Slow Coronary Flow Group Research Articles

Left Ventricular Twist Mechanics Are Impaired in Patients with Coronary Slow Flow.

Coronary slow flow (CSF) is a rare condition described as the delayed angiographic passage of a contrast agent in the absence of stenosis in epicardial coronary arteries. Left ventricular (LV) systolic and diastolic dysfunctions have been described in the presence of CSF. However, the effect of CSF on LV twist functions has not been assessed. We aimed to evaluate the effects of CSF on LV twist mechanics using speckle tracking echocardiography (STE). Twenty CSF patients (24-60years) were enrolled according to the exclusion criteria. Twenty subjects with similar demographic characteristics and normal coronary arteries were the controls. Participants were evaluated with conventional echocardiography and STE. The general characteristics of the two groups were similar. LV twist, LV torsion, and apical rotation were impaired in the CSF group (P=0.015, P=0.012, and P<0.001, respectively). Time to peak twist (TPT) and time to peak untwisting (TPU) were prolonged in CSF patients (P<0.001 and P<0.001, respectively). In the CSF group, rotation-deformation delay was shortened (P<0.001) and global longitudinal strain (GLS) was lower (P<0.001). The thrombolysis in myocardial infarction (TIMI) frame count was negatively correlated with LV twist, LV torsion and apical rotation (P=0.002, r=-0.624; P=0.002, r=-0.624; and P=0.002, r=-0.632, respectively). We demonstrated that LV twist mechanics are impaired in CSF patients. Worse LV twist parameters were associated with greater TIMI frame count.

Serum YKL-40 is increased in patients with slow coronary flow

There is accumulating evidence that inflammation plays a major role in the development of the slow coronary flow (SCF) phenomenon. YKL-40 has been suggested to be a potential biomarker of inflammation. In this study, we aimed to study YKL-40 as it relates to SCF. Patients who underwent coronary angiography before and had angiographically normal coronary arteries of varying coronary flow rates without any atherosclerotic lesion were enrolled in this study. Patients who had thrombolysis in myocardial infarction frame counts (TFC) above the normal cutoffs were considered to have SCF and those within normal limits were considered to have normal coronary flow (NCF). The YKL-40 levels and biochemical profiles of all patients were studied and analyzed. There were 41 patients in the SCF group and 209 patients in the NCF group. Compared with the NCF patients, SCF patients had higher serum high-sensitivity C-reactive protein (hs-CRP) (P=0.0003) and YKL-40 (P=0.0007) levels. A positive correlation was detected between the YKL-40 levels and hs-CRP (r=0.7021, P<0.001), and the mean TFC (r=0.4038, P=0.0088) in SCF patients. Our study showed that YKL-40 levels are higher and correlated positively with TFC and hs-CRP in SCF patients. This finding suggests that YKL-40 may be a useful marker and predictor for SCF.

Increased Platelet to Lymphocyte Ratio is Related to Slow Coronary Flow.

Previous studies showed that both inflammation and platelets have a role in development of slow coronary flow (SCF). Platelet to lymphocyte ratio (PLR) as an emerging inflammatory indicator was significantly associated with adverse cardiovascular events. Therefore, we aimed to assess the relationship between PLR and SCF. Patients who had angiographically normal coronary arteries were enrolled in this retrospective study (n = 221 as SCF group and n = 293 as control group). Patients who had thrombolysis in myocardial infarction frame counts (TFC) above the normal cutoffs were considered to have SCF. Both PLR and C-reactive protein (CRP) were significantly higher in the SCF group. In correlation analysis, PLR has a significantly positive correlation with the left anterior descending artery TFC (P = .001), circumflex artery TFC (P < .001), right coronary artery TFC (P < .001), and serum CRP level (P < .001). In multiple logistic regression analysis, PLR was independently associated with presence of SCF (odds ratio: 1.014, P < .001). In conclusion, higher PLR levels were significantly and independently related to the presence of SCF. Besides, PLR was positively correlated with serum CRP level as a conventional marker for systemic inflammation.

Low bilirubin levels are associated with coronary slow flow phenomenon.

