Effects of cardiac contraction and coronary sinus pressure elevation on collateral circulation

Abstract

Controlled coronary sinus occlusion was shown to retard necrosis of ischemic myocardium. To elucidate this mechanism, regional myocardial blood flow measurement was performed with and without coronary sinus pressure elevation to 30 mmHg (CS30). Colored microspheres were injected into left and right coronary arteries after coronary perfusion of the left anterior descending (LAD) coronary artery was stopped in seven isolated canine hearts with induced atrioventricular block, either paced at 120 beats/min by direct right ventricular stimulation [beating heart (B)] or during asystole induced by stopping pacing [nonbeating heart (NB)]. Regional myocardial blood flow in the LAD perfused area in the control state in the NB with normal coronary sinus pressure (NB-CScont; 0.27 +/- 0.13 ml.min-1.g-1, means +/- SE) was significantly greater than those in B-CScont (0.19 +/- 0.09 ml.min-1.g-1; P < 0.05) and in NB with CS30 (NB-CS30; 0.19 +/- 0.09 ml.min-1.g-1; P < 0.05). Regional myocardial blood flow of the LAD area in B with CS30 (B-CS30; 0.23 +/- 0.10 ml.min-1.g-1) was significantly greater in comparison with that at B-CScont and NB-CS30 (P < 0.05). The augmentative effect of the LAD area regional myocardial blood flow was observed only in the periphery of the ischemic region but not in its center. Cardiac contraction and CS30 impede regional myocardial blood flow in the ischemic bed independently. The coexistence of these two factors enhances regional myocardial blood flow. In conclusion, coronary sinus pressure elevation in B may participate in augmenting collateral flow.

Effects of coronary sinus occlusion on myocardial ischaemia in humans: role of coronary collateral function

“…Experimental work in the porcine animal model void of coronary collaterals supports this notion by revealing no effect of iCSO on the ligation-induced fall of perfusion in the LAD from 1.5 to <0.1 ml/min/g 22. Conversely, the canine model with a coronary artery anastomotic network similar to that in humans23 has shown an increase in the ischaemic LAD territory from 0.17–0.19 without iCSO to 0.23–0.33 ml/min/g with iCSO 21 24. In both the referenced canine studies, the effect of iCSO on myocardial perfusion was predominant in the penumbra and not the core of the ischaemic zone, thus indicating the transmit function of collaterals between adjacent supply areas and their role in diminishing the area at risk.…”

Safety and efficacy of a device to narrow the coronary sinus for the treatment of refractory angina: A single-centre real-world experience

“…However, two potential anti-ischaemic effects of elevation of CS pressure have been hypothesised, both related to the increased back pressure in the venules and capillaries caused by CS pressure elevation. Several studies observed increased flow in pre-existing collaterals between the non-ischaemic myocardium and ischaemic myocardium after CS narrowing/occlusion [10, 11, 20]. Enhanced coronary collateral flow may result from the back pressure exerted resistance to coronary flow into the non-ischaemic myocardium, leading to a shift of flow to the low pressure surroundings of the ischaemic myocardium [18].…”

“…This balloon-expandable stainless steel stent is designed to increase coronary venous pressure by creating a focal stenosis in the CS following its implantation. Coronary venous pressure elevation alleviates angina by improving perfusion of the ischaemic regions of the myocardium by increasing coronary collateral blood flow [10, 11], redirecting flow to the endocardium [11, 12], and possibly stimulating myocardial neovascularisation [13]. The principle of enhancing myocardial perfusion by elevating coronary venous pressure was already described in 1936 by Gross and colleagues [14] and was translated into clinical practice in 1954 by Beck and Leighninger [15], who performed surgical partial ligation of the CS in patients with angina pectoris (as part of the Beck I operation).…”

Coronary Sinus Reducer Stent for the Treatment of Chronic Refractory Angina Pectoris

“…The CS pressure elevation enhances coronary collateral flow and reduces subendocardial ischemia, with a positive correlation between the elevated CS pressure and the changes in collateral blood flow from nonischemic to ischemic territories of the myocardium (11). Clinical application of CS interventions during the early reperfusion period has shown improvement in regional myocardial function and salvaging of ischemic myocardium, especially by limiting the infarct from its border (13,14,20 -22).…”