Search Results (4,279)

Background: Erectile dysfunction (ED) is a common complication of type 2 diabetes and obesity and significantly affects patients’ quality of life. Nursing care for patients with metabolic multimorbidity requires a holistic, structured approach. The International Classification for Nursing Practice (ICNP^®) enables standardized formulation of nursing diagnoses, interventions, and outcomes and supports structured and individualized ICNP^®-based care planning. Aim: This study aimed to develop and present an ICNP^®-based nursing care plan for a patient with erectile dysfunction associated with type 2 diabetes and obesity and to demonstrate the applicability of ICNP^® in holistic nursing management of chronic disease. Methods: A descriptive single-case study was conducted in 2025 in a cardiology ward in Poland. Data were collected using a nursing interview, observation, medical documentation analysis, and standardized tools (IIEF-5, SF-36v2). Based on a comprehensive assessment of physical, psychological, and social status, nursing diagnoses, interventions, and expected outcomes were formulated according to ICNP^® terminology. Results: The patient presented with poorly controlled diabetes, class I obesity, moderate erectile dysfunction, reduced testosterone levels, and decreased quality of life, particularly in psychosocial domains. Key ICNP^® nursing diagnoses included erectile dysfunction, deficient knowledge, obesity, disturbed psychological status, impaired endocrine function, impaired cardiovascular function, and impaired adaptation. Individualized ICNP^®-based interventions focused on metabolic control, lifestyle modification, sexual health support, education, and psychosocial support. Implementation of the care plan was associated with improvements in health behaviors, disease knowledge, and psychological well-being. Conclusions: ICNP^® provides a useful framework for structured and comprehensive nursing care in patients with diabetes-related erectile dysfunction and multimorbidity. Case-based ICNP^® care planning supports holistic management, interdisciplinary collaboration, and quality improvement in chronic disease nursing. Full article

Background: Post-infarction heart failure (HF) remains a major contributor to morbidity and mortality despite advances in reperfusion and pharmacological management. However, the combined influence of clinical background, myocardial injury, neuro-hormonal activation, and angiographic disease on HF severity is not fully defined. Methods: We retrospectively analyzed 181 patients with confirmed myocardial infarction treated in a tertiary cardiology center. Demographics, cardiovascular risk factors, prior chronic HF, inflammatory markers (CRP, fibrinogen, ESR, leukocyte indices), and high-sensitivity troponin (hs-Tn) were measured at admission (pre-intervention), immediately after percutaneous coronary intervention (PCI), and at 48 h, angiographic lesion distributions were collected. HF severity was graded on a five-level scale and further dichotomized as no/mild HF (grade 0–1) versus moderate–severe HF (grade ≥ 2). Group comparisons and multivariable logistic regression were used to identify independent determinants of severe HF. Results: Moderate–severe HF occurred in 42.5% of patients (77/181). Compared to HF 0–1, the HF ≥ 2 group was older (64.0 vs. 60.5 years, p = 0.042) and exhibited substantially higher systemic inflammation (CRP 41.5 vs. 9.75 mg/L, p < 0.001; fibrinogen 435 vs. 346 mg/dL, p = 0.0002; ESR 28 vs. 18 mm/h, p = 0.0004). hs-Tn levels and NT-proBNP were significantly elevated in HF ≥ 2 (NT-proBNP 3449 vs. 1243 pg/mL, p = 0.0003), while left ventricular ejection fraction was reduced. Prior HF increased the likelihood of HF ≥ 2 (54.5% vs. 33.7%, p = 0.0078), and conservative therapy was associated with adverse outcomes (87.5% vs. 40.5%, p = 0.0235). In multivariable analysis, NT-proBNP remained the only independent predictor of moderate–severe HF, while CRP showed a positive but non-significant trend after adjustment. Conclusions: Post-MI HF severity reflects the combined influence of myocardial injury, neurohormonal stress, and systemic inflammatory activation. However, in multivariable analysis, NT-proBNP emerged as the dominant independent predictor of moderate–severe HF, while CRP reflected an associated but non-independent inflammatory signal. Full article

