Circulation: Cardiovascular Interventions最新文献

Background: Calcified nodules (CNs) remain a major challenge in percutaneous coronary intervention (PCI). We sought to compare procedural and clinical outcomes after orbital atherectomy (OA) versus intravascular lithotripsy (IVL)-facilitated PCI in patients with CNs.

Methods: We identified patients with optical coherence tomography (OCT)-defined CNs who underwent PCI with either OA or IVL between 2012 and 2022 and had both pre- and post-PCI OCT images available. The imaging end point was the minimal stent area on final post-PCI OCT. The clinical end point was 2-year target-lesion failure, a composite of cardiac death, target-vessel myocardial infarction, or clinically driven target-lesion revascularization. A multivariable Cox proportional hazards regression model was used to estimate hazard ratio and 95% CI. Sensitivity analyses were performed using propensity score matching, incorporating covariates such as age, sex, diabetes, and pre-PCI calcium burden assessed by OCT (length, arc, and thickness).

Results: Among 4856 patients with evaluable pre- and post-PCI OCT images, 493 patients (10.2%) had CNs, and 167 patients underwent PCI with either OA (n=83) or IVL (n=84). The 2 groups had similar baseline demographic and lesion characteristics. After PCI, final minimal stent area was comparable between the 2 groups (OA, 5.6 mm² [interquartile range, 4.8-6.7] versus IVL, 5.5 mm² [interquartile range, 4.8-7.0]; P=0.75). At a median follow-up of 2.4 years, there was no difference in target-lesion failure between the OA and IVL groups (12.0% versus 9.8%, respectively; log-rank P=0.64; adjusted hazard ratio, 1.10 [95% CI, 0.28-4.31]; P=0.89). Overall results remained consistent in the propensity score-matched population (n=68 per group), with similar minimal stent area (5.6 mm² [4.8-6.7] versus 5.5 mm² [4.7-6.8]; P=0.73) and comparable 2-year target-lesion failure rate (9.8% versus 8.8%; log-rank P=0.82).

Conclusions: In patients with OCT-defined CNs, OA- and IVL-assisted PCI resulted in comparable post-PCI minimal stent area and 2-year clinical outcomes.

Background: Platelet reactivity (PR) and clinical risk factors are known to have impact on outcomes in patients receiving percutaneous coronary intervention (PCI). We aimed to assess the interaction of PR and clinical risk assessment using the Thrombolysis in Myocardial Infarction Risk Score for Secondary Prevention (TRS2P) on adverse clinical outcomes following PCI.

Methods: From the PTRG-DES (Platelet function and Genotype-Related Long-Term Prognosis in Drug-Eluting Stent-Treated Patients With Coronary Artery Disease) registry, 11 714 patients who underwent PCI and had a mean platelet reactivity unit (PRU) value were studied. Clinical risk was stratified using the TRS2P as low clinical risk (score 0-1) or high clinical risk (≥2), and PR was stratified as high PR (HPR, PRU ≥252) and non-HPR (PRU <252). The primary outcome was a composite of cardiac death, myocardial infarction, and stent thrombosis. Landmark analysis was performed at 1- and 12 months after PCI.

Results: Among total population, mean PRU was 217.8±78.7, and mean TRS2P was 1.56±1.12. Over the long-term follow-up period, the primary outcome occurred in 335 (5.3%) patients. Patients with both high clinical risk and HPR had the highest incidence of the primary outcome (9.4%), followed by high clinical risk/non-HPR (5.9%), low clinical risk/HPR (4.8%), and low clinical risk/non-HPR (3.9%) (P<0.001). Compared with low clinical risk/non-HPR patients, those with both high clinical risk and HPR had a 3.25-fold higher risk of the primary outcome (hazard ratio, 3.25 [95% CI, 2.38-4.42]; P<0.001). Both PRU and TRS2P were independent predictors of the primary outcome. In landmark analyses, the risk of primary outcome within 1 month after PCI were mainly determined by PRU, while outcome beyond 1 month after PCI was mainly determined by TRS2P.

Conclusions: In the secondary prevention after percutaneous coronary intervention, platelet reactivity and clinical risk had additive value in predicting outcomes. Platelet reactivity had greater relative impact within 1 month while clinical risk had greater relative impact beyond 1 month.

Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT04734028.

Background: Among patients with intermediate-risk pulmonary embolism undergoing mechanical thrombectomy, the mean change in cardiac index (CI) is modest. We sought to identify variables associated with a hemodynamic super-response or a CI increase of ≥25% postthrombectomy.

Methods: This was a single-center retrospective study including patients with intermediate-risk pulmonary embolism undergoing mechanical thrombectomy with pulmonary artery catheter-derived hemodynamic indices obtained preprocedure and postprocedure.

