Finite element analysis of the biomechanical interaction between coronary sinus and proximal anchoring stent in coronary sinus annuloplasty

Recent clinical studies of the percutaneous transvenous mitral annuloplasty (PTMA) devices have shown a short-term reduction of mitral regurgitation after implantation. However, adverse events associated with the devices such as compression and perforation of vessel branches, device migration and fracture were reported. In this study, a finite element analysis was carried out to investigate the biomechanical interaction between the proximal anchor stent of a PTMA device and the coronary sinus (CS) vessel in three steps including: (i) the stent release and contact with the CS wall, (ii) the axial pull t the stent connector and (iii) the pressure inflation of the vessel wall. To investigate the impact of the material properties of tissues and stents on the interactive responses, the CS vessel was modelled with human and porcine material properties, and the proximal stent was modelled with two different Nitinol materials with one being stiffer than the other. The results indicated that the vessel wall stresses and contact forces imposed by the stents were much higher in the human model than the porcine model. However, the mechanical differences induced by the two stent types were relatively small. The softer stent exhibited a better fatigue safety factor when deployed in the human model than in the porcine model. These results underscored the importance of the CS tissue mechanical properties. Vessel wall stress and stent radial force obtained in the human model were higher than those obtained in the porcine model, which also brought up questions as to the validity of using the porcine model to assess device mechanical function. The quantification of these biomechanical interactions can offer scientific insight into the development and optimisation of the PTMA device design.     

Atresia of the right atrial ostium of the coronary sinus

A case of asymptomatic congenital occlusion of the ostium of the coronary sinus is described. The myocardial venous drainage was maintained via a persistent left superior vena cava as well via ectatic, widened atrial veins of the dorsal wall of the left atrium. The study shows that complete ostial occlusion of the coronary sinus does not reduce cardiac venous drainage. The view of the literature allows a comparison with the comprehensive classification of coronary sinus anomalies.     

Model of the haemodynamic reactions to intermittent coronary sinus occlusion

Coronary sinus pressure data have been obtained from anaesthetized dogs during pressure controlled intermittent coronary sinus occlusion. It is the main aim of this paper to provide a mathematical procedure for modelling the typical time course of sinus pressure after temporary obstruction of the sinus. The model is produced by fitting a parameterized function to the systolic and diastolic pressures in order to represent mathematically the shape of the curves. The parameters characterize the rise in coronary sinus pressure following occlusion, and are used to calculate ‘derived quantities’ which mimic the physician's visual assessment of trace recordings and their clinical implications in certain forms of coronary sinus pressure reaction. This procedure should be thought of as a kind of pattern recognition which reflects the changing state of the myocardium. The mathematical results are shown to bear a close resemblance to the clinical effects of coronary sinus occlusion.     

Simulation of coronary circulation with special regard to the venous bed and coronary sinus occlusion

The vascular beds of the left circumflex and the left anterior descending coronary arteries are modelled by means of coupled differential equations that consider an arterial, a capillary and a venous section. In a stepwise procedure, experimental data from normal coronary perfusion and coronary sinus occlusion are used to assess the model parameters. For venous distensibility, a non-linear form of pressure-volume relationship proved vital to reproduce the characteristics of the rise in venous pressure after the onset of coronary sinus occlusion. Numerical integration was carried out for normal perfusion and for coronary sinus occlusion, yielding time courses of flows, volumes and pressures within large coronary arteries, capillaries and coronary veins. Coronary sinus occlusion reduces total mean flow by 18% and divides intramyocardial flow between the capillaries and the veins into a forward component of 3.03 mls⁻¹ and a backward component of − 1.54 mls⁻¹. This result represents a prediction for a haemodynamic quantity which is therapeutically important but inacessible to measurement. Varying degrees of systolic myocardial squeezing are studied to display the impact of myocardial contractility and vessel collapse on the mean values and phasic components of intra-myocardial flows.     

A curious case of impossible coronary sinus cannulation

A 40-year-old male, diagnosed to have WPW syndrome and symptomatic with recurrent palpitations, was taken up for radiofrequency ablation. There was difficulty in coronary sinus cannulation. Coronary venogram revealed coronary sinus atresia with persistent left superior vena cava, and collateral venous pathways draining into the right atrium. This case is discussed for the rare coronary venous anomaly, its embryology and the difficulties in the management during electrophysiological studies.     

