A sanguineous pleuro pericardial effusion in a patient recently treated with Dabigatran.

Dabigatran, a direct thrombin inhibitor, is one of the new oral anticoagulants. As more patients receive treatment with Dabigatran, and as the clinical indications for Dabigatran use expand, reporting serious adverse effects is fundamental to future safety assessment. Although patients taking Dabigatran had fewer life-threatening bleeds when compared to Coumadin, those events continue to be reported. We describe, in the same patient, a sanguineous pleuro pericardial effusion that was diagnosed incidentally on a pre-ablation cardiac CT angiography. The diagnosis was made approximately two months after initiating Dabigatran treatment for non-valvular atrial fibrillation in a 63-year-old patient.

A rare case of silent transmural myocardial infarction with diffuse ST elevations complicated by concomitant severe hyperkalemia.

It is well described that certain group of patients do not display the typical symptoms of myocardial infarction (MI). Elderly patients, diabetics and those with previous coronary artery bypass graft surgery are at high risk for silent MI. The diagnosis of Acute MI in the emergency room (ER) is mainly based on the electrocardiogram (EKG) findings of ST elevations or new onset left bundle branch block which is supported by the clinical presentation and positive biomarkers when present. The diagnoses can sometimes become challenging when the patient is asymptomatic and has coincidental finding of hyperkalemia with diffuse ST segment elevations simulating that seen with electrolyte disturbance. Despite the well known pseudoinfarction pattern of hyperkalemia, acute MI should be ruled out first. A high index of suspicion is needed, especially in high risk patients. We think that in rare clinical situation when the diagnosis is in doubt, MI should be ruled out, as time has a high impact on patient mortality. An urgent bedside echocardiogram is very beneficial in excluding regional wall motion abnormalities and preventing any delay in destination therapy for transmural MI. We present a 67 years old female with history of diabetes and chronic kidney disease sent by her nephrologist to the ER for severe hyperkalemia (Potassium 7.2 milliequivalent/L). She was found to have ST elevations on EKG despite having no chest pain or distress. On cardiac catheterization she had a total occlusion of the proximal left circumflex artery, with a filling defect consistent with large thrombus.

A rare case of double-chambered right ventricle associated with ventricular septal defect and congenital absence of the pulmonary valve.

Double-chambered right ventricle (DCRV) is a rare congenital heart disorder involving 2 different right ventricle (RV) pressure compartments that is often associated with ventricular septal defect (VSD). Usually, the obstruction is caused by an anomalous muscle bundle crossing the RV from the interventricular septum to the RV free wall. We are reporting a case of double-chambered right ventricle associated with ventricular septal defect and congenital absence of the pulmonary valve, a rare form of congenital infundibular pulmonary stenosis. In addition to ventricular septal defect, our patient had congenital absence of the pulmonary valve, which is very unusual and has never been reported to our knowledge.

Hemidiaphragm paresis and granulomatous pneumonitis associated with adalimumab: a case report.

Adalimumab is a fully human monoclonal anti-TNF-alpha antibody. Reported adverse effects have raised a number of safety concerns associated with their prolonged use. A case of granulomatous pneumonitis and hemidiaphragm paresis associated with adalimumab therapy for rheumatoid arthritis is described. In May 2012, a 57 year old male presented with dry cough, dyspnea and orthopnea after 4 months of treatment with adalimumab for rheumatoid arthritis. The patient received adalimumab from November 2011 to February 2012. A right hemidiaphragm elevation was shown on chest radiograph. A right hemidiaphragm paresis was shown on chest fluoroscopy. Bilateral lower lobe interstitial disease was shown on the chest HRCT scan. Open lung biopsy of the right lower lobe showed subacute granulomatous pneumonitis. In July 2013, the patient's respiratory symptoms and the previous restrictive pattern on PFTs resolved. In a same patient, a rare association of hemidiaphragm paresis and granulomatous pneumonitis with adalimumab treatment is herein reported.

Isolated dysphagia unmasking bulbar neurosarcoidosis and pulmonary sarcoidosis.

