Introduction Atherosclerotic plaque healing is a dynamic process that promotes plaque repair after destabilization. Previous studies showed that healed plaques are more common in patients with chronic coronary syndrome than in those with acute coronary syndrome, suggesting that they might be a marker of clinical stability. The mechanisms underlying plaque healing are not completely understood. The aim of the present study was to evaluate sex-based differences in plaque phenotype and healing of non-culprit coronary lesions by optical coherence tomography. Methods In this observational, single-center cohort study, we enrolled patients from the OCT Registry of the Fondazione Policlinico A Gemelli IRCCS. A total of 205 patients with both acute coronary syndromes or chronic coronary syndromes undergoing coronary angiography and intravascular OCT imaging of non-culprit vessels were included in the analysis and divided into two groups according to gender. Results Of 205 patients, 153 were male (75%) and 52 (25%) female. Compared with male patients, female patients had lower prevalence of lipid-rich plaque (40.4% vs. 57.7%; p=0.030), plaque rupture (7.7% vs. 21.2%; p=0.028) and cholesterol crystal (13.5% vs. 29.5%; p=0.022). Mean lipid arc and calcium depht were significantly lower in female patients than in male ones (118.0° ± 79.9° vs. 135.5° ± 77.9°; p=0.011; and 52.7 µm ± 79.2 µm vs. 72.3 µm ± 93.5 µm; p=0.007) while fibrous cap tended to be thicker (108.2 µm ± 70.4 µm vs. 96.2 µm ± 72.9 µm; p=0.055). Healed plaques were significantly more frequent in female patients than in male patients (51.9% vs 34.6%; p = 0.027). The prevalence of fibrous plaque, thrombi, neovascularization, diffuse calcifications and spotty calcification was not different between the two groups. Conclusion Females have a distinct atherosclerotic phenotype and healing capacity compared with male patients, including lower prevalence of lipid-rich plaque, cholesterol crystals and plaque ruptures and higher prevalence of healed plaques in non-culprit coronary lesions.
Aim Adenosine has been tested in several randomized controlled trials (RCTs) to minimize the incidence of coronary microvascular obstruction (CMVO). The aim of the present study was to pool all the RCTs comparing intracoronary or intravenous adenosine versus placebo in patients with acute coronary syndrome (ACS) undergoing myocardial revascularization. Methods and results PubMed and Scopus electronic databases were scanned for eligible studies up to June 5th 2022. A total of 26 RCTs with 5843 patients were included. Efficacy endpoints were major adverse cardiac events (MACE), all-cause-death, non-fatal myocardial infarction and heart failure. Atrioventricular blocks and ventricular fibrillation/sustained ventricular tachycardia (VF/SVT) were the safety endpoints. Myocardial blush grade, Thrombolysis In Myocardial Infarction (TIMI) flow grade, left ventricular ejection fraction (LVEF), infarct size, and ST-segment resolution were also assessed. Adenosine administration was not associated with any clinical benefit in terms of MACE, all-cause death, non-fatal myocardial infarction, and heart failure. However, adenosine was associated with an increased rate of advanced atrioventricular blocks and of VF/SVT in studies with total mean ischemic time > 3 hours, compared to placebo. Remarkably, among patients undergoing percutaneous coronary intervention, adenosine was associated with reduced myocardial blush grade 0–1 and TIMI flow grade 0–2, compared to placebo. Furthermore, adenosine did not show favourable effects on LVEF and infarct size. Conclusion Adenosine infusion, as adjunctive therapy in ACS, was associated with an increased risk of advanced atrioventricular blocks and increased rates of adenosine-triggered ventricular arrhythmias in patients with long ischemic time, without providing any clinical benefit compared to placebo.
