Post-cardiac injury syndrome (PCIS) as a delayed complication of permanent pacemaker implantation has rarely been reported in the literature. A 67-year-old man who recently underwent a dual chamber permanent pacemaker implantation came to the hospital for increasing dyspnea and chest discomfort. A diagnosis of pericarditis was made, and the patient was discharged on ibuprofen therapy. He presented to our facility a month later with worsening dyspnea and chest discomfort despite recommended therapy. A computerized tomography (CT) scan of the chest revealed a large right-sided pleural effusion, requiring chest tube placement and drainage. A pleural fluid analysis revealed exudative effusion with elevated pH. The pleural fluid analysis was negative for infectious etiology. A perforation of the atrial wall was considered given the proximity of the atrial pacer lead and overlying pericardial effusion. However, no conclusive evidence of cardiac chamber perforation was found on echocardiogram or CT scan. A pacemaker interrogation was normal. A repeat CT scan showed the resolution of pleural effusion, and the chest tube was discontinued. A possible explanation for the absence of predominant pericardial findings may be the previous use of non-steroidal anti-inflammatory therapy.

Medical therapy has indisputably been the mainstay of management for chronic congestive heart failure. However, a significant percentage of patients continue to experience worsening heart failure (HF) symptoms despite treatment with multiple therapeutic agents. Recently, catheter-based interventional strategies that interrupt the renal sympathetic nervous system have shown promising results in providing better symptom control in patients with HF. In this article, we will review the pathophysiology of HF for better understanding of the interplay between the cardiovascular system and the kidney. Subsequently, we will briefly discuss pivotal renal denervation (RDN) therapy trials in patients with resistant hypertension and then present the available evidence on the role of RDN in HF therapy.

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We report a case of reversible nonischemic dilated cardiomyopathy in a male in his 60s who presented with an acute heart failure syndrome. Both conventional two-dimensional echocardiography and cardiac magnetic resonance imaging (cMRI) demonstrated severe left ventricular systolic dysfunction; however, both modalities were devoid of significant valvular heart disease as well as the presence of fibrosis, infiltration, inflammation, and scar. After six months of aggressive neurohumoral modulation, there was complete reverse remodeling and normalization of left ventricular function, which highlights the role of cMRI as an adjunct to two-dimensional echocardiography in the detection of a potentially reversible nonischemic cardiomyopathy.