Revista española de cardiología (English ed.)最新文献

Introduction and objectives: The ADALA trial showed a more favorable efficacy-safety profile with low-dose direct oral anticoagulation (LD-DOAC) vs dual antiplatelet therapy (DAPT) at 3 months after left atrial appendage occlusion (LAAO). However, outcomes after switching both regimens to single antiplatelet therapy (SAPT) remain uncertain. This study reports the 1-year results, focusing on outcomes after the switch to SAPT.

Methods: The ADALA trial was a multicenter, randomized clinical trial that enrolled 91 patients with atrial fibrillation and contraindications to oral anticoagulation. After successful LAAO, participants were randomized to receive LD-DOAC or DAPT for 3 months, after which all patients transitioned to SAPT. The primary endpoint was a composite of thromboembolic events, device-related thrombus (DRT), or major bleeding at 1-year.

Results: At 12 months, the primary endpoint was significantly lower in the LD-DOAC group compared with the DAPT group (9.1% vs 32.6%; HR, 0.25; 95%CI, 0.08-0.74; P=.013), mainly driven by a reduction in DRT (0% vs 11.6%; P=.023). Major bleeding was numerically lower with LD-DOAC (9.1% vs 19.6%; P=.167), and total bleeding events were significantly reduced (13.6% vs 37.0%; P=.013). Landmark analysis showed significant differences during the initial 3 months (P <.001) but not from 3 to 12 months (P=.195). All DRT cases treated with LD-DOAC (n=4) resolved completely without bleeding.

Conclusions: LD-DOAC reduced thromboembolic and bleeding events compared with DAPT during the first year after LAAO, driven by a marked reduction in early DRT. No DRT events occurred after LD-DOAC withdrawal, supporting a strategy of LD-DOAC for 3 months followed by SAPT in this high-risk population.

Introduction and objectives: The management of heart failure with improved ejection fraction remains unresolved, particularly after stabilization. This study aimed to determine whether maintenance with an angiotensin receptor-neprilysin inhibitor (ARNI) was superior to de-escalation to an angiotensin receptor blocker (ARB).

Methods: In this open-label, prospective pilot study conducted at the Samsung Medical Center in Seoul, South Korea, 98 patients with heart failure with improved ejection fraction who were stabilized on ARNI were randomized using a block allocation table to either switch to an ARB or continue with an ARNI. The primary outcome was a change in N-terminal pro b-type natriuretic peptide (NT-proBNP) during the follow-up period. The secondary outcomes were defined as: a) NT-proBNP increase, and b) heart failure admission. Additionally, a post-hoc composite outcome was evaluated, defined as the occurrence of any of the following: NT-proBNP increase, heart failure admission, left ventricular ejection fraction reduction, or left ventricular end-diastolic volume increase.

Results: Baseline characteristics did not differ significantly between the de-escalation group (n = 49) and the maintenance group (n = 49) including NT-proBNP levels (P = .765). During follow-up, NT-proBNP levels remained comparable at 6 and 12 months (P = .642 and P = .964). Secondary outcomes, including the post-hoc composite outcome, did not differ significantly between the groups.

Conclusions: This study demonstrates no significant difference in worsening heart failure indices or clinical outcomes between ARB de-escalation and ARNI maintenance in patients with heart failure with improved ejection fraction and stabilized NT-proBNP levels. These findings suggest the potential for flexible medication management, although further validation is needed. (ClinicalTrials.gov number: NCT04803175).

Introduction and objectives: To model the growth of pulmonary artery (PA) branches in children with a functionally univentricular heart between the Glenn procedure and total cavopulmonary connection (TCPC) and to assess whether anterograde pulmonary blood flow (APBF) promotes growth and influences morbidity and mortality.

Methods: Patients with a functionally univentricular heart who underwent cardiac catheterization prior to Glenn and TCPC between 2004 and 2024 were included. Growth was assessed by comparing pre-Glenn and pre-TCPC cross-sectional areas. PA growth was modeled using linear regression.

Results: A total of 180 children with a median follow-up of 8.8 years were included: 64 (35.6%) had maintained APBF. PA growth was linear over time (fractional polynomials; P=.20), with an estimated β=11.6mm/y; 95%CI, 5.8-17.4 mm²/y. Maintaining APBF was independently associated with increased PA growth (β=50.9mm; 95%CI, 25.3-76.5 mm²; P <.01), independent of TCPC timing. The multivariable model explained 21% of the variance in PA branch growth. Nine-year survival did not differ significantly between the APBF and non-APBF groups: 86.7% (95%CI, 71.9-93.9) vs 73.4% (95%CI, 61.3-82.3), respectively (P=.21). Morbidity outcomes, including length of hospital stay, hemodynamic contraindications to fenestration closure, and Fontan failure rates, were similar between groups.

Conclusions: PA growth between the Glenn procedure and TCPC is substantial and can be considered linear, suggesting that delaying TCPC optimizes growth potential. Maintaining APBF accelerates PA growth without increasing morbidity or mortality. Due to considerable interindividual variability, these findings are most meaningful at a group level and should be interpreted with caution when applied to individual patients.

Introduction and objectives: Despite the favorable prognosis associated with intravascular imaging (IVI)-guided percutaneous coronary intervention (PCI) for complex coronary lesions, it is still unclear whether IVI-guided PCI for such lesions provides clinical benefit in patients with acute myocardial infarction (AMI) according to the ACC/AHA lesion classification.

