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Andrew D Blann

Publications and source records attributed to Andrew D Blann.

At least 19 recordsLinked to original sources
PubMed2006

Circulating endothelial cells in cardiovascular disease.

Quantification of circulating endothelial cells (CECs) in peripheral blood is developing as a novel and reproducible method of assessing endothelial damage/dysfunction. The CECs are thought to be mature cells that have detached from the intimal monolayer in response to endothelial injury and are a different cell population to endothelial progenitor cells (EPCs). The EPCs are nonleukocytes derived from the bone marrow that are believed to have proliferative potential and may be important in vascular regeneration. Currently accepted methods of CEC quantification include the use of immunomagnetic bead separation (with cell counting under fluorescence microscopy) and flow cytometry. Several recent studies have shown increased numbers of CECs in cardiovascular disease and its risk factors, such as unstable angina, acute myocardial infarction, stroke, diabetes mellitus, and critical limb ischemia, but no change in stable intermittent claudication, essential hypertension, or atrial fibrillation. Furthermore, CEC quantification at 48 h after acute myocardial infarction has been shown to be an accurate predictor of major adverse coronary events and death at both 1 month and 1 year. This article presents an overview of the pathophysiology of CECs in the setting of cardiovascular disease and a brief comparison with EPCs.

Cardiovascular Diseases↗
PubMed2006

Changes in plasma vascular endothelial growth factor, angiopoietins, and their receptors following surgery for breast cancer.

BACKGROUND: Vascular endothelial growth factor (VEGF), a major angiogenic growth factor, is involved in the pathogenesis of cancer. Plasma VEGF is raised in breast cancer and falls after successful surgery. Less is known about angiopoietins 1 and 2 (Ang-1, Ang-2). All three growth factors act on cells via receptors; Flt-1 for VEGF and Tie-2 for the angiopoietins. Cancer is also marked by abnormalities in platelet activation (marked by soluble P selectin) and inflammation (interleukin-6 [IL6]). We hypothesised altered plasma Ang-1, Ang-2, Flt-1 and Tie-2 in breast cancer that would normalize after 3 and 12 months treatment (i.e., surgery plus chemo/radiotherapy). METHODS: Baseline venous blood was obtained from 40 women with breast cancer and 30 age-matched women with benign breast disease (BBD) also requiring surgery. Samples were taken again 3 months and 1 year later. Soluble P selectin, IL6, VEGF, Ang-1, Ang-2, Flt-1 and Tie-2 were measured in citrated plasma by ELISA. RESULTS: Women with breast cancer had raised VEGF (7-fold), Ang-1 (50% higher) and Tie-2 (2-fold), but lower Flt-1 (to 26%), compared to the BBD women that broadly correlated with markers of platelet activation and inflammation. A level of Tie-2 or VEGF >95th percentile of the BBD group correctly identified 68% and 52% of the women with breast cancer. After 3 months of treatment, VEGF and Ang-1 normalized (as did IL6 and soluble P selectin) but Tie-2 was significantly lower only after 1 year. There were no significant changes in the women with BBD. CONCLUSIONS: Treatment for breast cancer (surgery followed by chemotherapy and/or radiotherapy) is effective in reducing plasma VEGF, Tie-2 and Ang-1. These may be linked pathogenically with coagulation and inflammation.

Aged↗
PubMed2006

Circulating endothelial cells and endothelial progenitor cells: two sides of the same coin, or two different coins?

Circulating endothelial cells (CECs) and endothelial progenitor cells (EPCs) are two populations of recently discovered endothelioid cells present in the blood. The former are thought to arise from the intima, the latter from the bone marrow. However, it is becoming clear that these are not in fact homogenous populations (e.g. differing degrees of apoptosis, necrosis and viability, differing expression of monocyte markers) but do in fact represent more than one species of endothelioid cell. Thus whilst originally defined by different criteria (e.g. CD146 by immunobeads, CD34 by flow cytometry) and the perception of independence, there is also growing evidence of some degree of commonality, i.e. some cells co-expressing CD146 and CD34. Furthermore, relationships between these two cells types and, for example, plasma and physiological indicators of vascular damage, and the risk factors for atherosclerosis, suggest a potential role for these cells in the pathophysiology of this disease, possibly as markers. The current document reviews this evidence, presenting a view of some degree of shared ancestry that may have implications for pathophysiology and cell biology.

