Left Ventricular Minor Axis Diameter Research Articles

MDCT Bolus Tracking Data as an Adjunct for Predicting the Diagnosis of Pulmonary Hypertension and Concomitant Right-Heart Failure

The purpose of this study was to investigate the utility of bolus-triggering data from pulmonary CT angiography for predicting the diagnosis of pulmonary hypertension (PH) and right ventricular dysfunction (RVD) and to test its performance against previously established CT signs of PH. Automated bolus-triggering data from pulmonary CT angiograms of 101 patients were correlated with echocardiographic findings and a variety of CT-derived indexes of PH and RVD, including right and left ventricular minor axis diameter; pulmonary artery (PA), aortic, and superior vena caval diameters; right ventricular thickness; contrast reflux; and configuration of the interventricular septum. For bolus triggering, a region of interest was placed in the main PA. Time to threshold, defined as the time from the beginning of contrast injection to the time attenuation exceeded the threshold (100 HU), was measured. On the basis of results of two consecutive echocardiographic studies, subjects were divided into control and PH groups. The latter group was subdivided into PH without RVD and PH with RVD. Time to threshold values were compared between groups and correlated with standard CT-derived parameters. Significant differences between groups were found in time to threshold, PA and right ventricular diameters, and PA-to-aorta and right ventricular-to-left ventricular ratios. Time to threshold had an incremental pattern from the control group (6.6 ± 1.0 seconds) to PH without RVD (9.2 ± 2.4 seconds) and PH with RVD (12.1 ± 3.4 seconds) (p < 0.001). The optimal diagnostic performance of time to threshold for revealing the presence of PH and RVD was at cutoff values of 7.75 and 8.75 seconds, respectively. Time to threshold had a strong direct correlation with PA diameter. In multivariable analyses, time to threshold was identified as a significant predictor of PH and RVD. The specificity of time to threshold and PA diameter together was higher than that of PA diameter alone. Measurement of time to threshold of contrast enhancement derived from bolus-timing data at MDCT may be a useful adjunctive tool for diagnosing PH and consequent RVD.

Mechanical correlates of the third heart sound

In seven chronically instrumented conscious dogs, micromanometers measured left ventricular pressure, and ultrasonic dimension transducers measured left ventricular minor-axis diameter; the latter recording was filtered to examine data between 20 and 100 Hz. Acceptable external heart sounds were recorded with a phonocardiographic microphone in four of the seven dogs. With each dog sedatede, intubated and mechanically ventilated, data were obtained during hemodynamic alterations produced by volume loading, phenylephrine, calcium infusion and vena caval occlusion.Damped oscillations were noted consistently in the left ventricular diameter waveform toward the end of rapid ventricular filling. These wall vibrations, assessed by the Altered diameter, correlated well with the third heart sound (S3) on the phonocardiogram. The peak frequency of the wall vibrations increased with increased diastolic pressure (p = 0.004), probably reflecting an increase in myocardlal wall stiffness. In contrast, the amplitude of the vibrations varid directly with left ventricular filling rate (p = 0.0001).Thus, S3seemed to be related specifically to ventricular wall vibrations during rapid filling, and the spectra of the amplitude-frequency relation shifted toward the audible range with increases in diastolic pressure, wall stiffness or filling rate. Spectral analysis of S3may be useful in assessing pathologic chances in myocardial wall properties.

Effect of postextrasystolic potentiation on systolic bulging of ischemic myocardium

Because the extent of myocardial bulging after acute coronary occlusion is primarily dependent on wall tension, this study examined whether the decrease in systolic bulging with postextrasystolic potentiation was due to contractile reserve or to changes in loading conditions. Seven dogs were atrially paced at 100 beats/min after the sinus node was crushed and atrial extrasystoles were generated. The left ventricular minor axis diameter and segment lengths in the ischemic and nonischemic zones were measured with sonomicrometers. Wall tension was estimated using Laplace's law, and regional tension-length loops were determined.By 5 min after the left anterior descending coronary artery was occluded, there was regional bulging. Postextrasystolic potentiation diminished the extent of bulging by increasing both isovolumic and ejection percent systolic shortening (isovolumic −9.1 ± 2.0% to −5.9 ± 1.7%, p < 0.008; ejection 2.2 ± 0.7% to 4.3 ± 2.0%, p < 0.008). The tension-length loops after coronary occlusion showed an exponential upstroke and almost superimposed downstroke consistent with passive movement. The loops were unchanged by postextrasystolic potentiation. Wall tension data showed that bulging was reduced because of a shift down the tension-length curve as end-systolic wall tension was reduced by augmented nonischemic contraction. Similar results were seen at 60 min of coronary occlusion.This study demonstrates that the decrease in bulging seen with postextrasystolic potentiation is due to changes in loading conditions and not to contractile reserve.

The effect of changes in afterload on systolic bulging.

