RESUMO

Background: The prognosis for patients with chronic thromboembolic pulmonary hypertension (CTEPH) using their nutritional status has not been established. We investigated the relationship between the prognosis of patients with CTEPH and the Controlling Nutritional Status (CONUT) score, which is a nutritional assessment tool. Methods and Results: A total of 157 patients with CTEPH was enrolled in the study. The primary outcome was defined as the composite outcome of all-cause mortality and non-elective hospitalization due to heart failure. Receiver operating characteristic (ROC) curve analysis was used to determine the cutoff CONUT score for predicting the 1-year rate of the primary outcome. Patients were divided into 2 groups according to the significant cutoff value and compared. Undernutrition was observed in 51.6% of patients. ROC analysis revealed a significant cutoff CONUT score of 3.5 (area under the curve=0.789). The incidence rate of the primary composite outcome was higher in the high CONUT group (score ≥4) than in the low CONUT group (score ≤3; 20% vs. 2.2%; P<0.001). Cox analysis revealed the CONUT score per point increase was an independent risk factor for the primary composite outcomes (hazard ratio 2.301; 95% confidence interval 1.081-4.895; P=0.031). Conclusions: The CONUT score can predict the 1-year rate of all-cause death and non-elective hospitalization in patients with CTEPH.

RESUMO

Chronic fibrotic tissue disrupts various organ functions. Despite significant advances in therapies, mortality and morbidity due to heart failure remain high, resulting in poor quality of life. Beyond the cardiomyocyte-centric view of heart failure, it is now accepted that alterations in the interstitial extracellular matrix (ECM) also play a major role in the development of heart failure. Here, we show that protein kinase N (PKN) is expressed in cardiac fibroblasts. Furthermore, PKN mediates the conversion of fibroblasts into myofibroblasts, which plays a central role in secreting large amounts of ECM proteins via p38 phosphorylation signaling. Fibroblast-specific deletion of PKN led to a reduction of myocardial fibrotic changes and cardiac dysfunction in mice models of ischemia-reperfusion or heart failure with preserved ejection fraction. Our results indicate that PKN is a therapeutic target for cardiac fibrosis in heart failure.

Assuntos

Fibroblastos , Fibrose , Insuficiência Cardíaca , Miocárdio , Miofibroblastos , Proteína Quinase C , Animais , Insuficiência Cardíaca/patologia , Insuficiência Cardíaca/metabolismo , Insuficiência Cardíaca/genética , Miofibroblastos/metabolismo , Miofibroblastos/patologia , Fibroblastos/metabolismo , Fibroblastos/patologia , Camundongos , Miocárdio/patologia , Miocárdio/metabolismo , Proteína Quinase C/metabolismo , Proteína Quinase C/genética , Masculino , Humanos , Modelos Animais de Doenças , Camundongos Endogâmicos C57BL , Camundongos Knockout , Matriz Extracelular/metabolismo , Fosforilação , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo , Transdução de Sinais

RESUMO

AIMS: Impella has become a new option for mechanical circulatory support in patients with cardiogenic shock (CS); however, prognostic models for patients after Impella are lacking. We aimed to identify the factors that predict in-hospital mortality in patients with CS requiring Impella and develop a new risk prediction model. METHODS AND RESULTS: We utilized the J-PVAD registry, which includes all cases where Impella was implanted in Japan. Two-thirds of the patients in the J-PVAD registry were randomly assigned to the derivation cohort (n = 1701), and the other third was assigned to the validation cohort (n = 850). A backward stepwise logistic regression model was developed to identify factors associated with in-hospital mortality. In the derivation cohort, 956 patients were discharged alive, and 745 patients (43.8%) died during hospitalization. Among 29 candidate variables, 12 were independently associated with in-hospital mortality and were applied as components of the risk model, including age, sex, body mass index, fulminant myocarditis aetiology, cardiac arrest in hospital, baseline veno-arterial extracorporeal membrane oxygenation use, mean arterial pressure, lactate, lactate dehydrogenase, total bilirubin, creatinine, and albumin levels. The comparison of predicted and observed in-hospital mortality according to the 7th quantiles using the J-PVAD risk score showed good calibration. The area under the curve for the J-PVAD risk score was 0.76 (95% confidence interval 0.73-0.78). In the validation cohort, the J-PVAD risk score showed good calibration and discrimination ability. CONCLUSIONS: The J-PVAD risk score can be calculated using variables easily obtained in routine clinical practice. It helps the accurate stratification of mortality risk and facilitates clinical decision-making.

