Turbulent Blood Flow Research Articles

Where There's Smoke, There's Fire: A Case Report of Turbulent Blood Flow in Lower Extremity Point-of-care Ultrasound in COVID-19.

IntroductionCoronavirus disease 2019 (COVID-19) may predispose patients to increased risk of venous thromboembolism (VTE) due to various pathophysiological mechanisms, including but not limited to endothelial injury, inflammation, cytokine-mediated microvascular damage, and reactive thrombocytosis. A high risk of vessel thrombosis correlates with disease severity, making early identification and treatment of prime consideration.Although identification of a deep venous thrombosis (DVT) or pulmonary embolism warrants immediate treatment with anticoagulation, trying to predict which COVID-19 patients may be at increased risk for developing these pathologies is challenging.Case ReportsWe present two cases of patients with COVID-19 who had ultrasonographic findings of turbulent blood flow within the deep venous system, without clear evidence of acute proximal DVT, who were subsequently found to have significant VTE.ConclusionPoint-of-care lower extremity ultrasound has become one of the core applications used by emergency physicians. Typically we perform compression ultrasound for DVT evaluation. This novel finding of turbulent blood flow, or “smoke,” within the deep venous system, may serve as a marker of increased risk of clot development and could be an indication to consider early anticoagulation.

A year like no other: introduction to a special issue on COVID-19 and pain.

A year like no other: introduction to a special issue on COVID-19 and pain.

Extrasystolic arrhythmia: is it an additional risk factor of atherosclerosis?

Background Extrasystolic arrhythmia is not included in the list of risk factors of atherosclerosis. The aim of investigation is to determine the relationship between atherosclerosis of main arteries and extrasystolic arrhythmia. Methods We included 286 patients in our investigation. We performed 24-hours ECG monitoring, blood lipids analysis, transthoracic echocardiography, ultrasound Doppler of brachiocephalic arteries, abdominal aorta branches, lower extremities arteries, renal arteries. If prescribed we performed stress echocardiography, transesophageal echocardiography, coronary angiography, renal arteries angiography, pancerebral angiography. So the investigation was made for the active revealing of atherosclerotic signs. The main parameters of heart biomechanics and main arteries kinetics we calculated using apexcardiography and sphygmography and included: speed, acceleration, power, work in each phase of the cardiocycle by apexcardiography, as well as in period of prevalence of inflow over outflow and in period of prevalence of outflow over inflow in sphygmography. All the patients were divided into two main groups according to the quantity of extrasystoles per 24 hours: 1 group - less than 3000, 2 group -3000 extrasystoles and more per 24 hours. Results We determined that the atherosclerotic process was more advanced and more often in the group 2. The atherosclerosis was more severe in patients with extrasystoles before the mitral valve opening and in fast ventricles' filling phase in cardiocycle. The main parameters of heart biomechanics and main arteries kinetics (speed, acceleration, power, work) calculated by apexcardiography and sphygmography increased with the further tendency: if earlier extrasystole appears in cardiocycle, than more changes were observed. Analyzing the methods of physics for fluid movement - Newton equation for liquids and Reynold number - we demonstrated that in extrasystolic arrhythmia in first post-extrasystolic wave there are the conditions for the turbulent blood flow that can cause the onset and progressing of atherosclerotic process. Conclusions Extrasystolic arrhythmia is an additional risk factor of main arteries atherosclerosis. Especially this thesis is fair for the extrasystoles that appear in cardiocycle before the mitral valve opening and in fast ventricles' filling phase.

Extrasystolic arrhythmia: is it an additional risk factor of atherosclerosis?