Aims Atherosclerotic plaque healing is a dynamic process developing after plaque rupture or erosion, which aims to prevent lasting occlusive thrombus formation and to promote plaque repair. We hypothesized that diabetes mellitus, one of the major conventional cardiovascular risk factors, may influence the healing capacity after plaque destabilization. Methods and results In this single-centre observational cohort study, patients with acute coronary syndrome (ACS) or chronic coronary syndrome (CCS) who underwent optical coherence tomography (OCT) imaging at Fondazione Policlinico A. Gemelli–IRCCS, Rome, were included. Patients were divided into two groups (i.e. diabetes vs. no diabetes), and stratified based on diabetes medications (i.e. insulin, vs. oral antidiabetic drugs). OCT analysis of non-culprit coronary segments was performed. 105 patients were included (44 diabetes, 61 no diabetes). Prevalence of HCPs was not significantly different between patients with and without diabetes (3.6% vs. 3.8%, P = 0.854). However, patients with diabetes on insulin showed a lower prevalence of HCPs both at patient-based (7.1% vs. 26.4%, P = 0.116) and at segment-based analysis (1.2% vs. 4.2%, P = 0.020). When comparing HbA1c levels based on the presence or absence of healed plaque at the non-culprit lesions, patients with healed plaque showed significantly lower levels of HbA1c compared to patients without healed plaques (43.5 ± 12.1% vs. 61.2 ± 10.4%, P < 0.001). At segment-based analysis, normal vessel structure, pathological intimal thickening (PIT), and spotty calcifications were significantly less prevalent in diabetic patients (2.1% vs. 5.1%, P = 0.001; 7.2% vs. 9.5%, P = 0.05; 9.9% vs. 13.6%, P = 0.02, respectively), whereas neovascularization was significantly higher (19.2% vs. 15.6%, P = 0.035). Conclusions Patients with diabetes have a distinct coronary non-culprit plaque phenotype. Healing capacity may be impaired in patients with advanced diabetes on insulin therapy and in those with a suboptimal control of the disease. Further prospective, larger scale studies are warranted to confirm these findings.
Background Percutaneous coronary intervention (PCI) is the milestone of treatment for patients with acute coronary syndrome (ACS). However, a considerable number of patients do not achieve a complete myocardial reperfusion since coronary microvascular obstruction (CMVO) might occur. Adenosine is one of the pharmacological strategies tested in several randomized controlled trials (RCTs) to minimize the incidence of CMVO. However, conflicting results have been reported so far. The aim of the present study was to evaluate all the RCTs comparing intracoronary or intravenous adenosine versus placebo as adjunctive therapy in patients with ACS undergoing PCI or thrombolysis. Methods PubMed and Scopus electronic databases were scanned for eligible studies up to June 5th, 2022. Our meta-analysis included 26 randomized RCTs with a total of 5843 patients involved. Primary endpoints were the rate of clinical events, defined as major adverse cardiovascular events (MACE), heart failure (HF), all-cause-death and non-fatal myocardial infarction (MI). The rate of advanced atrioventricular (AV) blocks and ventricular fibrillation/sustained ventricular tachycardia (VF/SVT) were considered as safety endpoints. Further subgroup analyses and meta regressions were conducted to evaluate the role of different procedural and non-procedural factors influencing the results. Finally, a secondary analysis was conducted only including RCTs enrolling patients with ST-segment elevation myocardial infarction (STEMI). Results Adenosine administration did not confer any significant clinical benefit in terms of reduction of MACE (RR 0.91 CI 0.79-1.05, p 0.16), all-cause-death (RR 0.90 CI0.74-1.09, p 0.28), non-fatal MI (RR 1 CI 0.74 - 1.35, p 0.44) and HF (RR 0.94 CI 0.77-1.16, p 0.59). Remarkably, adenosine was associated with a significant reduction of post-procedural CMVO parameters such as Myocardial Blush Grade (MBG) 0-1 (RR 0.69 CI 0.53-0.90, p 0.01) and Thrombolysis In Myocardial Infarction (TIMI) flow grade 0-2 (RR 0.67 CI 0.53-0.85, p <0.01), when compared to placebo. Secondary analyses of STEMI patients showed similar results. As regards safety, adenosine therapy was associated with a higher rate of advanced AV blocks (RR 2.72 CI 1.57-4.74, p <0.01). A higher rate of VF/SVT was observed with adenosine in studies with total mean ischemic time >3 hours (RR 1.67 CI 1.14-2.42) Conclusions This is the most up-to-date meta-analysis summarizing the available evidence on adenosine safety and efficacy in the prevention or treatment of CMVO in ACS patients. Although adenosine improves surrogate parameters of myocardial perfusion, its use does not provide any clinical benefits. Additionally, adenosine infusion increases the risk of advanced AV blocks. Moreover, a longer ischemic time seems to be associated with a higher rate of adenosine-triggered ventricular arrhythmias, suggesting that higher myocardial ischemic damage may represent a substrate for adenosine arrhythmogenic effects.
