BACKGROUND: The coronary slow flow phenomenon (CSFP) is an angiographic finding characterized by Thrombolysis in Myocardial Infarction (TIMI)-2 flow in the absence of significant large vessel coronary disease. Although clinical and pathological features have been previously described, the underlying pathophysiology has not been fully elucidated. This study investigates the persistence of the phenomenon on serial angiographic studies, coronary hemodynamic findings at rest and during provocative stimuli, and biochemical evidence of inducible myocardial ischemia. METHODS: Twelve patients with CSFP underwent repeat angiography and coronary sinus canulation that allowed for the assessment of coronary blood flow, transmyocardial lactate, and oxygen extraction. Parameters were assessed at rest and during rapid atrial pacing, cold pressor stimulation, and acetylcholine infusion. Angiographic and coronary hemodynamic findings were compared with 47 patients who underwent angiography and 8 patients who were hemodynamic control subjects, respectively. RESULTS: Persistent TIMI-2 flow was demonstrated with repeat angiography in only 4 of the patients. However, the corrected TIMI frame count remained delayed compared with that in control subjects. Furthermore, resting coronary sinus oxygen saturation was low compared with control subjects (23% +/- 4% vs 31% +/- 4%; P <.01), reflecting an increased basal coronary vasomotor tone. The coronary vasodilatory response to atrial pacing was similar to that in control subjects; however, several patients exhibited abnormal vasomotor responsiveness to cold pressor and acetylcholine stimuli. There was no evidence of nett myocardial lactate production with atrial pacing. CONCLUSION: The CSFP is associated with a chronically elevated resting coronary microvascular tone, even when symptoms are relatively quiescent.
BACKGROUND: The coronary slow flow phenomenon (CSFP) is an angiographic finding characterized by Thrombolysis in Myocardial Infarction (TIMI)-2 flow in the absence of significant large vessel coronary disease. Although clinical and pathological features have been previously described, the underlying pathophysiology has not been fully elucidated. This study investigates the persistence of the phenomenon on serial angiographic studies, coronary hemodynamic findings at rest and during provocative stimuli, and biochemical evidence of inducible myocardial ischemia. METHODS: Twelve patients with CSFP underwent repeat angiography and coronary sinus canulation that allowed for the assessment of coronary blood flow, transmyocardial lactate, and oxygen extraction. Parameters were assessed at rest and during rapid atrial pacing, cold pressor stimulation, and acetylcholine infusion. Angiographic and coronary hemodynamic findings were compared with 47 patients who underwent angiography and 8 patients who were hemodynamic control subjects, respectively. RESULTS: Persistent TIMI-2 flow was demonstrated with repeat angiography in only 4 of the patients. However, the corrected TIMI frame count remained delayed compared with that in control subjects. Furthermore, resting coronary sinus oxygen saturation was low compared with control subjects (23% +/- 4% vs 31% +/- 4%; P <.01), reflecting an increased basal coronary vasomotor tone. The coronary vasodilatory response to atrial pacing was similar to that in control subjects; however, several patients exhibited abnormal vasomotor responsiveness to cold pressor and acetylcholine stimuli. There was no evidence of nett myocardial lactate production with atrial pacing. CONCLUSION: The CSFP is associated with a chronically elevated resting coronary microvascular tone, even when symptoms are relatively quiescent.