Weak and strong myocardium in series: implications for segmental dysfunction

Wiegner, Allen W.; Allen, Gregory; Bing, O. H. L.

doi:10.1152/ajpheart.1978.235.6.h776

Cited by 46 publications

(32 citation statements)

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“…For all 12 patients, the posterior wall endocardial and epicardial echoes were satisfactorily digitized and posterior wall thickness was computed every 5 msec throughout the cardiac cycle. A sixth-order polynomial was fitted to the posterior wall thickness-time data points from the time of peak thickness to give peak rates of left ventricular posterior wall thinning, as previously described.…”

Section: Methodsmentioning

confidence: 99%

Increased regional myocardial stiffness of the left ventricle during pacing-induced angina in man.

Bourdillon¹,

Lorell²,

Mirsky³

et al. 1983

Circulation

168

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SUMMARY The left ventricular diastolic pressure-volume.relationship shifts upward during angina, but why this happens is not known. To assess regional myocardial stiffness, we studied 12 patients who.had coronary artery disease using simultaneous left ventricular micromanometer pressure recording and Mmode echocardiography before and during angina induced. by pacing tachycardia. All patients had two-or three-vessel coronary artery disease that involved the posterior left ventricular wall circulation and had positive pacing stress tests, i.e., development of angina and a postpacing rise in left ventricular end-diastolic pressure (15 3 to 31 6 mm Hg, p < 0.001). A marked upward shift in the relationship between the diastolic left ventricular pressure and the posterior wall thickness (h) occurred after pacing tachycardia, but the change in left ventricular posterior wall end-diastolic thickness was minimal (8.9 2.1 to 9.2 2.1 mm, NS). After pacing, the peak rate of left ventricular posterior wall thinning decreased (82 37 to 48 27 mm/sec, p < 0.005) and the time constant of relaxation derived from the best exponential fit to the isovolumic left ventricular pressure decay increased (49 5 to 58 7 msec,.p < 0.001). Diastolic active left ventricular pressure decay, extrapolated from the exponential fit, was subtracted from the measured left ventricular pressure (which is equal in magnitude but opposite in sign to the radial stress at the endocardium) to calculate residual left ventricular pressure (PR) and hence residual stress (6R = -PR). A radial stifiness modulus (ER) was determined by the slope of the PR VS log h plots before and after pacing. Over the same range of residual radial stress (aR), ER was always higher during pacing-induced angina, indicating increased residual myocardial stiffness. Increased myocardial stiffness in addition to a decreased rate of wall thinning and slow active pressure decay contribute to the upward shift in left ventricular pressure-wall thickness and pressure-volume relationships during pacing-induced angina.DURING pacing-induced angina in patients with coronary artery disease, the left ventricular pressure-volume relationships shift upward during diastole. 1-The mechanisms by which these acute changes take place are not well understood and have been the subject of controversy.8' 9 Potential mechanisms include changes in the heart's geometry, 1012 persistent interaction of some contractile elements within the ischemic myocardium throughout diastole,"3 interaction between the two ventricles,8 changes in intrapericardial pressure8 9 and alterations in passive myocardial properties.1418The or the right ventricle in causing these shifts seems unlikely. Also, recent evidence shows that in an isolated canine heart model, left ventricular diastolic pressures are significantly altered by changes in the right ventricle only at very high levels of right ventricular end-diastolic pressure.21The effects of dyssynergistic contraction on diastolic pressure might be expected only during the early p...

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Section: Methodsmentioning

confidence: 99%

Increased regional myocardial stiffness of the left ventricle during pacing-induced angina in man.

Bourdillon¹,

Lorell²,

Mirsky³

et al. 1983

Circulation

168

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“…A similar pattern with late systolic lengthening has been observed in papillary muscle preparations exposed to hypoxemia. 19 Similarly, in myocardium with systolic akinesia, the pressure-segment length loop analysis indicated an active stress component that contributed to postsystolic shortening. The following qualitative approach is consistent with these inter- pretations: A segment that does not deform during the substantial rise in LV pressure during isovolumic contraction, but shortens markedly when pressure is falling during isovolumic relaxation, is not likely to be passive.…”

Section: Mechanism Of Postsystolic Shortening In Myocardium With Systmentioning

confidence: 97%

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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“…In isolated muscles put in series, of which one was made hypoxic while its loading was forced into a normal physiological pattern, deformation was similar as in an intact ventricle, with PST occurring after the active force started to reduce. 57,58 A similar setup, but with a constant nonphysiological load, only showed reduced contraction and bulging with no PST. 59 This clearly suggests that the interaction of the Figure 7.…”

Section: Postsystolic Thickening: What Is It and Why Does It Occur?mentioning

confidence: 97%

Investigating Cardiac Function Using Motion and Deformation Analysis in the Setting of Coronary Artery Disease

et al. 2007

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Weak and strong myocardium in series: implications for segmental dysfunction

Cited by 46 publications

References 0 publications

Increased regional myocardial stiffness of the left ventricle during pacing-induced angina in man.

Increased regional myocardial stiffness of the left ventricle during pacing-induced angina in man.

Postsystolic Shortening in Ischemic Myocardium

Investigating Cardiac Function Using Motion and Deformation Analysis in the Setting of Coronary Artery Disease

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