Extrasystolic arrhythmia is not included in the list of risk factors of atherosclerosis. The aim of this investigation was to determine the relationship between atherosclerosis of main arteries and extrasystolic arrhythmia. We included 286 patients in our investigation. We performed 24-hours ECG monitoring, blood lipids analysis, transthoracic echocardiography, ultrasound Doppler of brachiocephalic arteries, abdominal aorta branches, lower extremities arteries, renal arteries. If prescribed we performed stress echocardiography, transesophageal echocardiography, coronary angiography, renal arteries angiography, pancerebral angiography. So, the investigation was made for the active revealing of atherosclerotic signs. The main parameters of heart biomechanics and main arteries kinetics we calculated using apexcardiography and sphygmography and included: speed, acceleration, power, work in each phase of the cardiocycle by apexcardiography, as well as in period of prevalence of inflow over outflow and in period of prevalence of outflow over inflow in sphygmography. All the patients were divided into two main groups according to the quantity of extrasystoles per 24 hours: 1 group - less than 3000, 2 group -3000 extrasystoles and more per 24 hours. We determined that the atherosclerotic process was more advanced and more often the group 2. The atherosclerosis was more severe in patients with extrasystoles before the mitral valve opening and in fast ventricles' filling phase in cardiocycle. The main parameters of heart biomechanics and main arteries kinetics (speed, acceleration, power, work) calculated by apexcardiography and sphygmography increased with the further tendency: if earlier extrasystole appears in cardiocycle, than more changes were observed. Analyzing the methods of physics for fluid movement - Newton equation for liquids and Reynold number - we demonstrated that in extrasystolic arrhythmia in first post-extrasystolic wave there are the conditions for the turbulent blood flow that can cause the onset and progressing of atherosclerotic process. Extrasystolic arrhythmia is an additional risk factor of main arteries atherosclerosis. Especially this thesis is fair for the extrasystoles that appear in cardiocycle before the mitral valve opening and in fast ventricles' filling phase.

Intraluminal anatomy of the transverse sinus: implications for endovascular therapy.

Trabeculae or septations in the transverse sinus can have potentially life-threatening clinical significance. The current study demonstrates trabecula/septum patterning within the transverse sinus with measurements and distribution data supplemented by imaging, and describes the possible etiology of idiopathic intracranial hypertension and turbulent blood flow in the transverse sinus. Twenty-four sides from 12 cadaveric heads, all fresh-frozen, were used (five males, seven females; age at death 65–91 years, mean 79.1 years). The length and diameter of the transverse sinus were measured along with the number and locations of septations/trabeculae and their tensile strength. The mean length of the transverse sinus was 68.43 mm on the right side and 74.31 mm on the left. A total of 42 septations were found in the 24 transverse sinuses. The number of septations per side ranged from zero to four with a mean of 1.75. The septations were located in the proximal 1/3 in 54.8% (23/42), the middle 1/3 in 21.4% (9/42), and the distal 1/3 in 23.8% (10/42). The work presented here furthers our understanding of transverse sinus anatomy, including its detailed internal architecture. The measurements can provide a technical guide for neurosurgeons and influence instrument selection when a large thrombus forms or anchors in one of these trabeculae or septa and necessitates treatment.

Heart Murmurs

Key Points A Heart murmur results from turbulent blood flow. A complete history and physical examination are most important for evaluating a cardiac murmur. The intensity of a murmur does not necessarily reflect the severity of abnormality. Innocent murmurs are systolic, less than grade 3 in intensity, and louden when the patient moves from an upright position to a supine position. Electrocardiography and echocardiography are usually performed to define the cause of a pathological murmur.

