Could increased axial wall stress be responsible for the development of atheroma in the proximal segment of myocardial bridges?

<p>Abstract</p> <p>Background</p> <p>A recent model describing the mechanical interaction between a stenosis and the vessel wall has shown that axial wall stress can considerably increase in the region immediately proximal to the stenosis during the (forward) flow phases, so that abnormal biological processes and wall damages are likely to be induced in that region. Our objective was to examine what this model predicts when applied to myocardial bridges.</p> <p>Method</p> <p>The model was adapted to the hemodynamic particularities of myocardial bridges and used to estimate by means of a numerical example the cyclic increase in axial wall stress in the vessel segment proximal to the bridge. The consistence of the results with reported observations on the presence of atheroma in the proximal, tunneled, and distal vessel segments of bridged coronary arteries was also examined.</p> <p>Results</p> <p>1) Axial wall stress can markedly increase in the entrance region of the bridge during the cardiac cycle. 2) This is consistent with reported observations showing that this region is particularly prone to atherosclerosis.</p> <p>Conclusion</p> <p>The proposed mechanical explanation of atherosclerosis in bridged coronary arteries indicates that angioplasty and other similar interventions will not stop the development of atherosclerosis at the bridge entrance and in the proximal epicardial segment if the decrease of the lumen of the tunneled segment during systole is not considerably reduced.</p

Why can pulmonary vein stenoses created by radiofrequency catheter ablation worsen during and after follow-up ? A potential explanation

<p>Abstract</p> <p>Background</p> <p>Radiofrequency catheter ablation of excitation foci inside pulmonary veins (PV) generates stenoses that can become quite severe during or after the follow-up period. Since severe PV stenoses have most often disastrous consequences, it would be important to know the underlying mechanism of this temporal evolution. The present study proposes a potential explanation based on mechanical considerations.</p> <p>Methods</p> <p>we have used a mathematical-physical model to examine the cyclic increase in axial wall stress induced in the proximal (= upstream), non-stenosed segment of a stenosed pulmonary vein during the forward flow phases. In a representative example, the value of this increase at peak flow was calculated for diameter stenoses (DS) ranging from 1 to 99%.</p> <p>Results</p> <p>The increase becomes appreciable at a DS of roughly 30% and rise then strongly with further increasing DS value. At high DS values (e.g. > 90%) the increase is approximately twice the value of the axial stress present in the PV during the zero-flow phase.</p> <p>Conclusion</p> <p>Since abnormal wall stresses are known to induce damages and abnormal biological processes (e.g., endothelium tears, elastic membrane fragmentations, matrix secretion, myofibroblast generation, etc) in the vessel wall, it seems plausible that the supplementary axial stress experienced cyclically by the stenotic and the proximal segments of the PV is responsible for the often observed progressive reduction of the vessel lumen after healing of the ablation injury. In the light of this model, the only potentially effective therapy in these cases would be to reduce the DS as strongly as possible. This implies most probably stenting or surgery.</p

Schematic representation of a stenosed, non bridged coronary artery: a) When flow is zero, the intravascular pressure p exerts two axial, opposite, equal forces (Fand F) in the constriction and expansion cones, respectively

<p><b>Copyright information:</b></p><p>Taken from "Could increased axial wall stress be responsible for the development of atheroma in the proximal segment of myocardial bridges?"</p><p>http://www.tbiomed.com/content/4/1/29</p><p>Theoretical Biology & Medical Modelling 2007;4():29-29.</p><p>Published online 9 Aug 2007</p><p>PMCID:PMC2020464.</p><p></p> The vertical equidistant slashes indicate that the vessel wall does not pull (axially) at the surrounding myocardium. b) When blood flows through the stenosis, the proximal pressure pis greater than the distal pressure p, and the sum of the two forces pulling in downstream direction (Fand F, see Appendix) is greater than the sum of the two forces pulling in upstream direction (Fand F). If flow and proximal pressure do not reach their maximum simultaneously, the net force F = F+ F- F- Fis not necessarily maximal when flow or proximal pressure are maximal. The oblique slashes show where the vessel wall will elongate axially and pull at the myocardium

Axial wall stress (y-axis) at the entrance of the bridge considered in the numerical example versus diameter reduction values (DS; x-axis)

<p><b>Copyright information:</b></p><p>Taken from "Could increased axial wall stress be responsible for the development of atheroma in the proximal segment of myocardial bridges?"</p><p>http://www.tbiomed.com/content/4/1/29</p><p>Theoretical Biology & Medical Modelling 2007;4():29-29.</p><p>Published online 9 Aug 2007</p><p>PMCID:PMC2020464.</p><p></p> The stress values are the sum of "normal" axial wall stress (see text) and supplementary axial stress generated cyclically by the pressure drop across the bridge. The flow was set to 1 ml/s as long as the distal pressure did not fall below 10 mmHg. At high DS values (80, 85, 90, and 99%), it was appropriately reduced in order to respect this 10 mmHg limit. Axial stress begins to increase markedly at a DS value of approximately 60%; this corresponds to a lumen area reduction of roughly 80%

