RESUMEN
PURPOSE OF REVIEW: Speckle tracking echocardiography (STE)-derived measures of myocardial mechanics, referred to herewithin as strain measurements, directly assess myocardial contractility and provide a nuanced assessment of ventricular function. This review provides an overview of strain measurements and their current clinical value and utility in decision making in pediatric cardiology. RECENT FINDINGS: Strain measurements are advancing understanding of how cardiac dysfunction occurs in children with acquired and congenital heart disease (CHD). Global strain measurements can detect early changes in cardiac function and are reliable methods of serially monitoring systolic function in children. Global strain measurements are increasingly reported in echocardiographic assessment of ventricular function alongside ejection fraction. Research is increasingly focused on how strain measurements can help improve clinical management, risk stratification, and prognostic insight. Although more research is needed, preliminary studies provide hope that there will be clinical benefit for strain in pediatric cardiology management. SUMMARY: Strain measurements provide a more detailed assessment of ventricular function than conventional measures of echocardiographic functional assessment. Strain measurements are increasingly being used to advance understanding of normal and abnormal myocardial contractility, to increase sensitivity to detect early cardiac dysfunction, and to improve prognostic management in children with acquired and CHD.
Asunto(s)
Toma de Decisiones Clínicas , Ecocardiografía , Cardiopatías Congénitas , Humanos , Niño , Ecocardiografía/métodos , Cardiopatías Congénitas/diagnóstico por imagen , Cardiopatías Congénitas/fisiopatología , Contracción Miocárdica/fisiología , Pronóstico , Cardiopatías/diagnóstico por imagen , Cardiopatías/fisiopatologíaRESUMEN
In vitro cardiomyocyte mechano-sensing platform is crucial for evaluating the mechanical performance of cardiac tissues and will be an indispensable tool for application in drug discovery and disease mechanism study. Magnetic sensing offers significant advantages in real-time, in situ wireless monitoring and resistance to ion interference. However, due to the mismatch between the stiffness of traditional rigid magnetic material and myocardial tissue, sensitivity is insufficient and it is difficult to achieve cell structure induction and three-dimensional cultivation. Herein, a magnetic sensing platform that integrates a neodymium-iron-boron/polydimethylsiloxane (NdFeB/PDMS) flexible microbeam with suspended and ordered polycaprolactone (PCL) nanofiber membranes was developed, providing a three-dimensional anisotropic culture environment for cardiomyocyte growth and simultaneously realizing in situ wireless contractility monitoring. The as-prepared sensor presented an ultrahigh sensitivity of 442.2 µV/µm and a deflection resolution of 2 µm. By continuously monitoring the cardiomyocyte growth status and drug stimulation feedback, we verified the capability of the platform to capture dynamic changes in cardiomyocyte contractility. This platform provides a perspective tool for evaluating cardiomyocyte maturity and drug performance.
Asunto(s)
Miocitos Cardíacos , Nanofibras , Miocitos Cardíacos/citología , Miocitos Cardíacos/fisiología , Miocitos Cardíacos/efectos de los fármacos , Nanofibras/química , Animales , Ratas , Dimetilpolisiloxanos/química , Tecnología Inalámbrica , Contracción Miocárdica/efectos de los fármacos , Contracción Miocárdica/fisiología , Poliésteres/química , Neodimio/químicaAsunto(s)
Contracción Miocárdica , Humanos , Niño , Contracción Miocárdica/fisiología , Valores de ReferenciaRESUMEN
BACKGROUND: Cardiovascular magnetic resonance (CMR) derived global function index (GFI) and myocardial contraction fraction (MCF) were identified as useful imaging markers to assess left ventricular (LV) cardiac performance and can provide prognostic information for several cardiac diseases. As pediatric reference values are lacking, the aim of this retrospective study was to establish these values. METHODS: 154 CMR examinations of healthy children and adolescents (4-18 years) were included. LV end-diastolic, end-systolic and stroke volumes, ejection fraction (LVEF) and myocardial mass were measured using short axis stacks. Results were used to calculate LVGFI and LVMCF. Statistically, the Lambda-Mu-Sigma (LMS)-method was applied to create percentile curves and tables. RESULTS: The mean age (standard deviation) of the subjects was 13.8 (2.8) years, 102 were male (66%). Mean LVGFI was 46.3 (6.0)% and mean LVMCF was 110.6 (19.9) %. Both, LVGFI and LVMCF decreased significantly with age (LVGFI: r = -0.30, p < 0.001; LVMCF: -0.30, p < 0.001). There was no statistical difference between girls and boys (p all >0.05). Strong correlations between LVGFI and LVMCF (r = 0.78, p < 0.001) as well as between LVGFI and LVEF (r = 0.80, p < 0.001) were documented whereas the correlation of LVMCF and LVEF was weaker (r = 0.32, p < 0.001). Univariable and multivariable regression analysis demonstrated that LVGFI was strongly associated with age whereas LVMCF was associated with weight. Percentile curves and tables were created accordingly. CONCLUSION: We provide pediatric CMR reference values for the new cardiac functional markers LVGFI and LVMCF. These may improve the interpretation of clinical CMR studies and can be used for future research studies.
