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1.
Heart Vessels ; 38(9): 1172-1180, 2023 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-37074476

RESUMEN

Earlier intervention for pulmonary hypertension (PH) has been reported to improve the prognosis of patients with connective tissue disease (CTD). However, it is not fully elucidated how rapidly PH develops in patients showing normal mean pulmonary arterial pressure (mPAP) at the index investigation. We evaluated 191 CTD patients with normal mPAP retrospectively. The mPAP was estimated by the formerly defined method employing echocardiography (mPAPecho). We investigated predictive factors that predict increasing mPAPecho at follow-up transthoracic echocardiography (TTE) using uni- and multi variable analysis. The mean age was 61.5 years old, and 160 patients were female. The percentage of patients in whom mPAPecho exceeded 20 mmHg at follow-up TTE was 38%. Multivariable analysis revealed that acceleration time/ejection time (AcT/ET) measured at the right ventricular outflow tract at initial TTE was independently associated with the consequent increase of mPAPecho at the follow-up TTE. When using 0.43 of best cutoff value in AcT/ET calculated by receiver operating characteristic analysis, the change in mPAPecho in patients with low AcT/ET was significantly higher than in those with high AcT/ET (3.05 mmHg in patients with AcT/ET < 0.43 and 1.00 mmHg in patients with AcT/ET ≥ 0.43, p < 0.001). Thirty-eight percent of CTD patients who show the normal estimated mPAP by TTE develop gradual elevation of mPAP to the level to consider early intervention within 2 years. AcT/ET at initial TTE can predict increasing mPAP at follow-up TTE.


Asunto(s)
Enfermedades del Tejido Conjuntivo , Hipertensión Pulmonar , Humanos , Femenino , Persona de Mediana Edad , Masculino , Arteria Pulmonar/diagnóstico por imagen , Valores de Referencia , Estudios Retrospectivos , Cateterismo Cardíaco/métodos , Enfermedades del Tejido Conjuntivo/complicaciones , Enfermedades del Tejido Conjuntivo/diagnóstico , Ecocardiografía/métodos , Hipertensión Pulmonar/diagnóstico por imagen , Hipertensión Pulmonar/etiología
2.
Heart Vessels ; 32(11): 1410-1414, 2017 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-28669019

RESUMEN

The interaction among heart failure (HF), chronic kidney disease (CKD), and anemia is called cardio-renal anemia syndrome. The mechanism of anemia in cardio-renal anemia syndrome is complex and remains completely unknown. We have previously reported that impaired intestinal iron transporters may contribute to the mechanism of anemia in HF using in vivo HF model rats. In this study, we assessed intestinal iron transporters in CKD model rats to investigate the association of intestinal iron transporters in the mechanism of cardio-renal anemia syndrome. CKD was induced by 5/6 nephrectomy in Sprague-Dawley rats. Sham-operated rats served as a control. After 24-week surgery, CKD rats exhibited normocytic normochromic anemia and normal serum erythropoietin levels despite of anemia. Serum iron levels were decreased in CKD rats compared with the controls. Of interest, intestinal expression of critical iron importers, such as duodenal cytochrome b (Dcyt-b) and divalent metal transporter 1 (DMT-1), was decreased in CKD rats compared with the controls. On the other hand, intestinal expression of ferroportin, an intestinal iron exporter, was not different in the control and CKD groups. Moreover, hepatic expression of hepcidin, a regulator of iron homeostasis, did not differ between the control and CKD groups. These results suggest that impaired intestinal expression of Dcyt-b and DMT-1 might be associated with the reduction of an iron uptake in CKD. Taken together, impaired these intestinal iron transporters may become a novel therapeutic target for cardio-renal anemia syndrome.


Asunto(s)
Anemia/genética , Síndrome Cardiorrenal/genética , Proteínas de Transporte de Catión/genética , Citocromos b/genética , Duodeno/metabolismo , Regulación de la Expresión Génica , ARN/genética , Anemia/metabolismo , Animales , Síndrome Cardiorrenal/metabolismo , Proteínas de Transporte de Catión/biosíntesis , Citocromos b/biosíntesis , Modelos Animales de Enfermedad , Masculino , Ratas , Ratas Sprague-Dawley , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa
3.
Int Heart J ; 58(2): 232-237, 2017 Apr 06.
Artículo en Inglés | MEDLINE | ID: mdl-28320992

RESUMEN

Although adaptive servo-ventilation (ASV) therapy has beneficial effects on chronic heart failure (CHF), a relatively large number of CHF patients cannot undergo ASV therapy due to general discomfort from the mask and/or positive airway pressure. The present study aimed to clarify baseline patient characteristics which are associated with the smooth introduction of ASV treatment in stable CHF inpatients.Thirty-two consecutive heart failure (HF) inpatients were enrolled (left ventricular ejection fraction (LVEF) < 45%, estimated glomerular filtration rate (eGFR) > 10 mL/minute/1.73m2, and apnea-hypopnea index < 30/hour). After the patients were clinically stabilized on optimal therapy, they underwent portable polysomnography and echocardiography, and then received ASV therapy. The patients were divided into two groups: a smooth introduction group (n = 18) and non-smooth introduction group (n = 14). Smooth introduction of ASV treatment was defined as ASV usage for 4 hours and more on the first night. Univariate analysis showed that the smooth introduction group differed significantly from the non-smooth introduction group in age, hemoglobin level, eGFR, HF origin, LVEF, right ventricular (RV) diastolic dimension (RVDd), RV dp/dt, and RV fractional shortening. Multivariate analyses revealed that RVDd, eGFR, and LVEF were independently associated with smooth introduction. In addition, RVDd and eGFR seemed to be better diagnostic parameters for longer usage for ASV therapy according to the analysis of receiver operating characteristics curves.RV enlargement, eGFR, and LVEF are associated with the smooth introduction of ASV therapy in CHF inpatients.


