Mechanisms of augmented segment shortening in nonischemic areas during acute ischemia of the canine left ventricle.

Lew, Wilbur Y.W.; Chen, Z Y; Guth, Brian D.; Covell, JW

doi:10.1161/01.res.56.3.351

Cited by 121 publications

(63 citation statements)

References 60 publications

(87 reference statements)

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“…4) was higher than that in the healthy myocardial wall. This might be explained by the fact that different regions of the mouse heart are going through a process of differential remodeling and adaptation such as also observed in humans [51,52] and canines [53]. In contrast, Epstein et al [12] have found impairment of the remote myocardium in mice.…”

Section: Discussionmentioning

confidence: 98%

Magnetic resonance imaging of regional cardiac function in the mouse

Heijman

Strijkers

Habets

et al. 2004

MAGMA

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In this paper we introduce an improved harmonic phase (HARP) analysis for complementary spatial modulation of magnetization (CSPAMM) tagging of the mouse left ventricular wall, which enables the determination of regional displacement fields with the same resolution as the corresponding CINE anatomical images. CINE MRI was used to measure global function, such as the ejection fraction. The method was tested on two healthy mouse hearts and two mouse hearts with a myocardial infarction, which was induced by a ligation of the left anterior descending coronary artery. We show that the regional displacement fields can be determined. The mean circumferential strain for the left ventricular wall of one of the healthy mice was −0.09 ± 0.04 (mean ± standard deviation), while for one of the infarcted mouse hearts strains of −0.02 ± 0.02 and −0.10 ± 0.03 were found in the infarcted and remote regions, respectively.

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Section: Discussionmentioning

confidence: 98%

Magnetic resonance imaging of regional cardiac function in the mouse

Heijman

Strijkers

Habets

et al. 2004

MAGMA

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“…9 Infarct expansion causes the deformation of the border zone and remote myocardium, which alters Frank/Starling relations and augments shortening. 9 Perturbations in circulatory hemodynamics trigger the sympathetic adrenergic system, which stimulates catecholamine synthesis by the adrenals and spillover from sympathetic nerve terminals, activates the renin-angiotensin-aldosterone system, and stimulates the production of atrial and brain natriuretic peptides (ANP and BNP). 10 Augmented shortening and increased heart rate from sympathetic stimulation result in hyperkinesis of the noninfarcted myocardium and temporary circulatory compensation.…”

Section: Pathophysiology Postinfarction Left Ventricular Remodelingmentioning

confidence: 99%

Left Ventricular Remodeling After Myocardial Infarction

2000

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L eft ventricular remodeling is the process by which ventricular size, shape, and function are regulated by mechanical, neurohormonal, and genetic factors. 1,2 Remodeling may be physiological and adaptive during normal growth or pathological due to myocardial infarction, cardiomyopathy, hypertension, or valvular heart disease ( Figure 1). This article will review postinfarction remodeling, pathophysiological mechanisms, and therapeutic intervention. Pathophysiology Postinfarction Left Ventricular RemodelingThe acute loss of myocardium results in an abrupt increase in loading conditions that induces a unique pattern of remodeling involving the infarcted border zone and remote noninfarcted myocardium. Myocyte necrosis and the resultant increase in load trigger a cascade of biochemical intracellular signaling processes that initiates and subsequently modulates reparative changes, which include dilatation, hypertrophy, and the formation of a discrete collagen scar. Ventricular remodeling may continue for weeks or months until the distending forces are counterbalanced by the tensile strength of the collagen scar. This balance is determined by the size, location, and transmurality of the infarct, the extent of myocardial stunning, the patency of the infarct-related artery, and local tropic factors. 1,3 The myocardium consists of 3 integrated components: myocytes, extracellular matrix, and the capillary microcirculation that services the contractile unit assembly. Consideration of all 3 components provides important insights into the remodeling process and a rationale for future therapeutic strategies. The cardiomyocyte is terminally differentiated and develops tension by shortening. The extracellular matrix provides a stress-tolerant, viscoelastic scaffold consisting of type I and type III collagen that couples myocytes and maintains the spatial relations between the myofilaments and their capillary microcirculation. 4,5 The collagen framework couples adjacent myocytes by intercellular struts that align myofilaments to optimize force development, distribute force evenly to the ventricular walls, and prevent sarcomeric deformation. 5 Myocardial infarction results in the migration of macrophages, monocytes, and neutrophils into the infarct zone; this initiates intracellular signaling and neurohormonal activation, which localizes the inflammatory response. Changes in circulatory hemodynamics are determined primarily by the magnitude of myocyte loss, the stimulation of the sympathetic nervous system and renin-angiotensin-aldosterone system, and the release of natriuretic peptides.Postinfarction remodeling has been arbitrarily divided into an early phase (within 72 hours) and a late phase (beyond 72 hours). The early phase involves expansion of the infarct zone, 5 which may result in early ventricular rupture or aneurysm formation. Late remodeling involves the left ventricle globally and is associated with time-dependent dilatation, the distortion of ventricular shape, and mural hypertrophy. The failure to normalize increa...

