Mean TIMI Frame Count Research Articles

Effect of sodium-glucose co-transporter-2 inhibitors on coronary blood flow in patients with type 2 diabetes mellitus.

Type 2 diabetes mellitus (T2DM) is known to be associated with endothelial dysfunction (ED). Reducing ED can attenuate the occurrence of cardiovascular diseases. One of the indicators of ED is decreased coronary blood flow (CBF). Sodium-glucose co-transporter 2 inhibitors (SGLT-2is) are known to directly improve ED in both euglycemic and hyperglycemic conditions and have been shown to decrease the incidence of major cardiovascular events. We aimed to investigate whether SGLT-2is improves CBF in patients with T2DM, who have angiographically normal or nearly normal coronary arteries. In this single-center retrospective study, all patients who underwent coronary angiography between January 2017 and September 2022 were screened. We designed the study by dividing the patients into two groups - those who used conventional antidiabetic medications (CAM) together with SGLT-2is (patients using an SGLT-2 inhibitor for at least 3 months) and those who used only conventional antidiabetic medications. Of the 18,205 patients who underwent coronary angiography, 5,040 patients had T2DM. After exclusion, 288 patients were divided into two groups - those who used CAM together with SGLT-2is and those who used only CAM. CBF was assessed by thrombolysis in myocardial infarction (TIMI) frame counting. Two hundred eighty-eight patients who had T2DM and met the inclusion criteria were included in our study. The patients were divided into two groups - those who used CAM together with SGLT-2is (n = 75) and those who used only CAM (n = 213). The median age in the group that used CAM together with SGLT-2is was 55 (51-64), where 52 (69.3%) patients were female. The mean TIMI frame count (TFC) was 23.5 in the group using CAM + SGLT-2is and 27.5 in the group using only CAM. In the multivariable linear regression analysis, the mean TFC was significantly lower in the group using CAM together with SGLT-2is compared to the group using only CAM [β-coefficient = -12.766, 95% Cl: -5.304; -3.887, p < 0.001]. Moreover, there was a statistically significant correlation between an increase in BMI and hemoglobin with an increase in the mean TFC [β-coefficient = 3.018, 95% Cl 0.037-0.175, p = 0.003 and β-coefficient = 2.316, 95% Cl 0.033-0.405, p = 0.021, respectively]. We have demonstrated that the use of SGLT-2is improves coronary artery blood flow in patients with T2DM who have normal or nearly normal coronary angiography.

COMPARISON OF INTRACORONARY EPINEPHRINE TO STANDARD TREATMENTS ALONE FOR REFRACTORY CORONARY NO-REFLOW IN STEMI PATIENTS UNDERGOING PRIMARY PERCUTANEOUS CORONARY INTERVENTION

Refractory no-reflow is a serious primary percutaneous coronary intervention (PPCI) complication in ST-segment elevation myocardial infarction (STEMI) patients associated with worse clinical outcomes. Intracoronary epinephrine has been suggested as a potential adjunctive therapy to improve myocardial perfusion in these patients, but its efficacy and safety remain unclear. This study included 58 STEMI patients with refractory no-reflow during PPCI treated with either intracoronary epinephrine or conventional treatments alone. The primary outcome was the improvement in myocardial perfusion assessed by the TIMI frame count at the end of the procedure. Secondary outcomes included rates of adverse cardiovascular events and clinical outcomes at 30 days. Intracoronary epinephrine was associated with significantly improving myocardial perfusion compared to conventional treatments alone (mean TIMI frame count 24.1 ± 6.7 vs. 33.6 ± 7.9, p &lt; 0.001). This benefit was consistent across all subgroups of patients with TIMI 0-1 flow. Patients treated with intracoronary epinephrine had significantly lower rates of adverse cardiovascular events at 30 days than those who received conventional treatments alone (12.5% vs. 43.8%, p = 0.02). The two groups had no significant differences in major bleeding, recurrent myocardial infarction, or all-cause mortality. Based on the results, the use of intracoronary epinephrine during PPCI in STEMI patients with refractory no-reflow is associated with improved myocardial perfusion and lower rates of adverse cardiovascular events. These findings support the use of intracoronary epinephrine as a safe and effective adjunctive therapy in this population, but further studies are needed to determine optimal dosing and timing of administration.

Predictors of Long-Term Mortality in Patients with Stable Angina Pectoris and Coronary Slow Flow.

