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AIMS: We aim to assess the risk of thrombus-associated events (TAE) in patients with heart failure (HF) without atrial fibrillation (AF) and develop an effective scoring system for a risk stratification model. METHODS AND RESULTS: This retrospective study included 450 patients (median age 64.0 years, interquartile range [55.0, 75.0]; 31.6% women) hospitalized for HF without AF and atrial flutter, but with a left ventricular ejection fraction (LVEF) ≤ 55% and New York Heart Association (NYHA) functional class of III-IV. A median follow-up of 47 months was conducted. In the present study, TAE during follow-up was independently associated with both all-cause death [hazard ratio (HR) 1.756, 95% confidence interval (CI) 1.324-2.328, P < 0.001] and readmission for HF (HR 1.574, 95% CI 1.122-2.208, P = 0.009) after adjustment for covariates. Hypertension (HR 1.573, 95% CI 1.018-2.429, P = 0.041), atrial arrhythmia excluding AF (AAexAF) (HR 2.041, 95% CI 1.066-3.908, P = 0.031), previous ischaemic stroke (HR 2.469, 95% CI 1.576-3.869, P < 0.001), and vascular disease (HR 1.658, 95% CI 1.074-2.562, P = 0.023) were independently associated with TAE. Age (HR 1.021, 95% CI 1.008-1.033, P = 0.001), previous ischaemic stroke (HR 1.685, 95% CI 1.248-2.274, P = 0.001), LVEF ([10, 25] vs. [40, 55]) HR 1.925, 95% CI 1.311-2.826, P = 0.001; (25, 40] vs. (40, 55] HR 1.084, 95% CI 0.825-1.424, P = 0.563), and creatinine clearance rate (Ccr) (HR 0.991, 95% CI 0.986-0.996, P = 0.001) were independently associated with composite events of TAE and death (TAE-D). CHA2DS2VASc modestly predicted 5-year TAE [area under the receiver operating characteristic curves (AUC) 0.660, P < 0.001 compared with 0.5] and TAE-D (AUC 0.639, P < 0.001 compared with 0.5). (C)ACE, formed by incorporating AAexAF, LVEF, and Ccr into CHA2DS2VASc, had higher AUC for predicting 5-year TAE (0.694 vs. 0.660, P = 0.018) and TAE-D (0.708 vs. 0.639, P < 0.001) compared with CHA2DS2VASc. In patients with HF with reduced ejection fraction (HFrEF), (C)ACE and (C)ACEN [formed by incorporating NYHA into (C)ACE] had higher AUC compared with CHA2DS2VASc in predicting 5-year TAE (0.700 and 0.707 vs. 0.649, P = 0.013 and 0.030, respectively) and TAE-D (0.712 and 0.713 vs. 0.622, P < 0.001 and <0.001, respectively). The AUC did not improve statistically from (C)ACE to (C)ACEN (0.700 vs. 0.707, P = 0.600 for TAE; 0.712 vs. 0.713, P = 0.917 for TAE-D). CONCLUSIONS: In HF without AF, TAE during follow-up was associated with adverse prognoses. The independent risk factors of TAE or TAE-D improved CHA2DS2-VASc predictive ability, especially in patients with HFrEF. Our findings provide new evidence for TAE risk stratification in HF without AF, potentially guiding prophylactic anticoagulation.
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The high thrombus burden of the infarct-related artery (IRA) is associated with the adverse prognosis in ST-segment elevation myocardial infarction (STEMI) patients. Our objectives were to investigate the predictors and evaluate the prognosis of refractory thrombus in STEMI patients. A total of 1305 consecutive patients with STEMI who underwent primary percutaneous coronary intervention (pPCI) were screened. The refractory thrombus group (nâ =â 15) was defined as IRA thrombolysis in myocardial infarction flowâ <â grade 2 after multiple thrombus aspiration (TA). The control group (nâ =â 45) was age- and sex-matched and was selected from the same batch of patients. Baseline hematologic indices were measured before the pPCI. The major adverse cardiovascular events (MACE) were recorded during follow-up. The refractory thrombus group had significantly higher red cell distribution width (RDW) at baseline compared with the control group (13.1 [12.4-13.7] vs 12.6 [12.3-12.8], Pâ =â .008). In multivariate logistic regression analysis, RDW was an independent predictor of refractory thrombus (odds ratio: 8.799, 95% CI: 1.240-62.454, Pâ =â .030). The area under the receiver-operating characteristic curve of the RDW was 0.730 (95%CI: 0.548-0.912, Pâ =â .008). During a mean period of 26 months follow-up, patients in the refractory thrombus group tended to have higher percent MACEs compared with patients in the control group (53.3% vs 6.7%, Pâ <â .001). In the present study, we found that the refractory thrombus in STEMI patients was associated with the worse prognosis and the increased RDW might be a potential independent predictor.
