Impact of Polyvascular Disease in Patients Undergoing Unprotected Left Main Percutaneous Coronary Intervention.

Percutaneous coronary intervention (PCI) has demonstrated its safety and efficacy in treating left main (LM) coronary artery disease (CAD) in select patients. Polyvascular disease (PolyVD) is associated with adverse events in all-comers with CAD. However, there is little data examining the interplay between PolyVD and LM-PCI, which we sought to investigate in a retrospective single-center study. We included patients who underwent unprotected LM-PCI at a tertiary center from 2012 to 2019. The study population was stratified based on the presence or absence of PolyVD (i.e., medical history of cerebrovascular and/or peripheral artery disease in addition to LM-CAD). The primary outcome was major adverse cardiovascular events (MACE) combining all-cause mortality and spontaneous myocardial infarction within 1 year after index PCI. Overall, 869 patients were included, and 23.8% of the population had PolyVD. Subjects with PolyVD were older and had a greater burden of co-morbidities. After 1-year follow-up, PolyVD patients exhibited significantly higher rates of both MACE (22.8% vs 9.4%, p <0.001) and bleeding events compared with those without PolyVD. MACE was primarily driven by an increase in all-cause mortality (18.3% vs 7.1%, p <0.001). Results persisted after adjusting for confounders. In conclusion, in patients who underwent LM-PCI, the presence of PolyVD is linked to an increased risk of MACE and bleeding after 1 year of follow-up, which highlights the vulnerability of this population.

The AMPK activator ATX-304 alters cellular metabolism to protect against cisplatin-induced acute kidney injury.

Acute kidney injury (AKI) disrupts energy metabolism. Targeting metabolism through AMP-activated protein kinase (AMPK) may alleviate AKI. ATX-304, a pan-AMPK activator, was evaluated in C57Bl/6 mice and tubular epithelial cell (TEC) cultures. Mice received ATX-304 (1 mg/g) or control chow for 7 days before cisplatin-induced AKI (CI-AKI). Primary cultures of tubular epithelial cells (TECs) were pre-treated with ATX-304 (20 µM, 4 h) prior to exposure to cisplatin (20 µM, 23 h). ATX-304 increased acetyl-CoA carboxylase phosphorylation, indicating AMPK activation. It protected against CI-AKI measured by serum creatinine (control 0.05 + 0.03 mM vs ATX-304 0.02 + 0.01 mM, P = 0.03), western blot for neutrophil gelatinase-associated lipocalin (NGAL) (control 3.3 + 1.8-fold vs ATX-304 1.2 + 0.55-fold, P = 0.002), and histological injury (control 3.5 + 0.59 vs ATX-304 2.7 + 0.74, P = 0.03). In TECs, pre-treatment with ATX-304 protected against cisplatin-mediated injury, as measured by lactate dehydrogenase release, MTS cell viability, and cleaved caspase 3 expression. ATX-304 protection against cisplatin was lost in AMPK-null murine embryonic fibroblasts. Metabolomic analysis in TECs revealed that ATX-304 (20 µM, 4 h) altered 66/126 metabolites, including fatty acids, tricarboxylic acid cycle metabolites, and amino acids. Metabolic studies of live cells using the XFe96 Seahorse analyzer revealed that ATX-304 increased the basal TEC oxygen consumption rate by 38%, whereas maximal respiration was unchanged. Thus, ATX-304 protects against cisplatin-mediated kidney injury via AMPK-dependent metabolic reprogramming, revealing a promising therapeutic strategy for AKI.

Current Procedural Practices of Family Medicine Teaching Physicians.

BACKGROUND AND OBJECTIVES: Proficiency in procedural care achieved during residency is a major driver of family physician scope of practice. To date, no inventory exists of the advanced procedures and clinical skills performed by teaching family physicians. This study comprises the first such survey and assesses the attitude of respondents toward the importance of family physicians performing procedures. METHODS: We sent a clinical skills inventory to a convenience sample of teaching family physicians employed at 18 medical school-affiliated, community, and military residency programs across the United States. RESULTS: The overall response rate was 46% (N=337). Respondents performed a median of 12 advanced procedures and clinical skills (IQR: 8-18). Endorsed procedures ranged from skin biopsy (n=316, 93.8%) and joint injection (n=279, 82.8%) to colonoscopy (n=21, 6.2%) and cesarean delivery (n=23, 6.8%), and reported skills ranged from medication-assisted treatment (n=181, 53.7%) to highly active antiretrovial therapy (n=35, 10.4%). Gender and career stage were associated with statistically significant differences in endorsement of specific procedures. For example, fracture management was more likely to be performed by late- versus early-career faculty (54.1% vs 24.2%, P<.001) and by male versus female respondents (54.9% vs 24.2%, P<.001). Most respondents (84.3%) agreed that future family physicians should learn procedures and advanced clinical skills. CONCLUSIONS: Family medicine teaching faculty perform a wide array of procedures and advanced skills. Apparent differences by career stage and gender identity in the performance of some of the procedural and skill areas may portend a shift in the procedural training of future family physicians.

