Heart Vessels (2004) 19:23–26 DOI 10.1007/s00380-003-0722-z
© Springer-Verlag 2004
ORIGINAL ARTICLE Kubilay Senen · Ertan Yetkin · Hasan Turhan Ramazan Atak · Nasir Sivri · Bektas Battaloglu Izzet Tandogan · Mehmet Ileri · Feridun Kosar Ramazan Ozdemir · Sengul Cehreli
Increased thrombolysis in myocardial infarction frame counts in patients with isolated coronary artery ectasia
Received: September 2, 2002 / Accepted: June 6, 2003
Abstract The Thrombolysis in myocardial infarction (TIMI) frame count is a simple clinical tool for assessing quantitative indexes of coronary blood flow. This measurement has been significantly correlated with flow velocity measured with a flow-wire by several investigators during baseline conditions or hyperemia. In this study we aimed to evaluate the coronary flow in patients with isolated coronary artery ectasia by means of the TIMI frame count and to compare the results with those of patients with angiographically normal coronary arteries. The study population consisted of 37 patients with coronary artery ectasia only in the right coronary artery (RCA). The control group consisted of 31 patients with angiographically proven normal coronary arteries. Coronary artery ectasia was defined as nonobstructive lesions of the coronary arteries with a luminal dilatation 1.5-fold or more of the adjacent normal coronary segments. The TIMI frame count was determined for each major coronary artery in each patient according to the methods first described by Gibson et al. The TIMI frame count of RCA in the study group was significantly higher than in that of the control group (51 ⫾ 17 vs 25 ⫾ 8, P ⬍ 0.0001). The TIMI frame counts of the study group for the left anterior descending and left circumflex coronary artery were also significantly higher than those of the control group (corrected TIMI frame count for LAD ⫽ 42 ⫾ 11 vs 24 ⫾ 7, P ⬍ 0.001; TIMI frame count for LCx ⫽ 44 ⫾ 15 vs 25 ⫾ 9, P ⬍ 0.001). In patients with coronary artery ectasia, the TIMI frame count of the RCA was higher than that of
K. Senen · H. Turhan · R. Atak · M. Ileri Department of Cardiology, TYIH, Ankara, Turkey E. Yetkin (*) · N. Sivri · I. Tandogan · F. Kosar · R. Ozdemir · S. Cehreli Department of Cardiology, Inonu University Faculty of Medicine, Yesilevler 4, Blok No:35, Yesiltepe, Malatya, Turkey Tel. ⫹90-422-336-2429 e-mail:
[email protected] B. Battaloglu Department of Cardiovascular Surgery, Inonu University Faculty of Medicine, Malatya, Turkey
the left anterior descending and left circumflex coronary artery (51 ⫾ 17 vs 42 ⫾ 11 and 44 ⫾ 15, respectively, P ⬍ 0.05). We have shown increased TIMI frame counts in patients with isolated coronary artery ectasia and suggest that the pathophysiological mechanism of coronary artery ectasia is not a focal disease. TIMI frame counts can be regarded as an index of the severity of impaired coronary flow in patients with coronary artery ectasia. Key words Coronary artery ectasia · Thrombolysis in myocardial infarction frame count · Coronary flow
Introduction The thrombolysis in myocardial infarction (TIMI) frame count is a simple clinical tool for assessing quantitative indexes of coronary blood flow. This technique counts the number of cineangiographic frames from the initial contrast opacification of the proximal coronary artery to opacification of distal arterial landmarks.1 This measurement has been significantly correlated with flow velocity measured with a flow-wire by several investigators during baseline conditions or hyperemia.2,3 Coronary artery ectasia (CAE) is characterized by segmental or diffuse dilatation of the coronary arteries to ⬎1.5 the diameter of the adjacent segments of the same artery or of a different artery. CAE or localized aneurysmal dilatation of the coronary arteries is observed in 1.2%–4.7% of patients undergoing coronary angiography.4–7 In this study we aimed to evaluate the coronary flow in patients with isolated CAE by means of the TIMI frame count and to compare the results with those of patients with angiographically normal coronary arteries.
