Calculation of left ventricular wall stress.

Regen, David M.

doi:10.1161/01.res.67.2.245

Cited by 68 publications

(47 citation statements)

References 41 publications

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“…ESFS was calculated using the following formula: ESFS=1.35×P×bm×2h (expressed in g/cm 2 ), where P is the end-systolic pressure, 24 D is the end-systolic LV internal diameter (in cm), h is the end-systolic posterior wall thickness, and bm is the midwall minor semiaxis expressed as h/ln(0.5D+h)-ln(0.5D). 25 To assess the interobserver variability of volumetric analyses, a second expert (K.H.) performed the same analysis on subsets of 10 subjects.…”

Section: Image Analysismentioning

confidence: 99%

Occult Cardiotoxicity in Childhood Cancer Survivors Exposed to Anthracycline Therapy

Toro‐Salazar¹,

Gillan

O'Loughlin

et al. 2013

Circ: Cardiovascular Imaging

113

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Background-More than 50% of >270 000 childhood cancer survivors in the United States have been treated with anthracyclines and are therefore at risk of developing cardiotoxicity. Cardiac magnetic resonance (CMR) has demonstrated utility to detect diffuse interstitial fibrosis and changes in regional myocardial function. We hypothesized that CMR would identify occult cardiotoxicity characterized by structural and functional myocardial abnormalities in a cohort of asymptomatic pediatric cancer survivors with normal global systolic function. Methods and Results-Forty-six long-term childhood cancer survivors with a cumulative anthracycline dose ≥200 mg/m 2 and normal systolic function were studied 2.5 to 26.9 years after anthracycline exposure. Subjects underwent transthoracic echocardiography, CMR with routine cine acquisition, tissue characterization, and left ventricular strain analysis using a modified 16-segment model. Extracellular volume was measured in 27 subjects, all of whom were late gadolinium enhancement negative. End-systolic fiber stress was elevated in 45 of 46 subjects. Low average circumferential strain magnitude (ε cc ) −14.9±1.4; P<0.001, longitudinal strain magnitude (ε ll ) −13.5±1.9; P<0.001, and regional peak circumferential strain were seen in multiple myocardial segments, despite normal global systolic function by transthoracic echocardiography and CMR. The mean T1 values of the myocardium were significantly lower than that of control subjects at 20 minutes (458±69 versus 487±44 milliseconds; P=0.01). Higher mean extracellular volume was observed in female subjects (0.34 versus 0.22; P=0.01). The purpose of this study was to use CMR T1 mapping techniques and measures of myocardial strain by tagged cine MRI to detect interstitial disease and changes in regional myocardial function in childhood cancer survivors. We tested the hypothesis that individuals with a history of high-dose anthracycline therapy may have occult cardiotoxicity, manifested by a decrease in circumferential ε cc and longitudinal ε ll strain magnitude and changes in myocardial T1 and ECV, despite normal standard measures of global left ventricular (LV) systolic function. Conclusions-Asymptomatic Methods Study PopulationEligible subjects with a cumulative anthracycline dose ≥200 mg/m 2 and normal LV systolic function defined as TTE-based shortening fraction ≥29% were identified and prospectively enrolled through a registry of pediatric cancer survivors treated with anthracyclines between 1985 and January 2011. Inclusion criteria for this study are shown in Figure 1. Subjects with high-dose radiation exposure to the chest (>3000 cGy) were excluded from the study to minimize the known synergistic effect of therapeutic radiation on cardiotoxicity. 5,21This study was approved by the Institutional Review Board at the Connecticut Children's Medical Center. The medical records of all enrolled subjects were reviewed to identify known risk factors associated with cardiotoxicity. Conversions to isotoxic equivalents of anthracycline a...

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Section: Image Analysismentioning

confidence: 99%

Occult Cardiotoxicity in Childhood Cancer Survivors Exposed to Anthracycline Therapy

Toro‐Salazar¹,

Gillan

O'Loughlin

et al. 2013

Circ: Cardiovascular Imaging

113

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“…[11][12][13] The longitudinal and circumferential radii of curvature were calculated by fitting a circle to the 3 crystal positions in each direction. The positions of the crystals were calculated from all crystal-to-crystal distances.…”

Section: Calculationsmentioning

confidence: 99%

Postsystolic Shortening in Ischemic Myocardium

Skulstad¹,

Edvardsen²,

Urheim³

et al. 2002

Circulation

225

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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“…However, they will alter determinants of LV emptying. Left ventricular afterload, which may be defined as the LV wall stress during ejection [18], is directly proportional to the systolic transmural LV pressure. Since the pressure on the external surface of the LV is usually near zero, it is often ignored in clinical situations.…”

Section: Pal Pplmentioning

confidence: 99%

Heart-lung interactions: applications in the critically ill

Fessler¹

1997

Eur Respir J

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Since the circulatory and pulmonary systems are both driven by pressure and share space in the thorax, it is inevitable that they interact. These mechanical interactions, whilst relatively few in number, are protean in their manifestations.The circulatory system of the critically ill is often particularly susceptible to interference from respiration. Compensatory reserve is limited, ventilatory effort increased, and many critical care respiratory interventions place strain on the circulation, not seen in health.This review will examine the basic physiological mechanisms through which the pulmonary and circulatory systems interact. These mechanisms will then be applied to a variety of weaning, positive end-expiratory pressure (PEEP), and cardiopulmonary resuscitation techniques. It is hoped that this will provide the tools to understand clinical observations which would otherwise appear inexplicable.

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Calculation of left ventricular wall stress.

Cited by 68 publications

References 41 publications

Occult Cardiotoxicity in Childhood Cancer Survivors Exposed to Anthracycline Therapy

Occult Cardiotoxicity in Childhood Cancer Survivors Exposed to Anthracycline Therapy

Postsystolic Shortening in Ischemic Myocardium

Heart-lung interactions: applications in the critically ill

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