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Background. Chordal transposition is used in mitral valve repair, yet the effects of second-order chord transection on valve function have not been extensively studied. We evaluated leaflet coaptation, threedimensional anterior mitral valve leaflet shape, and valve competence after cutting anterior second-order chordae. Methods. In 8 sheep radiopaque markers were affixed to the left ventricle, mitral annulus, and leaflets. Animals were studied immediately with biplane videofluoroscopy and echocardiography before (Control) and after (Cut2) severing two anterior second-order “strut” chordae. Leaflet coaptation was assessed as separation between leaflet edge markers in the midleaflet and near each commissure (anterior commissure, posterior commissure). Anterior leaflet geometry was determined 100 milliseconds after end-diastole from three-dimensional coordinates of 13 markers. Results. Anterior leaflet geometry changed only slightly after chordal transection without inducing mitral regurgitation. Leaflet coaptation times were 79 6 17 and 87 6 22 milliseconds at the anterior commissure; 72 6 21, 72 6 19 milliseconds at midleaflet, and 71 6 12 and 75 6 8 milliseconds at the posterior commissure (p 5 NS) for Control and Cut2, respectively. Conclusions. Cutting anterior second-order chordae did not cause delayed leaflet coaptation, alter leaflet shape, or create mitral regurgitation. These data indicate that transposition of second-order anterior chordae (“strut” chordae) is not deleterious to anterior leaflet motion per se.

Objective: Incomplete mitral leaflet coaptation during acute left ventricular ischemia is associated with end-diastolic mitral annular dilatation and ischemic mitral regurgitation. Annular rings were implanted in sheep to investigate whether annular reduction alone is sufficient to prevent mitral regurgitation during acute posterolateral left ventricular ischemia. Methods: Radiopaque markers were inserted around the mitral anulus, on papillary muscle tips, and on the central meridian of both mitral leaflets in three groups of sheep: control (n = 5), Physio ring (n = 5) (Baxter Cardiovascular Div, Santa Ana, Calif), and Duran ring (n = 6) (Medtronic Heart Valve Div, Minneapolis, Minn). After 8 ± 1 days, animals were studied with biplane videofluoroscopy before and during left ventricular ischemia. Annular area was calculated from 3-dimensional marker coordinates and coaptation defined as minimal distance between leaflet edge markers. Results: Before ischemia, leaflet coaptation occurred just after end-diastole in all groups (control 17 ± 41, Duran 33 ± 30, Physio 33 ± 24 ms, mean ± SD, P > .2 by analysis of variance). During ischemia, regurgitation was detected in all control animals, and leaflet coaptation was delayed to 88 ± 8 ms after end-diastole (P = .02 vs preischemia). This was associated with increased end-diastolic annular area (8.0 ± 0.9 vs 6.7 ± 0.6 cm2, P = .004) and septal-lateral annular diameter (2.9 ± 0.1 vs 2.5 ± 0.1 cm, P = .02). Mitral regurgitation did not develop in Duran or Physio sheep, time to coaptation was unchanged (Duran 25 ± 25 ms, Physio 30 ± 48 ms [both P > .2 vs preischemia]), and annular area remained fixed. Conclusion: Mitral annular area reduction and fixation with an annuloplasty ring eliminated delayed leaflet coaptation and prevented mitral regurgitation during acute left ventricular ischemia after ring implantation. (J Thorac Cardiovasc Surg 2000;119:774-83)

Background —Recently, renewed interest in allograft and stentless “freehand” bileaflet xenograft mitral valve replacement has arisen. The variability of human papillary tip anatomy and scarcity of donors limit allograft availability, making xenograft mitral valves an attractive alternative; however, these valves require new surgical implantation techniques, and assessment of their hemodynamics and functional geometry is lacking. Methods —Seven sheep underwent implantation of a new stentless, glutaraldehyde-preserved porcine mitral valve (Physiological Mitral Valve [PMV], Medtronic) and were studied acutely under open-chest conditions. A new method of retrograde cardioplegia was developed. Hemodynamic valve function was assessed by epicardial Doppler echocardiography. 3D motion of miniature radiopaque markers sutured to the valve leaflets, annulus, and papillary tips was measured. Six other sheep with implanted markers served as controls. Results —Both papillary muscle tips avulsed in the first animal, leaving 6 other animals. Mitral regurgitation was not observed in any xenograft valve. The peak and mean transvalvular gradients were 4.6±1.8 mm Hg and 2.6±1.5 mm Hg, respectively. The average mitral valve area was 5.7±1.6 cm 2 . Valve closure in the xenograft group occurred later (30±11 ms, P P P P P Conclusions —Successful freehand stentless porcine mitral valve implantation is feasible in sheep and was associated with excellent early postoperative hemodynamics. Physiological mitral valve annular contraction and functional leaflet closure mechanics were preserved. Long-term valve durability, calcification, and hemodynamic performance remain to be determined in models.

