UNLABELLED: Percutaneous coronary intervention (PCI) with stent placement induces epicardial coronary vasoconstriction, which is resolved by intracoronary (IC) nitroglycerine (NTG). The effect of stenting on microvascular coronary circulation and coronary blood flow (CBF) is less well established, and the effect of NTG on CBF following stenting is unknown. We examined the time course, extent, and influence of NTG, on PCI induced coronary vasoconstriction. Secondarily we also did an explorative analysis to evaluate the effect of increased levels of low density lipoprotein cholesterol (LDL-Cholesterol) on CBF after stenting. METHODS: Single vessel PCI stent was performed in 19 patients (age 62+/-10 years). Immediately after PCI, a 0.014 Doppler flow-wire was positioned distal to the stent, and IC NTG 0.2 mg was given. Quantitative coronary angiography (QCA) and CBF measurements were taken at baseline, and at 10, 20 and 30 min following PCI. Further IC NTG 200 mug was given after the measurement at 30 min, and the measurements were repeated at 31 and 33 min. Coronary flow velocity reserve (CFVR) was measured with adenosine IC bolus. RESULTS: Compared to baseline, there were significant reductions in CBF (24.5+/-18.3%), (35+/-30 vs. 28+/-25 ml/min, p=0.001) and coronary arterial diameter (5.1+/-5.4%) (2.63+/-0.54 vs. 2.50 mm+/-0.53, p=0.008) within 30 min following PCI. Subsequent IC NTG reversed both small (28+/-25 vs. 44+/-30 ml/min, p<0.001) and large (2.50+/-0.53 vs. 2.80+/-0.59 mm, p=0.001) vessel PCI induced vasoconstriction. LDL-cholesterol was significantly correlated to the percent reduction of blood-flow within 30 min (r=0.515, p=0.024, n=19) and to the maximal CBF after NTG (r=0.520, p=0.022, n=19). CONCLUSION: Following PCI, both large and small vessel vasoconstriction are seen as manifest by a reduction in coronary conduit vessel diameter and in CBF. These effects are reversed by NTG. Serum levels of LDL are modestly related to the reduction of CBF and to the degree of NTG induced vasodilatation of coronary micro-vasculature.
UNLABELLED: Percutaneous coronary intervention (PCI) with stent placement induces epicardial coronary vasoconstriction, which is resolved by intracoronary (IC) nitroglycerine (NTG). The effect of stenting on microvascular coronary circulation and coronary blood flow (CBF) is less well established, and the effect of NTG on CBF following stenting is unknown. We examined the time course, extent, and influence of NTG, on PCI induced coronary vasoconstriction. Secondarily we also did an explorative analysis to evaluate the effect of increased levels of low density lipoprotein cholesterol (LDL-Cholesterol) on CBF after stenting. METHODS: Single vessel PCI stent was performed in 19 patients (age 62+/-10 years). Immediately after PCI, a 0.014 Doppler flow-wire was positioned distal to the stent, and IC NTG 0.2 mg was given. Quantitative coronary angiography (QCA) and CBF measurements were taken at baseline, and at 10, 20 and 30 min following PCI. Further IC NTG 200 mug was given after the measurement at 30 min, and the measurements were repeated at 31 and 33 min. Coronary flow velocity reserve (CFVR) was measured with adenosine IC bolus. RESULTS: Compared to baseline, there were significant reductions in CBF (24.5+/-18.3%), (35+/-30 vs. 28+/-25 ml/min, p=0.001) and coronary arterial diameter (5.1+/-5.4%) (2.63+/-0.54 vs. 2.50 mm+/-0.53, p=0.008) within 30 min following PCI. Subsequent IC NTG reversed both small (28+/-25 vs. 44+/-30 ml/min, p<0.001) and large (2.50+/-0.53 vs. 2.80+/-0.59 mm, p=0.001) vessel PCI induced vasoconstriction. LDL-cholesterol was significantly correlated to the percent reduction of blood-flow within 30 min (r=0.515, p=0.024, n=19) and to the maximal CBF after NTG (r=0.520, p=0.022, n=19). CONCLUSION: Following PCI, both large and small vessel vasoconstriction are seen as manifest by a reduction in coronary conduit vessel diameter and in CBF. These effects are reversed by NTG. Serum levels of LDL are modestly related to the reduction of CBF and to the degree of NTG induced vasodilatation of coronary micro-vasculature.