Consensus Statement on the Management of Nonthrombotic Iliac Vein Lesions From the VIVA Foundation, the American Venous Forum, and the American Vein and Lymphatic Society.

A nonthrombotic iliac vein lesion is defined as the extrinsic compression of the iliac vein. Symptoms of lower extremity chronic venous insufficiency or pelvic venous disease can develop secondary to nonthrombotic iliac vein lesion. Anatomic compression has been observed in both symptomatic and asymptomatic patients. Causative factors that lead to symptomatic manifestations remain unclear. To provide guidance for providers treating patients with nonthrombotic iliac vein lesion, the VIVA Foundation convened a multidisciplinary group of leaders in venous disease management with representatives from the American Venous Forum and the American Vein and Lymphatic Society. Consensus statements regarding nonthrombotic iliac vein lesions were drafted by the participants to address patient selection, imaging for diagnosis, technical considerations for stent placement, postprocedure management, and future research/educational needs.

Primary results of the SAVAL randomized trial of a paclitaxel-eluting nitinol stent versus percutaneous transluminal angioplasty in infrapopliteal arteries.

BACKGROUND: Effective and durable options for infrapopliteal artery revascularization for patients with chronic limb-threatening ischemia (CLTI) are limited. METHODS: The SAVAL trial is a prospective, multicenter, randomized trial of patients with CLTI and infrapopliteal artery lesions with total lesion length ⩽ 140 mm, stenosis ⩾ 70%, and Rutherford category 4-5 assigned 2:1 to treatment with the SAVAL self-expandable paclitaxel drug-eluting stent (DES) or percutaneous transluminal angioplasty (PTA) with an uncoated balloon. The primary effectiveness endpoint was primary vessel patency (i.e., core lab-adjudicated duplex ultrasound-based flow at 12 months in the absence of clinically driven target lesion revascularization or surgical bypass of the target lesion). The primary safety endpoint was the 12-month major adverse event (MAE)-free rate; MAEs were defined as a composite of above-ankle index limb amputation, major reintervention, and 30-day mortality. The endpoints were prespecified for superiority (effectiveness) and noninferiority (safety) at a one-sided significance level of 2.5%. RESULTS: A total of 201 patients were enrolled and randomly assigned to treatment (N = 130 DES, N = 71 PTA). Target lesion length was 68.1 ± 35.2 mm for the DES group and 68.7 ± 49.2 mm for the PTA group, and 31.0% and 27.6% of patients, respectively, had occlusions. The 12-month primary patency rates were 68.0% for the DES group and 76.0% for the PTA group (Psuperiority = 0.8552). The MAE-free rates were 91.6% and 95.3%, respectively (Pnoninferiority = 0.0433). CONCLUSION: The SAVAL trial did not show benefit related to effectiveness and safety with the nitinol DES compared with PTA in infrapopliteal artery lesions up to 140 mm in length. Continued innovation to provide optimal treatments for CLTI is needed. (ClinicalTrials.gov Identifier: NCT03551496).

A modified provisional stenting approach to coronary bifurcation lesions: clinical application of the "jailed-balloon technique".

OBJECTIVES: To demonstrate the application of a novel provisional side branch (SB) stenting strategy for coronary bifurcation lesions using a "jailed-balloon" technique (JBT). BACKGROUND: Adverse cardiac events are higher for percutaneous coronary intervention (PCI) of bifurcation lesions. Recent studies support the use of provisional SB stenting, but a risk of SB closure and a higher rate of target lesion revascularization (TLR) remain important limitations. METHODS: From December 2007 to August 2010, 100 patients with 102 bifurcation lesions underwent PCI using the JBT. Baseline and postprocedural quantitative coronary angiography (QCA) analysis were performed. Procedural and immediate clinical outcomes were reviewed. RESULTS: The majority of patients presented with acute coronary syndrome (68%) and had Medina class 1,1,1 bifurcation lesions (91%). TIMI 3 flow was established in 100% of main branch and 99% of SB lesions. QCA revealed preservation of the bifurcation angle after PCI (pre-PCI: 59.6 ± 30.0; post-PCI: 63.3 ± 26.8, P = 0.41). Nine patients (9%) had lesions that required rewiring and two patients (2%) required provisional stenting of the SB. SB loss occurred in one patient (1%). The jailed-balloon or wire was not entrapped during any PCI. One patient (1%) suffered a periprocedural myocardial infarction (MI). CONCLUSIONS: Provisional stenting of complex coronary bifurcation lesions using a JBT is associated with a high procedural success rate, improved SB patency, and a low rate of immediate cardiac events. Further study is warranted to evaluate the role of JBT in improving long-term clinical outcomes in PCI of complex bifurcation lesions.

Use of mechanical assist during high-risk PCI and STEMI with cardiogenic shock.

