Faculty Bibliography

PURPOSE/OBJECTIVE:The right ventricular outflow tract (RVOT) velocity time integral (VTI), an echocardiographic measure of stroke distance, correlates with cardiac index. We sought to determine the prognostic significance of low RVOT VTI on clinical outcomes among patients with acute pulmonary embolism (PE). MATERIALS AND METHODS/METHODS:We conducted a retrospective review of echocardiograms on Pulmonary Embolism Response Team (PERT) activations at our institution. The main outcome was a composite of death, cardiac arrest, or hemodynamic deterioration. RESULTS:Of 188 patients, 30 met the combined outcome (16%) and had significantly lower RVOT VTI measurements (9.0 cm v 13.4 cm, p < 0.0001). The AUC for RVOT VTI at a cutoff of 10 cm was 0.78 (95% CI 0.67-0.90) with a sensitivity, specificity, negative predictive value, and positive predictive value of 0.72, 0.81, 0.94, and 0.42, respectively. Fifty-two patients of the cohort were classified as intermediate-high-risk PE and 21% of those met the combined outcome. RVOT VTI was lower among outcome positive patients (7.3 cm v 10.7 cm, p = 0.02). CONCLUSIONS:Low RVOT VTI is associated with poor clinical outcomes among patients with acute PE.

The left ventricular outflow tract (LVOT) velocity time integral (VTI) is an easily measured echocardiographic stroke volume index analog. Low values predict adverse outcomes in left ventricular failure. We postulate the left ventricular VTI may be a signal of right ventricular dysfunction in acute pulmonary embolism, and therefore a predictor of poor outcomes. We retrospectively reviewed echocardiograms on all Pulmonary Embolism Response Team activations at our institution at the time of pulmonary embolism diagnosis. Low LVOT VTI was defined as ⩽ 15 cm. We examined two composite outcomes: (1) in-hospital death or cardiac arrest; and (2) shock or need for primary reperfusion therapies. Sixty-one of 188 patients (32%) had a LVOT VTI of ⩽ 15 cm. Low VTI was associated with in-hospital death or cardiac arrest (odds ratio (OR) 6, 95% CI 2, 17.9; p = 0.0014) and shock or need for reperfusion (OR 23.3, 95% CI 6.6, 82.1; p < 0.0001). In a multivariable model, LVOT VTI ⩽ 15 remained significant for death or cardiac arrest (OR 3.48, 95% CI 1.02, 11.9; p = 0.047) and for shock or need for reperfusion (OR 8.12, 95% CI 1.62, 40.66; p = 0.011). Among intermediate-high-risk patients, low VTI was the only variable associated with the composite outcome of death, cardiac arrest, shock, or need for reperfusion (OR 14, 95% CI 1.7, 118.4; p = 0.015). LVOT VTI is associated with adverse short-term outcomes in acute pulmonary embolism. The VTI may help risk stratify patients with intermediate-high-risk pulmonary embolism.

Non-bacterial thrombotic endocarditis in antiphospholipid syndrome presents a management dilemma. Large mobile valvular lesions pose an increased risk of stroke and arterial embolization. However, surgical excision or valve replacement in such patients carries high morbidity and mortality, while anticoagulation alone has limited data. We describe two patients with antiphospholipid syndrome presenting with neurologic events and large non-bacterial aortic valve vegetations. Both patients were successfully managed with anticoagulation and demonstrated rapid dissolution of lesions without evidence of recurrent embolic events. We provide a literature review describing additional cases managed with anticoagulation with dissolution of valvular lesions over time. Our cases further support the efficacy and safety of anticoagulation in patients with antiphospholipid syndrome and non-bacterial thrombotic endocarditis in the context of arterial embolization.

Learning Objective #1: Myocarditis is a potential complication of both Mesalamine and Ulcerative Colitis CASE: A 33-year-old male with a history of Ulcerative Colitis (UC) was recently started on mesalamine and budesonide 1 week prior to admission for a UC flare. He presented to the emergency department with central chest pressure radiating to the right arm associated with diaphoresis. Patient was hemodynamically stable with an intial troponin-I level of 1.55 ng/mL. Electrocardiogram demonstrated sinus rhythm with an incomplete right bundle branch block. A CT angiogram of the chest excluded pulmonary embolism. A transthoracic echocardiogram demonstrated a left ventricular ejection fraction of 55%, normal right ventricular function, and no valvular disease. The patient was admitted to the cardiology service and with ongoing episodes of chest pressure and rising cardiac biomarkers (Troponin-I of 5.18 ng/mL). Coronary angiography did not reveal any coronary disease. Myocarditis, either an extraintestinal manifestation of UC or mesalamine-induced, was thought to be the etiology. Cardiac magnetic resonance imaging (cMR) demonstrated patchy areas of mid wall late myocardial gadolinium enhancement in a non-vascular territory distribution, compatible with myocarditis. Gastroenterology was consulted, flexible sigmoidoscopy demonstrated active colitis, mesalamine was discontinued. His symptoms resolved over the next 36 hours and thereafter was treated with budesonide and infliximab. IMPACT: This was a case of myocarditis masqueraded by signs and symptoms of the more common diagnoses, acute coronary syndrome and pulmonary embolism, both associated with inflammatory bowel disease flares. Familiarity with this pathology may reduce alternative testing and leadto prompt treatment by discontinuation of the offending agent. DISCUSSION: Mesalamine, a 5-aminosalicylic acid derivative, is associated with a rare but potentially morbid and lethal myocarditis. Patients generally present 2-4 weeks after initiation of therapy with symptoms of chest pain or dyspnea, and may demonstrate leukocytosis, electrocardiographic abnormalities, or elevated cardiac biomarkers. Symptomatic resolution occurs after drug discontinuation. Rarely, peri-and myocarditis present as extraintestinal manifestations of UC. Precise mechanism of mesalamine induced myocarditis is unknown, however, thought to be a hypersensitivity reaction given report of myocardial biopsy-proven eosinophilic infiltrate in mesalamine myocarditis, improvement after drug discontinuation, and know hypersensitivity reactions involving other organs. Cardiac magnetic resonance imaging (cMR) has a unique advantage to characterize myocardial tissue and define edema, a hallmark of inflammation, and necrosis. Identification of regional edema in a non-ischemic distribution is compatible with the diagnosis of myocarditis in the appropriate clinical context. In our case cMR confirmed the diagnosis of myocarditis and time course made the association with mesalamine most likely