Coronary Collateral Development Research Articles

Prognostic Nutritional Index is Associated with the Degree of Coronary Collateral Circulation in Stable Angina Patients with Chronic Total Occlusion.

Coronary collateral circulation (CCC) can effectively improve myocardial blood supply to the area of CTO (chronic total coronary occlusion) and can, thus, improve the prognosis of patients with stable coronary syndrome (SCS). The degree of inflammation and some inflammation markers were associated with the development of collaterals. To investigate whether prognostic nutritional index (PNI) has an association with the development of CCC in patients with SCS. A total of 400 SCS patients with the presence of CTO in at least one major epicardial coronary artery were included in this study. The patients were divided into two groups according to the Rentrop score. Scores of 0 to 1 were considered poor developed CCC, and scores of 2 to 3 were accepted as good developed CCC. Statistical significance was set as a p-value < 0.05 for all analyses. The mean age of the study cohort was 63±10 years; 273 (68.3%) were males. The poor-developed CCC group had a significantly lower PNI level compared with the good-developed CCC group (38.29±5.58 vs 41.23±3.85, p< 0.001). In the multivariate analysis, the PNI (odds ratio 0.870; 95% confidence interval 0.822-0.922; p< 0.001) was an independent predictor of poorly developed CCC. The PNI can be used as one of the independent predictors of CCC formation. It was positively associated with the development of coronary collaterals in SCS patients with CTO.

Effect Of Fibroblast Growth Factor-21 Molecule On Coronary Collateral Development.

Collateral arteries provide an alternative source to myocardium resulting from ischemia due to occlusive coronary artery disease and may help preserve myocardial function in the case of coronary artery disease (CAD)[1]. Although the collateral development is so important, its pathophysiology has not been fully elucidated. Until now, there is no study investigating the relationship between Fibroblast growth factor-21(FGF-21) and coronary collateral. This study aims to investigate the pathophysiology of coronary collateral development. In our study, which we planned as a case control, 60 consecutive patients with ≥90 stenosis in at least one large coronary artery as a result of coronary angiography (CAG) and 30 patients with normal coronary angiography were included in the study cross-sectional. Demographic, echocardiographic and laboratory data were recorded. Coronary collateral circulation was evaluated using the Rentrop-Cohen method [2]. FGF-21 levels were measured in all individuals. In the analysis, no significant difference was observed between the two groups in basic biochemical parameters other than HDL (p>0.05 for all). FGF-21 level was found to be statistically significantly higher in the patient group compared to the control group (p:0.003). Also, FGF-21 level was found to be statistically significantly higher in the good collateral circulation group to the poor collateral circulation group (p:0.006). Univariate and multivariate logistic regression analysis was performed to predict the presence of collateral. We found that FGF-21(p=0.006), C-reactive protein (p=0.020) predicted the presence of collateral independently. Collateral formation and cardiac prognosis are closely related. Our study is the first to investigate the relationship between collateral formation and FGF-21. Our study showed that FGF-21 level is an independent predictor of collateral formation. In addition, there was a significant difference between bad and good collateral formation in terms of FGF-21 levels.

Elevated uric acid/albumin ratio as a predictor of poor coronary collateral circulation development in patients with non-ST segment elevation myocardial infarction.

Uric acid/albumin ratio (UAR) is a novel composite biomarker with superior predictive value for cardiovascular disease. To investigate the relationship between UAR and coronary collateral circulation (CCC) in patients with non-ST segment elevation myocardial infarction (NSTEMI). A total of 205 NSTEMI patients who underwent coronary arteriography with at least one major coronary stenosis, 95% were included. Patients were divided into two groups according to CCC development: poorly-developed CCC group (Rentrop 0-1) and well-developed CCC (Rentrop 2-3). Univariate analysis and logistic regression analysis were utilized to investigate the factors influencing adverse CCC formation in NSTEMI patients. The receiver operating characteristic (ROC) curve was plotted to evaluate the predictive value of UAR, C-reactive protein (CRP), uric acid, and albumin for patients with poorly developed CCC, and the area under the curve (AUC) was compared. The UAR values of NSTEMI patients were significantly higher in the poorly developed CCC group than those in the well-developed CCC group (10.19 [8.80-11.74] vs. 7.79 [6.28-9.55], p < .001). In the multiple logistic regression tests, UAR (odds ratio [OR]: 1.365, 95% confidence interval [CI]: 1.195-1.560, p < .001), CRP (OR: 1.149, 95% CI: 1.072-1.231, p < .001), and diabetes (OR: 2.924, 95% CI: 1.444-5.920, p = .003) were independent predictors of poorly developed CCC. The ROC curve analysis showed that the optimal cut-off value of UAR was 8.78 in predicting poorly developed CCC with a sensitivity of 76.8% and specificity of 62.4%, with the AUC of 0.737 (95% Cl: 0.668-0.805, p < .001). Elevated UAR may be an independent and effective biomarker for predicting poorly-developed CCC development in NSTEMI patients.

