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Biomedical subjects

N B Ingels

Publications and source records attributed to N B Ingels.

At least 73 records · Page 4Linked to original sources
PubMed1991

Mitral valve replacement in dilated canine hearts with chronic mitral regurgitation. Importance of the mitral subvalvular apparatus.

The importance of the mitral subvalvular apparatus in terms of left ventricular (LV) mechanics and energetic efficiency in the chronically dilated canine heart was assessed in nine dogs with surgically induced mitral regurgitation. Miniature radiopaque tantalum markers were implanted into the myocardium to measure LV volume. Biplane cinefluoroscopic images obtained 1 week and 3 months after creation of mitral regurgitation confirmed the presence of LV dilatation. Mitral valve replacement with preservation of all chordae tendineae was then performed. LV systolic function and derived energetics were then assessed during transient caval occlusion both before and after chordal division by using exteriorized snares. Global LV systolic mechanics, as assessed by the slopes of the end-systolic pressure volume (Ees) and end-systolic stress volume (Ms) relations, fell by 46% (11.7 +/- 2.8 versus 6.3 +/- 1.4 mm Hg/ml, p less than 0.001) and 33% (17.8 +/- 4.0 versus 12.0 +/- 5.1 kdyne/cm5, p = 0.0001), respectively, when the chordae were divided. Chordal severing also increased systolic LV wall stress or LV afterload. In terms of calculated myocardial energetics, the slopes of the stroke work-end-diastolic volume and pressure volume area-end-diastolic volume relations declined significantly by 20% (85 +/- 14 versus 68 +/- 16 mm Hg) and 11% (116 +/- 20 versus 104 +/- 20 mm Hg) after cutting the chordae, thereby indicating reduced external stroke work and mechanical energy generated at any given level of preload. Moreover, the efficiency of energy transfer from pressure volume area to external stroke work fell by 19% (p less than 0.001). Since effective systemic arterial elastance (Ea) did not change, the Ea/Ees ratio (index of ventriculoarterial [V-A] coupling) increased from 0.93 +/- 0.27 to 1.67 +/- 0.62 (p = 0.006). Therefore, chordal division in dilated dog hearts due to chronic mitral regurgitation resulted not only in deterioration of systolic LV mechanics but also deleterious changes in calculated LV energetics and efficiency due to exacerbated mismatch in V-A coupling between the left ventricle and the systemic arterial bed, unfavorable loading conditions, and exhaustion of preload reserve. These observations in the low-pressure, volume-overloaded heart due to chronic mitral regurgitation underscore the importance of the mitral subvalvular apparatus for optimal LV systolic performance and energetic efficiency.

Animals↗
PubMed1990

Three-dimensional left ventricular midwall dynamics in the transplanted human heart.

To quantify the three-dimensional regional dynamics of the left ventricular (LV) midwall and the centroid and cross-sectional shape of the LV chamber in the transplanted human heart, 12 miniature radiopaque tantalum markers were implanted in the LV midwall of the donor heart at the time of cardiac transplantation in 15 patients. Stereo cineradiography in the late postoperative period (mean, 52 days after surgery) allowed computer-aided measurements of the three-dimensional coordinates of multiple sites in anterior, inferior, lateral, and septal LV regions at 16.7-msec intervals throughout the cardiac cycle. In awake, supine patients, from maximum to minimum LV volume, group mean translations of free wall markers ranged from 0.80 to 1.24 cm, directed toward the LV interior, whereas translations of septal wall markers were significantly less, 0.46 and 0.34 cm (p less than 0.01), directed away from the LV interior. A component of this translation along the septal-lateral axis was also significantly less (p less than 0.01) in the septum (0.19 and 0.20 cm) than in the free wall, where it ranged from 0.32 to 0.97 cm. The LV cross section was not circular, and anterior-inferior dimensions (7.18 +/- 0.66 and 6.13 +/- 0.79 cm, at maximum and minimum volumes, respectively) were significantly greater (p less than 0.01) than septal-lateral dimensions (5.78 +/- 0.65 and 5.12 +/- 0.48 cm), yielding an unchanging transverse elliptical LV eccentricity (0.58 +/- 0.13). The position of the LV center of volume did not change significantly from maximum to minimum volume in the direction of either the LV long axis or the anterior-inferior axis, but it did change significantly (0.55 +/- 0.23 cm, p less than 0.01) along the septal-lateral axis. We conclude 1) as viewed in a fixed external reference system, midwall sites in the interventricular septum of the transplanted human heart move paradoxically yet are relatively immobile compared with the three-dimensional dynamics of midwall sites in the LV free wall; 2) the transverse cross-sectional shape of the LV in the transplanted human heart is decidedly oval, with significantly greater anterior-posterior than septal-lateral dimensions at the time of maximum and minimum LV volumes; and 3) the center of volume in the transplanted human LV is remarkably stable in the directions of the LV long axis and anterior-posterior axis, suggesting a balance of forces along these axes, yet it moves significantly toward the interventricular septum, presumably counterbalancing the opposite translation during systole of the right ventricular (RV) center of volume.(ABSTRACT TRUNCATED AT 400 WORDS)