RESUMO

Hereditary transthyretin cardiac amyloidosis (ATTRv-CA) after liver transplantation remains challenging to treat due to residual amyloid deposits in extrahepatic organs, including the heart. Tafamidis, a transthyretin tetramer stabilizer, has shown promise in the treatment of ATTRv-CA; however, its efficacy and safety after liver transplantation are uncertain. In this preliminary retrospective review, we assessed the efficacy and safety of tafamidis (80 mg) in three ATTRv-CA cases after liver transplantation. Following one year of treatment, all patients experienced improvement in dyspnea, New York Heart Association functional class, brain natriuretic peptide levels, and cardiac troponin T levels. No significant changes in echocardiographic parameters were observed. Notably, no cardiovascular or drug-related adverse events occurred during treatment. Our findings suggest that tafamidis may benefit post-liver transplant patients with ATTRv-CA and warrant further investigation through randomized controlled trials with larger cohorts. This study highlights a potential therapeutic avenue for the management of cardiovascular involvement in this challenging patient population.

RESUMO

Background: Guidelines recommend optimal medical therapy before cardiac resynchronization therapy (CRT) implantation. Herein, we report the potential effect of sodium-glucose cotransporter-2 inhibitors (SGLT2is) in improving the QRS duration and volume reduction in a patient with complete left bundle branch block (CLBBB) and reduced cardiac function. Case summary: A 68-year-old man with a history of ischaemic cardiomyopathy and decreased cardiac function had exacerbation of heart failure (HF) at an outpatient clinic. His QRS duration increased remarkably with a CLBBB of 143 ms on an electrocardiogram, and left ventricular desynchrony was assessed by echocardiography, suggesting an indication of CRT implantation. Administration of an SGLT2i and multimodal treatment for HF stabilized his HF condition and improved the QRS duration and volume reduction thereafter. The CLBBB recovered to incomplete LBBB with a QRS duration of 112 ms on electrocardiography after 6 months. The patient has been stably followed up with continuous medications, including SGLT2i, without requiring CRT implantation or worsening of HF for 12 months. Discussion: This case presents a unique scenario wherein electrical and mechanical reverse remodelling occurred in a patient with systolic HF and CLBBB, highlighting the potential benefits of SGLT2i in HF management. It may be important to carefully consider CRT indications when seeking other options to treat HF conditions and recognize an unusual phenomenon of reverse LBBB in clinical cases.

RESUMO

Primary Percutaneous Coronary Intervention (PCI) has significantly contributed to reducing the mortality of patients with ST-segment elevation myocardial infarction (STEMI) even in cardiogenic shock and is now the standard of care in most of Japanese institutions. The Task Force on Primary PCI of the Japanese Association of Cardiovascular Intervention and Therapeutics (CVIT) proposed an expert consensus document for the management of acute myocardial infarction (AMI) focusing on procedural aspects of primary PCI in 2018 and updated in 2022. Recently, the European Society of Cardiology (ESC) published the guidelines for the management of acute coronary syndrome in 2023. Major new updates in the 2023 ESC guideline include: (1) intravascular imaging should be considered to guide PCI (Class IIa); (2) timing of complete revascularization; (3) antiplatelet therapy in patient with high-bleeding risk. Reflecting rapid advances in the field, the Task Force on Primary PCI of the CVIT group has now proposed an updated expert consensus document for the management of ACS focusing on procedural aspects of primary PCI in 2024 version.