Background and Objectives: Coronary slow flow (CSF) is an angiographic phenomenon characterized by the slow progression of an injected contrast agent during diagnostic coronary angiography in the absence of significant stenosis. Although CSF is a common angiographic finding, the long-term outcomes and mortality rates are still unknown. This study aimed to investigate the underlying causes of mortality over a 10-year period in patients diagnosed with stable angina pectoris (SAP) and CSF. Materials and Methods: This study included patients with SAP who underwent coronary angiography from 1 January 2012 to 31 December 2012. All patients displayed CSF despite having angiographically normal coronary arteries. Hypertension (HT), diabetes mellitus (DM), hyperlipidaemia, medication compliance, comorbidities, and laboratory data were recorded at the time of angiography. Thrombolysis in myocardial infarction (TIMI) frame count (TFC) was calculated for each patient. The cardiovascular (CV) and non-CV causes of long-term mortality were assessed. Results: A total of 137 patients with CSF (93 males; mean age: 52.2 ± 9.36 years) were included in this study. Twenty-one patients (15.3%) died within 10 years of follow-up. Nine (7.2%) and 12 (9.4%) patients died of non-CV and CV causes, respectively. Total mortality in patients with CSF was associated with age, HT, discontinuation of medications, and high-density lipoprotein cholesterol (HDL-C) levels. The mean TFC was associated with CV mortality. Conclusion: Patients with CSF exhibited a notable increase in cardiovascular-related and overall mortality rates after 10 years of follow-up. HT, discontinuation of medications, HDL-C levels, and mean TFC were associated with mortality in patients with CSF.

Angiographic Profiles in Persistent Non-Valvular Atrial Fibrillation Patients

Abstract Funding Acknowledgements Type of funding sources: None. OnBehalf Cardiology dept. PGIMER, Chandigarh Background The relationship of atrial fibrillation (AF) with coronary artery disease (CAD) is well established. Atrial ischemia due to obstructive CAD has been identified as one of the key risk factors, leading to AF. However, sufficient evidence exists as to the presence of myocardial ischemia on stress imaging, even without the presence of obstructive CAD in AF patients. Slow flow and coronary tortuosity on angiogram can lead to downstream myocardial ischemia independent of CAD. Purpose We aimed to delineate the angiographic profiles in AF patients with attention to slow flow and tortuosity leading to ischemia in those without obstructive CAD. Methods The study was a nonrandomised, prospective, single-centre observational study of consecutive patients of persistent non valvular AF. Symptomatic patients despite optimal medical therapy (OMT) for 3 months were recruited and all underwent coronary angiograms (CAG). Patients with known CAD or prior history of myocardial infarction were excluded. Further angiographic analysis was done in those without obstructive CAD to determine incidence of slow flow (&amp;gt;27 corrected TIMI frame count) and tortuosity (presence of ≥3 fixed bends in an epicardial artery). Results A total of 70 patients were recruited and followed for a mean duration of 12 ± 1.4 months. The mean age of the study group was 66.07 (±11.49). Hypertension (74%) was the commonest comorbidity followed by obesity (35%) and diabetes (30%). At CAG, 32/70 (46%) had obstructive CAD, 17/70 (24%) had non obstructive (&amp;lt;50-70% stenosis) CAD and 21/70 (30%) had normal coronaries without atherosclerosis. Amongst patients without obstructive CAD (n = 38) slow flow was seen in 16/38 (42%) and coronary tortuosity in 11/38 (29%) patients. There ware no differences in terms of death, HF and FVR hospitalisations or stroke at follow up between the obstructive CAD vs no obstructive CAD. However in patients without obstructive CAD, hospitalisations for FVR was significantly increased in those having slow flow on CAG, 9/12 (75%) vs 7/26 (27%) in those without slow flow (p value = 0.005). The mean TIMI frame count was also significantly higher in those with FVR hospitalisations 35.3 ± 11 vs 25.8 ± 8.9 (p value = 0.005). TIMI frame count &amp;gt;31 had a sensitivity of 83% and a specificity of 69% for predicting hospitalisations for FVR on ROC curve(AUC = 0.71). Conclusions CAD is closely related to AF and majority (70%) of our patients had evidence of atherosclerotic CAD on CAG in our study. A large proportion of patients with no evidence of obstructive CAD on CAG had slow flow or coronary tortuosity. Significantly increased hospitalisation for FVR seen in the slow flow group shows its significance and may lead to newer treatment modalities in future. Further larger studies looking at these aspects on CAG may give further insight as to the nature and prognosis of these entities. Abstract Figure 1: Flow diagram showing the patie

Prolonged P Wave Peak Time May Be a Sign of LV Diastolic Dysfunction in the Coronary Slow Flow Phenomenon.