Platelet reactivity in patients with aortic stenosis depends on LV-AO angle

Abstract Background The pathogenesis of aortic stenosis (AS) is not fully understood. However, local inflammation of the valve appears to be a main player. Except haemostasis, platelets contribute to inflammatory processes in various ways. Furthermore, platelet function is altered in patients with AS. Moreover, a steep angle between the left ventricle and the aorta (LV-AO-angle) leads to turbulent blood flow. However, it is not known if platelet reactivity is associated with steep LV_AO angle in patients with AS. Methods We included 289 patients with severe AS and performed cardiac computertomography to assess the LV-AO-angle. Platelet function was evaluated by light transmission aggregometry by using collagen and adenosine-diphosphate to induce platelet activation Results ADP- and collagen induced aggregation showed a significant negative correlation with LV-AO-angle (ADP: r=−0.19, p=0.0009, R2=0.022; collagen: r=−0.21, p=0.0004, R2=0.027). ADP-induced MoA was significant higher in patients with a LV-AO-angle <160° in comparison to patients with an angle ≥160° (<160°: 66.99±20.72% vs. ≥160°: 60.66±19.85%, p=0.009). Collagen-induced platelet reactivity was significant higher in patients with a LV-AO-angle <160° in comparison to patients with an angle ≥160° (<160°: 78.67±13.19% vs. ≥160°: 73.85±14.44%, p=0.003). Multivariate cox-regression revealed that LV-AO angle <160 was a robust predictor of ADP- and collagen-induced platelet aggregation Conclusion A steep LV-AO-angle is associated with enhanced platelet reactivity in patients with AS. Platelet activation is known to lead to local inflammation. Therefore, enhanced platelet reactivity could play crucial in the progression of AS. The clinical significance of a steep LV-AO-angle needs be evaluated in further trials. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): German Research Foundation

Regulatory role of cardiomyocyte metabolism via AMPK activation in modulating atrial structural, contractile, and electrical properties following atrial fibrillation.

The number of patients diagnosed with atrial fibrillation (AF) has been rising due to increased incidence, enhanced detection methods, and greater survival rates following diagnosis. Due to this increase, AF is now the most commonly diagnosed arrhythmia in clinical practice. AF is characterized by irregular, high-frequency contractions of atrial myocytes that lead to turbulent blood flow and the potential for thrombus formation, stroke, or heart failure. These high-frequency contractions of the atrial myocytes cause an imbalance between metabolic supply and demand. Although advances have been made in understanding the pathophysiology of AF, the etiology and underlying pathogenic mechanism remain unknown. However, recent evidence suggests that cardiomyocyte metabolism involving 5' AMP-activated protein kinase (AMPK) activation is altered in patients with AF. Here, we critically reviewed the current understanding of AMPK activation in AF and how it could affect structural, contractile, and electrophysiological cellular properties in the pathogenesis of AF.

WHEN CATHETERIZATIONS GO "DOWNHILL"

SESSION TITLE: Medical Student/Resident Signs and Symptoms of Chest Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Downhill esophageal varices (DEV) are a rare cause of upper gastrointestinal bleeding secondary to superior vena cava (SVC) obstruction. While uphill varices from portal hypertension are commonly seen in practice, there are no current guidelines on the screening and management of downhill varices due to their unique pathophysiology. Here we present an underreported case of DEV from SVC obstruction after long-standing catheter placement. CASE PRESENTATION: A 65-year-old male patient presented to clinic with dysphagia. On upper endoscopy, an isolated upper esophageal varix was noted without varices in the lower esophagus. Chest CT revealed SVC stenosis close to the RA junction. Systemic collaterals were noted via branching to the intercostal and inferior phrenic vein. No significant stenosis of the SVC was present post-ballooning. Patient history indicated a long-term right-sided Port-A-Cath that had been removed a couple months prior due to a thrombus. DISCUSSION: DEV are found in the upper 2/3 of the esophagus as a result of SVC obstruction, from causes like thrombus, thyroid tumors, etc. Central venous catheters, typically in patients with end-stage renal disease, are an accepted cause of DEV from SVC obstruction. Mechanistically, SVC obstruction follows turbulent blood flow, endothelial injury, and thrombosis. This produces varices via dilation of venous drainage, specifically the azygous and hemiazygous systems. Obstruction precedes retrograde blood flow through collateral channels to the IVC. Varices form in the upper third of the esophagus if the stenosis is above the azygous vein and form in the entire esophagus if the stenosis is below or involves the azygous vein. Treatment focuses on the underlying cause of the SVC narrowing. Depending on the specific anatomy of the DEV, options include stenting, thrombolysis, angioplasty, tumor resection, variceal band ligation, or open surgery. In our case, a diagnosis of DEV rather than uphill varices was supported by the isolated upper varices without any lower varix presentation found on endoscopy. Further chest CT displayed SVC stenosis and systemic collaterals. Diagnosis of DEV was confirmed given the patient’s recent history of long-term right sided Port-A-Cath use. CONCLUSIONS: In patients with long-standing catheterizations, clinicians should be cognizant of potential DEV given risk of rupture and progression to hematemesis or hemoptysis. Due to the commonality of dilated collaterals on imaging, prior patient history indicative of SVC obstruction is critical in supporting diagnosis of DEV. The diverse pathophysiology & anatomy involved necessitates DEV treatment focus on the underlying source of the SVC obstruction. Reference #1: Chakinala, R. C., … Aronow, W. S. (2018). Downhill esophageal varices: a therapeutic dilemma. Annals of translational medicine, 6(23), 463. doi:10.21037/atm.2018.11.13 Reference #2: Berkowitz, J. C., Bhusal, S., Desai, D., Cerulli, M. A., & Inamdar, S. (2016). Downhill Esophageal Varices Associated With Central Venous Catheter-Related Thrombosis Managed With Endoscopic and Surgical Therapy. ACG case reports journal, 3(4), e102. doi:10.14309/crj.2016.75 Reference #3: Harwani, Y. P., Kumar, A., Chaudhary, A., Kumar, M., Choudeswari, P. R., Kankanala, V. V., … Tripathi, A. (2014). Combined uphill and downhill varices as a consequence of rheumatic heart disease: a unique presentation. Journal of clinical and experimental hepatology, 4(1), 63–65. doi:10.1016/j.jceh.2013.10.003 DISCLOSURES: No relevant relationships by jayanth keshavamurthy, source=Web Response No relevant relationships by Rohit Munagala, source=Web Response No relevant relationships by Moonkyung Schubert, source=Web Response