Cardiac Volume↗
PubMed1989

Relation between longitudinal, circumferential, and oblique shortening and torsional deformation in the left ventricle of the transplanted human heart.

The present study was designed to investigate the anisotropy of systolic chord shortening in the lateral, inferior, septal, and anterior regions of the human left ventricle. At the time of surgery, 12 miniature radiopaque markers were implanted into the left ventricular midwall of the donor heart in 15 cardiac transplant recipients. Postoperative biplane cineradiograms were computer-analyzed to yield the three-dimensional coordinates of these markers at 16.7-msec intervals. In each of the four left ventricular regions, chords were constructed from a central marker to outlying markers, and the percent systolic shortening of each chord was calculated. In each region, chord angles were measured with respect to the circumferential direction (positive angles counterclockwise) and each chord was assigned to one of four angular groups: I. oblique, -45 +/- 22.5 degrees or 135 +/- 22.5 degrees; II. circumferential, 0 +/- 22.5 degrees or 180 +/- 22.5 degrees; III. oblique, 45 +/- 22.5 degrees or -135 +/- 22.5 degrees; or IV. longitudinal, 90 +/- 22.5 degrees. In the lateral, inferior, and septal regions, respectively, systolic shortening (mean +/- SD%) was significantly greater in Group I chords (19 +/- 5%, 17 +/- 5%, and 15 +/- 4%) than those in Group II (15 +/- 5%, 12 +/- 4%, and 11 +/- 4%), Group III (12 +/- 4%, 12 +/- 5%, and 11 +/- 4%), or Group IV (13 +/- 5%, 13 +/- 6%, and 12 +/- 5%). The anterior region was unique in exhibiting equal shortening in both Group I and Group II chords (16 +/- 5%), although the shortening of these chords was significantly greater than that of Group III and Group IV (12 +/- 5%) in this region. A cylindrical mathematical model was developed to relate longitudinal, circumferential, and oblique systolic shortening to torsional deformation about the long axis of the left ventricle. Torsional deformations measured in these 15 hearts were of sufficient magnitude and correct sense to agree with model predictions. These data suggest that torsional deformations of the left ventricle are of fundamental importance in linking the one-dimensional contraction of the helically wound myocytes to the three-dimensional anisotropic systolic shortening encountered in the transplanted human heart.

Biomechanical Phenomena↗
PubMed1988

Torsional deformation of the left ventricular midwall in human hearts with intramyocardial markers: regional heterogeneity and sensitivity to the inotropic effects of abrupt rate changes.

