An Analysis of Segmental Ischemic Dysfunction Utilizing the Pressure-Length Loop

Tyberg, John V.; Forrester, James S.; Wyatt, H.L.; Goldner, S. J.; Parmley, William W.; Swan, H. J. C.

doi:10.1161/01.cir.49.4.748

Cited by 164 publications

(63 citation statements)

References 13 publications

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“…13 All values represent the mean of 3 consecutive heart cycles. In passive myocardial segments (Ͼ90% reduction in LVP-SL loop area compared with baseline), systolic myocardial compliance was calculated as systolic lengthening divided by systolic pressure rise (Figure 1, right).…”

Section: Calculationsmentioning

confidence: 99%

Myocardial Strain Analysis in Acute Coronary Occlusion

Lyseggen¹,

Skulstad²,

Helle-Valle³

et al. 2005

Circulation

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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 (nϭ6), for 4 hours with 3-hour reperfusion (nϭ6), or for 4 hours with no reperfusion (nϭ6). 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 (rϭ0.77, PϽ0.0001). In entirely passive myocardium, the L-S ratio approached 1 and was similar in viable (0.88Ϯ0.02) and necrotic (0.81Ϯ0.03) myocardium. Compliance, however, was reduced in necrotic myocardium owing to edema (0.07Ϯ0.01%/mm Hg) but was preserved in viable myocardium (0.

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Section: Calculationsmentioning

confidence: 99%

Myocardial Strain Analysis in Acute Coronary Occlusion

Lyseggen¹,

Skulstad²,

Helle-Valle³

et al. 2005

Circulation

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“…A common finding in ischemic myocardium is postsystolic (postejection) shortening and consequently delayed onset of diastolic lengthening (8,16,17). Therefore, in the ischemic ventricle, there may be substantial regional asynchrony in the onset of myocardial diastolic lengthening, and this in turn may have an impact on intraventricular flow.…”

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confidence: 99%

Postsystolic shortening of ischemic myocardium: a mechanism of abnormal intraventricular filling

Urheim¹,

Edvardsen²,

Steine³

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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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 Ϯ 1.6 cm/s). After LAD occlusion, the velocities reversed (Ϫ2.3 Ϯ 0.4 cm/s, P Ͻ 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 Ϯ 1.7% (P Ͻ 0.01) and 14.2 Ϯ 2.4% (P Ͻ 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. strain-Doppler echocardiography; two-dimensional color Doppler; myocardial ischemia; diastolic filling ASSESSMENT OF LEFT VENTRICULAR (LV) intracavitary filling by Doppler echocardiography is one of several noninvasive approaches for studying LV diastolic function. In the normal LV, the initial intraventricular filling wave propagates rapidly toward the apex, and, as demonstrated by color M-mode Doppler, there is near simultaneous onset of filling velocities along the entire LV inflow tract (7). However, in patients with reduced LV ejection fraction or impaired diastolic function, the early diastolic apical filling may be markedly delayed, and this can be measured as slowing of mitral-to-apical flow propagation (1, 13). This has been attributed to a decrease in rate of LV relaxation, which causes a decrease in the driving pressure for mitral-to-apical flow (1, 12, 13), to loss of "apical suction" (12), and enhanced vortex formations due to changes in LV and mitral valve geometry (10).There is, however, very limited insight into how regional wall motion interacts with intraventricular flow. A common finding in ischemic myocardium is postsystolic (postejection) shortening and consequently delayed onset of diastolic lengthening (8,16,17). Therefore, in the ischemic ventricle, there may be substantial regional async...

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“…[6][7][8][9][10] The changes are best characterized as a sequence that begins as late systolic outward motion and ends with total replacement of active shortening by passive expansion.4'5' Such a sequence is highly specific for regional ischemial 5 ' and invariably precedes electrocardiographic ST-segment shifts.4' It has been postulated4' 5that these alterations of regional function are directly analogous to qualitative angiographic contraction patterns such as "hypokinesis" and "dyskinesis.""' 12 If this is the case, clinical left ventriculography might be used as a quantitative measure of regional ischemia.…”

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confidence: 99%

“…mm Figure 4 summarizes these data in a conventional by 30 left ventriculographic format. Anterior segments [6][7][8][9][10][11][12][13][14][15][16][17][18] and apical-inferior segments 23 Segments 36-42 of the inferior wall, on the other hand, showed significant increase in wall motion compared with the control state.…”

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confidence: 99%

Analysis of regional ischemic left ventricular dysfunction by quantitative cineangiography.

Tzivoni¹,

Diamond²,

Pichler³

et al. 1979

Circulation

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An Analysis of Segmental Ischemic Dysfunction Utilizing the Pressure-Length Loop

Abstract: SUMMARYLeft ventricular (LV) pressure and myocardial segment length, determined by an epicardial mercury-in-silastic length gauge, were plotted simultaneously to obtain a pressure-length loop before and after left anterior descending artery (LAD) occlusion in 11 dogs. Previous

Cited by 164 publications

References 13 publications

Myocardial Strain Analysis in Acute Coronary Occlusion

Myocardial Strain Analysis in Acute Coronary Occlusion

Postsystolic shortening of ischemic myocardium: a mechanism of abnormal intraventricular filling

Analysis of regional ischemic left ventricular dysfunction by quantitative cineangiography.

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