[Expert Consensus document on angiotensin converting enzyme inhibitors in cardiovascular disease].
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Angiotensin-Converting Enzyme Inhibitors↗
Biomedical subjects
Otto A Smiseth
Publications and source records attributed to Otto A Smiseth.
Strain rate imaging: why do we need it?
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Animals↗
Postsystolic shortening of ischemic myocardium: a mechanism of abnormal intraventricular filling.
Acute myocardial ischemia has been associated with abnormal filling patterns in the left ventricular (LV) apex. We hypothesized that this may in part be due to postsystolic shortening of ischemic apical segments, which leads to reversal of early diastolic apical flow. Fourteen open-chest anesthetized dogs were instrumented with micromanometers in the LV apex and left atrium and myocardial sonomicrometers in the anterior apical LV wall. Intraventricular filling by color Doppler and wall motion by strain Doppler echocardiography (SDE) were assessed from an apical view. Measurements were taken before and after 5 min of left anterior descending coronary artery (LAD) occlusion. In four dogs, we measured the pressure difference between the LV apex and outflow tract. At baseline, peak early diastolic flow velocities in the distal one-third of the LV were directed toward apex (9.2 +/- 1.6 cm/s). After LAD occlusion, the velocities reversed (-2.3 +/- 0.4 cm/s, P < 0.01), indicating that blood was ejected from the apex toward the base during early filling. This interpretation was confirmed by wall motion analysis, which showed postsystolic shortening of apical myocardial segments. The postsystolic shortening represented 9.7 +/- 1.7% (P < 0.01) and 14.2 +/- 2.4% (P < 0.01) of end-diastolic segment length by SDE and sonomicrometry, respectively. Consistent with the velocity changes, we found reversal of the early diastolic pressure gradient from the LV apex to outflow tract. In the present model, acute LAD occlusion resulted in reversal of early diastolic apical flow, and this was attributed to postsystolic shortening of dyskinetic apical segments. The clinical diagnostic importance of this finding remains to be determined.
Animals↗
Postsystolic shortening in ischemic myocardium: active contraction or passive recoil?
BACKGROUND: Postsystolic shortening in ischemic myocardium has been proposed as a marker of tissue viability. Our objectives were to determine if postsystolic shortening represents active fiber shortening or passive recoil and if postsystolic shortening may be quantified by strain Doppler echocardiography (SDE). METHODS AND RESULTS: In 15 anesthetized dogs, we measured left ventricular (LV) pressure, myocardial long-axis strains by SDE, and segment lengths by sonomicrometry before and during LAD stenosis and occlusion. Active contraction was defined as elevated LVP and stress during postsystolic shortening when compared with the fully relaxed ventricle at similar segment lengths. LAD stenosis decreased systolic shortening from 10.4+/-1.2% to 5.9+/-0.9% (P<0.05), whereas postsystolic shortening increased from 1.1+/-0.3% to 4.2+/-0.7% (P<0.05). In hypokinetic and akinetic segments, LV pressure-segment length and LV stress-segment length loop analysis indicated that postsystolic shortening was active. LAD occlusion resulted in dyskinesis, and postsystolic shortening increased additionally to 8.2+/-1.0% (P<0.05). After 3 to 5 minutes with LAD occlusion, the dyskinetic segment generated no active stress, and the postsystolic shortening was attributable to passive recoil. Elevation of afterload caused hypokinetic segments to become dyskinetic, and postsystolic shortening remained partly active. Postsystolic shortening by SDE correlated well with sonomicrometry (r=0.83, P<0.01). CONCLUSIONS: Postsystolic shortening is a relatively nonspecific feature of ischemic myocardium and may occur in dyskinetic segments by an entirely passive mechanism. However, in segments with systolic hypokinesis or akinesis, postsystolic shortening is a marker of actively contracting myocardium. SDE was able to quantify postsystolic shortening and might represent a clinical method for identifying actively contracting and hence viable myocardium.
Animals↗
Quantitative assessment of intrinsic regional myocardial deformation by Doppler strain rate echocardiography in humans: validation against three-dimensional tagged magnetic resonance imaging.
