Cardiovascular Research Foundation

BACKGROUND:The pullback pressure gradient (PPG) is a novel physiological metric that quantifies coronary artery disease patterns as focal or diffuse on a scale from 0 to 1. This study assessed the relationship between PPG and residual angina at 1 year.METHODS:PPG Global is a prospective, investigator-initiated, single-arm, multicenter study that enrolled patients with at least 1 lesion with a fractional flow reserve ≤0.80 intended to be treated with percutaneous coronary intervention. After the PPG calculation, physicians could revise treatment assignment to medical therapy or coronary artery bypass graft surgery instead of percutaneous coronary intervention. Focal and diffuse disease were defined based on the median PPG value of 0.62. Patient-reported outcomes were assessed using the Seattle Angina Questionnaire at baseline and 1-year follow-up.RESULTS:The study included 947 patients with PPG and the Seattle Angina Questionnaire at 1 year. The mean age was 67.6±10.2 years, 24% were female, and 29% had diabetes. At 1 year, patients with focal coronary artery disease reported less angina than those with diffuse disease (Seattle Angina Questionnaire angina frequency score, 95.3±9.9 versus 92.5±15.0; P=0.006). PPG was independently associated with improvement in angina (P=0.017).CONCLUSIONS:In patients with flow-limiting coronary artery disease, a focal disease pattern defined by high PPG was associated with greater symptomatic relief at 1 year compared with diffuse disease (low PPG). By capturing the underlying pathophysiologic distribution of epicardial disease and its relation to post-treatment symptom relief, PPG may support a more tailored revascularization decision-making and percutaneous coronary intervention strategy.

The treatment of calcified coronary lesions requires optimal lesion preparation to achieve a larger minimal stent area (MSA), the strongest predictor of long-term outcomes. The comparative mechanisms of action of calcium-modifying therapies have not been well defined. In a prospective, multicenter ECLIPSE trial (Evaluation of Treatment Strategies for Severe Calcific Coronary Arteries: Orbital Atherectomy Versus Conventional Angioplasty Technique Before Implantation of Drug-Eluting Stents), 2005 patients with severely calcified lesions were randomized to vessel preparation with orbital atherectomy (OA) versus balloon angioplasty (BA) before drug-eluting stent implantation. The primary end point of the optical coherence tomography (OCT) substudy was the MSA at the site of maximal calcification; MSA across the entire stent was also assessed. Postprocedural OCT images were available in 286 lesions in 276 patients treated with OA and 292 lesions in 279 patients treated with BA. By angiographic core laboratory analysis, 567 (98.1%) of lesions were severely calcified. By postprocedural OCT, the maximal calcium arc, maximal calcium thickness, and total calcium length measured 204° (149°-268°), 0.85 mm (°0.69-1.03°), and 22.0 (16.0-31.0) mm. Compared with BA, calcium modification was greater in the OA group (greater number, total length, and maximal depth of calcium fractures), especially in lesions with thicker calcium. Nonetheless, the MSA at the site of maximal calcification was large in both groups and not different (median [interquartile range], 7.44 [6.03-8.94] mm2 versus 7.05 [5.78-8.66] mm2; P=0.08). Similar results were observed for the MSA across the entire stent (5.86 [4.60-7.38] mm2 versus 5.57 [4.50-6.97] mm2; P=0.10). Among patients in the OCT substudy, 1-year target-vessel failure rates were low and not different between the groups (7.8% with OA and 6.6% with BA, P=0.61). In lesions that are severely calcified by angiography, the extent of calcification by OCT was highly variable. Despite greater calcium modification after OA, the acute MSA and 1-year target-vessel failure rates were not different between OA and BA. URL: https://www.clinicaltrials.gov; Unique identifier: NCT03108456.

