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Published on: April 13, 2015
Coronary hemodynamic and metabolic studies of the coronary slow flow phenomenon
John F Beltrame1, Sananand B Limaye, Ronald D Wuttke
1Cardiology Unit, North Western Adelaide Health Service, Adelaide University, Adelaide, Australia. john.beltrame@adelaide.edu.au
Insights
The coronary slow flow phenomenon (CSFP) involves delayed blood flow in heart arteries. This study reveals CSFP is linked to chronically elevated resting coronary microvascular tone, even without active symptoms.
Area of Science:
- Cardiology
- Vascular Biology
- Diagnostic Imaging
Background:
- Coronary slow flow phenomenon (CSFP) is an angiographic finding of Thrombolysis in Myocardial Infarction (TIMI)-2 flow without significant coronary artery disease.
- The precise pathophysiology of CSFP remains incompletely understood.
- This study aimed to elucidate the underlying mechanisms of CSFP.
Purpose of the Study:
- To investigate the persistence of CSFP on serial angiographic studies.
- To assess coronary hemodynamic findings at rest and during provocative stimuli.
- To evaluate biochemical evidence of inducible myocardial ischemia in CSFP patients.
Main Methods:
- Twelve patients with CSFP underwent repeat angiography and coronary sinus catheterization.
- Coronary blood flow, transmyocardial lactate, and oxygen extraction were measured at rest and during pacing, cold pressor, and acetylcholine challenges.
- Findings were compared to control groups.
Main Results:
- Persistent TIMI-2 flow was observed in only 4 patients, but corrected TIMI frame count remained delayed.
- Resting coronary sinus oxygen saturation was significantly lower in CSFP patients, indicating increased basal coronary vasomotor tone.
- Abnormal vasomotor responses to cold pressor and acetylcholine stimuli were noted, with no evidence of myocardial lactate production during pacing.
Conclusions:
- CSFP is associated with chronically elevated resting coronary microvascular tone.
- This elevated tone persists even when patients are asymptomatic.
- The findings suggest a role for microvascular dysfunction in the pathophysiology of CSFP.
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.
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