Pressure-length loop area: Its components analyzed during graded myocardial ischemia

Safwat, Amira M.; Leone, Bruce J.; Norris, R. M.; Foëx, P.

doi:10.1016/s0735-1097(10)80199-8

Cited by 37 publications

(16 citation statements)

References 31 publications

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“…This is consistent with previous studies in different animal models. [15][16][17][18] As demonstrated in the present study, the relationship between regional myocardial deformation and severity of ischemia is not that clear. Whether an ischemic myocardial segment is hypokinetic or dyskinetic depends on the balance between the stress imposed on that segment and the sum of the active and passive stresses within the segment.…”

Section: Discussioncontrasting

confidence: 55%

Postsystolic Shortening in Ischemic Myocardium

Skulstad¹,

Edvardsen²,

Urheim³

et al. 2002

Circulation

223

143

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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 10.4Ϯ1.2% to 5.9Ϯ0.9% (PϽ0.05), whereas postsystolic shortening increased from 1.1Ϯ0.3% to 4.2Ϯ0.7% (PϽ0.05). 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 8.2Ϯ1.0% (PϽ0.05). 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 (rϭ0.83, PϽ0.01). 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.

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Section: Discussioncontrasting

confidence: 55%

Postsystolic Shortening in Ischemic Myocardium

Skulstad¹,

Edvardsen²,

Urheim³

et al. 2002

Circulation

223

143

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“…The consequence is dissipation and wasting of some energy produced by normal segments, which stretch the ischemic/scarred tissue and therefore does not contribute to ejection. 16 These changes explain the impaired pressure volume loops shown in Figure 4, which define global function that was ultimately changed by restoration.…”

Section: Mechanical Performance In Ischemic Cardiomyopathymentioning

confidence: 99%

Surgical Ventricular Restoration Improves Mechanical Intraventricular Dyssynchrony in Ischemic Cardiomyopathy

et al. 2004

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Background-In ischemic cardiomyopathy, dyssynchrony of left ventricular (LV) mechanical contraction produces adverse hemodynamic consequences. This study tests the capacity of geometric rebuilding by surgical ventricular restoration (SVR) to restore a more synchronous contractile pattern after a mechanical, rather than electrical, intervention. Methods and Results-A prospective study of the global and regional components of dyssynchrony was conducted in 30 patients (58Ϯ8 years of age) undergoing SVR at the Cardiothoracic Center of Monaco. The protocol used simultaneous measurements of ventricular volumes and pressure to construct pressure/volume (P/V) and pressure/length (P/L) loops. Angiograms were done before and after SVR to study a 600-ms cycle during atrial pacing at 100 bpm. Mean QRS duration was similar, at 100Ϯ17 ms preoperatively and 114Ϯ28 ms postoperatively (NS). Preoperative LV contraction was highly asynchronous, because P/V loops showed abnormal isometric phases with a right shifting. Endocardial time motion was either early or delayed at the end-systolic phase so that P/L loops were markedly abnormal in size, shape, and orientation. Postoperatively, SVR resulted in leftward shifting of P/V loops and increased area; endocardial time motion and P/L loops almost normalized to allow a better contribution of single regions to global ejection. The hemodynamic consequences of SVR were improved ejection fraction (30Ϯ13% to 45Ϯ12%; Pϭ0.001); reduced end-diastolic and end-systolic volume index (202Ϯ76 to 122Ϯ48 and 144Ϯ69 to 69Ϯ40 mL/m

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“…Assessment of regional pressure-dimension loops, however, has not been feasible in clinical studies. In animal models, however, one may analyze regional function from pressure-segment length loops obtained from micromanometers and implanted sonomicrometric crystals (1,3,7,10,14,15,17). Similar to sonomicrometry, SDE provides a continuous measure of changes in regional dimension, and regional pressure-strain loops may provide information similar to pressure-segment length loops.…”

mentioning

confidence: 99%

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

Urheim¹,

Rabben²,

Skulstad³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

364

495

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-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 ϭ 0.73x ϩ 0.21, r ϭ 0.82, P Ͻ 0.01). Volume loading caused an increase in RMWI from 1.3 Ϯ 0.2 to 2.2 Ϯ 0.1 kJ/m 3 (P Ͻ 0.05) by SDE and from 1.5 Ϯ 0.3 to 2.7 Ϯ 0.3 kJ/m 3 (P ϭ 0.066) by sonomicrometry. Short-term ischemia (1 min) caused a decrease in RMWI from 1.3 Ϯ 0.2 to 0.3 Ϯ 0.04 kJ/m 3 (P Ͻ 0.05) and from 1.3 Ϯ 0.3 to 0.5 Ϯ 0.2 kJ/m 3 (P Ͻ 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, Ϫ0.2 Ϯ 0.1 and Ϫ0.1 Ϯ 0.03 kJ/m 3 (P Ͻ 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.sonomicrometry; pressure-strain loop STRAIN DOPPLER ECHOCARDIOGRAPHY (SDE) has been introduced as a new clinical method to measure regional myocardial function (2, 5, 18). As a measure of systolic function, one may use peak systolic strain, recorded either in the LV long axis as shortening strain or in the short axis as thickening strain. However, peak systolic strain is load dependant and therefore may not reflect systolic function when there are changes in loading conditions (18). This is analogous to the problem with load dependency of LV ejection fraction. In the latter case, one may use LV pressure-volume relations to differentiate between load-induced changes in function and changes in intrinsic myocardial contractility. Assessment of regional pressure-dimension loops, however, has not been feasible in clinical studies. In animal models, however, one may analyze regional function from pressure-segment length loops obtained from micromanometers and implanted sonomicrometric crystals (1,3,7,10,14,15,17). Similar to sonomicrometry, SDE provides a continuous measure of changes in regional dimension, and regional press...

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Pressure-length loop area: Its components analyzed during graded myocardial ischemia

Cited by 37 publications

References 31 publications

Postsystolic Shortening in Ischemic Myocardium

Postsystolic Shortening in Ischemic Myocardium

Surgical Ventricular Restoration Improves Mechanical Intraventricular Dyssynchrony in Ischemic Cardiomyopathy

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

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