Rational The occurrence of stent thrombosis (ST) is a rare event, but it remains one of the most catastrophic complications following percutaneous coronary intervention (PCI). Coronary angiography has limited value in differentiating the causative factors responsible for ST. Technical resolutions We report a case of a 78-year-old male, hypertensive and dyslipidemic who underwent PCI with stenting of the mid left anterior descending artery (LAD) due to chronic coronary syndrome (CCD) two years before. He was admitted to our emergency department for syncopal episode occurred at rest followed by chest pain radiating to the left arm and to the neck. At the time of admission, his electrocardiogram showed diffuse ST-segment elevation in V2-V6 and DI-aVL, therefore patient was urgently sent to the cath lab. Coronary angiography showed LAD occlusion at the proximal edge of the previously implanted stent with TIMI flow grade 0 and TIMI thrombus grade 5. Multiple thrombus aspiration passes were performed with distal flow restoration, followed by intracoronary abciximab administration. After additional thrombus aspiration passes, ST-segment resolution was observed and chest pain improved significantly. OCT imaging of mid-to-proximal LAD was then performed to better characterize the cause of thrombosis. OCT revealed in stent-thrombosis with mixed thrombus (6 mm length, arc >270°) associated with major stent malapposition (maximum malapposition distance: 1.3 mm) at the proximal edge of the previous implanted stent, without evidence of neoatherosclerosis and/or residual disease with unstable features at the stent edges. Additional thrombus aspiration was performed, further reducing the thrombotic burden. As te patient was hemodynamically stable and asymptomatic, with TIMI flow grade 3 at coronary angiography, we decided to start dual antiplatelet therapy (ASA+ticagrelor) plus continuous heparin i.v. infusion, and to defer PCI, planning a control coronary angiography after 72 hours. After 72 hours, OCT revealed almost complete thrombus resolution, and guided PCI with a 4.0/8 mm everolimus-eluting stent in overlap with the previously implanted stent, postdilated with a 4.5 semi-compliant balloon at 18 atm. Revascularization was completed with an OCT-guided PCI of the proximal left circumflex during the same procedure. Clinical implications Our case demonstrates the utility of OCT in determining thrombus burden and assessing the causes of late stent failure, guiding PCI. In this case, OCT was useful as diagnostic tool to identify the mechanism underlying the very-late ST, and as guidance for treatment. It enabled to exclude neoatherosclerosis and/or unstable plaques at stent edges, leaving us more confident to defer PCI after 72 h of antithrombotic therapy. Perspectives The occurrence of ST is rare, but it remains one of the most catastrophic complications following PCI. Coronary angiography has limited value in differentiating the causative factors responsible for ST, while OCT allows to detect and characterize the causes of stent thrombosis (i.e., evaluate thrombus burden, presence of neoatherosclerosis, stent malapposition/underxpansion, uncovred stent struts, significant disease and/or unstable plaques at the stent edges, etc.). A better understanding of the pathophysiological mechanism underlying ST is an important clinical need. The increasing availability of high-resolution intravascular imaging techniques such as OCT provides new opportunities for tailoring treatment strategy and guiding PCI.
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