Increasing evidence suggests an inverse relationship between bilirubin levels and cardiovascular disease. The present study evaluated the effect of bilirubin level on the slow coronary flow (SCF) phenomenon. This study was cross-sectional and observational. We enrolled 222 consecutive patients who underwent coronary angiography for suspected ischaemic heart disease and were found to have normal or near-normal coronary arteries. Then, bilirubin levels were measured and coronary flow rate was assessed using the thrombolysis in myocardial infarction (TIMI) frame count. SCF was defined as a TIMI frame count > 27 frames. SCF was observed in at least one coronary vessel in 22 of the 222 subjects, indicating a prevalence of 10%. Serum bilirubin levels were significantly decreased in the SCF group. In multivariate logistic regression analysis, total bilirubin and diabetes mellitus were independent risk factors for SCF. Furthermore, after adjusting for age, sex, and cardiovascular disease risk factors, serum bilirubin level (B = -0.34, p < 0.001) was independently associated with TIMI frame count. These findings suggest that serum total bilirubin levels may be a useful marker for patients with the SCF phenomenon. We believe that further studies are needed to clarify the role of bilirubin in patients with SCF.

Anxiety, Depression, and General Psychological Distress in Patients with Coronary Slow Flow.

BackgroundThe relationship between psychiatric illness and heart disease has been frequently discussed in the literature. The aim of the present study was to investigate the relationship between anxiety, depression and overall psychological distress, and coronary slow flow (CSF).MethodsIn total, 44 patients with CSF and a control group of 50 patients with normal coronary arteries (NCA) were prospectively recruited. Clinical data, admission laboratory parameters, and echocardiographic and angiographic characteristics were recorded. Symptom Checklist 90 Revised (SCL-90-R), Beck Depression Inventory (BDI), and Beck Anxiety Inventory (BAI) scales were administered to each patient.ResultsThe groups were comparable with respect to age, sex, and atherosclerotic risk factors. In the CSF group, BAI score, BDI score, and general symptom index were significantly higher than controls (13 [18.7] vs. 7.5 [7], p = 0.01; 11 [14.7] vs. 6.5 [7], p = 0.01; 1.76 [0.81] vs. 1.1[0.24], p = 0.01; respectively). Patients with CSF in more than one vessel had the highest test scores. In univariate correlation analysis, mean thrombolysis in myocardial infarction (TIMI) frame counts were positively correlated with BAI (r = 0.56, p = 0.01), BDI (r = 0.47, p = 0.01), and general symptom index (r = 0.65, p = 0.01). The psychiatric tests were not correlated with risk factors for atherosclerosis.ConclusionOur study revealed higher rates of depression, anxiety, and overall psychological distress in patients with CSF. This conclusion warrants further studies.

Evaluation of serum prolidase activity in patients with slow coronary flow.

IntroductionSlow coronary flow (SCF) is described as the slow passage of contrast to distal coronaries despite anatomically normal coronary arteries. It has been shown that increased serum prolidase activity (SPA) correlates with collagen turnover. Increased collagen turnover might be associated with the development of atherosclerotic plaques.AimTo investigate the relationship between serum prolidase activity and slow coronary flow.Material and methodsThis cross-sectional study included 40 SCF patients (mean age: 55.0 ±9.5 years, 20 females) and 40 controls (mean age: 53.9 ±8.2 years, 21 females) with normal coronary anatomy and normal coronary flow. The Thrombolysis in Myocardial Infarction (TIMI) frame-count (TFC) method was used for SCF diagnosis. Serum prolidase activity was measured spectrophotometrically, and the relevant parameters were compared between the groups.ResultsThere were no statistically significant differences between the SCF and control groups in terms of basic demographic, clinical, and laboratory data. However, the SPA was significantly higher in the SCF group compared to the control (702.7 ±13.8 and 683.9 ±13.2 respectively, p<0.001). Serum prolidase activity was significantly correlated with the mean TFC (r=0.463, p<0.001). The overall findings of this study support the predictive accuracy of the serum prolidase activity in our cohort, with a statistically significant ROC value of 681.3.ConclusionsOur study showed that SPA was increased in SCF patients. The activity of this enzyme was significantly correlated with the mean TFC.

