Key result
Increasing coronary sinus outflow pressure increased subepicardial intramyocardial tissue pressure by 17 mmHg during systole and 10 mmHg during diastole (P<=0.001), independently of arterial pressure.
Why the study?
Does increasing coronary sinus outflow pressure affect intramyocardial tissue pressure and myocardial perfusion in open-chest dogs?
Does increasing coronary sinus outflow pressure affect intramyocardial tissue pressure and myocardial perfusion in open-chest dogs?
p-value: p=<= 0.001
Coronary sinus pressure can regulate intramyocardial tissue pressure independently of arterial pressure, influencing myocardial perfusion primarily in the subepicardial layer.
Does not support clinical translation; leaves open coronary sinus pressure effects on human myocardial perfusion.
To determine whether coronary sinus outflow pressure (Pcs) or intramyocardial tissue pressure (IMP) is the effective back pressure in the different layers of the left ventricular (LV) myocardium, we increased Pcs in 14 open-chest dogs under maximal coronary artery vasodilation. Circumflex arterial (flowmeter), LV total, and subendocardial and subepicardial (15-microns radioactive spheres) pressure-flow relationships (PFR) and IMP (needle-tip pressure transducers) were recorded during graded constriction of the artery at two diastolic Pcs levels (7 +/- 3 vs. 23 +/- 4 mmHg). At high Pcs, LV, aortic and diastolic circumflex arterial pressure, heart rate, myocardial oxygen consumption, and lactate extraction were unchanged; IMP in the subendocardium did not change (130/19 mmHg), whereas IMP in the subepicardium increased by 17 mmHg during systole and 10 mmHg during diastole (P < or = 0.001), independently of circumflex arterial pressure. Increasing Pcs did not change the slope of the PFR; however, coronary pressure at zero flow increased in the subepicardium (P < or = 0.008), whereas in the subendocardium it remained unchanged at 24 +/- 3 mmHg. Thus Pcs can regulate IMP independently of circumflex arterial pressure and consequently influence myocardial perfusion, especially in the subepicardial tissue layer of the LV.
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Cantin et al. (1992) studied this question. Increased coronary sinus outflow pressure (Pcs) vs. Low diastolic Pcs level (7 +/- 3 mmHg) was evaluated on Intramyocardial tissue pressure (IMP) and pressure-flow relationships (p=<= 0.001). Increasing coronary sinus outflow pressure increased subepicardial intramyocardial tissue pressure by 17 mmHg during systole and 10 mmHg during diastole (P<=0.001), independently of arterial pressure.
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