Materials and methods The study population consisted of 37 patients with CAE only in the right coronary artery (RCA). To be included in
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the study, patients also needed to have no significant stenotic lesion (⬎50%) in the coronary tree, no valvular heart disease, previous myocardial infarction, and no wall motion abnormalities with echocardiography. The control group consisted of 31 patients with angiographically proven normal coronary arteries. According to the angiographic definition of Hartnell et al.,6 CAE was defined as nonobstructive lesions of the coronary arteries with a luminal dilatation of 1.5-fold or more of the adjacent normal coronary segments. The TIMI frame count was determined for each major coronary artery in each patient according to the methods first described by Gibson et al.1 Briefly, the number of cineangiographic frames, recorded at 30 frames per second, required for the leading edge of the column of radiographic contrast to reach a predetermined landmark, is determined. The first frame is defined as the frame in which concentrated dye occupies the full width of the proximal coronary artery lumen, touching both borders of the lumen, and forward motion down the artery. The final frame is designated when the leading edge of the contrast column initially arrives at the distal landmark. In the left anterior descending coronary artery (LAD), the landmark used is the most distal branch nearest the apex of the left ventricle, commonly referred as the “pitchfork” or “whale’s tail.” The LAD is usually longer than the other major coronary arteries;8 the TIMI frame count for this vessel is often higher. To obtain a corrected TIMI frame count for the LAD, the TIMI frame count was divided by 1.7.1 The right coronary artery distal landmark is the first branch of the posterolateral right coronary artery after the origin of the posterior descending artery, regardless of the size of this branch. The branch of the circumflex artery (LCx) that
encompassed the greatest total distance traveled by contrast was used to define the distal landmark of the circumflex artery. The TIMI frame count in the left anterior descending and circumflex arteries was assessed in a right anterior oblique projection with caudal angulation and right coronary artery in a left anterior oblique projection. Continuous variables are presented as mean ⫾ SD, and categorical variables are presented as a percentage. Continuous variables were compared by using an unpaired t-test and paired t-test where appopriate, and categorical variables were compared by using the chi-square test. Pearson’s correlation coefficient was used to analyze the relation between the TIMI frame counts of the LAD, RCA, and LCx.
Results Characteristics of the study and control groups are presented in Table 1. There were no statistically significant differences between the two groups with respect to age, gender, presence of hypertension, and smoking (P ⬎ 0.05 for all). No statistically significant differences were detected between the diameters of the proximal segments of the LAD and LCx of the two groups (P ⬎ 0.05). The TIMI frame count of the RCA in the study group was significantly higher than that of the control group (51 ⫾ 17 vs 25 ⫾ 8, P ⬍ 0.0001). The TIMI frame counts of the study group for the LAD and the LCx were also significantly higher than those of the control group (corrected TIMI frame count for LAD ⫽ 42 ⫾ 11 vs 24 ⫾ 7, P ⬍ 0.001; TIMI frame count for LCx ⫽ 44 ⫾ 15 vs 25 ⫾ 9, P ⬍ 0.001). In patients with CAE,
Table 1. Baseline characteristics of patients with coronary artery ectasia and normal coronary arteries
Age (years ⫾ SD) M/F Systolic blood pressure (mmHg) Smoking Hypercholesterolemia (⬎240 mg/dl) Diameters of nonectasic coronary arteries Proximal LAD (mm) Proximal LCx (mm)
Patients with coronary artery ectasia (n ⫽ 37)
Patients with normal coronary artery (n ⫽ 31)
P
54 ⫾ 9 23/37 135 ⫾ 13 19/37 14/37
51 ⫾ 9 16/31 138 ⫾ 15 17/31 10/31
NS NS NS NS NS
3.4 ⫾ 0.62 2.9 ⫾ 0.56
3.3 ⫾ 0.74 2.7 ⫾ 0.64
NS NS
LAD, left anterior descending coronary artery; LCx, left circumflex coronary artery; NS, not significant
Table 2. Thrombosis in myocardial infarction (TIMI) frame counts of patients with isolated coronary artery ectasia and normal coronary arteries
Isolated coronary artery ectasia Normal coronary artery
Left anterior descending
Left circumflex
Right coronary artery
42 ⫾ 11*
44 ⫾ 15*
51 ⫾ 17*†
24 ⫾ 7
25 ⫾ 9
25 ⫾ 8
* P ⬍ 0.001 vs normal coronary artery, † P ⬍ 0.05 vs left anterior descending and left circumflex
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the TIMI frame count of the RCA was higher than that of the LAD and LCx (51 ⫾ 17 vs 42 ⫾ 11 and 44 ⫾ 15, respectively, P ⬍ 0.05, Table 2). The TIMI frame count of the RCA showed a significant correlation with that of the LAD (r ⫽ 0.422, P ⬍ 0.01) and LCx (r ⫽ 0.530, P ⬍ 0.01) in the CAE group.