Predictive value of the thrombotic risk criteria proposed in the 2023 ESC guidelines for the management of ACS: insights from a large PCI registry.

AIM: To assess the value of the thrombotic risk criteria proposed in the 2023 guidelines of the European Society of Cardiology (ESC) for the management of acute coronary syndrome (ACS) to predict the ischaemic risk after percutaneous coronary intervention (PCI). METHODS AND RESULTS: Consecutive patients with acute or chronic coronary syndrome undergoing PCI at a large tertiary-care center from 2014 to 2019 were included. Patients were stratified into low, moderate, or high thrombotic risk based on the ESC criteria. The primary endpoint was major adverse cardiovascular events (MACEs) at 1 year, a composite of all-cause death, myocardial infarction (MI), and stroke. Secondary endpoints included major bleeding. Among 11 787 patients, 2641 (22.4%) were at low-risk, 5286 (44.8%) at moderate risk, and 3860 (32.7%) at high-risk. There was an incremental risk of MACE at 1 year in patients at moderate (hazard ratios (HR) 2.53, 95% confidence interval (CI) 1.78-3.58) and high-risk (HR 3.39, 95% CI 2.39-4.80) as compared to those at low-risk, due to higher rates of all-cause death and MI. Major bleeding rates were increased in high-risk patients (HR 1.59, 95% CI 1.25-2.02), but similar between the moderate and low-risk group. The Harrell's C-index for MACE was 0.60. CONCLUSION: The thrombotic risk criteria of the 2023 ESC guidelines for ACS enable to stratify patients undergoing PCI in categories with an incremental 1 year risk of MACE; however, their overall predictive ability for MACE is modest. Future studies should confirm the value of these criteria to identify patients benefiting from an extended treatment with a second antithrombotic agent.

Interatrial Block Association With Adverse Cardiovascular Outcomes in Patients Without a History of Atrial Fibrillation.

BACKGROUND: Interatrial block (IAB) is associated with thromboembolism and atrial arrhythmias. However, prior studies included small patient cohorts so it remains unclear whether IAB predicts adverse outcomes particularly in context of atrial fibrillation (AF)/atrial flutter (AFL). OBJECTIVES: This study sought to determine whether IAB portends increased stroke risk in a large cohort in the presence or absence of AFAF/AFL. METHODS: We performed a 5-center retrospective analysis of 4,837,989 electrocardiograms (ECGs) from 1,228,291 patients. IAB was defined as P-wave duration ≥120 ms in leads II, III, or aVF. Measurements were extracted as .XML files. After excluding patients with prior AF/AFL, 1,825,958 ECGs from 458,994 patients remained. Outcomes were analyzed using restricted mean survival time analysis and restricted mean time lost. RESULTS: There were 86,317 patients with IAB and 355,032 patients without IAB. IAB prevalence in the cohort was 19.6% and was most common in Black (26.1%), White (20.9%), and Hispanic (18.5%) patients and least prevalent in Native Americans (9.2%). IAB was independently associated with increased stroke probability (restricted mean time lost ratio coefficient [RMTLRC]: 1.43; 95% CI: 1.35-1.51; tau = 1,895), mortality (RMTLRC: 1.14; 95% CI: 1.07-1.21; tau = 1,924), heart failure (RMTLRC: 1.94; 95% CI: 1.83-2.04; tau = 1,921), systemic thromboembolism (RMTLRC: 1.62; 95% CI: 1.53-1.71; tau = 1,897), and incident AF/AFL (RMTLRC: 1.16; 95% CI: 1.10-1.22; tau = 1,888). IAB was not associated with stroke in patients with pre-existing AF/AFL. CONCLUSIONS: IAB is independently associated with stroke in patients with no history of AF/AFL even after adjustment for incident AF/AFL and CHA2DS2-VASc score. Patients are at increased risk of stroke even when AF/AFL is not identified.

PFKFB2-mediated glycolysis promotes lactate-driven continual efferocytosis by macrophages.

