9 research outputs found

    Histomorphometric evaluation of the small coronary arteries in rats exposed to industrial noise

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    Morphological changes induced by industrial noise (IN) have been experimentally observed in several organs. Histological observations of the coronary arteries showed prominent perivascular tissue and fibrosis among IN-exposed rats. The effects on the small arteries are unknown. Objective: To evaluate the histomorphometric changes induced by IN on rat heart small arteries. Methods: Twenty Wistar rats exposed to IN during a maximum period of seven months and 20 age-matched controls were studied. Hearts were transversely sectioned from ventricular apex to atria and a mid-ventricular fragment was selected for analysis. The histological images were obtained with an optical microscope using 400× magnifications. A total of 634 arterial vessels (298 IN-exposed and 336 controls) were selected. The mean lumen-to-vessel wall (L/W) and mean vessel wall-to-perivascular tissue (W/P) ratios were calculated using image J software. Results: There were no differences between exposed and control animals in their L/W ratios (p = 0.687) and time variations in this ratio were non-significant (p = 0.110). In contrast, exposed animals showed lower W/P ratios than control animals (p < 0.001), with significant time variations (p = 0.004). Conclusions: Industrial noise induced an increase in the perivascular tissue of rat small coronary arteries, with significant development of periarterial fibrosis.info:eu-repo/semantics/publishedVersio

    Atrial fibrosis and decreased connexin 43 in rat hearts after exposure to high-intensity infrasound

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    Background: Noise is an important environmental risk factor. Industrial environments are rich in high-intensity infrasound (hi-IFS), which we have found to induce myocardial and coronary perivascular fibrosis in rats. The effects of exposure to IFS on the ventricles have been studied, but not on the atria. We hypothesized that rats exposed to hi-IFS develop atrial remodeling involving fibrosis and connexin 43, which we sought to evaluate. Material and methods: Seventy-two Wistar rats, half exposed to hi-IFS (120 dB, < 20 Hz) during a maximum period of 12 weeks and half age-matched controls, were studied. Atrial fibrosis was analyzed by Chromotropeaniline blue staining. The immunohistochemical evaluation of Cx43 was performed using the polyclonal antibody connexin-43 m diluted 1:1000 at 4 degrees C overnight. Digitized images were obtained with an optical microscope using 400 x magnifications. The measurements were performed using image J software. A two-way ANOVA model was used to compare the groups. Results: The mean values of the ratio "atrial fibrosis / cardiomyocytes" increased to a maximum of 0.1095 +/- 0,04 and 0.5408 +/- 0,01, and of the ratio "CX43 / cardiomyocytes" decreased to 0.0834 +/- 0,03 and 0.0966 +/- 0,03, respectively in IFS-exposed rats and controls. IFS-exposed rats exhibited a significantly higher ratio of fibrosis (p < .001) and lower ratio of Cx43 (p = .009). Conclusion: High-intensity infrasound exposure leads to an increase in atrial interstitial fibrosis and a decrease in connexin 43 in rat hearts. This finding reinforces the need for further experimental and clinical studies concerning the effects of exposure to infrasound

    The atrial fibrillation burden during the blanking period is predictive of time to recurrence after catheter ablation

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    © 2022 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/)Objective: This study aimed to assess whether atrial fibrillation (AF) occurrence or its corresponding daily mean burden (in minutes/day) during the mid to late blanking period after pulmonary vein isolation (PVI), predicts AF recurrence. Methods: Analysis of consecutive first PVI ablation patients undergoing prolonged electrocardiogram (ECG) monitoring during the second and third months after PVI. The clinical variables, total AF burden, and their relationship with time to recurrence were studied. Results: 477 patients with a mean age of 56.9 (SD = 12.3) years (63.7 % male; 71.7 % paroxysmal AF), from which 317 (66.5 %) had an external event recorder between 30 and 90 days after ablation. Median follow-up of 16.0 (P 25:12.0: P 75:33.0) months, 177 (37 %) patients had an AF recurrence, with 106 (22.2 %) having the first episode after 12 months of follow-up. In the group of patients with an event recorder, 80 (25.2 %) had AF documented during the blanking period. Multivariable analysis showed that AF during the blanking period was associated with a 4-fold higher risk of recurrence (HR: 3.98; 95 %CI: 2.95-5.37), and, compared to patients in sinus rhythm, those with an AF burden ≥ 23 min/day had an approximately 7-fold higher risk of recurrence (HR estimate: 6.79; 95 %CI: 4.56-10.10). Conclusions: The probability of experiencing AF recurrence can be predicted by atrial tachyarrhythmia episodes during the second and third months after PVI. Atrial arrhythmias burden > 23 min/day has a high predictive ability for recurrence.info:eu-repo/semantics/publishedVersio