Asunto(s)
Ventrículos Cardíacos , Imagen por Resonancia Cinemagnética , Contracción Miocárdica , Función Ventricular Izquierda , Humanos , Masculino , Niño , Femenino , Adolescente , Estudios Retrospectivos , Valores de Referencia , Preescolar , Función Ventricular Izquierda/fisiología , Imagen por Resonancia Cinemagnética/métodos , Imagen por Resonancia Cinemagnética/normas , Contracción Miocárdica/fisiología , Ventrículos Cardíacos/diagnóstico por imagen , Volumen Sistólico/fisiologíaRESUMEN
Aging is associated with cardiac contractile abnormalities, but the etiology of these contractile deficits is unclear. We hypothesized that cardiac contractile and regulatory protein expression is altered during aging. To investigate this possibility, left ventricular (LV) lysates were prepared from young (6 months) and old (24 months) Fischer344 rats. There are no age-related changes in SERCA2 expression or phospholamban phosphorylation. Additionally, neither titin isoform expression nor phosphorylation differed. However, there is a significant increase in ß-isoform of the myosin heavy chain (MyHC) expression and phosphorylation of TnI and MyBP-C during aging. In permeabilized strips of papillary muscle, force and Ca2+ sensitivity are reduced during aging, consistent with the increase in ß-MyHC expression and TnI phosphorylation. However, the increase in MyBP-C phosphorylation during aging may represent a mechanism to compensate for age-related contractile deficits. In isolated cardiomyocytes loaded with Fura-2, the peak of the Ca2+ transient is reduced, but the kinetics of the Ca2+ transient are not altered. Furthermore, the extent of shortening and the rates of both sarcomere shortening and re-lengthening are reduced. These results demonstrate that aging is associated with changes in contractile and regulatory protein expression and phosphorylation, which affect the mechanical properties of cardiac muscle.
Asunto(s)
Envejecimiento , Contracción Miocárdica , Miocitos Cardíacos , Ratas Endogámicas F344 , Animales , Masculino , Contracción Miocárdica/fisiología , Envejecimiento/metabolismo , Envejecimiento/fisiología , Ratas , Fosforilación , Miocitos Cardíacos/metabolismo , ATPasas Transportadoras de Calcio del Retículo Sarcoplásmico/metabolismo , Cadenas Pesadas de Miosina/metabolismo , Proteínas de Unión al Calcio/metabolismo , Conectina/metabolismo , Troponina I/metabolismo , Calcio/metabolismo , Proteínas de Unión a Calmodulina/metabolismo , Proteínas PortadorasRESUMEN
AIM: To evaluate the efficacy and safety of the advanced technique for positioning the endocardial electrodes of a cardiac contractility modulation (CCM) device. MATERIALS AND METHODS: The CCM system was implanted in 100 patients, of which 60 CCM electrodes were positioned in the most optimal zones of myocardial perfusion, in particular, in the zone of the minor focal-scar/fibrotic lesion (the Summed Rest Score of 0 to 1-2, the intensity of the radiopharmaceutical at least 30%), and in 40 patients according to the standard procedure. Before the implantation of the CCM system, 60 patients underwent tomography (S-SPECT) of the myocardium with 99mTc-methoxy-isobutyl-isonitrile at rest to determine the most optimal electrode positioning zones and 100 patients underwent transthoracic echocardiography at baseline and after 12 months to assess the effectiveness of surgical treatment. RESULTS: Improved ventricular electrode positioning technique is associated with the best reverse remodeling of the left ventricular myocardium, especially in patients with ischemic chronic heart failure, with less radiation exposure to the surgeon and the patient, and without electrode-related complications. CONCLUSION: At the preoperative stage, it is recommended to perform a synchronized single-photon emission computed tomography of the myocardium with 99mTc-methoxy-isobutyl-isonitrile at rest before implantation of the CCM device to assess the presence of scar zones/myocardial fibrosis in the anterior and inferior septal regions of the interventricular septum of the left ventricle, followed by implantation of ventricular electrodes in the zone of the minor scar/fibrous lesion, which will allow to achieve optimal stimulation parameters, increase the effectiveness of CCM therapy, reduce the radiation exposure on medical personnel and the patient during surgery.
