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1.
Life (Basel) ; 13(8)2023 Aug 18.
Artigo em Inglês | MEDLINE | ID: mdl-37629626

RESUMO

INTRODUCTION: Takotsubo cardiomyopathy (TCM) is a reversible form of cardiomyopathy characterized by transient regional systolic dysfunction of the left ventricle. CASE OUTLINE: A 78-year-old woman was admitted to the general hospital due to acute inferior STEMI late presentation. Two days after admission, the patient reported intense chest pain and an ECG registered diffuse ST-segment elevation in all leads with ST-segment denivelation in aVR. The patient also showed clinical signs of cardiogenic shock and was referred to a reference institution for further evaluation. Echocardiography revealed akinesia of all medioapical segments, dynamic obstruction of the left ventricular outflow tract (LVOT), moderate mitral regurgitation, and pericardial effusion. Coronary angiography showed the suboccluded right coronary artery, and a primary percutaneous coronary intervention was performed, which involved implanting a drug-eluting stent. The patient's condition worsened as pericardial effusion increased and led to tamponade. Pericardiocentesis was performed, resulting in the patient's stabilization. At this point, significant gradients at the LVOT and pericardial effusion were not registered. After eight days without symptoms and stable status, the patient was discharged. CONCLUSIONS: The simultaneous presence of AMI and TCM increases the risk of developing cardiogenic shock. The cardio-circulatory profile of these patients is different from those with AMI.

2.
Medicina (Kaunas) ; 59(7)2023 Jun 28.
Artigo em Inglês | MEDLINE | ID: mdl-37512025

RESUMO

Background: Pulmonary valve infective endocarditis (PVIE) is a rare form of infective endocarditis (IE) and is associated with high mortality and severe complications. Guidelines for treatment of this form of IE are scarce and based on general recommendations. We report a case series of PVE. Detailed Case Description: Case 1-A 36-year-old female with congenital pulmonary artery stenosis, dyspnea and leg edema symptoms for 2 months. Blood cultures yielded Staphylococcus spp. and Corynebacterium sp., and echocardiography revealed multiple floating vegetation at the pulmonic valve and surrounding structures. The clinical course was complicated with sepsis and multi-organ failure. Urgent surgery with pulmonary homograft implantation resulted in successful five-year outcome. Case 2-In a 38-year-old male with previous tetralogy of Fallot correction and symptoms of fatigue, fever, myalgia, and photophobia, echocardiography was suggestive of PVIE. The clinical course was complicated with septic shock, multi-organ failure, ischemic stroke with hemorrhagic transformation and death on the 12th day of hospitalization. Case 3-A 41-year-old male without previous medical history was hospitalized due to prolonged fatigue, fever, dyspnea, and leg edema. He was diagnosed with multi-valve infective endocarditis, affecting the aortic, tricuspid, and pulmonary valve. Acute heart failure and hemodynamic instability indicated urgent surgery with aortic valve replacement and reconstruction of the tricuspid and pulmonary valves. At four-year follow up he was doing well. Conclusion: Symptoms in PVIE may be versatile, and diagnosis is often delayed. High level of suspicion, early recognition, and echocardiography are cornerstones in diagnostics. Despite the standpoint that medical therapy is first-line, the role of surgery needs to be advocated in particular cases.


Assuntos
Endocardite Bacteriana , Endocardite , Valva Pulmonar , Masculino , Feminino , Humanos , Adulto , Endocardite/etiologia , Endocardite Bacteriana/complicações , Endocardite Bacteriana/cirurgia , Endocardite Bacteriana/tratamento farmacológico , Dispneia , Sistema de Registros , Progressão da Doença
3.
Int. j. morphol ; 40(5): 1236-1241, 2022. ilus, tab
Artigo em Inglês | LILACS | ID: biblio-1405279