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Índices de Eritrocitos , Intervención Coronaria Percutánea , Infarto del Miocardio con Elevación del ST , Humanos , Femenino , Infarto del Miocardio con Elevación del ST/sangre , Infarto del Miocardio con Elevación del ST/cirugía , Masculino , Persona de Mediana Edad , Pronóstico , Estudios de Casos y Controles , Intervención Coronaria Percutánea/métodos , Anciano , Trombosis/etiología , Trombosis/sangre , Curva ROC , Trombosis Coronaria/sangre , Trombectomía/métodosRESUMEN
The effect of Ryanodine receptor2 (RyR2) and its stabilizer on cardiac hypertrophy is not well known. C57/BL6 mice underwent transverse aortic contraction (TAC) or sham surgery were administered dantrolene, the RyR2 stabilizer, or control drug. Dantrolene significantly alleviated TAC-induced cardiac hypertrophy in mice, and RNA sequencing was performed implying calcineurin/NFAT3 and TNF-α/NF-κB/NLRP3 as critical signaling pathways. Further expression analysis and Western blot with heart tissue as well as neonatal rat cardiomyocyte (NRCM) model confirmed dantrolene decreases the activation of calcineurin/NFAT3 signaling pathway and TNF-α/NF-κB/NLRP3 signaling pathway, which was similar to FK506 and might be attenuated by calcineurin overexpression. The present study shows for the first time that RyR2 stabilizer dantrolene attenuates cardiac hypertrophy by inhibiting the calcineurin, therefore downregulating the TNF-α/NF-κB/NLRP3 pathway.
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Calcineurina , Dantroleno , Modelos Animales de Enfermedad , Regulación hacia Abajo , Ratones Endogámicos C57BL , Miocitos Cardíacos , FN-kappa B , Proteína con Dominio Pirina 3 de la Familia NLR , Canal Liberador de Calcio Receptor de Rianodina , Transducción de Señal , Factor de Necrosis Tumoral alfa , Animales , Transducción de Señal/efectos de los fármacos , Factor de Necrosis Tumoral alfa/metabolismo , Canal Liberador de Calcio Receptor de Rianodina/metabolismo , Canal Liberador de Calcio Receptor de Rianodina/genética , Canal Liberador de Calcio Receptor de Rianodina/efectos de los fármacos , Calcineurina/metabolismo , Proteína con Dominio Pirina 3 de la Familia NLR/metabolismo , Miocitos Cardíacos/efectos de los fármacos , Miocitos Cardíacos/metabolismo , Miocitos Cardíacos/patología , FN-kappa B/metabolismo , Dantroleno/farmacología , Masculino , Inhibidores de la Calcineurina/farmacología , Factores de Transcripción NFATC/metabolismo , Células Cultivadas , Cardiomegalia/metabolismo , Cardiomegalia/prevención & control , Cardiomegalia/patología , Cardiomegalia/tratamiento farmacológico , Ratas Sprague-Dawley , Ratas , Hipertrofia Ventricular Izquierda/prevención & control , Hipertrofia Ventricular Izquierda/metabolismo , Hipertrofia Ventricular Izquierda/patología , Hipertrofia Ventricular Izquierda/fisiopatologíaRESUMEN
Background: Factor Xa (FXa) not only plays an active role in the coagulation cascade but also exerts non-hemostatic signaling through the protease-activated receptors (PARs). This study aimed to investigate whether the FXa inhibitor, Rivaroxaban (RIV), attenuates adverse cardiac remodeling in rats with myocardial infarction (MI) and to identify the underlying molecular mechanisms it uses. Methods: An MI model was induced in eight-week-old, male Wistar rats, by permanent ligation of the left anterior descending coronary artery. MI rats were randomly assigned to receive RIV or protease-activated receptors 2-antagonist (PAR-2 antagonist, FSLLRY) treatment for four weeks. Histological staining, echocardiography and hemodynamics were used to assess the cardioprotective effects of RIV. Meanwhile, pharmacological approaches of agonist and inhibitor were used to observe the potential pathways in which RIV exerts antifibrotic effects in neonatal rat cardiac fibroblasts (CFs). In addition, real-time PCR and western blot analysis were performed to examine the associated signaling pathways. Results: RIV presented favorable protection of left ventricular (LV) cardiac function in MI rats by significantly reducing myocardial infarct size, ameliorating myocardial pathological damage and improving left ventricular (LV) remodeling. Similar improvements in the PAR-2 antagonist FSLLRY and RIV groups suggested that RIV protects against cardiac dysfunction in MI rats by ameliorating PAR-2 activation. Furthermore, an in vitro model of fibrosis was then generated by applying angiotensin II (Ang II) to neonatal rat cardiac fibroblasts (CFs). Consistent with the findings of the animal experiments, RIV and FSLLRY inhibited the expression of fibrosis markers and suppressed the intracellular upregulation of transforming growth factor ß1 (TGFß1), as well as its downstream Smad2/3 phosphorylation effectors in Ang II-induced fibrosis, and PAR-2 agonist peptide (PAR-2 AP) reversed the inhibition effect of RIV. Conclusions: Our findings demonstrate that RIV attenuates MI-induced cardiac remodeling and improves heart function, partly by inhibiting the activation of the PAR-2 and TGF-ß1 signaling pathways.
