Dynamic three-dimensional imaging of the mitral valve and left ventricle by rapid sonomicrometry array localization.

OBJECTIVES: The first objective was to develop a quantitative method for tracking the three-dimensional geometry of the mitral valve. The second was to determine the complex interrelationships of various components of the mitral valve in vivo. METHODS AND RESULTS: Sixteen sonomicrometry transducers were placed around the mitral vale anulus, at the tips and bases of both papillary muscles, at the ventricular apex, across the ventricular epicardial short axis, and on the anterior chest wall before and during cardiopulmonary bypass in eight anesthetized sheep. Animals were studied later on 17 occasions. Reproducibility of derived chord lengths and three-dimensional coordinates from sonomicrometry array localization, longevity of transducer signals, and the dynamics of the mitral valve and left ventricle were studied. Reproducibility of distance measurements averages 1.6%; Procrustes analysis of three-dimensional arrays of coordinate locations predicts an average error of 2.2 mm. Duration of serial sonomicrometry array localization signals ranges between 60 and 151 days (mean 114 days). Sonomicrometry array localization demonstrates the saddle-shaped mitral anulus, its minimal orifice area immediately before end-diastole, and uneven, apical descent during systole. Papillary muscles shorten only 3.0 to 3.5 mm. Sonomicrometry array localization demonstrates nonuniform torsion of papillary muscle transducers around a longitudinal axis and shows rotation of papillary muscular bases toward each other during systole. CONCLUSION: Tagging of ventricular structures in experimental animals by sonomicrometry array localization images is highly reproducible and suitable for serial observations. In sheep the method provides unique, quantitative information regarding the interrelationship of mitral valvular and left ventricular structures throughout the cardiac cycle.

Triiodothyronine optimizes sheep ventriculoarterial coupling for work efficiency.

BACKGROUND: Triiodothyronine (T3) administration after cardiopulmonary bypass has been shown to significantly improve cardiac performance. The present study was undertaken to elucidate the effects of T3, when administered as an intravenous bolus, on both cardiac energetics and stroke work-oxygen utilization (EW/LVVO2) efficiency. METHODS: In both unstressed and stressed hearts, energetics were evaluated at baseline and 2 hours after intervention in an in vivo sheep preparation. In the first group (n = 5) sheep received saline vehicle. In the second group (n = 9) sheep received an intravenous bolus of 1.2 micrograms/kg of T3. In the third group (n = 7) sheep received a 2-hour intravenous infusion of dobutamine at a rate of 5 micrograms/kg/min. RESULTS: In the unstressed heart, T3 improved cardiac function at no cost in oxygen consumption by decreasing afterload and hence improved EW/LVVO2 efficiency. In contrast, dobutamine improved unstressed cardiac function by increasing contractility at the cost of increased oxygen consumption and thus decreased EW/LVVO2 efficiency. Triiodothyronine optimized ventriculoarterial coupling for efficiency, but dobutamine optimized coupling for maximal work. In the stressed heart, T3 again improved EW/LVVO2 efficiency, but dobutamine had the opposite effect. CONCLUSIONS: The bolus administration of T3 improves unstressed cardiac performance through optimization of ventriculoarterial coupling for EW/LVVO2 efficiency, primarily through vasodilation. Triiodothyronine also increases efficiency in the stressed heart. This study supports the use of T3 in cardiac operations to improve cardiac performance with no cost in oxygen consumption characteristic of inotropic agents.

Use of sonomicrometry and multidimensional scaling to determine the three-dimensional coordinates of multiple cardiac locations: feasibility and initial implementation.

We describe a new method which uses sonomicrometry and the statistical technique of multidimensional scaling (MDS) to measure the three-dimensional (3-D) coordinates of multiple cardiac locations. We refer to this new method as sonomicrometry array localization (SAL). The new method differs from standard sonomicrometry in that each piezoelectric transducer element is used as both transmitter and receiver and the set of intertransducer element distances is measured. MDS calculates the 3-D coordinates of each sonomicrometry transducer element from the set of intertransducer element distances. The feasibility of this new method was tested with mathematical simulations which demonstrated the ability of MDS to compensate for signal error and missing intertransducer element distances. We describe the design elements of a modified digitally controlled sonomicrometer in which a single transducer element can sequentially broadcast to as many as eight receiver elements. That design is used to validate SAL in a water bath and in ex vivo and living hearts. Correlation with caliper measurement in the water bath (y int. = 3.91 +/- 3.36 mm, slope = 1.04 +/- 0.05, r2 = 0.969 +/- 0.027) and with radiography in ex vivo (y int. = -0.87 +/- 0.92 mm, slope = 0.97 +/- 0.02, r2 = 0.960 +/- 0.023) and in vivo hearts (y int. = 2.98 +/- 2.59 mm, slope = 1.01 +/- 0.06, r2 = 0.953 +/- 0.031) was excellent. Sonomicrometry array localization is able to accurately measure the 3-D coordinates of multiple cardiac locations. It can potentially measure myocardial deformation and remodeling after ischemic or valvular injury.

Pathogenesis of acute ischemic mitral regurgitation in three dimensions.