Antigens, CD34↗
PubMed2006

Endothelial activation, dysfunction, and damage in congestive heart failure and the relation to brain natriuretic peptide and outcomes.

Congestive heart failure (CHF) is associated with marked endothelial dysfunction. We hypothesized that acute and chronic CHF may manifest different degrees of endothelial damage/dysfunction and activation, as reflected by different plasma endothelial markers, such as von Willebrand factor (vWF) and soluble thrombomodulin (both are indexes of endothelial damage/dysfunction) and soluble E-selectin (an index of endothelial activation). Second, we hypothesized a relation between endothelial markers and B-type natriuretic peptide (BNP, an index of cardiac function) in acute and chronic CHF that could be linked to prognosis. To test this hypothesis, we studied 35 patients with acute CHF, 40 patients with chronic CHF, and 32 healthy controls. The patients with CHF were followed up for the combined outcomes of cardiovascular death, nonfatal myocardial infarction, stroke, thromboembolism, and recurrent admissions to the hospital. vWF (p = 0.001), soluble thrombomodulin, E-selectin, and BNP (all p <0.0001) were higher in patients with acute and chronic CHF compared with controls. When the 2 CHF groups were compared, no significant differences were found in vWF or E-selectin (p = NS), but soluble thrombomodulin was significantly elevated in acute CHF (Tukey's post hoc test, p <0.05). Only high vWF was associated with a poorer outcome (log-rank test, p = 0.0188). None of the endothelial indexes correlated with plasma BNP. After a median follow-up of 18 months, only high (median or higher) vWF levels were predictive of adverse outcomes in the patients with CHF (log-rank statistic = 5.52, degree of freedom 1, p = 0.0188). In conclusion, despite similar ejection fractions, patients with acute and chronic CHF have different degrees of endothelial damage/dysfunction and activation, which may be related to differences in pathophysiology. High levels of vWF were associated with a worse short-term outcome. These endothelial markers were unrelated to plasma BNP levels and may imply a different release mechanism.

Acute Disease↗
PubMed2006

Temporal and venepuncture-related decline in circulating endothelial cell capture from mixed venous blood.

BACKGROUND: The quantification of circulating endothelial cells (CECs) in whole blood has evolved as a novel method for the assessment of endothelial function, although major methodological issues remain. We hypothesized that there is a temporal decline in CEC counts in static venesected blood and that venepuncture itself may lead to increased CEC detachment. METHODS: CEC isolation was performed using the immunobead method. For the temporal decline experiment, we included 52 patients presenting with acute coronary syndrome (ACS). We performed CEC counts immediately and at 4 and 24 h later. For the venepuncture decline experiment, we studied 40 patients with stable cardiovascular disease (CVD). CEC counts were determined from the first 4 mL of aspirated venous blood and compared with counts obtained from a subsequent 4 mL sample of blood after at least 7.5 mL of blood had been collected. RESULTS: Among the ACS patients there was a significant temporal decline in CEC counts in static venous blood over a 24 h period (p = 0.013). Among the patients with stable CVD, the median CEC counts obtained from the initial 4 mL of aspirated venous blood were significantly higher (by 32%) than that obtained from the later 4 mL of aspirated venous blood (p = 0.041). CONCLUSIONS: We demonstrated a significant temporal fall in CEC numbers in static venous blood over 24 h following venesection. Furthermore, we have shown that CEC counts are higher in the initial aspirated blood compared with that aspirated from the same needle subsequently. These data would have implications for how CEC determination is undertaken by researchers in studies related to ACS or CVD.

Adult↗
PubMed2006

Effects of aspirin on intra-platelet vascular endothelial growth factor, angiopoietin-1, and p-selectin levels in hypertensive patients.