Coronary bifurcation lesions (CBL) are associated with lower procedural success, worse postprocedural outcomes, and greater unplanned repeat revascularization. We sought to better understand the impact of Impella support in patients undergoing percutaneous coronary intervention (PCI) of CBLs. We used data from the cVAD PROTECT III study (NCT04136392), an FDA-audited, single-arm study of patients undergoing high-risk PCI with Impella support, to examine the outcomes of patients undergoing PCI of CBLs. Patients with a Medina classification of 1.1.1, 1.0.1, or 0.1.1 were considered to have a true CBL, and were compared to patients with nontrue CBLs and/or no CBLs. The primary outcome was the rate of CEC-adjudicated major adverse cardiac and cerebrovascular events (MACCE: composite of all-cause death, myocardial infarction, stroke/transient ischemic attack, and repeat revascularization) at 90 days. Cox proportional hazards regression models were adjusted for age, sex, left main disease, and triple vessel disease. Of 1,044 patients, 523 had at least one true CBL treated. Baseline characteristics were comparable between groups except for age which was higher in patients with CBLs. Patients with CBLs had a significantly higher pre-PCI SYNTAX scores and number of treated lesions, more left main disease and triple vessel disease, and longer procedure duration. There was no difference in post-PCI SYNTAX score, PCI-related complications, or failure to achieve angiographic success. After adjustment for potential confounders, patients with CBLs had similar rates of 90-day MACCE. While patients with CBLs undergoing Impella-supported high-risk PCI had higher complexity, there were similar rates of PCI-related complications and 90-day MACCE. Trial Name: The Global cVAD Study (cVAD), ClinicalTrial.gov Identifier: NCT04136392, URL:https://clinicaltrials.gov/ct2/show/NCT04136392?term=cvad&draw=2&rank=2.

Introduction: Impella CP (Abiomed, Danvers, MA) microaxial flow pumps are commonly used in acute myocardial infarction (AMI) and heart failure (HF) cardiogenic shock (CS). Contemporary data from large, unselected populations are needed to understand differences between these groups. Hypothesis: Differences in patient and hospitalization characteristics such as device exposure and shock complications may contribute to differences in outcomes between those with AMI-CS compared to HF-CS. Methods: The Cardiogenic Shock Working Group (CSWG) registry enrolls patients with CS at 36 international sites. We analyzed patients with CS and Impella CP enrolled from 2019-2024, categorized by CS etiology and mechanical support device exposure. Baseline characteristics, complications, and outcomes were compared. Outcomes included survival to discharge, native heart survival, and heart replacement therapy. Multivariable analysis was performed to identify predictors of mortality and complications. Results: 1486 patients with CS (34.9% HF-CS, 57.9% AMI-CS) and Impella CP were analyzed. Patients with HF-CS were younger (60 vs 64 years), more often had chronic kidney disease (26.4% vs 13.6), less commonly had cardiac arrest (13.3% vs 27.6%), and less commonly had CSWG-SCAI stage E CS (45.7% vs 57.2%) than those with AMI-CS (p<0.001 for all). Impella CP alone was used in 38.3%. Multi-device strategies (sequential or concurrent) included CP+IABP in 9.8%, CP+Impella 5.0/5.5 in 8.3%, CP+ECMO in 23.1%, and CP+≥2 other devices in 20.4%. Impella CP alone was the most common device strategy in both HF-CS (37.9%) and AMI-CS (38.9%) followed by CP+ECMO (26.4% and 20.8%). Acute kidney injury and renal replacement therapy were more common in HF-CS than AMI-CS (66.5% vs 59.7%, p=0.03 for AKI; 40.5% vs 32.7%, p=0.002 for RRT). Acute limb ischemia was less common in HF-CS than in AMI-CS (11.0% vs 14.4%; p=0.05), with no difference in bleeding (36.8% vs 41.7%; p=0.08). Survival to discharge was 53.4% and was higher in HF-CS than AMI-CS (59.7% vs 49.8%; p<0.001). Patients supported by Impella CP+≥2 other devices had the lowest survival (43.8%). Multivariable modeling revealed several factors that were significantly associated with mortality, limb ischemia, and bleeding ( Figure ). Conclusion: Differences in baseline characteristics, shock severity, mechanical device exposure, and hospital complications between patients with HF-CS and AMI-CS supported by Impella CP may influence outcomes.

Abstract Background Coronary artery lipid accumulation is indicative of atherosclerosis. Purpose This study aimed to examine the clinical significance and prognostic value of residual lipid burden (RLB) after percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI). Methods Between January 2017 and December 2021, 1312 patients with AMI who underwent three-vessel optical coherence tomography (OCT) imaging after successful PCI were divided into low RLB group (n=656) and high RLB group (n=656) based on the median value of OCT-derived RLB (total lipid index of all non-culprit lesions). Patients were followed for up to 5 years. Major adverse cardiovascular events (MACE) were recorded. Results The average age was 57.0 years, and 74.9% were male. The high RLB group had more frequent multi-vessel disease (54.6% vs. 24.5%, P<0.001), non-culprit plaque rupture (28.4% vs. 6.1%, P<0.001), thin-cap fibroatheroma (TCFA: 53.8% vs. 11.0%, P<0.001), and other vulnerable plaque features (all P<0.001) compared to the low RLB group. After adjusting for clinical risk factors, a high RLB independently predicted non-culprit plaque rupture, TCFA, and vulnerable plaque features. Patients with a high RLB had a significantly greater incidence of 5-year non-culprit lesion-related MACE (8.4% vs. 2.6%, adjusted hazard ratio [HR]: 3.84, 95% confidence interval [CI]: 1.98-7.45, P<0.001) than patients with a low RLB; and most events were ischemia-driven revascularization (6.5% vs. 1.9%, P<0.001). Moreover, the predictive value of a high RLB was independent of non-culprit TCFA. Conclusions OCT-derived RLB was strongly associated with pancoronary plaque characteristics in AMI patients. A high RLB was predictive of 5-year adverse events independent of TCFA.