Auscultation System for Acquisition of Vascular Sounds - Towards Sound-Based Monitoring of the Carotid Artery.

IntroductionAtherosclerotic diseases of the carotid are a primary cause of cerebrovascular events such as stroke. For the diagnosis and monitoring angiography, ultrasound- or magnetic resonance-based imaging is used which requires costly hardware. In contrast, the auscultation of carotid sounds and screening for bruits – audible patterns related to turbulent blood flow – is a simple examination with comparably little technical demands. It can indicate atherosclerotic diseases and justify further diagnostics but is currently subjective and examiner dependent.MethodsWe propose an easy-to-use computer-assisted auscultation system for a stable and reproducible acquisition of vascular sounds of the carotid. A dedicated skin-transducer-interface was incorporated into a handheld device. The interface comprises two bell-shaped structures, one with additional acoustic membrane, to ensure defined skin contact and a stable propagation path of the sound. The device is connected wirelessly to a desktop application allowing real-time visualization, assessment of signal quality and input of supplementary information along with storage of recordings in a database. An experimental study with 5 healthy subjects was conducted to evaluate usability and stability of the device. Five recordings per carotid served as data basis for a wavelet-based analysis of the stability of spectral characteristics of the recordings.ResultsThe energy distribution of the wavelet-based stationary spectra proved stable for measurements of a particular carotid with the majority of the energy located between 3 and 40 Hz. Different spectral properties of the carotids of one individual indicate the presence of sound characteristics linked to the particular vessel. User-dependent parameters such as variations of the applied contact pressure appeared to have minor influence on the general stability.ConclusionThe system provides a platform for reproducible carotid auscultation and the creation of a database of pathological vascular sounds, which is a prerequisite to investigate sound-based vascular monitoring.

