Analysis of Retinal Vessel Pulsation with Electrographic Gating – Pulsation Amplitude and the Influence of Hyperoxia

2020 ◽  
Vol 237 (04) ◽  
pp. 469-473
Author(s):  
Yasemin Saruhan ◽  
Olivia Bollinger ◽  
Konstantin Gugleta

Abstract Purpose To analyse the amplitude of vessel pulsation in the retina and to determine whether constriction of the vessels by oxygen would decrease their pulsation amplitude and could thus be used to quantify the rigidity of the retinal vessels. Patients and Methods The study included 20 healthy young subjects. With the RVA (retinal vessel analyser), we aimed to quantify vessel pulsations under normal and hyperoxic conditions. Electrocardiographic (ECG)-gated RVA was used for this purpose, with change in vessel pulsation as the primary endpoint and shift in vessel pulsation during the heart cycle as the secondary endpoint. Furthermore, we assessed the correlation between the amplitude of retinal vessel wall pulsation and blood pressure. Descriptive statistics, paired t-tests, and correlation analysis were applied. Results Retinal veins in proximity to the optic disc demonstrated the highest pulsation amplitude under all conditions. All retinal vessels significantly constricted under hyperoxic conditions. There was no significant change in the amplitude of vessel pulsation nor a significant shift in the pulsation cycle under hyperoxic conditions in the examined cohort. No correlation was found between systemic blood pressure parameters and amplitude of retinal vessel wall pulsation or any change in this. Conclusion ECG-gated RVA recording is not able to detect any relevant change in vessel pulsation behaviour under oxygen, despite clearly observed vasoconstriction in retinal vessels. New approaches are necessary to reliably quantify the rigidity of the retinal vessels.

2021 ◽  
pp. 1098612X2199762
Author(s):  
Andra-Elena Enache ◽  
Ursula M Dietrich ◽  
Oscar Drury ◽  
Emanuele Trucco ◽  
Tom MacGillivray ◽  
...  

Objectives Early diagnosis of arterial hypertension is essential to prevent target organ damage. In humans, retinal arteriolar narrowing predicts hypertension. This blinded prospective observational study investigated the retinal vessel diameters in senior and geriatric cats of varying systolic blood pressure (SBP) status and evaluated retinal vascular changes in hypertensive cats after treatment. Methods Cats with a median age of 14 years (range 9.1–22 years) were categorised into five groups: group 1, healthy normotensive (SBP <140 mmHg; n = 40) cats; group 2, pre-hypertensive (SBP 140–160 mmHg; n = 14) cats; group 3, cats with chronic kidney disease (CKD) and normotensive (n = 26); group 4, cats with CKD and pre-hypertensive (n = 13); and group 5, hypertensive cats (SBP >160 mmHg, n = 15). Colour fundus images (Optibrand ClearView) were assessed for hypertensive lesions. Retinal vascular diameters and bifurcation angles were annotated and calculated using the Vascular Assessment and Measurement Platform for Images of the Retina annotation tool (VAMPIRE-AT). When available, measurements were obtained at 3 and 6 months after amlodipine besylate treatment. Results Ten hypertensive cats had retinal lesions, most commonly intraretinal haemorrhages and retinal exudates. Arteriole and venule diameters decreased significantly with increasing age (–0.17 ± 0.05 pixels/year [ P = 0.0004]; –0.19 ± 0.05 pixels/year). Adjusted means ± SEM for arteriole and venule diameter (pixels) were 6.3 ± 0.2 and 8.9 ± 0.2 (group 1); 7.6 ± 0.3 and 10.1 ± 0.4 (group 2); 6.9 ± 0.2 and 9.5 ± 0.3 (group 3); 7.4 ± 0.3 and 10.0 ± 0.4 (group 4); and 7.0 ± 0.3 and 9.8 ± 0.4 (group 5). Group 1 arteriole and venule diameters were significantly lower than those of groups 2 and 4. Group 2 arteriole bifurcation angle was significantly narrower than those of groups 1 and 3. Post-treatment, vessel diameters decreased significantly at 3 and 6 months in seven hypertensive cats. Conclusions and relevance Increased age was associated with reduced vascular diameters. Longitudinal studies are required to assess if vessel diameters are a risk indicator for hypertension in cats.


