George Giannakoulas

Spatial and phasic oscillation of non-newtonian wall shear stress in human left coronary artery bifurcation : an insight to atherogenesis

ObjectiveTo investigate the wall shear stress oscillation in a normal human left coronary artery bifurcation computational model by applying non-Newtonian blood properties and phasic flow. MethodsThe three-dimensional geometry of the investigated model included the left main coronary artery along with its two main branches, namely the left anterior descending and the left circumflex artery. For the computational analyses a pulsatile non-Newtonian flow was applied. To evaluate the cyclic variations in wall shear stress, six characteristic time-points of the cardiac cycle were selected. The non-Newtonian wall shear stress variation was compared with the Newtonian one. ResultsThe wall shear stress varied remarkably in time and space. The flow divider region encountered higher wall shear stress values than the lateral walls throughout the entire cardiac cycle. The wall shear stress exhibited remarkably lower and oscillatory values in systole as compared with that in diastole in the entire bifurcation region, especially in the lateral walls. Although the Newtonian wall shear stress experienced consistently lower values throughout the entire cardiac cycle than the non-Newtonian wall shear stress, the general pattern of lower wall shear stress values at the lateral walls, particularly during systole, was evident regardless of the blood properties. ConclusionsThe lateral walls of the bifurcation, where low and oscillating wall shear stress is observed, are more susceptible to atherosclerosis. The systolic period, rather than the diastolic one, favors the development and progression of atherosclerosis. The blood viscosity properties do not seem to qualitatively affect the spatial and temporal distribution of the wall shear stress.

N-Terminal Pro-Brain Natriuretic Peptide Levels Are Elevated in Patients with Acute Ischemic Stroke

Brain natriuretic peptide (BNP) is a counterregulatory hormone released by the ventricles of the heart. Its main actions are natriuresis and vasodilation. The authors studied N-terminal pro-brain natriuretic peptide (NT-proBNP) levels soon after an acute ischemic stroke. They compared plasma NT-proBNP concentrations in 30 patients with an acute ischemic stroke with those of 30 controls. The 2 groups were adjusted for age and gender, and there were no significant differences in vascular risk factors and left ventricular systolic and diastolic function. Venous samples were collected within the first 11.8 ±1.2 hours after the onset of symptoms and again on day 6. Brain computed tomography/magnetic resonance imaging (CT/MRI) was performed on the same days (day 0 and day 6) in order to assess the site (carotid or vertebrobasilar), cause (atherothrombotic, cardioembolic, or lacunar), and size (large, medium, or small) of the brain infarct. NT-proBNP levels were elevated in patients with acute stroke (129.9 ±9.9 fmol/mL) compared with the controls (90.8 ±6.3 fmol/mL, p<0.05). These levels remained elevated at day 6 (113.5 ±13.0 fmol/mL). NT-proBNP at admission was significantly higher in cardioembolic compared with atherothrombotic infarctions. There was no correlation between circulating NT-proBNP and stroke topography, infarct size, or severity as assessed by the National Institutes of Health Stroke Scale (NIHSS) at any of the 2 time points (admission and day 6). NT-proBNP levels were raised in patients with acute ischemic stroke; this effect persisted until day 6. The authors suggest that neurohumoral activation occurs in patients with acute ischemic stroke, either reflecting a counterbalancing vasodilating response to the cerebral ischemia or direct myocardial dysfunction.

Initial and Six-Year Results of Stent Implantation for Aortic Coarctation in Children

Although stenting has been used as a treatment option for aortic coarctation (CoA) at increasingly younger ages, limited information is available on the long-term follow-up of stent implantation for CoA in pediatric patients. A total of 74 patients with CoA (mean age 8 ± 3 years) underwent stent implantation; 42 were treated for isolated native CoA and 32 for recurrent CoA. A total of 87 stents were implanted (bare metal stents in 71 patients and covered stents in 3 patients). Redilation of a previously implanted stent was performed in 32 patients. Immediately after stenting, the peak systolic pressure gradient decreased from 68 ± 16 mm Hg to 8 ± 5 mm Hg (p <0.05), and the CoA diameter increased from 5 ± 3 mm to 16 ± 3 mm (p <0.05). The most important procedural complication was aneurysm formation in 1 patient that was successfully treated with implantation of a covered stent. No early or late deaths occurred and no evidence was found of late aneurysm formation during a follow-up period of 6 years. Late stent fracture was observed in 3 patients. At the end of follow-up, no cases of recoarctation were identified on multislice computed tomography or magnetic resonance imaging, and 67 (85%) of the 74 patients were normotensive, receiving no medications. In conclusion, stent implantation is an effective and safe treatment alternative to conventional surgical management for the treatment of CoA in selected pediatric patients.

Diabetes mellitus and cerebrovascular disease: which are the actual data?

Cerebrovascular disease (CeVD) represents a major cause of morbidity and mortality worldwide. Diabetes mellitus (DM) represents an independent risk factor for CeVD. The aim of the present review is to describe the epidemiology of CeVD in patients with DM and to explain how DM and diabetic autonomic neuropathy can increase the risk of CeVD. The prevention and management of CeVD in the diabetic population are also analyzed.

Adult congenital heart disease: A paradigm of epidemiological change

Increasing survival rates for patients with congenital heart disease (CHD) represent a major achievement of modern medicine. Despite incredible progress been made in diagnosis, follow-up, early treatment and management in adulthood, many patients are faced with long-term complications, such as arrhythmia, thromboembolism, heart failure, pulmonary hypertension, endocarditis and/or the need for reoperation. In parallel, half of the patients are female, most of childbearing age, and, thus warrant specialist reproductive counseling and appropriate obstetric care. It is not surprising therefore, that healthcare utilization has steadily increased for CHD in recent years. Furthermore, cardiology and other medical disciplines are now faced with new challenges, namely the provision of expert care and optimal, lifelong medical surveillance for these patients.