Asunto(s)
Insuficiencia Cardíaca/terapia , Respiración Artificial/métodos , Adulto , Anciano , Anciano de 80 o más Años , Enfermedad Crónica , Femenino , Tasa de Filtración Glomerular , Humanos , Hipertrofia Ventricular Derecha , Masculino , Persona de Mediana Edad , Estudios Prospectivos
4.
Int Heart J ; 58(3): 393-399, 2017 May 31.
Artículo en Inglés | MEDLINE | ID: mdl-28484123

RESUMEN

We hypothesized that the effects of adaptive servo-ventilation (ASV) therapy were influenced by right-sided heart performance. This study aimed to clarify the interaction between the effects of ASV and right-sided heart performance in patients with stable heart failure (HF) with reduced ejection fraction (HFrEF).Twenty-six stable HF inpatients (left ventricular ejection fraction < 0.45, without moderate to severe mitral regurgitation (MR) were analyzed. Echocardiography was performed before and after 30 minutes of ASV. ASV increased stroke volume index (SVI) in 14 patients (30.0 ± 11.9 to 41.1 ± 16.1 mL/m2) and reduced SVI in 12 patients (36.0 ± 10.1 to 31.9 ± 12.2 mL/m2). Multivariate linear regression analysis revealed that tricuspid annular plane systolic excursion (TAPSE) before ASV was an independent association factor for (SV during ASV - SV before ASV)/LVEDV × 100 (%) (%ΔSV/LVEDV). ROC analysis of TAPSE for %ΔSV/LVEDV > 0 showed that the cut-off point was 16.5 mm. All patients were divided into 2 groups according to the TAPSE value. Although no significant differences were found in the baseline characteristics and blood tests, there were significant differences in tricuspid lateral annular systolic velocity, TAPSE, right atrial area, and right ventricular (RV) area before ASV between patients with TAPSE ≤ 16.5 mm and those with TAPSE > 16.5 mm. Interestingly, ASV reduced RV area and increased TAPSE in patients with TAPSE ≤ 16.5 mm, while it reduced TAPSE in those > 16.5 mm.ASV therapy has the potential to increase SVI in stable HFrEF patients with low TAPSE.


Asunto(s)
Insuficiencia Cardíaca Sistólica/terapia , Ventrículos Cardíacos/fisiopatología , Insuficiencia de la Válvula Mitral/complicaciones , Respiración con Presión Positiva/métodos , Volumen Sistólico/fisiología , Válvula Tricúspide/fisiopatología , Función Ventricular Derecha/fisiología , Ecocardiografía , Femenino , Estudios de Seguimiento , Insuficiencia Cardíaca Sistólica/etiología , Insuficiencia Cardíaca Sistólica/fisiopatología , Ventrículos Cardíacos/diagnóstico por imagen , Humanos , Masculino , Persona de Mediana Edad , Válvula Mitral/diagnóstico por imagen , Válvula Mitral/fisiopatología , Insuficiencia de la Válvula Mitral/diagnóstico , Insuficiencia de la Válvula Mitral/fisiopatología , Estudios Prospectivos , Curva ROC , Sístole , Factores de Tiempo , Válvula Tricúspide/diagnóstico por imagen
5.
Heart Vessels ; 31(2): 222-9, 2016 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-25573257

RESUMEN

Several epidemiologic studies have reported that body iron status and dietary iron intake are related to an increased risk of acute myocardial infarction (MI). However, it is completely unknown whether dietary iron reduction impacts the development of left ventricular (LV) remodeling after MI. Here, we investigate the effect of dietary iron restriction on the development of LV remodeling after MI in an experimental model. MI was induced in C57BL/6 J mice (9-11 weeks of age) by the permanent ligation of the left anterior descending coronary artery (LAD). At 2 weeks after LAD ligation, mice were randomly divided into two groups and were given a normal diet or an iron-restricted diet for 4 weeks. Sham operation without LAD ligation was also performed as controls. MI mice exhibited increased LV dilatation and impaired LV systolic function that was associated with cardiomyocyte hypertrophy and interstitial fibrosis in the remote area, as compared with the controls at 6 weeks after MI. In contrast, dietary iron restriction attenuated LV dilatation and impaired LV systolic function coupled to cardiomyocyte hypertrophy and interstitial fibrosis in the remote area. Importantly, cardiac expression of cellular iron transport proteins, transferrin receptor 1 and divalent metal transporter 1 was increased in the remote area of MI mice compared with the controls. Dietary iron restriction attenuated the development of LV remodeling after MI in mice. Cellular iron transport might play a role in the pathophysiological mechanism of LV remodeling after MI.