Echo-Tracking Technology Assessment of Carotid Artery Stiffness in Patients with Coronary Slow Flow

Coronary slow flow (CSF) in coronary angiography (CAG) is a well-recognized clinical entity. Previous studies have suggested that microvascular abnormalities and endothelial dysfunction are responsible for CSF. Accordingly, we hypothesized that the CSF phenomenon is a form of atherosclerosis including both small vessels and epicardial coronary arteries. The echo-tracking (ET) technique is a non-invasive detection method for early prediction of arterial atherosclerosis. Therefore, we investigated carotid elasticity with the ET technique in patients with CSF. Fifty patients with CSF and 50 patients with normal coronary artery blood flow, as determined by CAG, with a similar distribution of risk factors were recruited. The stiffness parameter (β), pressure–strain elastic modulus (Ep), arterial compliance (AC), augmentation index (AIx) and local pulse-wave velocity (PWV) were determined at the level of the bilateral common carotid artery (CCA) with using the ET technique. Levels of serum high-sensitivity C-reactive protein (hs-HSCRP) were determined for the two groups. β, Ep and PWV were significantly higher in the CSF group than in the control group (β: 11.4 ± 3.76 vs. 9.22 ± 3.28, p < 0.01; Ep: 153.44 ± 47.85 vs. 126.40 ± 43.32, p < 0.01; PWV: 7.26 ± 1.10 vs. 6.55 ± 1.02, p < 0.01), but AC was lower in the CSF group than in the control group (0.62 ± 0.20 vs. 0.74 ± 0.24, p < 0.01). The elasticity parameters of the bilateral common carotid artery did not significantly differ. The level of hs-HSCRP was correlated positively with β (r = 0.306, p = 0.015), Ep (r = 0.358, p = 0.005) and PWV (r = 0.306, p = 0.015), but negatively with AC (r = −0.236, p = 0.049). In conclusion, the ET technique is a simple practical method for evaluating carotid artery elasticity, and there is a significant correlation between carotid artery stiffness and level of hs-HSCRP in patients with CSF.

The relationship between neutrophil gelatinase-associated lipocalin levels and the slow coronary flow phenomenon.

There is accumulating evidence that inflammation plays a major role in the development of the slow coronary flow (SCF) phenomenon. In this study, we aimed to study the biomarker neutrophil gelatinase-associated lipocalin (NGAL) as it relates to SCF. Patients who underwent coronary angiography before and had no significant epicardial coronary disease were included in the study. Patients who had Thrombolysis in Myocardial Infarction frame counts (TFCs) above the normal cutoffs were considered to have SCF and those within normal limits were considered to have normal coronary flow (NCF). The NGAL levels and biochemical profiles of all patients were studied and analyzed with coronary flow parameters. There were 50 patients in the SCF group and 50 patients in the NCF group. The serum NGAL level was higher in those patients in the SCF group versus the NCF group (75.2±39.7 vs. 50.6±24.2, P<0.001). There was a significant correlation between the NGAL levels and TFC (r=0.684, P<0.001). Multivariable regression analysis showed that the NGAL levels were an independent predictor of the SCF phenomenon (odds ratio=1.060, 95% confidence interval: 1.008-1.115, P=0.023). In this study, we show that patients with SCF have elevated levels of NGAL. We further show a strong correlation between the NGAL levels and coronary blood flow. We conclude that elevated NGAL levels might be a useful tool in predicting SCF in patients who undergo coronary angiography.

The association of serum albumin with coronary slow flow.

A number of inflammatory markers such as high-sensitivity C-reactive protein (Hs-CRP), interleukin-6 (IL-6), and fibrinogen have been shown to be associated with coronary slow flow (CSF). Our aim was to investigate the relationship between albumin, a long-acting negative acute-phase protein, and CSF. A total of 106 patients with angiographically proven slow coronary flow and 57 control subjects with normal coronary flow were included in the study. Serum levels of Hs-CRP and albumin were measured. CSF was defined by Thrombolysis In Myocardial Infarction (TIMI) frame count (TFC) method. Serum albumin (s-albumin) was significantly lower in the CSF group (3.79 ± 0.3 vs 4.17 ± 0.3, p < 0.001), whereas Hs-CRP level was significantly higher in the CSF group compared with the controls (1.22 ± 0.79 vs 0.76 ± 0.44, p < 0.001). S-albumin and Hs-CRP were correlated with the mean TFC in the whole study population (r= - 0.574, p < 0.001; r = 0.376, p < 0.001, respectively). Hs-CRP and low s-albumin were found to be significant predictors of CSF in the multivariate analysis. The comparison of receiver-operating characteristics curves for s-albumin and Hs-CRP demonstrated that s-albumin was the strongest predictor of CSF. We found that s-albumin levels decreased and Hs-CRP levels increased in patients with CSF. S-albumin was also found to have superior predictive value than Hs-CRP for diagnosing CSF. S-albumin, an inexpensive and easily measurable laboratory variable, may be a useful predictor of CSF, especially when other reasons which alter its serum levels were excluded.