Dysphagia is a rare manifestation of sarcoidosis. It is more commonly the result of esophageal compression by enlarged mediastinal lymph nodes rather than direct esophageal involvement and rarely secondary to neurosarcoidosis and oropharyngeal dysphagia. We report a 54 year old female presenting with a six month history of worsening dysphagia. She denied respiratory symptoms. Physical exam was normal. ESR was 61 mm/hr. Serum ACE level was 65 mcg/L. Chest X-ray was normal. Esophagram revealed a large amount of contrast pooling in pharyngeal recesses with intermittent laryngeal aspiration. Swallow videofluorography showed a decreased retraction of the base of the tongue, limited laryngeal elevation, and a large amount of contrast pooling in pharyngeal recesses with intermittent laryngeal aspiration. EGD showed a normal opening of the upper esophageal sphincter and the cricopharyngeus appeared normal. Proximal esophageal biopsies were normal. Brain MRI with gadolinium was normal. Lumbar puncture was performed. CSF showed a moderate pleocytosis, a WBC count of 19 with 97% lymphocytes, an elevated total protein level of 85 mg/dl (15-60). Neck CT scan showed no oropharyngeal tissue thickening or infiltration, no masses or enlarged lymph nodes. Chest CT scan showed enlarged intrathoracic lymph nodes and no esophageal compression. Bronchoscopy showed the vocal cords to be intact, and the CD4/CD8 ratio in BAL was 5.3. Subcarinal lymph node EBUS biopsy revealed non caseating granulomas. The patient was started on IV methylprednisolone. Three days later, the swallow videofluorography showed a near complete response to steroids. The patient tolerated regular consistency diet with thin liquids, and she was discharged on a slow taper of prednisone over a period of three months. A unique case of isolated dysphagia unmasking bulbar neurosarcoidosis and pulmonary sarcoidosis is herein reported.

High-density lipoprotein in uremic patients: metabolism, impairment, and therapy.

Several studies have shown that HDL has altered antioxidant and anti-inflammatory effects in chronic uremia, either by the reduction in its antioxidant enzymes or by the impairment of their activity. Systemic oxidative stress, which is highly prevalent in chronic kidney disease (CKD) patients, has been shown to decrease antioxidant and anti-inflammatory effects of HDL and even transform it into a pro-oxidant and pro-inflammatory agent. For this reason, we believe that the propensity for accelerated cardiovascular disease in CKD is facilitated by a few key features of this disease, namely, oxidative stress, inflammation, hypertension, and disorders of lipid metabolism. In a nutshell, oxidative stress and inflammation enhance atherosclerosis leading to increased cardiovascular mortality and morbidity in this population. In this detailed review, we highlight the current knowledge on HDL dysfunction and impairment in chronic kidney disease as well as the available therapy.

Effects of proton pump inhibitors and electrolyte disturbances on arrhythmias.

Several case reports have been written regarding the relationship between the use of proton pump inhibitors (PPI) and hypomagnesemia. Some of these reported cases have electrocardiogram abnormalities where electrolytes deficiencies were the contributing factor for these events. This study investigates the correlation between different arrhythmias and the use of PPI and hypomagnesaemia incidence. Four-hundred and twenty-one patients admitted to the critical care unit with unstable angina, non-ST elevation myocardial infarction, and ST-elevation myocardial infarction were included in this study. One-hundred and eighty-four patients (43.8%) received PPI and 237 patients (51.16%) did not, magnesium levels were low (<1.8 mg/dL) in 95 patients (22.5%), and 167 patients (39.6%) developed arrhythmias. The P-values for the regression coefficient association for the use of PPI and the level of magnesium were P = 1.31e(-29) and P = 8e(-102), respectively. The P-values indicate that there is a statistically significant association between the PPI use, magnesium levels, and the occurrence of cardiovascular events, with a strong correlation factor of 0.817. Patients receiving PPIs should be followed closely for magnesium deficiency, especially if they experience acute cardiovascular events, because this may contribute to worsening arrhythmias and further complications.