Background —Current surgical methods for treating aortic valve and aortic root pathology vary widely, and the basis for selecting one repair or replacement alternative over another continues to evolve. More precise knowledge of the interaction between normal aortic root dynamics and aortic valve mechanics may clarify the implications of various surgical procedures on long-term valve function and durability. Methods and Results —To investigate the role of aortic root dynamics on valve function, we studied the deformation modes of the left, right, and noncoronary aortic root regions during isovolumic contraction, ejection, isovolumic relaxation, and diastole. Radiopaque markers were implanted at the top of the 3 commissures (sinotubular ridge) and at the annular base of the 3 sinuses in 6 adult sheep. After a 1-week recovery, ECG and left ventricular and aortic pressures were recorded in conscious, sedated animals, and the 3D marker coordinates were computed from biplane videofluorograms (60 Hz). Left ventricular preload, contractility, and afterload were independently manipulated to assess the effects of changing hemodynamics on aortic root 3D dynamic deformation. The ovine aortic root undergoes complex, asymmetric deformations during the various phases of the cardiac cycle, including aortoventricular and sinotubular junction strain and aortic root elongation, compression, shear, and torsional deformation. These deformations were not homogeneous among the left, right, and noncoronary regions. Furthermore, changes in left ventricular volume, pressure, and contractility affected the degree of deformation in a nonuniform manner in the 3 regions studied, and these effects varied during isovolumic contraction, ejection, isovolumic relaxation, and diastole. Conclusions —These complex 3D aortic root deformations probably minimize aortic cusp stresses by creating optimal cusp loading conditions and minimizing transvalvular turbulence. Aortic valve repair techniques or methods of replacement using unstented autograft, allograft, or xenograft tissue valves that best preserve this normal pattern of aortic root dynamics should translate into a lower risk of long-term cusp deterioration.

Background —Asymmetrical mitral annular (MA) dilatation and papillary muscle dislocation are implicated in the pathogenesis of functional mitral regurgitation (MR). Methods and Results —To determine the mechanism by which annular and papillary muscle geometric alterations result in MR, we implanted radiopaque markers in the left ventricle, mitral annulus, anterior and posterior mitral leaflets, and papillary muscle tips and bases in 2 groups of sheep. One group served as controls (CTL, n=7); an experimental group (EXP, n=9) underwent topical phenol application to obliterate anterior annular and leaflet muscle (confirmed histologically ex vivo). After 1 week of recovery, markers were imaged with biplane videofluoroscopy, and hemodynamic data were recorded. MA area (computed from 3-dimensional marker coordinates) was 11% to 13% larger in the EXP group than in the CTL group ( P 1 cm) increases in both the intercommissural and septolateral annular axes. The anterior papillary muscle tip in EXP was displaced from CTL by 2.9±0.23 mm toward the anterolateral left ventricle and 2.5±0.12 mm toward the mitral annulus at end systole; the posterior papillary muscle geometry was unchanged. Transthoracic echocardiography revealed MR only in the heart exhibiting biaxial annular enlargement. Conclusions —MA dilatation in the intercommissural dimension with anterior papillary muscle tip displacement toward the annulus is insufficient to produce MR in sheep. Functional MR may require MA dilatation in the septolateral axis, as observed with proximal circumflex coronary occlusion.

The flow patterns in the human heart are complex and difficult to visualize using conventional two-dimensional (2D) modalities, whether they depict a single velocity component (Doppler echocardiography) or all three components in a few slices (2D phase contrast MRI). To avoid these shortcomings, a temporally resolved 3D phase contrast technique was used to derive data describing the intracardiac velocity fields in normal volunteers. The MRI data were corrected for phase shifts caused by eddy currents and concomitant gradient fields, with improvement in the accuracy of subsequent flow visualizations. Pathlines describing the blood pathways through the heart were generated from the temporally resolved velocity data, starting from user-specified locations and time frames. Flow trajectories were displayed as 3D particle traces, with simultaneous demonstration of morphologic 2D slices. This type of visualization is intuitive and interactive and may extend our understanding of dynamic and previously unrecognized patterns of intracardiac flow.