Left ventricular epicardial lead placement after Carillon placement in the coronary sinus

Netherlands Heart Journal -     

Rupture of right coronary sinus of Valsalva aneurysm into right ventricle

A sinus of Valsalva aneurysm is a rare cardiac anomaly that may be congenital or acquired; a coexisting cardiac lesion might be present. If the aneurysm ruptures, it causes acute symptoms of dyspnoea. Echocardiography and cardiac magnetic resonance imaging are useful for diagnosis. The treatment of choice is surgery. We present a case of a patient with acute onset of symptoms due to a ruptured sinus of Valsalva aneurysm. (Neth Heart J 2010;18:209-11)     

Snare technique for coronary sinus cannulation in cardiac resynchronization therapy

PurposeBiventricular pacing is a mainstay of therapy for patients with heart failure. However, lead implantations may fail due to anatomical reasons including the impossibility of coronary sinus cannulation.Methods and resultsA dual approach from the subclavian vein using a snare through a sheath and from the femoral vein using a steerable electrophysiology catheter was performed. Once the snare hooked the catheter, the latter was advanced into the coronary sinus and finally, the sheath could also be advanced in an “over-the-wire” technique.ConclusionThe snare technique for coronary sinus cannulation offers a “bail-out” strategy for left ventricular lead implantation.     

Effects of coronary sinus pressure elevation on coronary blood flow distribution in dogs with normal preload

Coronary sinus pressure (Pcs) elevation shifts the diastolic coronary pressure-flow relation (PFR) of the entire left ventricular myocardium to a higher pressure intercept. This finding suggests that Pcs is one determinant of zero-flow pressure (Pzf) and challenges the existence of a vascular waterfall mechanism in the coronary circulation. To determine whether coronary sinus or tissue pressure is the effective coronary back pressure in different layers of the left ventricular myocardium, the effect of increasing Pcs was studied while left ventricular preload was low. PFRs were determined experimentally by graded constriction of the circumflex coronary artery while measuring flow using a flowmeter. Transmural myocardial blood flow distribution was studied (15-micron radioactive spheres) at steady state, during maximal coronary artery vasodilatation at three points on the linear portion of the circumflex PFR both at low and high diastolic Pcs (7 +/- 3 vs. 22 +/- 5 mmHg; p less than 0.0001) (1 mmHg = 133.322 Pa). In the uninstrumented anterior wall the blood flow measurements were obtained in triplicate at the two Pcs levels. From low to high Pcs, mean aortic (98 +/- 23 mmHg) and left atrial (5 +/- 3 mmHg) pressure, percent diastolic time (49 +/- 7%), percent left ventricular wall thickening (32 +/- 4%), and percent myocardial lactate extraction (15 +/- 12%) were not significantly changed. Increasing Pcs did not alter the slope of the PFR; however, the Pzf increased in the subepicardial layer (p less than 0.0001), whereas in the subendocardial layer Pzf did not change significantly. Similar slopes and Pzf were observed for the PFR of both total myocardial mass and subepicardial region at low and high Pcs. Subendocardial:subepicardial blood flow ratios increased for each set of measurements when Pcs was elevated (p less than 0.0001), owing to a reduction of subepicardial blood flow; however, subendocardial blood flow remained unchanged, while starting in the subepicardium toward midmyocardium blood flow decreased at high Pcs. This pattern was similar for the uninstrumented anterior wall as well as in the posterior wall. Thus as Pcs increases it becomes the effective coronary back pressure with decreasing magnitude from the subepicardium toward the subendocardium of the left ventricle. Assuming that elevating Pcs results in transmural elevation in coronary venous pressure, these findings support the hypothesis of a differential intramyocardial waterfall mechanism with greater subendo- than subepi-cardial tissue pressure.     

Evidence for association of coronary sinus levels of hepatocyte growth factor and collateralization in human coronary disease

The therapeutic use of angiogenic factors to protect ischemic myocardium is limited by our incomplete understanding of their endogenous production. We determined the association between angiogenic factors and collateral formation in patients with coronary artery disease (CAD). A total of 71 patients underwent catheterization with sampling of the pulmonary artery, aorta, and coronary sinus (CS) to determine the levels of vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF). VEGF and HGF levels were not different in the three vascular sites, suggesting that the heart is not a major source of these cytokines in the circulation. CS VEGF and HGF levels were similar in patients with and without CAD. Elevated CS HGF levels were associated with collateral formation, whereas VEGF levels were not. Additionally, CS HGF was significantly elevated in patients with left ventricular dysfunction. These data map for the first time the concentration of endogenous angiogenic factors in the coronary circulation and support further studies to determine whether HGF may be an endogenous cardioprotective angiogenic factor.