MitraClip therapy in surgical high-risk patients: identification of echocardiographic variables affecting acute procedural outcome.

OBJECTIVES: The aim of the study was to assess predictors of acute procedural failure in surgical high-risk patients undergoing MitraClip (Abbott Vascular, Abbott Park, Illinois) therapy. BACKGROUND: MitraClip implantation is a novel percutaneous option to treat significant mitral regurgitation (MR). METHODS: In 300 patients (75 ± 9 years of age, 190 [63%] men), of whom 32 (10.7%) had been unsuccessfully treated (discharge MR grade of >2+), baseline clinical and echocardiographic variables were evaluated by exact logistic regression and classification tree analyses to assess their impact on acute procedural failure. Acute procedural failure was differentiated into aborted procedure (no MitraClip implanted; n = 11) and "clip failure" (inadequate MR reduction despite MitraClip implantation; n = 21). RESULTS: Multivariate logistic regression identified effective regurgitant orifice area (EROA), mitral valve orifice area (MVOA), and mean transmitral pressure gradient (TMPG) as independent predictors of overall acute procedural failure. Classification tree analysis revealed that an EROA >70.8 mm(2) (n = 28) was associated with a high rate (25%) of clip failures, whereas the combination of an MVOA ≤3.0 cm(2) and a TMPG ≥4 mm Hg (n = 16) was associated with a high rate (37.5%) of aborted procedures. Failure rates of ≤10% were observed in all patients with an EROA ≤70.8 mm(2) and either an MVOA >3.0 cm(2) (n = 217) or an MVOA ≤3.0 cm(2) in concert with a TMPG ≤3 mm Hg (n = 39). Multinomial logistic regression identified an EROA >70.8 mm(2) and a TMPG ≥4 mm Hg as independently predictive of clip failure, but an MVOA ≤3.0 cm(2) and a TMPG ≥4 mm Hg as independently predictive of procedure abortion. CONCLUSIONS: In surgical high-risk patients undergoing MitraClip therapy, a TMPG ≥4 mm Hg, an EROA ≥70.8 mm(2), and an MVOA ≤3.0 cm(2) carry an increased risk of procedural failure.

Aetiology of mitral regurgitation differentially affects 2-year adverse outcomes after MitraClip therapy in high-risk patients.

AIMS: To assess, and identify predictors of 2-year adverse outcomes of surgical high-risk patients after successful MitraClip therapy (MC), differentiated by the aetiology of mitral regurgitation (MR). METHODS AND RESULTS: Kaplan-Meier analysis was used to assess survival free from death, heart failure rehospitalization, and reintervention up to 2 years in 202 successfully treated patients [74 ± 9 years, 132 men (65%); secondary MR aetiology in 140 patients, primary MR in 62]. Predictors for study endpoints were determined using Cox regression analyses. Mortality was 20% at 1 year and 33% at 2 years in both primary and secondary MR patients; independent predictors of death were reduced forward stroke volume, impaired LV function, and renal failure in primary MR, yet only an increased logistic EuroSCORE in functional MR patients. The rate of rehospitalizations was not different between the patient subgroups for 6 months, but then diverged significantly in favour of primary MR patients (estimated 2-year incidence, primary MR 40% vs. secondary MR 66%). No predictor was found for primary MR patients, but increased LV end-diastolic volume significantly increased the risk of rehospitalization in functional MR patients. Reinterventions were overall rare (7.4% at 1 year, 9.7% at 2 years); primary MR patients required all except one reintervention within 2 months of MC, with again no predictors found, whereas secondary MR patients (all except one with discharge MR of 2+) exhibited a steadily declining freedom from reintervention curve throughout follow-up. CONCLUSION: MR aetiology affects rehospitalization and reintervention, but not mortality, differently after successful MC.

In vitro blockade of adhesion of breast cancer cells to endothelial cells using anti-inflammatory drugs.

BACKGROUND: Increasing evidence suggests that a pro-inflammatory microenvironment affects distant metastasis of breast cancer cells, in particular by favoring tumor cell adhesion to endothelium. The aim of this study was to investigate the potential of different anti-inflammatory drugs to inhibit this effect in vitro. MATERIALS AND METHODS: Breast cancer cells from the metastatic cell line KM22 were incubated with activated Human umbilical vein endothelial cells (HUVECs). Tumor cell adhesion was quantified by fluorescence microscopy. The anti-inflammatory drugs ibuprofen, aspirin (acetylsalicylic acid), diclofenac, and dexamethasone were used as inhibiting agents. RESULTS: Aspirin and dexamethasone significantly reduced breast cancer cell adhesion to HUVECs (20.3%, p<0.000; and 25%, p<0.05, respectively). Ibuprofen and diclofenac did not significantly reduce tumor cell adhesion. CONCLUSION: Aspirin and dexamethasone seem to be able to partly inhibit adhesion of breast cancer cells to endothelium. Future studies should attempt to optimize this effect in vitro, in preparation for potential in vivo trials.