PROFOUND ENDOTHELIAL DYSFUNCTION AS A CAUSE OF STROKE IN COVID-19: A CASE REPORT

SESSION TITLE: Medical Student/Resident Signs and Symptoms of Chest Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: There are recent reports of neurological manifestations (NMs) from COVID-191. We present a healthy male who developed multiple strokes likely from direct endothelial dysfunction (ED). CASE PRESENTATION: 66M with GERD presents with 5 days of cough, fever, and chills. He was febrile and hypoxic. Work-up revealed CRP 19 mg/dL, ferritin 594 ng/mL, D-dimer 2.01 mg/L, positive COVID-19 PCR, and normal lipid panel. He had wheezing and no NMs. He was treated with antibiotics, enoxaparin, and oxygen. On day 14 he acutely developed altered mental status, aphasia, and unilateral weakness. CT head revealed acute left ischemic infarct. CTA head/neck revealed proximal left ICA dissection. Aspirin and Atorvastatin were given. Further studies revealed D-dimer 0.4 mg/L, no inheritable hypercoagulopathy, and negative TTE and lower extremity venous duplex. MRI brain confirmed multiple acute infarcts. Left ICA thrombectomy and stent placement were performed. It was found that there was a pseudo-dissection with a ruptured plaque and an overlying thrombus resulting in a 75% stenosis. DISCUSSION: Arterial complications from COVID-19 have recently been reported.3 Studies from Wuhan, China showed that 36.7% of COVID-19 patients had NMs, most commonly dizziness (16.8%) and headache (13.1%); 5.7% had acute ischemic stroke. These patients had severe respiratory symptoms and developed neurologic signs in 1-2 days.1 Another study revealed that stroke occurred in elevated CRP (51.1 vs 12.1 ng/L) and D-dimer (6.9 vs 0.5 mg/L)2. It is believed that the virus directly invades and injures endothelial cells (ECs), changes prothrombotic factors, and promotes a hypercoagulable state secondary to a profound inflammatory response4. ACE-2-receptors on ECs are used for viral adhesion. Viral replication causes EC apoptosis, which promotes vasoconstriction, organ ischemia, tissue edema, and microvascular prothrombotic sequelae.5 In our case, COVID-19 had profound ED distal to the carotid artery bifurcation. Arterial bifurcations are sites of turbulent blood flow that are athero-prone.6 The stroke occurred in the setting of moderate elevations of D-dimer, suggesting an alternate mechanism.2 Plaque rupture occurred with prophylactic anticoagulation and normal lipid panel. At the time of the stroke, D-dimer and inflammatory markers largely normalized. His late onset NMs indicate that prothrombotic sequelae and ED persist after the cytokine storm has improved.1 Further studies are needed to investigate the duration of cytokine storm and prothrombotic state, and appropriate screening measures. CONCLUSIONS: Clinicians must be cognizant of NMs from COVID-19 such as thromboembolic strokes from direct ED. Reference #1: 1. Mao L et al. Neurologic Manifestations of Hospitalized Patients With Coronavirus Disease 2019 in Wuhan, China. JAMA Neurol. Epub 2020 Apr 10. Reference #2: 2. Li Y, Wang M, Zhou Y, Chang J. Acute Cerebrovascular Disease Following COVID-19: A Single Center, Retrospective, Observational Study. Available at SSRN: https://ssrn.com/abstract=3550025. 2020 Mar 3. Reference #3: 3. Oxley, Thomas et al. Large-Vessel Stroke as a Presenting Feature of Covid-19 in the Young. N Engl J Med. Epub 2020 Apr 28. 4. Connors JM, Levy JH. COVID-19 and its implications for thrombosis and anticoagulation. Blood. Epub 2020 Apr 27. 5. Ferrario CM et al. Effect of angiotensin-converting enzyme inhibition and angiotensin II receptor blockers on cardiac angiotensin-converting enzyme 2. Circulation. 2005;111:2605-10. 6. Ku DN, Giddens DP, Zarins CK, Glagov S. Pulsatile flow and atherosclerosis in the human carotid bifurcation: positive correlation between plaque location and low oscillating shear stress. Atherosclerosis. 1985 May-Jun; 5:293-302 DISCLOSURES: No relevant relationships by Krishna Akella, source=Web Response No relevant relationships by Luke Alessi, source=Web Response No relevant relationships by David Capone, source=Web Response No relevant relationships by Olga McAbee, source=Web Response No relevant relationships by Heidi Roppelt, source=Web Response No relevant relationships by Fredric Weinbaum, source=Web Response No relevant relationships by Daisy Young, source=Web Response