Resolving-type macrophages prevent chronic inflammation by clearing apoptotic cells through efferocytosis. These macrophages are thought to rely mainly on oxidative phosphorylation, but emerging evidence suggests a possible link between efferocytosis and glycolysis. To gain further insight into this issue, we investigated molecular-cellular mechanisms involved in efferocytosis-induced macrophage glycolysis and its consequences. We found that efferocytosis promotes a transient increase in macrophage glycolysis that is dependent on rapid activation of the enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 2 (PFKFB2), which distinguishes this process from glycolysis in pro-inflammatory macrophages. Mice transplanted with activation-defective PFKFB2 bone marrow and then subjected to dexamethasone-induced thymocyte apoptosis exhibit impaired thymic efferocytosis, increased thymic necrosis, and lower expression of the efferocytosis receptors MerTK and LRP1 on thymic macrophages compared with wild-type control mice. In vitro mechanistic studies revealed that glycolysis stimulated by the uptake of a first apoptotic cell promotes continual efferocytosis through lactate-mediated upregulation of MerTK and LRP1. Thus, efferocytosis-induced macrophage glycolysis represents a unique metabolic process that sustains continual efferocytosis in a lactate-dependent manner. The differentiation of this process from inflammatory macrophage glycolysis raises the possibility that it could be therapeutically enhanced to promote efferocytosis and resolution in chronic inflammatory diseases.

Mutation of regulatory phosphorylation sites in PFKFB2 does not affect the anti-fibrotic effect of metformin in the kidney.

The anti-fibrotic effect of metformin has been widely demonstrated. Fibrosis in the kidney after injury is associated with reduced expression of genes involved in both fatty acid and glycolytic energy metabolism. We have previously reported that the anti-fibrotic effect of metformin requires phosphoregulation of fatty acid oxidation by AMP-activated protein kinase (AMPK). To determine whether metformin also acts via regulation of glycolysis, we mutated regulatory phosphosites in the PFKFB2 isoform of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase (PFKFB2), a key regulator of glycolysis in the kidney. Mice with inactivating knockin (KI) mutations of the phosphorylation sites in PFKFB2 (PFKFB2 KI mice), which reduces the ability to increase the rate of glycolysis following stimulation, were used. Metformin was administered via drinking water to mice with a unilateral ureteric obstruction (UUO) model of renal fibrosis. In the PFKFB2 KI mice treated with metformin, there was decreased fibrosis and macrophage infiltration following UUO as assessed by Western blot for fibronectin and RT-PCR for α-smooth muscle actin, collagen 3, and F4.80, and confirmed by histology. Expression of the inducible PFKFB3 isoform was increased with metformin in UUO in both WT and PFKFB2 KI mice. There was no significant difference between WT and PFKFB2 KI mice treated with metformin in the degree of fibrosis following UUO in any of the Western blot or RT-PCR parameters that were measured. These data show that inhibition of the regulation of glycolysis by PFKFB2 does not diminish the anti-fibrotic effect of metformin in a model of renal fibrosis.

Understanding Donor-derived Cell-free DNA in Kidney Transplantation: An Overview and Case-based Guide for Clinicians.

Kidney transplant recipients undergo lifelong monitoring of allograft function and evaluation for transplant complications. The current monitoring paradigm utilizes blood, urine, and tissue markers that are insensitive, nonspecific, or invasive to obtain. As a result, problems are detected late, after significant damage has accrued, and often beyond the time at which complete resolution is possible. Indeed, most kidney transplants eventually fail, usually because of chronic rejection and other undetected injury. There is a clear need for a transplant-specific biomarker that enables a proactive approach to monitoring via early detection of reversible pathology. A biomarker that supports timely and personalized treatment would assist in achieving the ultimate goal of improving allograft survival and limiting therapeutic toxicity to the recipient. Donor-derived cell-free DNA (ddcfDNA) has been proposed as one such transplant biomarker. Although the test is presently utilized most in the United States, it is conceivable that its use will become more widespread. This review covers aspects of ddcfDNA that support informed use of the test by general nephrologists, including the basic biology of ddcfDNA, methodological nuances of testing, and general recommendations for use in the kidney transplant population. Clinical contexts are used to illustrate evidence-supported interpretation of ddcfDNA results and subsequent management. Finally, knowledge gaps and areas for further study are discussed.

Elevated serum urea-to-creatinine ratio is associated with adverse inpatient clinical outcomes in non-end stage chronic kidney disease.

