A novel strategy for increasing wall thickness of coronary venules prior to retroperfusion

Abstract

Choy, Jenny Susana, and Ghassan S. Kassab. A novel strategy for increasing wall thickness of coronary venules prior to retroperfusion. Am J Physiol Heart Circ Physiol 291: H972-H978, 2006. First published April 7, 2006 doi:10.1152/ajpheart.00235.2006.-The sudden exposure of veins to arterial pressures during coronary venous retroperfusion may cause rupture of small venules. Our rationale is to first occlude the coronary vein, which will cause an increase in pressure intermediate to arterial and venous values, and hence lead to remodeling and increased wall thickness of the veins prior to retroperfusion. To accomplish this objective, five pigs were subjected to left anterior descending (LAD) vein ligation while six pigs served as sham. Myocardial tissue samples were obtained from the area adjacent to the LAD vein at four transmural locations of the left ventricular free wall: epicardial surface, subepicardium, midmyocardium, and endocardium. Arterioles and venules from the experimental and sham control groups were photographed, and the following measurements were made: inner and outer circumferences, inner and outer areas, major and minor diameters, and intima-media thickness. Each vessel was categorized in four different orders according to lumen diameter. Our results show that intima-media thickness was larger in the experimental group in all four regions of the heart and in all four orders of the vessels, although venules from the epicardial region showed the largest increase in thickness. The intima-media thicknessto-radius ratio was also larger in the experimental group and decreased from epicardial to endocardial region of the heart and from order 1 to order 4 of the vessels. The present study provides a rationale for the development of coronary retroperfusion strategy that avoids vessel rupture and hemorrhage in the postcapillary venules. pressure overload; arterialization; rupture stress; remodeling; ligation BECAUSE THE CORONARY VEINS rarely develop arteriosclerosis (8,23,24), it is desirable to use these vessels as conduits for revascularization. The possibility of coronary retroperfusion was first suggested by Pratt (27) in 1898, when he was able to sustain the mechanical function of a cat's heart by delivering oxygenated blood through the coronary sinus. Almost 50 years after this seminal study, the first attempts at arterialization of the coronary sinus were made by Roberts et al. (30) and Beck et al. (5), independently. In 1943, Roberts et al. (30) suggested the use of coronary veins as conduits to deliver oxygenated blood in a retrograde manner in animal studies. In 1948, Beck and colleagues (5) performed the coronary retroperfusion procedure in humans. The method was abandoned, however, because of the high mortality rate from the edema and hemorrhage in the postcapillary venules that resulted from the elevated pressure (6,8,12,26). To remedy these difficulties, we propose to avoid raising the pressure in the left anterior descending (LAD) vein from venous (10 -20 mmHg) to arterial values (100 ...

Wall thickness of coronary vessels varies transmurally in the LV but not the RV: implications for local stress distribution

“…Recently, we showed that ligation of a coronary vein leads to an increase in wall thickness of large (7) and small (8) venous vessels in response to pressure overload. Furthermore, we found differential remodeling depending on vessel size and transmural location in the heart (8).…”

Morphological and biochemical characterization of remodeling in aorta and vena cava of DOCA-salt hypertensive rats

“…In general, an inflammation-based reaction in venous valves that includes an increase in MMP-2 expression has been observed. Neutrophil infiltration has also been observed in postthrombotic veins (32), as has a medial thickening of coronary venules and large veins exposed to arterial levels of pressure (11,12). More recently, veins have been described as remodeling in venous disease with the loss of venous valvular function (4), an idea that is difficult for us to investigate in the vena cava, which lacks valves.…”

Flow velocity is relatively uniform in the coronary sinusal venous tree: structure-function relation

“…The potential of coronary venous retroperfusion was proposed decades ago (4, 30) but abandoned because of structural damage of the coronary sinus wall as well as the intramyocardial vasculature caused by drainage disruption and elevated pressures (27,42). A rationale was proposed for reestablishment of coronary venous retroperfusion in that the ligation of a large coronary vein leads to an increase of venous pressure and further prearterialization of the venous tree (9,10). The pressure overload due to vein ligation induces an increase of ͑h ⁄r͒ ligation Ϫ ͑h ⁄r͒ sham ͑h ⁄r͒ sham (h/r refers to the wall thickness-toradius ratio in a vessel) from the smallest venules to the large coronary veins (9,10).…”

“…A rationale was proposed for reestablishment of coronary venous retroperfusion in that the ligation of a large coronary vein leads to an increase of venous pressure and further prearterialization of the venous tree (9,10). The pressure overload due to vein ligation induces an increase of ͑h ⁄r͒ ligation Ϫ ͑h ⁄r͒ sham ͑h ⁄r͒ sham (h/r refers to the wall thickness-toradius ratio in a vessel) from the smallest venules to the large coronary veins (9,10). Based on the relation between pressure ͫ P͑0͒ ϩ P͑L͒ 2 ͬ and vessel diameter and between CS ΄ P͑0͒ ϩ P͑L͒ 2 ͑h⁄r͒ ΅ and vessel diameter in normal swine hearts as shown in Figs.…”