Inquiring about the link between urotensin-II and coronary collateral development in coronary artery patients with and without diabetes

Aims: Coronary collateral circulation consists of vascular channels activated to maintain perfusion in major epicardial coronary arteries in severe stenosis or occlusion. Yet, coronary collateral development (CCD) in diabetic patients was previously proven to be poor. Urotesin-II (U-II) is famous for being the most potent vasoconstrictor agent, and plasma levels are known to elevate in diabetic patients and play an important role in diabetic complications. In this study, we inquired about the link between U-II levels and the development of coronary collaterals between diabetic and non-diabetic patients with coronary artery disease (CAD).&#x0D; Methods: We recruited 31 diabetic and 30 non-diabetic patients with 95% or more coronary artery stenosis or occlusion and considered Rentrop’s classification for grading collaterals. In this sense, while Rentrop grades 0-1 are regarded as poor CCD, Rentrop grades 2-3 correspond to well-developed collaterals. Moreover, we compared the patients’ serum levels of U-II by the degree of CCD.&#x0D; Results: The findings revealed that demographic characteristics did not significantly differ between the groups (p &gt;0.05). Although CCD seemed worse in diabetic patients than those without diabetes (DM), the finding was not statistically significant. However, the diabetic patients had significantly higher U-II levels than non-diabetic patients (388.1±314.2 vs. 229.8±216.9, p=0.026). Despite not being significant, U-II levels were higher in patients with poor CCD than those with well-developed collaterals in the non-diabetic group (370.6±298; 178.6±158.3, p=0.2). In the diabetic group, on the other hand, U-II levels were significantly higher in patients with poor CCD and significantly lower in patients with good CCD (582.7±316.4 and 180.4±121.6, respectively; p

Dedifferentiation and Proliferation of Artery Endothelial Cells Drive Coronary Collateral Development in Mice.

Collateral arteries act as natural bypasses which reroute blood flow to ischemic regions and facilitate tissue regeneration. In an injured heart, neonatal artery endothelial cells orchestrate a systematic series of cellular events, which includes their outward migration, proliferation, and coalescence into fully functional collateral arteries. This process, called artery reassembly, aids complete cardiac regeneration in neonatal hearts but is absent in adults. The reason for this age-dependent disparity in artery cell response is completely unknown. In this study, we investigated if regenerative potential of coronary arteries is dictated by their ability to dedifferentiate. Single-cell RNA sequencing of coronary endothelial cells was performed to identify differences in molecular profiles of neonatal and adult endothelial cells in mice. Findings from this in silico analyses were confirmed with in vivo experiments using genetic lineage tracing, whole organ immunostaining, confocal imaging, and cardiac functional assays in mice. Upon coronary occlusion, neonates showed a significant increase in actively cycling artery cells and expressed prominent dedifferentiation markers. Data from in silico pathway analyses and in vivo experiments suggested that upon myocardial infarction, cell cycle reentry of preexisting neonatal artery cells, the subsequent collateral artery formation, and recovery of cardiac function are dependent on arterial VegfR2 (vascular endothelial growth factor receptor-2). This subpopulation of dedifferentiated and proliferating artery cells was absent in nonregenerative postnatal day 7 or adult hearts. These data indicate that adult artery endothelial cells fail to drive collateral artery development due to their limited ability to dedifferentiate and proliferate.

The association of catestatin and endocan with the effects of cardiac shock wave therapy: Biomarker sub-study of the randomized, sham procedure-controlled trial.

