Impaired Systolic torsion in dilated cardiomyopathy: Reversal of apical rotation at mid-systole characterized with magnetic resonance tagging method

Kanzaki, Hideaki; Nakatani, Satoshi; Yamada, Naoaki; Urayama, Shin‐ichi; Miyatake, Kunio; Kitakaze, Masafumi

doi:10.1007/s00395-006-0603-6

Cited by 91 publications

(68 citation statements)

References 28 publications

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“…78 The impact of prolonged systolic forces during ejection was observed by Stuber et al, 74 employing tagging MRI studies in patients with aortic stenosis (Figure 12) and also in patients with dilated cardiomyopathy. 79 Systolic contraction extended into the isovolumic phase (previously termed early diastole), and a similar pattern was observed after transient ischemia 78 to produce diastolic dysfunction (Figures Xa, Xb, Xc, and XI in the online-only Data Supplement). Sonomicrometer crystal studies demonstrated that extended descending segment contraction limits the normal hiatus (Ϸ80 ms interval) between cessation of descending and ascending segment shortening to generate an abnormal pattern that is remedied by sodium-hydrogen exchange inhibitors.…”

Section: Discussionmentioning

confidence: 63%

Cardiac Mechanics Revisited

et al. 2008

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Abstract-The keynote to understanding cardiac function is recognizing the underlying architecture responsible for the contractile mechanisms that produce the narrowing, shortening, lengthening, widening, and twisting disclosed by echocardiographic and magnetic resonance technology. Despite background knowledge of a spiral clockwise and counterclockwise arrangement of muscle fibers, issues about the exact architecture, interrelationships, and function of the different sets of muscle fibers remain to be resolved. This report (1) details observed patterns of cardiac dynamic directional and twisting motions via multiple imaging sources; (2) summarizes the deficiencies of correlations between ventricular function and known ventricular muscle architecture; (3) correlates known cardiac motions with the functional anatomy within the helical ventricular myocardial band; and (4) defines an innovative muscular systolic mechanism that challenges the previously described concept of "isovolumic relaxation Key Words: diastole Ⅲ heart failure Ⅲ muscles Ⅲ ventricles C ongestive heart failure, due usually to both left ventricular (LV) and right ventricular failure, is an increasing problem worldwide. In the United States, Ϸ5 million patients suffer from congestive heart failure, and each year Ϸ500 000 new patients develop the condition. 1 Originally, this syndrome was believed to be due to failure of the LV to pump blood efficiently (ie, systolic ventricular failure). More recently, emphasis has been placed on diastolic ventricular failure, in which systolic function appears to be normal but diastolic ventricular function is impaired. 2-4 Diastolic dysfunction, in fact, may be the cause of congestive heart failure in up to 50% of these patients. 5,6 We have had treatment for systolic ventricular failure for many years, even if it is imperfect; at present, however, no agreement has been reached about the best ways of treating diastolic ventricular failure. To develop better treatments for congestive heart failure, both systolic and diastolic, we need first to understand the basic physiology of normal and abnormal ventricular contraction and relaxation.The heart is a muscular pump that supplies blood to the body. This goal is achieved by electric excitation that produces sequential ventricular emptying and filling. Figure 1a demonstrates the physiological sequence of ventricular function: an isovolumic contraction phase to develop preejection tension, ejection, a postejection isovolumic phase, and then rapid and slow periods for filling. LV volume decreases rapidly early in systole and slowly thereafter, corresponding to the rapid early acceleration in the flow curve. The volume then increases rapidly in early filling and more slowly during late filling.The information shown in Figure 1a is still correct, but it is only slightly more informative than the concept of William Harvey, who concluded, after dissecting cadaver hearts, that the heart squeezed by constriction to eject and dilated passively to fill. This accepted view of car...