Background: Standardised Ashwagandha root extract (SARE), characterised by its content of bioactive withanolides, is widely used for its antioxidant and adaptogenic properties; however, recent case reports have raised safety concerns, primarily involving non-standardised or multi-ingredient formulations. This systematic review evaluated the safety and tolerability of SARE in healthy adults, with a focus on clinical biomarkers and adverse event reporting. Methods: Randomised trials were identified through searches of PubMed, Web of Science and Google Scholar, published from 2010 to April 2026. Studies administering single-ingredient, standardised root-only extracts to generally healthy populations were included. Risk of bias was assessed using the Cochrane RoB 2 tool. Results: Twenty-three studies with a total of 2317 participants met the inclusion criteria, with doses ranging from 125 to 600 mg/day and intervention durations from a single dose to 180 days. Across studies, hepatic, renal, haematological, endocrine, and cardiovascular biomarkers remained within normal clinical ranges, with no clinically meaningful adverse alterations reported. Reductions in cortisol were consistently observed, while increases in testosterone remained within physiological ranges. No serious adverse events attributable to SARE were reported. Mild adverse events, including gastrointestinal discomfort, headache, and transient drowsiness, were infrequently reported and occurred in both intervention and comparator groups. Conclusions: SARE was well tolerated in healthy adults at the studied doses and durations. However, limited long-term data (>180 days) and heterogeneity in study design and reporting warrant further large-scale, standardised trials to confirm safety across extended use and diverse populations. The review is registered in the PROSPERO database with ID CRD420261337116. Full article

Sheng Mai San (SMS), a traditional Chinese medicine formula for treating qi and yin deficiency, is widely used in the management of conditions such as cardiovascular diseases and heatstroke. However, its role in mitigating heat stress (HS)-induced liver injury remains underexplored. In this study, a rat model of HS was established under high-temperature and high-humidity conditions, and SMS was administered as an intervention. The pharmacodynamic effects of SMS were comprehensively evaluated through histopathological examination, detection of heat shock protein 70 (HSP70) and heat shock protein 90(HSP90) expression, and analysis of liver function biomarkers (AST, ALT). Meanwhile, oxidative stress indicators were measured using biochemical assay kits (GSH, SOD, CAT, MDA, T-AOC), and transmission electron microscopy was employed to observe mitochondrial ultrastructure, thereby assessing the protective effects of SMS on hepatic oxidative stress and mitochondrial damage induced by HS. In vitro, BRL-3A cells were cultured, subjected to HS, and treated with SMS. Cell viability was assessed using the CCK-8 assay, and changes in mitochondrial reactive oxygen species (ROS) levels, mitochondrial permeability transition pore (MPTP) opening, and mitochondrial membrane potential (MMP) were evaluated using fluorescent probes. The results showed that SMS effectively restored HS-induced histopathological damage in rat liver tissues, reduced serum AST and ALT levels, and downregulated the mRNA expression of HSP70 and HSP90 in liver tissues. Meanwhile, SMS strengthened the hepatic antioxidant system by increasing the levels of GSH, SOD, T-AOC, and CAT, while decreasing MDA content. In vitro experiments confirmed that SMS increased the viability of BRL-3A cells, reduced ROS production, improved MPTP opening/closing regulation, and stabilized MMP. This study provides a clinical reference for its application in treating HS-related conditions in humans and animals. Full article

This study aimed to establish the first national diagnostic reference levels (DRLs) for coronary angiography (CAG) and interventional cardiology procedures in Korea, based on a nationwide patient-dose survey conducted in 2024. Radiation dose data were collected from 20 cardiovascular centers between April and December 2024 using a dedicated server system for radiation dose-structured reports, namely, Digital Imaging and Communications in Medicine. We classified 1980 procedures into the following seven procedural groups: CAG, CAG with percutaneous coronary intervention (CAG + PCI), CAG with percutaneous transluminal coronary angioplasty (CAG + PTCA), coronary spasm provocation, acute myocardial infarction (AMI), chronic total occlusion (CTO), and PCI alone. The DRLs were defined as the 75th percentile of the cumulative kerma–area product (KAP) and fluoroscopy time (FT). The established DRLs for KAP (Gy·cm²) were: CAG, 18.68; CAG + PCI, 63.40; AMI, 58.52; and CTO, 106.83. The corresponding DRLs for FT (s) were: CAG, 440.00; CAG + PCI, 1201.50; AMI, 947.64; and CTO, 2819.00. This study established the first official national DRLs for CAG and interventional cardiology procedures in Korea, using real-world clinical data. These reference levels provide a practical framework for institutions to benchmark radiation exposure, evaluate practice patterns, and optimize patient radiation safety. Full article