Infarct size may be reduced by left ventricular unloading after ST-segment elevation MI (STEMI) in addition to reperfusion therapy. Likewise, high-risk percutaneous coronary intervention (PCI) may benefit from periprocedural support especially in patients with low cardiac output at baseline or when periprocedural hemodynamic deterioration is anticipated. Traditionally, intraaortic balloon-pumps have been used in acute MI with cardiogenic shock. As this modality has limited hemodynamic benefits, new developments have focused on active hemodynamic assist devices. These devices actively unload the left ventricle increasing cardiac output by 2.5-5 L/min and are increasingly easier to implant and monitor. Thus, interventional cardiologists will be able to offer a safer more effective alternative to an increasing patient population with complex cardiac conditions and high-risk PCI.

Osteopontin promoter polymorphism is associated with increased carotid intima-media thickness.

BACKGROUND: Osteopontin (OPN)-transgenic mice exhibit increased carotid artery intima-media thickness (CIMT), smooth muscle cell proliferation, and atheroma formation. METHODS: An association of the human T-66G promoter variant with CIMT was examined in Caucasian adults grouped according to metabolic syndrome criteria: present (+MetS; n = 70) or absent (-MetS; n = 70). RESULTS: The G-allele frequency was 22%. For the entire cohort, the G group (TG and GG) was associated with significantly lower age-adjusted and gender-adjusted CIMT compared with the TT group (P = .008); similar analysis by metabolic syndrome group found a significant difference only in the -MetS group (P = .018). Stepwise multivariate regression showed that after age and waist circumference, the T-66G variant was the next most predictive of CIMT (P = .007). These data suggest that in a normoglycemic environment, human vascular OPN gene expression contributes to arterial structure, an effect diminished in dysmetabolic states. CONCLUSION: Humans with the OPN -66 TT genotype, particularly those without metabolic syndrome, exhibit thicker CIMT.

Role of tissue Doppler and color M-mode imaging for evaluation of diastolic function in ambulatory patients with LV systolic dysfunction.

INTRODUCTION: Tissue Doppler imaging (TDI) and color M-mode (CMM) indices provide assessment of left ventricular (LV) relaxation when combined with pulse-wave Doppler (PWD)-derived transmitral inflow, allows for estimation of LV filling pressures. However, use of these indices in patients with LV systolic dysfunction (LVSD) has not been well characterized. METHODS AND RESULTS: The study included 115 patients (age 58 +/- 11 years, 67% male) with LVSD (LV ejection fraction [LVEF] < 55%). Patients were grouped according to the diastolic LV filling pressure assessed by E/Em(septal) ratio as follows: 1) Normal (NFP), E/Em(septal) < 8; 2) Intermediate (IFP), E/Em(septal): 8-15; and 3) High (HFP), E/Em(septal) >15. Age-, gender-, and LVEF-adjusted analyses were performed. LV volumes and LVEF were significantly different between the groups (P < 0.01). PWD-derived E-wave velocity showed a significant stepwise increase across the three groups and the Em(septal) velocity demonstrated a stepwise decrease (P < 0.01 for both). CMM-derived diastolic intra-ventricular pressure gradient (IVPG) was significantly lower in the HFP compared to the other 2 groups (P < 0.01 for both); Vp was increased in the HFP compared to the other 2 groups (P < 0.01 for both), and Vp exhibited a U-shape relationship to LVEF. CONCLUSION: In patients with LVSD, abnormal LV relaxation is uniformly observed regardless of LV filling pressure. PWD-derived E-wave velocity and the TDI-derived Em velocity are important measurements to identify elevated LV filling pressures. CMM-derived Vp and IVPG were of limited incremental value for the evaluation of diastolic function in patients with LVSD.

Metabolic syndrome is associated with abnormal left ventricular diastolic function independent of left ventricular mass.

AIM: To characterize the extent to which metabolic syndrome criteria predict left ventricular (LV) structure and function. METHODS AND RESULTS: Metabolic syndrome criteria were assessed in 607 adults with normal LV function. The cohort was grouped according to the number of criteria satisfied: (1) Absent (0 criteria, n = 110); (2) Pre-Metabolic Syndrome (1-2 criteria, n = 311); and (3) Metabolic Syndrome (>or=3 criteria, n = 186). Echocardiography was used to assess LV structure (LV mass) and systolic (LVEF, Vs) and diastolic function, by pulse-wave Doppler (E/A ratio) and tissue Doppler imaging (Ve). LV volumes and LVEF were similar between groups. However, LV mass increased significantly and progressively (LVM/Ht(2.7), in g/m(2.7): 34.9 +/- 6.7, 41.0 +/- 9.5, 46.3 +/- 11.0, P < 0.001); LV relaxation decreased progressively (Ve(global'), in cm/s: 13.5 +/- 2.8, 12.1 +/- 3.0, 10.5 +/- 2.2, P < 0.001) from Absent to Pre-Metabolic Syndrome to Metabolic Syndrome groups, respectively. Multiple variable analyses showed that diastolic blood pressure, waist circumference, and triglyceride levels were independent predictors of Ve after adjustment for LV mass. CONCLUSION: Patients with metabolic syndrome have LV diastolic dysfunction independent of LV mass. These functional abnormalities may partially explain the increased cardiovascular morbidity and mortality associated with metabolic syndrome.