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Biomedical subjects

Otto A Smiseth

Publications and source records attributed to Otto A Smiseth.

At least 19 recordsLinked to original sources

Grading of myocardial dysfunction by tissue Doppler echocardiography: a comparison between velocity, displacement, and strain imaging in acute ischemia.

OBJECTIVES: The aim of the study was to compare the ability of the tissue Doppler echocardiographic imaging (TDI) modalities velocity, strain, and displacement to quantify systolic myocardial function. BACKGROUND: Several TDI modalities may be used to quantify regional myocardial function, but it is not clear how the different modalities should be applied. METHODS: In 10 anesthetized dogs we measured left ventricular pressure, longitudinal myocardial velocity, strain, and displacement by TDI at baseline and during left anterior descending coronary artery (LAD) stenosis and occlusion. Reference methods were segmental shortening by sonomicrometry and segmental work. In 10 patients with acute anterior wall infarction (LAD occlusion) and 15 control subjects, velocity, strain, and displacement measurements were performed. RESULTS: In the animal study, systolic strain correlated well with segmental shortening (r = 0.96, p < 0.01) and work (r = 0.90, p < 0.01), and differentiated well between non-ischemic (-13.5 +/- 3.2% [mean +/- SD]), moderately ischemic (-6.5 +/- 2.8%), and severely ischemic myocardium (7.1 +/- 13.2%). The ratio post-systolic strain/total strain also differentiated well between levels of ischemia. Displacement and ejection velocity had weaker correlations with segmental shortening (r = 0.92 and r = 0.74, respectively) and regional work (r = 0.85 and r = 0.69), and there was marked overlap between values at baseline and at different levels of ischemia. In the human study, systolic strain differentiated well between infarcted and normal myocardium (1.0 +/- 5.0% vs. -17.8 +/- 3.8%), whereas systolic displacement (-0.3 +/- 1.3 mm vs. -2.3 +/- 0.6 mm) and ejection velocity (0.9 +/- 0.6 cm/s vs. 2.2 +/- 0.6 cm/s) showed overlap. In the infarction group, strain was reduced in segments with infarcted tissue, while systolic velocity and displacement were reduced in all segments and did not reflect the extension of the infarct. CONCLUSIONS: Strain was superior to velocity and displacement for quantification of regional myocardial function. Provided technical limitations can be solved, strain Doppler is the preferred TDI modality for assessing function in ischemic myocardium.

Acute Disease↗

Noninvasive myocardial strain measurement by speckle tracking echocardiography: validation against sonomicrometry and tagged magnetic resonance imaging.

OBJECTIVES: The aim of this study was to validate speckle tracking echocardiography (STE) as a method for angle-independent measurement of regional myocardial strain, using sonomicrometry and magnetic resonance imaging (MRI) tagging as reference methods. BACKGROUND: Tissue Doppler imaging allows non-invasive measurement of myocardial strain in the left ventricle (LV), but is limited by angle dependency. METHODS: Strain measurements with STE were obtained by a custom-made program that allowed tracking of two-dimensional motion of speckle patterns in a B-mode image. In anesthetized dogs, we compared LV long- and short-axis measurements by STE to sonomicrometry during preload changes and regional myocardial ischemia. Measurements in the two orthogonal axes were obtained simultaneously in a single imaging plane. In human subjects, long-axis strain by STE and MRI tagging were compared in multiple segments of the LV. RESULTS: In the experimental study there was good correlation and agreement between STE and sonomicrometry for systolic strain in the long axis (r = 0.90, p < 0.001; 95% limits of agreement -4.4% to 5.0%) and systolic shortening in the short axis (r = 0.79, p < 0.001; -5.6% to 5.1%). In the clinical study, 80% of the segments could be analyzed, and correlation and agreement between STE and MRI tagging were good (r = 0.87, p < 0.001; -9.1% to 8.0%). CONCLUSIONS: Speckle tracking echocardiography provides accurate and angle-independent measurements of LV dimensions and strains and has potential to become a clinical bedside tool for quantifying myocardial strain.

Adult↗

Myocardial strain analysis in acute coronary occlusion: a tool to assess myocardial viability and reperfusion.