The relationship between coronary slow flow phenomenon and urotensin-II: A prospective and controlled study.

Objective:The underlying mechanism of coronary slow flow (CSF) has not yet been clarified, although many studies have been conducted to understand its pathophysiology. In this study, we investigated the role of a very potent vasoconstrictor, urotensin-II (UII), in the pathophysiology of CSF. This prospective and controlled investigation aimed to evaluate the association between CSF and serum levels of UII.Methods:Our study included 32 patients with slow flow in any coronary artery and 32 patients with normal coronary arteries. Coronary flow was calculated using the Thrombolysis in Myocardial Infarction (TIMI) frame count (TFC) method, and CSF was defined as TFC ≥39 for the left anterior descending artery, TFC ≥27 for the circumflex coronary artery, and TFC ≥24 for the right coronary artery. UII levels in blood samples obtained from both groups were measured by enzyme-linked immunosorbent assay (ELISA) method.Results:UII levels were significantly higher in the CSF group than in the control group [122 pg/mL (71-831), 95 pg/mL (21-635), respectively; p<0.001]. High-density lipoprotein (HDL) levels were lower in the CSF group, and leukocyte counts were significantly higher. A positive correlation between UII and mean TFC (r=0.524, p=0.002) was found in the CSF group. The multivariate logistic regression analysis determined that UII, HDL, and cigarette smoking were independent indicators in predicting CSF (OR=1.010, 95% confidence interval 1.002-1014, p=0.019; OR=0.927, 95% confidence interval 0.869-0.988, p=0.019; OR=5.755, 95% confidence interval 1.272-26.041, p=0.021, respectively).Conclusion:Serum UII levels were found to be significantly higher in the CSF group, suggesting that UII may be one of the underlying factors in the pathogenesis of CSF

Mean platelet volume is not associated with coronary slow flow: a retrospective cohort study.

Objective:To investigate mean platelet volume (MPV) levels in patients with coronary slow flow (CSF).Methods:465 stable angina pectoris cases with angiographically normal coronary arteries were recruited [coronary slow flow group (n=76), control group (n=389)] in the observational retrospective cohort study. Clinical, biochemical and demographic variables including MPV were noted and coronary blood flow was assessed with TIMI frame count (TFC).Results:Gender, smoking, height, serum creatinine, uric acid levels, hemoglobin, waist/hip ratio, systolic blood pressure but not MPV were significantly different among groups. Independent predictors of CSF were height (p=.029) and serum uric acid level (p=.045). Gender, height, weight, hip circumference, systolic blood pressure, fasting blood glucose, serum urea, creatinine, uric acid levels, hemoglobin and platelet count were associated with mean TFC whereas independent predictors of mean TIMI frame count were height (p=.010) and serum uric acid level (p=.041).Conclusion:Height and serum uric acid level but not MPV were independent predictors of both CSF and mean TFC.

Association of Glomerular Filtration Rate With Slow Coronary Flow in Patients With Normal to Mildly Impaired Renal Function

We evaluated the association between estimated glomerular filtration rate (eGFR) and slow coronary flow (SCF) in patients with normal to mildly impaired renal function; 211 patients with angiographically proven SCF and 219 controls were studied. Patients were categorized based on the angiographic findings as with or without SCF. We used the Modification of Diet in Renal Disease equation to calculate eGFR. The frequency of mildly decreased eGFR, serum uric acid levels, and eGFR was higher in the SCF group. Patients with mildly impaired renal function had higher thrombolysis in myocardial infarction frame counts in 3 major coronary arteries. In logistic regression analysis, uric acid (odds ratio [OR] = 1.323, 95% confidence interval [CI] = 1.109-1.572, P = .002) and eGFR (OR = 0.972, 95% CI = 0.957-0.987, P < .001) were independent correlates of SCF. In conclusion, eGFR was significantly correlated with SCF in patients with normal to mildly impaired renal function.