Background The coronary slow flow phenomenon (CSFP) is an atherosclerotic process that causes ischemia at the microvascular level. The CSFP may affect P wave durations, especially P wave peak time (PWPT), by microvascular ischemia, left ventricular diastolic dysfunction, and changes in the left atrial dimension. Therefore, in the present study, we aimed to assess PWPT in the CSFP. Method One hundred and ninety-five patients were included in this single-center, retrospective study. Ninety patients were enrolled in the CSFP group and 105 patients in the control group. PWPT was defined as the duration between the beginning and peak of the p wave and obtained from the leads Dıı and Vı. Results The mean age of the study population was 48.5 ± 9.5, and 108 (55.3%) of the patients were female. We found PWPT was longer in the CSFP group than in the control group. Correlation analysis showed a positive correlation between PWPT in both leads (DII, Vı) and left atrial anterior-posterior diameter, mean TIMI frame count (TFC), and E/e. A significant relationship was observed between mean TFC, E/e, EF, heart rate, and PWPT in lead Dıı (β coefficient = 0.33, 95% CI 0.44–1.33, p < 0.001, β coefficient = 0.23, 95% CI 0.25–1.85, p=0.01, β coefficient = -0.140, 95% CI −1.04–−0.53, p=0.03, and β coefficient = −0.13, 95% CI −0.29–−0.014, p=0.03, respectively) in multivariable linear analysis. Conclusion In the present study, we found prolonged PWPT in patients with the CSFP and found a relationship between PWPT and mean TFC.

Angiographic profiles in patients of persistent non-valvular atrial fibrillation from a tertiary care center in north india

Abstract Funding Acknowledgements Type of funding sources: None. Background The relationship of atrial fibrillation (AF) with coronary artery disease (CAD) is well established. Atrial ischemia due to obstructive CAD has been identified as one of the key risk factors, leading to AF. However, sufficient evidence exists as to the presence of myocardial ischemia on stress imaging, even without the presence of obstructive CAD in AF patients. Slow flow and coronary tortuosity on angiogram can lead to downstream myocardial ischemia independent of CAD. Purpose We aimed to delineate the angiographic profiles in AF patients with attention to slow flow and tortuosity leading to ischemia in those without obstructive CAD. Methods The study was a nonrandomised, prospective, single-centre observational study of consecutive patients of persistent non valvular AF. Symptomatic patients despite optimal medical therapy (OMT) for 3 months were recruited and all underwent coronary angiograms (CAG). Patients with known CAD or prior history of myocardial infarction were excluded. Further angiographic analysis was done in those without obstructive CAD to determine incidence of slow flow (&amp;gt;27 corrected TIMI frame count) and tortuosity (presence of ≥3 fixed bends in an epicardial artery). Results A total of 70 patients were recruited and followed for a mean duration of 12 ± 1.4 months. The mean age of the study group was 66.07 (±11.49). Hypertension (74%) was the commonest comorbidity followed by obesity (35%) and diabetes (30%). At CAG, 32/70 (45%) had obstructive CAD, 17/70 (24%) had non obstructive (&amp;lt;50-70% stenosis) CAD and 21/70 (30%) had normal coronaries without atherosclerosis. Amongst patients without obstructive CAD (n = 38) slow flow was seen in 16/38 (42%) and coronary tortuosity in 11/38 (29%) patients. There ware no differences in terms of death, HF and FVR hospitalisations or stroke at follow up between the obstructive CAD vs no obstructive CAD. However in patients without obstructive CAD, hospitalisations for FVR was significantly increased in those having slow flow on CAG, 9/12 (75%) vs 7/26 (27%) in those without slow flow (p value = 0.005). The mean TIMI frame count was also significantly higher in those with FVR hospitalisations 35.3 ± 11 vs 25.8 ± 8.9 (p value = 0.005). TIMI frame count &amp;gt;31 had a sensitivity of 83% and a specificity of 69% for predicting hospitalisations for FVR on ROC curve(AUC = 0.71). Conclusions CAD is closely related to AF and majority (70%) of our patients had evidence of atherosclerotic CAD on CAG in our study. A large proportion of patients with no evidence of obstructive CAD on CAG had slow flow or coronary tortuosity. Significantly increased hospitalisation for FVR seen in the slow flow group shows its significance and may lead to newer treatment modalities in future. Further larger studies looking at these aspects on CAG may give further insight as to the nature and prognosis of these entities.

Eosinophil cationic protein: A new diagnostic biomarker in coronary slow flow phenomenon.