BACKGROUND: Although aspirin is useful in reducing platelet activation and cardiovascular events, its effects on platelet levels of angiogenic factors, such as vascular endothelial growth factor (VEGF) and angiopoietin-1 (Ang-1), and markers of platelet activation in hypertension are unknown. The aim of this study was to study the effects of aspirin on the platelet morphology, plasma and platelet levels of VEGF (sVEGF and pVEGF respectively), Ang-1 (sAng-1 and pAng-1 respectively), and P-selectin (sPsel and pPsel respectively) in patients with well controlled hypertension. METHODS: A total of 35 aspirin-naive, hypertensive patients (29 male and six female; mean age 64 years) were compared with 30 (23 male, seven female, mean age 59 years) normotensive control subjects. Blood was collected for plasma VEGF, P-selectin, and Ang-1 (enzyme-linked immunoassay), intra-platelet levels of VEGF, Ang-1, and P-selectin, and platelet volume and mass. Research indices in hypertensive patients were studied before and after 3 months treatment with aspirin 75 mg daily. RESULTS: Hypertensive patients had significantly higher plasma levels of VEGF (P=.04), Ang-1 (P<.001), as well as pVEGF (P=.008), pAng-1(P=.001), sPsel (P=.02), pPsel (P<.001), and mean platelet mass (P=.01) when compared with control subjects. After treatment with aspirin for 3 months, there were significant reductions in plasma VEGF (P=.01), pAng-1 (P=.04), sPsel (P=.001), and pPsel (P<.001) levels, but not levels of platelet VEGF and plasma Ang-1. Neither pVEGF nor pAng-1 correlated with blood pressure or with their respective plasma levels. CONCLUSIONS: The use of aspirin in high-risk hypertensive patients leads to a reduction in intra-platelet angiogenic growth factors and platelet activation. This may have implications for the use of aspirin in conditions (such as vascular disease) that have been associated with an increase in angiogenesis and platelet activation.

Aged↗
PubMed2006

Detection and quantification of mature circulating endothelial cells using flow cytometry and immunomagnetic beads: a methodological comparison.

Mature circulating endothelial cells (CECs) are novel cellular markers of endothelial damage/dysfunction. The two main techniques of CEC enumeration are flow cytometry (FC) and immunomagnetic bead (IB) isolation. Both quantify CECs accurately, but a direct comparison of both methods has not been reported. We sought to assess the agreement between the two methods in two patient populations, and a group of healthy subjects, with emphasis given to methodological issues. We included 34 patients with acute coronary syndrome (ACS), 60 patients with primary breast cancer (PBC) and 30 healthy controls (HC). We quantified CECs using the IB method [CD146 and FITCUlex europaeus lectin-1] and FC [CD45, CD34 and CD146]. Bland-Altman plots suggested reasonable agreement (<5% of events >2 standard deviations from the mean) between FC and the IB methods for CEC quantification in whole blood in the two disease groups (ACS and PBC), but not among the HCs. There were no statistically significant differences in CEC levels by the two methods amongst all three patient groups. There is reasonable agreement between the FC and the IB methods for mature CEC quantification in whole blood, especially amongst disease groups. The agreement between the two methods appears to weaken in healthy controls, and at lower and higher absolute CEC counts.

Adult↗
PubMed2006

Plasma von Willebrand factor, thrombosis, and the endothelium: the first 30 years.

"It is quite useless to argue the questions concerning the development of intimal scleroses if we study and discuss the late stages of the disease alone. If we wish to gain insight into the complex question of arterio-sclerosis we must attempt to follow the lesion from its earliest beginning" (Klotz and Manning, J Path Bact 1911: 16; 211-20). Over thirty years ago Boneu and colleagues published a report of raised levels of plasma von Willebrand factor (vWf) in patients with arteritis, diabetes and sepsis. They concluded that raised levels of this molecule indicate endothelial damage, and may possibly be a contributory factor in thrombosis in arterial disease. The former aspect of this conclusion is now accepted, and numerous studies on the risk factors for atherosclerosis provide mechanisms for this damage. Other studies have demonstrated raised levels in cancer and in connective tissue disease. Numerous long-term follow-up studies have also demonstrated that increased vWf predicts major cardiovascular end points. However, the link between these studies, and the latter aspect of Boneu's conclusion, that raised vWf contributes to thrombosis is, although attractive, nevertheless unproven. Despite this, vWf remains the most important plasma marker of endothelial damage/dysfunction and as such attracts clinical attention.

Animals↗
PubMed2005

Inter-relationships of indices of endothelial damage/dysfunction [circulating endothelial cells, von Willebrand factor and flow-mediated dilatation] to tissue factor and interleukin-6 in acute coronary syndromes.

