Faculty Bibliography

Gordonia is a catalase-positive, aerobic, nocardioform, Gram-positive staining actinomycete that also shows weak acid-fast staining. Several Gordonia species are commonly found in the soil. The bacterium has been isolated from the saliva of domesticated/wild dogs as well. In hospitalized patients, most commonly it is found in the setting of intravascular catheter-related infections. However, recent reports show that it is being increasingly isolated from sternal wounds, skin/neoplastic specimens and from pleural effusions. Gordonia shares many common characteristics with Rhodococcus and Nocardia. Ergo, it is commonly misrecognized as Nocardia or Rhodococcus. Since this pathogen requires comprehensive morphological and biochemical testing, it is often difficult and cumbersome to isolate the species. Broad-range Polymerase Chain Reaction (PCR) and sequencing with genes like 16S rRNA or hsp65 are used to correctly identify the species. Identification is essential for choosing and narrowing the right antimicrobial agent. Herein, we report our experience with a patient who presented with sternal osteomyelitis after infection with this elusive bug.

A 52-year-old lady presented to the emergency department with recurrent episodes of dizziness and near-syncope on awakening up or swinging her left arm. Initial rhythm strips demonstrated intermittently non-conducted p waves corresponding to inappropriate pacemaker inhibition and oversensing malfunction. Pacemaker was interrogated in the ED showing ventricular lead noise and decreased lead impedance over a one year period. The patient was diagnosed with pacemaker lead failure supported by correlating pacemaker lead variation with homolateral arm movement. The patient was referred to an electrophysiologist and underwent new right ventricular lead placement with the resolution of symptoms.

BACKGROUND:Hypertrophic cardiomyopathy (HCM) with or without left ventricular apical aneurysm (LVA) had been studied in the past. Midventricular obstruction associated with HCM and LVA is a unique entity that has not been distinguished previously as a separate phenotypic disease in HCM patients. METHODS:A systematic review of Pubmed and Google Scholar was conducted from inception until September 2017 for all observational studies conducted on HCM with midventricular obstruction and LVA. RESULTS:A total of 94 patients from 39 studies were included in our analysis. The mean age of the patients was 58.05 ± 11.76 years with 59.6% being males. The most common electrocardiographic finding was T wave inversion occurring in 13.8% of the cases followed by ST elevation (9.5%). Maximal left ventricle (LV) wall thickness was reported 18.89 ± 5.19 mm on transthoracic echocardiography and paradoxical jet flow was detected in 29.8% of patients. Beta-blockers (58.5%) were the most common drug therapy at baseline and amiodarone (10.6%) was the most common antiarrhythmic used for ventricular tachycardia (VT). The most common complication, VT, occurred in 39.3% of cases and the incidence of all-cause mortality was 13.8 % over 16 ± 20.1 months follow-up. Implantable cardioverter defibrillator (ICD) was used in 37.2% of patients; 25.7% of patients with ICD received appropriate shock therapy. CONCLUSION:HCM with LVA and midventricular obstruction is a unique entity that appears to be associated with high incidence of morbidity and mortality. Thus, early diagnosis and therapeutic intervention is recommended for management of this condition.

Congenital inferior sinus venosus defect (SVD) is a rare congenital heart disease. Proper diagnosis of this disease is challenging and requires understanding of cardiac hemodynamics. Here, we discuss a patient with a late presentation of combined congenital inferior SVD associated with congenital pulmonary stenosis.

Thrombocytopenia is defined as a condition where the platelet count is below the lower limit of normal (<150 G/L), and it is categorized as mild (100-149 G/L), moderate (50-99 G/L), and severe (<50 G/L). We present here a 79-year-old man who developed severe thrombocytopenia with a platelet count of 6 G/L, less than 24 hours after intravenous tirofiban infusion that was given to the patient during a percutaneous transluminal coronary angioplasty procedure with placement of 3 drug-eluting stents. The patient's baseline platelet count was 233 G/L before the procedure. Based on the timeline of events during hospitalization and laboratory evidence, it was highly likely that the patient's thrombocytopenia was the result of tirofiban-induced immune thrombocytopenia, a type of drug-induced immune thrombocytopenia (DITP) which occurs due to drug-dependent antibody-mediated platelet destruction. Anticoagulant-mediated artefactual pseudothrombocytopenia was ruled out as no platelet clumping was seen on the peripheral blood smears. The treatment of DITP includes discontinuation of the causative drug; monitoring of platelet count recovery; or treatment of severe thrombocytopenia with glucocorticoids, IVIG, or platelet transfusions depending on the clinical presentation. The most likely causative agent of this patient's thrombocytopenia-tirofiban-was discontinued, and the patient did not develop any signs of bleeding during the remainder of his hospital stay. His platelet count gradually improved to 24 G/L, and he was discharged on the sixth hospital day.

Adult congenital heart diseases present a unique challenge in assessing right-sided cardiac chambers, where pressures can be mistakenly calculated using standard echocardiographic formulae. A challenging case is presented of a combined inlet ventricular septal defect and ventriculo-atrial Gerbode defect. The diagnosis of such adult congenital heart diseases requires an in-depth understanding of cardiac pathophysiology and hemodynamics. Video 1: Transthoracic echocardiography. Apical four-chamber view, showing a large inlet VSD with bidirectional shunt (Eisenmenger syndrome). Video 2: Transthoracic echocardiography showing the Gerbode defect in a short-axis view.