To better understand the role of the urea-to-creatinine ratio in chronic kidney disease patients, we assessed the epidemiology of the urea-to-creatinine ratio among hospitalised chronic kidney disease patients, and the association between the urea-to-creatinine ratio and inpatient clinical outcomes. This retrospective cohort study (n = 11,156) included patients with at least two eGFR values < 60 mL/min/1.73m2 measured greater than 90-days apart and admitted to a tertiary hospital between 2014 and 2019. Dialysis and renal transplant patients were excluded. Adjusted odds ratios for factors associated with an elevated urea-to-creatinine ratio were calculated. Multivariate regression was conducted to identify the relationship between elevated UCR and inpatient mortality, intensive care admission, hospital readmission and hospital length-of-stay. Urea-to-creatinine ratio > 100 was present in 27.67% of hospital admissions. Age ≥ 65 years, female gender, gastrointestinal tract bleeding, heart failure, acute kidney injury and lower serum albumin were associated with elevated urea-to-creatinine ratio. Higher urea-to-creatinine ratio level was associated with greater rates of inpatient mortality, hospital readmission within 30-days and longer hospital length-of-stay. Despite this, there was no statistically significant association between higher urea-to-creatinine ratio and intensive care unit admission. Elevated urea-to-creatinine ratio is associated with poor clinical outcomes in chronic kidney disease inpatients. This warrants further investigation to understand the pathophysiological basis for this relationship and to identify effective interventions.

An Exploration of Recent Intelligent Image Analysis Techniques for Visual Pavement Surface Condition Assessment.

Road pavement condition assessment is essential for maintenance, asset management, and budgeting for pavement infrastructure. Countries allocate a substantial annual budget to maintain and improve local, regional, and national highways. Pavement condition is assessed by measuring several pavement characteristics such as roughness, surface skid resistance, pavement strength, deflection, and visual surface distresses. Visual inspection identifies and quantifies surface distresses, and the condition is assessed using standard rating scales. This paper critically analyzes the research trends in the academic literature, professional practices and current commercial solutions for surface condition ratings by civil authorities. We observe that various surface condition rating systems exist, and each uses its own defined subset of pavement characteristics to evaluate pavement conditions. It is noted that automated visual sensing systems using intelligent algorithms can help reduce the cost and time required for assessing the condition of pavement infrastructure, especially for local and regional road networks. However, environmental factors, pavement types, and image collection devices are significant in this domain and lead to challenging variations. Commercial solutions for automatic pavement assessment with certain limitations exist. The topic is also a focus of academic research. More recently, academic research has pivoted toward deep learning, given that image data is now available in some form. However, research to automate pavement distress assessment often focuses on the regional pavement condition assessment standard that a country or state follows. We observe that the criteria a region adopts to make the evaluation depends on factors such as pavement construction type, type of road network in the area, flow and traffic, environmental conditions, and region's economic situation. We summarized a list of publicly available datasets for distress detection and pavement condition assessment. We listed approaches focusing on crack segmentation and methods concentrating on distress detection and identification using object detection and classification. We segregated the recent academic literature in terms of the camera's view and the dataset used, the year and country in which the work was published, the F1 score, and the architecture type. It is observed that the literature tends to focus more on distress identification ("presence/absence" detection) but less on distress quantification, which is essential for developing approaches for automated pavement rating.

Blocking AMPK signalling to acetyl-CoA carboxylase increases cisplatin-induced acute kidney injury and suppresses the benefit of metformin.

BACKGROUND: Acute kidney injury (AKI) is accompanied by dysregulation of cellular energy metabolism and accumulation of intracellular lipid. Phosphorylation of acetyl-CoA carboxylase (ACC) by AMP-activated protein kinase (AMPK) inhibits fatty acid synthesis and promotes fatty acid oxidation (FAO), vital for kidney tubular epithelial cells (TECs). The diabetes drug metformin is protective in models of AKI; however, it is not known whether ACC phosphorylation plays a role. METHODS: Cisplatin-induced AKI (CI-AKI) was established in ACC1/2 double knock-in (ACC1/2DKI) mice, harbouring mutations that disrupt fatty acid metabolism, and the role of metformin was studied in this model. Outcomes measured included serum biochemistry, expression of kidney injury markers such as neutrophil gelatinase-associated lipocalin (NGAL), and metabolomic analysis. FINDINGS: ACC1/2DKI mice demonstrated more severe CI-AKI than wild type (WT), as assessed by serum urea and creatinine, histological injury, and expression of NGAL and interleukin-6. Metformin protected against AKI in WT mice, shown by reduced NGAL, but this effect was absent in ACC1/2DKI mice. In cultured TECs exposed to cisplatin, metformin reduced expression of cleaved caspase-3, however, this effect was diminished in ACC1/2DKI TECs. Analysis of kidney polar metabolites found numerous differences between metformin-treated CI-AKI in ACC1/2DKI and WT mice, involving multiple pathways of amino acid, nucleoside, and energy metabolism. INTERPRETATION: Severity of CI-AKI is exacerbated by the inability to regulate metabolism via phosphorylation of ACC. ACC phosphorylation contributes to the protective effect of metformin against AKI, influencing multiple mechanisms involved in the pathogenesis of kidney injury.