Methods: This study was a patient-level pooled analysis of 2 nationwide Korean AMI registries. We identified 23 051 patients from KAMIR-V and KAMIR-NIH who underwent successful PCI for an infarct-related artery and stratified them by the ACC/AHA lesion classification. Clinical outcomes were compared between IVI-guided and angiography-guided PCI. The primary endpoint was major adverse cardiac events (MACE), a composite of cardiac death, AMI, repeat revascularization, and stent thrombosis, at 3 years.

Results: IVI-guided PCI demonstrated a lower incidence of MACE compared with angiography-guided PCI in patients with type B2/C lesions (adjusted HR, 0.78; 95%CI, 0.70-0.88; P <.001), but not in patients with type A/B1 lesions (adjusted HR, 0.81, 95%CI, 0.60-1.11; P=.190). In both non-ST-segment elevation myocardial infarction and ST-segment elevation myocardial infarction, a significantly lower risk of MACE following IVI-guided PCI than angiography-guided PCI was observed in patients with type B2/C lesions (non-ST-segment elevation myocardial infarction: adjusted HR, 0.73; 95%CI, 0.63-0.84; P <.001; ST-segment elevation myocardial infarction: adjusted HR, 0.86, 95%CI, 0.75-0.98; P=.027), but not in those with type A/B1 lesions.

Conclusions: Among patients with AMI, IVI-guided PCI was associated with a significantly lower risk of MACE in those with type B2/C lesions, but not in those with type A/B1 lesions. The prognostic benefit of IVI-guided PCI increased with greater lesion complexity in the infarct-related artery.

Introduction and objectives: Although widely used in clinical practice, pretreatment with a P2Y₁₂ inhibitor in patients with non-ST-segment elevation myocardial infarction (NSTEMI) remains controversial and is not recommended by current guidelines. This study aimed to evaluate the impact of P2Y₁₂ inhibitor pretreatment on the incidence of periprocedural (type 4a) myocardial infarction (MI) and in-hospital bleeding in NSTEMI patients undergoing percutaneous coronary intervention (PCI).

Methods: Consecutive NSTEMI patients undergoing PCI were enrolled from the AMIPE multicenter registry (NCT03883711) and stratified based on pretreatment strategy according to European Society of Cardiology (ESC) guideline timelines. Patients whose P2Y₁₂ inhibitor administration did not comply with contemporaneous ESC recommendations were excluded. The analysis compared patients treated before and after the 2020 ESC recommendation against routine pretreatment. The primary efficacy endpoint was type 4a MI, and the primary safety endpoint was in-hospital bleeding defined as Bleeding Academic Research Consortium (BARC) types 2, 3, and 5.

Results: A total of 1254 patients were included, of whom 740 (59.0%) received pretreatment, mainly with clopidogrel (91.2%). Type 4a MI occurred in 15.2% of patients, with no significant difference between the pretreatment and no pretreatment groups (15.9% vs 14.2%; aOR, 1.08; P=.638). In contrast, in-hospital bleeding was significantly higher in the pretreatment group (7.7% vs 3.9%; aOR, 2.17; P=.005), mainly due to BARC type 2 events.

Conclusions: In NSTEMI patients undergoing PCI, pretreatment with P2Y₁₂ inhibitors, mainly clopidogrel, did not reduce the incidence of type 4a MI but was associated with an increased risk of in-hospital bleeding.

Introduction and objectives: Dapagliflozin improves clinical outcomes in patients with chronic heart failure (HF), irrespective of left ventricular ejection fraction. However, its effects on circulating biomarkers that reflect distinct pathophysiological pathways remain incompletely understood.

Methods: DAPA-MODA is a prospective, multicenter, single-arm study that enrolled patients with stable chronic HF receiving optimized guideline-directed medical therapy, excluding sodium-glucose cotransporter-2 inhibitors. In a predefined biomarker substudy (n=156; 63.5% men; age 70.5±10.6 years; 67.9% with left ventricular ejection fraction > 40%), 11 biomarkers representing 5 key biological pathways (cardiac stress, inflammation, neurohormonal activation, congestion, and fibrosis) were measured at baseline, 1 month, and 6 months.

Results: At baseline, markers of myocardial stress were frequently elevated (NT-proBNP [95.5%] and MR-proANP [34.8%]), as was troponin for myocardial injury (73.5%). Inflammatory (IL-6 [40%], CRP [35%], GDF-15 [56%]) and neuro-endocrine stress (copeptin [43%]) markers were also commonly raised. In contrast, elevations in congestion (MR-proADM, CA-125) and fibrosis markers (ST2, PINP) were less frequent, reflecting diverse pathophysiological involvement. Dapagliflozin led to significant reductions in NT-proBNP and MR-proADM levels by 6 months. Reductions in MR-proANP, CRP, IL-6, copeptin, and PINP were confined to patients with elevated baseline levels. ST2 and CA-125 remained unchanged, while GDF-15 levels increased modestly.

Conclusions: Dapagliflozin favorably modulates several key pathophysiological pathways involved in chronic HF progression, with differential effects among biomarkers by acting particularly on those that are elevated at baseline.