Fall In Coronary Pressure Research Articles

The effect of coronary arterial pressure on myocardial distensibility. Absence of a “garden hose” effect during in-vivo conditions

The effect of the coronary perfusion pressure on myocardial distensibility was studied in 11 open-chest dogs. The left anterior descending coronary artery was cannulated, and coronary perfusion pressure and blood flow were measured. Regional myocardial segment length was measured using sonomicrometers. The temporal relationship between the phasic coronary pressure fall and change in myocardial segment length was analyzed during the early phase of coronary occlusion. Diastolic myocardial segment length was completely unaffected by the substantial fall in coronary pressure over a period of 9.3 +/- 0.8 s (20 +/- 2 heart beats). During this period, coronary pressure fell from 98 +/- 7 to 28 +/- 2 mm Hg. Subsequently, diastolic segment length increased, presumably due to ischemia rather than to a delayed compliance change. In order to differentiate between a possible long-time constant for coupling of the intravascular pressure to myocardial compliance versus a primary ischemic effect, regional cardiac contraction was abolished by an intracoronary potassium chloride infusion in three dogs. Coronary occlusion during regional cardioplegia produced no further segment length changes for a 1-min period, effectively excluding viscoelastic coupling time constants of up to 1 min. From these results we conclude that the coronary distending pressure does not contribute to passive myocardial properties over the physiological perfusion pressure range, and that the "garden hose" effect is not operative for the in vivo working heart.

Effect of nitroprusside-induced fall in systemic pressure on coronary stenoses

A fall in coronary pressure increases resistance across compliant coronary stenoses, probably because of passive collapse of the stenotic segment. The effects of a mechanically induced fall in coronary pressure were compared with the effects of a similar fall in pressure caused by intravenous sodium nitroprusside, a systemic and large coronary artery vasodilator. Seventeen dogs were studied in which a compliant circumflex coronary stenosis was produced by inflating an intracoronary balloon with saline. When coronary pressure was lowered from 105 ± 3 to 78 ± 3 mm Hg ( P < 0.001) by tightening a snare proximally on the circumflex coronary artery, the stenosis pressure gradient increased (9 ± 1 to 17 ± 3 mm Hg, P < 0.005), flow fell (21 ± 2 to 15 ± 2 ml/mm, P < 0.001) and stenosis resistance increased (0.67 ± 0.15 to 2.06 ± 0.68 units, P < 0.05). When nitroprusside caused pressure to fall from 112 ± 4 to 81 ± 4 mm Hg ( P < 0.001), the stenosis pressure gradient did not change (16 ± 1 to 16 ± 1 mm Hg), flow increased (42 ± 5 to 62 ± 6 ml/min, P < 0.001), and stenosis resistance decreased (0.46 ± 0.07 to 0.32 ± 0.06 units, P < 0.01). These findings demonstrate that nitroprusside prevented passive collapse of the compliant stenoses as pressure fell, possibly by nitroprusside actively dilating the stenotic segment. Therefore a moderate fall in systemic pressure caused by a coronary vasodilator may not have deleterious effects on stenosis severity.

Fixed vs nonfixed coronary stenosis: The response to a fall in coronary pressure in a canine model

The resistance of a coronary stenosis capable of passive vasomotion may change in response to alterations in intraluminal pressure. We studied the effects of a fall in perfusion pressure on the hemodynamics of two types of coronary stenosis in 12 open chest dogs: 1) a stenosis produced by placing a soft wire snare around the artery, and 2) a stenosis that was fixed in severity, produced by introducing and tying a short section of hollow plastic tubing into the coronary artery. Aortic pressure, coronary pressure proximal and distal to the stenosis, and coronary flow were measured. Pressure in the stenotic artery was lowered by tightening a snare placed very proximally on the artery. In arteries with a snare stenosis, lowering proximal coronary pressure by a mean of 31 mm Hg caused a rise in stenosis resistance from 0.86 +/- 0.06 to 1.38 +/- 0.14 units (p less than 0.001). However, in arteries with a fixed plastic stenosis, lowering the proximal coronary pressure by a mean of 30 mm Hg caused a fall in stenosis resistance from 0.36 +/- 0.04 to 0.21 +/- 0.03 units ( p less than 0.001). The increase in resistance of the snare stenoses as pressure was lowered may be attributed to passive narrowing of the stenotic segment, suggesting that these stenoses were not fixed in severity. However, the fixed plastic stenoses did not show an increase in resistance as pressure fell because the tubing was not capable of passively narrowing. Therefore, the hemodynamics of a coronary stenosis depend importantly on the type of stenosis that is present and whether it is capable of vasomotion.

Fixed vs. Non-fixed coronary stenosis: The response to a fall in coronary pressure

Fixed vs. Non-fixed coronary stenosis: The response to a fall in coronary pressure