The spiral orientation of left ventricular (LV) fibers suggests that twisting about the ventricular long axis of the apex with respect to the base, i.e., torsional deformation, may be characteristic of LV contraction. To demonstrate this twisting motion, 10 orthotopic human cardiac allograft recipients were studied with biplane cineradiography of tantalum helices implanted within the LV midwall at 12 specific sites. Counterclockwise twisting about the LV long axis (as reviewed from apex to base) accompanied ventricular ejection in all patients. Torsional deformation angles, measured relative to a reference minor axis at the base, were substantially smaller in the anteroapical wall, as compared with counterparts in the apical third of the inferior and lateral walls (anterior = 13.3 +/- 6.0 degrees, inferior = 18.7 +/- 6.3 degrees, and lateral = 23.4 +/- 10.7 degrees). Torsional angles at the midventricular level were roughly half as much and exhibited similar regional variabilities (anterior = 7.6 +/- 3.3 degrees, inferior = 9.0 +/- 3.3 degrees, lateral = 10.7 +/- 5.2 degrees, and septal = 8.8 +/- 3.8 degrees). Comparison of control beats and the initial beat after abrupt cessation of rapid atrial pacing (126 +/- 10 beats/min) with return to the control heart rate (96 +/- 9 beats/min) permitted the mild positive inotropic effect of tachycardia to be assessed at similar levels of ventricular load. Torsional deformation of the anteroapical and inferoapical sites increased significantly (p less than 0.05) over control values to 15.6 +/- 7.5 degrees and 21.2 +/- 5.5 degrees, respectively. In contrast, torsional deformation of the lateral wall was essentially unchanged. These data provide direct evidence for torsional deformation of the left ventricle in humans, demonstrate that torsion of the LV chamber is nonuniform, and suggest a dependence of LV torsion upon contractile strength that is attenuated in the lateral wall.

Heart↗
PubMed1987

Adaptation of human left ventricular volumes to the onset of supine exercise.

UNLABELLED: The purpose of this study was to measure the changes and rates of adaptation of left ventricular volumes at the onset of exercise. Eight asymptomatic subjects, in whom intramyocardial markers had been implanted 3-6 years previously during aortocoronary bypass surgery, exercised in the supine position at a constant workload of 73.6 W for 5 min. Six also exercised first at 16.4 W, and then against a workload which progressively increased by 8.2 W every 15 s. Cardiac volumes were measured by computer assisted analysis of the motion of the implanted markers. In the constant workload test, cardiac output increased rapidly from 5.7 +/- 1 min-1 to 10.3 +/- 1.9 1 min-1 by 2 min and then increased more slowly to 10.8 +/- 2.0 1 min-1 by 5 min. The cardiac output increase was mainly due to an increase in heart rate from 68 +/- 12 beats min-1 to 120 +/- 16 beats min-1 with minimal changes in stroke volume. The time constant for the early increase in cardiac output was 45s and for heart rate, 35s. With progressively increasing workloads, there was an almost linear increase of heart rate and cardiac output, but these increased at a slower rate than during the early phase of the constant load exercise test. IN CONCLUSION: rapid changes in cardiac output during supine exercise were produced by changes in heart rate; changes in stroke volume provided minor adjustments to cardiac output; the end-diastolic volume was almost constant.

Adaptation, Physiological↗
PubMed1985

Independence of left ventricular pressure-volume ratio from preload in man early after coronary artery bypass graft surgery.

The response of the maximum value of the left ventricular pressure-volume ratio to preload augmentation by blood or plasma expanders was studied in 11 patients during the first 24 hr after coronary artery bypass graft surgery. Increasing the mean left atrial pressure from 10 to 15 and 20 mm Hg resulted in no change in the maximum pressure-volume ratio in the group as a whole. In certain individual patients, however, the maximum pressure-volume ratio changed with volume infusion, and these changes were accompanied by simultaneous changes in afterload. The observed changes in pressure-volume ratio were in the same direction as the changes in afterload (systolic pressure), suggesting a dependence of maximum pressure-volume ratio on afterload. These results show that the maximum pressure-volume ratio is independent of preload in the first 24 hr after coronary artery bypass graft surgery with the pericardium open; thus the maximum pressure-volume ratio is a useful index of postoperative left ventricular function when afterload is unchanged. However, because this ratio (a single-point assessment of the pressure-volume relationship) may not be a good estimate of Emax, we recommend a more complete determination of the locus of the "upper left corners" of the pressure-volume loops for measurement of Emax to provide a more accurate indicator of the myocardial contractile state.

Adult↗
PubMed1985

Effect of early postoperative volume loading on left ventricular systolic function (including left ventricular ejection fraction determined by myocardial marker) after myocardial revascularization.