BACKGROUND: This study proposes 2 new echocardiographic indices with potential application in acute coronary artery occlusion to differentiate between viable and necrotic myocardium and to identify reperfusion. We investigated whether the ratio between systolic lengthening and combined late and postsystolic shortening (L-S ratio) could identify viable myocardium and whether systolic myocardial compliance, calculated as systolic lengthening divided by systolic pressure rise, could identify necrotic myocardium. METHODS AND RESULTS: In anesthetized dogs, we measured left ventricular (LV) pressure and long-axis strain by Doppler echocardiography (SDE) and sonomicrometry. The left anterior descending coronary artery was occluded for 15 minutes with 3-hour reperfusion (n=6), for 4 hours with 3-hour reperfusion (n=6), or for 4 hours with no reperfusion (n=6). Myocardial work was quantified by pressure-segment length analysis, necrosis by triphenyltetrazolium chloride staining, and edema by water content. L-S ratio and systolic compliance were calculated by SDE. The L-S ratio ranged between 0.00 and 1.00 and was well correlated with regional myocardial work (r=0.77, P<0.0001). In entirely passive myocardium, the L-S ratio approached 1 and was similar in viable (0.88+/-0.02) and necrotic (0.81+/-0.03) myocardium. Compliance, however, was reduced in necrotic myocardium owing to edema (0.07+/-0.01%/mm Hg) but was preserved in viable myocardium (0.15+/-0.01%/mm Hg, P<0.05). Reperfusion of viable myocardium caused a reduction of the L-S ratio after 15 minutes (0.57+/-0.06, P<0.05), reflecting recovery of function. Reperfusion of necrotic myocardium caused no change in the L-S ratio, but compliance was further reduced within 15 minutes (0.03+/-0.01%/mm Hg, P<0.05). CONCLUSIONS: Myocardial L-S ratio and compliance by SDE identified active contraction and necrosis, respectively. These indices should be tested clinically for assessment of myocardial viability and reperfusion.

Animals↗

New noninvasive method for assessment of left ventricular rotation: speckle tracking echocardiography.

BACKGROUND: Left ventricular (LV) torsion is due to oppositely directed apical and basal rotation and has been proposed as a sensitive marker of LV function. In the present study, we introduce and validate speckle tracking echocardiography (STE) as a method for assessment of LV rotation and torsion. METHODS AND RESULTS: Apical and basal rotation by STE was measured from short-axis images by automatic frame-to-frame tracking of gray-scale speckle patterns. Rotation was calculated as the average angular displacement of 9 regions relative to the center of a best-fit circle through the same regions. As reference methods we used sonomicrometry in anesthetized dogs during baseline, dobutamine infusion, and apical ischemia, and magnetic resonance imaging (MRI) tagging in healthy humans. In dogs, the mean peak apical rotation was -3.7+/-1.2 degrees (+/-SD) and -4.1+/-1.2 degrees, and basal rotation was 1.9+/-1.5 degrees and 2.0+/-1.2 degrees by sonomicrometry and STE, respectively. Rotations by both methods increased (P<0.001) during dobutamine infusion. Apical rotation by both methods decreased during left anterior descending coronary artery occlusion (P<0.007), whereas basal rotation was unchanged. In healthy humans, apical rotation was -11.6+/-3.8 degrees and -10.9+/-3.3 degrees, and basal rotation was 4.8+/-1.7 degrees and 4.6+/-1.3 degrees by MRI tagging and STE, respectively. Torsion measurement by STE showed good correlation and agreement with sonomicrometry (r=0.94, P<0.001) and MRI (r=0.85, P<0.001). CONCLUSIONS: The present study demonstrates that regional LV rotation and torsion can be measured accurately by STE, suggesting a new echocardiographic approach for quantification of LV systolic function.

Animals↗

Myocardial acceleration during isovolumic contraction: relationship to contractility.

