Influence of intermittent fasting on myocardial infarction-induced cardiac remodeling.

BACKGROUND: Information on the role of intermittent fasting (IF) on pathologic cardiac remodeling is scarce. We compared the effects of IF before and after myocardial infarction (MI) on rat cardiac remodeling and survival. METHODS: Wistar rats were intermittently fasted (food available every other day) or fed ad libitum for 12 weeks and then divided into three groups: AL - fed ad libitum; AL/IF - fed AL before MI and IF after MI; and IF - fed IF before and after MI. Echocardiogram was performed before MI and 2 and 12 weeks after surgery. Isolated hearts were evaluated in Langendorff preparations. RESULTS: Before surgery, body weight (BW) was lower in IF than AL. Final BW was lower in AL/IF and IF than AL. Perioperative mortality did not change between AL (31.3%) and IF (27.3%). Total mortality was lower in IF than AL. Before surgery, echocardiographic parameters did not differ between groups. Two weeks after surgery, MI size did not differ between groups. Twelve weeks after MI, left ventricular (LV) diastolic posterior wall thickness was lower in AL/IF and IF than AL. The percentage of variation of echocardiographic parameters between twelve and two weeks showed that MI size decreased in all groups and the reduction was higher in IF than AL/IF. In Langendorff preparations, LV volume at zero end-diastolic pressure (V0; AL: 0.41 ± 0.05; AL/IF: 0.34 ± 0.06; IF: 0.28 ± 0.05 mL) and at 25 mmHg end-diastolic pressure (V25; AL: 0.61 ± 0.05; AL/IF: 0.54 ± 0.07; IF: 0.44 ± 0.06 mL) was lower in AL/IF and IF than AL and V25 was lower in IF than AL/IF. V0/BW ratio was lower in IF than AL and LV weight/V0 ratio was higher in IF than AL. Myocyte diameter was lower in AL/IF and IF than AL (AL: 17.3 ± 1.70; AL/IF: 15.1 ± 2.21; IF: 13.4 ± 1.49 µm). Myocardial hydroxyproline concentration and gene expression of ANP, Serca 2a, and α- and ß-myosin heavy chain did not differ between groups. CONCLUSION: Intermittent fasting initiated before or after MI reduces myocyte hypertrophy and LV dilation. Myocardial fibrosis and fetal gene expression are not modulated by feeding regimens. Benefit is more evident when intermittent fasting is initiated before rather than after MI.

Myocardial myostatin in spontaneously hypertensive rats with heart failure.

BACKGROUND: Myostatin has been shown to regulate skeletal and cardiac muscle growth. However, its status on long-term hypertrophied myocardium has not been addressed. The purpose of this study was to evaluate the expression of myocardial myostatin and its antagonist follistatin in spontaneously hypertensive rats (SHR) with heart failure. METHODS: Eighteen-month-old SHR were evaluated to identify clinical features of heart failure such as tachypnea/labored respiration and weight loss. After heart failure was detected, rats were subjected to echocardiogram and euthanized. Age-matched normotensive Wistar-Kyoto (WKY) rats were used as controls. Myostatin and follistatin protein expression was assessed by Western blotting. Statistical analysis was performed by Student's t test. RESULTS: All SHR (n=8) presented right ventricular hypertrophy and five had lung congestion. SHR had left chambers hypertrophy and dilation (left atrial diameter: WKY 5.73±0.59; SHR 7.28±1.17mm; p=0.004; left ventricular (LV) diastolic diameter/body weight ratio: WKY 19.6±3.1; SHR 27.7±4.7mm/kg; p=0.001), and LV systolic dysfunction (midwall fractional shortening: WKY 34.9±3.31; SHR 24.8±3.20%; p=0.003). Myocyte diameter (WKY 23.1±1.50, SHR 25.5±1.33µm; p=0.004) and myocardial interstitial collagen fraction (WKY 4.86±0.01; SHR 8.36±0.02%; p<0.001) were increased in the SHR. Myostatin (WKY 1.00±0.16; SHR 0.77±0.23 arbitrary units; p=0.035) and follistatin (WKY 1.00±0.35; SHR 0.49±0.18 arbitrary units; p=0.002) expression was lower in SHR. Myostatin and follistatin expression negatively correlated with LV diastolic diameter-to-body weight ratio and LV systolic diameter, and positively correlated with midwall fractional shortening. CONCLUSION: Myostatin and follistatin protein expression is reduced in the long-term hypertrophied myocardium from spontaneously hypertensive rats with heart failure.

