Stenotic Severity Research Articles

Mechanism for dynamic changes in stenotic severity.

The mechanism responsible for rapid changes in stenotic severity or resistance due to alterations in perfusion pressure and distal resistance is addressed by this study. An in vitro, eccentric arterial stenosis model was created using 15 canine carotid arteries cannulated with silicone plugs containing special pressure-transducing catheters designed to measure pressure directly, within the stenosis. The vessels were perfused at perfusion pressures of 150, 100, and 75 mmHg and at two levels of distal resistance while perfusion pressure, distal pressure, stenotic pressure, and flow were recorded. Orthogonal arteriograms were performed. Stenotic resistance was calculated as (perfusion pressure--distal pressure)/flow. All variables changed significantly (P less than 0.05) with decreases in perfusion pressure. Stenotic resistance always increased (P less than 0.02) as perfusion pressure or distal resistance decreased. These dynamic changes in stenotic resistance occurred at stenotic pressures well above the atmospheric, extraluminal pressure. Arteriographic data demonstrated decreasing stenotic luminal area with decreasing stenotic pressure. These results confirm the assertion that rapid changes in stenotic resistance are related to changes in stenotic luminal area and are not due to extrinsic forces. The principles of the Starling resistor are, therefore, not applicable to dynamic arterial stenoses. This information is immediately relevant to clinical situations in which complaint, severe stenosis results in ischemia.

Hemodynamics of human arterial stenoses

We assessed the hemodynamic and geometric changes in compliant, human arterial stenoses in response to manipulation of vascular tone, perfusion pressure and distal resistance. Coronary and popliteal arteries were harvested from human cadavers shortly after death. Following incubation for several hours to permit recovery of physiologic energy stores and ion gradients, the vessels were attached to a perfusion apparatus and perfusion pressure (PP), distal pressure (DP), and flow (F) were recorded as perfusion pressure and distal resistance (DR) were varied. The experiments were then repeated in the presence of a vasoconstrictor (100 mM KCl). Orthogonal arteriograms were performed at maximums of vasoconstriction and vasodilation. Stenotic resistance (SR) was calculated as (PP-DP)F. Minimum cross-sectional area was determined by computer assisted analysis of the arteriograms. Stenosed vessels with normal wall segments at the stenosis responded to vasoconstriction with a large stenotic resistance increase (111 ± 15%; P < 0.05) and a flow decrease averaging 39.3 ± 6.2% ( P < 0.05). In addition, decreased perfusion pressure also increased stenotic resistance significantly ( P < 0.05). Stenotic resistance changes were of sufficient magnitude to be both statistically significant and clinically important. These results confirm the existence of dynamic arterial stenoses in humans and further support the assertion that dynamic stenotic severity changes elicited by manipulation of proximal and distal vascular tone and pressure are of sufficient magnitude to create acute ischemia. This information may apply to clinical situations in which compliant stenoses and acute ischemia coexist.

A theoretical model of a compliant arterial stenosis.

Recent clinical and experimental evidence indicates that coronary artery stenoses may rapidly change their size and shape in response to alterations in vasomotor tone and intraluminal pressure. This theoretical study models a partially compliant arterial stenosis to examine the hemodynamic impact of these alterations. In rigid vessels, a 98% reduction in luminal area would predictably produce subendocardial ischemia in the resting state. In contrast, stenoses, with part of the arterial wall normal by the underlying plaque, responded to vasoconstriction and to changes in intraluminal pressure. With part of the arterial wall normal by the plaque, both vasoconstriction and decreases in intraluminal pressure could increase the hemodynamic severity of the stenosis. Further, the more eccentrically positioned the underlying plaque was, the greater the effects of vasoconstriction and intraluminal pressure on stenotic severity. Thus the morphological configuration of the plaque and the normal wall segment in the stenosis appear to be important determinants of the hemodynamic response of the stenosis to vasoconstriction and blood pressure changes. In turn, these changes in stenotic severity can greatly influence flow through the vessel.

Effects of vasoconstriction and distal dilation on carotid stenoses in the dog.

Traditionally, arterial stenoses have been assumed to be inflexible, static obstructive lesions that could not acutely change their configuration or cross-sectional area. However, recent clinical and experimental observations have shown that coronary arterial stenoses can respond to vasoconstriction and intraluminal pressure changes. This experimental study evaluated whether similar dynamic changes could occur in a carotid artery stenosis. The effects of dilation distal to a circumferential snare were examined in 6 mongrel dogs. To eliminate collateral flow, the distal carotid artery was occluded and blood flow diverted through a 16 or 20 gauge needle. With no stenosis, distal dilation increased flow from 29.0 +/- 2.0 to 90.1 +/- 3.8 ml/min, (p less than 0.01). With moderate stenosis, the flow increase (25.5 +/- 1.3 to 56.4 +/- 3.7 ml/min, p less than 0.01 following dilation was attenuated. With severe stenosis, flow paradoxically decreased (20.4 +/- 1.0 to 11.4 +/- 1.0 ml/min, (p less than 0.01). This flow decrease was associated with a large stenotic resistance increase (2.13 +/- 0.51 to 18.93 +/- 5.58 mm Hg/ml . min-1, (p less than 0.01). In eight additional experiments, an in vitro preparation was used to examine the effects of vasoconstriction on stenotic severity. Vasoconstriction, induced by ergonovine, methoxamine, angiotensin, or vasopressin, resulted in a significant flow decrease and stenotic resistance increase. Thus, both vasoconstriction and intraluminal pressure were shown to affect stenotic severity, and thereby influence blood flow. These data illustrate hemodynamic factors which may be important in patients with severe carotid artery stenosis.

Impulse propagation in normal and stenosed vessels.

The propagation of a transient pressure impulse in a viscoelastic medium was investigated by experiments using water-filled latex rubber tubing and the aorta of anaesthetised dogs. A 5 ms pressure impulse was produced by the impact of a solenoid driven hammer. The propagation characteristics of the impulse (attenuation and propagation velocity) along the vessel were determined by means of a catheter-tip pressure manometer placed at various distances distal to the impulse generator. The presence of stenoses of varying degrees of severity resulted in reflection of the impulse and the appearance of reflected pulses whose magnitude depended on the stenotic severity. The experiments suggest that for the technique to be used in the detection of local reflecting sites such as might result from vascular occlusive disease, the lesions should occlude at least 70% of the lumen and should be no more than 0.20 m distal to the impulse generator.