Asunto(s)
Enfermedades Carenciales/metabolismo , Deficiencias de Hierro , Infarto del Miocardio/metabolismo , Miocardio/metabolismo , Función Ventricular Izquierda , Remodelación Ventricular , Animales , Cardiomegalia/metabolismo , Cardiomegalia/patología , Proteínas de Transporte de Catión/metabolismo , Modelos Animales de Enfermedad , Fibrosis , Masculino , Ratones Endogámicos C57BL , Infarto del Miocardio/patología , Infarto del Miocardio/fisiopatología , Miocardio/patología , Receptores de Transferrina/metabolismo
6.
Heart Vessels ; 31(11): 1826-1833, 2016 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-26825736

RESUMEN

Left ventricular (LV) diastolic dysfunction is associated with hypertension and hyperuricemia. However, it is not clear whether the L- and N-type calcium channel blocker will improve LV diastolic dysfunction through the reduction of uric acid. The aim of this study was to investigate the effects of anti-hypertensive therapy, the L- and N-type calcium channel blocker, cilnidipine or the L-type calcium channel blocker, amlodipine, on left atrial reverse remodeling and uric acid in hypertensive patients. We studied 62 patients with untreated hypertension, randomly assigned to cilnidipine or amlodipine for 48 weeks. LV diastolic function was assessed with the left atrial volume index (LAVI), mitral early diastolic wave (E), tissue Doppler early diastolic velocity (E') and the ratio (E/E'). Serum uric acid levels were measured before and after treatment. After treatment, systolic and diastolic blood pressures equally dropped in both groups. LAVI, E/E', heart rate and uric acid levels decreased at 48 weeks in the cilnidipine group but not in the amlodipine group. The % change from baseline to 48 weeks in LAVI, E wave, E/E' and uric acid levels were significantly lower in the cilnidipine group than in the amlodipine group. Larger %-drop in uric acid levels were associated with larger %-reduction of LAVI (p < 0.01). L- and N-type calcium channel blocker but not L-type calcium channel blocker may improve LV diastolic function in hypertensive patients, at least partially through the decrease in uric acid levels.


Asunto(s)
Amlodipino/uso terapéutico , Función del Atrio Izquierdo/efectos de los fármacos , Remodelación Atrial/efectos de los fármacos , Bloqueadores de los Canales de Calcio/uso terapéutico , Canales de Calcio Tipo L/efectos de los fármacos , Canales de Calcio Tipo N/efectos de los fármacos , Dihidropiridinas/uso terapéutico , Hipertensión/tratamiento farmacológico , Hiperuricemia/tratamiento farmacológico , Ácido Úrico/sangre , Disfunción Ventricular Izquierda/tratamiento farmacológico , Biomarcadores/sangre , Presión Sanguínea/efectos de los fármacos , China , Diástole , Regulación hacia Abajo , Ecocardiografía Doppler , Femenino , Humanos , Hipertensión/sangre , Hipertensión/diagnóstico por imagen , Hipertensión/fisiopatología , Hiperuricemia/sangre , Hiperuricemia/diagnóstico , Masculino , Persona de Mediana Edad , Factores de Tiempo , Resultado del Tratamiento , Disfunción Ventricular Izquierda/diagnóstico por imagen , Disfunción Ventricular Izquierda/fisiopatología , Función Ventricular Izquierda/efectos de los fármacos
7.
Heart Vessels ; 31(12): 2074-2079, 2016 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-27311944

RESUMEN

Several recent observations provide the association of iron deficiency with pulmonary hypertension (PH) in human and animal studies. However, it remains completely unknown whether PH leads to iron deficiency or iron deficiency enhances the development of PH. In addition, it is obscure whether iron is associated with the development of pulmonary vascular remodeling in PH. In this study, we investigate the impacts of dietary iron restriction on the development of hypoxia-induced pulmonary vascular remodeling in mice. Eight- to ten-week-old male C57BL/6J mice were exposed to chronic hypoxia for 4 weeks. Mice exposed to hypoxia were randomly divided into two groups and were given a normal diet or an iron-restricted diet. Mice maintained in room air served as normoxic controls. Chronic hypoxia induced pulmonary vascular remodeling, while iron restriction led a modest attenuation of this change. In addition, chronic hypoxia exhibited increased RV systolic pressure, which was attenuated by iron restriction. Moreover, the increase in RV cardiomyocyte cross-sectional area and RV interstitial fibrosis was observed in mice exposed to chronic hypoxia. In contrast, iron restriction suppressed these changes. Consistent with these changes, RV weight to left ventricular + interventricular septum weight ratio was increased in mice exposed to chronic hypoxia, while this increment was inhibited by iron restriction. Taken together, these results suggest that iron is associated with the development of hypoxia-induced pulmonary vascular remodeling in mice.