Embolización prostática: un nuevo campo de actuación de la radiología intervencionista

Objetivos: Presentar nuestra experiencia inicial con la embolización prostática como tratamiento para la hiperplasia prostática benigna (HPB) desde la perspectiva técnica, y establecer la contribución del Diagnóstico por Imágenes. Materiales y métodos: Dieciséis pacientes con trastornos del tracto urinario inferior debidos a HPB realizaron embolización prostática. Todos respondieron cuestionarios específicos para determinar la severidad de la sintomatología y su impacto en la calidad de vida y función eréctil. Además, fueron evaluados con ecografía y resonancia magnética de pelvis, flujometría urinaria y antígeno prostático específico (PSA) antes y 30 días después del procedimiento. Resultados: La embolización fue exitosa en todos los pacientes (10 en forma bilateral y 6 en unilateral). El tiempo medio de duración del procedimiento fue de 82 minutos y el de la radioscopia de 38,5 min. Todos los procedimientos se llevaron a cabo en forma ambulatoria, con un tiempo medio de estancia hospitalaria de 6,4 h. El consumo medio de contraste radiológico fue de 175 ml. A los 30 días se verificó una reducción media de volumen prostático del 21%. Adicionalmente, se constató una mejoría clínica caracterizada, en promedio, por una disminución de 8 puntos en el cuestionario que mide los síntomas prostáticos, de 2 puntos en el cuestionario que calcula la calidad de vida y de 4 puntos en el cuestionario que sondea la función eréctil. La flujometría mejoró un 39% y el PSA se redujo un 26%. No hubo complicaciones mayores y solo se observaron efectos adversos menores en 9 pacientes. Conclusión: La embolización prostática para el tratamiento de la HPB demostró ser segura y eficiente en esta serie preliminar de pacientes.(AU)

Purposes: To present the initial experience with prostatic embolization as an alternative treatment for benign prostatic hyperplasia (BPH) from a technical perspective to establish the contribution provided by diagnostic imaging. Materials and methods: Sixteen patients with lower urinary tract symptoms due to benign prostatic hyperplasia underwent prostatic embolization. All patients were evaluated with specific questionnaires to determine the severity of symptoms, impact on quality of life and erectile function, ultrasound and MRI of the pelvis, urinary flowmetry and PSA before and 30 days after the procedure. Results: Embolization was successful in all patients; in 10 cases the procedure was performed bilaterally and in six, only one side was embolized. The average time for completion of the procedure was 82 minutes and the average fluoroscopy time was 38.5 minutes. All procedures were performed on an outpatient basis with an average hospital stay of 6.4 hours. The mean contrast medium used was 175 ml. At 30 days there was a mean reduction on prostate volume of 21%. Clinical improvement was characterized by a mean 8-point improvement on IPSS, 2 points on QOL and 4 points on IIEF. The uroflowmetry improved 39% and PSA dropped 26%. No major complications that implied unscheduled hospitalization or performing additional surgical procedures were seen. Minor adverse events were verifi ed in 9 patients. Conclusion: The initial results of prostatic embolization as an alternative treatment for BPH indicate that it is a safe and effective procedure to be consolidated as a new field of action of interventional radiology.(AU)

Embolización prostática: nuevo campo de actuación radiología intervencionista / Prostate embolization: a new field of action interventional radiology