Definition of circumferential, axial, and radial wall stress (perspective view)

<p><b>Copyright information:</b></p><p>Taken from "Could increased axial wall stress be responsible for the development of atheroma in the proximal segment of myocardial bridges?"</p><p>http://www.tbiomed.com/content/4/1/29</p><p>Theoretical Biology & Medical Modelling 2007;4():29-29.</p><p>Published online 9 Aug 2007</p><p>PMCID:PMC2020464.</p><p></p> Division of the circumferential force Fby the area S of the cube face it pulls at yields the circumferential wall stress σ= F/S. Division of the axial force Fby the area S of the cube face it pulls at yields the axial wall stress σ= F/S. Division of the radial force Fby the area S of the cube face it pushes on yields the radial wall stress σ= F/S. These three orthogonal stresses are used to describe the mechanical state of the vessel wall at the considered location. The average axial wall stress over a wall cross-section is equal to the quotient "force pulling axially at that cross-section, divided by the area A of that cross-section" (A = π (R- R))

Thoracic aortic plaques, transoesophageal echocardiography and coronary artery disease

The purpose of this study was to assess whether the detection of atherosclerotic aortic plaques by transoesophageal echocardiography (TEE) could be used as a marker of coronary artery disease (CAD), relying on their number, cross-sectional surface, depth and localisation

Incidence of atrial fibrillation after percutaneous closure of patent foramen ovale and small atrial septal defects in patients presenting with cryptogenic stroke

OBJECTIVE: The occurrence of atrial fibrillation after percutaneous closure of a patent foramen ovale for cryptogenic stroke has been reported in a variable percentage of patients. However, its precise incidence and mechanism are presently unclear and remain to be elucidated. DESIGN: Prospective follow-up study. PATIENTS: Ninety-two patients undergoing a percutaneous patent foramen ovale closure procedure (closure group) for cryptogenic stroke were compared with a similar group of 51 patients, who were medically treated. METHODS: A systematic arrhythmia follow-up protocol to assess the incidence of AF was performed including a 7-day event-loop recording at day 1, after 6 and 12 months in patients of the closure group and compared with those of the medically treated group. RESULTS: The incidence of AF was similar in both study groups during a follow-up of 12 months, including 7.6% (95% CI: 3.1-15.0%) in the closure and 7.8% (95% CI: 2.18-18.9%) in the medically treated group (P=1.0). The presence of a large patent foramen ovale was the only significant risk factor for the occurrence of AF as demonstrated by a multivariate Cox regression analysis (95% CI, 1.275-20.018; P=0.021). CONCLUSIONS: Our findings indicate that patients with cryptogenic stroke and patent foramen ovale have a rather high incidence of AF during a follow-up of 12 months. Atrial fibrillation occurred with a similar frequency whether the patent foramen ovale/atrial septal defect was successfully percutaneously closed or was medically managed. The presence of a large patent foramen ovale was the only significant predictor of AF occurrence during follow-up

Altered expression of proteins of metabolic regulation during remodeling of the left ventricle after myocardial infarction.

Non-infarcted myocardium after coronary occlusion undergoes progressive morphological and functional changes. The purpose of this study was to determine whether non-infarcted myocardium exhibits (1) alteration of the substrate pattern of myocardial metabolism and (2) concomitant changes in the expression of regulatory proteins of glucose and fatty acid metabolism. Myocardial infarction was induced in rats by ligation of the left coronary artery. One day and eight weeks after coronary occlusion, glucose and palmitate oxidation were measured. Expression of selected proteins of metabolism were determined one day to 12 weeks after infarction. One day after coronary occlusion no difference of glucose and palmitate oxidation was detectable, whereas after eight weeks, glucose oxidation was increased (+84%, P&lt;0.05) and palmitate oxidation did not change significantly (-19%, P=0.07) in infarct-containing hearts, compared with hearts from sham-operated rats. One day after coronary occlusion, myocardial mRNA expression of the glucose transporter GLUT-1 was increased (+86%, P&lt;0.05) and the expression of GLUT-4 was decreased (-28%, P&lt;0.05) in surviving myocardium of infarct-containing hearts. Protein level of GLUT-1 was increased (+81%, P&lt;0.05) and that of GLUT-4 slightly, but not significantly, decreased (-16%, P=NS). mRNA expressions of heart fatty acid binding protein (H-FABP), and of medium chain acyl-CoA dehydrogenase (MCAD), were decreased by 36% (P&lt;0.05) and 35% (P=0. 07), respectively. Eight weeks after acute infarction, the left ventricle was hypertrophied and, at this time-point, there was no difference in the expression of GLUT-1 and GLUT-4 between infarcted and sham-operated hearts. However, myocardial mRNA and protein content of MCAD were decreased by 30% (P&lt;0.01) and 27% (P&lt;0.05), respectively. In summary, in surviving myocardium, glucose oxidation was increased eight weeks after coronary occlusion. Concomitantly, mRNA and protein expression of MCAD were decreased, compatible with a role of altered expression of regulatory proteins of metabolism in post-infarction modification of myocardial metabolism