BACKGROUND: Tissue Doppler echocardiography-derived strain rate and strain measurements (SDE) are new quantitative indices of intrinsic cardiac deformation. The aim of this study was to validate and compare these new indices of regional cardiac function to measurements of 3-dimensional myocardial strain by tagged MRI. METHODS AND RESULTS: The study population included 33 healthy volunteers, 17 patients with acute myocardial infarction, and 8 patients with suspected coronary artery disease who were studied during dobutamine stress echocardiography. Peak systolic myocardial velocities were measured by tissue Doppler echocardiography, peak systolic strain rates and strains by SDE, and strains by tagged MRI. In healthy individuals, longitudinal myocardial Doppler velocities decreased progressively from base to apex, whereas myocardial strain rates and strains were uniform in all segments. In patients with acute infarction, abnormal strains clearly identified dysfunctional areas. In infarcted regions, SDE showed 1.5+/-4.3% longitudinal stretching compared with -15.0+/-3.9% shortening in remote myocardium (P<0.001), and radial measurements showed -6.9+/-4.1% thinning and 14.3+/-5.0% thickening (P<0.001), respectively. During dobutamine infusion, longitudinal strains by SDE increased significantly from -13.5% to -23.8% (P<0.01) and radial strains increased from 13.1+/-3.1% to 29.3+/-11.5% (P<0.01). Comparisons between myocardial strains by SDE and tagged MRI in healthy individuals (n=11), in infarct patients (n=17), and during stress echo (n=4) showed excellent correlations (r=0.89 and r=0.96 for longitudinal and radial strains, respectively, P< 0.001). CONCLUSIONS: The present study demonstrates the ability of Doppler echocardiography to measure myocardial strains in a clinical setting. Myocardial strains by Doppler may represent a new powerful method for quantifying left ventricular function noninvasively in humans.
Adult↗
Quantification of left ventricular systolic function by tissue Doppler echocardiography: added value of measuring pre- and postejection velocities in ischemic myocardium.
BACKGROUND: Tissue Doppler imaging (TDI) is a potentially powerful method for diagnosing myocardial ischemia. This study was designed to investigate how velocity patterns in ischemic myocardium relates to regional function, and to determine whether timing of velocity measurements relative to ejection and isovolumic phases may increase the diagnostic power of TDI. METHODS AND RESULTS: In 17 open-chest anesthetized dogs we measured pressures by micromanometers, myocardial longitudinal segment lengths by sonomicrometry, and velocities by TDI. Myocardial longitudinal strain rate was calculated as velocity divided by distance to the left ventricle apex. Moderate ischemia (left anterior descending coronary artery stenosis) caused parallel reductions in regional systolic shortening by sonomicrometry (P<0.05) and in peak systolic velocities by TDI (P<0.05). Severe ischemia (left anterior descending coronary artery occlusion), however, induced systolic lengthening by sonomicrometry (P<0.001), whereas peak TDI velocity during ejection remained positive (P<0.05). When velocities during isovolumic contraction (IVC) and isovolumic relaxation (IVR) were included, TDI correlated well with sonomicrometry; ie, systolic lengthening occurred predominantly during IVC and was evident as negative velocities (r=0.70, P<0.001), and postsystolic shortening during IVR (r=0.72, P<0.001) as positive velocities. In nonischemic myocardium peak systolic strain rates were more uniform than velocities. CONCLUSION: The present results indicate that peak ejection velocity is an inappropriate measure of function in severely ischemic myocardium. Dyskinetic myocardium deforms predominantly during the isovolumic phases, and therefore IVC and IVR velocities are better markers of function. When isovolumic as well as ejection velocities are measured, TDI has excellent ability to quantify regional myocardial dysfunction. Longitudinal strain rates are more uniform than velocities and may further improve the diagnostic power of TDI.
Animals↗
Quantification of left ventricular diastolic pressure-volume relations during routine cardiac catheterization by two-dimensional digital echo quantification and left ventricular micromanometer.