Imaging of congenital heart disease in adults

Imaging is fundamental to the lifelong care of adult congenital heart disease (ACHD) patients. Echocardiography remains the first line imaging for inpatient, outpatient, or perioperative care. Cross-sectional imaging with cardiovascular magnetic resonance (CMR) or computed tomography (CT) provides complementary and invaluable information on cardiac and vascular anatomy and other intra-thoracic structures. Furthermore, CMR provides quantification of cardiac function and vascular flow. Cardiac catheterization is mostly reserved for assessment of pulmonary vascular resistance, ventricular end-diastolic pressure, and percutaneous interventions. There have been further advances in non-invasive imaging for ACHD including the application of advanced echocardiographic techniques, faster automated CMR imaging, and radiation dose reduction in CT. As a result ACHD, a heterogeneous population, benefit from appropriate application of multiple imaging modalities matched with tertiary ACHD expertise.

Blood biomarkers and their potential role in pulmonary arterial hypertension associated with congenital heart disease. A systematic review

BACKGROUND The development of pulmonary arterial hypertension (PAH) in patients with congenital heart disease (CHD) is multifactorial with a number of biomarkers serving as mediators of neurohormonal activation [B-type natriuretic peptide (BNP) and its N-terminal-pro-fragment (NT-proBNP)], endothelial dysfunction [asymmetric dimethylarginine (ADMA)] and cellular proliferation [vascular endothelial growth factor (VEGF)]. METHODS We systematically reviewed the literature for trials studying the role of these biomarkers in the clinical evaluation, prognosis and management of patients with PAH related to CHD (CHD-PAH). RESULTS Twenty-six studies were included in the systematic review, involving a total of 1113 patients with CHD-PAH. These patients had higher BNP, NT-proBNP and ADMA levels and higher VEGF expression when compared with healthy controls. Baseline and serial values of plasma levels of natriuretic peptides were shown to be significant predictors of survival. ADMA concentration was elevated in patients with CHD-PAH when compared with patients with simple CHD without PAH, whereas VEGF expression was particularly high in patients with CHD and persistent PAH after corrective surgery of the underlying heart disease. CONCLUSION Right heart dysfunction, endothelial inflammation and proliferation are mirrored by plasma levels of the corresponding biomarkers among patients with CHD-PAH. There is early evidence to suggest that natriuretic peptides, in particular, may be a simple and effective tool for determining prognosis and timing for therapeutic interventions in patients with CHD-PAH.

Is anemia a new cardiovascular risk factor

Anemia is frequent in patients with cardiovascular disease and is often characterized as the fifth cardiovascular risk factor. It is considered to develop due to a complex interaction of iron deficiency, cytokine production and impaired renal function, although other factors, such as blood loss, may also contribute. Unfortunately, treatment of anemia in cardiovascular disease lacks clear targets and specific therapy is not defined. Treatment with erythropoietin-stimulating agents in combination with iron is the basic strategy but clear guidelines are not currently available. This review aims to clarify poorly investigated and defined issues concerning the relation of anemia and cardiovascular risk--in particular in patients with acute coronary syndromes and chronic heart failure--as well as the current therapeutic strategies in these clinical conditions.

Micro- and macrovascular treatment targets in scleroderma heart disease

Cardiac involvement in systemic sclerosis (SSc) is a frequent visceral complication that considerably affects the prognosis of the disease. The pathophysiologic hallmark is myocardial fibrosis which can progress leading to arrhythmia, right and/or left heart dysfunction and failure. Symptoms range from unusual to prominent and from mild to dramatic, but clinically overt disease is a poor prognostic factor. Primary myocardial involvement is related to focal ischemia due to transient coronary spasm, and the available data support that microvascular functional and structural abnormalities rather than macrovascular coronary involvement represent the main underlying mechanism of the disease. However, the existence and prevalence of atherosclerotic coronary artery disease in SSc remain to be determined, as several studies have generated conflicting reports. Despite the lack of effective targeted therapy for SSc itself, sensitive and quantitative techniques have demonstrated the ability of vasodilators to improve myocardial function and perfusion and to prevent the evolution of subclinical heart involvement to decompensated heart failure. Further research will provide a better understanding of the disease by detecting the potent contribution of coronary artery involvement, explaining differences in accelerated atherosclerosis between SSc and other autoimmune disorders, and opening directions for the development of novel treatment strategies for this life-threatening complication of SSc.

Molecular Viscosity in the Normal Left Coronary Arterial Tree. Is It Related to Atherosclerosis

The purpose of this study is to elucidate, probably for the first time, the distribution of molecular viscosity in the entire left coronary artery (LCA) tree. The governing mass, momentum, and energy flow equations were solved by using a previously validated 3-dimensional numerical (finite-element analysis) code. High-molecular-viscosity regions occur at bifurcations in regions opposite the flow dividers, which are anatomic sites predisposed for atherosclerotic development. Furthermore, high-molecular-viscosity values appear in the proximal regions of the LCA tree, where atherosclerosis frequently occurs. The effect of blood flow resistance, due to increased blood viscosity, gives rise to increased contact time between the atherogenic particles of the blood and the endothelium, probably promoting atherosclerosis. Observations suggest that, whole viscosity distribution within the coronary artery tree may represent a risk factor for the resulting atherosclerosis. This distribution can become a possible tool for the location of atherosclerotic lesions.