It has been previously shown that after acute coronary occlusion, the extent of systolic bulging is dependent on preload and the function of the remote nonischemic myocardium is influenced by the motion of the ischemic myocardium as well as by the loading conditions. To examine the isolated effects of changing afterload on the movement of acutely ischemic and nonischemic myocardium, seven open-chest, anesthetized dogs were paced from the left atrium at a rate of 100 beats/min after crushing of the sinus node. The pulmonary artery was perfused artificially and the left ventricular end-diastolic pressure (LVEDP) was carefully controlled with a right heart bypass system. Twenty minutes after occlusion of the left anterior descending artery, the peak left ventricular pressure (LVP) was adjusted to three levels (70, 90, and 110 mm Hg) by blood withdrawal or aortic constriction, while the LVEDP was kept constant (8.3 +/- 2.3 mm Hg). Segment length in the ischemic (IZ) and nonischemic zones (NZ) were measured with sonomicrometers and total, isovolumetric, and ejection systolic shortening (% delta L) were calculated. Changes in left ventricular minor-axis diameter were measured with diameter crystals. Increasing the peak LVP increased the LVP both at aortic valve opening and closing. To keep the LVEDP constant as peak LVP was increased, the cardiac output had to be decreased (p less than .0001).(ABSTRACT TRUNCATED AT 250 WORDS)

A mechanism for the nitroglycerin-induced downward shift of the left ventricular diastolic pressure-diameter relation

Nitroglycerin has been shown to cause a downward shift in the left ventricular (LV) pressure-volume relation in patients. To test the hypothesis that this shift is mediated by an alteration in pericardial pressure, 13 patients undergoing diagnostic cardiac catheterization were studied. LV and right ventricular (RV) pressures (micromanometers) and LV diameter (2-dimensional echocardiography) were measured simultaneously before and after sublingual administration of 0.3 to 0.6 mg of nitroglycerin. In the 11 patients with hemodynamic effects from nitroglycerin, mean LV end-diastolic pressure decreased from 12.7 ± 5 mm Hg (mean ± standard deviation) to 7.3 ± 3 mm Hg (p < 0.002) and mean RV end-diastolic pressure declined from 7.7 ± 3 mm Hg to 5.0 ± 1 mm Hg (p < 0.001). However, nitroglycerin caused only a slight (6%) reduction in LV minor axis diameter, from 52 ± 8 mm to 49 ± 9 mm (p < 0.05). Diastolic pressure-diameter plots constructed from early and late diastolic measurements demonstrated a downward shift in the relation. However, when RV end-diastolic pressure was used as an estimate of pericardial pressure (a procedure validated by studies in our laboratory), the transmural pressure-diameter points before and after administration of nitroglycerin defined a single curve. These observations are in keeping with the conclusions that nitroglycerin did not alter the elastic properties of the myocardium and that the decrease in LV end-diastolic pressure induced by nitroglycerin was primarily attributable to a reduction in external constraint.

Increased myocardial contractility during endotoxin shock in dogs.

The slope of the left ventricular (LV) end-systolic pressure-diameter relationship (Ees) was analyzed in open-chest, pentobarbital-anesthetized dogs before and after endotoxin administration. A lead II electrocardiogram, systemic arterial pressure, LV pressure, LV dP/dt, and LV minor axis diameter were measured. After control measurements were taken, dogs were given either 1 mg/kg Salmonella enteritidis endotoxin (n = 5) or an equivalent volume of saline (n = 4). Control dogs were followed for 240 min. Endotoxic dogs were monitored until death (246 +/- 44 min). There were no significant changes in Ees in control dogs (17 +/- 3 mmHg/mm), which were hemodynamically stable for 4 h. Ees was significantly increased in endotoxic dogs even into the late stages of shock (41 +/- 11 mmHg/mm, P less than 0.01). Only during the terminal phase did Ees fall significantly below control (11 +/- 2 mmHg/mm, P less than 0.05). End-diastolic diameter decreased following endotoxin administration (P less than 0.05) but returned toward control by the terminal stage. Peak + LV dP/dt was depressed following endotoxin injection. Myocardial contractility was not depressed except as a terminal event. Early depression of cardiovascular performance in endotoxic dogs was therefore due to decreased preload and not cardiac dysfunction.

Left ventricular diastolic relaxation and pressure-diameter relations during ischaemic left ventricular failure in the dog.

The significance of severe ischaemic left ventricular (LV) failure on the LV isovolumic relaxation process and diastolic chamber stiffness has been investigated in nine open-chest pentobarbital-anaesthetized dogs. LV failure was induced by bolus injections of 50 micron microspheres into left coronary vascular bed until LV minor axis diameter had increased about 25% and end-diastolic pressure about 20 mmHg. Such ischaemic LV failure did not shift the relation between diastolic LV pressure and minor axis diameter compared with pressure-diameter curves obtained before induction of failure. Neither inotropic nor chronotropic stimulation evoked such shifts. Assuming exponential pressure decline, LV relaxation was significantly slower during failure, but proceeded in all experimental conditions at rates which indicated complete relaxation in late diastole. Analysis of the pressure decline during LV relaxation demonstrated that this process proceeded faster than assumed by an exponential function both before and during LV failure.