Assuntos

Síndrome Coronariana Aguda , Consenso , Intervenção Coronária Percutânea , Humanos , Intervenção Coronária Percutânea/métodos , Síndrome Coronariana Aguda/terapia , Síndrome Coronariana Aguda/cirurgia , Inibidores da Agregação Plaquetária/uso terapêutico , Japão , Infarto do Miocárdio com Supradesnível do Segmento ST/cirurgia , Infarto do Miocárdio com Supradesnível do Segmento ST/terapia

RESUMO

Many studies have reported a relationship between various lipids, such as cholesterol, fatty acids, and lipoproteins, and cardiovascular events. Low-density lipoprotein cholesterol (LDL-C) is often cited as a representative marker. However, there is still room for discussion regarding which markers, among other lipids, should take clinical precedence.This observational study focused on patients without residual stenosis on post-coronary angiography. It was based on blood tests, including lipid profiles at that time, and assessed the association with the subsequent occurrence of major adverse cardiovascular events (MACE, a composite of all-cause mortality, hospitalization due to heart failure, myocardial infarction, stroke, and all revascularizations).Of the 375 patients analyzed, 134 experienced MACE (median follow-up duration: 1031 days). When comparing the MACE and non-MACE groups, significant differences were observed in lipid markers such as non-high-density lipoprotein cholesterol (non-HDL-C) and remnant-like particle cholesterol (RLP-C) (non-HDL-C; P = 0.003, RLP-C; P < 0.001). Furthermore, the area under the curve for RLP-C was 0.656 (95% CI: 0.598-0.714). Improvement in MACE risk discrimination was observed when LDL-C was replaced with non-HDL-C or RLP-C, in addition to atherosclerosis risk factors (non-HDL-C; net reclassification improvement (NRI) = 0.366, 95% CI: 0.159-0.572, RLP-C; NRI = 0.224, 95% CI: 0.016-0.433).It is highly likely that non-HDL-C and RLP-C can serve as significant lipid markers for predicting the occurrence of MACE.

Assuntos

Biomarcadores , Humanos , Masculino , Feminino , Biomarcadores/sangue , Idoso , Pessoa de Meia-Idade , LDL-Colesterol/sangue , Doenças Cardiovasculares/sangue , Doenças Cardiovasculares/epidemiologia , Lipídeos/sangue , Colesterol/sangue , Angiografia Coronária , Lipoproteínas/sangue , Triglicerídeos/sangue , Infarto do Miocárdio/sangue , Infarto do Miocárdio/epidemiologia , Medição de Risco/métodos , HDL-Colesterol/sangue

RESUMO

BACKGROUND: The number of older people in Japan is increasing more quickly than in other countries; with this aging of society, the number of elderly patients hospitalized for acute heart failure (HF) is also increasing. The treatment and prognosis of acute HF may be changing, but there are insufficient recent data, especially for octogenarian and older patients. METHODS AND RESULTS: This study investigated the characteristics and treatment of acute HF patients in Japan. From 2018 to 2020, 1,146 patients from 7 Tokai area hospitals were followed for at least 1 year. The mean age was 78 years. Compared with patients aged <80 years, those aged ≥80 years were more likely to be female (57.4% vs. 34.2%), have a lower body mass index (22.2 vs. 24.9 kg/m2), and have HF with preserved ejection fraction (43.1% vs. 21.4%), and less likely to have HF with reduced ejection fraction (38.9% vs. 61.7%). During hospitalization, 6.5% died. After discharge, patients faced high risks of rehospitalization for HF and death (27.6 and 14.2 per 100 patient-years, respectively). Notably, prescription rates of HF medications have declined over time for all patients, but especially for those aged ≥80 years. CONCLUSIONS: Guideline-directed medical therapy should be provided based on a thorough understanding of an individual's background rather than withheld simply because of clinical inertia due to a patient's advanced age.

