Pressure–Diameter Relationship in Human Coronary Arteries

Abstract

Background-To quantify the changes in arterial dimensions after the acute changes in pressure associated with percutaneous coronary intervention (PCI). Methods and Results-Forty-eight patients with one angiographically moderate-to-severe stenosis were included in the study. The pressure proximal and distal to the stenosis and the arterial diameter proximal and distal to the stenosis were measured at baseline, after intracoronary nitrates, and after stent PCI. In addition, in 8 patients distal pressure and coronary diameter were assessed while graded, controlled stenoses were created in the stented segment by progressive inflation of a balloon catheter. The mean diameter of the proximal coronary segment was 2.75±0.08 mm, 2.92±0.08 mm (+7.4%), and 3.10±0.07 mm (+14.7%) at baseline, after nitrates and after PCI, respectively (P<0.001). The mean diameter of the distal coronary segment was 2.07±0.09 mm, 2.23±0.09 mm (+9.7%), and 2.5±0.07 mm (+28.4%) at baseline, after nitrates and after PCI, respectively (P<0.001). The increase in distal diameter correlated significantly with the increase in distal pressure after PCI (r 2 =0.57; P<0.001). When graded stenoses were created, a decrease in diameter of 18±4% was observed with a pressure drop of 43±5 mm Hg. Conclusions-The diameter of coronary arteries markedly varies with their distending pressure. After re-establishment of a normal distending pressure by stenting of severe coronary stenoses, a proportional increase in vessel diameter is observed. This should be taken into account when choosing the stent diameter and is an argument to discourage direct stenting. (Circ Cardiovasc Interv. 2012;5:791-796.)

Preprocedural fractional flow reserve and microvascular resistance predict increased hyperaemic coronary flow after elective percutaneous coronary intervention

“…The mechanism of the increased hyperaemic MR that decreased after PCI in the present study remains to be elucidated. The coronary resistance vessels, similar to epicardial coronary arteries, are reportedly pressure‐distensible at maximal hyperaemic vasodilation . Because MR is significantly correlated with vessel radius and the vessel size depends on vessel perfusion pressure, impaired distal perfusion pressure secondary to progression of epicardial stenosis severity will result in a progressive increase in MR at maximal vasodilation and thus in increased MR .…”

Impact of hyperaemic microvascular resistance on fractional flow reserve measurements in patients with stable coronary artery disease: insights from combined stenosis and microvascular resistance assessment

“…Although it may be explained by an increase in passive resistance in the microvascular bed due to extensive microvascular disease, it must be borne in mind that microvascular resistance at maximal vasodilation will also increase when the magnitude of epicardial disease increases. Although increasing epicardial disease severity will dictate progressive vasodilation of the coronary resistance vessels under resting conditions when coronary autoregulation is active, the coronary resistance vessels, similar to epicardial coronary arteries,15 are pressure-distensible at maximal vasodilation, when most active coronary tone is abolished. Because resistance increases as a function of the fourth power of the vessel radius, and the latter, in turn, depends on vessel perfusion pressure,16 17 a progressive impairment of distal perfusion pressure secondary to progression of epicardial stenosis severity will lead to a progressive increase in microvascular resistance at maximal vasodilation, and thus in an increase in HMR 18…”

Improvement in coronary haemodynamics after percutaneous coronary intervention: assessment using instantaneous wave-free ratio

“…However, it is possible despite successful anatomical resolution of a coronary stenosis, unwanted or unaccounted for effects of PCI itself may pose difficulties for post-PCI physiological evaluation. Such effects included altered haemodynamics,13 changes in microcirculatory resistance,14 and altered responsiveness to adenosine due to microembolisation 15. The impact may vary according to initial lesion severity,16 17 the stenting strategy18 and even concomitant drugs 19.…”