickness value of 0.74 ± 0.26 cm at the LAD artery level and 0.71 ± 0.27 cm at the LCx artery level. We observed a positive correlation between BMI and EAT thickness at the LAD level (r = 0.260, p < 0.001) and similarly at the LCx level (r = 0.260, p < 0.001). Additionally, advancing age is associated with an increase in EAT thickness at both the LAD level (r = 0.188, p = 0.003) and the LCx level (r = 0.242, p < 0.001). Furthermore, we observed a higher EAT thickness at the LAD level (p = 0.0019) and the LCx level (p = 0.0225) among subjects with unstable atherosclerotic plaques. In the logistic regression analysis, the elevated value of EAT thickness was associated with unstable atherosclerotic plaque at LAD (OR: 1.88, p = 0.002) and LCx (OR: 1.51, p = 0.010) for the entire study cohort. Conclusions: Our data revealed that higher baseline values of EAT LCx and EAT LAD are associated with unstable plaque at the level of the left coronary arteries. Furthermore, our findings indicate that male individuals are more susceptible to developing unstable plaques in the coronary arteries. Full article