Asunto(s)
Hipertensión Pulmonar/etiología , Hipoxia/complicaciones , Hierro de la Dieta/metabolismo , Hierro/metabolismo , Arteria Pulmonar/metabolismo , Remodelación Vascular , Animales , Modelos Animales de Enfermedad , Hipertensión Pulmonar/metabolismo , Hipertensión Pulmonar/patología , Hipertensión Pulmonar/fisiopatología , Hipertrofia Ventricular Derecha/etiología , Hipertrofia Ventricular Derecha/metabolismo , Hipertrofia Ventricular Derecha/fisiopatología , Hipertrofia Ventricular Derecha/prevención & control , Hipoxia/metabolismo , Hipoxia/patología , Hipoxia/fisiopatología , Deficiencias de Hierro , Masculino , Ratones Endogámicos C57BL , Arteria Pulmonar/patología , Arteria Pulmonar/fisiopatología , Factores de Tiempo , Disfunción Ventricular Derecha/etiología , Disfunción Ventricular Derecha/metabolismo , Disfunción Ventricular Derecha/fisiopatología , Disfunción Ventricular Derecha/prevención & control , Función Ventricular Derecha , Remodelación Ventricular
8.
J Card Fail ; 20(5): 295-301, 2014 May.
Artículo en Inglés | MEDLINE | ID: mdl-24462960

RESUMEN

BACKGROUND: Theoretically, salt supplementation should promote diuresis through increasing the glomerular filtration rate (GFR) during treatment of acute decompensated heart failure (ADHF) even with low-dose furosemide; however, there is little evidence to support this idea. METHODS AND RESULTS: This was a prospective, randomized, open-label, controlled trial that compared the diuretic effectiveness of salt infusion with that of glucose infusion supplemented with low-dose furosemide in 44 consecutive patients with ADHF. Patients were randomly administered 1.7% hypertonic saline solution supplemented with 40 mg furosemide (salt infusion group) or glucose supplemented with 40 mg furosemide (glucose infusion group). Our major end points were 24-hour urinary volume and GFR. Urinary volume was greater in the salt infusion group than in the glucose infusion group (2,701 ± 920 vs 1,777 ± 797 mL; P < .001). There was no significant difference in the estimated GFR at baseline. Creatinine clearance for 24 h was greater in the salt infusion group than in the glucose infusion group (63.5 ± 52.6 vs 39.0 ± 26.3 mL min(-1) 1.73 m(-2); P = .048). CONCLUSIONS: Salt supplementation rather than salt restriction evoked favorable diuresis through increasing GFR. The findings support an efficacious novel approach of the treatment of ADHF.


Asunto(s)
Furosemida/administración & dosificación , Insuficiencia Cardíaca/diagnóstico , Insuficiencia Cardíaca/tratamiento farmacológico , Cloruro de Sodio/administración & dosificación , Enfermedad Aguda , Anciano , Anciano de 80 o más Años , Quimioterapia Combinada , Femenino , Tasa de Filtración Glomerular/efectos de los fármacos , Tasa de Filtración Glomerular/fisiología , Glucosa/administración & dosificación , Insuficiencia Cardíaca/fisiopatología , Humanos , Infusiones Intravenosas , Masculino , Persona de Mediana Edad , Estudios Prospectivos , Solución Salina Hipertónica , Resultado del Tratamiento
9.
Heart Vessels ; 29(3): 343-53, 2014 May.
Artículo en Inglés | MEDLINE | ID: mdl-23660866

RESUMEN

The mitral early to late diastolic flow velocity ratio (E/A ratio) is age-dependent. It has been considered that its age dependency reflects the age-related lengthening of left ventricular (LV) relaxation; however, the change in E/A ratio is far larger than that expected from those in LV relaxation. We hypothesized that an age-related reduction of the parasympathetic activity increases left atrial (LA) contractility, and that this accounts for the age-related change in E/A ratio. (1) Exercise stress test was performed in 61 normal subjects (age range, 8-80 years, mean, 40 years) to assess heart rate (HR) recovery because slowed HR recovery indicates lowered parasympathetic activity. There were good interrelations among age, E/A ratio, and HR recovery. Among those aged ≤30 years, the age no longer correlated with E/A ratio or HR recovery, but there was a significant correlation between HR recovery and E/A ratio (r = 0.44, p < 0.05). (2) Pulsed Doppler and two-dimensional speckle tracking echocardiography (2DSTE) were performed before and after administration of parasympathetic blockade (atropine) in ten young healthy subjects. LA booster pump function was assessed with LA emptying index calculated by 2DSTE. LA emptying index was calculated from ([LA volume before the atrial contraction - minimal LA volume]/LA volume before the atrial contraction) × 100. Atropine increased mitral A velocity (p < 0.001) and LA emptying index (p < 0.05) along with a decrease in E/A ratio (p < 0.001). Parasympathetic withdrawal enhances LA contraction and increases mitral A velocity, which likely cause a reciprocal decrease in mitral E velocity and E/A ratio. Thus, parasympathetic deactivation with aging should be closely involved in the age-related change in mitral E/A ratio.