BACKGROUND: Increased circulating endothelial cells (CECs, reflecting endothelial damage) in acute coronary syndromes (ACS) has been reported. However, the inter-relationships of indices of endothelial damage/injury with development of vascular (dys)function, plasma levels of tissue factor (TF, an index of coagulation) and interleukin-6 (IL-6, a pro-inflammatory cytokine) have not been investigated in ACS. We hypothesized that increased CECs can be related to impaired flow-mediated vasodilatation (FMD, an index of endothelial dysfunction) and elevated plasma von Willebrand factor (vWf, also marking endothelial damage/dysfunction), TF and IL-6 in patients with ACS. METHODS: We studied 120 patients with ACS (80 acute myocardial infarction and 40 unstable angina; 86 male, age 65+/-12 years) and 40 matched patients with stable CAD and 40 healthy controls (HC) in a cross-sectional analysis. Plasma vWf, TF and IL-6 levels were measured by ELISA. CECs were quantified using epifluorescence microscope after immunomagnetic separation with CD146. Brachial artery FMD was assessed in a subset of 39 ACS patients. RESULTS: ACS patients had significantly higher CECs, vWf, TF and IL-6 levels, but lower FMD, when compared to stable CAD and HC (all p<0.001) and all were inter-correlated significantly. In ACS, CECs was strongly correlated with FMD (r=-0.64, p<0.001) and TF (r=0.7, p<0.001). In stable CAD, significant correlations were again found between many indices, but on multivariate analysis, IL-6 and vWf were both independently related to FMD. CONCLUSIONS: Increased CECs in ACS patients are closely associated with endothelial damage/dysfunction (vWf and FMD), coagulation (TF) and inflammation (IL-6). These inter-relationships support the concept of a central role of endothelial damage/injury in the activation of vascular and coagulation abnormalities in ACS.

Aged↗
PubMed2005

The effects of direct current cardioversion for persistent atrial fibrillation on indices of endothelial damage/dysfunction.

BACKGROUND: Atrial fibrillation is associated with increased thromboembolic risk, and this risk may occur even following cardioversion. Atrial fibrillation has been hypothesised to cause alterations in endothelial cell function through the influences of altered flow dynamics, and resultant endothelial dysfunction may be contributory to the generation of a prothrombotic state. The aim of this study was therefore to assess endothelial function before and after electrical cardioversion. METHODS: We studied 30 consecutive patients undergoing elective cardioversion for AF and compared them with 20 healthy controls. Plasma levels of endothelial damage/dysfunction [von Willebrand factor (vWF), E-selectin (E-sel), soluble thrombomodulin (sTM)] and Circulating Endothelial Cells (CECs, an index of endothelial damage) in whole blood were measured in all subjects and on the AF group at baseline (pre-cardioversion) and at 2 h and 4 weeks following cardioversion. RESULTS: Plasma levels of vWf were significantly increased in persistent AF at baseline compared to healthy controls (p<0.001). With restoration of sinus rhythm, vWF levels were significantly decreased at 4 weeks (p=0.0001), whilst levels of CECs (p=0.01) and sTM (p=0.022), although not increased at baseline, were significantly increased following cardioversion. CONCLUSION: Although plasma vWF levels decreased post-cardioversion, suggesting some improvement in vascular endothelial function, the increases in sTM and CECs at 4 weeks may indicate endothelial injury sustained peri-cardioversion. This (delayed) injury and shedding of endothelial cells post-cardioversion may contribute to late thromboembolic risk.

Aged↗
PubMed2005

Increased circulating endothelial cells in acute heart failure: comparison with von Willebrand factor and soluble E-selectin.

BACKGROUND: Circulating endothelial cells (CECs) in the peripheral blood, probably representing the most direct evidence of endothelial cell damage, are increased in myocardial infarction, unstable angina and critical limb ischaemia. As chronic heart failure is also associated with endothelial abnormalities, we hypothesised that CECs are raised in acute heart failure and that they would correlate with plasma indices of endothelial perturbation, that is, von Willebrand factor (vWf) and soluble E-selectin. METHODS: We studied 30 patients with acute heart failure (venesected within 24 h of emergency hospital admission), 30 patients with chronic stable heart failure (venesected as out-patients, all patients in sinus rhythm with ejection fraction < or = 40%) and 20 healthy controls. CECs were quantified using epifluorescence microscopy after CD146-immunomagnetic separation and phenotyped by streptavidin/biotin immunocytochemistry. Citrated plasma was analysed for soluble E-selectin and vWf by ELISA. RESULTS: Levels of CECs, vWf and soluble E-selectin were significantly higher (all p<0.01) in patients with heart failure compared to controls, with no significant differences between acute and chronic heart failure. CECs correlated with plasma vWf (p<0.0001) and soluble E-selectin (p = 0.022) but not ejection fraction or NYHA class. In multiple regression analysis, heart failure was the only independent predictor of raised CECs (p<0.0001). Immunoperoxidase-defined surface expression of CD34, CD45 and CD36 by CECs was <2%, 0% and 8%, respectively. CONCLUSION: CECs, a possibly heterologous population, may be used as a novel measure of endothelial damage in acute heart failure and may have implications for the thrombotic risk associated with acute and chronic heart failure and prognosis in this condition.

