27 research outputs found

    Complete revascularization with multivessel PCI for myocardial infarction

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    BACKGROUND In patients with ST-segment elevation myocardial infarction (STEMI), percutaneous coronary intervention (PCI) of the culprit lesion reduces the risk of cardiovascular death or myocardial infarction. Whether PCI of nonculprit lesions further reduces the risk of such events is unclear. METHODS We randomly assigned patients with STEMI and multivessel coronary artery disease who had undergone successful culprit-lesion PCI to a strategy of either complete revascularization with PCI of angiographically significant nonculprit lesions or no further revascularization. Randomization was stratified according to the intended timing of nonculprit-lesion PCI (either during or after the index hospitalization). The first coprimary outcome was the composite of cardiovascular death or myocardial infarction; the second coprimary outcome was the composite of cardiovascular death, myocardial infarction, or ischemia-driven revascularization. RESULTS At a median follow-up of 3 years, the first coprimary outcome had occurred in 158 of the 2016 patients (7.8%) in the complete-revascularization group as compared with 213 of the 2025 patients (10.5%) in the culprit-lesion-only PCI group (hazard ratio, 0.74; 95% confidence interval [CI], 0.60 to 0.91; P=0.004). The second coprimary outcome had occurred in 179 patients (8.9%) in the complete-revascularization group as compared with 339 patients (16.7%) in the culprit-lesion-only PCI group (hazard ratio, 0.51; 95% CI, 0.43 to 0.61; P<0.001). For both coprimary outcomes, the benefit of complete revascularization was consistently observed regardless of the intended timing of nonculprit-lesion PCI (P=0.62 and P=0.27 for interaction for the first and second coprimary outcomes, respectively). CONCLUSIONS Among patients with STEMI and multivessel coronary artery disease, complete revascularization was superior to culprit-lesion-only PCI in reducing the risk of cardiovascular death or myocardial infarction, as well as the risk of cardiovascular death, myocardial infarction, or ischemia-driven revascularization. (Funded by the Canadian Institutes of Health Research and others; COMPLETE ClinicalTrials.gov number, NCT01740479. opens in new tab.

    Influenza H1N1 infection leading to cardiac tamponade in a previously healthy patient: A case report

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    Introduction: The cardiac manifestations of influenza A are broad, ranging from self-limited pericarditis to fatal cardiomyopathy. The 2009 H1N1 influenza A (H1N1) strain is a rare cause of pericarditis, and its role in developing a pericardial effusion leading to tamponade has infrequently been reported. Case Presentation: We describe a case of a young female with no prior cardiovascular history who presents with a pericardial effusion and shock secondary to cardiac tamponade from pericarditis due to H1N1 influenza A. Conclusions: This case highlights the potential severity of H1N1 infections and the utility of considering cardiac tamponade in patients presenting with influenza symptoms and circulatory collapse

    Potent P2Y12 Inhibitor Selection and De-escalation Strategies in Acute Coronary Syndrome Patients Undergoing Percutaneous Coronary Intervention: Systematic Review and Meta-analysis

