Comparison of vascular closure devices for access site closure after transfemoral aortic valve implantation.

BACKGROUND: The majority of transcatheter aortic valve implantation (TAVI) procedures are currently performed by percutaneous transfemoral approach. The potential contribution of the type of vascular closure device to the incidence of vascular complications is not clear. AIM: To compare the efficacy of a Prostar XL- vs. Perclose ProGlide-based vascular closure strategy. METHODS: The ClOsure device iN TRansfemoral aOrtic vaLve implantation (CONTROL) multi-center study included 3138 consecutive percutaneous transfemoral TAVI patients, categorized according to vascular closure strategy: Prostar XL- (Prostar group) vs. Perclose ProGlide-based vascular closure strategy (ProGlide group). Propensity-score matching was used to assemble a cohort of patients with similar baseline characteristics. RESULTS: Propensity matching identified 944 well-matched patients (472 patient pairs). Composite primary end point of major vascular complications or in-hospital mortality occurred more frequently in Prostar group when compared with ProGlide group (9.5 vs. 5.1%, P = 0.016), and was driven by higher rates of major vascular complication (7.4 vs. 1.9%, P < 0.001) in the Prostar group. However, in-hospital mortality was similar between groups (4.9 vs. 3.5%, P = 0.2). Femoral artery stenosis occurred less frequently in the Prostar group (3.4 vs. 0.5%, P = 0.004), but overall, Prostar use was associated with higher rates of major bleeding (16.7 vs. 3.2%, P < 0.001), acute kidney injury (17.6 vs. 4.4%, P < 0.001) and with longer hospital stay (median 6 vs. 5 days, P = 0.007). CONCLUSIONS: Prostar XL-based vascular closure in transfemoral TAVI procedures is associated with higher major vascular complication rates when compared with ProGlide; however, in-hospital mortality is similar with both devices.

Correlation between trans and intra-thoracic impedance and conductance in patients with chronic heart failure.

AIMS: In chronic heart failure, changes of intra-thoracic impedance (Z0IT) may suggest impending pulmonary congestion; a similar result has been found by measuring trans-thoracic conductance (TFCTT = 1/Z0 = 1/kΩ). We assumed that a relationship could exist between Z0IT and TFCTT. METHODS: We collected 140 measurements from 70 patients carrying an implantable cardioverter-defibrillator/cardiac resynchronization device with the CareLink function (71 ± 9 years, New York Heart Association (NYHA) 2.4 ± 0.9, ejection fraction 31 ± 8%, optimal treatment); they were studied during system alarms and after appropriate treatment (diuretics and/or vasodilators, n = 42) or during clinical stability and at the time of a system alarm (n = 28); correspondent BNP values were obtained. We related Z0IT obtained by the device, with TFCTT obtained with a commercial system. RESULTS: A strong relationship was found between Z0IT and TFCTT. Changes in the variables after treatment or during worsening conditions were of the same direction and order of magnitude, and were related to BNP levels obtained simultaneously. CONCLUSIONS: Trans-thoracic conductance, similarly to intra-thoracic impedance, may noninvasively point to pulmonary congestion and be useful in patients not carrying an implanted device. The possibility of remotely obtaining this variable should be evaluated for the telemonitoring of heart failure patients.

Acute effects of levosimendan on mitral regurgitation and diastolic function in patients with advanced chronic heart failure.

BACKGROUND: We analyzed the inodilator properties of levosimendan in patients with chronic heart failure and severe functional mitral regurgitation. METHODS: We studied 20 patients under optimal treatment and in stable clinical condition (New York Heart Association 3.19 + or - 0.66; 70 + or - 7 years). Levosimendan was infused as a bolus (12 microg/kg in 10 min) followed by a 24-h infusion (0.1-0.2 microg/kg per min). Before and after infusion, Doppler echocardiography, brain natriuretic peptide determination and noninvasive hemodynamic monitoring with bioimpedance cardiography were performed. RESULTS: Levosimendan improved left ventricular ejection fraction (ejection fraction 31 + or - 4 from 27 + or - 4, P < 0.05), decreased brain natriuretic peptide (333 + or - 139 from 629 + or - 63 pg/ml, P < 0.01), reduced mitral valve effective regurgitant orifice area to 27 + or - 5 from 36 + or - 7 mm (P < 0.01) and the velocity of displacement of mitral annulus [ratio between E and E' waves on Doppler and tissue Doppler (E/E') from 22.7 + or - 1.6 to 13.1 + or - 0.6, P < 0.01]. Noninvasive hemodynamic monitoring showed increased acceleration index (a marker of inotropism), and reduced peripheral resistances and thoracic fluid content (P < 0.01). After 4 weeks of washout, some of these effects were still evident. CONCLUSION: In patients with chronic heart failure and functional mitral regurgitation, levosimendan acutely improved systolic and diastolic function, reduced mitral regurgitation and modulated neurohormonal activation, with a tendency for these changes to persist over a short-term follow-up.