Asunto(s)
Envejecimiento , Válvula Mitral/inervación , Sistema Nervioso Parasimpático/fisiología , Adolescente , Adulto , Factores de Edad , Anciano , Anciano de 80 o más Años , Función del Atrio Izquierdo , Atropina/administración & dosificación , Niño , Ecocardiografía Doppler de Pulso , Prueba de Esfuerzo , Femenino , Voluntarios Sanos , Frecuencia Cardíaca , Humanos , Masculino , Persona de Mediana Edad , Válvula Mitral/diagnóstico por imagen , Antagonistas Muscarínicos/administración & dosificación , Contracción Miocárdica , Sistema Nervioso Parasimpático/efectos de los fármacos , Recuperación de la Función , Factores de Tiempo , Adulto Joven
10.
Phys Ther Res ; 27(1): 21-34, 2024.
Artículo en Inglés | MEDLINE | ID: mdl-38690533

RESUMEN

OBJECTIVE: There are few analyses of the current status of and responses to acute deteriorations encountered by physiotherapists, occupational therapists, and speech-language pathologists (rehabilitation professions [RPs]). The purpose of this study was to analyze the responses of RPs to acute deterioration in patients using the functional resonance analysis method (FRAM) based on the descriptions in "the Medical Accident Database". METHODS: Subjects were 413 cases with medical incidents reported by RPs to the database from 2012 to 2021. Life-threatening cases with changes in consciousness, circulation, and respiration were selected. Descriptions regarding findings assessed by RPs and support team, and requests for assistance were extracted. We also attempted to construct appropriate respond in RPs by using the FRAM. RESULTS: Thirty-nine cases of acute deterioration were included in the analysis, and descriptions by RPs of consciousness (35 cases), circulation (18 cases), and respiration (36 cases) were identified. Blood pressure and percutaneous oxygen saturation measurement were frequently presented in the assessment by RPs, whereas the support team assessed cardiac arrest and respiratory arrest in high frequency. The FRAM analysis indicated that appropriate and rapid post-response by RPs requires patient information in prior, appropriate assessment and integration/interpretation. CONCLUSION: We attempted to identify problems analyzing the response by RPs to acute deterioration using the database and construct an appropriate response model. It resulted that RPs need to obtain patient information in advance and integrate/interpret it appropriately based on accurate assessment of conscious, circulation and respiration for rapid response. A model including integration/interpretation for appropriate post-response by RPs was constructed using the FRAM.

11.
Biochem Biophys Res Commun ; 436(2): 145-51, 2013 Jun 28.
Artículo en Inglés | MEDLINE | ID: mdl-23707944

RESUMEN

Pulmonary hypertension (PH) is characterized by pulmonary vascular remodeling leading to right ventricular (RV) failure. Recently, iron deficiency is reported to be prevalent in patients with PH. However, the mechanism by which iron deficiency occurs in patients with PH remains unknown. Here, we investigated the effects of dietary iron restriction on the development of monocrotaline-induced pulmonary vascular remodeling and the involved mechanisms. Male Sprague-Dawley rats were subcutaneously injected with monocrotaline (60mg/kg). Afterwards, monocrotaline-injected rats were randomly divided into two groups and were given a normal diet (n=6) or an iron-restricted diet (n=6) for 4weeks. Saline-injected rats given a normal diet were served as controls (n=6). Monocrotaline-injected rats showed pulmonary vascular remodeling, increased RV pressure, RV hypertrophy, and decreased RV ejection fraction, followed by RV failure after 4weeks. In contrast, iron restriction attenuated the development of pulmonary vascular remodeling and RV failure. Of interest, expression of cellular iron transport protein, transferrin receptor 1 was increased in the pulmonary remodeled artery and the failing right ventricle of monocrotaline-injected rats, as compared with the controls. Moreover, a key regulator of iron homeostasis, hepcidin gene expression was increased in the failing right ventricle of monocrotaline-injected rats. Iron restriction attenuated the development of monocrotaline-induced pulmonary vascular remodeling and RV failure. Cellular iron transport might be involved in the pathophysiology of PH and PH induced RV failure.


Asunto(s)
Hipertensión Pulmonar/fisiopatología , Hipertrofia Ventricular Derecha/fisiopatología , Hierro de la Dieta/farmacología , Pulmón/efectos de los fármacos , Disfunción Ventricular Derecha/fisiopatología , Animales , Péptidos Catiónicos Antimicrobianos/genética , Péptidos Catiónicos Antimicrobianos/metabolismo , Expresión Génica/efectos de los fármacos , Hepcidinas , Hipertensión Pulmonar/inducido químicamente , Hipertrofia Ventricular Derecha/inducido químicamente , Inmunohistoquímica , Hierro de la Dieta/administración & dosificación , Estimación de Kaplan-Meier , Pulmón/metabolismo , Pulmón/fisiopatología , Masculino , Monocrotalina , Arteria Pulmonar/efectos de los fármacos , Arteria Pulmonar/metabolismo , Arteria Pulmonar/fisiopatología , Distribución Aleatoria , Ratas , Ratas Sprague-Dawley , Receptores de Transferrina/genética , Receptores de Transferrina/metabolismo , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Disfunción Ventricular Derecha/inducido químicamente , Función Ventricular Derecha/efectos de los fármacos
12.
Heliyon ; 9(2): e13181, 2023 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-36747544

