Impaired coronary vasodilator reserve in the immediate postcoronary angioplasty period: Analysis of coronary artery flow velocity indexes and regional cardiac venous efflux

Abstract

The ratio of peak hyperemic/basal mean coronary flow velocity, an index of coronary vasodilator reserve, immediately after coronary angioplasty normalizes in less than 50% of patients. To evaluate other indexes of coronary vasodilator capacity, both intracoronary arterial velocity and cardiac venous efflux were measured at rest and during vasodilator-induced coronary hyperemia (intracoronary nitroglycerin and papaverine) before and after angioplasty in 27 patients; 17 patients had measurements of intracoronary velocity alone and 10 had thermodilution measurements of great cardiac vein flow. Coronary flow velocity responses were also measured in 6 angiographically normal segments in patients undergoing angioplasty and in 10 normal left coronary artery segments in patients with normal coronary arteries or isolated right coronary artery disease. Despite significant angiographic (72 +/- 12 to 23 +/- 11% diameter narrowing) and hemodynamic (49 +/- 12 to 19 +/- 12 mm Hg aortocoronary gradient) improvement, coronary vasodilator reserve ratios for both arterial velocity and venous flow after angioplasty were only minimally affected. Angioplasty did not significantly increase rest coronary vein flow or artery flow velocities, but did result in significantly higher papaverine responses after angioplasty. Mean and phasic coronary velocity, diastolic coronary flow velocity integral and measured great cardiac vein flow ratios were significantly lower when compared with those in 16 angiographically normal coronary artery segments. These data indicate that maximal hyperemic coronary flow velocity is increased after angioplasty, but the reserve ratios, calculated by any of several flow velocity indexes, remain minimally improved. Angiographic correlations (percent coronary diameter, absolute diameter or cross-sectional area) with variables of coronary blood flow or velocity suggest that no single variable is useful in assessing angioplasty results. However, postangioplasty arterial mean velocity and diastolic flow velocity integral are nearly normalized in most patients, whereas relative changes remain attenuated. These findings are important in studies assessing coronary vasomotor responses in patients with atherosclerotic coronary disease, especially after angioplasty.

Impaired Coronary Autoregulation Is Associated With Long-term Fatal Events in Patients With Stable Coronary Artery Disease

“…[15][16][17] This increase in baseline flow velocity was repeatedly ascribed to disturbed coronary autoregulation. 15,17 Under physiological circumstances, coronary autoregulation regulates vasodilation and vasoconstriction of the coronary resistance vessels to maintain stable coronary blood flow to the distal myocardium within a physiological range of perfusion pressures.…”

Role of Coronary Vasoconstriction in Ischemic Heart Disease and Search for Novel Therapeutic Targets

“…16 The pharmacological blockade of this inappropriate vasoconstriction would restore residual coronary flow reserve to its maximum value, but different drugs might be required for blocking epicardial arteries and small vessel constriction. Indeed, about 50% of the patients with stable coronary disease continue to have angina and positive exercise tests in spite of successful coronary interventional revascularization, 17,18 which does not appear to have significant impact on prognosis in these patients. 19 …”

Immediate and Long-Term Effect of Balloon Angioplasty or Stent Implantation on the Absolute and Relative Coronary Blood Flow Velocity Reserve

“…These findings are in accordance with other studies that demonstrated an impaired coronary flow reserve immediately after balloon angioplasty, compared with normal values of the control group, due to an increased baseline coronary blood flow. 10,16 Several mechanisms have been postulated for the observed increase in baseline flow velocity after PTCA, such as (1) failure of the peripheral arterial vascular bed to vasoconstrict appropriately on the sudden increase in distal coronary pressure produced by coronary angioplasty, (2) epicardial vasoconstriction at the site of the Doppler guidewire tip mediated by a myogenic response and/or neural mechanisms, 17,18 or (3) the influence of drug therapy. 19,20 However, all patients were treated with nitroglycerin during the procedure, and there was no difference in drug therapy (nitrates, calcium antagonists, ␤-blockers, or ACE inhibitors) between patients with and without impaired CFR after PTCA.…”