Asunto(s)
Fibrilación Atrial , Insuficiencia Cardíaca , Humanos , Masculino , Femenino , Persona de Mediana Edad , Insuficiencia Cardíaca/fisiopatología , Insuficiencia Cardíaca/terapia , Fibrilación Atrial/fisiopatología , Fibrilación Atrial/terapia , Fibrilación Atrial/cirugía , Anciano , Resultado del Tratamiento , Electrodos Implantados , Volumen Sistólico/fisiología , Tomografía Computarizada de Emisión de Fotón Único/métodos , Ecocardiografía/métodos , Contracción Miocárdica/fisiologíaRESUMEN
BACKGROUND: The primary genetic risk factor for heritable pulmonary arterial hypertension is the presence of monoallelic mutations in the BMPR2 gene. The incomplete penetrance of BMPR2 mutations implies that additional triggers are necessary for pulmonary arterial hypertension occurrence. Pulmonary artery stenosis directly raises pulmonary artery pressure, and the redirection of blood flow to unobstructed arteries leads to endothelial dysfunction and vascular remodeling. We hypothesized that right pulmonary artery occlusion (RPAO) triggers pulmonary hypertension (PH) in rats with Bmpr2 mutations. METHODS AND RESULTS: Male and female rats with a 71 bp monoallelic deletion in exon 1 of Bmpr2 and their wild-type siblings underwent acute and chronic RPAO. They were subjected to full high-fidelity hemodynamic characterization. We also examined how chronic RPAO can mimic the pulmonary gene expression pattern associated with installed PH in unobstructed territories. RPAO induced precapillary PH in male and female rats, both acutely and chronically. Bmpr2 mutant and male rats manifested more severe PH compared with their counterparts. Although wild-type rats adapted to RPAO, Bmpr2 mutant rats experienced heightened mortality. RPAO induced a decline in cardiac contractility index, particularly pronounced in male Bmpr2 rats. Chronic RPAO resulted in elevated pulmonary IL-6 (interleukin-6) expression and decreased Gdf2 expression (corrected P value<0.05 and log2 fold change>1). In this context, male rats expressed higher pulmonary levels of endothelin-1 and IL-6 than females. CONCLUSIONS: Our novel 2-hit rat model presents a promising avenue to explore the adaptation of the right ventricle and pulmonary vasculature to PH, shedding light on pertinent sex- and gene-related effects.
Asunto(s)
Receptores de Proteínas Morfogenéticas Óseas de Tipo II , Modelos Animales de Enfermedad , Hemodinámica , Mutación , Arteria Pulmonar , Animales , Receptores de Proteínas Morfogenéticas Óseas de Tipo II/genética , Receptores de Proteínas Morfogenéticas Óseas de Tipo II/metabolismo , Femenino , Masculino , Arteria Pulmonar/fisiopatología , Arteria Pulmonar/metabolismo , Hipertensión Pulmonar/fisiopatología , Hipertensión Pulmonar/genética , Hipertensión Pulmonar/etiología , Hipertensión Pulmonar/metabolismo , Ratas , Ratas Sprague-Dawley , Remodelación Vascular/genética , Hipertensión Arterial Pulmonar/fisiopatología , Hipertensión Arterial Pulmonar/genética , Hipertensión Arterial Pulmonar/metabolismo , Hipertensión Arterial Pulmonar/etiología , Estenosis de Arteria Pulmonar/genética , Estenosis de Arteria Pulmonar/fisiopatología , Estenosis de Arteria Pulmonar/metabolismo , Presión Arterial , Contracción Miocárdica/fisiologíaRESUMEN
Hypertrophic cardiomyopathy (HCM) is a genetic disease of the heart characterized by thickening of the left ventricle (LV), hypercontractility, and impaired relaxation. HCM is caused primarily by heritable mutations in sarcomeric proteins, such as ß myosin heavy chain. Until recently, medications in clinical use for HCM did not directly target the underlying contractile changes in the sarcomere. Here, we investigate a novel small molecule, RLC-1, identified in a bovine cardiac myofibril high-throughput screen. RLC-1 is highly dependent on the presence of a regulatory light chain to bind to cardiac myosin and modulate its ATPase activity. In demembranated rat LV trabeculae, RLC-1 decreased maximal Ca2+-activated force and Ca2+ sensitivity of force, while it increased the submaximal rate constant for tension redevelopment. In myofibrils isolated from rat LV, both maximal and submaximal Ca2+-activated force are reduced by nearly 50%. Additionally, the fast and slow phases of relaxation were approximately twice as fast as DMSO controls, and the duration of the slow phase was shorter. Structurally, x-ray diffraction studies showed that RLC-1 moved myosin heads away from the thick filament backbone and decreased the order of myosin heads, which is different from other myosin inhibitors. In intact trabeculae and isolated cardiomyocytes, RLC-1 treatment resulted in decreased peak twitch magnitude and faster activation and relaxation kinetics. In conclusion, RLC-1 accelerated kinetics and decreased force production in the demembranated tissue, intact tissue, and intact whole cells, resulting in a smaller cardiac twitch, which could improve the underlying contractile changes associated with HCM.
