This study looks at pulsatile blood flow through four different right coronary arteries, which have been reconstructed from bi-plane angiograms. A non-Newtonian blood model (the Generalised Power Law), as well as the usual Newtonian model of blood viscosity, is used to study the wall shear stress in each of these arteries over the entire cardiac cycle. The difference between Newtonian and non-Newtonian blood models is also studied over the whole cardiac cycle using the recently generalised global non-Newtonian importance factor. In addition, the flow is studied by considering paths of massless particles introduced into the flow field.The study shows that, when studying the wall shear stress distribution for transient blood flow in arteries, the use of a Newtonian blood model is a reasonably good approximation. However, to study the flow within the artery in greater detail, a non-Newtonian model is more appropriate.

This study looks at pulsatile blood flow through four different right coronary arteries, which have been reconstructed from biplane angiograms. A non-Newtonian blood model (the Generalised Power Law), as well as the usual Newtonian model of blood viscosity, is used to study the wall shear stress in each of these arteries over the entire cardiac cycle. The difference between Newtonian and non-Newtonian blood models is also studied over the whole cardiac cycle using the recently generalised global non-Newtonian importance factor. In addition, the flow is studied by considering paths of massless particles introduced into the flow field. The study shows that, when studying the wall shear stress distribution for transient blood flow in arteries, the use of a Newtonian blood model is a reasonably good approximation. However, to study the flow within the artery in greater detail, a non-Newtonian model is more appropriate.

No abstract

SummaryHip fracture surgery is associated with a high rate of mortality and morbidity; heart disease is the leading cause and is often unrecognised and inadequately treated. Pre-operative focused transthoracic echocardiography by anaesthetists frequently influences management, but mortality outcome studies have not been performed to date. Mortality over the 12 months after hip fracture surgery, in 64 patients at risk of cardiac disease who received pre-operative echocardiography, was compared with 66 randomised historical controls who did not receive echocardiography. Mortality was lower in the group that received echocardiography over the 30 days (4.7% vs 15.2%, log rank p = 0.047) and 12 months after surgery (17.1% vs 33.3%, log rank p = 0.031). Hazard of death was also reduced with pre-operative echocardiography over 12 months after adjustment for known risk factors (hazard ratio 0.41, 95% CI 0.2-0.85, p = 0.016). Pre-operative echocardiography was not associated with a delay in surgery. These data support a randomised controlled trial to confirm these findings.

Abstract-To clarify the source of electrocardiographic ST depression associated with ischemia, a sheep model of subendocardial ischemia was developed in which simultaneous epicardial and endocardial ST potentials were mapped, and a computer model using the bidomain technique was developed to explain the results. To produce ischemia in different territories of the myocardium in the same animal, the left anterior descending coronary artery and left circumflex coronary artery were partially constricted in sequence. Results from 36 sheep and the computer simulation are reported. The distributions of epicardial potentials from either ischemic source were very similar (rϭ0.77Ϯ0.14, PϽ0.0001), with both showing ST depression on the free wall of the left ventricle and no association between the ST depression and the ischemic region. However, endocardial potentials showed that ST elevation was directly associated with the region of reduced blood flow. Insulating the heart from the surrounding tissue with plastic increased the magnitude of epicardial ST potentials, which was consistent with an intramyocardial source. Increasing the percent stenosis of a coronary artery increased epicardial ST depression at the lateral boundary and resulted in ST elevation starting from the ischemic center as ischemia became transmural. Computer simulation using the bidomain model reproduced the epicardial ST patterns and suggested that the ST depression was generated at the lateral boundary between ischemic and normal territories. ST depression on the epicardium reflected the position of this lateral boundary. The boundaries of ischemic territories are shared, and only those appearing on the free wall contribute to external ST potential fields. These effects explain why body surface ST depression does not localize cardiac ischemia in humans.(Circ Res. 1998;82;957-970.)Key Words: ST depression Ⅲ potential mapping Ⅲ bidomain model Ⅲ subendocardial ischemia Ⅲ regional myocardial blood flow E lectrocardiographic ST-segment depression has long been recognized as a sign of ischemia, 1,2 but the explanations of the responsible mechanisms have been controversial. [3][4][5][6] Much of the current opinion regarding the genesis of ST-segment depression is derived from interpretations based on certain theoretical considerations 7,8 and indirect evidence from animal experiments. 1,2 Ischemic muscle generates intracellular currents, which effectively cause TQ depression and ST elevation over the ischemic area 9,10 and which conventional electrocardiography with AC-coupled amplifiers reflects as ST elevation. ST-segment depression recorded at the epicardium has been considered to be secondary to an injury current in the underlying subendocardium. [11][12][13][14] In conventional stress testing, as myocardial demand exceeds the ability of the narrowed coronary arterial bed to increase blood flow, the ischemic threshold is exceeded, and reversible ST-segment depression is produced. However, the location of this ST depression does not enable us to localize...