Cardiac shock-wave therapy (CSWT) is a non-invasive regenerative treatment method based on low-frequency ultrasound waves, which stimulate angiogenesis. Current data about the effects of revascularization procedures on angiogenesis biomarkers is limited. Recently, an association of catestatin and endocan with coronary collateral development was shown in several trials. In this study, we aimed to evaluate the impact of CSWT on the dynamics of catestatin and endocan levels and to assess their correlation with parameters of myocardial perfusion and function. Prospective, randomized, triple-blind, sham procedure-controlled study enrolled 72 adult subjects who complied with defined inclusion criteria (NCT02339454). We measured biomarkers in 48 patients with stable angina (24 patients of CSWT group, 24 patients of sham-procedure group). Additionally, patients were divided into responders and non-responders according to improvement in myocardial perfusion and/or contractility assessed by myocardial scintigraphy and dobutamine echocardiography (30 and 13 patients, respectively). The blood samples were collected at baseline, after the last treatment procedure (9th treatment week) and at 6-month follow-up to evaluate biomarkers concentration and stored at -80° until analysis. Serum catestatin and endocan levels were determined by commercially available ELISA kits. Serum catestatin concentration significantly increased in all patients. While endocan levels significantly decreased in the responders sub-group. The increase in catestatin levels at 9th week and 6 months was positively associated with improvement in summed difference score (rho = 0.356, p = 0.028) and wall motion score, WMS (rho = 0.397, p = 0.009) at 6 months in the whole study population. Meanwhile, the decrease in endocan levels over 6 months was positively correlated with improvement in WMS at 3- and 6- months (r = 0.378, p = 0.015 and r = 0.311, p = 0.045, respectively). ROC analysis revealed that a change at 6 months in catestatin and endocan levels significantly predicted improvement in myocardial perfusion and contractile function with 68.9% sensitivity and 75.0% specificity (p = 0.039) and 51.7% sensitivity, and 91.7% specificity (p = 0.017), respectively. Baseline endocan concentration and its change at 6 months predicted response to CSWT with 68.8% sensitivity and 83.3% specificity (p = 0.039) and 81.3% sensitivity and 100% specificity (p < 0.0001), respectively. This study demonstrates the association of increase in catestatin and decrease in endocan levels with the improvement of myocardial perfusion and contractile function. The potential predictive value of catestatin and endocan dynamics for the response to regenerative therapy is shown.

Past Myocardial Infarctions and Gender Predict the LVEF Regardless of the Status of Coronary Collaterals: An AI-Informed Research

BACKGROUND: The degree of the development of coronary collaterals is long considered an alternate – that is, a collateral – source of blood supply to an area of the myocardium threatened with vascular ischemia or insufficiency. Hence, the coronary collaterals are beneficial but can also promote harmful (adverse) effects. For instance, the coronary steal effect during the myocardial hyperemia phase and that of restenosis following coronary angioplasty. OBJECTIVES: Our study explores the contribution of coronary collaterals – if any exist – while considering other potential predictors, including demographics and medical history, toward the left ventricular (LV) dysfunction measured through the LV ejection fraction (LVEF). METHODS: Our cross-sectional design study used convenience sampling of 100 patients (n = 100; a male-to-female ratio of 4:1). We conducted frequentist inference statistics using IBM-SPSS version 24 and Microsoft Office Excel 2016 with the analysis ToolPak plugin; we ran parallel neural networks (supervised machine learning (ML)) and a two-step clustering (non-supervised ML) for robust conjoint inference with frequentist statistics. RESULTS: The past incidents of myocardial infarction (p = 0.036) and gender (p = 0.072) influenced the LVEF; both are significant predictors at a 90% confidence interval. We found that gender and past incidents of MI influenced the LVEF regardless of the status of coronary collaterals. Our study did not yield any positive or significant findings concerning the status of coronary collaterals or the coronary circulation dominance patterns. CONCLUSION: Regardless of the status of coronary collaterals, we verified that the female gender is protective of the LV function, contrary to the past infarction incidents that predispose to a deteriorated LV function. Our study’s innovation relates to its status as the first study from India to explore the coronary collaterals and the ejection fraction while incorporating frequentist statistics and narrow artificial intelligence to infer reliable results.