Asunto(s)
Contracción Miocárdica , Animales , Ratas , Contracción Miocárdica/efectos de los fármacos , Contracción Miocárdica/fisiología , Cadenas Ligeras de Miosina/metabolismo , Bovinos , Miofibrillas/metabolismo , Miosinas Cardíacas/metabolismo , Ratas Sprague-Dawley , Masculino , Calcio/metabolismoRESUMEN
Chronic heart failure is one of the most common reasons for hospitalization. Current risk stratification is based on ejection fraction, whereas many arrhythmic events occur in patients with relatively preserved ejection fraction. We aim to investigate the mechanistic link between proarrhythmic abnormalities, reduced contractility and diastolic dysfunction in heart failure, using electromechanical modelling and simulations of human failing cardiomyocytes. We constructed, calibrated and validated populations of human electromechanical models of failing cardiomyocytes, that were able to reproduce the prolonged action potential, reduced contractility and diastolic dysfunction as observed in human data, as well as increased propensity to proarrhythmic incidents such as early afterdepolarization and beat-to-beat alternans. Our simulation data reveal that proarrhythmic incidents tend to occur in failing myocytes with lower diastolic tension, rather than with lower contractility, due to the relative preserved SERCA and sodium calcium exchanger current. These results support the inclusion of end-diastolic volume to be potentially beneficial in the risk stratifications of heart failure patients.
Asunto(s)
Potenciales de Acción , Arritmias Cardíacas , Insuficiencia Cardíaca , Miocitos Cardíacos , Humanos , Miocitos Cardíacos/metabolismo , Insuficiencia Cardíaca/fisiopatología , Arritmias Cardíacas/fisiopatología , Arritmias Cardíacas/etiología , Diástole/fisiología , Modelos Cardiovasculares , Contracción Miocárdica/fisiología , Simulación por Computador , ATPasas Transportadoras de Calcio del Retículo Sarcoplásmico/metabolismoRESUMEN
Evaluation of the fetal heart involves two approaches. The first describes a screening protocol in which the heart is imaged in transverse planes that includes the four-chamber view (4CV), left and right outflow tracts, and the 3-vessel-tracheal view. The second approach is a fetal echocardiogram that requires additional cardiac images as well as evaluating ventricular function using diagnostic tools such as M-mode and pulsed Doppler ultrasound. Speckle tracking analysis of the ventricular and atrial endocardium of the fetal heart has focused primarily on computing longitudinal global strain. However, the technology enabling this measurement to occur has recently been adapted to enable the clinician to obtain numerous additional measurements of the size, shape, and contractility of the ventricles and atrial chambers. By using the increased number of measurements derived from speckle tracking analysis, we have reported the ability to screen for tetralogy of Fallot, D-transposition of the great arteries (D-TGA), and coarctation of the aorta by only imaging the 4CV. In addition, we have found that measurements derived from speckle tracking analysis of the ventricular and atrial chambers can be used to compute the risk for emergent neonatal balloon atrial septostomy in fetuses with D-TGA. The purpose of this review is to consolidate our experience in one source to provide perspective on the benefits of speckle tracking analysis to measure the size, shape, and contractility of the ventricles and atria imaged in the 4CV in fetuses with congenital heart defects.