Infective endocarditis (IE) carries a high risk of morbidity and mortality. Rapid diagnosis, effective treatment, and prompt recognition of complications are essential to good patient outcome. Therapy of IE caused by the more commonly encountered organisms, including streptococci, enterococci, staphylococci, and the HACEK organisms ( Hemophilus parainfluenzae, Hemophilus aphrophilus, Actinobacillus [Hemophilus] actinomycetemcomitans, Cardiobacterium hominis, Eikenella species , and Kingella species), has been addressed previously by this committee.1 Likewise, the antimicrobial prevention of endocarditis has also been previously addressed.2 In this article, we review and update the current literature with respect to diagnostic challenges and strategies, difficult therapeutic situations, and management choices in patients with IE. This article focuses predominantly on adults with IE. A separate article, currently in preparation, will address the issues of IE in childhood. ### Clinical Criteria The diagnosis of IE is straightforward in those patients with classic oslerian manifestations: bacteremia or fungemia, evidence of active valvulitis, peripheral emboli, and immunologic vascular phenomena. In other patients, however, the classic peripheral stigmata may be few or absent.3 This may occur during acute courses of IE, particularly among intravenous drug abuse (IVDA) patients in whom IE is often due to Staphylococcus aureus infection of right-sided heart valves, or in patients with IE caused by microorganisms such as HACEK. Acute IE evolves too quickly for the development of immunologic vascular phenomena, which are more characteristic of subacute IE. In addition, acute right-sided IE valve lesions do not create the peripheral emboli and immunologic vascular phenomena that can result from left-sided valvular involvement.3 The variability in the clinical presentation of IE requires a diagnostic strategy that will be both sensitive for disease detection and specific for its exclusion across all the forms of the disease. In 1981, von Reyn et al4 proposed a scheme for strict case definitions of IE …

Background: The mechanism by which incomplete mitral leaflet coaptation develops during ischemic mitral regurgitation is debated, with recent studies suggesting that incomplete mitral leaflet coaptation may be due to apically displaced papillary muscle tips. Yet quantitative in vivo three-dimensional mitral leaflet motion during ischemic mitral regurgitation has never been described. Methods: Radiopaque markers (sutured around the mitral anulus, to the central free mitral leaflet edges, and to both papillary muscle tips and bases) were imaged with the use of biplane videofluoroscopy in six closed-chest, sedated sheep before (control) and during induction of acute ischemic mitral regurgitation. Leaflet coaptation was defined as the minimum distance measured between edge markers during control conditions. Results: During control, leaflet coaptation occurred 23 ± 7 msec (mean ± standard error of the mean) after end-diastole, when left ventricular pressure was 27 ± 6 mm Hg. During ischemic mitral regurgitation, coaptation was delayed to 115 ± 19 msec after end-diastole (p 0.01 {abs2}vs control [n = 4]) when left ventricular pressure was 88 ± 4 mm Hg. At end-diastole during ischemic mitral regurgitation, the mitral anulus area was 14% ± 2% larger than control (7.4 ± 0.3 cm 2 vs 6.5 ± 0.2 cm 2, p 0.005) as the result of the lengthening of muscular annular regions (76.0 ± 2.5 mm vs 70.5 ± 1.4 mm, p 0.01). Mitral anulus shape (ratio of two diameters) at end-diastole was more circular during ischemic mitral regurgitation (0.79 ± 0.01 vs 0.71 ± 0.02, p < 0.01). At end-diastole during ischemic mitral regurgitation, the posterior papillary muscle tip was displaced 1.5 ± 0.5 mm laterally and 2.0 ± 0.6 mm posteriorly (p 0.02 vs control), but there was no apical displacement of either papillary muscle tip. Conclusions: Incomplete mitral leaflet coaptation during acute ischemic mitral regurgitation occurred early in systole, not at end-systole, and was due to “loitering” of the leaflets associated with posterior mitral anulus enlargement and circularization, as well as some posterolateral, but not apical, posterior papillary muscle tip displacement. These data suggest that early systolic mitral anulus dilatation and shape change and altered posterior papillary muscle motion are the primary mechanisms by which incomplete mitral leaflet coaptation occurs during acute ischemic mitral regurgitation. (J Thorac Cardiovasc Surg 1998;116:193-205)

In this issue of the Journal , Hoffmann et al. ([1][1]) report on their comparison of conventional and contrast-enhanced echocardiography, biplane cine angiography, and cardiac magnetic resonance for the detection of regional wall motion abnormalities. Their effort to acquire three or four of these

The benefit of left ventricular (LV) unloading for preserving LV function is commonly accepted, but its efficacy remains incompletely defined.We studied the influence of complete LV unloading on LV systolic and diastolic mechanics using an in situ isovolumic preparation with two different coronary perfusion pressures (CPPs) in 12 dogs during prolonged normothermic cardiopulmonary bypass.Multivariate analysis of covariance with time as a covariate revealed that a high CPP (143 +/- 36 mm Hg; n = 6) was associated with better preservation of systolic LV function over time as assessed by LV end-systolic elastance (p0.001) and the end-systolic pressure-volume relation physiologic intercept (p0.001) compared with a moderate CPP (107 +/- 18 mm Hg; p0.005 versus a high CPP by t-test; n = 6). Dobutamine (2 micrograms.kg-1.min-1) improved LV end-systolic elastance (p0.005) and LV physiologic intercept (p0.01) only in the high-CPP group. Conversely, impaired LV diastolic function (as measured by LV stiffness) was observed (p0.001) with a high CPP, but did not change with a moderate CPP.These observations in canine hearts suggest that complete LV unloading may not preserve LV systolic function adequately over time when CPP is maintained in the accepted clinical range. A higher CPP is required to prevent deterioration over prolonged cardiopulmonary bypass times, but diastolic dysfunction still occurs.