RESUMO

Identifying specific markers of adipose stem and progenitor cells (ASPCs) in vivo is crucial for understanding the biology of white adipose tissues (WAT). PDGFRα-positive perivascular stromal cells represent the best candidates for ASPCs. This cell lineage differentiates into myofibroblasts that contribute to the impairment of WAT function. However, ASPC marker protein(s) that are functionally crucial for maintaining WAT homeostasis are unknown. We previously identified Meflin as a marker of mesenchymal stem cells (MSCs) in bone marrow and tissue-resident perivascular fibroblasts in various tissues. We also demonstrated that Meflin maintains the undifferentiated status of MSCs/fibroblasts. Here, we show that Meflin is expressed in WAT ASPCs. A lineage-tracing experiment showed that Meflin+ ASPCs proliferate in the WAT of obese mice induced by a high-fat diet (HFD), while some of them differentiate into myofibroblasts or mature adipocytes. Meflin knockout mice fed an HFD exhibited a significant fibrotic response as well as increases in adipocyte cell size and the number of crown-like structures in WAT, accompanied by impaired glucose tolerance. These data suggested that Meflin expressed by ASPCs may have a role in reducing disease progression associated with WAT dysfunction.

Assuntos

Tecido Adiposo Branco , Fibrose , Animais , Camundongos , Fibrose/metabolismo , Tecido Adiposo Branco/metabolismo , Humanos , Biomarcadores/metabolismo , Camundongos Endogâmicos C57BL , Diferenciação Celular , Masculino , Dieta Hiperlipídica/efeitos adversos , Camundongos Knockout , Células-Tronco/metabolismo , Células-Tronco Mesenquimais/metabolismo , Adipócitos/metabolismo

RESUMO

Hyperuricemia is an independent predictor of mortality in patients with chronic heart failure (CHF). To determine whether febuxostat, a urate-lowering agent, may improve clinical outcomes in CHF patients, we conducted a multicenter, prospective, randomized, open-label, blinded endpoint study with a treatment period of 24 weeks. We randomly assigned Japanese outpatients diagnosed with both CHF with reduced left ventricular ejection fraction (LVEF < 40%) and asymptomatic hyperuricemia (serum uric acid [UA] levels > 7.0 mg/dl and < 10.0 mg/dl) to either a febuxostat group (n = 51) or a control group (n = 50). The primary efficacy endpoint was the change in log-transformed plasma B-type natriuretic peptide (BNP) levels from baseline to week 24 (or at discontinuation). The secondary efficacy endpoints were the changes in LV systolic or diastolic function evaluated by echocardiography, New York Heart Association (NYHA) class, hemoglobin, and estimated glomerular filtration rate from baseline to week 24, and the change in log-transformed plasma BNP levels or serum UA levels from baseline to weeks 4, 8, 12, 16 and 20 (BNP) or weeks 4, 8, 12, 16, 20 and 24 (serum UA). The primary safety endpoints were occurrence of all-cause death or major cardiovascular events. The mean age of participants was 70 years; 14% were female. The febuxostat group and the control group did not differ with respect to the primary efficacy endpoint (p = 0.13), although the decrease in log-transformed plasma BNP levels from baseline to each of weeks 4, 8, 12, 16 and 20 was greater in the febuxostat group. There were no significant differences between the two groups in the primary safety endpoints or the secondary efficacy endpoints except reduced serum UA levels in the febuxostat group. Febuxostat did not reduce plasma BNP levels at week 24 in patients with CHF, but it appeared safe with no increase in major cardiovascular events and all-cause or cardiovascular mortality.