RESUMEN

Plasma renin activity (PRA) level at admission is reported to be a prognostic predictor of acute decompensated heart failure (ADHF) patients. Although PRA is affected during hospitalization by several factors including fluid volume and drug titration, whether the changes in PRA levels during hospitalization (ΔPRA) are associated with prognosis of ADHF patients are largely unknown. PURPOSE: Investigate the predictive impact of ΔPRA on the prognosis of ADHF patients with reduced ejection fraction (HFrEF) and mildly reduced ejection fraction (HFmrEF). METHODS: Retrospectively analyzed consecutive 116 HFrEF and HFmrEF patients admitted for ADHF. PRA measurements were acquired at admission and at discharge. The primary outcome was a composite of cardiovascular death and HF re-hospitalization. RESULTS: Out of 116 patients, 85 had PRA measurements both at admission and at discharge. Compared to admission, PRA level was significantly higher at discharge (0.8 (IQR 0.3-2.2) to 2.8 (IQR 1.0-7.2), p < 0.001). Tertiary groups ranked by PRA level on admission showed trend of poor prognosis in order of high, mid, and low PRA level (p = 0.07). On the contrary, PRA level at discharge significantly differentiated the prognosis and was poor in order of high, low, and mid (p = 0.026). Next, when the participants were divided into tertiary groups ranked by ΔPRA, prognosis worsened in the order of "minimal", "decreasing", and the "increasing" tier. Cubic splines analysis also indicate a similar tendency. CONCLUSIONS: In ADHF patients with HFrEF and HFmrEF, patients with minimal ΔPRA showed the better prognosis over the those with either increasing or decreasing.

13.
Eur J Echocardiogr ; 10(2): 278-81, 2009 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-18786948

RESUMEN

AIMS: We assessed the comparative value of measurements of tissue Doppler early diastolic mitral annular velocity (E'), left atrial diameter (LAD), and left atrial volume (LAV) in patients with possible heart failure (HF) but with normal left ventricular (LV) ejection fraction (EF) and mitral flow velocity pattern. METHODS AND RESULTS: We determined LAV and LAD indexes in addition to the ratio of peak early diastolic mitral flow velocity (E) to E' (E/E' ratio) in 91 patients with all three of the followings: HF, LVEF of greater than 55%, and normal mitral E/A ratio between 0.8 and 1.5. Twenty healthy subjects were used as controls. E/E' ratio was abnormal (>1.5) in 38 of the 91 patients (sensitivity=44%). LAV index was 32 mL/m(2) or greater in 71 of the 91 patients (sensitivity=78%), while LAD index was 27 mm/m(2) or greater in 81 of 91 patients (sensitivity=89%). The area under the curve by receiver-operator curve analyses was 0.995 for LA volume index, 0.998 for LAD index, and 0.885 for E/E' ratio. CONCLUSION: LAV and LAD indexes are more useful in detecting with HF and normal EF patients than E' related parameters.


Asunto(s)
Reserva del Flujo Fraccional Miocárdico , Atrios Cardíacos/patología , Insuficiencia Cardíaca/patología , Válvula Mitral/patología , Volumen Sistólico , Función Ventricular Izquierda , Diástole , Femenino , Insuficiencia Cardíaca/diagnóstico por imagen , Humanos , Masculino , Persona de Mediana Edad , Curva ROC , Estudios Retrospectivos , Sensibilidad y Especificidad , Ultrasonografía
15.
Int J Cardiol ; 243: 396-403, 2017 Sep 15.
Artículo en Inglés | MEDLINE | ID: mdl-28526544

RESUMEN

BACKGROUND: Interleukin-18 (IL-18) neutralization protects against lipopolysaccharide (LPS)-induced injuries, including myocardial dysfunction. However, the mechanism is yet to be fully elucidated. The aim of the present study was to determine whether IL-18 gene deletion prevents sepsis-induced cardiac dysfunction and to elucidate the potential mechanisms underlying IL-18-mediated cardiotoxicity by LPS. METHODS AND RESULTS: Ten-week-old male wild-type (WT) and IL-18 knockout (IL-18 KO) mice were intraperitoneally administered LPS. Serial echocardiography showed better systolic pump function and less left ventricular (LV) dilatation in LPS-treated IL-18 KO mice compared with those in LPS-treated WT mice. LPS treatment significantly decreased the levels of phospholamban (PLN) and Akt phosphorylation in WT mice compared with those in saline-treated WT mice, while the LPS-induced decrease in the phosphorylation levels was attenuated in IL-18 KO mice compared with that in WT mice. IL-18 gene deletion also attenuated an LPS-induced increase of type 2 protein phosphatase 2A (PP2A) activity, a molecule that dephosphorylates PLN and Akt. There was no difference in type 1 protein phosphatase (PP1) activity. To address whether IL-18 affects PLN and Akt phosphorylation via PP2A activation in cardiomyocytes, rat neonatal cardiac myocytes were cultured and stimulated using 100ng/ml of recombinant rat IL-18. Exogenous IL-18 decreased the level of PLN and Akt phosphorylation in cardiomyocytes. PP2A activity but not PP1 activity was increased by IL-18 stimulation in cardiomyocytes. CONCLUSIONS: IL-18 plays a pivotal role in advancing sepsis-induced cardiac dysfunction, and the mechanisms underlying IL-18-mediated cardiotoxicity potentially involve the regulation of PLN and Akt phosphorylation through PP2A activity.