Background Left ventricular (LV) unloading with mechanical support devices alters biventricular geometry and impairs right ventricular (RV) contractility, but its effect on septal systolic function remains unknown. Methods and Results To evaluate the effects of LV volume and pressure unloading on septal geometry and function, LV preload was abruptly reduced by clamping left atrial pressure between 0 and −2 mm Hg in seven open-chest, anesthetized dogs by use of a pressure-control servomechanism to withdraw blood from the left atrium. With left atrial pressure clamping, maximal LV pressure decreased 30±12% (mean±SD) ( P P P P P P P P Conclusions LV unloading not only altered interventricular septal geometry but also reduced septal systolic thickening and output, all of which may contribute to impaired RV contractility during mechanical LV support.

Objectives. Mitral valve homografts, despite theoretical advantages, are not widely used, in part because of lack of basic information about the three-dimensional geometry of the mitral apparatus. Methods: Radiopaque markers were used in the study of eight closed-chest dogs under four conditions: (1) baseline, (2) caval occlusion, (3) tachycardia (atrial pacing), and (4) nitroprusside infusion. Using a cylindrical coordinate system, defined with the origin at the midpoint between the anterior and posterior commissures, and the left ventricular long axis (z-axis), defined by the origin and the left ventricular apex, DTIP-MA (the z-coordinate [millimeters] of the papillary muscle tip), was measured at 10 time points throughout the entire cardiac cycle. DBASE-MA (the z-coordinate of the papillary muscle base) and LPM (the length of the papillary muscle [millimeters]) were also measured. Results: DTIP-MA varied slightly with time (p < 0.001 by analysis of variance), but the magnitude of change was negligible (

Autores/Miembros del Grupo de Trabajo Presidentes: Kristian Thygesen (Dinamarca), Joseph S. Alpert (Estados Unidos), Harvey D. White (Nueva Zelanda); Subcomite sobre Biomarcadores: Allan S. Jaffe (Estados Unidos), Hugo A. Katus (Alemania), Fred S. Apple (Estados Unidos), Bertil Lindahl (Suecia) y David A. Morrow (Estados Unidos); Subcomite del ECG: Bernard R. Chaitman (Estados Unidos), Peter M. Clemmensen (Dinamarca), Per Johanson (Suecia) y Hanoch Hod (Israel); Subcomite de Imagen: Richard Underwood (Reino Unido), Jeroen J. Bax (Paises Bajos), Robert O. Bonow (Estados Unidos), Fausto Pinto (Portugal) y Raymond J. Gibbons (Estados Unidos); Subcomite de Clasificacion: Keith A. Fox (Reino Unido), Dan Atar (Noruega), L. Kristin Newby (Estados Unidos), Marcello Galvani (Italia) y Christian W. Hamm (Alemania); Subcomite de Intervencion: Barry F. Uretsky (Estados Unidos), P. Gabriel Steg (Francia), William Wijns (Belgica), Jean-Pierre Bassand (Francia), Phillippe Menasche (Francia) y Jan Ravkilde (Dinamarca); Subcomite de Ensayos y Registros: E. Magnus Ohman (Estados Unidos), Elliott M. Antman (Estados Unidos), Lars C. Wallentin (Suecia), Paul W. Armstrong (Canada) y Maarten L. Simoons (Paises Bajos); Subcomite de Insuficiencia Cardiaca: James L. Januzzi (Estados Unidos), Markku S. Nieminen (Finlandia), Mihai Gheorghiade (Estados Unidos) y Gerasimos Filippatos (Grecia); Subcomite de Epidemiologia: Russell V. Luepker (Estados Unidos), Stephen P. Fortmann (Estados Unidos), Wayne D. Rosamond (Estados Unidos), Dan Levy (Estados Unidos) y David Wood (Reino Unido); Subcomite de Perspectivas Globales: Sidney C. Smith (Estados Unidos), Dayi Hu (China), Jose Luis Lopez-Sendon (Espana), Rose Marie Robertson (Estados Unidos), Douglas Weaver (Estados Unidos), Michal Tendera (Polonia), Alfred A. Bove (Estados Unidos), Alexander N. Parkhomenko (Ucrania), Elena J. Vasilieva (Rusia) y Shanti Mendis (Suiza)