BACKGROUND: Acceleration of the mitral ring during isovolumic contraction has been proposed as a load-independent index of global left ventricular (LV) contractility. This study investigates whether myocardial isovolumic acceleration (IVA) reflects regional contractility. METHODS AND RESULTS: In acutely instrumented, anesthetized dogs, we measured LV pressure, myocardial long-axis velocities, and IVA by tissue Doppler imaging (TDI) and sonomicrometry at different levels of global LV contractility and preload and during regional myocardial ischemia (reduced flow in the left anterior descending coronary artery). Dobutamine caused dose-dependent increments in IVA from 3.6+/-0.6 (mean+/-SEM) to a maximum of 7.1+/-1.4 m/s2 (P<0.01) by TDI, and there were parallel increments in LV dP/dt(max) (P<0.01). However, volume loading decreased IVA from 3.6+/-0.6 to 2.5+/-0.4 m/s2 (P<0.05), whereas LV dP/dt(max) was unchanged, and LV pressure-segment length loop analysis confirmed unchanged regional contractility. During myocardial ischemia, sonomicrometry indicated severely depressed regional function, whereas IVA remained unchanged. These findings were confirmed when IVA was measured by sonomicrometry. In contrast to peak ejection velocity that increased from apex toward the LV base, peak IVC velocity was maximum midway between apex and base. The onset of IVA coincided with onset of the first heart sound by phonocardiography. Peak IVA occurred at a LV pressure of 14+/-1 mm Hg, ie, close to end-diastole. CONCLUSIONS: There was no consistent relationship between peak IVA and regional myocardial contractility. Peak IVA was markedly load dependent and did not reflect impaired myocardial function during ischemia. Peak IVA may reflect late-diastolic events and possibly wall oscillations that are related to global LV function. Peak IVA seems to have limited potential in the assessment of regional myocardial function.

Animals↗

Regional myocardial work by strain Doppler echocardiography and LV pressure: a new method for quantifying myocardial function.

There is a need for better methods to quantify regional myocardial function. In the present study, we investigated the feasibility of quantifying regional function in terms of a segmental myocardial work index as derived from strain Doppler echocardiography (SDE) and invasive pressure. In 10 anesthetized dogs, we measured left ventricular (LV) pressure by micromanometer and myocardial longitudinal strains by SDE and sonomicrometry. The regional myocardial work index (RMWI) was calculated as the area of the pressure-strain loop. As a reference method for strain, we used sonomicrometry. By convention, the loop area was assigned a positive sign when the pressure-strain coordinates rotated counterclockwise. Measurements were done at baseline and during volume loading and left anterior descending coronary artery (LAD) occlusion, respectively. There was a good correlation between RMWI calculated from strain by SDE and strain by sonomicrometry (y = 0.73x + 0.21, r = 0.82, P < 0.01). Volume loading caused an increase in RMWI from 1.3 +/- 0.2 to 2.2 +/- 0.1 kJ/m3 (P < 0.05) by SDE and from 1.5 +/- 0.3 to 2.7 +/- 0.3 kJ/m3 (P = 0.066) by sonomicrometry. Short-term ischemia (1 min) caused a decrease in RMWI from 1.3 +/- 0.2 to 0.3 +/- 0.04 kJ/m3 (P < 0.05) and from 1.3 +/- 0.3 to 0.5 +/- 0.2 kJ/m3 (P < 0.05) by SDE and sonomicrometry, respectively. In the nonischemic ventricle and during short-term ischemia, the pressure-strain loops rotated counterclockwise, consistent with actively contracting segments. Long-term ischemia (3 h), however, caused the pressure-strain loop to rotate clockwise, consistent with entirely passive segments, and the loop areas became negative, -0.2 +/- 0.1 and -0.1 +/- 0.03 kJ/m3 (P < 0.05) by SDE and sonomicrometry, respectively. A RMWI can be estimated by SDE in combination with LV pressure. Furthermore, the orientation of the loop can be used to assess whether the segment is active or passive.

Animals↗

Mechanisms of elevated plasma endothelin-1 in CHF: congestion increases pulmonary synthesis and secretion of endothelin-1.

