Dialysis-related constrictive pericarditis: old enemies may sometimes come back / Pericardite Constritiva relacionada a diálise: velhos inimigos podem, às vezes, voltar

ABSTRACT Cardiovascular disease is the main cause of death in patients with chronic kidney disease (CKD). Several heart conditions have been associated with CKD, including myocardial and pericardial diseases. This paper describes a case of Dialysis-related constrictive pericarditis in a patient diagnosed with sudden hypotension during a hemodialysis session. A 65-year-old man diagnosed with hypertension, diabetes, obesity, and cirrhosis on hemodialysis for two years complained of symptoms during one of his sessions described as malaise, lipothymia, and confusion. The patient had a record of poor compliance with the prescribed diet and missed dialysis sessions. He was sluggish during the physical examination, and presented hypophonetic heart sounds, a blood pressure of 50/30mmHg, and a prolonged capillary refill time. The patient was referred to the intensive care unit and was started on antibiotics and vasoactive drugs. His workup did not show signs of infection, while electrocardiography showed low QRS-wave voltage. His echocardiogram showed signs consistent with a thickened pericardium without pericardial effusion. Cardiac catheterization showed equalization of diastolic pressures in all heart chambers indicative of constrictive pericarditis. The patient underwent a pericardiectomy. Examination of surgical specimens indicated he had marked fibrosis and areas of dystrophic calcification without evidence of infection, consistent with Dialysis-related constrictive pericarditis. Hypotension for unknown causes must be considered in the differential diagnosis of dialysis patients.

RESUMO A doença cardiovascular é a principal causa de morte em pacientes com doença renal crônica (DRC). Várias formas de acometimento cardíaco têm sido associadas. à DRC, incluindo doenças miocárdicas e pericárdicas. Este artigo descreve um caso de pericardite constritiva relacionada a em um paciente diagnosticado com hipotensão súbita durante uma sessão de hemodiálise. Um homem de 65 anos com diagnósticos prévios de hipertensão, diabetes, obesidade e cirrose em hemodiálise por dois anos queixou-se de sintomas durante uma de suas sessões, descritos como mal-estar, lipotímia e confusão mental. Apresentava histórico de baixa adesão à dieta prescrita e faltas frequentes às sessões de diálise. Ele estava fraco durante o exame físico e apresentava bulhas cardíacas hipofonéticas, pressão arterial de 50/30mmHg e tempo de enchimento capilar prolongado. O paciente foi encaminhado para a unidade de terapia intensiva e iniciou o tratamento com antibióticos e drogas vasoativas. Investigação laboratorial não mostrou sinais de infecção, enquanto o eletrocardiograma mostrou baixa voltagem de complexo QRS. Seu ecocardiograma evidenciou sinais consistentes com um pericárdio espessado, sem derrame pericárdico. O cateterismo cardíaco mostrou equalização das pressões diastólicas em todas as câmaras cardíacas, indicativo de pericardite constritiva. O paciente foi submetido a uma pericardiectomia. O exame anatomopatológico mostrou sinais de acentuada fibrose acentuada fibrose e áreas de calcificação distrófica sem evidência de infecção, consistente com pericardite constritiva relacionada a por diálise. A hipotensão por causas desconhecidas deve ser considerada no diagnóstico diferencial de pacientes em diálise.

Dialysis-related constrictive pericarditis: old enemies may sometimes come back.

Cardiovascular disease is the main cause of death in patients with chronic kidney disease (CKD). Several heart conditions have been associated with CKD, including myocardial and pericardial diseases. This paper describes a case of Dialysis-related constrictive pericarditis in a patient diagnosed with sudden hypotension during a hemodialysis session. A 65-year-old man diagnosed with hypertension, diabetes, obesity, and cirrhosis on hemodialysis for two years complained of symptoms during one of his sessions described as malaise, lipothymia, and confusion. The patient had a record of poor compliance with the prescribed diet and missed dialysis sessions. He was sluggish during the physical examination, and presented hypophonetic heart sounds, a blood pressure of 50/30mmHg, and a prolonged capillary refill time. The patient was referred to the intensive care unit and was started on antibiotics and vasoactive drugs. His workup did not show signs of infection, while electrocardiography showed low QRS-wave voltage. His echocardiogram showed signs consistent with a thickened pericardium without pericardial effusion. Cardiac catheterization showed equalization of diastolic pressures in all heart chambers indicative of constrictive pericarditis. The patient underwent a pericardiectomy. Examination of surgical specimens indicated he had marked fibrosis and areas of dystrophic calcification without evidence of infection, consistent with Dialysis-related constrictive pericarditis. Hypotension for unknown causes must be considered in the differential diagnosis of dialysis patients.

Oxidant generation predominates around calcifying foci and enhances progression of aortic valve calcification.

OBJECTIVE: We hypothesized that reactive oxygen species (ROS) contribute to progression of aortic valve (AV) calcification/stenosis. METHODS AND RESULTS: We investigated ROS production and effects of antioxidants tempol and lipoic acid (LA) in calcification progression in rabbits given 0.5% cholesterol diet +10(4) IU/d Vit.D2 for 12 weeks. Superoxide and H2O2 microfluorotopography and 3-nitrotyrosine immunoreactivity showed increased signals not only in macrophages but preferentially around calcifying foci, in cells expressing osteoblast/osteoclast, but not macrophage markers. Such cells also showed increased expression of NAD(P)H oxidase subunits Nox2, p22phox, and protein disulfide isomerase. Nox4, but not Nox1 mRNA, was increased. Tempol augmented whereas LA decreased H2O2 signals. Importantly, AV calcification, assessed by echocardiography and histomorphometry, decreased 43% to 70% with LA, but increased with tempol (P < or = 0.05). Tempol further enhanced apoptosis and Nox4 expression. In human sclerotic or stenotic AV, we found analogous increases in ROS production and NAD(P)H oxidase expression around calcifying foci. An in vitro vascular smooth muscle cell (VSMC) calcification model also exhibited increased, catalase-inhibitable, calcium deposit with tempol, but not with LA. CONCLUSIONS: Our data provide evidence that ROS, particularly hydrogen peroxide, potentiate AV calcification progression. However, tempol exhibited a paradoxical effect, exacerbating AV/vascular calcification, likely because of its induced increase in peroxide generation.