Changes in the geometric and intravalvular relationships between subunits of the ovine mitral valve were measured before and after acute posterior wall myocardial infarction in three dimensions by means of sonomicrometry array localization. In 13 sheep, nine sonomicrometer transducers were attached around the mitral anulus and to the tip and base of each papillary muscle. Five additional transducers were placed on the epicardium. Snares were placed around three branches of the circumflex coronary artery. One to 2 weeks later, echocardiograms, dimension measurements, and left ventricular pressures were obtained before and after the coronary arteries were occluded. Data were obtained from seven sheep. Coronary occlusion infarcted 32% of the posterior left ventricle and produced 2 to 3+ mitral regurgitation by Doppler color flow mapping. Multidimensional scaling of dimension measurements obtained from sonomicrometry transducers produced three-dimensional spatial coordinates of each transducer location throughout the cardiac cycle before and after infarction and onset of mitral regurgitation. After posterior infarction, the mitral anulus enlarges asymmetrically along the posterior anulus, and the tip of the posterior papillary muscle moves 1.5 +/- 0.3 mm closer to the posterior commissure at end-systole. The posterior papillary muscle also elongates 1.9 +/- 0.3 mm at end-systole. The left ventricle enlarges asymmetrically and ventricular torsion along the long axis changes. The development of postinfarction mitral regurgitation appears to be the consequence of multiple small changes in ventricular shape and contractile deformation and in the spatial relationship of mitral valvular subunits.

Large animal model of ischemic mitral regurgitation.

A large animal model of ischemic mitral regurgitation (MR) that resembles the multiple presentations of the human disease was developed in sheep. In 76 sheep hearts, the anatomy of the coronary arterial circulation was determined by observation and polymer casts. Two variations, types A and B, which differed by the vessel that supplied the left ventricular apex, were found. In all hearts, the circumflex coronary artery has three marginal branches and terminates in the posterior descending coronary artery. The amount and location of left ventricular (LV) mass supplied by each marginal circumflex branch was determined by dye injection and planimetry. In type A hearts, ligation of the first and second marginal branches infarcts 23% +/- 3.0% of the LV mass, does not infarct either papillary muscle, significantly (p < 0.001) increases LV cavity size 48% at the high papillary muscle level by 8 weeks, and does not cause MR. Ligation of the second and third marginal branches infarcts 21.4% +/- 4.0% of the LV mass, includes the posterior papillary muscle, significantly increases (p < 0.001) LV cavity size 75%, and causes severe MR by 8 weeks. Ligation of the second and third marginal branches and the posterior descending coronary artery infarcts 35% to 40% of the LV mass, increases LV cavity size 39% within 1 hour, and causes massive MR. After moderate (21% to 23%) LV infarction, development of ischemic MR requires both LV dilatation and posterior papillary muscle infarction; neither condition alone produces MR. Large posterior wall infarctions (35% to 40%) that include the posterior papillary muscle produce immediate, severe MR.(ABSTRACT TRUNCATED AT 250 WORDS)

Pathogenesis of ischemic mitral insufficiency.

We developed a new animal model of ischemic mitral insufficiency in sheep and used it to test the hypothesis that the combination of posterior papillary muscle infarction and left ventricular dilatation was required to produce mitral regurgitation after acute inferior myocardial infarction of moderate size. In 12 sheep, ligation of the first two circumflex marginal coronary arteries infarcted 23% of the left ventricular mass, increased left ventricular cavitary area from 13.2 +/- 1.2 cm2 to 20.0 +/- 2.7 cm2 by 8 weeks and did not produce ischemic mitral regurgitation. In 13 sheep, ligation of the second and third circumflex marginal arteries infarcted 21% of the left ventricular mass and, in 11 of these sheep, the posterior papillary muscular mass as well. When the papillary muscle was included, this infarction produced progressively severe mitral regurgitation over 8 weeks, as left ventricular cavitary area increased from 12.5 +/- 2.6 cm2 to 22.8 +/- 3.8 cm2. We conclude that neither posterior papillary muscle infarction nor left ventricular dilatation alone produces ischemic mitral regurgitation after moderate-sized inferior wall infarction, but that the combination does.

Recovery of oxygen utilization efficiency after global myocardial ischemia.

The time required for myocardial oxygen utilization to recover from 12 minutes of warm ischemia was studied in 15 sheep. Five control animals had 42 minutes of cardiopulmonary bypass at 37 degrees C with the heart beating and vented. In 10 experimental animals, the aorta was clamped for 12 minutes during bypass with the heart vented, and the animals were perfused 30 additional minutes after removal of the clamp. In both groups, measurements of left ventricular coronary arterial blood flow, oxygen consumption (LVO2), peak systolic pressure, circumferential systolic stress integral (CSI), and pressure volume area (PVA) were made 30 minutes after and hourly for 5 more hours after cardiopulmonary bypass ended. Reversible ischemia significantly increases the relationship between LVO2/PVA and LVO2/CSI 1 hour after the clamp is released, but the relationships return to prebypass values by 2 hours. Ischemia significantly decreases end-systolic elastance, which remains depressed thereafter. Cardiopulmonary bypass without myocardial ischemia significantly decreases total ventricular mechanical energy output and oxygen utilization efficiency of the working sheep heart but does not significantly alter end-systolic elastance or the LVO2/PVA and LVO2/CSI relationships. Twelve minutes of warm ischemia impairs oxygen utilization efficiency in the reperfused sheep heart for more than 60 minutes but less than 120 minutes.