Presentar nuestra experiencia inicial con la embolización prostática como tratamiento para la hiperplasia prostática benigna (HPB) desde la perspectiva técnica, y establecer lacontribución del Diagnóstico por Imágenes. Materiales y métodos: Dieciséis pacientes con trastornos del tracto urinario inferior debidos a HPB realizaron embolización prostática. Todos respondieron cuestionarios específicos para determinar la severidad de la sintomatología y su impacto en la calidad de vida y función eréctil. Además, fueron evaluados con ecografía y resonancia magnética de pelvis, flujometría urinariay antígeno prostático específico (PSA) antes y 30 días después del procedimiento. Resultados: La embolización fue exitosa en todos los pacientes (10 en forma bilateral y 6 enunilateral). El tiempo medio de duración del procedimiento fue de 82 minutos y el de la radioscopia de 38,5 min. Todos los procedimientos se llevaron a cabo en forma ambulatoria, con un tiempo medio de estancia hospitalaria de 6,4 h. El consumo medio de contraste radiológico fue de 175 ml. A los 30 días se verificó una reducción media de volumen prostático del 21%. Adicionalmente,se constató una mejoría clínica caracterizada, en promedio, por una disminución de 8 puntos en el cuestionario que mide los síntomas prostáticos, de 2 puntos en el cuestionarioque calcula la calidad de vida y de 4 puntos en el cuestionario que sondea la función eréctil. La flujometría mejoró un 39% y el PSA se redujo un 26%. No hubo complicaciones mayores y solo seobservaron efectos adversos menores en 9 pacientes. Conclusión: La embolización prostática para el tratamiento de la HPB demostró ser segura y eficiente en esta serie preliminar de pacientes...

Incidence of positive surgical margins after robotic assisted radical prostatectomy: Does the surgeon's experience have an influence on all pathological stages?

OBJECTIVE: The aim of this study is to analyze the clinical and surgical features of patients who underwent robotic-assisted radical prostatectomy (RARP) at our institution, and the impact of the surgeon's experience in the oncological results related to pathological stage. MATERIAL AND METHODS: An analysis of 300 RARP consecutively performed by the same urologist was conducted. Patients were divided into 3 groups of 100 patients in chronological order, according to surgery date. All patients had organ-confined clinical stage. Variables which could impact in positive margins rates were analyzed. Finally, positive surgical margins (PSM) in regard to pathological stage and surgeon's experience were compared and analyzed. RESULTS: No significant differences were found in variables which could impact in PSM rates. The overall PSM rate was 21%, with 28% in the first group, 20% in the second, and 16% in the third (P = .108). Significant lineal decreasing tendency was observed (P = .024). In pT2 patients, the overall PSM rate was 16.6%, with 27%, 13.8%, and 7.3% in each group respectively (P = .009). A significant difference was found between group 1 and group 3 (P = .004). In pT3 patients, the surgeon's experience was not significantly associated with margin reductions with an overall PSM rate of 27.7% (28.2%, 28.6%, and 26.7% in each group respectively). CONCLUSIONS: Clinical and surgical features in our patients did not vary over time. We found a significant reduction of PSM related to surgeon's experience in pT2 patients. Contrariwise, the margin status remained stable despite increasing experience in pT3 patients.

Heart failure-induced skeletal myopathy in spontaneously hypertensive rats.