Asunto(s)
Corazón Fetal , Cardiopatías Congénitas , Contracción Miocárdica , Ultrasonografía Prenatal , Humanos , Cardiopatías Congénitas/fisiopatología , Cardiopatías Congénitas/diagnóstico por imagen , Cardiopatías Congénitas/embriología , Ultrasonografía Prenatal/métodos , Corazón Fetal/diagnóstico por imagen , Corazón Fetal/fisiopatología , Contracción Miocárdica/fisiología , Ecocardiografía/métodos , Diagnóstico por Imagen de Elasticidad/métodos , Interpretación de Imagen Asistida por Computador/métodos , FemeninoAsunto(s)
Corazón , Humanos , Corazón/fisiología , Animales , Contracción Miocárdica/fisiología , Modelos CardiovascularesRESUMEN
The cardiac extracellular matrix (cECM) is fundamental for organ morphogenesis and maturation, during which time it undergoes remodeling, yet little is known about whether mechanical forces generated by the heartbeat regulate this remodeling process. Using zebrafish as a model and focusing on stages when cardiac valves and trabeculae form, we found that altering cardiac contraction impairs cECM remodeling. Longitudinal volumetric quantifications in wild-type animals revealed region-specific dynamics: cECM volume decreases in the atrium but not in the ventricle or atrioventricular canal. Reducing cardiac contraction resulted in opposite effects on the ventricular and atrial ECM, whereas increasing the heart rate affected the ventricular ECM but had no effect on the atrial ECM, together indicating that mechanical forces regulate the cECM in a chamber-specific manner. Among the ECM remodelers highly expressed during cardiac morphogenesis, we found one that was upregulated in non-contractile hearts, namely tissue inhibitor of matrix metalloproteinase 2 (timp2). Loss- and gain-of-function analyses of timp2 revealed its crucial role in cECM remodeling. Altogether, our results indicate that mechanical forces control cECM remodeling in part through timp2 downregulation.
Asunto(s)
Matriz Extracelular , Corazón , Inhibidor Tisular de Metaloproteinasa-2 , Pez Cebra , Animales , Pez Cebra/embriología , Pez Cebra/metabolismo , Matriz Extracelular/metabolismo , Inhibidor Tisular de Metaloproteinasa-2/metabolismo , Inhibidor Tisular de Metaloproteinasa-2/genética , Corazón/embriología , Proteínas de Pez Cebra/metabolismo , Proteínas de Pez Cebra/genética , Contracción Miocárdica/fisiología , Miocardio/metabolismo , Morfogénesis , Atrios Cardíacos/embriología , Atrios Cardíacos/metabolismo , Fenómenos Biomecánicos , Regulación del Desarrollo de la Expresión Génica , Ventrículos Cardíacos/metabolismo , Ventrículos Cardíacos/embriologíaRESUMEN
Cardiovascular disease (CVD) remains the leading cause of death worldwide. Patients often fail to recognize the early signs of CVDs, which display irregularities in cardiac contractility and may ultimately lead to heart failure. Therefore, continuously monitoring the abnormal changes in cardiac contractility may represent a novel approach to long-term CVD surveillance. Here, a zero-power consumption and implantable bias-free cardiac monitoring capsule (BCMC) is introduced based on the triboelectric effect for cardiac contractility monitoring in situ. The output performance of BCMC is improved over 10 times with nanoparticle self-adsorption method. This device can be implanted into the right ventricle of swine using catheter intervention to detect the change of cardiac contractility and the corresponding CVDs. The physiological signals can be wirelessly transmitted to a mobile terminal for analysis through the acquisition and transmission module. This work contributes to a new option for precise monitoring and early diagnosis of CVDs.
Asunto(s)
Contracción Miocárdica , Porcinos , Animales , Monitoreo Fisiológico/instrumentación , Monitoreo Fisiológico/métodos , Contracción Miocárdica/fisiología , Nanopartículas/química , Tecnología Inalámbrica , Enfermedades Cardiovasculares/diagnóstico , Diseño de EquipoRESUMEN
Human induced pluripotent stem cell (hiPSC)-derived cardiomyocytes (CMs) have found utility for conducting in vitro drug screening and disease modelling to gain crucial insights into pharmacology or disease phenotype. However, diseases such as atrial fibrillation, affecting >33 M people worldwide, demonstrate the need for cardiac subtype-specific cells. Here, we sought to investigate the base characteristics and pharmacological differences between commercially available chamber-specific atrial or ventricular hiPSC-CMs seeded onto ultra-thin, flexible PDMS membranes to simultaneously measure contractility in a 96 multi-well format. We investigated the effects of GPCR agonists (acetylcholine and carbachol), a Ca2+ channel agonist (S-Bay K8644), an HCN channel antagonist (ivabradine) and K+ channel antagonists (4-AP and vernakalant). We observed differential effects between atrial and ventricular hiPSC-CMs on contractile properties including beat rate, beat duration, contractile force and evidence of arrhythmias at a range of concentrations. As an excerpt of the compound analysis, S-Bay K8644 treatment showed an induced concentration-dependent transient increase in beat duration of atrial hiPSC-CMs, whereas ventricular cells showed a physiological increase in beat rate over time. Carbachol treatment produced marked effects on atrial cells, such as increased beat duration alongside a decrease in beat rate over time, but only minimal effects on ventricular cardiomyocytes. In the context of this chamber-specific pharmacology, we not only add to contractile characterization of hiPSC-CMs but propose a multi-well platform for medium-throughput early compound screening. Overall, these insights illustrate the key pharmacological differences between chamber-specific cardiomyocytes and their application on a multi-well contractility platform to gain insights for in vitro cardiac liability studies and disease modelling.
