Use of an argatroban systemic infusion and purge solution in a patient with a percutaneous ventricular assist device with suspected heparin-induced thrombocytopenia.

PURPOSE: Thrombocytopenia can occur when using an Impella percutaneous ventricular assist device (pVAD), and heparin-induced thrombocytopenia (HIT) is often suspected. Data on heparin- and anticoagulant-free purge solutions in these devices are limited. Previous case reports have described argatroban-based purge solutions, both with and without systemic argatroban, at varying concentrations in patients with known or suspected HIT. SUMMARY: A 33-year-old male was transferred to our institution and emergently initiated on life support with venoarterial extracorporeal membrane oxygenation (ECMO), an Impella pVAD, and continuous venovenous hemofiltration to receive an urgent aortic valve replacement. Over the next several days, the patient's platelet count declined with a nadir of 17 × 103/µL on hospital day 13. The patient's 4T score for probability of HIT was calculated as 4. All heparin products were discontinued on hospital day 15, and the patient was initiated on systemic infusion with argatroban 1,000 µg/mL at a rate of 0.2 µg/kg/min with a purge solution of argatroban 0.05 mg/mL. The systemic infusion remained at a rate of 0.2 µg/kg/min, and the total argatroban dose was, on average, less than 0.25 µg/kg/min. On hospital day 21, the patient was transferred to another institution. CONCLUSION: Systemic infusion and a purge solution with argatroban were used in a patient with an Impella pVAD with multisystem organ dysfunction and suspected HIT. The patient achieved therapeutic activated partial thromboplastin times without adjustment of the systemic argatroban infusion and did not experience bleeding or thrombosis. Further studies concerning the safety and effectiveness of argatroban-based purge solutions in patients with pVADs are needed.

Left ventricular volume shifts and aortic root expansion during isovolumic contraction.

BACKGROUND AND AIM OF THE STUDY: Aortic valve opening involves conformational changes of the aortic root, including the ventricular-aortic junction (VAJ), sinotubular junction (STJ), and cusps. Moreover, the aortic root is contiguous with the left ventricular outflow tract (LVOT), which changes diameter throughout the cardiac cycle. Aortic root expansion prior to valve opening facilitates outward displacement of aortic cusp attachments, which helps flatten the cusps, thereby reducing cusp stress and fatigue, ultimately enhancing functional valve durability. The mechanisms underlying aortic root expansion prior to valve opening, however, remain incompletely characterized. The study aim was to establish a link between such aortic root expansion and intraventricular volume shifts into the LVOT during isovolumic contraction (IVC). METHODS: Miniature radiopaque markers were implanted on the left ventricle, VAJ, STJ, and aortic cusps of six sheep. After one week, 3-D marker coordinates were obtained using biplane videofluoroscopy (60 Hz). Triangular areas at the VAJ and STJ were calculated; LV main chamber (non-LVOT) and LVOT volumes were calculated using multiple tetrahedra. End-diastole was defined as the peak of the electrocardiogram R-wave, and end-IVC when aortic cusp separation began. RESULTS: During IVC, blood within the left ventricle was redistributed to the LVOT: mean LVOT volume was increased (+0.2 +/- 0.1 ml, p = 0.009) as non-LVOT volume fell (-0.8 +/- 0.4 ml, p = 0.006). Concomitantly, the aortic root expanded as both VAJ and STJ areas increased (+0.23 +/- 0.12 cm2 (p = 0.005) and +0.25 +/- 0.14 cm2 (p = 0.007), respectively) prior to aortic cusp separation. CONCLUSION: Aortic root expansion prior to valve opening is closely related to intraventricular volume shifts into the LVOT during IVC. Such volume shifts may 'prime' the aortic valve for ejection. These findings expand our understanding of cardiac dynamics by showing that blood acts as a coupling link between various cardiac units. Preservation of these normal aortic root dynamics may enhance the efficacy and durability of aortic surgical interventions.

Aorto-mitral annular dynamics.

BACKGROUND: The aortic and mitral valves are coupled through fibrous aorto-mitral continuity, but their synchronous dynamic physiology has not been completely characterized. METHODS: Seven sheep underwent implantation of five radiopaque markers on the left ventricle, 10 on the mitral annulus, and 3 on the aortic annulus. One of the mitral annulus markers was placed at the center of aorto-mitral continuity (mitral annulus "saddle horn"). Animals were studied with bi-plane videofluoroscopy 7 to 10 days postoperatively. Total circumference and lengths of mitral fibrous annulus, mitral muscular annulus, aortic fibrous annulus, and aortic muscular annulus were calculated throughout the cardiac cycle from three dimensional marker coordinates as was mitral annular area and aortic annular area. Aorto-mitral angle was determined as the angle between the centroid of the aortic annulus markers, the saddle horn, and the centroid of the mitral annulus markers. Aortic annulus and mitral annulus flexion was expressed as the difference between maximum and minimum values of the aortic and mitral annulus angles during the cardiac cycle. RESULTS: Mitral and aortic annular areas changed in roughly a reciprocal fashion during late diastole and early systole with an overall 32 +/- 8% change in aortic annular area and a 13 +/- 13% change in mitral annular area. Aortic fibrous annulus changed much less than aortic muscular annulus (6 +/- 2% vs 18 +/- 4%; p = 0.0003) as did mitral fibrous annulus relative to mitral muscular annulus (4 +/- 1% vs 8 +/- 2%; p = 0.004). Aortic annulus and mitral annulus flexion was 8 +/- 2 degrees and increased to 11 +/- 2 degrees (p = 0.009) with inotropic stimulation. CONCLUSIONS: Dynamic aortic and mitral annular area changes were not mediated through the anatomic fibrous continuity. Aorto-mitral flexion, which increased with enhanced contractility, may facilitate left ventricle ejection. The effect of valvular surgical interventions on aorto-mitral flexion needs further investigation.