Independent of Renox, NOX5 Promotes Renal Inflammation and Fibrosis in Diabetes by Activating ROS-Sensitive Pathways.

Excessive production of renal reactive oxygen species (ROS) plays a major role in diabetic kidney disease (DKD). Here, we provide key findings demonstrating the predominant pathological role of the pro-oxidant enzyme NADPH oxidase 5 (NOX5) in DKD, independent of the previously characterized NOX4 pathway. In patients with diabetes, we found increased expression of renal NOX5 in association with enhanced ROS formation and upregulation of ROS-sensitive factors early growth response 1 (EGR-1), protein kinase C-α (PKC-α), and a key metabolic gene involved in redox balance, thioredoxin-interacting protein (TXNIP). In preclinical models of DKD, overexpression of NOX5 in Nox4-deficient mice enhances kidney damage by increasing albuminuria and augmenting renal fibrosis and inflammation via enhanced ROS formation and the modulation of EGR1, TXNIP, ERK1/2, PKC-α, and PKC-ε. In addition, the only first-in-class NOX inhibitor, GKT137831, appears to be ineffective in the presence of NOX5 expression in diabetes. In vitro, silencing of NOX5 in human mesangial cells attenuated upregulation of EGR1, PKC-α, and TXNIP induced by high glucose levels, as well as markers of inflammation (TLR4 and MCP-1) and fibrosis (CTGF and collagens I and III) via reduction in ROS formation. Collectively, these findings identify NOX5 as a superior target in human DKD compared with other NOX isoforms such as NOX4, which may have been overinterpreted in previous rodent studies.

Cardiovascular Complications of Interatrial Conduction Block: JACC State-of-the-Art Review.

Interatrial block (IAB) is an electrocardiographic pattern describing the conduction delay between the right and left atria. IAB is classified into 3 degrees of block that correspond to decreasing conduction in the region of Bachmann's bundle. Although initially considered benign in nature, specific subsets of IAB have been associated with atrial arrhythmias, elevated thromboembolic stroke risk, cognitive impairment, and mortality. As the pathophysiologic relationships between IAB and stroke are reinforced, investigation has now turned to the potential benefit of early detection, atrial imaging, cardiovascular risk factor modification, antiarrhythmic pharmacotherapy, and stroke prevention with oral anticoagulation. This review provides a contemporary overview of the epidemiology, pathophysiology, diagnosis, and management of IAB, with a focus on future directions.

SGLT-2 inhibitors and cardiovascular outcomes in patients with and without a history of heart failure: a systematic review and meta-analysis.

AIMS: Sodium-glucose cotransporter 2 (SGLT-2) inhibitors have cardiovascular (CV) benefits in patients with heart failure with reduced ejection fraction (HFrEF). Whether these medications improve CV outcomes irrespective of heart failure history or left ventricular ejection fraction (LVEF) in HFrEF remains unknown. METHODS AND RESULTS: All randomized, placebo-controlled trials of SGLT-2 inhibitors reporting similar CV outcomes were searched in PubMed from 1 January 2010 to 1 October 2021. The primary outcome was the composite of hospitalization for heart failure or CV death. Secondary outcomes included all-cause mortality. Pooled hazard ratios (HRs) and 95% confidence intervals (CIs) were used as effect estimates and calculated with a random-effects model. Data from 11 trials and a total of 66 957 patients (n = 36 758 SGLT-2 group, n = 30 199 placebo group) were included. SGLT-2 inhibitors reduced the risk of hospitalization for heart failure or CV death in patients with (HR 0.76, 95% CI 0.71-0.80) and without (HR 0.76, 95% CI 0.68-0.86; Pinteraction = 0.69) heart failure. Patients with (HR 0.87, 95% CI 0.80-0.95) and without (HR 0.84, 95% CI 0.73-0.95; Pinteraction = 0.67) heart failure treated with SGLT-2 inhibitors had a reduction in all-cause mortality. Reduction in the primary outcome was consistently observed in HFrEF patients with (HR 0.68, 95% CI 0.59-0.78) and without (HR 0.84, 95% CI 0.71-0.99; Pinteraction = 0.13) severely reduced LVEF, and in heart failure with preserved ejection fraction patients (HR 0.80, 95% CI 0.70-0.92; Pinteraction = 0.65). CONCLUSION: SGLT-2 inhibitors improved CV outcomes irrespective of heart failure history or type, and severity of LVEF reduction.

