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

Abstract

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.

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

“…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]. Other studies also suggest that elevated back pressure promotes blood flow to the ischaemia-prone endocardium [11, 12]. Endocardial blood flow is often diminished in the presence of epicardial coronary stenosis because of decreased perfusion pressure and dysfunctional physiological mechanisms to preserve endocardial flow during exercise (i. e. the lack of sympathetically mediated constriction of subepicardial vessels) [21].…”

“…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 vasoregulation in health and disease

“…Modulation of coronary sinus outflow pressure in normal canine hearts affects intramyocardial tissue pressure and has been shown to reduce blood flow in the subepicardial tissue layer independently of coronary artery pressure (3,4). This is of clinical relevance following the Fontan operation, in which right atrial and coronary sinus pressures are often elevated (5).…”

Comparison between Diastolic Subendocardial Tissue Pressures Measured Directly or Calculated from Pressure-Flow Relations

“…Secondly, the selected experimental model accounted for most factors that modulate myocardial perfusion with the exception of coronary sinus and LV intracavity pressure. Thirdly, experiments were performed during pharmacologic vasodilatation to minimize potential coronary artery capacitance effects [19]. Finally, potential problems related to measurement of intramyocardial tissue pressures are known; for instance, tissue damage and oedema may occur during placement of sensors [40].…”

“…The atria, ventricles and interventricular septum were sectioned and blood flow analyzed as previously described [18] [19]. Myocardial oxygen consumption (MVO 2 ; ml/min/100 g) was calculated as the product of total myocardial blood flow (microspheres) and the artero-coronary sinus oxygen content difference.…”