Savage, Michael P.

Background Optimal duration and choice of antiplatelet therapy in patients with acute coronary syndrome undergoing percutaneous coronary intervention remain controversial. Methods and Results Digital databases (PubMed, Cochrane, and Embase) were queried to select all randomized controlled trials on a post–percutaneous coronary intervention population with acute coronary syndrome. Dual‐antiplatelet therapy (DAPT) with aspirin and clopidogrel for 12 months was compared with 4 major strategies: high‐potency, high‐ to low‐potency, low‐dose, and short‐duration DAPT. A network meta‐analysis was performed to compare the safety and efficacy of different antiplatelet strategies. This study was the second updated manuscript under the International Prospective Register of Systematic Review registration (CRD42021286552). Thirty‐two randomized controlled trials comprising 103 459 (51 750 experimental, 51 709 control) patients were included. Compared with DAPT with aspirin and clopidogrel for 12 months, high‐ to low‐potency DAPT (risk ratio [RR], 0.69 [95% CI, 0.52–0.92]) and aspirin+prasugrel containing DAPT for 12 months (RR, 0.84 [95% CI, 0.72–0.98]) had a significantly lower, whereas DAPT for 1 month followed by clopidogrel only (RR, 1.59 [95% CI, 1.06–2.39]) had a higher, incidence of major adverse cardiovascular events at 1 year (median follow‐up). Prasugrel (RR, 1.35 [95% CI, 1.09–1.66]) and ticagrelor (RR, 1.38 [95% CI, 1.17–1.62]) containing DAPT for 12 months had significantly higher rates, whereas high‐ to low‐potency DAPT (RR, 0.85 [95% CI, 0.63–1.15]) had no significant risk of major bleeding. Conclusions Aspirin and ticagrelor for 3 months, followed by aspirin and clopidogrel for the remaining duration, can be considered the optimal strategy for treating post–percutaneous coronary intervention patients with acute coronary syndrome because of a significantly reduced risk of major adverse cardiovascular events without increasing the risk of bleeding.

Purpose: To compare left-ventricular and aortic pressures obtained using fluid-filled and high-fidelity solid-state pressure catheters in subjects undergoing left heart catheterization. Methods: Twenty subjects scheduled for a left heart catheterization were enrolled and 18 subjects completed this IRB-approved study. During catheterization, left-ventricular (LV) and aortic (AO) pressures were obtained using a fluid-filled pressure catheter (standard-of-care) and a high-fidelity solid-state pressure catheter synchronously. The pressure tracings were analyzed by two independent readers to measure LV systolic (LVSP), LV minimum diastolic (LVMDP), LV end diastolic (LVEDP), AO systolic (AOSP), and AO diastolic (AODP) pressures. Derivatives of the pressure waveforms were computed to estimate the isovolumic contraction and relaxation rates (peak ± dp/dt). The measurements were made over multiple cardiac cycles and averaged results were used for comparisons using repeated measures analysis of variance, post-hoc tests with Bonferroni corrections and Bland-Altman plots. Results: A significant main effect of the pressure catheter was noted for LVSP, LVMDP and AOSP (p < 0.025). The LVSP and AOSP measured with fluid-filled pressure catheters were higher by 6.6 ± 6.9 mmHg and 4.6 ± 5.2 mmHg in comparison to the high-fidelity solid-state pressure catheter assessments. In contrast, the LVMDP measurements were 3.5 ± 5.7 mmHg lower than the solid-state pressure catheter measurements. When evaluating the differences between readers, the maximum difference was noted for LVEDP measurements (3.1 ± 2.4 mmHg; p ≤ 0.001). The differences in isovolumic contraction rate (66.4 ± 116.0 mmHg/s) and relaxation rate (60.5 ± 113.5 mmHg/s) were not significantly different between the two catheter systems after Bonferroni corrections for multiple comparisons (p > 0.06). Bland-Altman analysis revealed a bias ranging from 0.8 to 6.6 mmHg for all the pressure measurements. Conclusions: There are differences in LVSP, LVMDP, and AOSP measured using fluid-filled and high-fidelity solid-state pressure catheters. Clinicians should be aware that the fluid-filled catheters commonly overestimate the true systolic pressures in the left ventricle and aorta.

Background— Restenosis after percutaneous coronary intervention (PCI) is a major problem affecting 15% to 30% of patients after stent placement. No oral agent has shown a beneficial effect on restenosis or on associated major adverse cardiovascular events. In limited trials, the oral agent tranilast has been shown to decrease the frequency of angiographic restenosis after PCI. Methods and Results— In this double-blind, randomized, placebo-controlled trial of tranilast (300 and 450 mg BID for 1 or 3 months), 11 484 patients were enrolled. Enrollment and drug were initiated within 4 hours after successful PCI of at least 1 vessel. The primary end point was the first occurrence of death, myocardial infarction, or ischemia-driven target vessel revascularization within 9 months and was 15.8% in the placebo group and 15.5% to 16.1% in the tranilast groups ( P =0.77 to 0.81). Myocardial infarction was the only component of major adverse cardiovascular events to show some evidence of a reduction with tranilast (450 mg BID for 3 months): 1.1% versus 1.8% with placebo ( P =0.061 for intent-to-treat population). The primary reason for not completing treatment was ≥1 hepatic laboratory test abnormality (11.4% versus 0.2% with placebo, P <0.01). In the angiographic substudy composed of 2018 patients, minimal lumen diameter (MLD) was measured by quantitative coronary angiography. At follow-up, MLD was 1.76±0.77 mm in the placebo group, which was not different from MLD in the tranilast groups (1.72 to 1.78±0.76 to 80 mm, P =0.49 to 0.89). In a subset of these patients (n=1107), intravascular ultrasound was performed at follow-up. Plaque volume was not different between the placebo and tranilast groups (39.3 versus 37.5 to 46.1 mm 3 , respectively; P =0.16 to 0.72). Conclusions— Tranilast does not improve the quantitative measures of restenosis (angiographic and intravascular ultrasound) or its clinical sequelae.