A CASE OF VENTRICULAR SEPTAL RUPTURE AFTER ACUTE MYOCARDIAL INFARCTION

When ventricular septal rupture (VSR) complicates acute myocardial infarction the mortality is usually high. Reperfusion therapy has reduced its incidence. However if VSR has developed then rapid diagnosis, aggressive medical management, and surgical intervention are required to optimize recovery and survival. In the era before reperfusion therapy, septal rupture complicated 1 to 3 percent of acute myocardial infarctions. Among the 41,021 patients in the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) trial, ventricular septal rupture was suspected in 140 patients (0.34 percent) and confirmed by a retrospective review in 84 (0.2 percent). Thus, reperfusion therapy has decreased the incidence of septal rupture. Septal rupture occurs more frequently with anterior wall acute myocardial infarction than other types of acute myocardial infarction. Risk factors for septal rupture included hypertension, advanced age (60 to 69 years), female sex and the absence of a history of angina or myocardial infarction. Angina or previous infarction may lead to myocardial preconditioning as well as to the development of coronary collaterals, both of which reduce the likelihood of septal rupture. In patients undergoing thrombolysis advanced age, female sex, and the absence of smoking are often associated with an increased risk of septal rupture, whereas the absence of antecedent angina has not been associated with an increased risk. In the GUSTO-I trial, there was a nonlinear relation between the systolic and diastolic blood pressures at enrolment and septal rupture, since hypertension and extensive myocardial infarction and right ventricular infarction are also risk factors for septal rupture

Diabetic dyslipidemia impairs coronary collateral formation: An update.

Coronary collateralization is substantially impaired in patients with type 2 diabetes and occlusive coronary artery disease, which leads to aggravated myocardial ischemia and a more dismal prognosis. In a diabetic setting, altered serum lipid profiles and profound glycoxidative modification of lipoprotein particles induce endothelial dysfunction, blunt endothelial progenitor cell response, and severely hamper growth and maturation of collateral vessels. The impact of dyslipidemia and lipid-lowering treatments on coronary collateral formation has become a topic of heightened interest. In this review, we summarized the association of triglyceride-based integrative indexes, hypercholesterolemia, increased Lp(a) with its glycoxidative modification, as well as quantity and quality abnormalities of high-density lipoprotein with impaired collateral formation. We also analyzed the influence of innovative lipid-modifying strategies on coronary collateral development. Therefore, clinical management of diabetic dyslipidemia should take into account of its effect on coronary collateralization in patients with occlusive coronary artery disease.

Effect of obstructive sleep apnoea on coronary collateral vessel development in patients with ST-segment elevation myocardial infarction.

The impact of obstructive sleep apnoea (OSA) in the setting of acute ST-segment elevation myocardial infarction (STEMI) is complex and divergent. This study aimed to investigate the association between OSA and coronary collateral vessel (CCV) development in patients with STEMI. The present study prospectively screened 282 STEMI patients with an overnight sleep study. OSA was defined as apnoea-hypopnoea index (AHI) ≥15 events/h. The coronary angiograms were used for the assessment of Rentrop grades representing CCVs. Among 119 patients enrolled, 60 patients had OSA (50.4%). The prevalence of CCV development (Rentrop grade ≥ 2) was significantly higher in OSA group than in the non-OSA group (43.3% vs. 5.1%, p < 0.001). There was a parallel increase in the Rentrop grades associated with OSA severity and worsening of hypoxaemia indicators (minimum arterial oxygen saturation [SaO2 ], mean SaO2 and time with SaO2 below 90%). After adjustment for clinical and angiographic characteristics, and pre-procedure medications that might interact with OSA, AHI as a continuous variable (OR 1.11, 95% CI 1.08-1.21, p < 0.001) and the presence of OSA (OR 11.41, 95% CI 2.70-48.15, p=0.001) were both associated with dramatically higher incidence of CCV development. Our study demonstrated that the presence of OSA might augment CCV development in STEMI patients. The potential protective effects and mechanisms of OSA in the acute setting of STEMI should be further investigated in larger studies.

Correlation of serum vascular endothelial growth factor and cardiovascular risk factors on collateral formation in patients with acute coronary artery syndrome.