A heart murmur - a frequent incidental finding

A heart murmur - a frequent incidental finding Abstract. Heart murmurs are very common and are present in up to 80 % of school children and 52 % of adults. They originate from the transition from laminar to turbulent blood flow in patients with a structural cardiomyopathy (so-called "organic" murmurs) or in patients with normal hearts (so-called "innocent" murmurs). A detailed history and physical examination help to discriminate innocent from organic murmurs. With the wide availability of transthoracic echocardiography (TTE) cardiac auscultation has lost a lot of its importance, although it remains an important skill for the initial evaluation and triage. An innocent murmur is a minor (1 / 6 - 2 / 6), crescendo-decrescendo, mostly position-dependent, mid-systolic murmur without radiation, which needs no further workup in asymptomatic patients with normal physical capacity. A TTE should be ordered if signs for a cardiac disease are present based on history, physical examination or other tests. Diastolic and continuous murmurs are mostly pathologic and warrant further workup.

Turbulent Systolic Flow Downstream of a Bioprosthetic Aortic Valve: Velocity Spectra, Wall Shear Stresses, and Turbulent Dissipation Rates.

Every year, a quarter million patients receive prosthetic heart valves in aortic valve replacement therapy. Prosthetic heart valves are known to lead to turbulent blood flow. This turbulent flow field may have adverse effects on blood itself, on the aortic wall and on the valve performance. A detailed characterization of the turbulent flow downstream of a valve could yield better understanding of its effect on shear-induced thrombocyte activation, unphysiological wall shear stresses and hemodynamic valve performance. Therefore, computational simulations of the flow past a bioprosthetic heart valve were performed. The computational results were validated against experimental measurements of the turbulent flow field with tomographic particle image velocimetry. The turbulent flow was analyzed for disturbance amplitudes, dissipation rates and shear stress distributions. It was found that approximately 26% of the hydrodynamic resistance of the valve was due to turbulent dissipation and that this dissipation mainly took place in a region about one valve diameter downstream of the valve orifice. Farther downstream, the turbulent fluctuations became weaker which was also reflected in the turbulent velocity spectra of the flow field. Viscous shear stresses were found to be in the range of the critical level for blood platelet activation. The turbulent flow led to elevated shear stress levels along the wall of the ascending aorta with strongly fluctuating and chaotic wall shear stress patterns. Further, we identified leaflet fluttering at 40 Hz which was connected to repeated shedding of vortex rings that appeared to feed the turbulent flow downstream of the valve.

Physiologic blood flow is turbulent

Contemporary paradigm of peripheral and intracranial vascular hemodynamics considers physiologic blood flow to be laminar. Transition to turbulence is considered as a driving factor for numerous diseases such as atherosclerosis, stenosis and aneurysm. Recently, turbulent flow patterns were detected in intracranial aneurysm at Reynolds number below 400 both in vitro and in silico. Blood flow is multiharmonic with considerable frequency spectra and its transition to turbulence cannot be characterized by the current transition theory of monoharmonic pulsatile flow. Thus, we decided to explore the origins of such long-standing assumption of physiologic blood flow laminarity. Here, we hypothesize that the inherited dynamics of blood flow in main arteries dictate the existence of turbulence in physiologic conditions. To illustrate our hypothesis, we have used methods and tools from chaos theory, hydrodynamic stability theory and fluid dynamics to explore the existence of turbulence in physiologic blood flow. Our investigation shows that blood flow, both as described by the Navier–Stokes equation and in vivo, exhibits three major characteristics of turbulence. Womersley’s exact solution of the Navier–Stokes equation has been used with the flow waveforms from HaeMod database, to offer reproducible evidence for our findings, as well as evidence from Doppler ultrasound measurements from healthy volunteers who are some of the authors. We evidently show that physiologic blood flow is: (1) sensitive to initial conditions, (2) in global hydrodynamic instability and (3) undergoes kinetic energy cascade of non-Kolmogorov type. We propose a novel modification of the theory of vascular hemodynamics that calls for rethinking the hemodynamic–biologic links that govern physiologic and pathologic processes.