RESUMO

BACKGROUND: The fibrosis-5 (FIB-5) index is a noninvasive marker for assessing the progression of liver fibrosis and predictor in patients with heart failure (HF). This study investigated the association between the FIB-5 index and response to cardiac resynchronization therapy (CRT) and evaluated its predictive value for prognosis. METHODS: In total, 203 patients who underwent CRT/CRT-defibrillator (CRT-D) implantation were retrospectively included. The FIB-5 index was calculated using blood samples obtained before and after CRT/CRT-D. Response to CRT was defined as a relative reduction in left ventricular end-systolic volume of ≥15% 6 months after CRT/CRT-D. We compared the prognosis after CRT/CRT-D between the groups according to the FIB-5 index. RESULTS: One hundred and twenty-three patients (61%) responded to CRT. The responder group demonstrated a significantly higher FIB-5 index than the nonresponder group (-2.76 ± 3.85 vs. -4.67 ± 3.29, p < 0.001). Receiver-operating characteristic analysis demonstrated that the area under the curve of the FIB-5 index was 0.660 with a cutoff value of -4.00 for responders. In multivariate analysis, FIB-5 index ≥ -4.00 was an independent predictor for CRT response (odds ratio: 3.665, p = 0.003), in addition to QRS duration ≥ 150 ms and echocardiographic dysynchrony. The FIB-5 index increased significantly after 6 months in the responder group but not in the nonresponder group. The FIB-5 index ≥ -4.00 group showed a significantly better prognosis for cardiac death, HF hospitalization, and composite endpoint than the FIB-5 index < -4.00 group. CONCLUSION: The FIB-5 index in addition to classical predictors may be a useful marker for predicting response to CRT.

Assuntos

Biomarcadores , Terapia de Ressincronização Cardíaca , Insuficiência Cardíaca , Cirrose Hepática , Humanos , Masculino , Feminino , Terapia de Ressincronização Cardíaca/métodos , Insuficiência Cardíaca/terapia , Insuficiência Cardíaca/fisiopatologia , Insuficiência Cardíaca/mortalidade , Insuficiência Cardíaca/sangue , Cirrose Hepática/terapia , Cirrose Hepática/sangue , Cirrose Hepática/fisiopatologia , Cirrose Hepática/complicações , Prognóstico , Estudos Retrospectivos , Biomarcadores/sangue , Idoso , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Resultado do Tratamento

RESUMO

Background: Outcomes in patients with relatively high His-bundle (HB) capture thresholds at implantation are unknown. This study aimed to compare changes in the HB capture threshold and prognosis between patients with a relatively high threshold and those with a low threshold. Methods and Results: Forty-nine patients who underwent permanent HB pacing (HBP) were divided into two groups: low (<1.25 V at 1.0 ms; n=35) and high (1.25-2.49 V; n=14) baseline HB capture threshold groups. The HB capture threshold was evaluated at implantation, and after 1 week, 1, 3, and 6 months, and every 6 months thereafter. HB capture threshold rise was defined as threshold rise ≥1.0 V at 1.0 ms compared with implantation measures. We compared outcomes between the groups. During a mean follow-up period of 34.6 months, the high-threshold group showed a trend toward a higher incidence of HB capture threshold of ≥2.5 V (50% vs. 14%; P=0.023), HBP abandonment (29% vs. 8.6%; P=0.091), lead revision (21% vs. 2.9%; P=0.065), and clinical events (all-cause death, heart failure hospitalization, and new-onset or progression of atrial fibrillation; 50% vs. 23%; P=0.089) than the low-threshold group. A baseline HB capture threshold of ≥1.25V was an independent predictor of clinical events. Conclusions: A relatively high HB capture threshold is associated with increased risk of HBP abandonment, lead revision, and poor clinical outcomes.

RESUMO

The adult mammalian heart has extremely limited cardiac regenerative capacity. Most cardiomyocytes live in a state of permanent cell-cycle arrest and are unable to re-enter the cycle. Cardiomyocytes switch from cell proliferation to a maturation state during neonatal development. Although several signaling pathways are involved in this transition, the molecular mechanisms by which these inputs coordinately regulate cardiomyocyte maturation are not fully understood. Retinoic acid (RA) plays a pivotal role in development, morphogenesis, and regeneration. Despite the importance of RA signaling in embryo heart development, little is known about its function in the early postnatal period. We found that mRNA expression of aldehyde dehydrogenase 1 family member A2 (Aldh1a2), which encodes the key enzyme for synthesizing all-trans retinoic acid (ATRA) and is an important regulator for RA signaling, was transiently upregulated in neonatal mouse ventricles. Single-cell transcriptome analysis and immunohistochemistry revealed that Aldh1a2 expression was enriched in cardiac fibroblasts during the early postnatal period. Administration of ATRA inhibited cardiomyocyte proliferation in cultured neonatal rat cardiomyocytes and human cardiomyocytes. RNA-seq analysis indicated that cell proliferation-related genes were downregulated in prenatal rat ventricular cardiomyocytes treated with ATRA, while cardiomyocyte maturation-related genes were upregulated. These findings suggest that RA signaling derived from cardiac fibroblasts is one of the key regulators of cardiomyocyte proliferation and maturation during neonatal heart development.