Coronary collaterals serve as an alternative source of blood flow in obstructive coronary heart disease. Coronary collateral development is induced by various angiogenic growth factors, including vascular endothelial growth factor-A (VEGF-A). Cardiovascular risk factors strongly associated with coronary artery disease include age, sex, elevated serum cholesterol, disturbed carbohydrate metabolism, and elevated blood pressure. A better understanding of the effects of these cardiovascular risk factors and serum VEGF-A level on collateral recruitment is necessary for a better prognosis in coronary artery diseases and new insight for further therapeutic promotion of coronary collaterals.220 consecutive patients undergoing coronary angiography with a mean age of 61 ± 9.83 were selected for the analysis. Two milliliters of blood were taken from the patients for analysis. The blood serum VEGF concentration was quantified via the ELISA method. Angiograms and other clinical reports were collected. Significant coronary artery disease was diagnosed in those with ≥ 70% of stenosis in at least one of the coronary arteries. The angiographic and clinical data were documented. The collateral grading was done according to the Rentrop Scoring system. The serum vascular endothelial growth factor level was correlated with the collateral score and cardiovascular risk factors like age, sex, type II diabetes, blood pressure, and cholesterol level. An increase in the level of the collateral score was noted with an increase in the level of VEGF in blood serum. A significant association was founded between serum VEGF level and cardiovascular risk factors on collateral formation in patients with diabetes and hypertension.

The prognostic value of the CHA2DS2-VASc score in coronary collateral circulation and long-term mortality in coronary artery disease.

The CHA2DS2-VASc score is used to determine thromboembolic risk in cases of atrial fibrillation. The predictive value of this score in predicting coronary collateral circulation in chronic total occlusion is unknown. The aim of this study was to investigate the relationship between the CHA2DS2-VASc score and coronary collateral circulation in patients with chronic total occlusion. A total of 189 patients, who underwent coronary angiography and had a chronic total occlusion in at least one coronary artery, were enrolled in this study. The Rentrop scoring system was used for grouping the patients, and patients were classified as having poorly developed coronary collateral circulation (Rentrop grade 0 or 1) or well-developed coronary collateral circulation (Rentrop grade 2 or 3). The CHA2DS2-VASc score of the good coronary collateral circulation group was significantly lower than the other group (3.1±1.7 vs. 3.7±1.7, p=0.021). During the follow-up period, 30 (32.2%) patients in the poorly developed coronary collateral circulation group and 16 (16.7%) patients in the well-developed coronary collateral circulation group died (p=0.028). According to the multivariable Cox regression model, the CHA2DS2-VASc score [hazard ratio (HR): 1.262, p=0.009], heart rate (HR: 1.049, p=0.003), LVEF (HR: 0.975, p=0.039), mean platelet volume (HR: 1.414, p=0.028), and not taking acetylsalicylic acid during admission (HR: 0.514, p=0.042) were independently associated with a higher risk of mortality. The CHA2DS2-VASc score is closely related to coronary collateral development and predicts mortality in patients with chronic total occlusion.

Hemoglobin A1c, Koroner Kronik Total Oklüzyonu Olan Diyabetik Olmayan Hastalarda Zayıf Kollateral Gelişiminin Bir Prediktörüdür: Retrospektif Klinik Çalışma

Objective: Collateral circulation plays an important role for the nutrition of the myocardium in the region of chronic total occlusion (CTO), and affects clinical prognosis. It has been accepted that increased hemoglobin A1c (HbA1c) is a risk factor for cardiovascular events and subclinical atherosclerosis in individuals without diabetes mellitus. In this study, we aimed to reveal the effect of HbA1c level on coronary collateral development in the non-diabetic adult population with CTO. Material and Methods: The study included 208 non-diabetic patients out of 487 patients diagnosed with CTO on coronary angiography between March 2014 and January 2019. The patients were classified into two groups based on the Rentrop classification. Group 1 (Rentrop 0-1) (poor collateral) (90 patients) and Group 2 (Rentrop 2-3) (good collateral) (118 patients). This is a retrospective analysis. Results: The two groups were similar in terms of male gender, age, hypertension and previous history of myocardial infarction (78.9% vs. 75.4%, p=0.557; 58.9±9.9 vs. 60.8±11.2, p=0.194; 26.7% vs. 33.0%, p=0.321; and 18.9% vs. 12.7%, p=0.221; respectively). HbA1c value was statistically higher in Group 1 (5.85±0.45) than in Group 2 (5.22±0.84) (p<0.001). The ideal HbA1c cut-off value was 5.65 that was calculated by the Youden index had 77% sensitivity, and 75% specificity (Receiver operating characteristic area under curve: 0.780, 95% confidence interval: 0.717-0.844, p<0.001) for poor collateral development of CTO. Conclusion: HbA1c is a parameter that affects coronary collateral development even in non-diabetic patients. In non-diabetic patients with CTO, high HbA1c levels correlate with poor collateral development.