Background/Objectives: Diabetes is a prevalent chronic condition and a major contributor to morbidity, mortality, and healthcare costs in the U.S., particularly among older adults with comorbidities such as hypertension and dyslipidemia. Complex medication regimens increase the risk of nonadherence, which can worsen glycemic control, cardiovascular outcomes, and healthcare utilization. This study assessed longitudinal adherence patterns to oral antidiabetic medications among high-risk older adults and identified predictors using group-based trajectory modeling (GBTM). Methods: This retrospective cohort study used 2016–2017 Texas Medicare Advantage claims. Participants were older adults with diagnoses of diabetes, hypertension, and hyperlipidemia who had continuous plan coverage throughout the study period and at least one prescription fill for an oral antidiabetic, a statin, and a renin–angiotensin system (RAS) antagonist. Adherence was measured monthly over 12 months using the proportion of days covered (PDC). GBTM identified adherence trajectories, and multinomial logistic regression, based on the Andersen Behavioral Model, evaluated predictors using perfect adherence as the reference. Results: Among 7847 patients, three trajectories were observed: perfect adherence (59.50%), near-perfect adherence (29.21%), and rapid decline (11.29%). Female sex (OR, 1.38; 95% CI, 1.19–1.60) and absence of health plan subsidy (OR, 0.79; 95% CI, 0.68–0.92) were associated with rapid decline. Female sex (OR, 1.13; 95% CI, 1.02–1.25) and age ≥ 75 years (OR, 1.20; 95% CI, 1.00–1.43) were associated with near-perfect adherence. Conclusions: Older adults with diabetes and comorbidities exhibit distinct medication adherence patterns. Trajectory-based methods can identify those at risk for declining adherence and guide interventions to improve outcomes. Full article

Background/Objectives: Coronary artery ectasia (CAE) presents challenges, specifically in the context of percutaneous coronary intervention (PCI), and has been associated with adverse events, particularly in the setting of acute myocardial infarction (AMI). The objective of the present study was to assess whether CAE is associated with increased occurrence of major adverse cardiovascular events (MACEs) in patients with AMI. Methods: A systematic review and meta-analysis of observational studies were conducted. We systematically searched MEDLINE via PubMed, Scopus, the Cochrane Library (CENTRAL), ClinicalTrials.gov, and reference lists to identify eligible studies. Baseline characteristics, comorbidities, angiographic data, and rates of MACEs and their individual components (all-cause or cardiovascular mortality, repeat AMI, repeat revascularization, stroke, and heart failure) have been extracted. The results were synthesized as odds ratios (ORs) using random-effects models. Results: Ten studies and 13,908 patients were included. CAE was found to be predictive of higher odds of MACEs [OR: 2.12, 95% CI: 1.34 to 3.36]. No difference was found regarding the odds of all-cause and cardiac death. The presence of ectasia was associated with higher odds of recurrent AMI, compared with controls [OR: 2.76, 95% CI:1.62 to 4.71]. The groups were comparable regarding the need for repeat revascularization, while the reports on stroke and heart failure were scarce. Conclusions: The results highlight the compounding effect of CAE on future MACE events in patients with AMI. Patients with AMI and CAE have higher odds of repeat AMI compared to patients without CAE, while mortality and repeat revascularization rates are similar. This might indicate the need for more aggressive treatment strategies in these patients. Full article