The presence of fragmented QRS on 12-lead ECG in patients with coronary slow flow

Coronary slow flow (CSF) is characterised by delayed opacification of coronary arteries in the absence of epicardial occlusive disease. It has been reported that CSF may cause angina, myocardial ischaemia, and infarction. Fragmentation of QRS complex (fQRS) is an easily evaluated non-invasive electrocardiographic parameter. It has been associated with alternation of myocardial activation due to myocardial scar and/or ischaemia. Whether CSF is associated with fQRS is unknown. The presence of fQRS on ECG may be an indicator of myocardial damage in patients with CSF. To investigate the presence of fQRS in patients with CSF. Sixty patients (mean age 55.5 ± 10.5 years) with CSF and 44 patients with normal coronary arteries without associated CSF (mean age 53 ± 8.4 years) were included in this study. The fQRS was defined as the presence of an additional R wave or notching of R or S wave or the presence of fragmentation in two contiguous leads corresponding to a major coronary artery territory. The presence of fQRS was higher in the CSF group than in the controls (p = 0.005). Hypertension was significantly more common in the CSF group (p < 0.001). There was no significant association between the presence of fQRS and an increasing number of vessel involvements. Logistic regression analysis demonstrated that the presence of CSF was the independent determinant of fQRS (OR = 10.848; 95% CI 2.385-49.347; p = 0.002). Fragmented QRS, indicating increased risk for arrhythmias and cardiovascular mortality, was found to be significantly higher in patients with CSF. We have not found an association between the presence of fragmented QRS and the degree of CSF. Further prospective studies are needed to establish the significance as a possible new risk factor in patients with CSF.

Slow coronary flow phenomenon and increased platelet volume indices.

Background and ObjectivesWe sought to determine the relationship between mean platelet volume (MPV), platelet distribution width (PDW), and platelet larger cell ratio (P-LCR) with slow coronary flow (SCF).Subjects and MethodsEighty participants who underwent coronary angiography were divided into two groups, 50 participants with SCF as case group, and 30 with normal coronary flow (NCF) as control group. Baseline characteristics and laboratory data were collected before angiography.ResultsPlatelet volume indices MPV (10.8±1.2 fL), PDW (14.5±2.2 fL), and P-LCR (30.5±8.1%) in the SCF group were significantly (p<0.05) higher than those (10.1±0.9 fL, 13.2±1.8 fL, and 26.8±6.8%, respectively) in the NCF group. The patients with three SCF arteries had significantly higher platelet volume indices compared to those with NCF arteries; however, the patients with one SCF artery did not. Based on linear regression model, MPV, PDW, and P-LCR were independent predictors of mean infarction frame counting (TFC). In multivariate analysis, MPV {odds ratio (OR)=32.393, 95% confidence interval (CI)=1.189-882.606, p=0.039} and P-LCR (OR=0.566, 95% CI=0.330-0.937, p=0.028) were independent predictors of SCF.ConclusionPlatelet volume indices MPV, PDW, and P-LCR were associated with both the presence and extent of SCF.

Endothelial nitric oxide synthase levels and their response to exercise in patients with slow coronary flow

SummaryBackgroundEndothelial dysfunction plays a key role in the aetiopathogenesis of slow coronary flow (SCF) even if there is no obstructive epicardial lesion. Reduced plasma levels of endothelial nitric oxide synthase (eNOS) are an important indicator of endothelial dysfunction. We aimed to determine plasma levels of eNOS and their relationship with exercise in patients with SCF.MethodsTwenty-two patients with SCF in at least one coronary artery and 17 healthy individuals were included in this study. The TIMI frame count method was used to determine SCF. Plasma levels of eNOS before and after effort were determined in the patient and control groups.ResultsBasal eNOS levels in the patient group were lower than in the control group (p = 0.040), and plasma eNOS levels after exercise decreased more significantly in the patient group compared to the control group (p = 0.002). Median decreases of eNOS in response to exercise were higher in the SCF group than in the control group (p < 0.001), and the decrease observed in the control group was not statistically significant (p = 0.35). There were significantly negative correlations between TIMI frame count and plasma levels of eNOS at baseline and after exercise (r = –0.51, p = 0.015, r = –0.58, p = 0.005, respectively). Moreover, there was also a positive correlation between the rate–pressure product and plasma levels of eNOS after exercise in patients with SCF (r = 0.494, p = 0.019).ConclusionOur findings indicate an important pathophysiological relationship between the severity of SCF in which endothelial dysfunction plays a role in its pathogenesis and the level of circulating plasma levels of eNOS.