Prognostic Nutritional Index as a New Prediction Tool for Coronary Collateral Development.

Nutritional status is a predictor of the prognosis of cardiovascular diseases. The association between the Prognostic Nutritional Index (PNI), which is an immunonutritional parameter, and cardiovascular diseases has been extensively studied in the literature. The aim of this study was to investigate whether PNI is associated with coronary collateral development. This retrospective study included 172 patients with chronic total occlusion. The patients were diagnosed with stable coronary artery disease, and all patients underwent coronary angiography. PNI was calculated using serum albumin level and lymphocyte count. Collateral circulation was classified according to Rentrop grade. There was a positive correlation between PNI and Rentrop grade (r = 0.168, p = 0.026) and a negative correlation between C-reactive protein and PNI (r = -0.353, p < 0.001). Multivariate logistic regression analysis showed that uric acid and PNI were independent predictors of Rentrop grade (p = 0.008 and p = 0.037, respectively). This study showed that PNI, which can easily be calculated using serum albumin level and lymphocyte count, was a predictor of coronary collateral development in terms of Rentrop grade.

Visfatin and 25-Hydroxyvitamin D3 Levels Affect Coronary Collateral Circulation Development in Patients with Chronic Coronary Total Occlusion

Background: Coronary collateral circulation (CCC) plays a vital role in the myocardial blood supply, especially for ischemic myocardium. Evidence suggests that the visfatin and 25-hydroxyvitamin D3 [25(OH)D3] levels are related to the degree and incidence of vascular stenosis associated with coronary artery disease; however, few studies have evaluated the effect of visfatin and 25(OH)D3 on CCC development in patients with chronic total occlusion (CTO). This study aimed to evaluate the relationship between the serum visfatin and 25(OH)D3 levels and CCC in patients with CTO. Methods: A total of 189 patients with CTO confirmed by coronary angiography were included. CCC was graded from 0 to 3 according to the Rentrop-Cohen classification. Patients with grade 0 or grade 1 collateral development were included in the poor CCC group (n=82), whereas patients with grade 2 or grade 3 collateral development were included in the good CCC group (n=107). The serum visfatin and 25(OH)D3 levels were measured by ELISA. Results: The visfatin level was significantly higher in the poor CCC group than in the good CCC group, and the 25(OH)D3 level was significantly lower in the poor CCC group than in the good CCC group (P=0.000). Correlation analysis showed that the Rentrop grade was negatively correlated with the visfatin level (r=−0.692, P=0.000) but positively correlated with the 25(OH)D3 level (r=0.635, P=0.000). Logistic regression analysis showed that the visfatin and 25(OH)D3 levels were independent risk factors for CCC (odds ratio 1.597, 95% confidence interval 1.300–1.961, P=0.000 and odds ratio 0.566, 95% confidence interval 0.444–0.722, P=0.000, respectively). The visfatin and 25(OH)D3 levels can effectively predict the CCC status. Conclusion: Serum visfatin and 25(OH)D3 levels are related to CCC development and are independent predictors of poor CCC.

Monocyte High-Density Lipoprotein cholesterol Ratio and coronary collateral circulation development in patients with stable coronary artery disease and no history of revascularization

Monocyte High-Density Lipoprotein cholesterol Ratio and coronary collateral circulation development in patients with stable coronary artery disease and no history of revascularization

New Research Is Shining Light on How Collateral Arteries Form in the Heart: a Future Therapeutic Direction?