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Infarto del Miocardio , Rivaroxabán , Ratas , Animales , Masculino , Rivaroxabán/farmacología , Factor de Crecimiento Transformador beta1/metabolismo , Factor Xa/metabolismo , Remodelación Ventricular , Ratas Wistar , Transducción de Señal , Infarto del Miocardio/tratamiento farmacológico , Fibrosis , Receptores Proteinasa-ActivadosRESUMEN
BACKGROUND: The deterioration of thyroid health is involved in the progression of heart failure (HF). This is usually a lengthy process, so there are almost no reports on its rapid development. Here we report a case of a young male who rapidly developed hypothyroid cardiomyopathy secondary to radioactive iodine treatment, suggesting that severe HF might occur even after a short period of hypothyroidism. CASE SUMMARY: A 26-year-old man was referred to our hospital for HF presenting with dyspnea on exertion and chest discomfort lasting for 1 mo. He received radioactive iodine treatment for hyperthyroidism 1 year ago and had an almost normal echocardiogram 6 mo ago. Admission echocardiogram and cardiac magnetic resonance (CMR) revealed left ventricle (LV) global hypokinesia and severely depressed systolic function. In addition, late gadolinium enhancement indicated no obvious changes in the myocardium. Thyroid function tests showed decreased serum levels of thyroid hormone (TH) and elevated thyroid-stimulating hormone. Based on an exclusionary examination, the patient was diagnosed with hypothyroid cardiomyopathy and was started on replacement therapy. His HF symptoms were completely relieved during the six-month follow-up, and echocardiogram and CMR revealed recovered LV size and ejection fraction. CONCLUSION: This report demonstrates that severe fluctuations in TH levels may lead to acute HF, which can completely recover with timely thyroid hormone replacement. In addition, our findings highlight the importance of routinely detecting cardiac function in patients treated with radioactive iodine.
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BACKGROUND: Contemporary data regarding the clinical characteristics and prognosis of left ventricular thrombus (LVT) in older adults (aged ≥ 65 years old) are lacking. In this study, we characterized elderly patients with LVT (aged ≥ 65 years old) and investigated the long-term prognosis in this highly vulnerable patient population. METHODS: This single-center, retrospective study was conducted from January 2017 to December 2022. Patients with a reported LVT were assessed primarily by transthoracic echocardiography (TEE) and classified into two groups: elderly LVT groups and younger LVT groups. All patients were treated with anticoagulant treatment. Major adverse cardiovascular event (MACE) was defined as the composite of all-cause mortality, systemic embolism, and rehospitalization for cardiovascular events. Survival analyses were performed with the Kaplan-Meier method and Cox proportional-hazard model. RESULTS: A total of 315 eligible patients were included. Compared to the younger LVT group (n = 171), the elderly LVT group (n = 144) had a lower proportion of males and lower serum creatinine clearance, as well as a higher level of NT-proBNP, and a higher rate of history of systemic embolism. LVT resolution occurred in 59.7% and 69.0% of patients in the elderly LVT group and younger LVT group, respectively, with no significant difference (adjusted HR, 0.97; 95% CI, 0.74-1.28; P = 0.836). Yet, elderly patients with LVT, had higher prevalence rates of MACE (adjusted HR, 1.52; 95% CI, 1.10-2.11; P = 0.012), systemic embolism (adjusted HR, 2.81; 95% CI, 1.20-6.59; P = 0.017) and all-cause mortality (adjusted HR, 2.20; 95% CI, 1.29-3.74; P = 0.004) compared with younger patients with LVT. After adjusting for mortality in the Fine-Gray model, similar results were observed. Additionally, patients treated with different anticoagulation therapies (DOACs vs. warfarin) achieved a similar improvement in prognosis (P > 0.05) or LVT resolution (P > 0.05) in elderly patients with LVT. CONCLUSIONS: Our results found that elderly patients experiencing LVT have a poor prognosis compared with the younger ones. Clinical prognosis in elderly patients did not significantly differ with the type of anticoagulant used. With aging societies worldwide, further evidence of antithrombotic therapy in elderly individuals with LVT is necessary.
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Intracardiac echocardiography (ICE) is a novel tool for estimating cardiac anatomy during pulmonary vein isolation procedures, particularly the left atrium (LA) anatomy and pulmonary vein structures. ICE is widely used to establish a three-dimensional (3D) left atrial structural model during ablation procedures. However, it is unclear whether using ICE in a precise 3D modeling method can provide a more accurate left atrial 3D model and the transseptal approach. This study proposes a protocol to model the left atrium and pulmonary veins with ICE and fast anatomical mapping (FAM) catheter remodeling. It evaluates the accuracy of the models produced using the two methods through observer scoring. We included 50 patients who underwent ICE-based 3D remodeling and 45 who underwent FAM 3D remodeling based on pulmonary vein isolation procedures. The pulmonary vein antrum remodeling is estimated by comparing the antrum area acquired by remodeling and left atrial computed tomography angiography (CTA). The observer scores for the modeling in the ICE and FAM groups were 3.40 ± 0.81 and 3.02 ± 0.72 (P < 0.05), respectively. The pulmonary vein antrum area obtained using the ICE- and FAM-based methods showed a correlation with the area acquired by left atrium CT. However, the 95% confidence interval bias was narrower in ICE-acquired models than in FAM-acquired models (-238 cm2 to 323 cm2 Vs. -363 cm2 to 386 cm2, respectively) using Bland-Altman analysis. Therefore, precise ICE possesses high accuracy in estimating the left atrial structure, becoming a promising approach for future cardiac structure estimation.