Computational studies of comparative and cumulative effects of turbulence, fluid–structure interactions, and uniform magnetic fields on pulsatile non-Newtonian flow in a patient-specific carotid artery

Clinical evidence has shown that hemodynamics plays an important role in vascular diseases that hemodynamic parameters are highly dependent on the elasticity of the artery wall. Since so far, no study has not been done about turbulent and non-Newtonian blood flow in carotid artery under a magnetic field, in this study we use computational fluid dynamics and fluid–structure interaction (FSI) models to study the hemodynamics of a patient-specific carotid artery. The comparative and cumulative effects of turbulence modeling, arterial wall elasticity, and magnetic field intensities are investigated by quantifying their effects on different variables of interest. These variables include blood pressure, time-averaged wall shear stress, relative residence time (RRT), and oscillating shear index (OSI), which are important in the onset and development of atherosclerosis. The results showed that the effects of turbulence are significant for predictions of OSI, while for other variables the turbulent simulation results were comparable to laminar simulations. The effects of wall elasticity were significant for all variables, such that FSI modeling will be essential for an accurate computational framework. The effects of magnetic fields were also found to be relatively significant. By increasing Hartman number from zero to five, the maximum shear stress was reduced by about 10%. Other effects of increased intensity of magnetic field included reduction in the average amount of RRT, sharp decrease in the OSI > 0 region, and transfer of maximum OSI from distal part of carotid sinus to the proximal part.

Dysregulation of Endothelial Nitric Oxide Synthase Does Not Depend on Hemodynamic Alterations in Bicuspid Aortic Valve Aortopathy.

BackgroundBicuspid aortic valves (BAVs) predispose to ascending aortic aneurysm. Turbulent blood flow and genetic factors have been proposed as underlying mechanisms. Endothelial nitric oxide synthase (eNOS) has been implicated in BAV aortopathy, and its expression is regulated by wall shear stress. We hypothesized that if turbulent flow induces aneurysm formation in patients with a BAV, regional differences in eNOS expression would be observed in BAVs.Methods and ResultsAscending aortic specimens were harvested intraoperatively from 48 patients with tricuspid aortic valve (19 dilated, 29 nondilated) and 38 with BAV (28 dilated, 10 nondilated) undergoing cardiac surgery. eNOS mRNA and protein concentration were analyzed at the convex and concave aortic wall. In nondilated aortas, eNOS mRNA and protein concentration were decreased in BAV compared with tricuspid aortic valve (all P<0.05). eNOS expression was increased in association with dilation in BAV aortas (P=0.03), but not in tricuspid aortic valve aortas (P=0.63). There were no regional differences in eNOS mRNA or protein concentration in BAV aortas (all P>0.05). However, eNOS expression was increased at the concave wall (versus convexity) in tricuspid aortic valve dilated aortas (all P<0.05).ConclusionsDysregulated eNOS occurs independent of dilation in BAV aortas, suggesting a potential role for aberrantly regulated eNOS expression in the development of BAV‐associated aneurysms. The absence of regional variations of eNOS expression suggests that eNOS dysregulation in BAV aortas is the result of underlying genetic factors associated with BAV disease, rather than changes stimulated by hemodynamic alterations. These findings provide insight into the underlying mechanisms of aortic dilation in patients with a BAV.

Doppler characteristics of hepatic venous hemodynamics in adult healthy camels (Camelus dromedarius)

Abstract The present study was designed to describe the Doppler measurements of hepatic venous blood flow in camels (Camelus dromedarius). A total number of 9 adult healthy camels underwent hepatic Doppler examinations on the right side between the 11th and 9th intercostal spaces. The splenic and cranial mesenteric veins showed turbulent blood flows at their fusion to form the main portal trunk. At porta hepatis, the main portal vein exhibited turbulent blood flows and the mean velocities ranged from 21 to 28 cm/sec. In contrast, the intrahepatic branches of portal veins revealed smooth laminar spectral patterns with low blood velocities ranged from 12 to 22 cm/sec. In addition, hepatic veins and caudal vena cava have laminar blood flows. In conclusion, as a non-invasive clinical tool, Doppler ultrasonography is a simple and easy applicable method for assessment of hepatic hemodynamics in camels (Camelus dromedaries). The present findings have the potential to serve as references for evaluating the health status of the liver from camels. Therefore; a further research study, including comparative evaluation of Doppler findings in camels with various hepatic diseases, may be required.

