Relationships of the Thrombolysis in Myocardial Infarction Frame Count With Clinical, Hemodynamic and Medicine Variables in Syndrome X Patients

Abstract

The thrombolysis in myocardial infarction (TIMI) frame count was reported to reflect coronary blood flow and have prognostic value. However, such data in syndrome X was lacking. The purpose of this study was to examine the prognostic value of the TIMI frame count in syndrome X patients, compared with the normal population. The TIMI frame count was measured in 2,049 consecutive patients referred for coronary angiography from March 2003 to February 2005. Among 308 patients with normal coronary angiograms, 44 undergoing the procedure for electrophysiologic studies or valvular heart disease surveys other than angina were designated normal controls. Another 155 patients with positive stress test results were diagnosed as syndrome X. Comparisons of the two groups showed that the syndrome X patients had higher frame counts in the left anterior descending artery (40.9 ± 15.7 vs. 47.8 ± 25.4; p < 0.05) and left circumflex artery (35.2 ± 11.7 vs. 42.0 ± 18.7; p < 0.05). A similar trend was found in the right coronary artery (29.3 ± 13.5 vs. 31.9 ± 15.9; p = 0.2). The TIMI frame count in each artery of the syndrome X group was related to the patients' variables (sex, age, and body mass index), clinical variables (medication use, diabetes, hypertension, hypercholesterolemia, smoking, and family history), and hemodynamic variables (aortic systolic blood pressure and left ventricular end-diastolic pressure). By multivariate analysis, the TIMI frame counts in all arteries were significantly higher in women and lower with angiotensin-converting enzyme inhibitor (ACEI) use (both p < 0.05). The frame count in the left anterior descending was associated with diuretics use ( p < 0.05). Our TIMI frame count data confirm the presence of slow coronary flow in syndrome X patients, especially women. ACEI use shortens the counts in these patients, suggesting that ACEIs have the potential to correct the underlying hemodynamic defects in such patients.