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Fibrilación Atrial , Ablación por Catéter , Venas Pulmonares , Humanos , Fibrilación Atrial/cirugía , Venas Pulmonares/diagnóstico por imagen , Venas Pulmonares/cirugía , Atrios Cardíacos/diagnóstico por imagen , Atrios Cardíacos/cirugía , Angiografía , Ecocardiografía/métodosRESUMEN
Background: Severe coronary artery calcification increases the difficulty of percutaneous coronary intervention procedures and impairs stent expansion. Herein, we report a case of a patient who was successfully treated with rotational atherectomy using a stepped burr strategy combined with intravascular lithotripsy for plaque modification under intracoronary imaging. Case summary: A 65â year-old woman presented to our hospital with recurrent chest pain evolving for 1â year. Coronary angiography showed approximately 80% stenosis of the proximal mid-left anterior descending artery. Intravascular ultrasound (IVUS) and optical coherence tomography (OCT) revealed a 360° annular calcification. The calcification was rotablated with 1.5 and 1.75â burrs, and the lesion was undilatable with a 3.0â mm non-compliant balloon at 14â atm. Subsequently, the intravascular lithotripsy was reset for the modification of the calcified lesion. A shockwave balloon measuring 3.0â mm × 12â mm was delivered, and 40â pulses were performed at 6â atm. Intravascular imaging modalities (IVUS and OCT) revealed a circumferential calcified plaque with deep fractures. After post-balloon expansion followed by drug-eluting stent placement with a final stent expansion of 84%, there were no intraoperative complications and no major adverse cardiovascular events within 90â days postoperatively. Conclusion: A combination of rotational atherectomy and intravascular lithotripsy may be an effective and complementary strategy for the treatment of severely calcified lesions that cannot be resolved using a single procedure. However, more clinical studies are required to clarify this finding.
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BACKGROUND: Cardiac fibrosis increases with age. Fibroblast activation plays an essential role in cardiac fibrosis. Histone modifications are involved in various chromatin-dependent processes. Attenuation of the histone H3 trimethylation on lysine 27 demethylase UTX by RNA interference or heterozygous mutation extends lifespan in worm. The objective of this study was to explore whether epigenetic silencing of UTX mitigates aging-associated cardiac fibrosis. METHODS: Middle-aged mice (15 months old) were used and started to receive adeno-associated virus-scrambled-small hairpin RNA and adeno-associated virus-UTX-small hairpin RNA every 3 months from 15 months to 21 months, respectively. The mice were euthanized at 24 months of age (length of the study). RESULTS: Adeno-associated virus-UTX-small hairpin RNA delivery significantly attenu-ated aging-associated increase in blood pressure, especially in diastolic blood pressure, indicating silencing of UTX rescued aging-associated cardiac dysfunction. Aging-associated cardiac fibrosis is characterized by fibroblast activation and abundant extracellular matrix deposition, including collagen deposition and alpha smooth muscle actin activation. Silencing of UTX abolished collagen deposition and alpha smooth muscle actin activation, decreased serum transforming growth factor ß, blocked cardiac fibro blast s-to- myofi brobl asts trans-differentiation by elevation of cardiac resident mature fibroblast markers, TCF21, and platelet-derived growth factor receptor alpha, which are important proteins for maintaining cardiac fibroblast physiological function. In the mechanistic study, adeno-associated virus-UTX-small hairpin RNA blocked transforming growth factor ß-induced cardiac fibro blast s-to- myofi brobl asts trans-differentiation in isolated fibroblasts from 24-month-old mouse heart. The same results demonstrated as the in vivo study. CONCLUSIONS: Silencing of UTX attenuates aging-associated cardiac fibrosis via blocking cardiac fibroblasts-to-myofibroblasts transdifferentiation and consequently attenuates aging-associated cardiac dysfunction and cardiac fibrosis.