Inverse correlation between coronary and retinal blood flows in patients with normal coronary arteries and slow coronary blood flow

BackgroundThe “Slow Coronary Flow” (SCF) phenomenon in the presence of angiographically normal coronaries is attributed to microvascular and endothelial dysfunction. The microcirculation can be non-invasively assessed by measuring retinal blood flow velocity.The aim of the present study was to evaluate the efficacy of the “Retinal Functional Imager” (RFI) device as a noninvasive method of diagnosing patients with slow coronary flow. MethodsCoronary blood flow velocity assessed by corrected TIMI Frame Count and retinal arterioles blood flow assessed by RFI were measured in 28 consecutive patients with normal coronary arteries. The patients were divided into 2 groups: a slow coronary flow (SCF) and a normal coronary flow (NCF) groups. ResultsInverse correlation was found between retinal and coronary blood flows so that higher retinal arterial flow velocity was observed in the SCF group (3.8 ± 1.1 mm/s vs. 2.9 ± 0.61 mm/s, respectively, p = 0.022). RFI provided 73% sensitivity and 77% specificity for diagnosing SCF using ROC analysis. Additionally, patients with SCF had higher values of serum LDL cholesterol (104.7 ± 18.93 mg/dl vs. 81.55 ± 14.62 mg/dl in NCF, p = 0.005), Glucose (96.9 ± 23.0 mg/dl vs. 83.55 ± 9.7 mg/dl in NCF, p = 0.024), and lower percentage of statin consumption (40.0% vs. 76.9% in NCF, p = 0.049). ConclusionsSlow coronary blood flow can be non-invasively diagnosed with Retinal Functional Imager. Patients with normal coronary arteries and slow coronary blood flow have high retinal arteriolar blood flow. Early non-invasive diagnosis of SCF might help detect individuals who are at higher risk to develop coronary atherosclerosis, and to provide them with early preventive measures.

The Effect of Slow Coronary Flow on Right and Left Ventricular Performance

Objective: To evaluate left and right ventricular functions using tissue Doppler echocardiography (TDE) and myocardial performance index (MPI) methods in patients with slow coronary flow (SCF) and to determine the relationship between these parameters and thrombolysis in myocardial infarction frame count in SCF patients. Subjects and Methods: Thirty-five patients (20 males and 15 females) with SCF who underwent coronary angiography and 35 age- and sex-matched controls (14 males and 21 females) without SCF who underwent elective coronary angiography were enrolled in the study. Left ventricular (LV) and right ventricular (RV) functions were examined using conventional echocardiography and TDE. Results: LV systolic myocardial velocity (Sm), early myocardial velocity (Em), late myocardial velocity (Am), and Em/Am ratio were similar in both the SCF and control groups; however, isovolumetric relaxation time (IRT) was higher in the SCF group compared to the control group (IRT: 99 ± 17 vs. 88 ± 20; p = 0.01). In patients with SCF, LV MPI was higher than in the control group, but this was not statistically significant (0.61 ± 0.11 vs. 0.56 ± 0.12; p = 0.07). The RV tricuspid annular velocities and MPI were similar in the SCF and control groups. Conclusion: This study showed that SCF affected LV functions echocardiographically and could cause partially reduced LV performance. In addition, SCF did not affect RV functions echocardiographically.