Results: Overall, 105 intermediate-risk patients had complete hemodynamic profiles, with 41 patients (39%) classified as super-responders. Super-responders had a lower baseline CI (1.9±0.7 versus 2.3±0.6 L/min per m²). The mean change in CI postthrombectomy was 0.8±0.4 L/min per m² among super-responders versus 0.1±0.4 L/min per m² among non-super-responders. Several established indices of poor right ventricular function were associated with a significant increase in the CI in a univariable model. A left ventricular outflow tract velocity-time integral ≤15 cm, tricuspid annular plane systolic excursion/pulmonary artery systolic pressure ≤0.34 mm/mm Hg, and substantial inferior vena cava contrast reflux were associated with a hemodynamic super-response with an odds ratio of 16.19 (95% CI, 1.97-133.24,), 6.5 (95% CI, 2.13-19.83), and 2.53 (95% CI, 1.09-5.88), respectively. In a multivariable model, a preprocedure CI ≤2.2 L/min per m² was associated with a hemodynamic super-response (odds ratio, 3.76 [95% CI, 1.09-13.0]).

Conclusions: Patients with intermediate-risk pulmonary embolism with the more severe hemodynamic derangements had the greatest improvement in CI post thrombectomy. This group can be identified with commonly available noninvasive indices of right ventricular dysfunction.

Mitral regurgitation is the most common valve disease worldwide. Despite its wide success in inoperable or high-risk surgical patients, transcatheter edge-to-edge repair remains limited by some anatomic features and the non-negligible rate of significant residual regurgitation. Transcatheter mitral valve replacement has emerged as a viable alternative that promises to overcome these issues, but its development has been progressing slowly. This review aims to provide a comprehensive overview of the current state of transcatheter mitral valve replacement, including patient selection, procedural techniques, and currently available outcomes.

Background: Patients with peripheral artery disease experience walking impairment that is incompletely explained by large-artery atherosclerotic occlusive disease and abnormal ankle-brachial index (ABI). Microvascular dysfunction is associated with adverse outcomes, including amputation, but its effect on ambulation is unknown. We tested the hypothesis that skeletal muscle microvascular function directly associates with walking distance, is a more sensitive indicator of walking distance than conduit artery blood inflow, and correlates with ambulatory improvement following peripheral artery disease interventions.

Methods: Sixty-eight participants, including 50 with peripheral artery disease (ABI ≤0.85) and 18 healthy controls, underwent vascular function assessment after sphygmomanometer cuff-induced calf ischemia using magnetic resonance imaging measures of blood oxygenation level-dependent reactivity and arterial spin labeling perfusion reactivity. Functional status was assessed using the 6-minute walk test. A subgroup of patients with peripheral artery disease underwent repeat testing after supervised exercise therapy (n=14) or revascularization (n=14). Multivariable linear regression models were used to assess the association of macrovascular reactive hyperemic blood inflow within the conduit arteries, skeletal muscle microvascular blood oxygenation level-dependent reactivity, and walking distance.

Results: Resting large-artery pressure by ABI (R=0.74; P<0.001), macrovascular blood inflow (R=0.40; P<0.001), and skeletal muscle microvascular blood oxygenation level-dependent reactivity (R=0.66; P<0.001) significantly correlated with the 6-minute walk test distance in univariable vascular testing. In multivariable analysis of each vascular parameter, however, calf skeletal muscle microvascular reactivity was most strongly associated with the 6-minute walk test (β=825.3; P=0.023). In those with repeat testing after intervention, the change in microvascular reactivity, but not ABI or macrovascular blood inflow, significantly correlated with the change in the 6-minute walk test distance (R=0.46; P=0.014).

Conclusions: Microvascular reactivity after ischemia directly associates with walking distance and was a stronger predictor of walking distance than macrovascular blood inflow and ABI. After supervised exercise therapy or revascularization, improvements in microvascular function, but not macrovascular inflow or ABI, correlate with improvement in walking distance. Further study of microvascular dysfunction as a mechanistic driver of ambulatory function is warranted.

Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03490968.

Background: External drainage of the thoracic duct can temporarily reduce tissue congestion and improve symptoms in patients with heart failure. However, loss of fluid limits the duration of this approach. Here, we report on our initial experience with thoracic duct drainage and autotransfusion in patients with elevated central venous pressure.

Methods: This is a retrospective review of medical records of 8 patients who underwent percutaneous thoracic duct drainage with autotransfusion as part of their medical care. We reviewed clinical and procedural outcomes, laboratory data, and imaging.

Results: In 5 (62.5%) patients, central venous pressure was elevated secondary to congenital heart disease, 1 (12.5%) had a lymphatic conduction disorder and trisomy 21, 1 (12.5%) had a lymphatic conduction disorder with Noonan syndrome and congenital heart disease, and 1 (12.5%) patient had severe chronic lung disease due to prematurity. Median central venous pressure was 15.5 mm Hg (range, 12-28), and all patients presented with severe multicompartment lymphatic failure including plastic bronchitis (12.5%), pleural effusions (37.5%), protein-losing enteropathy (62.5%), ascites (75%), and anasarca (100%). Over 7 (87.5%) patients survived to decannulation, and the median duration of autotransfusion was 11.5 days (range, 6-126). There was a significant reduction in creatinine from a median of 0.63 (0.3-2.4) to 0.36 (0.16-0.8) mg/dL (P=0.017). There was also a significant reduction in weight (P=0.017) and drainage output (P=0.017). There were no intraprocedural or autotransfusion-related deaths.

Conclusions: Thoracic duct drainage with autotransfusion can improve fluid status and end-organ function without significant complications and presents a new therapeutic option. Further studies are needed to better define indications for this procedure and long-term outcomes.