Taquicardia ventricular incessante: causa rara e reversível de miocardiopatia dilatada / Incessant ventricular tachycardia: rare and reversible cause of dilated cardiomyopathy

INTRODUÇÃO: A taquicardiomiopatia é definida por disfunção ventricular esquerda reversível atribuída ao aumento da frequência ventricular, independente da origem da taquicardia, na ausência de outra etiologia mais provável. Apresenta-se geralmente por disfunção biventricular moderada a severa, com dilatação das cavidades e ausência de hipertrofia do ventrículo esquerdo (VE). Fibrilação atrial e Flutter de alta resposta ventricular são as mais comuns, no entanto taquicardias ventriculares (TV) também podem ser responsáveis. Os sintomas se apresentam mais precocemente nos pacientes com frequências cardíacas mais elevadas e são principalmente dispneia NYHA III-IV, palpitações e síncope. O tratamento é baseado na supressão da arritmia com medicações antiarrítmicas e/ou ablação além da terapêutica medicamentosa padrão para insuficiência cardíaca (IC). O diagnóstico é confirmado após a recuperação ou melhora da disfunção ventricular dentro de 1 a 6 meses após a resolução da taquiarritmia. MÉTODOS: Estudo de série de casos, retrospectivo e observacional. RESULTADOS: Foram avaliados três pacientes, masculinos, cujas idades eram 19, 23 e 61 anos, todos brancos. A apresentação inicial encontrada foi insuficiência cardíaca inicialmente manejada com betabloqueador, IECA e espironolactona. Disponibilizamos mais dados na tabela 1. Após ablação da TV, os pacientes evoluíram com melhora significativa de classe funcional e incremento da fração de ejeção de VE. O tempo médio de melhora foi de 5 meses e 20 dias após o procedimento e não houve complicações ou mesmo óbitos. CONCLUSÃO: A taquicardia ventricular incessante deve ser lembrada como possibilidade etiológica da disfunção ventricular. A ablação dos focos arritmogênicos pode resultar em recuperação rápida e significativa da disfunção ventricular, mostrando-se uma terapia segura e eficaz.

Blockade of angiotensin AT1 receptors prevents arterial remodelling and stiffening in iron-overloaded rats.

BACKGROUND AND PURPOSE: Damage to the vasculature caused by chronic iron-overload in both humans and animal models, is characterized by endothelial dysfunction and reduced compliance. In vitro, blockade of the angiotensin II AT1 receptors reversed functional vascular changes induced by chronic iron-overload. In this study, the effect of chronic AT1 receptor blockade on aorta stiffening was assessed in iron-overloaded rats. EXPERIMENTAL APPROACH: Male Wistar rats were treated for 15 days with saline as control group, iron dextran 200 mg·kg-1 ·day-1 , 5 days a week (iron-overload group), losartan (20 mg·kg-1 ·day-1 in drinking water), and iron dextran plus losartan. Mechanical properties of the aorta were assessed in vivo. In vitro, aortic geometry and biochemical composition were assessed with morphometric and histological methods. KEY RESULTS: Thoracoabdominal aortic pulse wave velocity (PWV) increased significantly, indicating a decrease in aortic compliance. Co-treatment with losartan prevented changes on PWV, ß-index, and elastic modulus in iron-overloaded rats. This iron-related increase in PWV was not related to changes in aortic geometry and wall stress. but to increased elastic modulus/wall stress ratio, suggesting that a change in the composition of the wall was responsible for the stiffness. Losartan treatment also ameliorated the increase in aorta collagen content of the iron-overload group, without affecting circulating iron or vascular deposits. CONCLUSIONS AND IMPLICATIONS: Losartan prevented the structural and functional indices of aortic stiffness in iron-overloaded rats, implying that inhibition of the renin-angiotensin system would limit the vascular remodelling in chronic iron-overload.

Chronic iron overload intensifies atherosclerosis in apolipoprotein E deficient mice: Role of oxidative stress and endothelial dysfunction.

AIMS: We previously demonstrated that iron overload induces endothelial dysfunction and oxidative stress, which could increase the risk for atherosclerosis. However, the iron-related harmfulness under a genetic predisposition to atherosclerosis is still unclear. Here, we have tested the hypothesis that chronic iron overload may change vascular reactivity associated with worsening of the atherosclerotic process in apolipoprotein E knockout (apoE(-/-)) mice. MAIN METHODS: Serum and aortas of wild-type (WT) and apoE(-/-) mice injected with iron-dextran (IO, 10 mg/mouse/day, ip) or saline 5 times a week for 4 weeks, were used. KEY FINDINGS: Iron overload increased serum levels of iron and biomarkers of liver injury and oxidative stress, and iron deposition in the aorta in both lines, but only apoE(-/-) IO mice had intensified hypercholesterolemia and atherosclerosis. By scanning electron microscopy, the small endothelial structural damage caused by iron in WT was worsened in the apoE(-/-) group. However, endothelial dysfunction was found only in the apoE(-/-) IO group, identified by impaired relaxation to acetylcholine and hyperreactivity to phenylephrine associated with reduced nitric oxide modulation. Moreover, tiron and indomethacin attenuated reactivity to phenylephrine with greater magnitude in aortas of the apoE(-/-) IO group. Confirming, there were changes in the antioxidant (superoxide dismutase and catalase) activity, increased expression of cyclooxygenase-2 in the aorta and elevated levels of thromboxane A2 and prostacyclin metabolites in the urine of apoE(-/-) IO. SIGNIFICANCE: Our results showed that chronic iron overload intensifies the atherosclerotic process and induces endothelial dysfunction in atherosclerotic mice, probably due to the oxidative stress and the imbalance between the relaxing and contractile factors synthesized by the damaged endothelium.