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Cardiomiopatías , Cardiopatías , Ratones , Animales , Miofibroblastos/metabolismo , Miofibroblastos/patología , Miocardio/patología , Actinas/metabolismo , Transducción de Señal , Cardiomiopatías/genética , Cardiomiopatías/patología , Fibroblastos/metabolismo , Fibroblastos/patología , Colágeno/metabolismo , Envejecimiento , Cardiopatías/metabolismo , Factor de Crecimiento Transformador beta/metabolismo , Fibrosis , ARN Interferente Pequeño , Transdiferenciación Celular , Factor de Crecimiento Transformador beta1 , Células CultivadasRESUMEN
Background: Doxorubicin-induced cardiomyopathy (DICM) is one of the complications that can limit treatment for a significant number of cancer patients. In animal models, the administration of statins can prevent the development of DICM. Therefore, the use of statins with anthracyclines potentially could enable cancer patients to complete their chemotherapy without added cardiotoxicity. The precise mechanism mediating the cardioprotection is not well understood. The purpose of this study is to determine the molecular mechanism by which rosuvastatin confers cardioprotection in a mouse model of DICM. Methods: Rosuvastatin was intraperitoneally administered into adult male mice at 100 µg/kg daily for 7 days, followed by a single intraperitoneal doxorubicin injection at 10 mg/kg. Animals continued to receive rosuvastatin daily for an additional 14 days. Cardiac function was assessed by echocardiography. Optical calcium mapping was performed on retrograde Langendorff perfused isolated hearts. Ventricular tissue samples were analyzed by immunofluorescence microscopy, Western blotting, and quantitative polymerase chain reaction. Results: Exposure to doxorubicin resulted in significantly reduced fractional shortening (27.4% ± 1.11% vs 40% ± 5.8% in controls; P < 0.001) and re-expression of the fetal gene program. However, we found no evidence of maladaptive cardiac hypertrophy or adverse ventricular remodeling in mice exposed to this dose of doxorubicin. In contrast, rosuvastatin-doxorubicin-treated mice maintained their cardiac function (39% ± 1.26%; P < 0.001). Mechanistically, the effect of rosuvastatin was associated with activation of Akt and phosphorylation of phospholamban with preserved sarcoplasmic/endoplasmic reticulum Ca2+ transporting 2 (SERCA2)-mediated Ca2+ reuptake. These effects occurred independently of perturbations in ryanodine receptor 2 function. Conclusions: Rosuvastatin counteracts the cardiotoxic effects of doxorubicin by directly targeting sarcoplasmic calcium cycling.
Contexte: La cardiomyopathie induite par la doxorubicine (CMID) est l'une des complications pouvant limiter le traitement d'un nombre considérable de patients atteints de cancer. Dans des modèles animaux, l'administration de statines peut prévenir l'apparition d'une CMID. Ainsi, l'utilisation de statines avec les anthracyclines pourrait vraisemblablement permettre aux patients de compléter leur chimiothérapie en évitant une cardiotoxicité supplémentaire. Le mécanisme précis qui sous-tend cet effet cardioprotecteur n'est pas entièrement élucidé. Cette étude a pour objectif de déterminer dans un modèle murin de CMID le mécanisme moléculaire par lequel la rosuvastatine confère une cardioprotection. Méthodologie: La rosuvastatine a été administrée par voie intrapéritonéale à des souris adultes mâles à une dose de 100 µg/kg par jour pendant sept jours, suivie d'une dose unique de doxorubicine de 10 mg/kg administrée par injection intrapéritonéale. Les animaux poursuivaient ensuite le traitement par la rosuvastatine une fois par jour pendant 14 jours supplémentaires. La fonction cardiaque a été mesurée par échocardiographie. Une cartographie optique du calcium a été réalisée sur des cÅurs isolés soumis à une perfusion rétrograde selon la méthode de Langendorff. Des échantillons de tissu ventriculaire ont été analysés par microscopie en immunofluorescence, par buvardage de western et par mesure quantitative de l'amplification en chaîne par polymérase. Résultats: L'exposition à la doxorubicine a entraîné une diminution significative de la fraction de raccourcissement (27,4 % ± 1,11 % vs 40 % ± 5,8 % dans le groupe témoin; p < 0,001) et la réexpression du programme génique fÅtal. Toutefois, aucune hypertrophie cardiaque inadaptée ni aucun remodelage ventriculaire indésirable n'ont été observés chez les souris ayant été exposées à la dose de doxorubicine étudiée. En revanche, la fonction cardiaque a été préservée chez les souris traitées par l'association rosuvastatine-doxorubicine (39 % ± 1,26 %; p < 0,001). Sur le plan du mode d'action, l'effet de la rosuvastatine a été associé à une activation de l'Akt et à une phosphorylation du phospholambane, avec préservation du recaptage de Ca2+ médié par la pompe SERCA2 (sarcoplasmic/endoplasmic reticulum Ca 2+ transporting 2). Ces effets sont survenus indépendamment des perturbations de la fonction du récepteur RyR2 (ryanodine receptor 2). Conclusions: La rosuvastatine neutralise les effets cardiotoxiques de la doxorubicine en ciblant directement la circulation sarcoplasmique du calcium.