    Infrasound induces coronary perivascular fibrosis in rats

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    Background: Chronic exposure to industrial noise is known to affect biological systems, namely, by inducing fibrosis in the absence of inflammatory cells. In rat hearts exposed to this environmental hazard, we have previously found myocardial and perivascular fibrosis. The acoustic spectrum of industrial environments is particularly rich in high-intensity infrasound (<20 Hz), whose effects on the heart are unknown. We evaluated the morphological changes induced by IFS in rat coronaries in the presence and absence of dexamethasone. Methods: Adult Wistar rats were divided into three groups: group A (GA)-IFS (<20 Hz, 120 dB)-exposed rats for 28 days treated with dexamethasone; group B (GB)-IFS-exposed rats; group C (GC)-age-matched controls. The midventricle was prepared for observation with an optical microscope using 100x magnification. Thirty-one arterial vessels were selected (GA 8, GB 10, GC 13). The vessel caliber, thickness of the wall, and perivascular dimensions were quantified using image j software. Mann-Whitney and Kruskal-Wallis tests were used to compare the groups for lumen-to-vessel wall (LW) and vessel wall-to-perivascular tissue (W/P) ratios. Results: IFS-exposed rats exhibited a prominent perivascular tissue. The median L/W and median W/P ratios were 0.54 and 0.48, 0.66 and 0.49, and 0.71 and 0.68, respectively, in GA, GB, and GC. The W/P ratio was significantly higher in GC compared with IFS-exposed animals (P=.001). The difference was significant between GC and GB (P=.008) but not between GC and GA. Conclusion: IFS induces coronary perivascular fibrosis that differs under treatment with corticosteroid

    Infrasound exposure promotes development of atrial fibrosis in rats

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    INTRODUCTION: Recent data has shown a significant association between noise exposure and atrial fibrillation (AF) in a large cohort [1] but the pathophysiology remains unclear. The acoustic spectrum of industrial environments is particularly rich in high-intensity infrasound (IFS), which we have previously found to induce coronary perivascular fibrosis in rat hearts [2–4]. The role of atrial fibrosis in AF is well documented and remains the cornerstone of atrial pathology in patients with this arrhythmia [5]. The aim of this study was to evaluate and measure the atrial interstitial fibrosis in rats exposed to high-intensity IFS. MATERIAL AND METHODS: Twelve Wistar rats exposed to high-intensity IFS (110 dB, <20Hz) during a period of 6 weeks and 12 age-matched controls were studied. All the handling and care of the experimental animals was performed by authorised researchers and was done in accordance with the EU Commission on Animal Protection for Experimental and Scientific Purposes (2010/63/EU). Hearts were transversely sectioned and the atrial fragment was selected for analysis. Chromotrope-aniline blue staining was used for histological observation and the images were obtained with an optical microscope using 400× magnifications. For each atrium, three optical fields containing more prominent fibrotic development in the absence of any arterial vessel were selected. The measurement of fibrosis was performed using Image J software. Mann–Whitney test was used to compare the groups. RESULTS: The mean values of atrial interstitial fibrosis were 8.96 ± 4.08 and 4.91 ± 1.46, respectively, in IFS-exposed rats and controls. IFS-exposed rats exhibited a significant increase in atrial interstitial fibrosis (p = .005). DISCUSSION AND CONCLUSION: High-intensity IFS induces atrial interstitial fibrosis in rats. This finding reinforces the need for further experimental and clinical studies concerning the effects of IFS on the heart

    Metastização pulmonar na apresentação de angiossarcoma cardíaco: Caso clínico e discussão Pulmonary metastasis in a cardiac angiosarcoma: Case report and discussion

