Oxidative stress and inflammation in heart failure: Mechanisms of damage and therapeutic alternatives (Rev Méd Chile 2007; 135: 1056-63 so hemodinámico de retención de agua y sal, sino como un síndrome complejo con importantes alteraciones neurohumorales que contribuyen a los síntomas y progresión de la enfermedad 1 .La búsqueda de terapias efectivas para IC, ha impulsado la investigación de los mecanismos fisiopatológicos subyacentes. Actualmente, la IC es vista como un fenómeno complejo resultante de la interacción de alteraciones locales a nivel del cardiomiocito (por ejemplo, trastornos en la homeostasis de calcio o de la activación de proteínas contráctiles) y alteraciones sistémicas resultantes P ese a los avances en diagnóstico y terapia, la insuficiencia cardiaca (IC) sigue siendo una de las causas más importantes de hospitalización, morbilidad y mortalidad a nivel mundial 1 .En la actualidad entendemos que la IC se produce no sólo como consecuencia de un proce-

(Rev Med Chile 2011; 139: 864-871).

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Catastrophic antiphospholipid syndrome and acute heart failure. Report of one case A 33 years old woman was admitted to the hospital after four days with cough, dyspnea, orthopnea and hemoptysis. Blood pressure was 170/90 mmHg, pulse was 112 and temperature was normal. She had cyanosis and a left ventricular gallop, without heart murmurs. A chest radiograph revealed pulmonary edema and echocardiogram showed a global left ventricular systolic disfunction. Oxygen and furosemide were started, but cardiopulmonary collapse ensued. The patient was supported with mechanical ventilation and treated with inotropic drugs. A right sided cardiac catheterization showed pulmonary wedge pressure of 18 mmHg and a cardiac index of 3 l/min/m 2. The levels of creatinine and urea nitrogen were elevated and a urine protein was 97 mg/dl. Coagulation tests were normal except by a positive lupic anticoagulant. Markers of connective tissue diseases or vasculitis were negatives. The clinical evolution suggested that a catastrophic antiphospholipid syndrome was ongoing. Intravenous corticoids, gammaglobulin and cyclofosfamide were administered with transient improvement. On her fourth day of treatment, the patient presented sudden pulmonary bleeding and embolism. A plasmapheresis was performed with improvement of renal, cardiac and pulmonary function. After this episode, the patient has been treated with prednisone and oral anticoagulants treatment for the last two years, without further clinical events (Rev Méd Chile 2003; 131: 1037-41).