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Section: Discussionmentioning

confidence: 63%

Cardiac Mechanics Revisited

et al. 2008

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“…In addition to the balance of endocardial and epicardial forces, rotation patterns are influenced by the electric activation sequence, with an earlier electrical depolarization of the subendocardial fibers (33). LV geometry also likely plays a role in LV twist through relative change in LV fiber orientation secondary to LV remodelling as has been shown in adults with myocardial disease (8,18). Given the observations of the current study, we postulate that the differences in LV twist mechanics between NPs and YPs would suggest fundamental differences in LV myocardial architecture, which may contribute to the enhanced response of the NP LV to tachycardia.…”

Section: Discussionmentioning

confidence: 98%

Postnatal neonatal myocardial adaptation is associated with loss of tolerance to tachycardia: a simultaneous invasive and noninvasive assessment

Fortin-Pellerin

Khoo

Mills

et al. 2016

American Journal of Physiology-Heart and Circulatory Physiology

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Fortin-Pellerin E, Khoo NS, Mills L, Coe JY, Serrano-Lomelin J, Cheung PY, Hornberger LK. Postnatal neonatal myocardial adaptation is associated with loss of tolerance to tachycardia: a simultaneous invasive and noninvasive assessment. Am J Physiol Heart Circ Physiol 310: H598 -H607, 2016. First published December 30, 2015; doi:10.1152/ajpheart.00595.2015-Doppler studies at rest suggest left ventricular (LV) diastolic function rapidly improves from the neonate to infant. Whether this translates to its response to hemodynamic challenges is uncertain. We sought to explore the impact of early LV maturation on its ability to tolerate atrial tachycardia. As tachycardia reduces filling time, we hypothesized that the neonatal LV would be less tolerant of atrial tachycardia. Landrace cross piglets of two age groups (1-3 days; NPs; 14 -17 days, YPs; n ϭ 7/group) were instrumented for an atrial pacing protocol (from 200 to 300 beats/min) and assessed by invasive monitoring and echocardiography. NPs maintained their LV output and blood pressure, whereas YPs did not. Although negative dP/dt in NPs at baseline was lower than that of YPs (Ϫ1,599 Ϯ 83 vs. Ϫ2,470 Ϯ 226 mmHg/s, respectively, P ϭ 0.007), with increasing tachycardia negative dP/dt converged between groups and was not different. Both groups had similar preload reduction during tachycardia; however, NPs maintained shortening fraction while YPs decreased (NPs: 35.4 Ϯ 1.4 vs. 31.8 Ϯ 2.2%, P ϭ 0.35; YPs: 31.4 Ϯ 0.8 vs. 22.9 Ϯ 0.8%, P Ͻ 0.001). Contractility measures did not differ between groups. Peak LV twist and untwisting rate also did not differ; however, NPs tended to augment LV twist through increased apical rotation and YPs through increasing basal rotation (P ϭ 0.009). The NPs appear more tolerant of atrial tachycardia than the YPs. They have at least similar diastolic performance, enhanced systolic performance, and different LV twist mechanics, which may contribute to improved tachycardia tolerance of NPs. HEMODYNAMIC MANAGEMENT OF the critically ill term newborn is complex. Understanding the functional nature of the neonatal myocardium and how it evolves through the first few weeks and months after birth is key to optimizing care. Although many authors have provided their opinions regarding clinical management strategies (1, 12, 32), more translational and clinical studies are needed to provide insight into the functional capacity of the early postnatal heart. In particular, changes in diastolic reserve during the first few weeks and months of life in relation to the known disproportionate left ventricular (LV) growth (3, 27) have been poorly explored.In human infants, most of our understanding of the evolution of diastolic function has been derived from noninvasive Doppler-based studies (16,26,31). These investigations have suggested that the neonatal LV myocardium has less robust diastolic relaxation (16) with greater dependency on atrial contraction for filling, much like that of the diseased adult heart with diastolic dysfunction (15). In the first few mo...

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“…Peak rotation at the apex may range from 5.7º to 11.2º. Maximum systolic torsion in normal hearts has then been found to range from 6.1º to 14.5º (Helle-Valle et al 2005;Kanzaki et al 2006;Nakai et al 2006;Takeuchi et al 2006). An example of the rotational motion of a normal, healthy heart is presented in Figure 5 below.…”

Section: Rotational Motionmentioning

confidence: 98%

“…Using the same short axis images, rotational motion around a central point in the LV can be measured with STE. Both radial and rotational motion measurements, derived from STE, have recently been used in a variety of settings to assess cardiac function (Borg et al 2008;Chung et al 2006;Delhaas et al 2004;Dohi et al 2008;Kanzaki et al 2006;Suffoletto et al 2006;Tops et al 2007). …”

Section: Speckle Tracking Echocardiographymentioning

confidence: 99%