Cardiometabolic disease is increasingly shaped by the overlap among obesity, type 2 diabetes, chronic kidney disease, heart failure, and atherosclerotic cardiovascular disease, underscoring the need for prevention strategies that extend beyond glucose-centered care. This narrative review critically examines the mechanistic rationale, clinical evidence, guideline evolution, and practical implementation of sodium-glucose cotransporter-2 inhibitors (SGLT-2 inhibitors) and glucagon-like peptide-1 receptor agonists (GLP-1 receptor agonists) within the cardiorenal–metabolic continuum. A structured literature search was conducted in PubMed, Scopus, and Web of Science, focusing primarily on publications from January 2019 to March 2026, with selected landmark studies from earlier years included for context. Priority was given to randomized controlled trials, major cardiovascular and kidney outcome trials, meta-analyses, clinical practice guidelines, scientific statements, and expert consensus documents. The reviewed evidence indicates that SGLT-2 inhibitors show the most consistent benefits in reducing heart failure events, slowing chronic kidney disease progression, and lowering cardiorenal risk, whereas GLP-1 receptor agonists are more strongly associated with reductions in major adverse cardiovascular events, residual atherosclerotic risk, and body weight. Emerging data also support extension of this therapeutic paradigm beyond diabetes, particularly in obesity-associated cardiovascular risk. Contemporary care is increasingly moving toward phenotype-informed treatment selection, earlier organ-protective intervention, and multidisciplinary management, although cost, access, tolerability, and implementation barriers remain important limitations. SGLT-2 inhibitors and GLP-1 receptor agonists are therefore central to modern cardiovascular prevention across the cardiovascular–kidney–metabolic spectrum. In this context, the proposed Cardiometabolic 2.0 framework may serve as a clinically oriented model for integrating these therapies within contemporary organ-protective care. Full article

Background/Objectives: Excessive trabeculation of the left ventricle, previously known as left ventricular non-compaction (LVNC), is a rare phenotypic trait whose mechanisms and pathogenesis still remain conflictual. Its presentations may range from heart failure to embolism and, most importantly, ventricular arrhythmias (VAs). This study aims to find novel predictive factors for the occurrence of potentially fatal VAs in patients with left ventricular hypertrabeculation. Methods: All consecutive patients meeting the echocardiographic (Chin, Jenny or Stöllberger) and/or MRI criteria (Petersen) for hypertrabeculation were prospectively enrolled from October 2009 to December 2023. The primary outcome was a composite of sudden cardiac death, sustained ventricular tachycardias (sVTs), ventricular fibrillation (VF) or appropriate implantable cardioverter defibrillator (ICD) interventions. The secondary outcome was a composite of cardiovascular death and cardiovascular hospitalizations. Results: Overall, 64 patients (41 males, mean age 46 ± 19 years old) were enrolled and followed for a median time of 2.2 years. Six patients (9.4%) experienced a composite outcome at eight years, three with previous sVTs and three with previous non-sustained VTs (nsVTs). The strongest predictor of the primary endpoint was the anamnesis of nsVTs and sVTs before LVNC diagnosis. In addition, nsVTs and sVTs were significantly associated with the secondary outcome. Conclusions: Hypertrabeculation of the left ventricle is a complex and poorly understood condition whose status of cardiomyopathy is currently challenged. In our population, patients with a trabecular pattern experienced a high incidence of VAs, cardiovascular death and hospitalizations. VAs before LVNC diagnosis were predictive of the outcome independently from systolic function. Full article

Hypertension is the leading global risk factor for cardiovascular diseases, and its pathogenesis is closely linked to excessive sympathetic activation, which markedly elevates the risk of stroke, heart failure and other adverse cardiovascular events. Traditional therapies mainly target peripheral mechanisms, whereas the clinical efficacy of renal denervation highlights the critical role of central regulation in sympathetic hyperactivity. This review focuses on the core sympathetic nuclei including the rostral ventrolateral medulla (RVLM) and paraventricular nucleus (PVN), with epigenetic regulation as a key innovative perspective. We systematically summarize the upstream driving effects of reactive oxygen species (ROS) and neuroinflammation, and emphasize lncRNA/miRNA-mediated post-transcriptional regulation and the modulatory actions of gasotransmitters. Under stress conditions, aberrant activation of ROS and neuroimmune pathways, epigenetic reprogramming, and hyperexcitability of central sympathetic neurons act as key events in sympathetic overactivation, which interact synergistically to promote hypertension. Integrating evidence from multiple hypertensive animal models and clinical studies, we discuss multimodal interventions including pharmacotherapy, nanozyme biotechnology and neuromodulation, analyze current translational challenges, and provide a theoretical framework for developing central-targeted antihypertensive therapies. Full article