Background. It has been suggested that ischemic mitral regurgitation results, at least in part, from generalized end-systolic mitral annulus (MA) dilatation, but the role of the MA is incompletely understood and the segmental dynamics of the MA during left ventricular ischemia have not been described. Methods. We used radiopaque markers and simultaneous biplane videofluoroscopy to measure threedimensional in vivo lengths of eight MA segments in 7 sedated dogs before and after induction of ischemic MR (produced by circumflex coronary artery balloon occlusion and verified by Doppler echocardiography). As viewed from the left atrium, the MA segment between markers 1 and 2 (S 12 ) was defined as starting at the posteromedial commissure, and remaining segments were numbered sequentially clockwise around the MA (ie, the posterior MA encompassed S 12 , S 23 , S 34 , S 45 ; the anterior MA included S 56 , S 67 , S 78 , S 81 ). Marker images obtained 7 to 12 days after implantation were used to construct x, y , and z coordinates of each marker at end-diastole and end-systole. Results. During regional (posterolateral walls) left ventricular ischemia, the end-systolic MA area increased (4.9 ± 0.8 cm 2 [control] versus 5.9 ± 0.6 cm 2 ; p = 0.005). End-systolic MA segment lengths were as follows (control, ischemia [mm, mean ± standard deviation]): S 12 = 9 ± 2, 10 ± 3; S 23 = 10 ± 2, 12 ± 3; S 34 = 13 ± 1, 15 ± 1; S 45 = 8 ± 2, 9 ± 2; S 56 = 11 ± 2, 11 ± 2; S 67 = 12 ± 2, 12 ± 2; S 78 = 10 ± 3, 11 ± 2; and S 81 = 11 ± 1, 12 ± 1. Values for S 12 , S 23 , S 34 , and S 81 were significant ( p ≤ 0.05 for control versus ischemia by paired t test). Conclusions. During ischemic mitral regurgitation, the MA enlarged at end-systole, but in an asymmetric manner; most posterior annular segments lengthened, whereas most anterior annular segment lengths did not change. These data suggest that alterations in regional MA mechanics may be important in the pathogenesis of ischemic mitral regurgitation. Further three-dimensional studies of MA dynamics and shape should be conducted so that new knowledge may result in improved mitral valve surgical techniques.

We investigated left ventricular (LV) diastolic volume changes (suction inflows) with left atrial pressure (LAP) clamped to ambient pressure in six open-chest, anesthetized dogs. The left atrium was cannulated and connected to a servo pump, and LAP was clamped to a set point near 0 mmHg for four beats by withdrawing blood. LAP averaged 5.88 +/- 1.44 mmHg before the clamp and fell to 0.74 +/- 0.61 mmHg (P < 0.0001) after the clamp. During the first clamped beat a transmitral pressure gradient of 1.0 +/- 0.6 mmHg was observed, resulting in LV filling of 2.6 +/- 1.8 ml. Subsequent beats developed suction-driven (mean negative LV pressure: -1.5 +/- 1.3 mmHg; P < 0.005 vs. zero) LV filling of 4.5 +/- 2.8 ml/beat with a peak transmitral pressure gradient of 1.7 +/- 0.6 mmHg. These data are consistent with the hypothesis that LV suction can be an important filling mechanism under condition in which LV end-systolic volume is reduced, e.g., reduced filling pressures, high heart rates, exercise, or increased inotropic drive.

It is not known how best to resuspend the mitral chordae tendineae during mitral valve replacement to optimize postoperative left ventricular (LV) systolic and diastolic function.Six different techniques to preserve the chordae during mitral valve replacement were compared in 12 dogs using a nondistorting isovolumic technique: conventional, all chordae severed; anterior, all chordae preserved anteriorly; partial, anterior papillary muscle chordae preserved anteriorly; posterior, all chordae preserved posteriorly; oblique, anterior papillary muscle chordae directed anteriorly and posterior papillary muscle chordae posteriorly; and counter, opposite of oblique chordal direction. Control measurements (no chordal tension) were recorded between each experimental condition.The oblique method tended to have the best LV systolic function versus the conventional method (Emax = 4.0 +/- 1.8 versus 3.3 +/- 1.2 mm Hg/mL [mean +/- standard deviation]; p = 0.08 by repeated-measures analysis of variance; physiologic intercept Ees100 = 20.3 +/- 8.6 mL [p0.05 versus control]), with no major change in LV diastolic stiffness. The posterior method had a lower Emax (3.3 +/- 1.2 mm Hg/mL) than the oblique method, but a similar Ees100 (20.8 +/-8.1 mL; p0.05 versus control) and the best diastolic LV performance (LV diastolic stiffness = 0.46 +/- 0.23 mm Hg/mL). The counter method also had good systolic function (Emax = 3.8 +/- 1.2 mm Hg/mL; Ees100 = 19.7 +/- 7.5 mL; p0.05 versus control), but had less favorable diastolic properties (0.65 +/- 0.37 mm Hg/mL; p0.05 by repeated-measures analysis of variance versus posterior).In this isovolumic preparation in normal canine hearts, the oblique method of chordal resuspension was associated with the best LV systolic function, whereas the counter technique impaired LV diastolic function. These preliminary results warrant further study in ejecting and failing hearts to determine conclusively which chordal orientation best preserves LV performance after mitral valve replacement.