The effects of early volume loading in terms of isovolumetric-phase and ejection-phase indexes of left ventricular systolic function were studied in 12 patients 5 hr after myocardial revascularization, with myocardial markers used to measure left ventricular volume directly and with simultaneous transmural left ventricular pressure measurements by micromanometers. Volume loading (increasing transmural left ventricular end-diastolic pressure from 11 +/- 4 to 15 +/- 5 mm Hg) induced a significant 14% increase in left ventricular end-diastolic volume index (LVEDVI), which was associated (as expected) with significant (p less than .005) augmentation of stroke work (+26%), left ventricular pressure-volume loop area (+35%), and stroke volume index (+22%) and with increments in left ventricular dP/dt and mean velocity of circumferential fiber shortening despite a simultaneous increase in left ventricular afterload. In contrast to previous radionuclide studies, however, left ventricular ejection fraction increased significantly (+9%) and the left ventricular end-systolic pressure-volume ratio did not fall. The relative change in ejection fraction was directly proportional to the increment in LVEDVI (r = .54, p = .03) and inversely related to the change in left ventricular end-systolic volume index (r = -.71, p = .0005). Patients who demonstrated a small or no increase in ejection fraction generally had a larger simultaneous increase in afterload, but one patient exhibited exhaustion of preload reserve. Ejection fraction, as an ejection-phase index of left ventricular performance, is highly dependent on afterload; therefore, interpretation of postoperative changes in ejection fraction must be undertaken only with strict caution.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Output↗
PubMed1984

Dobutamine and dopamine after cardiac surgery: greater augmentation of myocardial blood flow with dobutamine.

Left ventricular hemodynamics, dimensions and coronary sinus blood flows were measured simultaneously after infusions of dobutamine and dopamine. Ten patients were studied 6, 10 to 15, and 24 hr after cardiopulmonary bypass surgery. The dose of each drug was adjusted to increase cardiac output by 25%. Heart rate was held constant with atrial pacing. Dobutamine and dopamine increased peak left ventricular dP/dt from baseline values by 72% vs 58% during the early study, 77% vs 78% in the intermediate study, and 95% vs 79% in the late study (all NS, difference between drugs). Similarly, there were no significant differences in hemodynamic response or in cardiac dimensions after the two drugs in any period. Both drugs increased myocardial oxygen uptake during the intermediate and late studies (32% vs 33% and 34% vs 25%). With dobutamine this increase was matched by a similar increase in coronary blood flow; however, failure of the expected increase in coronary blood flow with dopamine suggested coronary constriction. Although dobutamine and dopamine have similar hemodynamic effects, dobutamine has the advantage of not limiting the increase in coronary blood flow associated with increased oxygen demand.

Catecholamines↗
PubMed1980

Left ventricular response to isometric exercise in patients with denervated and innervated hearts.

Patients with cardiac denervation resulting from allograft transplantation have been observed to increase their diastolic and systolic blood pressure during isometric exercise without concomitant cardioacceleration. To determine the mechanism for the blood pressure increase, heart rate, blood pressure, and ventricular volumes (measured using fluoroscopy of tantalum midwall myocardial markers) were recorded before and after a 50% maximal voluntary contraction. Seven cardiac transplant recipients (denervated heart) and seven nontransplant patients (innervated heart) were studied. Innervated and denervated heart patients increased systolic blood pressure by 16% and 21% and total peripheral resistance by 20% and 12%, respectively. The percentage responses were not significantly different between groups, except for heart rate, which increased 17% in innervated heart patients and 2% in denervated heart patients (p less than 0.05). Neither group had enhanced contractility or increases in cardiac output, suggesting that the blood pressure increases resulted in both groups from increased peripheral resistance.

Adult↗
PubMed1980

Evaluation of methods for quantitating left ventricular segmental wall motion in man using myocardial markers as a standard.