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Background: Post-defibrillation myocardial contractile dysfunction adversely affects the survival of patients after cardiac arrest. Attenuation of diastolic calcium (Ca2+) overload by stabilization of the cardiac ryanodine receptor (RyR2) is found to reduce refibrillation after long-duration ventricular fibrillation (LDVF). Objective: In the present study, we explored the effects of RyR2 stabilization by azumolene on systolic Ca2+ release synchrony and myocardial contractility. Methods: After completion of baseline optical mapping, Langendorff-perfused rabbit hearts were subjected to global ischemia followed by reperfusion with azumolene or deionized distilled water (vehicle). Following reperfusion, LDVF was induced with burst pacing. In the first series of experiments (n = 16), epicardial Ca2+ transient was analyzed for Ca2+ transient amplitude alternans and dispersion of Ca2+ transient amplitude alternans index (CAAI). In the second series of experiments following the same protocol (n = 12), ventricular contractility was assessed by measuring the left ventricular pressure. Results: Ischemic LDVF led to greater CAAI (0.06 ± 0.02 at baseline vs 0.12 ± 0.02 post-LDVF, P < .01) and magnitude of dispersion of CAAI (0.04 ± 0.01 vs 0.09 ± 0.01, P < .01) in control hearts. In azumolene-treated hearts, no significant changes in CAAI (0.05 ± 0.01 vs 0.05 ± 0.01, P = .84) and dispersion of CAAI (0.04 ± 0.01 vs 0.04 ± 0.01, P = .99) were noted following ischemic LDVF. Ischemic LDVF was associated with reduction in left ventricular developed pressure (100% vs 36.8% ± 6.1%, P = .002) and dP/dtmax (100% vs 45.3% ± 6.5%, P = .003) in control hearts, but these reductions were mitigated (left ventricular developed pressure: 100% vs 74.0% ± 8.1%, P = .052, dP/dtmax: 100% vs 80.8% ± 7.9%, P = .09) in azumolene-treated hearts. Conclusion: Treatment with azumolene is associated with improvement of systolic Ca2+ release synchrony and myocardial contractility following ischemic LDVF.
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Background: The role of rivaroxaban in patients with heart failure (HF) combined with left ventricular (LV) thrombus remains unknown in current guideline-directed anticoagulant therapy. The aim of this study was to investigate the impact on clinical outcomes of rivaroxaban compared to vitamin K antagonists (VKAs) in patients with HF combined with LV thrombus. Methods: We retrospectively extracted clinical, echocardiographic and follow-up data of HF patients (all classifications) admitted at China-Japan Union Hospital of Jilin University from January 2017 to June 2021. A total of 198 patients with HF were identified with LV thrombus by echocardiography, 78 of them were managed with VKAs, 109 with rivaroxaban. Results: The median follow-up was 17.0 months (interquartile range: 6.0-24.0 months). High rates of major cardiovascular adverse events (MACEs) were observed in both the rivaroxaban and VKAs groups (49.5% vs. 57.7%). However, rivaroxaban versus VKAs observed a decrease in MACEs (adjusted HR:0.636; 95%CI:0.418-0.970; p = 0.035) and systemic embolism (4.6% vs. 12.8%; adjusted HR:0.318; 95%CI:0.108-0.933; p = 0.037; Gray's test p = 0.041) but was not found to have a benefit with regard to LV thrombus resolution (59.6% vs. 70.6%; adjusted HR: 1.303; 95% CI:0.898-1.890; p = 0.163; Gray's test p = 0.073). Additionally, there was no significant between-group difference in the rate of International Society on Thrombosis and Hemostasis (ISTH) bleeding events. Conclusion: Our data found that in populations with HF combined with LV thrombus, the overall prognosis in both the rivaroxaban and VKAs groups was catastrophic. Although rivaroxaban improved the prognosis to some extent, a considerable need remains for new treatments to improve their clinical course.
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INTRODUCTION: Left-sided accessory pathway (AP) with atrial insertion away from the annulus is an atypical variation. Conventional mapping and ablation performed along mitral annulus (MA) is usually ineffective. METHODS: A 14-year-old girl without structural heart disease presented with recurrent episodes of sudden onset palpitations and electrocardiogram (ECG) showed a narrow QRS complex tachycardia. RESULTS: Electrophysiology study (EPS) was done and anterograde atrioventricular reentrant tachycardia (AVRT) with AP was diagnosed. Conventional mapping and ablation performed along TA and MA was failed. 3D-activation mapping found the retrograde atrial insertion site of AP on the left atrium fossa ovalis (FO), and AP was successfully abolished by radiofrequency ablation at that site. CONCLUSION: As reported, this patient is the first report of ablating a left-sided AP with retrograde atrial insertion on the left atrium FO.
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Fascículo Atrioventricular Accesorio , Ablación por Catéter , Taquicardia por Reentrada en el Nodo Atrioventricular , Fascículo Atrioventricular Accesorio/cirugía , Adolescente , Electrocardiografía , Femenino , Atrios Cardíacos/diagnóstico por imagen , Atrios Cardíacos/cirugía , Humanos , Taquicardia/cirugía , Taquicardia por Reentrada en el Nodo Atrioventricular/diagnóstico , Taquicardia por Reentrada en el Nodo Atrioventricular/cirugíaAsunto(s)
Cardiopatías Congénitas , Cardiopatías , Trombosis , Cardiopatías/diagnóstico por imagen , Cardiopatías/etiología , Cardiopatías/prevención & control , Ventrículos Cardíacos/diagnóstico por imagen , Humanos , Trombosis/diagnóstico por imagen , Trombosis/etiología , Trombosis/prevención & control , Resultado del TratamientoRESUMEN
OBJECTIVES: The aim of this study was to investigate the effects of rivaroxaban on left ventricle thromboprophylaxis in patients with anterior ST-segment elevation myocardial infarction (STEMI). BACKGROUND: Anterior STEMI is associated with an increased risk of left ventricular thrombus (LVT) formation. The contemporary role of prophylactic rivaroxaban therapy remains unclear. METHODS: We randomly assigned 279 patients with anterior STEMI who had undergone primary percutaneous coronary intervention to receive, in a 1:1 ratio, low-dose rivaroxaban (2.5 mg twice daily for 30 days) and dual antiplatelet therapy (DAPT) or only DAPT. The primary efficacy outcome was the LVT formation within 30 days. Net clinical adverse events were assessed at 30 days and 180 days, including all-cause mortality, LVT, systemic embolism, rehospitalization for cardiovascular events, and bleeding. RESULTS: The addition of low-dose rivaroxaban to DAPT reduced LVT formation within 30 days compared with only DAPT (0.7% vs 8.6%; HR: 0.08; 95% CI: 0.01-0.62; P = 0.015; P < 0.001 for superiority). Net clinical adverse events were lower within 30 days in the rivaroxaban group versus those in the only DAPT group and remained relatively low throughout the follow-up period. There were no significant differences in bleeding events between the 2 groups in 30 days and 180 days. However, 1 case of intracranial hemorrhage (major bleeding) occurred in the rivaroxaban group within 30 days. CONCLUSIONS: Our results supported that the short-duration addition of low-dose rivaroxaban to DAPT could prevent LVT formation in patients with anterior STEMI following primary percutaneous coronary intervention. A larger multiple-institution study is necessary to determine the generalizability.
