Background: Cardiogenic shock (CS) complicating acute coronary syndrome (ACS) remains a leading cause of in-hospital cardiovascular mortality. Systemic inflammatory cytokines may contribute to CS pathophysiology but remain incompletely characterized. We aimed to delineate profiles of ACS patients with and without CS and evaluate their utility for CS identification. Methods: In this single-centre observational study with a comparator sampling design, 150 ACS patients (August 2024-December 2025) were enrolled as ACS-CS (n = 60) and ACS-noCS (n = 90). A 13-analyte cytokine panel, selected a priori from an independent bioinformatics analysis of six GEO datasets, was quantified in serum by Luminex multiplex immunoassay within 24 hours of admission and before definitive therapy. Analyses comprised group comparison with Benjamini–Hochberg false discovery rate (FDR) correction, receiver operating characteristic (ROC) analysis, random-forest classification and multivariable logistic regression with Firth-penalised sensitivity analysis. Results: ACS-CS patients were more frequently female (46.7% vs 22.2%; p = 0.002) and had higher diabetes prevalence (68.3% vs 37.8%; p < 0.001). Median SBP was lower (85 vs 127 mmHg; p < 0.001), LVEF reduced (27.5% vs 44.5%), BNP elevated (1009 vs 237.5 pg/mL; p < 0.001) and in-hospital mortality higher (35.0% vs 6.7%; p < 0.001). Eleven cytokines met both pre-specified criteria (FDR < 0.05 and log₂FC > 0.5). IL-6 was the strongest individual discriminator (log₂FC 2.62; AUC 0.870). A random-forest model incorporating the 13-cytokine panel achieved an internally cross-validated AUC of 0.958 (95% CI 0.92-0.98). IL-6, IL-10 and TNF-α remained independently associated with CS after adjustment for age and sex. Conclusion: CS complicating ACS is accompanied by broad, coordinated systemic immune activation alongside hemodynamic failure. Multi-cytokine modelling showed high discrimination within this cohort, but all performance estimates are internal and potentially optimistic. These findings are hypothesis-generating and support prospective external validation of inflammatory profiling for risk stratification and as a rationale for immunomodulatory strategies.
Background: Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) is a rare congenital anomaly in which coronary steal causes progressive left ventricular ischemia, dysfunction, and secondary mitral regurgitation. Direct reimplantation into the aorta is the gold standard. However, it is technically hazardous when the left coronary artery (LCA) arises from the distant non-facing pulmonary sinus, because tension on the transferred vessel risks occluding it. The Takeuchi procedure is an established alternative, but it has limitations, particularly when the anomalous ostium lies close to a pulmonary valve commissure.Technique: We describe the “Aswan Drawbridge” technique in an asymptomatic 8-year-old girl whose anomalous LCA ostium lay immediately adjacent to a pulmonary valve commissure. The commissure was partially detached to maximize the harvested coronary button. A long aortic flap was then created in the left coronary sinus and reflected inferiorly, like a drawbridge, to form the floor of the tunnel. The lateral flaps of the button were sutured to this aortic flap, creating a tension-free tunnel of autologous arterial tissue between the LCA and the aorta. The pulmonary artery defect was reconstructed with an autologous pericardial patch, and the detached commissure was resuspended to it.Outcome: The postoperative course was uneventful, and the patient was discharged on postoperative day 7. Cardiac computed tomography at 1 month showed a patent 5-mm tunnel without kinking, stenosis, or compression. At 3 years, the patient remained asymptomatic, with normal biventricular function and regression of mitral regurgitation from moderate to mild, consistent with left ventricular reverse remodeling.Conclusion: The Aswan Drawbridge technique is a feasible option for ALCAPA arising from the non-facing pulmonary sinus. Longer follow-up is needed to establish the tunnel’s durability.
Specialist cardiac care makes unusual demands on buildings. It requires a small number of tightly controlled environments in which intervention can be performed safely, and a much larger territory of ordinary spaces in which patients are screened, prepared, educated, rehabilitated and followed up for years afterwards. In low- and middle-income countries, hospital design has often responded by importing high-income specifications at a level of technical and constructional dependency that local building, procurement and maintenance capacity cannot always sustain. The result can be a facility that opens at one standard but gradually settles towards the standard its context can actually hold - not through any single failure, but because of the accumulated drift of systems operating without the maintenance they require, adjacencies disrupted by later additions, and local capacity that the original design did not develop or enhance. This paper reports the design of the Rwanda Egypt Heart Centre (REHC), now under construction in Kigali as the country’s first dedicated cardiac teaching, treatment and research hospital and conceived as a national and regional centre of excellence in cardiac care. Building on the model established at the Aswan Heart Centre, Egypt, the project subsequently extends beyond the specialist hospital through the Village Integrated Plug-In (VIPI), a community platform combining preventive healthcare and patient follow-up with shared social, educational and digital facilities, designed for future integration with Rwanda’s national health data systems. We analyse the design process itself as evidence, tracing how local and international clinicians, architects, policymakers and engineers arrived at key design decisions through project records, design iterations and co-design workshop deliberations. From this analysis we introduce the concept of “Appropriate Complexity”: a framework for designing a centre of excellence in which the highest specification is located precisely where clinical intervention demands it, while the wider infrastructure is designed to be operated, maintained and adapted within its context. Complexity is therefore located rather than reduced. Neither project is yet operational. We therefore present Appropriate Complexity as a design-derived hypothesis rather than as evidence of clinical or operational outcomes, and specify the post-occupancy indicators, reference points and assessment schedule against which it can be tested.
[No abstract, showing first paragraph of letter] Dear Editor, We read with interest the meta-analysis by Ahmed et al. evaluating vutrisiran in transthyretin amyloidosis (ATTR) [1]. While the review addresses a clinically important question, we wish to raise several methodological concerns not addressed in the manuscript's limitations section.
Cardiovascular diseases (CVDs) remain the leading cause of global morbidity and mortality, emphasizing the need for sensitive biomarkers and effective therapeutic strategies. Extracellular vesicles (EVs) are membrane-bound nanoparticles released by virtually all cell types that mediate intercellular communication through the transfer of proteins, lipids, messenger RNAs, microRNAs and DNA. Increasing evidence indicates that alterations in EV cargo contribute to the initiation and progression of multiple cardiovascular disorders, while also offering opportunities for minimally invasive diagnosis and targeted therapy. This review summarizes current evidence on the molecular mechanisms, diagnostic significance and therapeutic applications of EVs across major cardiovascular diseases, including atherosclerosis, coronary artery disease, myocardial infarction, heart failure, atrial fibrillation, valvular heart disease and cardiomyopathies. Disease-specific EV-associated proteins and non-coding RNAs, particularly microRNAs, are discussed as candidate biomarkers for diagnosis, risk stratification, prognosis and treatment monitoring. The review also highlights emerging EV-based therapeutic approaches, including regenerative medicine, engineered EVs and targeted drug delivery systems, while critically discussing translational challenges such as EV heterogeneity, lack of standardized isolation and characterization protocols, scalability, regulatory considerations and the need for robust clinical validation. Most mechanistic and therapeutic evidence remains preclinical and EV biomarker assays are not yet established for routine care. In conclusion, EVs represent a promising platform for advancing precision cardiovascular medicine by integrating molecular diagnostics with innovative therapeutic strategies. Although substantial progress has been achieved, overcoming current technical, regulatory and clinical challenges through standardized methodologies and large-scale validation studies is essential for translating EV-based technologies into routine cardiovascular practice.