RESUMO

SUMMARY: Statins inhibit cholesterol synthesis, but also have other pleiotropic effects. There are indications that they affect macrophage survival trough the regulation of apoptosis. We analyzed 50 samples of aortic wall, selected based on statins in patients' therapy (n=25, Th-S group) or statin-free therapy (n=25, Th-nonS group). Each group had 5 samples of healthy aortic tissue, 10 samples of mild and 10 samples of severe atherosclerotic changes in aortic wall. Tissue was stained with hematoxylin-eosin and immunohistochemical methods (anti-Bcl-2 antibody). Presence of Bcl2-positive macrophages (Bcl-2+ MP) was determined semiquantitatively, and data were processed in Microsoft Excell and IMB SPSS 23 Statistics. 60 % of patients in the Th-S group had a mild increase of Bcl-2+ MP The use of statins leads to a significantly more frequent increase in Bcl2+ macrophages in the intima of the healthy aortic tissue. Analysis of all aortic samples with pathohistological diagnosis showed that statin therapy was statistically significantly more often leading to a markedly increased presence of Bcl-2+ MP. In the media, all samples of the Th-S group have a mild increase of Bcl-2+ MP, and in adventitia 40 % of patients. The use of statins more often leads to a markedly increased presence of Bcl-2+ MP in aortic tissue with diagnosed mild and severe atherosclerosis. In samples of severe atherosclerosis, statins lead to a markedly increased presence of Bcl-2+ MP in the parts of the plaque towards the intima and towards the media. Statins lead to an increased presence of Bcl-2+ macrophages, prolong their life, both in healthy and atherosclerotic altered aortic tissue. This indicates potentiation of inflammation and damage to the aortic wall, and calls into question the positive effect of statins on the aortic wall with atherosclerosis.


RESUMEN: Las estatinas inhiben la síntesis de colesterol, pero también tienen otros efectos pleiotrópicos. Hay indicios de que afectan la supervivencia de los macrófagos a través de la regulación de la apoptosis.Se analizaron 50 muestras de pared aórtica, seleccionadas en base a estatinas en tratamiento de pacientes (n=25, grupo Th-S) o en tratamiento libre de estatinas (n=25, grupo Th- nonS). Cada grupo tenía 5 muestras de tejido aórtico sano, 10 muestras de cambios ateroscleróticos leves y 10 muestras de cambios ateroscleróticos severos en la pared aórtica. El tejido se tiñó con hematoxilina-eosina y métodos inmunohistoquímicos (anticuerpo anti-Bcl-2). La presencia de macrófagos positivos para Bcl2 (Bcl- 2+ MP) se determinó semicuantitativamente y los datos se procesaron en Microsoft Excell e IMB SPSS 23 Statistics. El 60 % de los pacientes del grupo Th-S tuvo un aumento leve de Bcl-2+ MP. El uso de estatinas conduce a un aumento significativamente más frecuente de macrófagos Bcl2+ en la íntima del tejido aórtico sano. El análisis de todas las muestras aórticas con diagnóstico anatomopatológico mostró que la terapia con estatinas fue significativamente más frecuente desde el punto de vista estadístico, lo que condujo a una presencia marcadamente mayor de Bcl-2+ MP. En los medios, todas las muestras del grupo Th-S tienen un leve aumento de Bcl-2+ MP, y en adventicia en el 40 % de los pacientes. El uso de estatinas con mayor frecuencia conduce a una presencia marcadamente mayor de MP Bcl-2+ en el tejido aórtico con aterosclerosis leve y grave diagnosticada. En muestras de aterosclerosis severa, las estatinas conducen a una presencia aumentada de Bcl-2+ MP en las partes de la placa hacia la íntima y hacia la media. Las estatinas conducen a una mayor presencia de macrófagos Bcl-2+, prolongan su vida, tanto en tejido aórtico sano como aterosclerótico alterado. Esto indica la potenciación de la inflamación y el daño a la pared aórtica y pone en duda el efecto positivo de las estatinas en la pared aórtica con aterosclerosis.


Assuntos
Humanos , Inibidores de Hidroximetilglutaril-CoA Redutases/administração & dosagem , Aterosclerose/metabolismo , Aorta/efeitos dos fármacos , Fatores de Risco , Apoptose/efeitos dos fármacos , Medição de Risco , Genes bcl-2/fisiologia , Aterosclerose/tratamento farmacológico , Proteína bcl-X/metabolismo , Placa Aterosclerótica , Macrófagos/efeitos dos fármacos
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