Assuntos

Família Aldeído Desidrogenase 1 , Proliferação de Células , Miócitos Cardíacos , Retinal Desidrogenase , Transdução de Sinais , Tretinoína , Animais , Tretinoína/farmacologia , Tretinoína/metabolismo , Miócitos Cardíacos/metabolismo , Miócitos Cardíacos/citologia , Miócitos Cardíacos/efeitos dos fármacos , Camundongos , Família Aldeído Desidrogenase 1/metabolismo , Família Aldeído Desidrogenase 1/genética , Retinal Desidrogenase/metabolismo , Retinal Desidrogenase/genética , Proliferação de Células/efeitos dos fármacos , Ratos , Humanos , Regulação para Cima , Animais Recém-Nascidos , Ciclo Celular/efeitos dos fármacos , Diferenciação Celular/efeitos dos fármacos , Coração/efeitos dos fármacos , Coração/crescimento & desenvolvimento , Células Cultivadas

RESUMO

AIMS: Hospitalizations are common in patients with heart failure and are associated with high mortality, readmission and economic burden. Detecting early signs of worsening heart failure may enable earlier intervention and reduce hospitalizations. The HeartLogic algorithm is designed to predict worsening heart failure using diagnostic data from multiple device sensors. The main objective of this analysis was to evaluate the sensitivity of the HeartLogic alert calculation in predicting worsening heart failure events (HFEs). We also evaluated the false positive alert rate (FPR) and compared the incidence of HFEs occurring in a HeartLogic alert state to those occurring out of an alert state. METHODS: The HINODE study enrolled 144 patients (81 ICD and 63 CRT-D) with device sensor data transmitted via a remote monitoring system. HeartLogic alerts were then retrospectively simulated using relevant sensor data. Clinicians and patients were blinded to calculated alerts. Reported adverse events with HF symptoms were adjudicated and classified by an independent HFE committee. Sensitivity was defined as the ratio of the number of detected usable HFEs (true positives) to the total number of usable HFEs. A false positive alert was defined as an alert with no usable HFE between the alert onset date and the alert recovery date plus 30 days. The patient follow-up period was categorized as in alert state or out of alert state. The event rate ratio was the HFE rate calculated in alert to out of alert. RESULTS: The patient cohort was 79% male and had an average age of 68 ± 12 years. This analysis yielded 244 years of follow-up data with 73 HFEs from 37 patients. A total of 311 HeartLogic alerts at the nominal threshold (16) occurred across 106 patients providing an alert rate of 1.27 alerts per patient-year. The HFE rate was 8.4 times greater while in alert compared with out of alert (1.09 vs. 0.13 events per patient-year; P < 0.001). At the nominal alert threshold, 80.8% of HFEs were detected by a HeartLogic alert [95% confidence interval (CI): 69.9%-89.1%]. The median time from first true positive alert to an adjudicated clinical HFE was 53 days. The FPR was 1.16 (95% CI: 0.98-1.38) alerts per patient-year. CONCLUSIONS: Results suggest that signs of worsening HF can be detected successfully with remote patient follow-up. The use of HeartLogic may predict periods of increased risk for HF or clinically significant events, allowing for early intervention and reduction of hospitalization in a vulnerable patient population.