Acute Disease↗
PubMed2005

Effects of omega-3 polyunsaturated fatty acids on plasma indices of thrombogenesis and inflammation in patients post-myocardial infarction.

OBJECTIVE: To determine the effects of n-3 PUFAs supplementation on plasma indices of coagulation (fibrinogen), fibrin D-Dimer (an index of thrombogenesis and fibrin turnover), endothelial damage/dysfunction (von Willebrand factor (vWf)), platelet activation (soluble P-selectin (sP-sel)) and inflammation (interleukin-6, IL-6) in patients following acute myocardial infarction. METHODS: Open-labelled randomised controlled trial. Seventy-seven post-myocardial infarction (MI) patients stabilized on standard secondary prevention therapy were randomised either to 3 months' treatment with Omacor 1 g/day (n=37) or 'usual care' control (n=40). Plasma levels of fibrinogen, D-Dimer, vWf, sP-sel, IL-6 and plasma viscosity at baseline and after 3 months were determined. RESULTS: At baseline, there were no significant differences between the groups in all research indices, except vWf levels were higher in patients allocated to Omacor supplementation. After 3 months, there were no significant changes in the levels of any research indices in either the Omacor supplemented or the 'usual care' control patients when compared to baseline. Patients who received Omacor experienced a fall in total cholesterol (p=0.019), total/HDL-cholesterol ratio (p=0.009) and LDL-cholesterol (p=0.023). However, the relative changes in plasma lipids and lipoproteins did not differ between the two groups. CONCLUSIONS: Three-month supplementation of Omacor at 1 g per day in post-MI patients is not associated with an improvement in the levels of peripheral indices of coagulation potential, endothelial function, platelet reactivity and inflammation.

Dietary Supplements↗
PubMed2005

Hemodynamic, hemostatic, and endothelial reactions to psychological and physical stress in coronary artery disease patients.

Episodes of psychological and physical stress may elicit thrombotic cardiac events, such as myocardial infarction. These events are triggered when there are concurrent hemodynamic, hemostatic, and endothelial abnormalities. Hemodynamic, hemostatic, and endothelial reactions of 72 (15 women, 57 men) coronary artery disease patients to psychological and physical stress were examined. Blood pressure, electrocardiography, and impedance cardiography were recorded during rest, mental arithmetic, and exercise. Blood was collected, via catheter, at rest and after each task. Mental arithmetic elicited increases in blood pressure, heart rate, cardiac output, and cardiac contractility, but no consistent changes in hemostatic and endothelial markers. In contrast, exercise, in addition to increasing blood pressure, heart rate, cardiac output, cardiac contractility, and lowering peripheral resistance, elicited increases in plasma viscosity, hematocrit, platelets, and tissue plasminogen activator together with a decrease in plasminogen activator inhibitor. This pattern of hemodynamic, hemostatic, and endothelial reactions suggests that acute psychological and physical stress influence the thrombotic system differently in these high risk patients. Future research is needed to investigate how these stress responses are prospectively related to acute cardiac events.

Acute Disease↗
PubMed2005

Platelet activation in pregnancy-induced hypertension.

BACKGROUND: Although excess platelet activation, as indicated by increased plasma beta thromboglobulin (beta-TG), has been shown in pregnancy-induced hypertension (PIH), platelet adhesion, platelet morphology and a comparison of platelet and soluble (plasma) levels of the adhesion molecules P-selectin (pPsel and sPsel, respectively) have not been studied. METHODS: We conducted a cross-sectional study of 35 consecutive women with PIH (age 31+/-6 years), 31 consecutive women with normotensive pregnancies (age 29+/-5 years) and 30 normotensive non pregnant women (age 30+/-5 years). Platelet adhesion was studied in vitro by binding to fibrinogen-coated microwells, platelet morphology [mass and volume by flow cytometry], whole-platelet P-selectin (pPsel) by ELISA of the lysate of 2 x 10(8) cells, and the plasma markers soluble P-selectin (sP-sel) and beta-TG, by ELISA. RESULTS: The women with PIH had significantly raised sPsel, pPsel and (as expected) beta-TG (all p<0.05), when compared to the normotensive pregnant women and controls. However, in PIH platelet adhesion was similar to that in the normotensive pregnancy, but still higher than the normal controls (p<0.001). There was no difference among the three groups with respect to platelet mass and volume. pPsel and platelet adhesion correlated with gestational age and with systolic and diastolic blood pressure (all p<0.05). CONCLUSIONS: Increased platelet activation and adhesion develop during normal pregnancy, with some indices being further altered in PIH.