This study has investigated the role of eosinophil cationic protein (ECP), released by eosinophils, in the coronary slow flow phenomenon. This study included sixty patients with coronary slow flow (CSF) and sixty patients with normal coronary flow. The coronary flow rate was evaluated with TIMI frame count (TFC). ECP level, blood count and biochemical parameters were assessed. The ECP levels (18.9±7.5 vs 13.1±6.4 ng/ml, p<0.001) and eosinophil counts (0.25±0.14 vs 0.18±0.09 10³/mm³, p=0.001) were higher in the CSF group. Multivariable regression analysis showed that ECP level and eosinophil counts were independent predictors the presence of CSF (p=0.003 and p=0.006). There was a weak but important correlation among the ECP level, eosinophil count and mean TFC (p=0.001, p=0.003, respectively). The ROC analysis showed a cut off value of 14.05 ng/ml for ECP level to diagnose CSF with 73.3 % sensitivity and 66.7 % specificity, and area under the ROC curve was 0.745 (95% CI: 0.657-0.833, p<0.001). ECP levels were increased in CSF patients and this increasing correlated with coronary artery flow rates. The ECP level was independent predictor for the presence of SCF and it may be use as suitable diagnostic biomarker for CSF (Tab. 3, Fig. 3, Ref. 30).

Intracoronary Versus Intravenous Administration of Eptifibatide During Percutaneous Coronary Intervention in Patients With Acute Coronary Syndromes

Platelet activation and aggregation play a major role in thrombosis formation of coronary arteries in patients with Acute Coronary Syndrome (ACS) and is responsible for most ischemic complications during PCI. There is little information on the benefits and side effects of intracoronary and intravenous injection of Eptifibatide, a potent antiplatelet agent; therefore, this study was performed with the aim to compare coronary blood flow velocity by measurement of TIMI frame count. In intravenous versus intracoronary bolus administration of Eptifibatide during PCI in ACS patients. This non-randomized clinical trial study was performed on 103 patients with acute coronary syndromes who referred to the cardiac emergency ward of Ghaem hospital, Mashhad University of Medical Sciences, and were candidates for urgent coronary angiography and PCI. Forty-eight cases received intracoronary bolus Eptifibatide and 55 intravenous Eptifibatide. TIMI Frame Count and Corrected TIMI Frame Count were used to comparing the effect of these two methods on coronary blood flow velocity. Data were analyzed by SPSS software (version 22). To compare the quantitative variables in the two groups, according to the distribution of variables, the t-test was used if it was normal or the Mann-Whitney test was used if it was not normal. A Chi-square test was also used to compare qualitative variables into two groups. P&lt;0.05 was considered statistically significant. Mean of age, gender, and cardiovascular risk factors were similar in the two groups. There was no significant difference in terms of serum Creatine Kinase MB (CKMB) level, Left Ventricular Ejection Fraction (LVEF), coronary artery lesion length, coronary artery diameter, coronary thrombosis, and coronary artery thrombectomy in two groups. Based on Student's t-test, there was no significant difference between mean TIMI Frame Count in different coronary arteries in the intracoronary and intravenous injection groups (In LAD, P=0.518; For LCX, P=0.576; and in RCA, P=0.964). The complications were observed in 11 patients (22.9%) of the intracoronary injection group and 9 (16.4%) of the intravenous injection group; the difference was not significant (P=0.402). The effects and complications of Eptifibatide were not significantly different in Intracoronary and intravenous administration in ACS patients during PCI and at the time of patients' hospitalization.

Coronary Slow Flow Phenomenon: The Role of New Echo cardiographic Indices

Abstract Background: The Coronary Slow Flow Phenomenon (CSFP) is defined as a delayed distal vessel contrast opacifi-cation in the absence of obstructive epicardial coronary artery disease during coronary angiography. There is conflicting data in medical literature regarding the effects of CSFP on the left ventricular functions assessed by conventional echocar-diography or tissue Doppler imaging. Aim of Study: To evaluate whether there is impairement of Global Longitudinal Strain (GLS) of the Left Ventricle (LV) obtained by Speckle Tracking Echocardiography (STE) in patients with CSFP and the role of GLS of the left ventricle in prediction of CSFP. Patients and Methods: Patients with chronic stable angina referred for coronary angiography from February 2015 to Augusts 2017 at the Department of Cardiology, Faculty of Medicine; Zagazig University Hospitals were examined. 31 patients with CSFP and 52 age and sex matched controls without CSFP were enrolled in the study. Diagnosis of CSFP was made by TIMI Frame Count (TFC). GLS of LV was measured by two dimensional (2D) STE in addition to other conventional and tissue Doppler parameters to assess LV diastolic and systolic functions. Results: LV GLS was lower in CSFP group patients (–15 ±2.73) compared to control group (–17.19±2.54) (p=0.001). There was statistically significant negative correlation between mean TFC and LV GLS (r=–0.33, p=0.002). LVEF by modified Simpson method was lower in CSFP group (57.77±5.66%) compared to control group (59.29±3.32%) but with no statis-tical significance (p=0.18). Left atrial diameter, LAVI were larger in CSFP group compared to control group (p < 0.05). MV E/Ep and TV E/Ep was higher in CSFP group compared to control group (p < 0.001). Smoking was the only risk factors that showed statistical significance being more common in CSFP patients (p=0.003) with positive correlation between mean TFC and smoking index (r=0.28, p=0.002). Conclusion: CSFP impaires LV systolic and diastolic function, RV diastolic function. We found significant negative correlation between mean TFC and GLS of LV.