Assuntos

Desfibriladores Implantáveis , Insuficiência Cardíaca , Humanos , Insuficiência Cardíaca/fisiopatologia , Insuficiência Cardíaca/terapia , Insuficiência Cardíaca/diagnóstico , Insuficiência Cardíaca/epidemiologia , Masculino , Feminino , Idoso , Estudos Retrospectivos , Pessoa de Meia-Idade , Seguimentos , Algoritmos , Incidência , Valor Preditivo dos Testes , Progressão da Doença , Prognóstico

Assuntos

Inibidores da Enzima Conversora de Angiotensina , COVID-19 , Doenças Cardiovasculares , Sistema Renina-Angiotensina , Humanos , Sistema Renina-Angiotensina/efeitos dos fármacos , Inibidores da Enzima Conversora de Angiotensina/uso terapêutico , Inibidores da Enzima Conversora de Angiotensina/efeitos adversos , Doenças Cardiovasculares/prevenção & controle , SARS-CoV-2 , Tratamento Farmacológico da COVID-19 , Antagonistas de Receptores de Angiotensina/uso terapêutico , Antagonistas de Receptores de Angiotensina/efeitos adversos , Hipertensão/tratamento farmacológico

RESUMO

Improvements in therapies for heart failure with preserved ejection fraction (HFpEF) are crucial for improving patient outcomes and quality of life. Although HFpEF is the predominant heart failure type among older individuals, its prognosis is often poor owing to the lack of effective therapies. The roles of the spleen and bone marrow are often overlooked in the context of HFpEF. Recent studies suggest that the spleen and bone marrow could play key roles in HFpEF, especially in relation to inflammation and immune responses. The bone marrow can increase production of certain immune cells that can migrate to the heart and contribute to disease. The spleen can contribute to immune responses that either protect or exacerbate heart failure. Extramedullary hematopoiesis in the spleen could play a crucial role in HFpEF. Increased metabolic activity in the spleen, immune cell production and mobilization to the heart, and concomitant cytokine production may occur in heart failure. This leads to systemic chronic inflammation, along with an imbalance of immune cells (macrophages) in the heart, resulting in chronic inflammation and progressive fibrosis, potentially leading to decreased cardiac function. The bone marrow and spleen are involved in altered iron metabolism and anemia, which also contribute to HFpEF. This review presents the concept of an interplay between the heart, spleen, and bone marrow in the setting of HFpEF, with a particular focus on extramedullary hematopoiesis in the spleen. The aim of this review is to discern whether the spleen can serve as a new therapeutic target for HFpEF.

Assuntos

Medula Óssea , Insuficiência Cardíaca , Hematopoese Extramedular , Baço , Humanos , Insuficiência Cardíaca/fisiopatologia , Insuficiência Cardíaca/metabolismo , Hematopoese Extramedular/fisiologia , Baço/imunologia , Baço/metabolismo , Volume Sistólico/fisiologia , Miocárdio/metabolismo , Miocárdio/patologia , Miocárdio/imunologia , Inflamação

RESUMO

BACKGROUND: In an aging society, percutaneous coronary intervention (PCI) for super-elderly patients is commonly performed in clinical practice. However, data are scarce regarding the clinical features and outcomes of this population. METHODS: This multicenter observational study enrolled patients aged over 90 years who underwent PCI across 10 hospitals between 2011 and 2020. The study included patients presenting with acute coronary syndrome (ACS) and chronic coronary syndrome (CCS). The occurrence of all-cause and cardiac deaths during hospitalization and after discharge was investigated. RESULTS: In total, 402 patients (91.9 ±â€¯2.0 years, 48.3 % male) participated in the study, of whom 77.9 % presented with ACS. The rate of in-hospital death was significantly higher in patients with ACS compared to patients with CCS (15.3 % vs. 2.2 %, p < 0.001). The estimated cumulative incidence rates of all-cause death were 24.3 %, 39.5 %, and 60.4 % at 1, 3, and 5 years, respectively. No significant difference was observed in the occurrence of all-cause death between patients with ACS and CCS. Regarding causes of death after discharge, non-cardiac deaths accounted for just over half of the cases. CONCLUSION: This study highlights the clinical features and long-term clinical course of patients aged over 90 years who underwent PCI in a real-world setting. Patients presenting with ACS exhibited a higher rate of in-hospital mortality compared to those with CCS. Following discharge, both ACS and CCS patients experienced comparable and substantial increases in the incidence rates of both cardiac and non-cardiac mortality over time, and a more holistic management approach is warranted.