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    Apresenta-se um caso clínico referente a doente de 35 anos, do sexo masculino sem antecedentes pessoais relevantes, admitido no serviço de urgência por quadro de toracalgia e tosse produtiva com alterações electrocardiograficas sugestivas de pericardite. Inicialmente admitido pelo Serviço de Cardiologia, com melhoria do quadro clínico apos terapêutica anti-inflamatória; contudo, no internamento houve como intercorrencia pneumonia de provável etiologia bacteriana, complicada por derrame pleural. Após a alta, foi referenciado a consulta de pneumologia, onde se manteve o estudo etiológico do derrame persistente, tendo vindo a complicar-se o seu quadro com alterações das cavidades cardíacas e múltiplos nódulos pulmonares, sugestivos de endocardite subaguda com embolização séptica pulmonar. Internado no serviço de Pneumologia e submetido a videotoracoscopia, foi-lhe diagnosticado angiossarcoma cardíaco com metastização pulmonar. Assistiu-se a uma rápida evolução do quadro clínico, quase fulminante, com falência cardíaca e óbito do doente sem ter iniciado radioterapia ou quimioterapia adjuvante.We present a case report of a 35 year-old male without any relevant former pathology admitted to the emergency room with atypical chest pain, cough and sputum with ECG changes suggesting pericarditis. He was initially admitted to the cardiology ward and experienced clinical improvement after initiating anti- inflammatory treatment. As intercurrence he had bacterial origin pneumonia complicated by pleural effusion (PE). After discharge patient was referred to a pulmonology appointment where aetiological investigation of the PE was instigated. Investigation revealed changes in the cardiac cavities and multiple lung nodules, suggesting subacute endocarditis with septic pulmonary embolism. Admitted to the pulmonology unit patient underwent videothoracsopy which diagnosed cardiac angiosarcoma with pulmonary metastisation. Within a few days there was a rapid evolution of the clinical picture, with cardiac failure and death of the patient without radiotherapy or adjuvant chemotherapy being started

    Metastização pulmonar na apresentação de angiossarcoma cardíaco â Caso clínico e discussão

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    Resumo: Apresenta-se um caso clínico referente a doente de 35 anos, do sexo masculino sem antecedentes pessoais relevantes, admitido no serviço de urgência por quadro de toracalgia e tosse produtiva com alterações electrocardiográficas sugestivas de pericardite. Inicialmente admitido pelo Serviço de Cardiologia, com melhoria do quadro clínico após terapêutica anti-inflamatória; contudo, no internamento houve como intercorrência pneumonia de provável etiologia bacteriana, complicada por derrame pleural. Após a alta, foi referenciado à consulta de pneumologia, onde se manteve o estudo etiológico do derrame persistente, tendo vindo a complicar-se o seu quadro com alterações das cavidades cardiacas e múltiplos nódulos pulmonares, sugestivos de endocardite subaguda com embolização séptica pulmonar. Internado no serviço de Pneumologia e submetido a videotoracoscopia, foi-lhe diagnosticado angiossarcoma cardíaco com metastização pulmonar. Assistiu-se a uma rápida evolução do quadro clínico, quase fulminante, com falência cardíaca e óbito do doente sem ter iniciado radioterapia ou quimioterapia adjuvante.Rev Port Pneumol 2009; XV (6): 1175-1184 Abstract: We present a case report of a 35 year-old male without any relevant former pathology admitted to the emergency room with atypical chest pain, cough and sputum with ECG changes suggesting pericarditis. He was initially admitted to the cardiology ward and experienced clinical improvement after initiating anti-inflammatory treatment. As intercurrence he had bacterial origin pneumonia complicated by pleural effusion (PE). After discharge patient was referred to a pulmonology appointment where aetiological investigation of the PE was instigated. Investigation revealed changes in the cardiac cavities and multiple lung nodules, suggesting subacute endocarditis with septic pulmonary embolism. Admitted to the pulmonology unit patient underwent videothoracsopy which diagnosed cardiac angiosarcoma with pulmonary metastisation. Within a few days there was a rapid evolution of the clinical picture, with cardiac failure and death of the patient without radiotherapy or adjuvant chemotherapy being started.Rev Port Pneumol 2009; XV (6): 1175-1184 Palavras-chave: Angiossarcoma cardíaco, metástases pulmonares, derrame pleural, pericardite, Key-words: Heart angiosarcoma, pulmonary metastasis, pleural effusion, pericarditi
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