Transient integral boundary layer method to calculate the translesional pressure drop and the fractional flow reserve in myocardial bridges

BACKGROUND: The pressure drop – flow relations in myocardial bridges and the assessment of vascular heart disease via fractional flow reserve (FFR) have motivated many researchers the last decades. The aim of this study is to simulate several clinical conditions present in myocardial bridges to determine the flow reserve and consequently the clinical relevance of the disease. From a fluid mechanical point of view the pathophysiological situation in myocardial bridges involves fluid flow in a time dependent flow geometry, caused by contracting cardiac muscles overlying an intramural segment of the coronary artery. These flows mostly involve flow separation and secondary motions, which are difficult to calculate and analyse. METHODS: Because a three dimensional simulation of the haemodynamic conditions in myocardial bridges in a network of coronary arteries is time-consuming, we present a boundary layer model for the calculation of the pressure drop and flow separation. The approach is based on the assumption that the flow can be sufficiently well described by the interaction of an inviscid core and a viscous boundary layer. Under the assumption that the idealised flow through a constriction is given by near-equilibrium velocity profiles of the Falkner-Skan-Cooke (FSC) family, the evolution of the boundary layer is obtained by the simultaneous solution of the Falkner-Skan equation and the transient von-Kármán integral momentum equation. RESULTS: The model was used to investigate the relative importance of several physical parameters present in myocardial bridges. Results have been obtained for steady and unsteady flow through vessels with 0 – 85% diameter stenosis. We compare two clinical relevant cases of a myocardial bridge in the middle segment of the left anterior descending coronary artery (LAD). The pressure derived FFR of fixed and dynamic lesions has shown that the flow is less affected in the dynamic case, because the distal pressure partially recovers during re-opening of the vessel in diastole. We have further calculated the wall shear stress (WSS) distributions in addition to the location and length of the flow reversal zones in dependence on the severity of the disease. CONCLUSION: The described boundary layer method can be used to simulate frictional forces and wall shear stresses in the entrance region of vessels. Earlier models are supplemented by the viscous effects in a quasi three-dimensional vessel geometry with a prescribed wall motion. The results indicate that the translesional pressure drop and the mean FFR compares favourably to clinical findings in the literature. We have further shown that the mean FFR under the assumption of Hagen-Poiseuille flow is overestimated in developing flow conditions

The effect of electrical neurostimulation on collateral perfusion during acute coronary occlusion

<p>Abstract</p> <p>Background</p> <p>Electrical neurostimulation can be used to treat patients with refractory angina, it reduces angina and ischemia. Previous data have suggested that electrical neurostimulation may alleviate myocardial ischaemia through increased collateral perfusion. We investigated the effect of electrical neurostimulation on functional collateral perfusion, assessed by distal coronary pressure measurement during acute coronary occlusion. We sought to study the effect of electrical neurostimulation on collateral perfusion.</p> <p>Methods</p> <p>Sixty patients with stable angina and significant coronary artery disease planned for elective percutaneous coronary intervention were split in two groups. In all patients two balloon inflations of 60 seconds were performed, the first for balloon dilatation of the lesion (first episode), the second for stent delivery (second episode). The Pw/Pa ratio (wedge pressure/aortic pressure) was measured during both ischaemic episodes. Group 1 received 5 minutes of active neurostimulation before plus 1 minute during the first episode, group 2 received 5 minutes of active neurostimulation before plus 1 minute during the second episode.</p> <p>Results</p> <p>In group 1 the Pw/Pa ratio decreased by 10 ± 22% from 0.20 ± 0.09 to 0.19 ± 0.09 (p = 0.004) when electrical neurostimulation was deactivated. In group 2 the Pw/Pa ratio increased by 9 ± 15% from 0.22 ± 0.09 to 0.24 ± 0.10 (p = 0.001) when electrical neurostimulation was activated.</p> <p>Conclusion</p> <p>Electrical neurostimulation induces a significant improvement in the Pw/Pa ratio during acute coronary occlusion.</p

Fractional flow reserve after previous myocardial infarction

Marques and colleagues have conducted an interesting study on microvascular resistance of viable tissue within an infarcted area. 1 This study is important, not only from a conceptual point of view, but also because it has several relevant implications for the applicability of MIBI spect and fractional flow reserve (FFR) measurement in patients with previous myocardial infarction and a residual or recurrent stenosis in the infarct-related coronary artery. The use of these methods, one non-invasive and the other invasive, has been supported by theoretical and empirical data, but the present study corroborates their usefulness in patients with previous myocardial infarctions. To understand the clinical implications of the study by Marques et al., it is paramount to understand microvascular resistance, which so far has been hard to assess in conscious humans. Microvascular resistance equals the ratio of distal coronary pressure divided by myocardial blood flow. As surrogates for the numerator and denominator of that ratio, sometimes aortic pressure and coronary blood flow or flow velocity, respectively, have been used, which might be correct in healthy persons. However, in patients with coronary artery disease, the first number overestimates distal coronary pressure and the second one underestimates myocardial blood flow, and therefore use of these surrogates leads to progressive overestimation of myocardial resistance in the case of a stenotic coronary artery. 2– 4 As a consequence, our knowledge about microvascular resistance in patients with coronary disease, and especially after previous myocardial infarction, has remained questionable. Furthermore, from a clinical point of view, i.e. the question of whether inducible ischaemia is still present or present again, the interesting index to study is hyperaemic blood flow, corresponding to minimal resistance of the viable myocardium within the infarcted zone, not the resistance of the scar tissue

The crux of maximum hyperemia:the last remaining barrier for routine use of fractional flow reserve

In the decision-making process of revascularization of coronary artery stenoses by percutaneous coronary intervention (PCI) or coronary artery bypass graft surgery (CABG), the presence and extent of reversible ischemia associated with such particular stenoses is of paramount importance (1, 2, 3). A stenosis associated with reversible ischemia (also called functionally significant or hemodynamically significant stenosis) causes symptoms of angina pectoris and has a negative influence on outcome (1, 2). Therefore, the general feeling is that such lesions should be revascularized if technically feasible. On the contrary, functionally nonsignificant stenoses do not cause symptoms by definition and have an excellent outcome with medical therapy (3, 4, 5). Therefore, revascularization of such lesions is generally not indicated