Predictors of Treatment Response Following Ultrasound-Facilitated Catheter-Directed Thrombolysis for Submassive and Massive Pulmonary Embolism: A SEATTLE II Substudy.

BACKGROUND: Little is known about which factors predict improvement in clinical and imaging parameters among patients undergoing catheter-directed thrombolysis for submassive or massive pulmonary embolism. The identification of such predictors may allow for more appropriate patient selection for ultrasound-facilitated catheter-directed thrombolysis. METHODS: We conducted a retrospective cohort analysis of patients from the SEATTLE II trial (Prospective, Single-Arm, Multi-Center Trial of EkoSonic Endovascular System and Activase for Treatment of Acute Pulmonary Embolism) to identify clinical characteristics that independently predict pulmonary artery pressures, right ventricular-to-left ventricular (RV/LV) diameter ratio, and modified Miller angiographic index following ultrasound-assisted catheter-directed thrombolysis. Eligible patients had submassive or massive pulmonary embolism and an RV/LV diameter ratio ≥0.9 on chest computed tomography. Multivariable linear regression was used to identify independent clinical predictors of each outcome. RESULTS: One hundred fifty patients with massive (n=31) or submassive (n=119) pulmonary embolism were enrolled. Mean (±SD) baseline and postprocedure RV/LV diameter ratio, pulmonary artery systolic pressure, and modified Miller Score were 1.59 (±0.39) and 1.14 (±0.2), 51.45 (±16.0), and 37.47 (±11.9), and 23.0 (±5.7) and 15.7 (±5.9), respectively. The multivariable model adjusted R2 for absolute change in RV/LV ratio, pulmonary artery systolic pressure, modified Miller Score was 0.71, 0.57, and 0.43, respectively. After adjusting for age, gender, and baseline RV/LV ratio, pulmonary artery systolic pressure, and modified Miller Score, patients with higher body mass index, renal or hepatic dysfunction, active smoking, or a higher baseline heart rate showed less improvement. CONCLUSIONS: Patients with more life-threatening pulmonary embolism may derive the greatest benefit from ultrasound-assisted, catheter-directed thrombolysis.

Pulmonary Embolism in 2017: Increasing Options for Increasing Incidence.

Scope of the problem - An increasing burden of disease Acute pulmonary embolism (PE) is a problem encountered by a majority of medical and surgical specialties in their scope of practice. Acute PE is currently the 3rd leading cause of cardiovascular death in the United States, resulting in 100,000 deaths annually as estimated by the Centers for Disease Control (CDC (1). There is a paucity of data and a broad range of estimates for both incidence and morbidity due to acute PE. The mortality of all patients presenting with acute PE is estimated between 10-30% at 90 days utilizing current treatment regimens (2). The incidence of acute symptomatic PE seems to be increasing from 3/100 to more than 6.5/100 in the past 15 years (2). The increasing burden of disease has led to a period of intense investigation into new therapies and strategies to treat acute PE. [Full article available at http://rimed.org/rimedicaljournal-2017-05.asp].

Transcatheter aortic valve replacement: a review of current indications and outcomes.

In patients with symptomatic severe aortic stenosis, surgical aortic valve replacement (SAVR) improves survival, quality of life, and functional status compared with medical therapy. Based on the results of the randomized PARTNER Trial, Transcatheter Aortic Valve Replacement (TAVR) using the Edwards Sapien balloon expandable valve is now available in the United States for patients who are either inoperable due to anatomic concerns or severe medical co-morbidities, or as an alternative in patients considered high risk for SAVR. Fifty-six patients have been treated with TAVR at Rhode Island Hospital from March 2012 through October 2013 with similar outcomes to The PARTNER Trial and several large European registries. Second- generation valves and lower profile delivery systems designed to reduce the incidence of vascular complications, stroke, and perivalvular leak; and extension of TAVR to intermediate risk surgical patients, are under investigation.

Increased local cytokine production at culprit superficial femoral artery plaques.

Characterization of local inflammation at culprit superficial femoral artery (SFA) stenosis has not been studied. We hypothesized that arterial cytokine concentrations would be greater at sites of stenosis. Twenty patients with ≥50 % angiographic stenosis of the SFA had blood drawn just proximal to the lesion and from a contralateral site free of disease. A microplate immunoassay was used to determine the concentrations of 42 distinct cytokines and growth factors. Exact conditional logistic analysis was used to compare measures at the two sites with interaction terms describing clinical factors used to identify difference mediators. Interaction terms identified clinical factors that could predict cytokine levels. The concentrations of soluble CD40 ligand (sCD40L; mean 212 and 177 pg/ml, p = 0.01) and tumor necrosis factor beta (TNF-B; mean 16.6 and 15.9 pg/ml, p = 0.04) were increased immediately proximal to areas of stenosis. Factors associated with greater concentrations at sites of stenosis were bilateral ankle-brachial index ≤0.90 (p = 0.04), no statin use (p = 0.02), claudication (p = 0.03), low leukocyte count (p = 0.03), absence of limb ischemia (p = 0.04) and lack of aspirin or clopidogrel therapy (p ≤ 0.06). Greater concentrations of sCD40L and TNF-B at sites of stenosis suggest that these cytokines play a role in the pathogenesis of symptomatic SFA disease. Our results also suggest that statin, aspirin and clopidogrel therapy may attenuate localized inflammation in the SFA, though due to a small sample size and the use of multiple comparisons across groups, these findings can be viewed as hypothesis generating only. In conclusion, selected cytokines are heightened at culprit SFA lesions and inflammation may be modulated by statin and antiplatelet therapy.

Bleeding complications with regional adaptation of a prolonged bivalirudin regimen for ST-elevation acute myocardial infarction.

Bivalirudin (BIV) is superior to a heparin/glycoprotein IIb/IIIa receptor inhibitor (GPI) strategy with respect to net adverse cardiovascular events for ST-segment elevation myocardial infarction (STEMI) percutaneous coronary intervention (PCI), albeit with an increased risk of acute stent thrombosis. We hypothesized that a 2-hour BIV infusion after PCI (BIV + 2) could be used without increased bleeding risk as a potential method of mitigating early thrombotic risk. We analyzed a 6-center regional protocol involving routine therapy with aspirin, clopidogrel, and bolus heparin followed by primary PCI for STEMI using BIV. All consecutive patients presenting with STEMI requiring primary PCI were included (2009 to 2011). We compared baseline characteristics and clinical outcomes of the University of Vermont Regional Registry to the historical groups of BIV (BIV terminated at end of PCI) or unfractionated heparin/GPI from the HORIZONS trial and determined independent predictors of bleeding. Of 346 patients undergoing PCI for STEMI, 98% received BIV; 82% of patients received BIV + 2, and 13.3% of all patients receiving BIV received GPI bailout. All-cause mortality was 3.1%. Overall bleeding rates were 50% less than in the HORIZONS GPI arm and similar to the HORIZONS BIV arm. Acute stent thrombosis occurred in <1.0% of patients. Bailout GPI was a potent independent predictor of bleeding complications. In conclusion, BIV + 2 is a feasible regional pharmacologic algorithm for STEMI PCI; BIV + 2 for STEMI PCI is not associated with increased bleeding risk and warrants further study as a mechanism of mitigating very early thrombosis risk.