2001 ◽  
Vol 239 (9) ◽  
pp. 673-677 ◽  
Author(s):  
Gabriele Fuchsjäger-Mayrl ◽  
Kaija Polak ◽  
Alexandra Luksch ◽  
Elzbieta Polska ◽  
Guido T. Dorner ◽  
...  

2009 ◽  
Vol 65 (2) ◽  
pp. 206-212 ◽  
Author(s):  
Olaf Brinchmann-Hansen ◽  
Kjell Myhre ◽  
Leiv Sandvik

1986 ◽  
Vol 61 (1) ◽  
pp. 185-191 ◽  
Author(s):  
C. A. Hales ◽  
R. D. Brandstetter ◽  
C. F. Neely ◽  
M. B. Peterson ◽  
D. Kong ◽  
...  

Acute pulmonary and systemic vasomotor changes induced by endotoxin in dogs have been related, at least in part, to the production of eicosanoids such as the vasoconstrictor thromboxane and the vasodilator prostacyclin. Steroids in high doses, in vitro, inhibit activation of phospholipase A2 and prevent fatty acid release from cell membranes to enter the arachidonic acid cascade. We, therefore, administered methylprednisolone (40 mg/kg) to dogs to see if eicosanoid production and the ensuing vasomotor changes could be prevented after administration of 150 micrograms/kg of endotoxin. The stable metabolites of thromboxane B2 (TxB2) and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) were measured by radioimmunoassay. Methylprednisolone by itself did not alter circulating eicosanoids but when given 2.5 h before endotoxin not only failed to inhibit endotoxin-induced eicosanoid production but actually resulted in higher circulating levels of 6-keto-PGF1 alpha (P less than 0.05) compared with animals receiving endotoxin alone. Indomethacin prevented the steroid-enhanced concentrations of 6-keto-PGF1 alpha after endotoxin and prevented the greater fall (P less than 0.05) in systemic blood pressure and systemic vascular resistance with steroid plus endotoxin than occurred with endotoxin alone. Administration of methylprednisolone immediately before endotoxin resulted in enhanced levels (P less than 0.05) of both TxB2 and 6-keto-PGF1 alpha but with a fall in systemic blood pressure and vascular resistance similar to the animals pretreated by 2.5 h. In contrast to the early steroid group in which all of the hypotensive effect was due to eicosanoids, in the latter group steroids had an additional nonspecific effect. Thus, in vivo, high-dose steroids did not prevent endotoxin-induced increases in eicosanoids but actually increased circulating levels of TxB2 and 6-keto-PGF1 alpha with a physiological effect favoring vasodilation.


2021 ◽  
Vol 2021 (1) ◽  
Author(s):  
Yang Yu ◽  
Hongqing Zhu

AbstractDue to the complex morphology and characteristic of retinal vessels, it remains challenging for most of the existing algorithms to accurately detect them. This paper proposes a supervised retinal vessels extraction scheme using constrained-based nonnegative matrix factorization (NMF) and three dimensional (3D) modified attention U-Net architecture. The proposed method detects the retinal vessels by three major steps. First, we perform Gaussian filter and gamma correction on the green channel of retinal images to suppress background noise and adjust the contrast of images. Then, the study develops a new within-class and between-class constrained NMF algorithm to extract neighborhood feature information of every pixel and reduce feature data dimension. By using these constraints, the method can effectively gather similar features within-class and discriminate features between-class to improve feature description ability for each pixel. Next, this study formulates segmentation task as a classification problem and solves it with a more contributing 3D modified attention U-Net as a two-label classifier for reducing computational cost. This proposed network contains an upsampling to raise image resolution before encoding and revert image to its original size with a downsampling after three max-pooling layers. Besides, the attention gate (AG) set in these layers contributes to more accurate segmentation by maintaining details while suppressing noises. Finally, the experimental results on three publicly available datasets DRIVE, STARE, and HRF demonstrate better performance than most existing methods.