Asunto(s)
Eliminación de Gen , Cardiopatías/metabolismo , Interleucina-18/deficiencia , Interleucina-18/genética , Proteína Fosfatasa 2/metabolismo , Sepsis/metabolismo , Animales , Células Cultivadas , Activación Enzimática/fisiología , Cardiopatías/genética , Cardiopatías/prevención & control , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados , Miocitos Cardíacos/metabolismo , Proteína Fosfatasa 2/antagonistas & inhibidores , Ratas , Ratas Sprague-Dawley , Sepsis/genética , Sepsis/prevención & control
16.
Gynecol Oncol Rep ; 16: 11-3, 2016 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-27331128

RESUMEN

•An ovarian clear cell carcinoma patient showed malignant pericardial and pleural effusion.•She subsequently experienced pulmonary embolism due to cancer progression.•Pericardial and pleural effusion were successfully treated using bevacizumab.

17.
Int J Cardiol ; 221: 302-9, 2016 Oct 15.
Artículo en Inglés | MEDLINE | ID: mdl-27404696

RESUMEN

BACKGROUND: In contrast to loop diuretics, tolvaptan does not cause neurohormonal activation in several animal heart failure models. However, it remains unknown whether chronic vasopressin type 2 receptor blockade exerts beneficial effects on mortality in murine heart failure after myocardial infarction (MI). In an experimental heart failure model, we tested the hypothesis that tolvaptan reduces myocardial remodeling and mortality. METHODS AND RESULTS: MI was induced in 9-week-old male C57Bl6/J by the left coronary artery ligation. In study 1, animals were randomly assigned to treatment with placebo or tolvaptan starting 14days post-MI. In study 2, animals were randomized to tolvaptan or furosemide+tolvaptan starting 14days post-MI. Interestingly, results showed lower survival rate in tolvaptan group compared to placebo. Tolvaptan group had higher serum osmolality, heavier body weight, more severe myocardial remodeling, and lung congestion at day 28 of drug administration compared to placebo. In study 2, addition of furosemide significantly reduced mortality rate seen with tolvaptan, and presented with decreased osmolality, myocardial remodeling, and lung congestion compared to tolvaptan-treated mice. Increase in proximal tubular expression of aquaporin 1, Angiotensin II, and vasopressin seen with tolvaptan treatments were normalized to basal levels, similar to levels in placebo-treated mice. CONCLUSIONS: Contrary to our hypothesis, tolvaptan was associated with increased mortality in murine heart failure after MI. This increase in lung congestion, myocardial remodeling, could be prevented by co-administration of furosemide, which resulted in normalized serum osmolality, neurohormonal activation, and renal aquaporin 1 expression, and hence decreased mortality post-MI.


Asunto(s)
Benzazepinas/administración & dosificación , Modelos Animales de Enfermedad , Insuficiencia Cardíaca/diagnóstico por imagen , Insuficiencia Cardíaca/mortalidad , Infarto del Miocardio/diagnóstico por imagen , Infarto del Miocardio/mortalidad , Remodelación Ventricular/efectos de los fármacos , Animales , Antagonistas de los Receptores de Hormonas Antidiuréticas/administración & dosificación , Antagonistas de los Receptores de Hormonas Antidiuréticas/efectos adversos , Benzazepinas/efectos adversos , Insuficiencia Cardíaca/inducido químicamente , Enfermedades Pulmonares/inducido químicamente , Enfermedades Pulmonares/diagnóstico por imagen , Enfermedades Pulmonares/mortalidad , Masculino , Ratones , Ratones Endogámicos C57BL , Mortalidad/tendencias , Infarto del Miocardio/inducido químicamente , Distribución Aleatoria , Factores de Tiempo , Tolvaptán , Remodelación Ventricular/fisiología
18.
Hypertens Res ; 39(12): 832-839, 2016 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-27439494

RESUMEN

Iron is a catalyst in the formation of reactive oxygen species. Oxidative stress is associated with the pathogenesis of both human and experimental animal models of renovascular hypertension. We hypothesized that iron is involved in the pathogenesis of renovascular hypertension and that iron restriction may affect the pathogenesis of renovascular hypertension via the inhibition of oxidative stress. Herein, we investigated the effect of iron restriction on hypertension and renal damage in a rat model of two-kidney one-clip (2K1C) renovascular hypertension. Renovascular hypertension was induced by 2K1C in male Sprague-Dawley rats. At the day of clipping, 2K1C rats were divided into untreated (2K1C) and dietary iron-restricted groups (2K1C+IR). The 2K1C rats showed hypertension after the day of clipping, whereas dietary iron restriction attenuated the development of hypertension. Vascular hypertrophy and the increased fibrotic area were suppressed in the 2K1C+IR group. The clipped kidney developed renal atrophy in both the 2K1C and 2K1C+IR groups after clipping. However, the unclipped kidney showed renal hypertrophy in the 2K1C and 2K1C+IR groups, and the extent was less in the 2K1C+IR group. The 2K1C rats exhibited glomerulosclerosis and tubulointerstitial fibrosis in the unclipped kidney, whereas these changes were attenuated by an iron-restricted diet. Importantly, proteinuria was decreased in the 2K1C+IR group, along with decreased urinary 8-hydroxy-2'-deoxyguanosine excretion and superoxide production of the unclipped kidney. Moreover, the expression of nuclear mineralocorticoid receptor in the unclipped kidney of the 2K1C rats was attenuated by iron restriction. These data indicate a novel effect of iron restriction on hypertension and renal damage in renovascular hypertension.


