Project description:A right atrial (RA) mass was incidentally found by transthoracic echocardiography in a 79-year-old man with atrial fibrillation rhythms but without a history of anticoagulation. Transesophageal echocardiography revealed a pedunculated immobile mass in the RA appendage. In addition, some calcification was detected in computed tomography. The mass was excised, and pathological examinations revealed organized thrombosis. Accordingly, in the presence of predisposing factors, thrombi, which may mimic some imaging features of tumors, should be considered in the differential diagnosis of RA masses.
Project description:Purpose: This study aims to identify IHD-associated signature RNAs from the atrial myocardium and evaluate their ability to reflect disease severity or cardiac surgery outcomes. Methods: We collected right atrial appendage (RAA) biopsies from 40 patients with invasive coronary angiography (ICA)-positive IHD undergoing coronary artery bypass surgery and from 8 patients ICA-negative for IHD (non-IHD) undergoing valvular surgery. Following RNA sequencing, RAA transcriptomes were analyzed against those 429 donors from the GTEx project without cardiac background. Results: The IHD transcriptome was characterized using repressed RNA expressions in pathways for cell–cell contacts and mitochondrial dysfunction. Specifically, we identified the increased expressions of the CSRNP3, FUT10, SHD, NAV2-AS4, and hsa-mir-181 genes to correlate with the complexity of coronary artery obstructions or with a functional cardiac benefit from bypass surgery. Conclusions: Our results provide an atrial myocardium–focused insight into IHD signature RNAs. The specific gene expression changes we characterized here pave the way for disease mechanism–based identification of biomarkers allowing for the early detection and treatment of IHD.
Project description:The left atrial appendage (LAA) of the adult heart has been shown to contain cardiac and myeloid progenitor cells. The resident myeloid progenitor population expresses an array of pro-regenerative paracrine factors. Cardiac constructs have been shown to inhibit deleterious remodeling of the heart using physical support. Due to these aspects, LAA holds promise as a regenerative transplant. LAAs from adult mT/mG mice were transplanted to the recipient 129X1-SvJ mice simultaneously as myocardial infarction (MI) was performed. A decellularized LAA patch was implanted in the control group. Two weeks after MI, the LAA patch had integrated to the ventricular wall, and migrated cells were seen in the MI area. The cells had two main phenotypes: small F4/80+ cells and large troponin C+ cells. After follow-up at 8 weeks, the LAA patch remained viable, and the functional status of the heart improved. Cardiac echo demonstrated that, after 6 weeks, the mice in the LAA-patch-treated group showed an increasing and statistically significant improvement in cardiac performance when compared to the MI and MI + decellularized patch controls. Physical patch-support (LAA and decellularized LAA patch) had an equal effect on the inhibition of deleterious remodeling, but only the LAA patch inhibited the hypertrophic response. Our study demonstrates that the LAA transplantation has the potential for use as a treatment for myocardial infarction. This method can putatively combine cell therapy (regenerative effect) and physical support (inhibition of deleterious remodeling).
Project description:BackgroundStenoses of the left atrial appendage (LAA) represent a common complication after incomplete surgical ligation. However, the idiopathic entity is very rare. So far, there is uncertainty about the thromboembolic risk and potential benefit of anticoagulation in these patients. We report on congenital ostial stenosis of the LAA as a secondary finding in a patient with myocardial infarction.Case summaryA 56-year-old patient presented with acute heart failure secondary to ST elevation myocardial infarction (STEMI) and eventually progressed to cardiogenic shock. A percutaneous coronary intervention and stent placement in the first diagonal branch and in the left anterior descending artery was performed in two sessions. There was a new onset of typical atrial flutter and paroxysmal atrial fibrillation with haemodynamically relevant tachycardia. Before synchronized electrical cardioversion, we performed transoesophageal echocardiography. Left atrial thrombi were ruled out. Surprisingly, we found membranous ostial stenosis of the LAA, resulting in a bidirectional flow pattern. After 28 days of treatment in the intensive care unit the patient had full clinical recovery.DiscussionGiven the very rare cases of congenital LAA ostial stenosis, there is uncertainty about the thrombogenicity and the potential benefit of anticoagulation or even a percutaneous closure of the LAA. We discuss possible similarities regarding the thromboembolic risk of patients with an idiopathic narrowing of the LAA to patients with incomplete surgical ligation and patients with a device leak after percutaneous LAA closure. Congenital ostial LAA stenosis represents a clinically relevant condition and may be considered as a potential hazard for thromboembolism.