2021 ◽  
Vol 23 (6) ◽  
Author(s):  
A. Maud ◽  
G. J. Rodriguez ◽  
A. Vellipuram ◽  
F. Sheriff ◽  
M. Ghatali ◽  
...  

Abstract Purpose of Review In this review article we will discuss the acute hypertensive response in the context of acute ischemic stroke and present the latest evidence-based concepts of the significance and management of the hemodynamic response in acute ischemic stroke. Recent Findings Acute hypertensive response is considered a common hemodynamic physiologic response in the early setting of an acute ischemic stroke. The significance of the acute hypertensive response is not entirely well understood. However, in certain types of acute ischemic strokes, the systemic elevation of the blood pressure helps to maintain the collateral blood flow in the penumbral ischemic tissue. The magnitude of the elevation of the systemic blood pressure that contributes to the maintenance of the collateral flow is not well established. The overcorrection of this physiologic hemodynamic response before an effective vessel recanalization takes place can carry a negative impact in the final clinical outcome. The significance of the persistence of the acute hypertensive response after an effective vessel recanalization is poorly understood, and it may negatively affect the final outcome due to reperfusion injury. Summary Acute hypertensive response is considered a common hemodynamic reaction of the cardiovascular system in the context of an acute ischemic stroke. The reaction is particularly common in acute brain embolic occlusion of large intracranial vessels. Its early management before, during, and immediately after arterial reperfusion has a repercussion in the final fate of the ischemic tissue and the clinical outcome.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
K.A Dumont ◽  
R Persson ◽  
J.P Kvitting ◽  
R Lundblad ◽  
R Haaverstad ◽  
...  

Abstract Background Barlow's disease provides both diagnostic and therapeutic challenges. The impact of systemic blood-pressure on severity of regurgitation is still unclear. Purpose We hypothesized that mitral annulus behaves passively with enlargement during ventricular systole, and secondly, we tested the hypothesis that severity of regurgitation correlates to systemic blood-pressure (BP) of the patient. Methods Ten patients with Barlow's disease were compared with 10 healthy controls. Brachial blood-pressure was measured according to guidelines. Transthoracic 3D echo was obtained from an apical view (38.6±8.2 frames per second). Data was analyzed using a holographic display. We measured commissure width (CW), septallateral length (SL) and mitral annular surface area throughout the cardiac cycle. Aortic flow ejection time was derived from continuous Doppler across the aortic valve. Timing of aortic valve closure was visually assessed by 3D echo. Onset and end of mitral regurgitation was derived from continuous wave Doppler of transmitral flow. Results Systolic BP in controls and patients were 122±5 and 133±12 mmHg, respectively (p&lt;0.05). Enddiastolic volume was 87±7 ml/m2 (controls) and 100±14 ml/m2 (Barlow), p&lt;0.02. Left ventricular EF in controls and patients were 59±5 and 62±5%, respectively, p=NS. Barlow patients had moderate or severe late systolic regurgitation with mean regurgitation volume of 51±18 ml. Annular surface area, CW and SL behaved passively with enlargement during ventricular systole (Figure 1). Peak systolic surface area, CW and SL in healthy controls and Barlow patients were 8.7±0.5 vs 20.7±3.2 cm2 (p&lt;0.001), 30.1±1.5 vs 49.5±4.9 mm (p&lt;0.001) and 30.9±1.5 vs 44.9±3.3 mm (p&lt;0.001). Peak annular surface area and regurgitation volume in patients showed a positive correlation with systolic BP (y = 0.156x − 0.077, r=0.60 and y = 1.136x − 99.7, r=0.80, respectively). Conclusions We have demonstrated pressure constrained mitral annular dysfunction in Barlow's disease, indicating that systemic blood pressure may modify the severity of regurgitation. The study provides novel insights into mechanisms of mitral regurgitation and potential therapeutic actions in the future. Figure 1 Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): Grieg Foundation


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