OBJECTIVE: The pulmonary circulation may contribute to elevated plasma levels of endothelin-1 (ET-1) in congestive heart failure (CHF). The aims of the present study were to determine the mechanisms of increased secretion of ET-1 from the pulmonary circulation in CHF. METHODS: Juvenile pigs were subjected to sham operation (n=9) or rapid cardiac pacing-induced CHF (215-240 bpm, n=15). RESULTS: Three weeks of rapid pacing led to significant left ventricular dilatation, increased cardiac filling pressures, and reduced contractility (CHF pigs). Arterial plasma ET-1 levels in the CHF pigs were increased 4-fold compared to sham pigs (P<0.001). Single-bolus multiple indicator-dilution experiments revealed that pulmonary synthesis and release of ET-1 was increased in CHF, while pulmonary clearance of plasma ET-1 remained unaltered despite significant reduction of pulmonary fractional extraction of plasma ET-1. Pulmonary ECE-1 isozyme activity (pmol.min-1.mg protein-1) was selectively increased in lower lobe segments of CHF pigs (2.0+/-0.3) compared to lower lobe segments of controls (1.1+/-0.1, P<0.02), and to upper lobe segments of CHF pigs (1.1+/-0.1, P<0.005), and correlated significantly with the wet/dry weight ratios of the pulmonary tissue samples (R=0.75, P<0.001), i.e. a marker of pulmonary congestion. Furthermore, alveolar macrophages in congested lobe segments were identified as likely sites of increased synthesis and release of ET-1. CONCLUSIONS: In rapid pacing-induced CHF, a complex cardiopulmonary interaction revealed by pulmonary congestion causes increased pulmonary production and secretion of ET-1 due to enhanced pulmonary ECE-1 activities. Pulmonary secretion of ET-1 during evolving CHF is an important contributor to elevated plasma ET-1 levels in the systemic circulation.

Animals↗

An ultrasound-based method for determining pulse wave velocity in superficial arteries.

In this paper, we present a method for estimating local pulse wave velocity (PWV) solely from ultrasound measurements: the area-flow (QA) method. With the QA method, PWV is estimated as the ratio between change in flow and change in cross-sectional area (PWV = dQ/dA) during the reflection-free period of the cardiac cycle. In four anaesthetized dogs and 21 human subjects (age 23-74) we measured the carotid flow and cross-sectional area non-invasively by ultrasound. As a reference method we used the Bramwell-Hill (BH) equation which estimates PWV from pulse pressure and cross-sectional area. Additionally, we therefore measured brachial pulse pressure by oscillometry in the human subjects, and central aortic pulse pressure by micro-manometry in the dogs. As predicted by the pressure dependency of arterial stiffness, the estimated PWV decreased when the aortic pressure was lowered in two of the dogs. For the human subjects, the QA and BH estimates were correlated (R=0.43, p<0.05) and agreed on average (mean difference of -0.14 m/s). The PWV by the BH method increased with age (p<0.01) whereas the PWV by the QA method tended to increase with age (p<0.1). This corresponded to a larger residual variance (residual = deviation of the estimated PWV from the regression line) for the QA method than for the BH method, indicating different precisions for the two methods. This study illustrates that the simple equation PWV = dQ/dA gives estimates correlated to the PWV of the reference method. However, improvements in the basic measurements seem necessary to increase the precision of the method.

Adult↗

Tissue Doppler imaging for the diagnosis of coronary artery disease.

PURPOSE OF REVIEW: Tissue Doppler imaging (TDI) is a diagnostic method that provides quantitative data about myocardial function. The present review discusses the most recent developments in the application of TDI in coronary artery disease. RECENT FINDINGS: The most widely used TDI modality is velocity imaging, and systolic function is measured as peak velocity during LV ejection. Several recent studies show that TDI measurements during the LV isovolumic phases provide unique information regarding myocardial dysfunction. Since velocity imaging is confounded by influence from velocities in other segments, the TDI-based modalities strain- and strain rate imaging (SRI) have been introduced to measure regional shortening fraction and shortening rate, respectively.Velocity imaging during stress echocardiography has been validated clinically and appears equivalent, but not superior to conventional visual assessment of grey scale images. Potentially, more comprehensive evaluation that includes the use of SRI may improve the diagnostic power of TDI further. Preliminary reports suggest that TDI may have an important role in the assessment of viability in acute coronary occlusion, but this needs to be demonstrated in appropriately designed clinical trials. SUMMARY: At the present time tissue Doppler velocity imaging can be recommended for clinical use, especially the pulsed mode. Strain rate imaging may be useful as additional imaging, but needs further refinement before it is ready for routine clinical use.

Acute Disease↗