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Rivaroxabán , Infarto del Miocardio con Elevación del ST , Trombosis , Terapia Antiplaquetaria Doble/efectos adversos , Hemorragia/inducido químicamente , Humanos , Intervención Coronaria Percutánea , Inhibidores de Agregación Plaquetaria/efectos adversos , Rivaroxabán/efectos adversos , Infarto del Miocardio con Elevación del ST/complicaciones , Infarto del Miocardio con Elevación del ST/tratamiento farmacológico , Trombosis/epidemiología , Trombosis/prevención & control , Resultado del TratamientoRESUMEN
BACKGROUND: Left ventricular thrombus (LVT) can complicate ST-Elevation myocardial infarction (STEMI) and is associated with poor outcomes. Conventional triple anticoagulation [Vitamin K Antagonists (VKA) plus dual-antiplatelet therapy (DAPT)] is the first-line therapy for LVT after STEMI. In patients with LVT following STEMI, contemporary data of triple therapy with rivaroxaban are lacking. METHODS: We conducted a retrospective cohort study involving 1335 STEMI patients who underwent primary percutaneous coronary intervention (PCI). Among patients who developed LVT after STEMI, we observed differences in efficacy between rivaroxaban plus DAPT therapy and VKA plus DAPT. The time of LVT resolution was also evaluated, as well as net clinical adverse events, and rates of bleeding events. RESULTS: In 1335 patients with STEMI, a total of 77 (5.7%) developed LVT over the follow-up period (median 25.0 months). Of the patients diagnosed with LVT, 31 patients were started on triple therapy with VKA, 33 patients on triple therapy with rivaroxaban. There was a consistent similarity in LVT resolution with rivaroxaban application compared to VKA application during the follow-up period [HR (log-rank test) 1.57(95% CI 0.89-2.77), p = 0.096; Adjusted HR 1.70(95% CI 0.90-3.22), p = 0.104]. Triple therapy with rivaroxaban showed quicker resolution than with VKA (6 months: p = 0.049; 12 months: p = 0.044; 18 months: p = 0.045). Similar risks of ISTH bleeding were not significantly different between the 2 groups [VKA 9.7% vs Rivaroxaban 6.1%, Adjusted HR 0.48 (95% CI 0.73-3.20); p = 0.444)]. Fewer net adverse clinical events (NACE) were observed in the rivaroxaban group [VKA 58.1% vs Rivaroxaban 24.2%; HR (log-rank test) 0.31(95% CI 0.14-0.68), p = 0.003; Adjusted HR 0.23(95% CI 0.09-0.57), p = 0.001]. CONCLUSION: In the observational study, triple therapy with rivaroxaban has similar and quicker LVT resolution in patients with LVT after STEMI, compared with triple therapy with VKA, and perhaps was associated with a better clinical benefit. Larger sample sizes and randomized controlled trials are needed to confirm this observation.
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Intervención Coronaria Percutánea , Infarto del Miocardio con Elevación del ST , Trombosis , Anticoagulantes/efectos adversos , Humanos , Intervención Coronaria Percutánea/efectos adversos , Estudios Retrospectivos , Rivaroxabán/efectos adversos , Infarto del Miocardio con Elevación del ST/complicaciones , Trombosis/diagnóstico , Trombosis/tratamiento farmacológico , Trombosis/etiología , Resultado del Tratamiento , Vitamina K/uso terapéutico , Warfarina/efectos adversosRESUMEN
OBJECTIVE: In the current era of primary percutaneous coronary intervention (PPCI), the prognosis of the left ventricular thrombus (LVT) is not well assessed. METHODS: We performed a retrospective, single-center study of 1305 consecutive ST-segment-elevation myocardial infarction (STEMI) patients treated with PPCI. During a mean period of 27 months of follow-up, the major adverse cardiovascular and cerebrovascular events (MACCE) were recorded. RESULTS: The incidence of LVT (n = 47) was 3.60%. The independent risk factors of LVT included anterior STEMI, left ventricular (LV) aneurysm, reduced LV ejection fraction (LVEF), dilated LV end-diastolic dimension (LVEDD), and delayed door-to-balloon time (DTBT). During follow-up, LVT was an independent risk factor for MACCE [hazard ratio (HR)=3.46; 95% confidence interval (CI) = 2.23-3.38; P < 0.01]. Patients with LVT were more likely to have the following complications: heart failure (P < 0.001), embolic events (P = 0.034), and all-cause mortality (P = 0.020). Notably, the regression of LVT was not independently associated with those three adverse events (P > 0.05). CONCLUSION: In the era of PPCI, the presence of early LVT following STEMI was associated with adverse events. Furthermore, the prognosis of patients with LVT did not improve even if the LVT regressed. LVT was likely a generalized indicator of impaired cardiac performance, rather than the cause. This indicated that prophylactic therapy and identifying individuals with a high risk of developing LVT were of substantial importance.