Collateral arteries create artery-artery anastomoses that could serve as natural bypasses that in the heart could relieve the various complications of ischemia heart disease. Recent work using animal models have begun to reveal details of how coronary collateral arteries form. Mouse genetics has been used to study the cellular and molecular mechanisms of collateral artery development. Collateral arteries are not pre-existing in the mouse heart, and only form in response to injury. Myocardial infarction creates tissue hypoxia that triggers the expression of growth factors and chemokines that guide collaterogenesis. Collateral development is more robust in neonatal hearts when compared with adults, and contributes to neonatal heart regeneration. The identification of signaling pathways and cellular responses underlying coronary collateral artery development suggests potential translational strategies. Continued investigation into this subject could lead to the identification of targetable pathways that induce collateral arteries for cardiac revascularization.

Total bilirubin and fasting plasma glucose levels are associated with coronary collateral development in elderly patients

Background and objective: We aimed to investigate biochemical factors affecting coronary collateral circulation development in an elderly population aged 75 years and over. Material and methods: The study group consisted of patients with a prior coronary angiography for stable coronary artery disease (CAD). Patients with total occlusion of at least one vessel were included in the study. Enrolled patients were divided into two groups, good collateral (GC; n = 73) and bad collateral (BC; n = 55), in accordance with the Cohen-Rentop's classification system. Results: In comparison to the GC group, bilirubin levels were significantly lower (p &lt; 0.001), and fasting plasma glucose (FPG) levels were significantly higher in the BC group (p = 0.026). Low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) levels were significantly lower in the BC group when compared to the GC group (p = 0.002 and p &lt; 0.001, respectively). Backward elimination stepwise logistic regression analysis identified bilirubin and FPG as variables that strongly predicted the presence of a well-developed coronary collateral circulation and a poorly developed coronary collateral circulation, respectively. Conclusion: Bilirubin and FPG were seemed as the most important factors affecting coronary collateral circulation development in patients with stable CAD who were older than 75 years.

Dating thrombus organization with eosinophil counts in deep venous thrombosis

ObjectiveIt is known that eosinophils (EOS) are essential for thrombus formation. Studies have demonstrated the association of EOS with coronary artery disease, stent thrombosis, coronary collateral development, and vasospastic angina. However, there is little data about the association of hemogram parameters, especially EOS counts, with deep venous thrombosis (DVT) subgroups. MethodsThe present study comprised 243 patients diagnosed with DVT (of whom 86 were acute, 72 were indeterminate, and 85 were chronic) and 75 control patients. Medical records of all the patients were reviewed, and relevant data were collected retrospectively. The baseline characteristics, as well as hemogram and biochemistry parameters, were recorded. ResultsThe patients with DVT had significantly lower median EOS count yet higher median neutrophil to lymphocyte ratio (NLR) than those of control patients (P < .001). Similarly, acute DVT patients had lower EOS count yet higher NLR values compared with those of indeterminate and chronic DVT patients. However, EOS count was not significantly different between chronic DVT and control groups. While NLR ratio was significantly correlated with acute DVT (r = 0.34; P < .001), Spearman's correlation test revealed that EOS count was inversely correlated with the presence of acute DVT (r = –0.52; P < .001). ConclusionsLow EOS count may lead the physician to a higher probability of acute DVT rather than indeterminate and chronic DVT.

Exercise Training as a Mediator for Enhancing Coronary Collateral Circulation: A Review of the Evidence.

Coronary collateral vessels supply blood to areas of myocardium at risk after arterial occlusion. Flow through these channels is driven by a pressure gradient between the donor and the occluded artery. Concomitant with increased collateral flow is an increase in shear force, a potent stimulus for collateral development (arteriogenesis). Arteriogenesis is self-limiting, often ceasing prematurely when the pressure gradient is reduced by the expanding lumen of the collateral vessel. After the collateral has reached its self-limited maximal conductance, the only way to drive further increases is to re-establish the pressure gradient.During exercise, the myocardial oxygen demand is increased, subsequently increasing coronary flow. Therefore, exercise may represent a means of driving augmented arteriogenesis in patients with stable coronary artery disease. Studies investigating the ability of exercise to drive collateral development in humans are inconsistent. However, these inconsistencies may be due to the heterogeneity of assessment methods used to quantify change. This article summarises current evidence pertaining to the role of exercise in the development of coronary collaterals, highlighting areas of future research.