Chronic kidney disease (CKD) is associated with a markedly increased risk of cardiovascular (CV) morbidity and mortality that cannot be fully explained by traditional risk factors. Emerging evidence highlights the central role of the gut–kidney–heart axis, whereby gut microbiota dysbiosis promotes the generation and systemic accumulation of uremic toxins, including indoxyl sulfate (IS), p-cresyl sulfate (PCS), and trimethylamine N-oxide (TMAO). These metabolites contribute to endothelial dysfunction, oxidative stress, inflammation, and vascular remodeling, thereby accelerating CV disease progression in CKD. Dietary patterns represent a key modifiable factor influencing gut microbiota composition and metabolic activity. The Mediterranean diet, characterized by high intake of plant-based foods, dietary fiber, and polyphenols, and low consumption of red and processed meats, has emerged as a promising microbiota-targeted strategy. It promotes saccharolytic fermentation, enhances short-chain fatty acid production, and reduces proteolytic pathways responsible for uremic toxin generation. Accumulating evidence from observational studies, meta-analyses, and dietary intervention trials suggests that adherence to Mediterranean and plant-based dietary patterns is associated with reduced uremic toxin burden, improved renal outcomes, and lower CV risk in CKD populations. However, direct interventional evidence linking Mediterranean diet adherence to changes in specific uremic toxin levels remains limited. This narrative review summarizes current evidence on diet–microbiota interactions in CKD and highlights the Mediterranean diet as a biologically plausible strategy for targeting the gut–kidney–heart axis. Future well-designed randomized controlled trials (RCTs) are needed to confirm causal relationships and support clinical implementation. Full article

Background: Extracorporeal membrane oxygenation (ECMO) is lifesaving in pediatric patients with respiratory and/or cardiovascular failure. Cardiac catheterization is an important diagnostic and therapeutic tool in patients with congenital heart disease supported by ECMO, allowing the assessment of residual lesions, hemodynamically significant anatomical abnormalities, and unexplained indications for ongoing ECMO support. The timing and clinical contribution of cardiac catheterization in these patients are still debated. Objective: This study aimed to evaluate the indications, safety, and impact of cardiac catheterization on clinical management in pediatric patients receiving postoperative ECMO support. Methods: This single-center, retrospective study examined 39 pediatric patients under the age of 18 who underwent postoperative cardiac catheterization with ECMO support between January 2022 and December 2025. Demographic data, procedure characteristics, and clinical outcomes were analyzed. Results: Of the 190 patients under postoperative ECMO support, 39 underwent catheterization. The median age of the patients was 2.5 months (range, 6 days–180 months) and median weight was 4.2 kg (range, 2.8–57 kg). The most frequent diagnoses were ventricular septal defect-pulmonary atresia (VSD-PA) in 20.5% (n = 8) and transposition of the great arteries (TGA) in 15.3% (n = 6). The indication for catheterization was to investigate the reason for ECMO placement in 26 patients (66.6%). Most patients underwent catheterization within the first 24 h after ECMO initiation. Patients who underwent catheterization represented a higher-risk subgroup, with a greater proportion of STAT 4-5 procedures (59% vs. 40%) compared with the overall ECMO cohort. Cardiac catheterization resulted in a change in clinical management in 25.6% of patients through catheter-based intervention or surgical revision. Survival in the catheterized subgroup was 12.8%, reflecting the high-risk nature of this population. Conclusions: Cardiac catheterization in pediatric patients on postoperative ECMO support can be performed with a low complication rate and can significantly alter clinical management. Cardiac catheterization should be considered an important diagnostic and therapeutic modality, particularly in the presence of suspected residual lesions or unexplained hemodynamic instability. Additionally, we recommend that cardiac catheterization be performed promptly within the first 24–48 h in this patient group on ECMO support. Full article