Asunto(s)
Atrios Cardíacos , Ventrículos Cardíacos , Células Madre Pluripotentes Inducidas , Contracción Miocárdica , Miocitos Cardíacos , Miocitos Cardíacos/efectos de los fármacos , Miocitos Cardíacos/fisiología , Humanos , Células Madre Pluripotentes Inducidas/efectos de los fármacos , Atrios Cardíacos/efectos de los fármacos , Atrios Cardíacos/citología , Contracción Miocárdica/efectos de los fármacos , Contracción Miocárdica/fisiología , Ventrículos Cardíacos/efectos de los fármacos , Ventrículos Cardíacos/citología , Receptores Acoplados a Proteínas G/metabolismo , Receptores Acoplados a Proteínas G/agonistas , Desarrollo de Medicamentos/métodos , Canales Iónicos/efectos de los fármacos , Células Cultivadas , Evaluación Preclínica de Medicamentos/métodos , Carbacol/farmacología , Sistemas MicrofisiológicosRESUMEN
INTRODUCTION: Cardiac implantable electrical devices are able to affect kidney function through hemodynamic improvements. The cardiac contractility modulation (CCM) is a device-based therapy option for patients with symptomatic chronic heart failure (HF) despite optimized medical treatment. The long-term cardiorenal interactions for CCM treated patients are yet to be described. METHODS: CCM recipients (n = 187) from the Mannheim Cardiac Contractility Modulation Observational Study (MAINTAINED) were evaluated in the long-term (up to 60 months) for changes in serum creatinine, estimated glomerular filtration rate (eGFR), other surrogate markers of kidney function, and the chronic kidney disease (CKD) stage distribution. With regard to kidney function at baseline, the patients were furthermore grouped to either advanced CKD (aCKD, CKD stage ≥3, eGFR≤59 mL/min/1.73 m2, n = 107) or preserved kidney function and mild CKD (pCKD, CKD stages 1-2, eGFR≥60 mL/min/1.73 m2, n = 80). The groups were compared for differences regarding kidney function, New York Heart Association classification (NYHA), biventricular systolic function, HF hospitalizations and other parameters in the long-term (60 months). RESULTS: CKD stage distribution remained stable during the entire follow-up (p = 0.65). An increase in serum creatinine (1.47 ± 1 vs. 1.6±1 mg/dL) with a corresponding decline of eGFR (58.2 ± 23.4 vs. 54.2 ± 24.4 mL/min/1.73 m2, both p < 0.05) were seen after 60 months but not before for the total cohort, which was only significant in pCKD patients in terms of group comparison. Mean survival (54.3 ± 1.3 vs. 55.3 ± 1.2 months, p = 0.53) was comparable in both groups. Improvements in NYHA (3.11 ± 0.46 vs. 2.94 ± 0.41-2.28 ± 0.8 vs. 1.94 ± 0.6) and LVEF (24.8 ± 7.1 vs. 22.9 ± 6.6-31.1 ± 11.4 vs. 35.5 ± 11.1%) were likewise similar after 60 months (both p < 0.05). The aCKD patients suffered from more HF hospitalizations and ventricular tachycardias during the entire follow-up period (both p < 0.05). CONCLUSIONS: The kidney function parameters and CKD stage distribution might remain stable in CCM treated HF patients in the long-term, who experience improvements in LVEF and functional status, regardless of their kidney function before. An impaired kidney function might be associated with further cardiovascular comorbidities and more advanced HF before CCM, and could be an additional risk factor of HF complications afterward.