Faculty Bibliography

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

Although loperamide has been widely used for the treatment of diarrhea, there is growing popularity over its abuse potential in alleviating opioid-withdrawal symptoms and achieving euphoria. Toxic levels of loperamide have been associated with life-threatening ventricular tachyarrhythmias and cardiac arrest. We report a case of high-dose loperamide ingestion in a patient presenting initially with unstable bradycardia followed by episodes of polymorphic ventricular tachycardia, and an unmasked Brugada ECG pattern. This is the first such report of the Brugada pattern being unmasked on ECG with loperamide ingestion. The patient stabilized with supportive care without the need for inotropic support. We discuss potential mechanisms of toxicity leading to conduction abnormalities and provide a literature review of all published cases of loperamide toxicity to describe proposed treatment options. Recognition of the abuse potential and hazards of this over-the-counter anti-diarrheal therapy will alert the clinician of associated toxidromes and management strategies

OBJECTIVES: This study sought to evaluate variability in aortic measurements with multiple imaging modalities in clinical centers by comparing with a standardized measuring protocol implemented in a core laboratory. BACKGROUND: In patients with aortic disease, imaging of thoracic aorta plays a major role in risk stratifying individuals for life-threatening complications and in determining timing of surgical intervention. However, standardization of the procedures for performance of aortic measurements is lacking. METHODS: To characterize the diversity of methods used in clinical practice, we compared aortic measurements performed by echocardiography, computed tomography (CT), and magnetic resonance imaging (MRI) at the 6 GenTAC (National Registry of Genetically Triggered Thoracic Aortic Aneurysms and Cardiovascular Conditions) clinical centers to those performed at the imaging core laboratory in 965 studies. Each center acquired and analyzed their images according to local protocols. The same images were subsequently analyzed blindly by the core laboratory, on the basis of a standardized protocol for all imaging modalities. Paired measurements from clinical centers and core laboratory were compared by mean of differences and intraclass correlation coefficient (ICC). RESULTS: For all segments of the ascending aorta, echocardiography showed a higher ICC (0.84 to 0.93) than CT (0.84) and MRI (0.82 to 0.90), with smaller mean of differences. MRI showed higher ICC for the arch and descending aorta (0.91 and 0.93). In a mixed adjusted model, the different imaging modalities and clinical centers were identified as sources of variability between clinical and core laboratory measurements, whereas age groups or diagnosis at enrollment were not. CONCLUSIONS: By comparing core laboratory with measurements from clinical centers, our study identified important sources of variability in aortic measurements. Furthermore, our findings with regard to CT and MRI suggest a need for imaging societies to work toward the development of unifying acquisition protocols and common measuring methods.

BACKGROUND: There is a lack of uniformity across echocardiographic society guidelines as to how the diameter of the ascending aorta is to be measured. The aims of this study were to compare measurements done using the diastolic leading edge-to-leading edge and systolic inner edge-to-inner edge (SIE) techniques in a large cohort of healthy adult individuals and to report the normal values for adults using the SIE technique. METHODS: Aortic diameters obtained according to the two guideline recommendations at the aortic annuls, sinuses of Valsalva, sinotubular junction, and ascending aorta in 1,148 healthy adult volunteers were compared. Bland-Altman analysis, paired t tests, and intraclass correlation coefficients were evaluated at each segment. SIE values are reported as normative data, according to age, gender, and body surface area. RESULTS: The diastolic leading edge-to-leading edge convention yielded smaller diameters (compared with SIE) at the aortic annulus and ascending aorta and larger diameters at the sinus of Valsalva and sinotubular junction (P < .001 for all). There was excellent correlation between these techniques, with intraclass correlation coefficients of 0.88 to 0.96. Interobserver variability was minimal and similar for both techniques. Using the SIE technique, diameters were larger for men and increased with age and larger body surface area. CONCLUSIONS: Although there was a statistically significant difference in aortic diameter measures between the two conventions used, this difference was very small and correlations were excellent, suggesting that the difference has no clinical significance. The authors recommend that a standard convention be adopted within the American Society of Echocardiography and across all professional cardiovascular imaging societies for consistency and improved communication.

Atrial fibrillation (AF) is prevalent in patients with type 2 diabetes mellitus (DM) and is associated with markers of poor glycemic control; however, the impact of glycemic control on incident AF and outcomes is unknown. The aims of this study were to prospectively evaluate if intensive glycemic control in patients with DM affects incident AF and to evaluate morbidity and mortality in patients with DM and incident AF. A total of 10,082 patients with DM from the Action to Control Cardiovascular Risk in Diabetes (ACCORD) cohort were studied in a randomized, double-blind fashion. Participants were randomized to an intensive therapeutic strategy targeting a glycated hemoglobin level of <6.0% or a standard strategy targeting a glycated hemoglobin level of 7.0% to 7.9%. Incident AF occurred in 159 patients (1.58%) over the follow-up period, at a rate of 5.9 per 1,000 patient-years in the intensive-therapy group and a rate of 6.37 per 1,000 patient-years in the standard-therapy group (p = 0.52). In a multivariate model, predictors of incident AF were age, weight, diastolic blood pressure, heart rate, and heart failure history. Patients with DM and new-onset AF had a hazard ratio of 2.65 for all-cause mortality (95% confidence interval 1.8 to 3.86, p <0.0001), a hazard ratio of 2.1 for myocardial infarction (95% confidence interval 1.33 to 3.31, p = 0.0015), and a hazard ratio of 3.80 for the development of heart failure (95% confidence interval 2.48 to 5.84, p <0.0001). In conclusion, intensive glycemic control did not affect the rate of new-onset AF. Patients with DM and incident AF had an increased risk for morbidity and mortality compared with those without AF.