This investigation was designed to elucidate the dynamics of the left ventricular (LV) papillary muscles. Miniature tantalum myocardial markers were placed on the tip and base of each papillary muscle in six dogs. Markers were also implanted into the LV myocardium to define two orthogonal equatorial diameters and the long-axis dimension. Two weeks later, after recovery from thoracotomy, markers were visualized by biplane fluoroscopy, and video images were recorded during control conditions, after autonomic blockade, after inotropic stimulation with calcium, after methoxamine infusion (to increase afterload), and after blood volume augmentation (to increase preload). Two days later, radiographic recordings were made before and after occlusion of the left circumflex coronary artery. Computer-aided analysis of the video recordings was used to determine three-dimensional coordinates of the markers. It was found that before circumflex coronary occlusion, the dynamics of both papillary muscles closely mimicked the dynamics of the LV as a whole. The papillary muscles shortened during ejection and lengthened during diastole. Their lengths changed minimally during the isovolumic periods, and this behavior was not altered by any of the interventions except coronary occlusion. During circumflex coronary artery occlusion, the ischemic posterior papillary muscle lengthened during isovolumic contraction and most of ejection and shortened only when LV pressure began to fall. Hence, we believe that previous studies demonstrating papillary muscle lengthening during isovolumic contraction and shortening during isovolumic relaxation may have been confounded by coexistent myocardial ischemia or stunning.

Intraoperative epicardial echocardiography and color flow Doppler were performed before and after cardiopulmonary bypass in 17 consecutive patients undergoing 20 freehand allograft aortic valve replacements. Native aortic valves were replaced in 12, and prostheses in 8 patients. Precardiopulmonary bypass echocardiography estimates of annular diameter guided allograft selection and predicted length of allograft aortic root required, defined coronary situs, and revealed other cardiac abnormalities. These included unanticipated severe mitral regurgitation (which precluded allograft aortic valve replacements in one patient), left-to-right shunts in the membranous septum, ascending aortic dissection, and aortic root pathology requiring coronary reimplantation or bypass. Postcardiopulmonary bypass echocardiography demonstrated acceptable competency of 18/19 allograft valves (mild or no aortic insufficiency), and successful repair of 3/4 shunts. Mild mitral regurgitation was detected more often at postcardiopulmonary bypass than precardiopulmonary bypass (15 vs 11 cases) and postcardiopulmonary bypass estimates of mitral regurgitation severity corollated well with subsequent postoperative follow-up. IOE allows selection and thawing of the allograft valves prior to aortic cross clamping, minimizing cross-clamp time. It detects important concomitant cardiac abnormalities, and predicts postoperative allograft valve and mitral competency. Intraoperative echocardiography Doppler, is therefore, a useful adjunct for allograft aortic valve replacements or aortic root replacement.

Purpose HIV-associated morbidity and mortality have decreased following the introduction of highly active antiretroviral therapy. Previous studies have shown that HIV-infected patients are at increased risk for atherosclerosis, independent of other risk factors. Measurement of carotid artery intima media thickness (IMT) is a noninvasive method of assessing atherosclerosis that predicts myocardial infarction and stroke even after adjustment for traditional risk factors. Wherease some studies of HIV patients have shown increased carotid IMT measurements, others have not. We hypothesized that the disparity between these studies may result from different methods used to measure carotid IMT, namely, either including or excluding the bifurcation region. Methods Carotid IMT data were available from 230 HIV-infected individuals. Measurements were taken on both right and left sides at a total of 12 sites per subject. These included the near and far walls of the common carotid artery (CCA), the bifurcation (BIF), and the internal carotid artery (ICA). A carotid plaque was defined as IMT ≥ 1.5 mm. Results The mean IMT of all sites (0.97 mm ± 0.40) was significantly higher than the mean taken from only the CCA (0.74 mm ± 0.30; p Conclusion These data suggest that the different results from recent carotid IMT studies in HIV patients may result from important differences in IMT measurement protocols, some of which exclude the most common sites for plaque formation. A standard procedure should be established to be able to compare the results from different centers. As the majority of disease in our HIV patients was found at the BIF region, we recommend a measurement protocol that includes this specific region.

Reversal of blood flow in the descending aorta : Implications for Doppler quantitation of aortic insufficiency

To determine the value of transesophageal ultrasound in the assessment of cardiac valve prostheses, 14 patients with clinically suspected mitral prosthesis malfunction were studied by transthoracic and transesophageal two-dimensional imaging as well as by color Doppler flow velocity mapping (color Doppler). Patients underwent left ventricular angiography (n = 13), surgery (n = 11), or both angiography and surgery (n = 10). Nine patients had only mitral valve replacement, four patients had both mitral and aortic valve replacement, and one patient had mitral, aortic, and tricuspid valve replacement. There were 16 biological and four mechanical prostheses. The degree of mitral regurgitation was graded by both transthoracic and transesophageal color Doppler according to the area of the regurgitant jet visualized and was compared with a three-point classification of mitral regurgitation by left ventricular angiography judged by observers blinded to the echocardiographic results. All transesophageal studies were performed without complication and were well tolerated. The pathological morphology of the mitral prosthesis was additionally or more clearly visualized by transesophageal two-dimensional imaging and subsequently proven at surgery in three patients with flail leaflets and one patient with a vegetation compared with images obtained by the transthoracic approach. Valvular regurgitation was graded by the transthoracic approach as absent in four patients, mild in two patients, moderate in five patients, and severe in only three patients. The transesophageal assessment showed absence of mitral regurgitation in two patients, moderate regurgitation in two patients, and severe regurgitation in 10 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

