Stress echocardiography for identifying patients at risk after myocardial infarction

Iliceto, Sabino; Amico, Antonio; Caiati, Carlo; Piccinni, Giovanni; Tota, Francesco; Marangelli, Vito; Memmola, Cataldo; Rizzon, Paolo

doi:10.1007/978-94-009-0611-2_19

Cited by 4 publications

(3 citation statements)

References 26 publications

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“…Although the evaluation of CFV by transesophageal Doppler is not feasible in every patient, in our study adequate Doppler recordings were obtained in 66% of our patients, a results similar to that in a previous study [12]. The technique cannot be considered noninvasive, since it does entail a certain level of discomfort for the patient.…”

Section: Discussionsupporting

confidence: 71%

Coronary flow reserve and exercise capacity in hypertrophic cardiomyopathy

et al. 1996

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The aim of this study was to evaluate the relation of coronary flow velocity (CFV) and coronary flow reserve (CFR) to exercise capacity in ten verapamil-treated patients with hypertrophic cardiomyopathy (HC). Using Doppler transesophageal echocardiography, we assessed diastolic CFV in the proximal left anterior descending coronary artery at baseline and after administering 0.56 mg/kg intravenous dipyridamole. The CFR was calculated as the post-dipyridamole/baseline diastolic CFV ratio. A maximal symptom-limited exercise treadmill test was performed according to a modified Bruce protocol and the exercise capacity was expressed as metabolic equivalents. The mean value for baseline diastolic CFV was 59 +/- 27 cm/s; this increased after dipyridamole to 134 +/- 57 cm/s. The CFR was 2.37 +/- 0.67. Baseline diastolic CFV correlated negatively with both exercise duration (r = -0.69; P < 0.05) and value for metabolic equivalents (r = -0.70; P < 0.05). CFR was weakly and non-significantly related to exercise duration (r = 0.40; P > 0.05) and to the value for metabolic equivalents (r = 0.32; P > 0.05). Shortening of exercise time and decreasing metabolic equivalents were correlated with increased baseline diastolic CFV. Dipyridamole-assessed CFR, was weakly related to parameters of exercise capacity.

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Section: Discussionsupporting

confidence: 71%

Coronary flow reserve and exercise capacity in hypertrophic cardiomyopathy

et al. 1996

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“…ð3:3Þ where u 0 is the mean inlet velocity as the average of the mean diastolic and systolic velocities in the left anterior descending coronary artery, in accordance with the experimental data given by Iliceto et al [46]. R is the internal radius of the artery and r is the radius of the artery at the axial location.…”

Section: Governing Equationssupporting

confidence: 79%

Mathematical modelling of atheroma plaque formation and development in coronary arteries

Cilla

Peña

Martı́nez

2014

J. R. Soc. Interface.

114

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Atherosclerosis is a vascular disease caused by inflammation of the arterial wall, which results in the accumulation of low-density lipoprotein (LDL) cholesterol, monocytes, macrophages and fat-laden foam cells at the place of the inflammation. This process is commonly referred to as plaque formation. The evolution of the atherosclerosis disease, and in particular the influence of wall shear stress on the growth of atherosclerotic plaques, is still a poorly understood phenomenon. This work presents a mathematical model to reproduce atheroma plaque growth in coronary arteries. This model uses the Navier-Stokes equations and Darcy's law for fluid dynamics, convectiondiffusion-reaction equations for modelling the mass balance in the lumen and intima, and the Kedem-Katchalsky equations for the interfacial coupling at membranes, i.e. endothelium. The volume flux and the solute flux across the interface between the fluid and the porous domains are governed by a three-pore model. The main species and substances which play a role in early atherosclerosis development have been considered in the model, i.e. LDL, oxidized LDL, monocytes, macrophages, foam cells, smooth muscle cells, cytokines and collagen. Furthermore, experimental data taken from the literature have been used in order to physiologically determine model parameters. The mathematical model has been implemented in a representative axisymmetric geometrical coronary artery model. The results show that the mathematical model is able to qualitatively capture the atheroma plaque development observed in the intima layer.

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“…As shown in figure 1, flow transport equations (2.2) -(2.3) and (2.8) -(2.9) are subject to the following boundary conditions: BC-A: At the inlet of the lumen of the arterial segment, the flow is set as a fully developed ( parabolic) velocity profile. The mean velocity is chosen to be 0.24 m s 21 as the average of the mean diastolic and systolic velocities in the LAD, so that the resulting mean Reynolds number (Re) based on the diameter of the artery is approximately 270 [33].…”

Section: Boundary Conditionsmentioning

confidence: 99%

Nitric oxide transport in an axisymmetric stenosis

Liu

Fan

et al. 2012

J. R. Soc. Interface.

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To test the hypothesis that disturbed flow can impede the transport of nitric oxide (NO) in the artery and hence induce atherogenesis, we used a lumen -wall model of an idealized arterial stenosis with NO produced at the blood vessel -wall interface to study the transport of NO in the stenosis. Blood flows in the lumen and through the arterial wall were simulated by Navier -Stokes equations and Darcy's Law, respectively. Meanwhile, the transport of NO in the lumen and the transport of NO within the arterial wall were modelled by advection -diffusion reaction equations. Coupling of fluid dynamics at the endothelium was achieved by the Kedem -Katchalsky equations. The results showed that both the hydraulic conductivity of the endothelium and the non-Newtonian viscous behaviour of blood had little effect on the distribution of NO. However, the blood flow rate, stenosis severity, red blood cells (RBCs), RBC-free layer and NO production rate at the blood vessel -wall interface could significantly affect the transport of NO. The theoretical study revealed that the transport of NO was significantly hindered in the disturbed flow region distal to the stenosis. The reduced NO concentration in the disturbed flow region might play an important role in the localized genesis and development of atherosclerosis.

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Stress echocardiography for identifying patients at risk after myocardial infarction

Cited by 4 publications

References 26 publications

Coronary flow reserve and exercise capacity in hypertrophic cardiomyopathy

Coronary flow reserve and exercise capacity in hypertrophic cardiomyopathy

Mathematical modelling of atheroma plaque formation and development in coronary arteries

Nitric oxide transport in an axisymmetric stenosis

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