Asunto(s)
Hipertensión Renovascular/terapia , Deficiencias de Hierro , Hierro de la Dieta , Riñón/patología , 8-Hidroxi-2'-Desoxicoguanosina , Animales , Presión Sanguínea/fisiología , Desoxiguanosina/análogos & derivados , Desoxiguanosina/metabolismo , Frecuencia Cardíaca/fisiología , Hipertensión Renovascular/metabolismo , Hipertensión Renovascular/patología , Hipertensión Renovascular/fisiopatología , Riñón/fisiopatología , Masculino , Ratas , Ratas Sprague-Dawley , Receptores de Mineralocorticoides/metabolismo , Superóxidos/metabolismo , Resultado del Tratamiento
19.
Am J Hypertens ; 29(6): 713-8, 2016 06.
Artículo en Inglés | MEDLINE | ID: mdl-26419445

RESUMEN

BACKGROUND: Iron is associated with the pathophysiology of several cardiovascular diseases, including pulmonary hypertension (PH). In addition, disrupted pulmonary iron homeostasis has been reported in several chronic lung diseases. Transferrin receptor 1 (TfR1) plays a key role in cellular iron transport. However, the role of TfR1 in the pathophysiology of PH has not been well characterized. In this study, we investigate the role of TfR1 in the development of hypoxia-induced pulmonary vascular remodeling. METHODS: PH was induced by exposing wild-type (WT) mice and TfR1 hetero knockout mice to hypoxia for 4 weeks and evaluated via assessment of pulmonary vascular remodeling, right ventricular (RV) systolic pressure, and RV hypertrophy. In addition, we assessed the functional role of TfR1 in pulmonary artery smooth muscle cells in vitro. RESULTS: The morphology of pulmonary arteries did not differ between WT mice and TfR1 hetero knockout mice under normoxic conditions. In contrast, TfR1 hetero knockout mice exposed to 4 weeks hypoxia showed attenuated pulmonary vascular remodeling, RV systolic pressure, and RV hypertrophy compared with WT mice. In addition, the depletion of TfR1 by RNA interference attenuated human pulmonary artery smooth muscle cells proliferation induced by platelet-derived growth factor-BB (PDGF-BB) in vitro. CONCLUSIONS: These results suggest that TfR1 plays an important role in the development of hypoxia-induced pulmonary vascular remodeling.


Asunto(s)
Hipertensión Pulmonar/fisiopatología , Receptores de Transferrina/fisiología , Remodelación Vascular , Animales , Hipertensión Pulmonar/patología , Hipoxia/fisiopatología , Masculino , Ratones Noqueados , Miocitos del Músculo Liso/fisiología , Arteria Pulmonar/patología
20.
PLoS One ; 10(5): e0126611, 2015.
Artículo en Inglés | MEDLINE | ID: mdl-25962140

RESUMEN

BACKGROUND: Deep vein thrombosis (DVT) is a major cause of pulmonary thromboembolism and sudden death. Thus, it is important to consider the pathophysiology of DVT. Recently, iron has been reported to be associated with thrombotic diseases. Hence, in this study, we investigate the effects of dietary iron restriction on the process of thrombus resolution in a rat model of DVT. METHODS: We induced DVT in 8-week-old male Sprague-Dawley rats by performing ligations of their inferior venae cavae. The rats were then given either a normal diet (DVT group) or an iron-restricted diet (DVT+IR group). Thrombosed inferior venae cavae were harvested at 5 days after ligation. RESULTS: The iron-restricted diet reduced venous thrombus size compared to the normal diet. Intrathrombotic collagen content was diminished in the DVT+IR group compared to the DVT group. In addition, intrathrombotic gene expression and the activity of matrix metalloproteinase-9 were increased in the DVT+IR group compared to the DVT group. Furthermore, the DVT+IR group had greater intrathrombotic neovascularization as well as higher gene expression levels of urokinase-type plasminogen activator and tissue-type plasminogen activator than the DVT group. The iron-restricted diet decreased intrathrombotic superoxide production compared to the normal diet. CONCLUSIONS: These results suggest that dietary iron restriction affects the process of thrombus resolution in DVT.


Asunto(s)
Hierro de la Dieta/administración & dosificación , Trombosis/metabolismo , Trombosis de la Vena/metabolismo , Alimentación Animal , Animales , Quimiotaxis de Leucocito/inmunología , Colágeno/metabolismo , Modelos Animales de Enfermedad , Fibrinolisina/metabolismo , Hierro/metabolismo , Leucocitos/inmunología , Leucocitos/metabolismo , Masculino , Neovascularización Patológica/metabolismo , Estrés Oxidativo , Ratas , Superóxidos/metabolismo , Trombosis de la Vena/patología
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