The purpose of this science advisory is to summarize the currently available data concerning thiazolidinediones and cardiovascular risk, with a focus on ischemic heart disease (IHD) events, and to provide practical recommendations to healthcare workers seeking to minimize the burden of cardiovascular disease (CVD) and other complications in their patients with type 2 diabetes mellitus. On May 21, 2007, the US Food and Drug Administration (FDA) released a safety alert concerning a possible increased risk of ischemic cardiovascular events in patients prescribed the thiazolidinedione rosiglitazone. This safety alert was prompted by the results of a large meta-analysis that reported that treatment with rosiglitazone resulted in a 43% increase in risk for myocardial infarction (MI) and a possible increase in risk for cardiovascular death.1 These data were particularly alarming because the metabolic effects of thiazolidinediones were widely presumed, although not proven, to reduce the risk for IHD. Subsequently, a number of additional reports using alternative meta-analytic techniques,2,3 new meta-analyses,4–10 recently published results of new clinical trials,11–15 and observational studies of both rosiglitazone and pioglitazone16–24 have provided variable evidence regarding an adverse cardiovascular effect of these agents. On November 14, 2007, after a specially convened FDA Advisory Panel meeting on July 30, 2007, the FDA decided not to withdraw rosiglitazone from the market. They issued new prescribing information that included a new boxed warning regarding the potential risk for myocardial ischemia, particularly in patients with heart disease taking nitrates, and in patients for whom rosiglitazone was added to established insulin therapy.25 Diabetes mellitus is increasing in prevalence in the United States and worldwide. An estimated 23.6 million people in the United States, 7.8% of the population, had diabetes in 2007, with more than 90% of cases being type 2 diabetes mellitus. Diabetes increases the risk of …

Objectives: The purpose of this study was to explore whether geometric changes that predispose to left ventricular outflow tract obstruction after mitral ring annuloplasty are coupled to subvalvular apparatus disturbances. Methods: Radiopaque markers were implanted in sheep: 9 in the ventricle, 1 in the high interventricular septum, 1 on each papillary muscle tip, 8 around the mitral anulus, 4 on the anterior mitral leaflet, and 2 on the posterior leaflet. One group served as control (n = 5); the others were randomized to undergo annuloplasty with the Duran ring (n = 6; Medtronic, Inc, Minneapolis, Minn) or Carpentier-Edwards Physio ring (n = 6; Baxter Healthcare Corp, Irvine, Calif). After a 7- to 10-day recovery period, 3-dimensional marker coordinates were measured with biplane videofluoroscopy. Results: At the beginning of ejection, (1) the anterior leaflet was displaced toward the left ventricular outflow tract; (2) the normal atrially flexed anterior anulus was flattened into the left ventricular outflow tract; (3) the posterior anulus was displaced toward the left ventricular outflow tract; (4) the anterior papillary muscle was displaced septally; and (5) the posterior papillary muscle was dislocated inwardly toward the anterior papillary muscle in the Physio ring group compared with the control group. During ejection, all these structures moved septally, encroaching further on the left ventricular outflow tract. In the Duran ring group, only the posterior anulus was displaced toward the left ventricular outflow tract; the anterior leaflet was not displaced toward the left ventricular outflow tract, and it did not move septally during ejection. Conclusions: The semirigid Physio ring was associated with perturbations in annular dynamics that caused changes in papillary muscle geometry. We propose an integrated valvular–subvalvular mechanism to explain displacement of the anterior leaflet into the left ventricular outflow tract after mitral ring annuloplasty. (J Thorac Cardiovasc Surg 1999;117:472-80)