Severe aortic stenosis (AS) induces a disproportional pressure gradient across the aortic valve causing increased left ventricular (LV) afterload. Transcatheter Aortic Valve Replacement (TAVR) aims to immediately alleviate the aortic pressure gradient and thereby changing LV cardiac mechanics. The aim was to describe by in-vivo assessment of LV pressure-volume (PV) relationships how TAVR acutely affects LV cardiac mechanics. In this prospective observational study in patients with severe AS, LV cardiac mechanics were evaluated with an LV conductance catheter before and after TAVR. The effects of transcatheter valve design, pre and postdilatation, use of rapid pacing (≥180 bpm) and LV ejection fraction (EF) were specifically addressed. In-vivo LV PV reconstructions were obtained in 61 patients. Stroke work (SW) and pressure volume area (PVA) were significantly lower following TAVR (decrease from median [25th-75th percentile] of 10,935.6 [6877.5-13490.8] to 6,878.0 [4,870.8-8,613.8] mmHg/mL, P < .001 and from 17,831.5 [12,414.9-22,416.8] to 11,024.9 [8364.7-14705.0] mmHg/mL, P < .001, respectively) with stable SW/PVA ratios. Overall, end-systolic and end-diastolic pressures and volumes were significantly lower after TAVR. Arterial Elastance, as an index for LV afterload also decreased (2.66 [2.01-3.87]-1.96 [1.25-2.72] mmHg/mL, P < .001). LV contractility declined as illustrated by a reduction in End-systolic Elastance (2.22 [1.50-3.10]-1.58 [1.08-2.43] mmHg/mL, P < .001). The trends in changing LV cardiac mechanics were similar for balloon- and self-expanding valves and were not affected by pre/post dilatation, rapid pacing or LV EF. TAVR for severe AS resulted in immediate LV unloading, lower myocardial metabolic demand and impaired contractility. This observational study was registered at URL: https://www. gov with unique identifier: NCT06204783.

BackgroundFive-year data from the PARTNER 3 trial showed that among low-risk patients with severe, symptomatic aortic stenosis, outcomes were similar among patients who had undergone transcatheter aortic-valve replacement (TAVR) and those who had undergone surgical aortic-valve replacement. Longer-term assessments of clinical outcomes and valve durability are needed.MethodsPatients were randomly assigned in a 1:1 ratio to undergo transfemoral TAVR or surgery. The first primary end point was a nonhierarchical composite of death, stroke, or rehospitalization related to the procedure, the valve, or heart failure. The second primary end point was a hierarchical composite of death, disabling stroke, nondisabling stroke, and the number of rehospitalization days related to the procedure, the valve, or heart failure, analyzed with the use of a win ratio analysis. Clinical, echocardiographic, valve-durability, and health-status end points were assessed through 7 years.ResultsA total of 1000 patients underwent randomization. In the analysis of the first primary end point, the Kaplan–Meier estimate of the incidence of an end-point event was 34.6% with TAVR and 37.2% with surgery (difference, −2.6 percentage points; 95% confidence interval [CI], −9.0 to 3.7). The win ratio for the second primary end point was 1.04 (95% CI, 0.84 to 1.30). In the TAVR and surgery groups, respectively, the Kaplan–Meier estimates for the incidence of components of the first primary end point were as follows: death, 19.5% and 16.8%; stroke, 8.5% and 8.1%; and rehospitalization, 20.6% and 23.5%. The mean (±SD) aortic-valve gradients assessed by echocardiography at 7 years were 13.1±8.5 mm Hg after TAVR and 12.1±6.3 mm Hg after surgery. The percentage of bioprosthetic valves that failed was 6.9% in the TAVR group and 7.5% in the surgery group. Patient-reported outcomes were similar in the two groups.ConclusionsAmong low-risk patients with severe, symptomatic aortic stenosis, no significant differences with respect to two primary composite end points involving death, stroke, and rehospitalization were observed at 7 years between those who had undergone TAVR and those who had undergone surgery. (Funded by Edwards Lifesciences; PARTNER 3 ClinicalTrials.gov number, NCT02675114.)