Radiopaque markers were implanted in the left ventricular myocardial midwall in 58 patients and studied in the 30 degrees right anterior oblique projection by computer-aided fluoroscopy. Marker motion was used as a standard of segmental wall motion against which the accuracy of five methods for measuring left ventricular wall motion was assessed: two methods using hemiaxial measurements in rectangular coordinates, two using radial measurements in polar coordinates (all with frame-by-frame axial reindexing) and one using radial measurements in fixed external polar coordinates. The latter method showed significantly less error (25.9%, p less than 10(-6)) in measuring midwall marker motion than the other four methods (range 42.5--47.5%) in the group as a whole and in subgroups that had abnormalities of posterior, apical and anterior wall motion. This method also had the best correlation of marker motion and motion of adjacent endocardial border (of the overall left ventricle and the posterior, apical, and anterior walls separately) as visualized by ventriculography in 29 patients. The bulk of the reduction in error using this method was due to the use of a fixed external reference system, with a small additional increment of error removed by proper selection of the polar origin at a point 69% of the distance from the anterolateral edge of the aortic valve to the ventricular apex at end-systole.

Coronary Artery Bypass↗
PubMed1980

Contribution of asynergic contraction to halothane-induced myocardial depression.

We investigated the possibility that myocardial asynergy (dyscoordinate contraction) is a contributing mechanism to the impairment of cardiac function produced by halothane. Coronary cineangiograms were performed in seven dogs, awake and at 1, 2, and 3 MAC halothane. The relative motions between four arterial bifurcations (six segments) were plotted as an indication of changing ventricular dimensions. To quantitate ventricular asynergy, we calculated anisotropy (AI) and asynchrony (AS), the coefficient of variation of mean shortening (S-) and of mean time to half shortening (T-50), respectively, of the six segments. From these a myocardial performance index (MPI) was derived: MPI = S-/AI + T-50 + AS. In general, S- and MPI decreased with increasing halothane concentration. Anisotropy showed a trend, although usually insignificant, toward increasing, while AS did not change. These observations have two implications. First, asynergy of contraction contributes little, if anything, to halothane-induced impairment of myocardial performance. Second, changes in measurements of intact cardiac performance, such as dP/dtmax, may be reasonably valid during halothane, provided loading conditions are taken into account.

Anesthesia, Inhalation↗
PubMed1979

Effect of intrathoracic pressure on left ventricular performance.

Left ventricular dysfunction is common in respiratory-distress syndrome, asthma and obstructive lung disease. To understand the contribution of intrathoracic pressure to this problem, we studied the effects of Valsalva and Müller maneuvers on left ventricular function in eight patients. Implantation of intramyocardial markers permitted beat-by-beat measurement of the velocity of fiber shortening (VCF) and left ventricular volume. During the Müller maneuver, VCF and ejection fraction decreased despite an increase in left ventricular volume and a decline in arterial pressure. In addition, when arterial pressure was corrected for changes in intrapleural pressure during either maneuver it correlated better with left ventricular end-systolic volumes than did uncorrected arterial pressures. These findings suggest that negative intrathoracic pressure affects left ventricular function by increasing left ventricular transmural pressures and thus afterload. We conclude that large intrathoracic-pressure changes, such as those that occur in acute pulmonary disease, can influence cardiac performance.

Cardiac Output↗
PubMed1979

Effects of digitalis on normal and abnormal left ventricular segmental dynamics.

To study the effects of digoxin on regional left ventricular performance, continuous ventricular dynamics were assessed in nine patients with stable coronary disease. Computer-assisted analysis of the fluoroscopic motion of surgically implanted mid wall myocardial markers was used. The markers define six minor ventricular radii and outline the left ventricle. One and one-half hours after administration of 1 mg of intravenous digoxin, mean velocity of circumferential fiber shortening for all segments increased 19 percent, from 0.67 +/- 0.06 to 0.78 +/- 0.06 circumference/sec (P less than 0.01) and ejection fraction increased 4.5 percent, from 0.50 +/- 0.03 to 0.53 +/- 0.03 (P less than 0.05). Segmental velocity of circumferential fiber shortening, total segmental shortening and early segmental systolic shrtening increased in 83 percent to 91 percent of normal segments, depending on which index was used. Only 45 to 55 percent of initially abnormal segments benefited from digoxin. In general, segmental dyssynergy increased even when net ventricular function was enhanced. These results suggest that in pateints with chronic left ventricular contraction abnormalities due to coronary disease, deterioration of performance in abnormal regions after administration of digoxin may result from increased stress imposed by increased afterload and by improved segmental dynamics in more normal areas.

Adult↗