Relationship between plasma miR-126 and coronary slow flow phenomenon

Objective: To investigate the relationship between miR-126 in plasma and coronary slow flow (CSF) phenomenon. Methods: A total of 109 patients without coronary artery disease who underwent coronary angiography at Beijing Anzhen Hospital Affiliated to Capital Medical University from August 2016 to March 2018 were enrolled. The patients were divided into CSF groups (53 cases) and the control group (56 cases) according to CSF existing or not. Clinical data and blood samples of the participants in two groups were collected. Real-time quantitative PCR (RT-qPCR) was used to determine the expression of miR-126 in plasma, and the relationship between miR-126 and CSF and its predictive effect were analyzed. Results: Mean TIMI frame counts (34±4 vs 20±3), left anterior descending TIMI frame counts (35±5 vs 21±3), left gyroscopic TIMI frame counts (36±5 vs 20±3), right coronary TIMI frame counts (34±5 vs 20±35) and expression level of hypersensitive C-reactive protein (hs-CRP, (3.0±1.2) mg/L vs (2.1±0.9) mg/L) and plasma miR-126 (0.25±0.09 vs 0.19±0.10) of the CSF group were significantly higher than those of the control group (P<0.05). Correlation analysis showed that miR-126 and hs-CRP levels were significantly correlated with mean TIMI frame count (r=0.367, P<0.05), and miR-126 was also significantly associated with the hs-CRP level (r=0.388, P<0.05). Logistic regression analysis showed that miR-126 (OR=2.513) and hs-CRP (OR=1.568) were independent risk factors for coronary slow flow. The area under the ROC curve of miR-126 predicting for CSF was 0.661. When the cutoff value was set at 0.225, the Youden index reached the maximum with a sensitivity of 0.660 and a specificity of 0.714. Conclusion: The expression level of miR-126 in plasma is significantly correlated with CSF, and miR-126 can be used as a predictor of coronary slow flow phenomenon.

Low Serum Adropin Levels are Associated with Coronary Slow Flow Phenomenon.

Adropin is a peptide hormone expressed in coronary artery endothelial cells, which plays a potential endothelial protective role. We sought to assess whether serum adropin levels are correlated with the coronary slow flow phenomenon (CSFP). We enrolled 82 patients with angiographically confirmed CSFP and 184 age-matched controls. Serum adropin levels were measured by enzyme-linked immunosorbent assay (ELISA), and coronary flow rate was assessed using thrombolysis in myocardial infarction (TIMI) frame count (TFC). CSFP was defined as a corrected TIMI-TFC greater than two standard deviations from the normal range. Serum adropin levels were significantly lower in the CSFP patients (n = 82) than in the controls (n = 184) (4.03 ± 1.99 vs. 4.86 ± 1.88 ng/ml, p = 0.001). Multivariate logistic regression analysis revealed that serum adropin was the only independent negative predictor of CSFP (odds ratio 0.758, 95% confidence interval 0.647-0.888, p = 0.001). Serum adropin levels were independently and negatively correlated with mean TFC (r = -0.387, p < 0.001). We demonstrated that decreased serum adropin levels were independently associated with the presence and severity of angiographically proven CSFP. These findings suggest that serum adropin may be a potential biomarker to provide valuable information regarding the prediction of CSFP.

Effect of fibrillatory wave amplitude on coronary blood flow as assessed by thrombolysis in myocardial infarction frame count in patients with atrial fibrillation.