The effects of beta 1-adrenoceptor partial agonist ICI 118.587 on left ventricular function in patients with coronary heart disease

We investigated the effects of a new selective beta 1-adrenoceptor partial agonist, ICI 118.587, on left ventricular function in 14 patients with coronary heart disease and a history of stable angina pectoris. The drug (0.2 mg/kg) increased peak left ventricular dp dt from 1518 to 1993 mm Hg/sec ( P < 0.001) and left ventricular V max from 1.63 to 2.08 circ/sec ( P < 0.001), while left ventricular end-diastolic pressure decreased ( P < 0.05). Measured by echocardiography, the fractional shortening of the left ventricular minor axis diameter and the mean velocity of the left ventricular circumferential fiber shortening increased ( P < 0.001) and the cardiac index increased by 36%, reflecting increased contractility mainly in the normal left ventricular wall areas. In coronary heart disease, ICI 118.587 increased left ventricular muscle contractility and output without untoward side effects in the majority of the patients.

Value of positive myocardial technetium-99m-pyrophosphate scintigraphy in the noninvasive diagnosis of cardiac amyloidosis

Ten consecutive patients with tissue-proven amyloidosis, seven of whom presented with congestive heart failure, were found to exhibit intense diffuse uptake of technetium-99m-pyrophosphate (Tc-99m-PYP) on cardiac radionuclide imaging. The patients exhibited echocardiographic and systolic time interval abnormalities suggesting combined restrictive and congestive cardiomyopathic changes. On M-mode echocardiograms, there was symmetrically increased thickness of the interventricular septum and left ventricular (LV) posterior wall in diastole (10 of 10), decreased fractional shortening of the LV minor axis diameter in systole (eight of nine), and decreased percent thickening of the septum (eight of nine) and LV posterior wall (10 of 10) in systole. Three patients demonstrated enlarged LV end-diastolic diameter. All 10 patients had abnormal PEP LVET and eight had shortened LVETI. When combined with noninvasive tests of LV performance, positive myocardial pyrophosphate (PYP) scanning provides a new and useful adjunct in the diagnosis of amyloid heart disease.

Effect of graded narrowing of left main coronary artery on left ventricular function

The relationship between left ventricular function and coronary blood flow was studied in 16 chloralose-anesthetized dogs with an intact coronary circulation and left ventricle. Left ventricular dimensions, hemodynamic function indices, and coronary blood flow were measured simultaneously as the origin of the left coronary artery was narrowed by a calibrated snare. With a left coronary blood flow reduction of 17% (average), left ventricular minor axis diameter increased and maximum aortic blood flow acceleration and maximum rate of rise of left ventricular pressure decreased. Other measured indices of ventricular function did not change significantly. Larger coronary flow decrements caused a decrease in aortic systolic and diastolic pressures, stroke volume and cardiac output and an increase in heart rate and left ventricular end-diastolic pressure. These results confirm a close relationship between left ventricular function and blood supply.

Ventricular response to isometric and isotonic exercise. Echocardiographic assessment.

The effects of supine isometric handgrip and graded isotonic bicycle ergometer exercise on left ventricular performance were studied echocardiographically in 20 normal subjects, aged 18 to 36. Measurements of the left ventricular minor axis diameter were taken from recordings performed at rest, during each form of exercise, and during recovery. At the completion of isometric exercise, the pressure-rate product increased significantly. There was no significant change in percentage of fractional shortening (%deltaD), while there was a small but significant fall in peak velocity of circumferential fibre shortening (peak Vcf). Isotonic exercise resulted in a significant increase in %deltaD and peak Vcf. The pressure-rate product also increased and showed a positive correlation with peak Vcf. Isotonic exercise produced a much greater stimulus to left ventricular contractility than isometric exercise and may be a useful means of detecting latent left ventricular dysfunction echocardiographically.

Evaluation of the force-frequency relationship as a descriptor of the inotropic state of canine left ventricular myocardium.

The short-term force-frequency characteristics of canine left ventricular myocardium were examined in both isolated and intact preparations by briefly pertubing the frequency of contraction with early extrasystoles. The maximum rate of rise of isometric tension (Fmas) of the isolated trabeculae carneae was potentiated by the introduction of extrasystoles. The ratio of Fmas of potentiated to control beats (force-frequency ratio) was not altered significantly by a change in muscle length. However, exposure of the trabeculae to isoproterenol (10(-7)M) significantly changed the force-frequency ratio obtained in response to a constant frequency perturbation. Similar experiments were performed on chronically instrumented conscious dogs. Left ventricular minor axis diameter was measured with implanted pulse-transit ultrasonic dimension transducers, and intracavitary pressure was measured with a high fidelity micromanometer. Atrial pacing was performed so that the end-diastolic diameters of the beats preceding and following the extrasystole could be made identical. Large increases in the maximum rate of rise of pressure (Pmas) were seen in the contraction after the extrasystole. The ratio of Pmax of the potentiated beat to that of the control beat was not changed by a 9% increase in the end-diastolic diameter, produced by saline infusion. Conversely, isoproterenol significantly altered this relationship in the same manner as in the isolated muscle. Thus, either in vitro or in situ, left ventricular myocardium exhibits large functional changes in response to brief perturbations in rate. The isoproterenol and length data indicate that the force-frequency ratio reflects frequency-dependent changes in the inotropic state, independent of changes in length.