BACKGROUND—Abnormal flow patterns in the left atrium in atrial fibrillation or mitral stenosis are associated with an increased risk of thrombosis and systemic embolisation; the characteristics of normal atrial flow that avoid stasis have not been well defined. OBJECTIVES—To present a three dimensional particle trace visualisation of normal left atrial flow in vivo, constructed from flow velocities in three dimensional space. METHODS—Particle trace visualisation of time resolved three dimensional magnetic resonance imaging velocity measurements was used to provide a display of intracardiac flow without the limitations of angle sensitivity or restriction to imaging planes. Global flow patterns of the left atrium were studied in 11 healthy volunteers. RESULTS—In all subjects vortical flow was observed in the atrium during systole and diastolic diastasis (mean (SD) duration of systolic vortex, 280 (77) ms; and of diastolic vortex, 256 (118) ms). The volume incorporated and recirculated within the vortices originated predominantly from the left pulmonary veins. Inflow from the right veins passed along the vortex periphery, constrained between the vortex and the atrial wall. CONCLUSIONS—Global left atrial flow in the normal human heart comprises consistent patterns specific to the phase of the cardiac cycle. Separate paths of left and right pulmonary venous inflow and vortex formation may have beneficial effects in avoiding left atrial stasis in the normal subject in sinus rhythm. Keywords: atrium; blood flow; magnetic resonance imaging; haemodynamics

Method Seven dilated cardiomyopathy (DCM) patients (4 female, aged 52 ± 14 years, ejection fraction 43 ± 5% [mean ± SD]) and six healthy subjects (3 female, aged 58 ± 4 years) were studied. 4D velocity data and morphological b-SSFP images were acquired on a 1.5 T MRI-scanner (Philips Achieva). The LV endocardium was segmented (http:// segment.heiberg.se) from the short axis images at the times of isovolumetric contraction (IVC) and isovolumetric relaxation (IVR). Pathlines were emitted from the IVC LV blood volume and traced forward and backward in time until IVR, thus including the entire cardiac cycle. The IVR volume was used to determine if and where the traces left the LV. This information was used to automatically separate inflow pathlines into two components [1]: direct flow that enters and leaves the LV within the same cardiac cycle, and retained inflow that does not leave the LV within a single cardiac cycle. By knowing the volume occupied by each trace, its velocity and the density of blood, the change in KE was calculated from the time of the traces' entrance into the LV (by crossing a plane at the mitral annulus) until the time of IVC. from 13th Annual SCMR Scientific Sessions Phoenix, AZ, USA. 21-24 January 2010

Summary Although total left ventricular (LV) stroke volume (SV) is equal in healthy subjects and heart failure patients with mild LV remodeling, the SV’s transventricular flow paths to ejection and diastolic energetics are different. These flow-specific markers of inefficiency of the failing heart are detectable prior to clinical decompensation, and might be predictors of progressive adverse cardiac remodeling. Background Heart failure is a common disorder with a dismal prognosis. Cardiac remodeling is a key component of heart failure that progresses from adaptive to maladaptive as the disease worsens, and is associated with increased risks of symptoms and mortality. In earlier stages of heart failure with adaptive remodeling, patients may remain clinically compensated and the failing heart’ sl eft ventricular (LV) stroke volume (SV) remains the same as in the normal heart. Recently, time-varying and complex three-dimensional flow patterns and energetics within the normal LV have been demonstrated. Based on such 4D flow-specific measures, we hypothesized that while the SV of normal and failing LVs may be equal, the SV’s diastolic kinetic energy (KE) and transventricular routes to ejection are different in the two states. Methods In ten patients with dilated cardiomyopathy (DCM) (6 females, 49±14 years [mean±SD]) and ten healthy subjects (4 female, 44±17 years), 4D phase-contrast CMR velocity data and morphological data were acquired at 1.5T (Philips Achieva). A previously validated method was used for the analysis: The LV endocardium was segmented from the morphological images at end-diastole (ED) and end-systole. Pathlines were emitted from the ED blood volume and traced forward and backward in time until end-systole, allowing separation of the Total SV into two flow components (figure 1): 1) Blood that enters and leaves the LV during the analyzed cardiac cycle (Direct SV), and 2) Blood that leaves but does not enter the LV during the analyzed cardiac cycle (Delayed SV). The KE was calculated over the cardiac cycle for these flow components based on the volume occupied by each pathline, its velocity, and blood density. Results The LV ED volume was larger and LV ejection fraction was smaller in DCM compared to healthy (179±33 vs 147±22 ml, p=0.021, and 42±5 vs 54±6 %, p

Background Left bundle branch block (LBBB) leads to dyssynchronous left ventricular (LV) contraction and relaxation which may contribute to LV dysfunction and ultimately heart failure. LBBB-related mechanical dyssynchrony often responds to cardiac resynchronization therapy (CRT). However, this therapy is expensive and the number of non-responders remains significant. Reliable functional markers of dyssynchronous LV pumping that can predict response to CRT have proved elusive. Almost all studies of LV mechanical dyssynchrony focus on wall motion properties rather than aspects of intraventricular flow. 4D flow CMR specific measures have recently emerged as markers of LV function in failing hearts. Reduced volume and kinetic energy (KE) of the portion of LV inflow which passes directly to outflow (Direct Flow) has been demonstrated in failing LVs compared to normal LVs. In this study we hypothesized that the volume and KE of Direct Flow would be further reduced in myopathic LVs with LBBB compared to similarly dysfunctional and remodeled LVs without LBBB.