Project description:Background: Right ventricular (RV) function is a known predictor of adverse events in heart failure and following acute myocardial infarction (AMI). While right atrial (RA) involvement is well characterized in pulmonary arterial hypertension, its relative contributions to adverse events following AMI especially in patients with heart failure and congestion need further evaluation. Methods: In this cardiovascular magnetic resonance (CMR)-substudy of AIDA STEMI and TATORT NSTEMI, 1235 AMI patients underwent CMR after primary percutaneous coronary intervention (PCI) in 15 centers across Germany (n = 795 with ST-elevation myocardial infarction and 440 with non-ST-elevation MI). Right atrial (RA) performance was evaluated using CMR myocardial feature tracking (CMR-FT) for the assessment of RA reservoir (total strain εs), conduit (passive strain εe), booster pump function (active strain εa), and associated strain rates (SR) in a blinded core-laboratory. The primary endpoint was the occurrence of major adverse cardiac events (MACE) 12 months post AMI. Results: RA reservoir (εsp = 0.061, SRs p = 0.049) and conduit functions (εep = 0.006, SRe p = 0.030) were impaired in patients with MACE as opposed to RA booster pump (εap = 0.579, SRa p = 0.118) and RA volume index (p = 0.866). RA conduit function was associated with the clinical onset of heart failure and MACE independently of RV systolic function and atrial fibrillation (AF) (multivariable analysis hazard ratio 0.95, 95% confidence interval 0.92 to 0.99, p = 0.009), while RV systolic function and AF were not independent prognosticators. Furthermore, RA conduit strain identified low- and high-risk groups within patients with reduced RV systolic function (p = 0.019 on log rank testing). Conclusions: RA impairment is a distinct feature and independent risk factor in patients following AMI and can be easily assessed using CMR-FT-derived quantification of RA strain.
Project description:A 67-year-old man underwent left atrial appendage (LAA) exclusion concomitant with mitral valve surgery and radiofrequency ablation maze procedure. On transoesophageal echocardiography anticipating ablation for left atrial tachycardia, an echodense thrombus was visualised in the LAA location with apparent intracavitary extension into the left atrium. Based on CT imaging findings, the echo represented thrombosis of a large left atrial appendage with probable extension into the left atrium.
Project description:Background: Although many pathological changes have been associated with ischemic heart disease (IHD), molecular-level alterations specific to the ischemic myocardium and their potential to reflect disease severity or therapeutic outcome remain unclear. Currently, diagnosis occurs relatively late and evaluating disease severity is largely based on clinical symptoms, various imaging modalities, or the determination of risk factors. This study aims to identify IHD-associated signature RNAs from the atrial myocardium and evaluate their ability to reflect disease severity or cardiac surgery outcomes. Methods and Results: We collected right atrial appendage (RAA) biopsies from 40 patients with invasive coronary angiography (ICA)-positive IHD undergoing coronary artery bypass surgery and from 8 patients ICA-negative for IHD (non-IHD) undergoing valvular surgery. Following RNA sequencing, RAA transcriptomes were analyzed against 429 donors from the GTEx project without cardiac disease. The IHD transcriptome was characterized by repressed RNA expression in pathways for cell-cell contacts and mitochondrial dysfunction. Increased expressions of the CSRNP3, FUT10, SHD, NAV2-AS4, and hsa-mir-181 genes resulted in significance with the complexity of coronary artery obstructions or correlated with a functional cardiac benefit from bypass surgery. Conclusions: Our results provide an atrial myocardium-focused insight into IHD signature RNAs. The specific gene expression changes characterized here, pave the way for future disease mechanism-based identification of biomarkers for early detection and treatment of IHD.
Project description:BackgroundGuidelines suggest statin use after acute myocardial infarction (AMI) should be close to universal in patients without safety concerns yet rates are much lower than recommended, decline with patient complexity, and display substantial geographic variation. Trial exclusions have resulted in little evidence to guide statin prescribing for complex patients.ObjectiveTo assess the benefits and risks associated with higher rates of statin use after AMI by baseline patient complexity.Research designSample includes Medicare fee-for-service patients with AMIs in 2008-2009. Instrumental variable estimators using variation in local area prescribing patterns by statin intensity as instruments were used to assess the association of higher statin prescribing rates by statin intensity on 1-year survival, adverse events, and cost by patient complexity.ResultsProviders seem to have individualized statin use across patients based on potential risks. Higher statin rates for noncomplex AMI patients were associated with increased survival rates with little added adverse event risk. Higher statin rates for complex AMI patients were associated with tradeoffs between higher survival rates and higher rates of adverse events.ConclusionsHigher rates of statin use for noncomplex AMI patients are associated with outcome rate changes similar to existing evidence. For the complex patients in our study, who were least represented in existing trials, higher statin-use rates were associated with survival gains and higher adverse event risks not previously documented. Policy interventions promoting higher statin-use rates for complex patients may need to be reevaluated taking careful consideration of these tradeoffs.