Venous thromboembolism (VTE) is responsible for the hospitalization of >250 000 Americans annually and represents a significant risk for morbidity and mortality. Despite the publication of evidence-based clinical practice guidelines to aid in the management of VTE in its acute and chronic forms, the clinician is frequently confronted with manifestations of VTE for which data are sparse and optimal management is unclear. In particular, the optimal use of advanced therapies for acute VTE, including thrombolysis and catheter-based therapies, remains uncertain. This report addresses the management of massive and submassive pulmonary embolism (PE), iliofemoral deep vein thrombosis (IFDVT),and chronic thromboembolic pulmonary hypertension (CTEPH). The goal is to provide practical advice to enable the busy clinician to optimize the management of patients with these severe manifestations of VTE. Although this document makes recommendations for management, optimal medical decisions must incorporate other factors, including patient wishes, quality of life, and life expectancy based on age and comorbidities. The appropriateness of these recommendations for a specific patient may vary depending on these factors and will be best judged by the bedside clinician.

Renal artery stenting is an effective treatment for renovascular hypertension, with a low angiographic restenosis rate. Stent placement appears to be a very attractive therapy in patients with lesions difficult to treat with balloon angioplasty such as renal aorto-ostial lesions and restenotic lesions, as well as after a suboptimal balloon angioplasty result.

Percutaneous stent placement for the treatment of CMI can be performed with a high procedural success and a low complication rate. The long-term freedom from symptoms and vascular patency are comparable with surgical results. The inherent lower procedural morbidity and mortality makes the endovascular approach the preferred revascularization technique for these patients.

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Background-A significant number (20% to 40%) of hypertensive patients with renal artery stenosis will not have blood pressure improvement after successful percutaneous revascularization. Identifying a group of patients with refractory hypertension and renal artery stenosis who are likely to respond to renal stent placement would be beneficial. Methods and Results-Brain natriuretic peptide (BNP) was measured in 27 patients with refractory hypertension and significant renal artery stenosis before and after successful renal artery stent placement. This neuropeptide was elevated (median, 187 pg/mL; 25th to 75th percentiles, 89 to 306 pg/mL) before stent placement and fell within 24 hours of the successful stent procedure (96 pg/mL; 25th to 75th percentiles, 61 to 182 pg/mL; Pϭ0.002), remaining low (85 pg/mL; 25th to 75th percentiles, 43 to 171 pg/mL) at follow-up. Clinical improvement in hypertension was observed in the patients with a baseline BNP Ͼ80 pg/mL (nϭ22) in 17 patients (77%) compared with 0% of the patients with a baseline BNP Յ80 pg/mL (nϭ5) (Pϭ0.001). After correction for glomerular filtration rate, BNP was strongly correlated with improvement in hypertension. Conclusions-BNP is increased in patients with severe renal artery stenosis and decreases after successful stent revascularization. In addition, an elevated baseline BNP level of Ͼ80 pg/mL appears to be a good predictor of a blood pressure response after successful stent revascularization. (Circulation. 2005;111:328-333.)

Catheter-based revascularization with stents for symptomatic S/IA lesions is safe and effective with excellent patency rates and sustained symptom resolution in the majority (>80%) of patients over 3 years of follow-up. Percutaneous primary stent therapy is the preferred method of revascularization in patients with suitable anatomy.

We performed percutaneous transluminal intervention in 20 consecutive patients (21 limbs) with common femoral artery (CFA) lesions causing symptomatic limb ischemia. In 12 limbs, concurrent additional percutaneous intervention proximal or distal to the target CFA lesion was performed. Angiographic success was obtained in 100%, with procedural success (angiographic success without a major in-hospital complications) in 90% and clinical success (procedural success and in-hospital improvement by at least one Fontaine functional class) in 81% of the limbs. The in-hospital Fontaine class improved by at least one functional class in 17 of 19 patients (89%), and the overall in-hospital event-free survival was 90% (18 of 20 patients). At follow-up (11.4 +/- 6 months), the overall event-free survival was 90% (18 of 20 patients) and 17 of 19 patients (89%) continue to show improvement by at least one functional (Fontaine) class. Percutaneous intervention of the CFA can be performed with a rate of high technical success and a low complication rate. It provides excellent clinical results at mid-term follow-up and appears to be a reasonable alternative to surgical therapy in patients at high risk for surgery.

BackgroundZofenopril, a sulfhydrylated angiotensin‐converting enzyme inhibitor (ACEI), reduces mortality and morbidity in infarcted patients to a greater extent than do other ACEIs. Zofenopril is a unique ACEI that has been shown to increase hydrogen sulfide (H2S) bioavailability and nitric oxide (NO) levels via bradykinin‐dependent signaling. Both H2S and NO exert cytoprotective and antioxidant effects. We examined zofenopril effects on H2S and NO bioavailability and cardiac damage in murine and swine models of myocardial ischemia/reperfusion (I/R) injury.Methods and ResultsZofenopril (10 mg/kg PO) was administered for 1, 8, and 24 hours to establish optimal dosing in mice. Myocardial and plasma H2S and NO levels were measured along with the levels of H2S and NO enzymes (cystathionine β‐synthase, cystathionine γ‐lyase, 3‐mercaptopyruvate sulfur transferase, and endothelial nitric oxide synthase). Mice received 8 hours of zofenopril or vehicle pretreatment followed by 45 minutes of ischemia and 24 hours of reperfusion. Pigs received placebo or zofenopril (30 mg/daily orally) 7 days before 75 minutes of ischemia and 48 hours of reperfusion. Zofenopril significantly augmented both plasma and myocardial H2S and NO levels in mice and plasma H2S (sulfane sulfur) in pigs. Cystathionine β‐synthase, cystathionine γ‐lyase, 3‐mercaptopyruvate sulfur transferase, and total endothelial nitric oxide synthase levels were unaltered, while phospho‐endothelial nitric oxide synthase1177 was significantly increased in mice. Pretreatment with zofenopril significantly reduced myocardial infarct size and cardiac troponin I levels after I/R injury in both mice and swine. Zofenopril also significantly preserved ischemic zone endocardial blood flow at reperfusion in pigs after I/R.ConclusionsZofenopril‐mediated cardioprotection during I/R is associated with an increase in H2S and NO signaling.