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Coronary slow flow phenomenon: Not only low in flow rate but also in myocardial energy expenditure.
BACKGROUND AND AIM: Coronary slow flow phenomenon (CSFP) is a miscellaneous clinical entity leading to angina-like symptoms, and electrocardiographic and scintigraphic evidence of ischemia. The impact of this syndrome on myocardial performance has not been comprehensively evaluated. In this study, we sought to evaluate the myocardial energy expenditure (MEE) in patients with CSFP and its relationship with exercise capacity.
METHODS AND RESULTS: A total of 64 patients (64.1% male, mean age 53.2 ± 10.3 years) with CSFP and 64 patients (60.9% male, mean age 52.2 ± 10.9 years) with normal coronary artery as control group were included. MEE was calculated by a validated formula that uses transthoracic echocardiography (TTE) parameters, including left ventricular circumferential end-systolic stress, stroke volume, and ejection time CSFP patients had significantly lower MEE (0.79 cal/systole ± 0.15 vs. 0.91 cal/systole ± 0.09, p < 0.001). In correlation analysis, MEE had a significant negative correlation with mean corrected TIMI frame count (mTFC) (β = -0.523; p < 0.001) and positive correlations with metabolic equivalents (METs) (β = 0.560; p < 0.001), rate pressure product (β = 0.649; p < 0.001), and exercise duration (β = 0.408; p < 0.001). At multivariate analysis, MEE was demonstrated as an independent predictor of CSFP (OR 1.863, CI 95% 1.485-2.338 p < 0.001).
CONCLUSION: Myocardial energy consumption, as a calculation obtained from TTE parameters, was reduced in patients with CSFP, and it had a significant relationship with exercise capacity. Considering its significant correlation with exercise capacity, myocardial energy consumption seemed to use evaluation of myocardial performance and functional status in another cardiovascular disease.
METHODS AND RESULTS: A total of 64 patients (64.1% male, mean age 53.2 ± 10.3 years) with CSFP and 64 patients (60.9% male, mean age 52.2 ± 10.9 years) with normal coronary artery as control group were included. MEE was calculated by a validated formula that uses transthoracic echocardiography (TTE) parameters, including left ventricular circumferential end-systolic stress, stroke volume, and ejection time CSFP patients had significantly lower MEE (0.79 cal/systole ± 0.15 vs. 0.91 cal/systole ± 0.09, p < 0.001). In correlation analysis, MEE had a significant negative correlation with mean corrected TIMI frame count (mTFC) (β = -0.523; p < 0.001) and positive correlations with metabolic equivalents (METs) (β = 0.560; p < 0.001), rate pressure product (β = 0.649; p < 0.001), and exercise duration (β = 0.408; p < 0.001). At multivariate analysis, MEE was demonstrated as an independent predictor of CSFP (OR 1.863, CI 95% 1.485-2.338 p < 0.001).
CONCLUSION: Myocardial energy consumption, as a calculation obtained from TTE parameters, was reduced in patients with CSFP, and it had a significant relationship with exercise capacity. Considering its significant correlation with exercise capacity, myocardial energy consumption seemed to use evaluation of myocardial performance and functional status in another cardiovascular disease.
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