BACKGROUND: Currently there is no simple clinical method for quantifying the left ventricular (LV) diastolic pressure-volume relation. Echocardiographic-automated endocardial border detection, however, may be combined with LV micromanometer to construct LV pressure-volume loops. We investigated the feasibility of on-line display and sampling of LV pressure-volume loops by such an approach. For this purpose we used a new echocardiographic digital echo quantification (DEQ) method in combination with LV pressures on-line and in real-time. METHODS: Eighteen patients were screened by conventional echocardiography and DEQ. Ten of the patients with high quality images were included in the study. Left ventricular pressures and volumes were recorded simultaneously and were displayed on-line as pressure-volume loops. Changes in LV volume were induced by intravenous saline. Left ventricular chamber compliance was estimated as change in volume divided by change in pressure from minimum diastolic pressure to end-diastolic pressure (average LV chamber compliance). RESULTS: Left ventricular pressure-volume loops were displayed on-line during the examination. When compared with the Simpson's method, DEQ underestimated end-diastolic volume (EDV) by 35% and overestimated end-systolic volume (ESV) by 14%. Beat-to-beat variability for ESV and EDV were 7.4% +/- 0.8% and 7.2% +/- 0.7 %, respectively. Volume loading increased LV end-diastolic pressure (LVEDP) from 14.0 +/- 1.6 to 24.7 +/- 2.0 mm Hg (P <.05) and EDV from 79 +/- 10 to 85 +/- 11 mL (NS), and decreased LV chamber compliance from 4.0 +/- 0.7 to 2.0 +/- 0.3 mL/mm Hg (P <.05). CONCLUSION: The current study demonstrates that LV pressure-volume loops can be displayed and evaluated in real-time during routine cardiac catheterization. This may represent a clinically useful method for identifying patients with reduced chamber compliance. The underestimation of the volumes by DEQ compared with the Simpson's method suggests that further refinements should be performed to improve the endocardial border detection algorithm.
Aged↗
Effects of acute volume loading and hemorrhage on intestinal vascular capacitance: a mechanism whereby capacitance modulates cardiac output.
BACKGROUND: Changes in intestinal vascular capacitance during acute volume loading and hemorrhage have not been described. OBJECTIVES: To determine the effects of volume loading and hemorrhage on the intestinal vascular pressure-volume relationship and cardiac output. PATIENTS AND METHODS: In 11 alpha-chloralose-anesthetized dogs, a pneumatic portal venous constrictor and catheter were positioned to increase and measure portal venous pressure (Ppv), respectively. Relative changes in intestinal blood volume (IBV) were determined by blood-pool scintigraphy and expressed as the percentage change from control values (taken as 100%). Ppv-IBV relationships were constructed by graded portal vein constriction. RESULTS: IBV and cardiac output increased by 60 6% and 178 48%, respectively, and Ppv increased from 5.8 0.9 mmHg to 13.2 1.8 mmHg after initial volume loading (40 mL/kg of an isotonic glucose-saline solution over 7 min). IBV gradually decreased and reached near-control values after 75 min. In seven dogs, hemorrhage (sufficient to decrease mean aortic pressure by 56 4%) decreased IBV and cardiac output to 88 4% and 52 3% of control values, respectively, and Ppv decreased to 3.2 0.8 mmHg. CONCLUSIONS: A sigmoid function curve defined the relationship between cardiac output and IBV. Cardiac output remained constant over a wide range (between approximately 95% and 135% of control IBV). Outside this range, insufficient dilation or constriction resulted in a marked increase or decrease in venous pressures and cardiac output. These data indicate that vasculature capacitance modulates cardiac output during acute volume loading and hemorrhage, thereby maintaining cardiac output relatively constant over a wide range of total vascular blood volume.
Animals↗
Systolic dysfunction in heart failure with normal ejection fraction: speckle-tracking echocardiography.
Left ventricular (LV) ejection fraction (EF) and LV end-systolic volumes are important measures of LV global function. However, in many patients with symptoms of heart failure, these measures are within normal limits. This condition is classified as heart failure with normal ejection fraction (HFNEF). Reduced EF and increased end-systolic volume, however, require impaired function in a number of LV segments. Therefore, apparently normal systolic function in HFNEF may reflect limited sensitivity of global EF, and assessment of regional systolic function may provide important diagnostic information. The recently introduced method, speckle-tracking echocardiography (STE), represents a simplified, objective, and angle-independent modality for quantification of regional myocardial deformation. The software uses conventional gray-scale B-mode recordings and tracks myocardial speckles, which serve as natural acoustic markers. Radial and longitudinal myocardial deformation can be measured simultaneously from long-axis recordings, radial and circumferential deformation from short-axis recordings, and LV torsion from assessment of apical and basal short-axis rotation. Experimental and clinical studies have demonstrated that the STE method can assess myocardial function accurately in healthy subjects in the settings of acute and chronic ischemia, dyssynchrony, and cardiomyopathy. So far, no STE studies have been performed regarding HFNEF. The purpose of this article is therefore to illustrate the potential of this novel method.
Diastole↗