Objectives We sought to assess the clinical value of adding intravascular ultrasound (IVUS) evaluation to coronary angiography (CA) to guide extrinsic left main coronary artery (LMCA) compression diagnosis and treatment in pulmonary hypertension (PH). Background LMCA compression due to a pulmonary artery aneurysm (PAA) is a severe complication of PH. Although guidelines encourage the use of IVUS for LMCA disease evaluation, it has hardly been used in this scenario. Methods We analyzed morbimortality of type 1 and 4 PH patients with clinically suspected LMCA compression by a PAA between 2010 and 2018 in a reference unit. LMCA compression was prospectively assessed with CA ± IVUS. Angiographic‐LMCA compression was considered conclusive when LMCA stenosis>50% was present in four predetermined projections; inconclusive, when LMCA stenosis>50% was present in <4 projections and negative if no stenosis>50% was present. Patients with conclusive and inconclusive CA underwent IVUS. IVUS‐LMCA compression was defined as systolic minimum lumen area < 6 mm2. Results LMCA compression was suspected in 23/796 patients (3%). CA was conclusive for compression in 7(30.5%), inconclusive in 9(39%), and negative in 7(30.5%). IVUS confirmed LMCA compression in 6/7(86%) patients with conclusive CA and in 2/9(22%) with inconclusive CA. Patients fulfilling IVUS criteria for LMCA compression underwent stent implantation. At 20 months follow‐up a composite end‐point of death, stent restenosis/thrombosis, or lung transplant was reported in three patients (13%). Conclusions CA can misdiagnose LMCA extrinsic compression. IVUS discriminates better whether significant compression by a PAA exists or not, avoiding unnecessary LMCA stenting. Patients treated following this strategy show a low rate of major clinical events at 20 months follow‐up.
The limited availability of red cells with extremely rare blood group phenotypes is one of the global challenges in transfusion medicine that has prompted the search for alternative self‐renewable pluripotent cell sources for the in vitro generation of red cells with rare blood group types. One such phenotype is the Rh null , which lacks all the Rh antigens on the red cell membrane and represents one of the rarest blood types in the world with only a few active blood donors available worldwide. Rh null red cells are critical for the transfusion of immunized patients carrying the same phenotype, besides its utility in the diagnosis of Rh alloimmunization when a high‐prevalence Rh specificity is suspected in a patient or a pregnant woman. In both scenarios, the potential use of human‐induced pluripotent stem cell (hiPSC)‐derived Rh null red cells is also dependent on ABO compatibility. Here, we present a CRISPR/Cas9‐mediated ABO gene edition strategy for the conversion of blood type A to universal type O, which we have applied to an Rh null donor‐derived hiPSC line, originally carrying blood group A. This work provides a paradigmatic example of an approach potentially applicable to other hiPSC lines derived from rare blood donors not carrying blood type O.
Biological circadian rhythms in living organisms are regulated by molecular clocks. Several of these clocks are present in blood vessels, peripheral tissues, and immune cells. There is strong evidence linking dysregulation of circadian rhythms to the development of cardiovascular disease. Dysregulation of circadian rhythms is believed to activate inflammatory processes at specific times of day, leading to an increased risk of thrombosis and atherosclerosis progression. Research into circadian clock genes and molecular networks has the potential to identify therapeutic targets to reduce cardiovascular risk. In this review, we summarize the evidence linking circadian rhythms to thrombosis and atherothrombotic events and discuss potential therapeutic implications.
Background There is a lack of evidence regarding the benefits of β-blocker treatment after invasively managed acute myocardial infarction (MI) without reduced left ventricular ejection fraction (LVEF). Methods and results TREatment with Beta-blockers after myOcardial infarction withOut reduced ejection fraction (REBOOT) trial is a pragmatic, controlled, prospective, randomized, open-label blinded endpoint (PROBE design) clinical trial testing the benefits of β-blocker maintenance therapy in patients discharged after MI with or without ST-segment elevation. Patients eligible for participation are those managed invasively during index hospitalization (coronary angiography), with LVEF >40%, and no history of heart failure (HF). At discharge, patients will be randomized 1:1 to β-blocker therapy (agent and dose according to treating physician) or no β-blocker therapy. The primary endpoint is a composite of all-cause death, nonfatal reinfarction, or HF hospitalization over a median follow-up period of 2.75 years (minimum 2 years, maximum 3 years). Key secondary endpoints include the incidence of the individual components of the primary composite endpoint, the incidence of cardiac death, and incidence of malignant ventricular arrhythmias or resuscitated cardiac arrest. The primary endpoint will be analyzed according to the intention-to-treat principle. Conclusion The REBOOT trial will provide robust evidence to guide the prescription of β-blockers to patients discharged after MI without reduced LVEF.