BACKGROUND: Although skeletal muscle atrophy and changes in myosin heavy chain (MyHC) isoforms have often been observed during heart failure, their pathophysiological mechanisms are not completely defined. In this study we tested the hypothesis that skeletal muscle phenotype changes are related to myogenic regulatory factors and myostatin/follistatin expression in spontaneously hypertensive rats (SHR) with heart failure. METHODS: After developing tachypnea, SHR were subjected to transthoracic echocardiogram. Pathological evidence of heart failure was assessed during euthanasia. Age-matched Wistar-Kyoto (WKY) rats were used as controls. Soleus muscle morphometry was analyzed in histological sections, and MyHC isoforms evaluated by electrophoresis. Protein levels were assessed by Western blotting. STATISTICAL ANALYSIS: Student'st test and Pearson correlation. RESULTS: All SHR presented right ventricular hypertrophy and seven had pleuropericardial effusion. Echocardiographic evaluation showed dilation in the left chambers and left ventricular hypertrophy with systolic and diastolic dysfunction in SHR. Soleus weight and fiber cross sectional areas were lower (WKY 3615 ± 412; SHR 2035 ± 224 µm(2); P<0.001), and collagen fractional volume was higher in SHR. The relative amount of type I MyHC isoform was increased in SHR. Myogenin, myostatin, and follistatin expression was lower and MRF4 levels higher in SHR. Myogenin and follistatin expression positively correlated with fiber cross sectional areas and MRF4 levels positively correlated with I MyHC isoform. CONCLUSION: Reduced myogenin and follistatin expression seems to participate in muscle atrophy while increased MRF4 protein levels can modulate myosin heavy chain isoform shift in skeletal muscle of spontaneously hypertensive rats with heart failure.

Obesity induces upregulation of genes involved in myocardial Ca2+ handling.

Obesity is a complex multifactorial disorder that is often associated with cardiovascular diseases. Research on experimental models has suggested that cardiac dysfunction in obesity might be related to alterations in myocardial intracellular calcium (Ca2+) handling. However, information about the expression of Ca2+-related genes that lead to this abnormality is scarce. We evaluated the effects of obesity induced by a high-fat diet in the expression of Ca2+-related genes, focusing the L-type Ca2+ channel (Cacna1c), sarcolemmal Na+/Ca2+ exchanger (NCX), sarcoplasmic reticulum Ca2+ ATPase (SERCA2a), ryanodine receptor (RyR2), and phospholamban (PLB) mRNA in rat myocardium. Male 30-day-old Wistar rats were fed a standard (control) or high-fat diet (obese) for 15 weeks. Obesity was defined as increased percent of body fat in carcass. The mRNA expression of Ca2+-related genes in the left ventricle was measured by RT-PCR. Compared with control rats, the obese rats had increased percent of body fat, area under the curve for glucose, and leptin and insulin plasma concentrations. Obesity also caused an increase in the levels of SERCA2a, RyR2 and PLB mRNA (P < 0.05) but did not modify the mRNA levels of Cacna1c and NCX. These findings show that obesity induced by high-fat diet causes cardiac upregulation of Ca2+ transport_related genes in the sarcoplasmic reticulum.

Obesity induces upregulation of genes involved in myocardial Ca2+ handling

Obesity is a complex multifactorial disorder that is often associated with cardiovascular diseases. Research on experimental models has suggested that cardiac dysfunction in obesity might be related to alterations in myocardial intracellular calcium (Ca2+) handling. However, information about the expression of Ca2+-related genes that lead to this abnormality is scarce. We evaluated the effects of obesity induced by a high-fat diet in the expression of Ca2+-related genes, focusing the L-type Ca2+ channel (Cacna1c), sarcolemmal Na+/Ca2+ exchanger (NCX), sarcoplasmic reticulum Ca2+ ATPase (SERCA2a), ryanodine receptor (RyR2), and phospholamban (PLB) mRNA in rat myocardium. Male 30-day-old Wistar rats were fed a standard (control) or high-fat diet (obese) for 15 weeks. Obesity was defined as increased percent of body fat in carcass. The mRNA expression of Ca2+-related genes in the left ventricle was measured by RT-PCR. Compared with control rats, the obese rats had increased percent of body fat, area under the curve for glucose, and leptin and insulin plasma concentrations. Obesity also caused an increase in the levels of SERCA2a, RyR2 and PLB mRNA (P < 0.05) but did not modify the mRNA levels of Cacna1c and NCX. These findings show that obesity induced by high-fat diet causes cardiac upregulation of Ca2+ transport_related genes in the sarcoplasmic reticulum.