Atrial fibrillation (AF) is the most common arrhythmia, characterized by a lack of atrial contraction and an irregular ventricular rhythm. We assessed the effect of fibrillatory wave amplitude on coronary blood flow in patients with AF using the thrombolysis in myocardial infarction (TIMI) frame count. Sixty-one patients with AF persisting for longer than 30days were included. For controls, 61 age- and sex-matched patients with sinus rhythm were selected. Coarse AF was defined as any fibrillatory wave≥1mm and fine AF as any fibrillatory wave<1mm. Mean TIMI frame count was significantly higher in patients with AF than in those with sinus rhythm (18±4 vs 30±11, p<0.001). Multivariate analysis showed that AF was the only determinant of mean TIMI frame count (β=0.48, p<0.001). Among patients with AF, 32 had coarse AF and 29 had fine AF. Left atrial volume index (54±14 vs 64±21ml/m2, p=0.03) was significantly larger, and mean TIMI frame count (26±7 vs 35±12, p<0.001) was significantly higher in patients with fine AF than in those with coarse AF. Multivariate analysis showed that hypertension (β=-0.29, p=0.01) and a fine fibrillatory wave (β=0.33, p=0.007) were determinants of mean TIMI frame count. Our data suggest that coronary blood flow is reduced in patients with AF compared with those with sinus rhythm, and that a fine fibrillatory wave is a major determinant of reduced coronary blood flow in patients with AF.

Relationship Between Angiographic Coronary Slow Flow Phenomenon and Subfoveal Choroidal Thickness: What is The Effect of Atorvastatin Therapy?

Objective: Although the pathophysiological mechanisms underlying coronary slow flow (CSF) phenomenon still remains uncertain, the microvascular dysfunction has been first implicated. The CSF phenomenon may not only affect the coronary arteries but it may also be a part of vascular problem that affect other arteries. The aim of the present study is to evaluate the relationship between CSF phenomenon and subfoveal choroidal thickness (SFCT) and to investigate the effect of short-term atorvastatin therapy on SFCT in patients with CSF. Methods: The study population consisted of 48 patients with CSF and 41 healthy control participants. Coronary flow patterns of the patients were determined by thrombolysis in myocardial infarction (TIMI) frame count method. Spectral-domain optical coherence tomography (SD-OCT) measurements of SFCT and lipid parameters were obtained before and after 2 weeks of daily single dose of 80 mg atorvastatin therapy. Results: We found that patients with CSF had thinner SFCT compared with control group. There was a significant negative correlation between mean TIMI frame count and baseline SFCT (r=-0.69, p=0.001). ROC curve analysis revealed that SFCT <259 m predicted CSF with a 85% sensitivity and 88% specificity. The SFCT significantly increased after the short-term atorvastatin therapy. Conclusion: There was a close negative correlation between CSF phenomenon and SFCT. Endothelial dysfunction (ED) and the resultant microvascular dysfunction might be operative on both coronary and ocular choriocapillary arteries in patients with CSF. Increase of SFCT after the short-term atorvastatin therapy might be an indicator of microvascular dysfunction improvement in patients with CSF.

Characteristics of coronary microcirculatory function in patients with Takotsubo syndrome.

Takotsubo syndrome (TS) is a recently described cardiac syndrome whose pathogenesis is still unclear. We investigated the characteristics of coronary microcirculatory function in patients with TS through the analysis of the TIMI frame count (TFC) compared to normal subjects and with to subjects with microvascular angina (MA). We enrolled 71 TS patients (F:M =69:2, mean age of 65.27±9.53 years), 70 controls (F:M =34:36, mean age of 56.63±13.5 years) and 71 patients with MA, (F:M =69:2, mean age of 65.9±9.2 years). The assessment of the microcirculation was carried out through the TFC. microcirculation was significantly altered in patients with TS compared with healthy controls [left anterior descending coronary artery (LAD) 25.16±6.91 vs. 17.30±3.76, P<0.001; circumflex artery (CX) 25.48±6.10 vs. 17.05±4.60, P<0.001; right coronary artery (RCA) 26.43±8.95 vs. 15.74±4.27, P<0.001, average TFC in TS 25.70±5.34 vs. 16,70±3.26, P<0.001). A TFC >20 frames was able to discriminate TS patients from controls with a specificity of 88.57% and sensitivity of 85.92% (AUC 0.927, P<0.0001). Microvascular dysfunction was diffuse in TS as well as in MA and slightly more severe in this last (mean TFC in MA 28.25±9.3 vs. 25.7±5.34 in TS, P<0.046). Coronary microcirculation in TS patients is diffuse and milder compared to MA patients. Cut-off values >20 frames discriminate between patients with normal microcirculation and patients with TS.

Evaluation of ghrelin levels and endothelial functions in patients with coronary slow flowphenomenon.