Influence of anterior mitral leaflet second-order chordae tendineae on left ventricular systolic function.

BACKGROUND: The contribution of anterior mitral leaflet second-order ("strut") chordae tendineae to left ventricular (LV) systolic mechanics is debated; we measured the in vivo contribution of anterior chordae tendineae (ACT) and posterior chordae tendineae (PCT) to regional and global LV contractile function. METHODS AND RESULTS: Eight sheep had radiopaque markers implanted in the LV epicardium, partitioning the ventricle into 12 regions. Microminiature force transducers and snares were sutured to anterior leaflet "strut" chordae originating from ACT and PCT papillary muscles. Chordal tension, marker images, and hemodynamic data were acquired before and after (CUT) severing ACT and PCT. Fractional area shrinkage and slope of the regional end-diastolic area-regional stroke work relation (r-PRSW) were computed for each LV region. CUT did not affect global LV systolic function but reduced FAS in LV segments near the PCT insertion site: equatorial posterior lateral (19+/-2% versus 16+/-2%, P<0.05), apical posterior lateral (23+/-4% versus 19+/-4%, P<0.05), and posterior medial LV segments (16+/-2% versus 13+/-2%, P<0.05). r-PRSW fell near both the ACT (equatorial anterior medial [84+/-8 versus 62+/-11 mm Hg, P<0.05] and lateral [73+/-7 versus 53+/-9 mm Hg, P<0.05]) and PCT (apical posterior medial [91+/-12 versus 67+/-17 mm Hg, P<0.05] and lateral [72+/-8 versus 59+/-9 mm Hg, P<0.05]) LV insertion sites. Maximum tension in PCT was higher than in ACT (0.81+/-0.1 versus 0.52+/-0.08N, P<0.01). CONCLUSIONS: Dividing anterior leaflet strut chordae in sheep was associated acutely with regional LV systolic dysfunction near the chordal insertion sites. Caution is necessary when embarking on procedures that cut second-order chordae to treat ischemic mitral regurgitation, since this may compromise LV systolic function in ventricles that are already impaired.

The effects of mitral annuloplasty rings on mitral valve complex 3-D geometry during acute left ventricular ischemia.

OBJECTIVE: Annuloplasty rings are used to treat ischemic mitral regurgitation (IMR), but their exact effects on 3-D geometry of the overall mitral valve complex during acute left ventricular (LV) ischemia remain unknown. METHODS: Radiopaque markers were sutured to the mitral leaflet edges, annulus, papillary muscle tips, and ventricle in three groups of sheep. One group served as control (n = 5), and the others underwent Duran (n = 6) or Physio (n = 5) ring annuloplasty. One week later, 3-D marker coordinates at end-systole were obtained before and during balloon occlusion of the circumflex artery. RESULTS: In all control animals, acute LV ischemia was associated with: (i) septal-lateral separation of the leaflet edges, which was predicted by lateral displacement of the lateral annulus during septal-lateral mitral annular dilatation; (ii) apical restriction of the posterior leaflet edge, which was predicted by displacement of the lateral annulus away from the non-ischemic anterior papillary muscle; (iii) displacement of the posterior papillary muscle, which was not predictive of either septal-lateral leaflet separation or leaflet restriction; and (iv) mitral regurgitation. In the Duran group during ischemia, the posterior leaflet edge shifted posteriorly due to posterior movement of the lateral annulus, but no IMR occurred. In the Physio group during ischemia, neither the posterior leaflet edge nor the lateral annulus changed positions, and there was no IMR. In both the Duran and Physio groups, displacement of the posterior papillary muscle did not lead to IMR. CONCLUSIONS: Either annuloplasty ring prevented the perturbations of mitral leaflet and annular--but not papillary muscle tip--3-D geometry during acute LV ischemia. By fixing the septal-lateral annular dimension and preventing lateral displacement of the lateral annulus, annuloplasty rings prevented systolic septal-lateral leaflet separation and posterior leaflet restriction, and no acute IMR occurred. The flexible ring allowed posterior displacement of the posterior leaflet edge and the lateral annulus, which was not observed with a semi-rigid ring.

Surgical relocation of the posterior papillary muscle in chronic ischemic mitral regurgitation.

Mitral annuloplasty is the preferred surgical treatment for chronic ischemic mitral regurgitation. Although this is usually successful, leaflet restriction by apical displacement of the posterior papillary muscle tip may cause residual mitral regurgitation. Ventricular remodeling surgery is an effective procedure for surgical relocation of the posterior papillary muscle tip in the setting of a severely dilated left ventricle. Direct relocation of the posterior papillary muscle may be useful for patients with a minimally dilated left ventricle or regional left ventricular geometric changes causing mitral regurgitation. Such a surgical procedure is described.