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Primary vascular tumors such as vascular leiomyosarcomas are rare, but exhibit markedly different characteristics than tumors that invade the vasculature from a secondary source. Establishing a diagnosis is essential in determining the appropriate treatment plan, but obtaining a histologic specimen may prove challenging and carry significant risks. Minimally invasive endovascular biopsy techniques can be pivotal in the diagnosis-and thus in the management-of vascular tumors. We present a case of a primary inferior vena cava leiomyosarcoma, not able to be adequately assessed by noninvasive imaging and deemed too risky to be approached with traditional percutaneous biopsy techniques. Accurate diagnosis of such tumors is critical, as the success of surgical resection, although high risk, depends greatly upon the type, location, and extent of malignancy.

Background Vasodilator stress computed tomography perfusion (sCTP) imaging is complementary to coronary CT angiography (CCTA), used to determine the hemodynamic significance of coronary artery disease. However, it requires a separate image acquisition due to motion artifacts caused by higher heart rates during stress, resulting in increased iodine contrast dose and radiation. We sought to determine whether a novel motion correction algorithm applied to stress images would improve the visualization of the coronary arteries to potentially allow CCTA + sCTP evaluation in a single scan. Methods 28 patients referred for clinically indicated CCTA (iCT, Philips) underwent sCTP imaging (retrospective-gating with dose modulation; 100 kVp and 250 mA; 5.2 ± 4.3 mSv) after regadenoson (0.4 mg, Astellas). Stress images were reconstructed using standard filtered back-projection (FBP) and also processed to generate interaction-free coronary motion-compensated back-projection reconstructions (MCR). Each coronary artery from standard FBP and MCR images was viewed side-by-side by a reader blinded to the reconstruction technique, who graded severity of motion artifact by segment (scale 0–5, with 3 as the threshold for diagnostic quality) and to measure signal-to-noise and contrast-to-noise ratios (SNR, CNR). Results Visualization scores were higher with MCR for all coronary segments, including 14/86 (16%) segments deemed as non-diagnostic on FBP images. SNR (7 ± 2) and CNR (15 ± 8) were unchanged by motion-correction (7 ± 3, p = 0.88 and 15 ± 5, p = 0.94, respectively). Conclusions MCR improves the visualization of coronary anatomy on sCTP images without degrading image characteristics. This algorithm is an important step towards the combined assessment of coronary anatomy and myocardial perfusion in a single scan, which will reduce study time, radiation exposure and contrast dose.

The significance of cardiac troponin I (TnI) levels in patients with acute ischemic stroke remains unclear.Data were prospectively collected on 1718 patients with acute ischemic stroke (2009-2010). Patients with positive TnI (peak TnI ≥0.1 μg/L) were assigned to the myocardial infarction (MI) group if they met diagnostic criteria. The remaining patients with positive TnI were assigned to the no-MI group. Patients were followed up for 1.4 ± 1.1 years. Primary outcome was inhospital and long-term all-cause mortality.Positive TnI was present in 309 patients (18%), 119 of whom (39%) were classified as having MI. Positive TnI was independently associated with older age, hypertension, smoking, peripheral arterial disease, heart failure, higher systolic blood pressure, higher serum creatinine, and lower heart rate (P.01). Patients with MI had the highest inpatient mortality (P.001) and the lowest survival rate by Kaplan-Meier analysis (P.0001). Peak TnI greater than or equal to 0.5 μg/L, particularly if satisfying criteria for MI, was independently associated with long-term mortality (P.0001); peak TnI less than 0.5 μg/L alone was not when adjusted for covariates.Positive TnI greater than or equal to 0.5 μg/L in patients with acute ischemic stroke was independently associated with worse outcomes. Patients with diagnosis of MI represent a particularly high-risk subgroup.

Echocardiographic assessment of left ventricular (LV) filling pressures is performed using a multi-parametric algorithm. Left atrial (LA) strain was recently found to accurately classify the degree of diastolic dysfunction. We hypothesized that LA strain could be used as a stand-alone marker and sought to identify and test a cutoff, which would accurately detect elevated LV pressures. We studied 76 patients with a spectrum of LV function who underwent same-day echocardiogram and invasive left-heart catheterization. Speckle tracking was used to measure peak LA strain. The protocol involved a retrospective derivation group (N = 26) and an independent prospective validation cohort (N = 50) to derive and then test a peak LA strain cutoff which would identify pre-A-wave LV diastolic pressure > 15 mmHg. The guidelines-based assessment of filling pressures and peak LA strain were compared side-by-side against invasive hemodynamic data. In the derivation cohort, receiver-operating characteristic analysis showed area under curve of 0.76 and a peak LA strain cutoff

Background Recent American Society of Echocardiography (ASE)/European Association of Cardiovascular Imaging (EACVI) guidelines for echocardiographic evaluation of left ventricular (LV) diastolic function provide a practical, simplified diagnostic algorithm for estimating LV filling pressure. The aim of this study was to test the accuracy of this algorithm against invasively measured pressures and compare it with the accuracy of the previous 2009 guidelines in the same patient cohort. Methods Ninety patients underwent transthoracic echocardiography immediately before left heart catheterization. Mitral inflow E/A ratio, E/e′, tricuspid regurgitation velocity, and left atrial volume index were used to estimate LV filling pressure as normal or elevated using the ASE/EACVI algorithm. Invasive LV pre-A pressure was used as a reference, with >12 mm Hg defined as elevated. Results Invasive LV pre-A pressure was elevated in 40 (44%) and normal in 50 (56%) patients. The 2016 algorithm resulted in classification of 9 of 90 patients (10%) as indeterminate but estimated LV filling pressures in agreement with the invasive reference in 61 of 81 patients (75%), with sensitivity of 0.69 and specificity of 0.81. The 2009 algorithm could not definitively classify 4 of 90 patients (4.4%), but estimated LV filling pressures in agreement with the invasive reference in 64 of 86 patients (74%), with sensitivity of 0.79 and specificity of 0.70. Conclusions The 2016 ASE/EACVI guidelines for estimation of filling pressures are more user friendly and efficient than the 2009 guidelines and provide accurate estimates of LV filling pressure in the majority of patients when compared with invasive measurements. The simplicity of the new algorithm did not compromise its accuracy and is likely to encourage its incorporation into clinical decision making.

Elevated cardiac troponin (cTn) signals myocardial necrosis and injury but does not specify the mechanism of that injury. The measurement of cardiac troponins is widely used to diagnose myocardial infarction and has become an important tool for the risk stratification and clinical management of patients with acute coronary syndrome

Acute ischemic stroke is a cause of troponin elevation which is often attributed to demand, type 2 myocardial infarction (MI). The incidence of spontaneous, type 1 MI is unknown. We reviewed our prospective hospital registry of acute ischemic stroke (2009–2010). All patients had ≥3 troponin I (

Cardiomyopathy (CM) in patients admitted with acute ischemic stroke has not been investigated previously. A prospective registry of 1,761 patients admitted with diagnosis of acute ischemic stroke from 2009-2010 was used to identify patients with systolic CM. Echocardiography was performed on 1,594

Acute ischemic strokes are often accompanied by cardiac events. The prevalence, associated factors, and implications of elevated troponin I (TnI) in acute ischemic stroke merit further study. We reviewed our prospective registry of hospitalized patients with acute ischemic stroke from 2009 to 2010