BackgroundGhrelin has recently been reported to have beneficial effects on cardiac contractile functions and coronary blood flow. The main purpose of this study was to investigate the role of ghrelin in the pathogenesis of coronary slow flow (CSF) together with endothelial functions.MethodsTwenty-five patients having normal coronary arteries with CSF and 25 controls with normal coronary flow were included into the study. The quantitative measurement of coronary blood flow was performed for each coronary artery using the thrombolysis in myocardial infarction (TIMI) frame count (TFC) method. Ghrelin levels were measured using the enzyme-linked immunosorbent assay method from venous blood samples. Endothelial functions were evaluated from the brachial artery with the flow-mediated dilation (FMD) and nitrate-related dilation methods.ResultsThere was a significant difference in terms of mean TFC values between the control and CSF groups (p < 0.001 for all coronary arteries). The mean FMD percentage among patients with CSF was lower than that of the control group (5.9 ± 0.8 vs. 10.7% ± 1.1%; p < 0.001). A moderate negative correlation was observed between the FMD percentages and the TFCs. There was no relationship between the TFC and ghrelin levels.ConclusionPlasma ghrelin levels seem to be uninfluential while impaired endothelial functions play an important role in the etiopathogenesis of CSF.

Evaluation of Plasma Thrombomodulin in Patients with Coronary Slow Flow

Background: It has been reported that coronary slow flow (CSF) is associated with acute myocardial infarction, ventricular tachycardia, ventricular fibrillation, and even sudden cardiac death. Although studies concerning the etiopathogenesis of CSF are scarce, diffuse atherosclerosis and endothelial dysfunction are thought to play important roles. It has been suggested that a high plasma thrombomodulin (TM) level seems to play an important role in the pathogenesis of atherosclerosis and endothelial dysfunction. Objectives: We hypothesized that a high plasma TM level might be associated with CSF and aimed to research the relationship between plasma TM level and CSF. Methods: Fifty-two CSF patients with angiographically proven CSF and 44 cases with normal coronary flow were included in this study. Coronary flow velocity was determined by the thrombolysis in myocardial infarction (TIMI) frame count method. Plasma TM levels were measured in all the study subjects. Results: Plasma TM levels were significantly higher in the CSF group compared to the control group (3.9 ± 0.5 vs. 3.6 ± 0.3 ng/mL, p = 0.01). There was a positive relationship (r = 0.31, p = 0.002) between plasma TM level and mean TIMI frame count (TFC). Factors associated with mean TFC were plasma TM level (β = 0.206, p = 0.038) and red cell distribution width (β = 0.088, p = 0.009) in multiple linear regression analysis. Conclusions: Patients with CSF have a higher plasma TM level, and this may play an important role in the pathogenesis of CSF. An elevated plasma TM level may be a predictor of CSF. Future studies are needed to confirm these results.

Impaired coronary blood flow may be related to elevated homocysteine levels in patients with metabolic syndrome.

Metabolic syndrome (MS) refers to a group of cardiovascular risk factors associated with endothelial dysfunction and impaired coronary blood flow (CBF). Homocysteine (Hcy) is another risk factor for the development of insulin resistance and endothelial dysfunction. However, the relationship between Hcy levels and CBF in patients with MS has not been investigated specifically. In the present study, we aimed to evaluate the relationship between Hcy levels and CBF in MS patients with normal coronary arteries. The study population included 36 patients with MS (20 males, 16 females; mean age = 55 ± 9 years) and 36 control subjects (20 males, 16 females; mean age = 51 ± 7 years). All subjects had angiographically proven normal coronary arteries. Plasma Hcy concentrations were evaluated after a fast of 12 h or longer. The CBF rates of all subjects were documented by the thrombolysis in myocardial infarction (TIMI) frame count method. The TIMI frame counts for each major epicardial coronary artery and mean TIMI frame count were found to be significantly higher in the MS group compared with the control group (left anterior descending coronary artery (LAD): 53 ± 26 vs. 39 ± 17; p = 0.01, left circumflex artery (LCx): 32 ± 12 vs. 26 ± 11; p = 0.01, right coronary artery (RCA): 33 ± 14 vs. 26 ± 12; p = 0.02, mean TIMI frame count: 39 ± 16 vs. 20 ± 12; p = 0.01). Plasma Hcy levels in patients with MS were significantly higher compared with controls (MS group = 11.6 ± 4 and control group = 9.6 ± 2.6; p = 0.01). Additionally, plasma Hcy levels were positively correlated with each calculated TIMI frame count value in the MS group (LAD, r: 0.28 and p = 0.006; LCx, r: 0.25 and p = 0.022; RCA, r: 0.26 and p = 0.042; mean TIMI frame count, r: 0.28 and p = 0.004). Plasma Hcy levels and TIMI frame counts were significantly higher in patients with MS. Impaired CBF in MS may be related to elevated levels of Hcy, even if Hcy levels are normal.

Assessment of the relationship between a narrow fragmented QRS complex and coronary slow flow.