Background Balance between embolic and bleeding risk is challenging in patients with cancer. There is a lack of specific recommendations for the use of antithrombotic therapy in oncologic patients with atrial fibrillation (AF). We aimed to evaluate the effectiveness and safety of direct oral anticoagulants (DOACs) and vitamin K antagonists (VKAs) within patients with breast cancer. We also compared the embolic and bleeding risk, the preventive management and the incidence of events between patients with and without cancer. Methods It is an ambispective observational multicentric study that analysed patients with non-valvular AF treated in Oncology and Cardiology Departments in Spain in the period 2011–2018. A total of 1237 female patients with AF were enrolled: 637 with breast cancer and 599 without cancer. The incidence of thromboembolic and major bleeding events according to the antithrombotic strategy with VKAs or DOACs was evaluated in the cohort of 637 patients with cancer. Analysis were conducted using SPSS software V.22.0 and R V.3.5.1, with a two-tailed significance value of 0.05. Results Mean follow-up was 3.1 years. Both groups were similar in age, CHA2DS2-VASc and HASB-LED scores. There was no evidence that the incidence of ischemic stroke/systemic embolism differed between patients with cancer treated with AVK and DOAC after CHA2DS2-VASc adjustment: HR 0.91 (95% CI, 0.42–1.99). In addition, no significant differences in the incidence of major bleeding events were found between DOACs and VKA after adjustment for HAS-BLED score: HR 1.53 (95% CI, 0.93–2.53) (Figure 3). Gastrointestinal bleeding was the main source of haemorrhages in both groups (45% of bleedings among patients treated with DOACs and, 37% in VKAs group). Metastatic disease or active chemotherapy were studied as potential covariates but none of them posed any relevant change in the result. Kaplan-Meier analysis Conclusions Cancer patients treated with DOACs did not differ versus those treated with VKAs with regards to stroke or systemic embolism in a model adjusted for CHA2DS2-VASc. Neither significant differences were found for bleeding events in a model adjusted for baseline HASBLED.
Aims Balance between embolic and bleeding risk is challenging in patients with cancer. There is a lack of specific recommendations for the use of antithrombotic therapy in oncologic patients with atrial fibrillation (AF). We compared the embolic and bleeding risk, the preventive management and the incidence of events between patients with and without cancer. We further evaluated the effectiveness and safety of direct oral anticoagulants (DOACs) and vitamin K antagonists (VKAs) within patients with cancer. Methods The AMBER-AF registry is an observational multicentre study that analysed patients with non-valvular AF treated in Oncology and Cardiology Departments in Spain. 1237 female patients with AF were enrolled: 637 with breast cancer and 599 without cancer. Mean follow-up was 3.1 years. Results Both groups were similar in age, CHA2DS2-VASc and HASB-LED scores. Lack of guidelines recommended therapies was more frequent among patients with cancer. Compared with patients without cancer, adjusted rates of stroke (hazard ratio [95% confidence interval]) in cancer patients were higher (1.56 [1.04–2.35]), whereas bleeding rates remained similar (1.25 [0.95–1.64]). Within the group of patients with cancer, the use of DOACs vs VKAs did not entail differences in the adjusted rates of stroke (0.91 [0.42–1.99]) or severe bleedings (1.53 [0.93–2.53]). Follow-up events Conclusions Antithrombotic management of AF frequently differs in patients with breast cancer. While breast cancer is associated with a higher risk of incident stroke, bleeding events remained similar. Patients with cancer treated with DOACs experienced similar rates of stroke and bleeding as those with VKAs.
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