Background and Objectives: Residual coronary anatomical complexity following culprit-lesion-only percutaneous coronary intervention (PCI) remains a major determinant of clinical outcomes in patients with multivessel coronary artery disease (CAD). Platelet distribution width (PDW), a marker of platelet heterogeneity and activation, has been associated with adverse cardiovascular outcomes; however, its relationship with post-procedural residual disease burden remains unclear. This study aimed to evaluate the association between PDW and residual SYNTAX (Synergy between Percutaneous Coronary Intervention with Taxus and Cardiac Surgery) score and to determine its incremental predictive value beyond established clinical variables. Materials and Methods: In this retrospective, single-center study, 140 patients with multivessel CAD undergoing culprit-lesion-only PCI followed by planned staged revascularization were included. Clinical presentation was categorized as chronic coronary syndrome (CCS), non-ST-elevation myocardial infarction (NSTEMI), or ST-elevation myocardial infarction (STEMI). Residual SYNTAX score was calculated after the index procedure, and patients were stratified into low (≤22) and high (≥23) groups. Associations between PDW and residual SYNTAX score were assessed using correlation and regression analyses. Model discrimination and incremental predictive value were evaluated using ROC analysis, hierarchical logistic regression, and reclassification metrics. Nonlinear relationships were explored using restricted cubic spline analysis, and clinical utility was assessed by decision curve analysis. Results: PDW was significantly correlated with residual SYNTAX score (Spearman ρ = 0.503, p < 0.001) and increased progressively across SYNTAX severity strata and clinical presentation groups. In multivariable analysis, PDW remained independently associated with high residual SYNTAX score (OR 1.38, 95% CI 1.07–1.82, p = 0.016). The addition of PDW to a hierarchical clinical model significantly improved model performance (ΔR² = 0.049, p = 0.012). Although the improvement in area under the curve (AUC) was modest, reclassification analyses demonstrated significant net reclassification and discrimination improvements. Spline analysis revealed a nonlinear relationship, with a marked increase in risk beyond PDW levels of approximately 13 fL. Decision curve analysis confirmed the clinical utility of PDW across a range of threshold probabilities. Conclusions: PDW is independently associated with post-procedural coronary anatomical complexity and provides incremental predictive value beyond established clinical variables. However, PDW should be interpreted as a biomarker reflecting platelet heterogeneity within a thromboinflammatory context, without the ability to distinguish between acute and chronic components. Full article

Fatty acids serve dual roles in cardiac physiology: as energy substrates and as precursors of bioactive lipid mediators (prostaglandins, leukotrienes, oxylipins) from n-3/n-6 PUFAs that regulate inflammation, thrombosis, and remodeling. Saturated, monounsaturated, and trans fatty acids modulate metabolism and membrane function, thereby shaping these pathways. Clinically, n-3 long-chain PUFAs (EPA and DHA) reduce cardiovascular mortality and aid postischemic remodeling; however, high doses increase the risk of atrial fibrillation. By contrast, trans and saturated fatty acids promote dyslipidemia, dysfunction, and higher rates of coronary artery disease and heart failure. Mechanistically, fatty acid uptake via FABPpm, CD36 (FAT), and FATPs, along with β-oxidation and PPAR signaling, regulates metabolism, while COX/LOX/CYP pathways generate eicosanoids and resolvins that influence inflammation and repair. This review synthesizes evidence on the roles of fatty acids and oxylipins in lipotoxicity, heart failure, ischemia–reperfusion, and arrhythmias, and evaluates dietary and supplemental interventions to optimize cardiac lipid metabolism, aligning with fatty acid signaling. Full article

Growing evidence indicates that myocardial infarction (MI) is the clinical manifestation of heterogeneous plaque substrates with distinct molecular, cellular, and biomechanical mechanisms. Acute coronary thrombosis (ACT) most commonly arises from plaque rupture (PR), plaque erosion (PE), and calcified nodules (CNs), each associated with different inflammatory profiles, thrombus composition, clinical presentation, and prognosis. This comprehensive review provides a clinician-oriented synthesis of the pathophysiological mechanisms underlying these three principal plaque phenotypes and discusses their implications for the contemporary management of acute coronary syndromes (ACS). We examine the molecular and cellular determinants of plaque instability and highlight how systemic factors such as plaque burden, impaired healing responses, and myocardial jeopardy modulate clinical risk. The role of intracoronary and non-invasive imaging is discussed primarily as a tool to elucidate plaque biology with direct clinical relevance rather than merely as a procedural guide. Building on these insights, we propose a conceptual framework for integrating plaque biology into clinical decision-making across the acute phase, secondary prevention, and long-term follow-up. In particular, recognizing the biological heterogeneity of plaque substrates may support more personalized therapeutic strategies, enabling clinicians to tailor pharmacological and interventional approaches according to the underlying plaque phenotype and patient-specific risk profile. Finally, we briefly address emerging perspectives, including the potential role of artificial intelligence (AI) in refining plaque characterization, risk stratification, and precision cardiovascular prevention. Overall, recognition of PR, PE, and CNs as biologically distinct entities supports a shift toward mechanism-informed and personalized management of MI, aligning advances in plaque biology with the principles of precision cardiovascular medicine. Full article