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    Background: Balancing the effects of dual antiplatelet therapy (DAPT) in the era of potent purinergic receptor type Y, subtype 12 (P2Y12) inhibitors remains a challenge in the management of acute coronary syndrome (ACS). Methods: We conducted a systematic review and meta-analysis following a 2-stage process consisting of searching for systematic reviews published between 2019 and November 2022. We included randomized controlled trials (RCTs) of ACS patients treated with percutaneous coronary intervention comparing (i) ticagrelor- vs prasugrel-based DAPT and (ii) P2Y12 inhibitor de-escalation strategies. Outcomes of interest were major adverse cardiovascular events (MACE), all-cause death, stent thrombosis, and major bleeding. We estimated risk ratios (RRs) and 95% confidence intervals (CIs) using a random-effects model. Results: Eight RCTs (n = 5571) compared ticagrelor to prasugrel. Ticagrelor was associated with an increased risk of MACE compared to prasugrel (RR 1.23, 95% CI 1.01-1.49, moderate certainty), without significant differences in death, stent thrombosis, or major bleeding. In 2 RCTs (n = 3343) comparing clopidogrel-based DAPT de-escalation after 1 month to potent P2Y12 inhibitor–based DAPT continuation, clopidogrel de-escalation did not significantly alter the incidence of MACE, death, or stent thrombosis, but reduced that of major bleeding (RR 0.51, 95% CI 0.28-0.92, high certainty). The effect of prasugrel dose de-escalation was inconclusive for all outcomes based on one trial. Conclusions: Ticagrelor was associated with an increase in MACE compared with prasugrel, based on low-certainty evidence, whereas de-escalation to clopidogrel after 1 month of potent P2Y12 inhibitor was associated with a decrease in incidence of major bleeding without increasing thrombotic outcomes in ACS patients post-percutaneous coronary intervention. RĂ©sumĂ©: Contexte: Équilibrer les effets de la bithĂ©rapie antiplaquettaire (BTAP) Ă  l’ùre des puissants inhibiteurs du rĂ©cepteur purinergique de type Y, sous-type 12 (P2Y12) demeure un dĂ©fi dans la prise en charge du syndrome coronarien aigu (SCA). MĂ©thodologie: Nous avons procĂ©dĂ© Ă  un examen systĂ©matique et Ă  une mĂ©ta-analyse, tout d’abord en recherchant les revues systĂ©matiques publiĂ©es entre 2019 et 2022, puis en mettant Ă  jour la recherche la plus complĂšte de ces revues jusqu’en novembre 2022. Nous avons inclus des essais contrĂŽlĂ©s randomisĂ©s (ECR) menĂ©s chez des patients ayant subi un SCA traitĂ© par intervention coronarienne percutanĂ©e qui comparaient i) une BTAP comportant du ticagrĂ©lor Ă  une BTAP Ă  base de prasugrel, et ii) les stratĂ©gies de rĂ©duction graduelle de la dose de l’inhibiteur de P2Y12. Les rĂ©sultats d’intĂ©rĂȘt comprenaient les Ă©vĂ©nements cardiovasculaires indĂ©sirables majeurs (ECIM), les dĂ©cĂšs toutes causes confondues, les thromboses de l’endoprothĂšse et les saignements majeurs. Nous avons estimĂ© les rapports de risques (RR) et les intervalles de confiance (IC) Ă  95 % Ă  l’aide d’un modĂšle Ă  effets alĂ©atoires. RĂ©sultats: Huit ECR (n = 5 571) ont comparĂ© le ticagrĂ©lor au prasugrel. Le ticagrĂ©lor Ă©tait associĂ© Ă  un risque accru d’ECIM comparativement au prasugrel (RR de 1,23, IC Ă  95 % de 1,01 Ă  1,49, certitude modĂ©rĂ©e), sans diffĂ©rence significative quant au dĂ©cĂšs, Ă  la thrombose de l’endoprothĂšse ou au saignement majeur. Dans deux ECR (n = 3 343) comparant la rĂ©duction graduelle de la BTAP Ă  base de clopidogrel aprĂšs 1 mois Ă  la poursuite de la BTAP comportant un inhibiteur puissant de P2Y12, la rĂ©duction graduelle de la dose de clopidogrel n’a pas modifiĂ© de maniĂšre significative la frĂ©quence des ECIM, des dĂ©cĂšs ou des thromboses de l’endoprothĂšse, mais a rĂ©duit celle des saignements majeurs (RR de 0,51, IC Ă  95 % de 0,28 Ă  0,92, certitude Ă©levĂ©e). L’effet de la rĂ©duction graduelle de la dose de prasugrel n’a pas Ă©tĂ© concluant pour tous les rĂ©sultats sur la base d’un seul essai. Conclusions: Si l’on se fie aux donnĂ©es probantes de faible certitude, le ticagrĂ©lor a Ă©tĂ© associĂ© Ă  une augmentation des ECIM comparativement au prasugrel, tandis que la rĂ©duction graduelle de la dose de clopidogrel aprĂšs 1 mois d’administration d’un puissant inhibiteur de P2Y12 a Ă©tĂ© associĂ©e Ă  une diminution de la frĂ©quence des saignements majeurs sans augmentation des Ă©vĂ©nements thrombotiques chez les patients ayant subi une intervention coronarienne percutanĂ©e pour traiter un SCA

    Implications of ischaemic area at risk and mode of reperfusion in ST-elevation myocardial infarction

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    OBJECTIVE: Uncertainty exists concerning the relative merits of pharmacological versus mechanical coronary reperfusion in patients presenting early with ST-elevation myocardial infarction (STEMI) with extensive myocardium at risk. Accordingly, we investigated whether the extent of baseline ST-segment shift was related to the response of either reperfusion modality in patients with STEMI presenting within 3 h of symptoms. METHODS: We analysed baseline ECGs from 1859 patients enrolled in the STrategic Reperfusion Early After Myocardial Infarction (STREAM) trial. The sum of ST-segment elevation (∑STE) and ST-segment deviation (∑STD) was categorised into quartiles and associations with the primary endpoint (30-day death/shock/congestive heart failure/re-myocardial infarction) for each reperfusion strategy (early fibrinolysis vs primary percutaneous coronary intervention) were explored. RESULTS: Overall, there was a progressive rise in the 30-day primary endpoint according to quartiles of baseline ∑STE (10.3% (0-5 mm), 12.4% (5.5-8.5 mm), 12.1% (9-13.5 mm), 17.6% (> 14.0 mm), p = 0.008) and ∑STD (9.0% (0-9 mm), 13.5% (9.5-14 mm), 14.7% (14.5-20 mm), 15.3% (> 20 mm), p = 0.019). Both ∑STE and ∑STD were associated with the primary endpoint (∑STE: p = 0.071; ∑STD: p = 0.024). However, there was no interaction between quartiles of baseline ∑STE or ∑STD and efficacy of either reperfusion strategy on the 30-day clinical outcomes (∑STE: p (interaction) = 0.696; ∑STD: p (interaction) = 0.542). CONCLUSIONS: These data demonstrate an association between ∑STE or ∑STD on the baseline ECG and clinical events at 30 days following reperfusion therapy in STEMI. More importantly, the response to different reperfusion strategies was not influenced by the extent of jeopardised myocardium. TRIAL REGISTRATION NUMBER: NCT00623623; Post-results.status: publishe
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