Rheumatoid arthritis (RA) is a chronic inflammatory disease of the joints. Extra-articular features are very common. We report a case of RA first diagnosed after an episode of congestive heart failure (CHF) and the evolution of left ventricular function after conventional treatment of CHF and immunosuppressive drugs. The patient, a 52-year-old man, with history of epilepsy and a stroke 6 years before, presented to the emergency department with increasing dyspnea. He had polyarthralgia 2 months before. The lower extremities had mild pitting edema. The musculoskeletal examination revealed synovial thickening of the metacarpophalangeal and proximal interphalangeal joints, but there was no joint tenderness. The patient’s alanine aminotransferase, troponin levels and CRP were slightly elevated. His renal function was preserved. The electrocardiogram (EKG) was normal. An echocardiogram performed in showed a global hypokinetic dilated cardiomyopathy with an ejection fraction of 15–20%, with apical thrombus. The patient was diagnosed with exacerbation of congestive heart failure (CHF) and was treated with intravenous diuretics. This led to symptomatic improvement. He got a conventional heart failure treatment with vit K antagonists. Coronarography was normal. Viral serologies were negative. The martial, phosphocalcic and thyroid markers were normal. However, the immunologic tests showed positive rheumatoid factor and anti-CCP. The diagnosis of dilated cardiomyopathy due to rheumatoid arthritis was retained. The patient was treated by corticosteroids and immunosuppressive agents. Patient was seen during routine follow-up after 6 months. Interestingly, echocardiographic findings were totally normal with left ventricular ejection fraction >50% and normal LV size.
Pericardial decompression syndrome (PDS) is an unusual, potentially fatal complication that occurs after pericardial drainage for cardiac tamponade. either by needle pericardiocentesis or surgical pericardiostomy. It manifests with paradoxical hemodynamic deterioration and/or pulmonary edema, commonly associated with ventricular dysfunction. PDS usually begins after initial clinical amelioration after pericardiocentesis. It is largely under-reported and may be neglected in clinical practice. While the precise mechanisms behind PDS are not well understood, it seems to be strongly related to patients with preexisting ventricular dysfunction. Doctors who perform pericardial drainage should be mindful of the associated high-risk factors for the intervention, taking into consideration the uncommon possibility of PDS formation.
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