RESUMEN
BACKGROUND: Loeffler endocarditis is a relatively rare and potentially life-threatening heart disease. This study aimed to identify the characteristic features of Loeffler endocarditis with intracardiac thrombus on a background of hypereosinophilic syndrome (HES). CASE PRESENTATION: We described a 57-year-old woman with Loeffler endocarditis and intracardiac thrombus initially presenting with neurological symptoms, who had an embolic stroke in the setting of HES. After cardiac magnetic resonance (CMR), corticosteroids and warfarin were administered to control eosinophilia and thrombi, respectively. During a 10-month follow-up, the patient performed relatively well, with no adverse events. We also systematically searched PubMed and Embase for cases of Loeffler endocarditis with intracardiac thrombus published until July 2021. A total of 32 studies were eligible and included in our analysis. Further, 36.4% of recruited patients developed thromboembolic complications, and the mortality rate was relatively high (27.3%). CMR was a powerful noninvasive modality in providing diagnostic and follow-up information in these patients. Steroids were administered in 81.8% of patients, achieving a rapid decrease in the eosinophil count. Also, 69.7% of patients were treated with anticoagulant therapy, and the thrombus was completely resolved in 42.4% of patients. Heart failure and patients not treated with anticoagulation were associated with poor outcomes. CONCLUSIONS: Cardiac involvement in HES, especially Loeffler endocarditis with intracardiac thrombus, carries a pessimistic prognosis and significant mortality. Early steroids and anticoagulation therapy may be beneficial once a working diagnosis is established. Further studies are needed to provide evidence-based evidence for managing this uncommon manifestation of HES.
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Cardiopatías/etiología , Síndrome Hipereosinofílico/complicaciones , Trombosis/etiología , Adolescente , Corticoesteroides/uso terapéutico , Adulto , Anciano , Anticoagulantes/uso terapéutico , Niño , Preescolar , Accidente Cerebrovascular Embólico/etiología , Femenino , Cardiopatías/diagnóstico , Cardiopatías/tratamiento farmacológico , Humanos , Síndrome Hipereosinofílico/diagnóstico , Síndrome Hipereosinofílico/tratamiento farmacológico , Masculino , Persona de Mediana Edad , Trombosis/diagnóstico , Trombosis/tratamiento farmacológico , Resultado del Tratamiento , Warfarina/uso terapéutico , Adulto JovenRESUMEN
BACKGROUND Diabetes is one of the most commonly reported comorbidities among patients infected with SARS-CoV-2. This retrospective study of patients with SARS-CoV-2 infection was conducted to evaluate the association between blood glucose levels and the severity of COVID-19 pneumonia and patient mortality. MATERIAL AND METHODS A total of 268 patients with confirmed SARS-CoV-2 infection were included in this retrospective study. We obtained demographic characteristics, clinical symptoms, laboratory data, and survival information from patients' electronic medical records. Blood glucose was measured on admission to the hospital. Comorbidities, including hypertension, diabetes, chronic kidney disease, chronic liver disease, chronic obstructive pulmonary disease, and cardiovascular disease, were collected by self-reported medical history. RESULTS Significantly higher risks of severe COVID-19 were found in patients with blood glucose levels ranging from 5.53 to 7.27 mmol/L (odds ratio [OR], 3.98; 95% confidence interval [CI], 1.81-8.75) and in patients with blood glucose ≥7.27 mmol/L (OR, 12.10; 95% CI, 5.53-26.48) than in those with blood glucose <5.53 mmol/L. There was a trend toward better survival in patients with blood glucose <5.53 mmol/L than in patients with blood glucose from 5.53 to 7.27 mmol/L (hazard ratio [HR], 6.34; 95% CI, 1.45-27.71) and ≥7.27 mmol/L (HR, 19.37; 95% CI, 4.68-80.17). Estimated 10-day overall survival rates were 96.8%, 90.6%, and 69.3% in patients with blood glucose <5.53 mmol/L, 5.53 to 7.27 mmol/L, and ³7.27 mmol/L, respectively. CONCLUSIONS Hyperglycemia was association with severity of COVID-19 pneumonia and with increased patient mortality. These findings support the need for blood glucose monitoring and control of hyperglycemia in patients with COVID-19 pneumonia.