Effect of Elevated C-Reactive Protein on Outcomes After Complex Percutaneous Coronary Intervention for Angina Pectoris.

Inflammation and procedural complexity are individually associated with adverse outcomes after percutaneous coronary intervention (PCI). We aimed to evaluate the association of high sensitivity C-reactive protein (hsCRP) with adverse events according to PCI complexity. We included patients with available hsCRP levels who underwent PCI at our center from 2012 to 2017. We compared patients with hsCRP ≥3 versus <3 mg/L. Complex PCI was defined as having ≥1 of the following: ≥3 different target vessels, ≥3 lesions treated, ≥3 stents implanted, bifurcation lesion treated with 2 stents, chronic total occlusion as target lesion, or total stent length >60 mm. The primary end point was major adverse cardiac events (MACEs) (composite of all-cause death, myocardial infarction, or target vessel revascularization) at 1 year. A total of 11,979 patients were included, of which 2,840 (24%) underwent complex PCI. In those, 767 (27%) had hsCRP ≥3 mg/L. The 1-year incidence of MACE was 6% (noncomplex PCI, low hsCRP), 10% (noncomplex PCI, high hsCRP), 10% (complex PCI, low hsCRP), and 15% (complex PCI, high hsCRP). Overall, hsCRP ≥3 mg/L was associated with an increased risk of MACE compared with hsCRP <3 mg/L; this was independent of the number of complex PCI features: 0 (adjusted hazard ratio [HR] 1.53; 95% confidence interval [CI] 1.27 to 1.86), 1 (adjusted HR 1.77; 95% CI 1.21 to 2.60), or ≥2 (adjusted HR 1.21; 95% CI 0.80 to 1.83) (pinteraction = 0.42). In conclusion, in patients who underwent PCI, elevated hsCRP is associated with an increased risk of ischemic events. The effect of elevated hsCRP on cardiovascular risk is consistent regardless of PCI complexity.

Outcomes of intravascular ultrasound versus optical coherence tomography guided percutaneous coronary angiography: A meta regression-based analysis.

BACKGROUND: Studies comparing clinical outcomes with intravascular ultrasound (IVUS) versus optical coherence tomography (OCT) guidance for percutaneous coronary intervention (PCI) in patients presenting with coronary artery disease, including stable angina or acute coronary syndrome, are limited. METHODS: We performed a detailed search of electronic databases (PubMed, Embase, and Cochrane) for randomized controlled trials and observational studies that compared cardiovascular outcomes of IVUS versus OCT. Data were aggregated for the primary outcome measure using the random-effects model as pooled risk ratio (RR). The primary outcome of interest was major adverse cardiac events (MACE), cardiac mortality, and all-cause mortality. Secondary outcomes included myocardial infarction (MI), stent thrombosis (ST), target lesion revascularization (TLR), and stroke. RESULTS: A total of seven studies met the inclusion criteria, comprising 5917 patients (OCT n = 2075; IVUS n = 3842). OCT-PCI versus IVUS-guided PCI comparison yielded no statistically significant results for all the outcomes; MACE (RR 0.78; 95% confidence interval [CI], 0.57-1.09; p = 0.14), cardiac mortality (RR 0.97; 95% CI, 0.27-3.46; p = 0.96), all-cause mortality (RR 0.74; 95% CI, 0.39-1.39; p = 0.35), MI (RR 1.27; 95% CI, 0.52-3.07; p = 0.60), ST (RR 0.70; 95% CI, 0.13-3.61; p = 0.67), TLR (RR 1.09; 95% CI, 0.53-2.25; p = 0.81), and stroke (RR 2.32; 95% CI, 0.42-12.90; p = 0.34). Furthermore, there was no effect modification on meta-regression including demographics, comorbidities, lesion location, lesion length, and stent type. CONCLUSIONS: In this meta-analysis, OCT-guided PCI was associated with no difference in clinical outcomes compared with IVUS-guided PCI.