Thrombin activatable fibrinolysis inhibitor

The slow coronary flow (SCF) phenomenon is characterized by slow progression of angiographic contrast medium in the coronary arteries in the absence of stenosis in the epicardial vessels. The pathophysiological mechanisms of SCF phenomenon remain uncertain. Several hypotheses, however, have been suggested for SCF phenomenon, including an early form of atherosclerosis, small vessel dysfunction, dilatation of coronary vessels, imbalance between vasoconstrictor and vasodilatory factors, platelet function disorder, and inflammation. Atherosclerosis and inflammation are the most accepted mechanisms for the pathogenesis of SCF. Thrombin activatable fibrinolysis inhibitor (TAFI) was described as a new inhibitor of fibrinolysis recently and plays an important role in coagulation and fibrinolysis. In previous studies, the role of TAFI was associated with inflammation and evolution of atherosclerosis in coronary artery disease. There are no data available about TAFI levels in patients with SCF phenomenon investigated by angiography. Our goal was to evaluate TAFI antigen (Ag) levels in patients with SCF and to determine the association of the TAFI Ag level with traditional cardiovascular risk factors in our study. The study group constituted 41 patients with angiographically confirmed SCF and 46 patients with normal coronary flow as the control group. The TAFI Ag levels of each patient were determined. Between the control and study group, a statistical difference in the levels of TAFI Ag (p < 0.05) was observed. The TAFI Ag level was significantly higher in the SCF group than the control group (132.21 ± 21.14 versus 122.15 ± 21.59). We have demonstrated that TAFI might be a risk factor for the development of SCF independently of conventional cardiovascular risk factors. In addition, TAFI Ag levels were positively correlated with C-reactive protein (CRP) known as an acute phase reactant. Our findings support the reports of previous studies that increased TAFI levels may be associated with inflammation. Further large studies are required to evaluate the importance of TAFI antigen levels in relation to the development of SCF.

Evaluation of coronary microvascular function and nitric oxide synthase intron 4a/b polymorphism in patients with coronary slow flow

Slow coronary flow (SCF) is reported to be associated with increased risk of cardiovascular disease. We have used coronary flow reserve measurement by transthoracic Doppler echocardiography to determine coronary microvascular function in patients with SCF and to determine whether the intron 4a/b polymorphism of the eNOS gene influences coronary endothelial function. Overall, 96 patients with SCF and 79 controls were enrolled in the study. Coronary flow was quantified according to the thrombolysis in myocardial infarction (TIMI) frame count (TFC) on angiogram. Coronary diastolic peak flow velocities (DPFV) were measured with color Doppler flow mapping at baseline and after dipyridamole infusion. Coronary flow reserve was calculated as the ratio of hyperemic to baseline DPFV. The eNOS 4a/b polymorphism was detected by PCR. Patients with diabetes were excluded from the study. The SCF group was comparable to the control group in terms of demographic and clinical characteristics, except for hemoglobin and HDL-cholesterol levels, TFC of the left anterior descending artery, the circumflex artery, and the right coronary artery; the mean TFC was higher in the SCF group. Hyperemic DPFV and the hyperemic/baseline DPFV ratio were significantly lower in the SCF group when compared with the control group. However, baseline DPFV were similar in both groups. The number of patients with eNOS4 a/a and eNOS4 a/b phenotypes was statistically higher in SCF groups. The frequency of allele 'a' of the eNOS4 gene was also statistically higher in the SCF group. When patients were grouped according to the presence or absence of allele 'a' of the eNOS4 gene, statistically significant differences were found in the TFC of the left anterior descending artery, the circumflex artery; mean TFC; baseline DPFV; and hyperemic/baseline DPFV. Univariate analysis in which eNOS4 b/b was used as the referent group showed that the presence of allele 'a' of the eNOS4 gene significantly predicted SCF (odds ratio: 2.79, 95% confidence interval: 1.32-5.89; P=0.007). In multivariate analysis using a model adjusted for variables with a P value lower than 0.10 in univariate analyses, the presence of allele 'a' of the eNOS4 gene was found to be an independent predictor of SCF (odds ratio: 3.22, 95% confidence interval: 1.28-8.82; P=0.013). The presence of allele 'a' may be a risk factor for microvascular endothelial dysfunction and higher TFCs in SCF patients.

GW24-e0451 Evaluation of myocardial perfusion in patients with coronary slow flow by myocardial contrast echocardiography

ObjectivesTo explore myocardial perfusion of patients with coronary slow flow (CSF) using myocardial contrast echocardiography.MethodsMyocardial contrast echocardiography was performed in coronary artery angiography diagnosed CSF patients (n = 20) and...