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“…In the work of Akaishi et al 4 and that of Lew et al ,8 the influence of preload on the movement of ischemic and nonischemic myocardium was demonstrated. In the present study we undertook the analysis of the influence of afterload on systolic bulging and augmentation of nonischemic myocardium.…”

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confidence: 96%

The effect of changes in afterload on systolic bulging.

et al. 1988

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It has been previously shown that after acute coronary occlusion, the extent of systolic bulging is dependent on preload and the function of the remote nonischemic myocardium is influenced by the motion of the ischemic myocardium as well as by the loading conditions. To examine the isolated effects of changing afterload on the movement of acutely ischemic and nonischemic myocardium, seven open-chest, anesthetized dogs were paced from the left atrium at a rate of 100 beats/min after crushing of the sinus node. The pulmonary artery was perfused artificially and the left ventricular end-diastolic pressure (LVEDP) was carefully controlled with a right heart bypass system. Twenty minutes after occlusion of the left anterior descending artery, the peak left ventricular pressure (LVP) was adjusted to three levels (70, 90, and 110 mm Hg) by blood withdrawal or aortic constriction, while the LVEDP was kept constant (8.3 + 2.3 mm Hg). Segment length in the ischemic (IZ) and nonischemic zones (NZ) were measured with sonomicrometers and total, isovolumetric, and ejection systolic shortening (%zXL) were calculated. Changes in left ventricular minor-axis diameter were measured with diameter crystals. Increasing the peak LVP increased the LVP both at aortic valve opening and closing. To keep the LVEDP constant as peak LVP was increased, the cardiac output had to be decreased (p < .0001).In the IZ, increasing the peak LVP increased isovolumetric bulge (-13.6 + 3.4%, -14.4 ± 3.7%, and -15.0 3.7% at LVP 70, 90, and 110 mm Hg, respectively, p < .00005) and decreased ejection %AL (4.8 4.6%, 4.1 ± 4.3%, and 3.3 ± 4.4%, p < .05) so that total %AL was decreased (p < .001). In the NZ, increasing the peak LVP decreased both isovolumetric %AL (8.4 ± 2.7%, 7.1 + 2.9% and 6.3 ± 2.8%, p < .0005) and ejection %zSL (10.8 ± 6.5%, 9.6 + 4.4%, and 8.8 ± 4.2%, p < .05) so total %AL was reduced (p < .0005). We conclude that increasing afterload increases the extent of the bulge in the ischemic zone and hypothesize that these changes are caused directly by an increase in wall tension. Increasing afterload also decreases shortening in nonischemic myocardium. Circulation 77, No. 1, 221-226, 1988

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Mechanisms of augmented segment shortening in nonischemic areas during acute ischemia of the canine left ventricle.

Cited by 121 publications

References 60 publications

Magnetic resonance imaging of regional cardiac function in the mouse

Magnetic resonance imaging of regional cardiac function in the mouse

Left Ventricular Remodeling After Myocardial Infarction

The effect of changes in afterload on systolic bulging.

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