OBJECTIVE: An under-recognized cause of chest pain, the coronary slow-flow (CSF) phenomenon is characterized by delayed coronary opacification during diagnostic angiography in the absence of epicardial coronary artery disease (CAD). Given its angiographic resemblance to no-reflow during percutaneous coronary intervention, a condition associated with microvascular spasm responsive to calcium-channel blockers, we hypothesized that spontaneous CSF may similarly be reversed by intracoronary (IC) nicardipine. METHODS: The effect of IC nicardipine was evaluated in 30 patients. CSF was defined as spontaneously delayed flow (<TIMI 3) during diagnostic coronary angiography in the absence of obstructive epicardial CAD or other conditions associated with impaired flow. Nicardipine was administered as a 200 μg IC bolus, after which repeat angiography was performed. Coronary flow before and after nicardipine was evaluated by TIMI flow grade and corrected TIMI frame count (TFC) assessments. RESULTS: The study population consisted of 22 men and 8 women (mean age, 54 ± 11 years). Clinical presentation was rest angina in 21 patients (70%). At baseline, CSF with <TIMI 3 flow was observed in 49 vessels. TFC was prolonged (>27) in 68/90 vessels (76%). IC nicardipine produced markedly accelerated coronary filling, which was corroborated by TFC analysis. TFC was 47 ± 17 before vs 15 ± 5 after nicardipine (P<.001). All vessels demonstrated TIMI 3 flow and TFC <28 after nicardipine treatment. CONCLUSIONS: IC nicardipine appears highly effective in reversing spontaneous CSF. These findings implicate microvascular spasm in the pathogenesis of CSF. Future studies of oral calcium-channel blockers in the long-term management of CSF are needed.
OBJECTIVE: An under-recognized cause of chest pain, the coronary slow-flow (CSF) phenomenon is characterized by delayed coronary opacification during diagnostic angiography in the absence of epicardial coronary artery disease (CAD). Given its angiographic resemblance to no-reflow during percutaneous coronary intervention, a condition associated with microvascular spasm responsive to calcium-channel blockers, we hypothesized that spontaneous CSF may similarly be reversed by intracoronary (IC) nicardipine. METHODS: The effect of IC nicardipine was evaluated in 30 patients. CSF was defined as spontaneously delayed flow (<TIMI 3) during diagnostic coronary angiography in the absence of obstructive epicardial CAD or other conditions associated with impaired flow. Nicardipine was administered as a 200 μg IC bolus, after which repeat angiography was performed. Coronary flow before and after nicardipine was evaluated by TIMI flow grade and corrected TIMI frame count (TFC) assessments. RESULTS: The study population consisted of 22 men and 8 women (mean age, 54 ± 11 years). Clinical presentation was rest angina in 21 patients (70%). At baseline, CSF with <TIMI 3 flow was observed in 49 vessels. TFC was prolonged (>27) in 68/90 vessels (76%). IC nicardipine produced markedly accelerated coronary filling, which was corroborated by TFC analysis. TFC was 47 ± 17 before vs 15 ± 5 after nicardipine (P<.001). All vessels demonstrated TIMI 3 flow and TFC <28 after nicardipine treatment. CONCLUSIONS: IC nicardipine appears highly effective in reversing spontaneous CSF. These findings implicate microvascular spasm in the pathogenesis of CSF. Future studies of oral calcium-channel blockers in the long-term management of CSF are needed.