Haemolysis induced by mechanical circulatory support devices: unsolved problems.

Since the use of continuous flow blood pumps as ventricular assist devices is standard, the problems with haemolysis have increased. It is mainly induced by shear stress affecting the erythrocyte membrane. There are many investigations about haemolysis in laminar and turbulent blood flow. The results defined as threshold levels for the damage of erythrocytes depend on the exposure time of the shear stress, but they are very different, depending on the used experimental methods or the calculation strategy. Here, the results are resumed and shown in curves. Different models for the calculation of the strengths of erythrocytes are discussed. There are few results reported about tests of haemolysis in blood pumps, but some theoretical approaches for the design of continuous flow blood pumps according to low haemolysis have been investigated within the last years.

Simulations of Frictional Losses in a Turbulent Blood Flow Using Three Rheological Models

Blood flow rate is a crucial factor in transporting an oxygen and depends on several parameters like heart pressure, blood properties like density and viscosity, frictional loss and diameter and shape of vein. Frictional loss is a main challenge of current engineering. Therefore, simulation of dependence of blood properties on frictional loss is very important. When blood properties are considered the first step is to find proper rheological model. It is well known that human blood demonstrates a yield shear stress. Therefore, the research is focused on simulating frictional losses in a turbulent flow of human blood, which demonstrates a yield stress. Three arbitrarily chosen rheological models were considered, namely Bingham, Casson and Herschel-Bulkley. Governing equations describing turbulent blood flow were developed to axially symmetrical an aorta. The mathematical model constitutes three partial differential equations, namely momentum equation, kinetic energy of turbulence and its dissipation rate. The main objective of the research is examining influence of the yield shear stress on frictional losses in a human blood in an aorta when flow becomes turbulent. Simulation of blood flow confirmed marginal influence of a yield shear stress on frictional losses when flow becomes turbulent. Results of simulations are discussed and final conclusions are stated.

Heart murmurs in apparently healthy cats caused by iatrogenic dynamic right ventricular outflow tract obstruction.

BackgroundHeart murmurs are detected commonly in apparently healthy cats during routine physical examination, and Doppler echocardiography ultimately is required to identify the source of flow turbulence causing the murmur. However, in some cases, the origin of the murmur cannot be identified on echocardiographic examination, even by experienced clinicians. The application of gentle pressure with the ultrasound transducer against the chest wall of a cat can induce temporary narrowing of the mid‐right ventricular (RV) lumen, causing blood flow turbulence even in the absence of cardiac abnormalities.Objectives/HypothesesTo evaluate the effect of pressure of the ultrasound transducer against the chest wall of cats during echocardiography (provocative testing) on RV blood flow. The main hypothesis is that provocative testing can increase RV outflow velocity and cause flow turbulence. The second hypothesis is that the effect of this maneuver is independent of changes in heart rate during testing.AnimalsSixty‐one client‐owned, apparently healthy cats with heart murmurs on physical examination.MethodsRetrospective review of echocardiographic examinations of 723 cats presented for investigation of a heart murmur.ResultsOutflow systolic velocity increased from 1.05 ± 0.26 to 1.94 ± 0.51 m/s during provocative testing (P < .0001); no correlation was found between RV outflow peak velocity and heart rate during provocative testing (P = .34; r = 0.1237).Conclusions and Clinical RelevanceRight ventricular outflow tract obstruction and associated heart murmur can be iatrogenically induced in apparently healthy cats by increasing pressure on the right chest wall with an ultrasound probe.