Dynamic device properties of pulse contour cardiac output during transcatheter aortic valve implantation.

This prospective single-center study aimed to determine the responsiveness and diagnostic performance of continuous cardiac output (CCO) monitors based on pulse contour analysis compared with invasive mean arterial pressure (MAP) during predefined periods of acute circulatory deterioration in patients undergoing transcatheter aortic valve implantation (TAVI). The ability of calibrated (CCO(CAL)) and self-calibrated (CCO(AUTOCAL)) pulse contour analysis to detect the hemodynamic response to 37 episodes of balloon aortic valvuloplasty enabled by rapid ventricular pacing was quantified in 13 patients undergoing TAVI. A "low" and a "high" cut-off limit were predefined as a 15 or 25 % decrease from baseline respectively. We found no significant differences between CCO(CAL) and MAP regarding mean response time [low cut-off: 8.6 (7.1-10.5) vs. 8.9 (7.3-10.8) s, p = 0.76; high cut-off: 11.4 (9.7-13.5) vs. 12.6 (10.7-14.9) s, p = 0.32] or diagnostic performance [area under the receiver operating characteristics curve (AUC): 0.99 (0.98-1.0) vs. 1.0 (0.99-1.0), p = 0.46]. But CCOCAL had a significantly higher amplitude response [95.0 (88.7-98.8) % decrease from baseline] than MAP [41.2 (30.0-52.9) %, p < 0.001]. CCOAUTOCAL had a significantly lower AUC [0.83 (0.73-0.93), p < 0.001] than MAP. Moreover, CCO(CAL) detected hemodynamic recovery significantly earlier than MAP. In conclusion, CCO(CAL) and MAP provided equivalent responsiveness and diagnostic performance to detect acute circulatory depression, whereas CCO(AUTOCAL) appeared to be less appropriate. In contrast to CCO(CAL) the amplitude response of MAP was poor. Consequently even small response amplitudes of MAP could indicate severe decreases in CO.

Stroke volume determination using transcardiopulmonary thermodilution and arterial pulse contour analysis in severe aortic valve disease.

PURPOSE: Transcardiopulmonary thermodilution (TPTD, SVTD) as well as calibrated (SVPC CAL) and uncalibrated (SVPC UNCAL) arterial pulse contour analysis (PC) are increasingly promoted as less-invasive technologies to measure stroke volume (SV) but their reliability in aortic valve disease was unknown. The objective of this prospective study was to investigate the validity of three less-invasive techniques to assess SV in conditions involving aortic stenosis (AS) and valvuloplasty-induced aortic insufficiency (AI) compared with transesophageal echocardiography. METHODS: In 18 patients undergoing transcatheter aortic valve implantation, SVTD and SVPC CAL were determined using a central pressure signal via the brachial artery and SVPC UNCAL using a peripheral radial signal. RESULTS: In aortic valve dysfunction TPTD achieved adequate reproducibility (concordance correlation coefficient (CCC): AS 0.84; AI 0.82) and agreement (percentage error (PE): AS 26.3 %; AI 26.2 %) with the reference technique. In severe AS, SVPC CAL (PE 25.7 %; CCC 0.85) but not SVPC UNCAL (PE 50.4 %; CCC 0.38) was reliable. Neither calibrated nor uncalibrated PC (SVPC CAL: PE 51.5 %; CCC 0.49; SVPC UNCAL: PE 61.9 %; CCC 0.22) was valid in AI. Trending ability to hemodynamic changes, quantified by the ΔSV vector and the angle θ, was acceptable for each measurement modality. CONCLUSIONS: Transcardiopulmonary thermodilution is valid in aortic valve dysfunction. Calibration of PC substantially improves reliability in aortic valve disease. Calibrated PC is valid in severe AS. Valvuloplasty-induced AI seriously confounds PC measurements. In uncalibrated PC approaches, the relative SV trend is superior to single absolute values.

Different mechanisms of increased luminal stenosis after arterial injury in mice deficient for urokinase- or tissue-type plasminogen activator.

BACKGROUND: Tissue-type plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA) are thought to play critical roles in vascular remodeling after injury, with tPA mediating intravascular clot lysis and uPA modulating cell migration within the vessel wall. In human vascular disease, however, thrombus organization and neointimal formation are closely interrelated processes. This study examines the differential roles of tPA and uPA in these processes in mice. METHODS AND RESULTS: Carotid artery injury and thrombosis were induced in wild-type (WT), uPA-deficient (uPA(-/-)), and tPA-deficient (tPA(-/-)) mice with the use of ferric chloride. The expression of uPA and tPA was significantly upregulated in the vessel wall of WT mice 1 week after injury, and compared with WT mice, uPA(-/-) and tPA(-/-) mice had lower carotid patency rates after injury. At 3 weeks, only 55% of uPA(-/-) mouse vessels were patent compared with 81% in tPA(-/-) mice and 100% in WT mice (P=0.014). Morphometric analysis of injured arterial segments revealed severe luminal stenosis (62+/-28%) in uPA(-/-) mice compared with their tPA(-/-) (16+/-12%) and WT (6.3+/-3.6%, P<0.001) counterparts. Moreover, although the vascular walls of WT mice and, particularly, tPA(-/-) mice developed a cell-rich multilayered neointima and media, the lumen of uPA(-/-) vessels remained obstructed with acellular unorganized thrombotic material, and their medial areas did not expand. CONCLUSIONS: These results indicate that the roles of uPA and tPA in the arterial response to injury are different and more complex than previously assumed and emphasize the critical role of thrombus organization and resolution in neointimal formation and vascular pathology.