The coronary slow flow (CSF) phenomenon is a delayed antegrade progression of contrast agent to the distal branch of a coronary artery in the absence of obstructive coronary artery disease (CAD). A narrow fragmented QRS (fQRS) has been reported as a significant predictor of sudden cardiac death in patients with idiopathic dilated cardiomyopathy. The present study aimed to investigate the relationship between a narrow fQRS on the admission electrocardiogram (ECG) and CSF on coronary angiography. This study included 165 consecutive patients (112 CSF, 53 controls) who underwent first-time diagnostic conventional coronary angiography for suspected CAD. Coronary flow was quantified by thrombolysis in myocardial infarction (TIMI) frame count (TFC). The patients were divided into two groups according to the presence or absence of a narrow fQRS complex on the admission ECG. Forty four patients were in the fQRS group (mean age, 52.97 ± 3.13 years). There was no difference between the two groups with respect to age, gender, body mass index, family history, hyperlipidemia, hypertension, or diabetes mellitus. The extent of CSF was significantly greater in the fQRS group compared to the non-fragmented group (p < 0.001). A significant correlation was also found between mean TFC values and fQRS (p < 0.001). On multivariate analysis, only CSF (p = 0.03) was a significant independent predictor for narrow fQRS, after adjustment for other parameters. The narrow fQRS is a simple, inexpensive, and readily available noninvasive ECG parameter that may be a new potential indicator of myocardial damage in patients with CSF.

Assessment of left and right ventricular diastolic and systolic functions using two-dimensional speckle-tracking echocardiography in patients with coronary slow-flow phenomenon.

ObjectiveCoronary slow-flow phenomenon (CSFP) is an angiographic diagnosis characterised by a low rate of flow of contrast agent in the normal or near-normal epicardial coronary arteries. Many of the patients with CSFP may experience recurrent acute coronary syndromes. However, current clinical practice tends to underestimate the impact of CSFP due to the yet unknown effect on the cardiac function. This study was performed to evaluate left ventricular (LV) and right ventricular (RV) diastolic and systolic functions, using two-dimensional (2D) longitudinal strain and strain rate, in patients with CSFP, and to determine the relationships between the thrombolysis in myocardial infarction (TIMI) frame count (TFC) and LV and RV diastolic and systolic functions.MethodsSixty-three patients with CSFP and 45 age- and sex-matched controls without CSFP were enrolled in the study. Diagnosis of CSFP was made by TFC. LV and RV diastolic and systolic functions were assessed by 2D speckle-tracking echocardiography.ResultsLV peak early diastolic longitudinal strain rate (LSRe) was lower in patients with CSFP than in controls (P = 0.01). LV peak systolic longitudinal strain (LS) and LV peak systolic longitudinal strain rate (LSRs) were lower in patients with CSFP than in controls (P = 0.004 and P = 0.03, respectively). There was no difference in LV ejection fraction. RV peak early diastolic longitudinal strain rate (RSRe) was lower in patients with CSFP than in controls (P = 0.03). There were no differences in RV peak systolic longitudinal strain (RS), RV peak systolic longitudinal strain rate (RSRs), or RV fractional area change among the groups. The mean TFC correlated negatively with LSRe and RSRe in patients with CSFP (r = −0.26, P = 0.04 and r = −0.32, P = 0.01, respectively).ConclusionsLV diastolic and systolic functions were impaired in patients with CSFP. CSFP also affected RV diastolic function, but not RV systolic function.

Relationship between Serum Uric Acid and Coronary Blood Flow in Patients with Atrial Fibrillation

Objectives: Atrial Fibrillation (AF) is associated with impaired coronary flow by means of Thrombolysis in Myocardial Infarction (TIMI) Frame Count (TFC). The Serum Uric Acid (SUA) level is elevated in patients with AF. In the present study we aimed to investigate the relationship between serum uric acid and TFC in patients with AF in the absence of obstructive Coronary Artery Disease (CAD). Methods: This observational study enrolled 185 AF patients and 189 control subjects, all with angiographically documented normal coronary arteries. Serum uric acid was measured at baseline and mean TFC was assessed after diagnostic coronary angiography. Results: The SUA was 6.3 ± 1.0 mg in the AF group and 4.9 ± 1.1 mg in the control group (p<0.001). In AF patients,SUA was significantly correlated with mean TFC (r=0.477, p<0.001). In linear regression analysis, SUA and low-density lipoprotein were found to be independently associated with mean TFC (p<0.001 and p<0.05 respectively). Conclusion: Serum uric acid seems to be independently associated with coronary blood flow in patients with atrial fibrillation in the absence of obstructive coronary artery disease.