Adult↗
PubMed2005

Markers of inflammation in acute coronary syndromes: association with increased heart rate and reductions in heart rate variability.

BACKGROUND: Systemic and vascular inflammation is at the heart of the thrombotic occlusion of coronary arteries. HYPOTHESIS: The study was undertaken to determine the relationship between established inflammatory markers (interleukin-6 [IL-6] and high-sensitivity C-reactive protein [hs-CRP]), neutrophil or white cell count, and concomitant autonomic tone in patients with coronary artery disease soon after occlusive events. METHODS: We tested the linkage between autonomic tone (as defined using both time domain and frequency domain estimates of heart rate variability [HRV]) and circulating markers of inflammation (white cell counts, hs-CRP, and IL-6) in a sample of 100 patients with proven acute coronary syndrome and compared these with healthy controls (n = 49) and the relationships on repeated measures at 4 months in recovery (n = 51). RESULTS: We demonstrated predictable depressed HRV in acute patients who tended to show recovery by 4 months. The acute changes in HRV indices (e.g., triangular index) showed modest negative correlation (r = -0.2-0.3) with the acute elevation of white cell count, IL-6, and hs-CRP. These associations did not persist on multivariate analysis of data gathered at 4 months post event. CONCLUSION: These observational data, while limited, are the first to link autonomic tone and in particular sympathetic tone (as indicated by HRV), to the process of acute leukocytosis and systemic inflammation common in acute coronary syndromes.

Biomarkers↗
PubMed2005

Impaired tissue Doppler diastolic function in patients with coronary artery disease: relationship to endothelial damage/dysfunction and platelet activation.

BACKGROUND: Pulsed tissue Doppler imaging (TDI) allows direct measurement of systolic and diastolic function of the left ventricle. In patients with coronary artery disease (CAD), myocardial ischemia-related impaired diastolic function may be linked to systemic endothelial damage/dysfunction and increased thrombogenesis. We hypothesized relationships between TDI-defined diastolic dysfunction and plasma von Willebrand factor (vWf, marking endothelial damage/dysfunction), soluble P-selectin (sP-sel, reflecting platelet activation), fibrin D dimer (an index of fibrin turnover and thrombogenesis), fibrinogen, and plasma viscosity (PV) in CAD. METHODS: Conventional 2-dimensional Doppler echocardiography and TDI were performed in 75 stable CAD patients (55 men, 59 +/- 11 years) and 40 age- and sex-matched healthy controls. Peak systolic (Sm), peak early (Em), and late (Am) diastolic mitral annular velocities measured at 4 sites (septal, lateral, inferior, and anterior) were averaged as global systolic and diastolic left ventricular function, respectively. The mean TDI velocities were dichotomized into low and high (below/above median) groups. Plasma vWf, sP-sel, D dimer (enzyme-linked immunosorbent assay), fibrinogen (modified Clauss), and PV levels were measured. RESULTS: CAD patients had significantly lower Sm, Em, Em/Am ratio, and a higher ratio of early transmitral flow E-velocity over Em (E/Em) when compared with controls (all P < .05). On multivariate analysis, adjusted for age, ejection fraction, and clinical variables, the differences in the group means of vWf, sP-sel, and fibrinogen remained significantly different between the low and high TDI indexes. D-dimer levels were unrelated to any TDI indexes. None of the transmitral flow indexes were independently related to the research indexes. CONCLUSIONS: In patients with CAD, diastolic dysfunction was closely associated with increased platelet activation and endothelial damage/dysfunction independent of systolic function. TDI-derived indexes are more sensitively related to plasma hemostatic markers than transmitral indexes in middle-aged patients with CAD.

Blood Flow Velocity↗