Discussion There are several main findings of our study: (1) using the TIMI frame count method, patients with CAE in RCA had significantly higher TIMI frame counts for all three coronary arteries than control subjects, (2) in patients with CAE, TIMI frame counts of the RCA in which CAE was found were significantly higher than that of the LAD and the LCx in those where CAE were absent, and lastly, (3) there was a significant correlation between the TIMI frame counts of the LAD, the RCA, and the LCx. Although it has been suggested that ectasia is a variant of obstructive coronary artery disease,7–9 its pathogenesis remains poorly understood. Histology of the ectatic segments has demonstrated extensive atherosclerotic changes and destruction of media of the vessel wall.9,10 Williams and Stewart11 have suggested that in most patients coronary ectasia is a diffuse disease of the coronary arteries rather than a localized abnormality of a single arterial segment. This conclusion has been supported by the high proportion of patients who had involvement of multiple segments in one or more vessels.5,9,12 In patients with coronary artery disease the cause is probably destruction of the musculoelastic elements by the atherosclerotic process.5 It has been suggested that there is an imbalance between the benefical effects of nitric oxide on coronary dilatation and the potentially detrimental effects of chronic overstimulation by this endothelium-derived relaxation factor. Nitric oxide stimulates the relaxation of vascular smooth muscle via the guanylate cyclase pathway and release of calcium from the endoplasmic reticulum. There is indirect evidence that chronic vascular relaxation may lead to a clinical syndrome similar to that seen in ectasia.13–15 The chronic relaxation stimulus may also be an underlying mechanism of CAE. Angiographic signs of an impaired coronary blood flow in these isolated CEA are delayed antegrade coronary dye filling, a segmental backflow phenomenon, and local deposition of dye in the dilated coronary segments.5,16 However, this explanation seems to be invalid for the nonectasic coronary artery of the same patient in which we have shown slow coronary flow by the increased TIMI frame count. Increased TIMI frame counts of the ectasic coronary artery compared with those of nonectasic coronary artery and a significant positive correlation between the TIMI frame counts of the ectasic and nonectasic coronary arteries in the same patients have suggested that the mechanism underlying the CAE is a diffuse rather than a focal process and the presence of CAE is an additional factor for increased TIMI frame counts in the affected patients. Coronary flow velocity in apparently normal coronary arteries is mainly deter-
mined by microvascular resistance and endothelial function in conduit vessels.17,18 The slow flow phenomenon observed in apparently normal coronary arteries in patients with isolated CAE in the RCA might be related to high microvascular resistance preceding the development of CAE in these arteries. Another possible mechanism involved in the slow flow phenomen in apparently normal coronary arteries is the diffuse nature of the pathologic changes in CAE. Papadakis et al.19 have also demonstrated slow coronary flow in patients with isolated CAE using the TIMI frame count. The TIMI frame counts for all three coronary arteries were noticed to be lower in that study when compared with our results. The distrubution of the CAE in the coronary territory was not clearly defined in that study. Therefore, the inclusion of highly selected patients who had marked ectasia in the RCA in the present study might be a possible explanation for this difference. In conclusion, we have shown increased TIMI frame counts in patients with isolated CAE and suggest that the pathophysiological mechanism of CAE is not a focal disease. TIMI frame counts can be regarded as an index of severity of impaired coronary flow in patients with CAE.
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