A System for Accurate Deployment of Unconstrained Triple-Fenestrated Aortic Arch Endografts

Purpose: To achieve accurate rotational orientation and the axial position of unconstrained triple-fenestrated physician-modified endografts upon deployment in the aortic arch during total arch thoracic endovascular aortic repair (TA-TEVAR). Materials and Methods: Following a detailed study of reconstructed computerized tomography angiography images of patients’ arch anatomy, customized, sealable fenestrations with radio-opaque margins are created onsite on Valiant Captivia (Medtronic) endografts, transposing the arch branch ostial anatomic interrelationship onto the endograft precisely. Radio-opaque figure-of-8 markers, indicating the 12 o’clock (superior) position, are attached to the endograft on the surface and brought up to the surface under the endograft cover during resheathing. Resheathing without any twist in the endograft is achieved by lining up the welds in each endograft stent segment in a straight line. The fluoroscopic working view for arch endograft delivery and deployment is the left anterior oblique view that is orthogonal to the plane of the arch, which, in turn, is the right anterior oblique view in which parts of a stiff indwelling guidewire in the ascending and descending aorta precisely overlap. During introduction in the working view, the endograft delivery system is rotated in the descending thoracic aorta so that the 12 o’clock figure-of-8 markers are viewed on the edge and situated at the outer aortic curvature; continued advancement into the arch without any further rotation will ensure superior orientation of the figure-of-8 markers and, consequently, correct endograft rotational orientation. Proper axial endograft positioning requires locating the left common carotid artery (LCCA) fenestration just proximal to a taut externalized LCCA-femoral guidewire loop marking the posterior limit of the LCCA ostium. After endograft deployment during rapid cardiac pacing, the target arch branches are cannulated through their respective fenestrations using hydrophilic 0.035-inch guidewires that are externalized via distal sheaths to create femoral-arch branch (through-and-through) loops over which covered fenestrated stents are introduced and deployed. Results: This technique was used successfully in 31 consecutive patients undergoing TA-TEVAR; systemic blood pressure was obtained in all arch branches immediately after endograft deployment, indicating adequate blood flow. All arch branches were successfully cannulated and stented. Conclusion: This system enables accurate deployment of unconstrained triple-fenestrated arch endografts simply and reliably during TA-TEVAR.

Left atrial Appendage Rupture Following Intraoperative Hypertensive Crisis

The acute and severe rise in systemic blood pressure during or after cardiac operations may be life-threatening and result in end-organ injury. This case is the first report of spontaneous left atrial appendage rupture following the hypertensive crisis in cardiac surgery

Variation of intraocular pressure comparing rebound (TONOVET Plus®) and applanation (TONO-PEN VET®) tonometry in New Zealand rabbits treated with Amlodipine®

Rabbits have played an important role in ophthalmological research processes, however in the environment there has been a deficiency of sensitive equipment in measurement of intraocular pressure for this species. To compare intraocular pressure (IOP) measured with rebound (TONOVET Plus®) and applanation (TONO-PEN VET®) tonometry in healthy New Zealand rabbits treated with Amlodipine. Twelve healthy male New Zealand white rabbits, 5 months old; two groups with 6 individuals were used in this study. The experimental group was given Amlodipine® at a dose of 5 mg/kg, once a day for a month. Blood pressure and intraocular pressure were measurement before treatment and 6 h after treatment in a period of one month. A trend is noted where the group of animals treated with amlodipine® presents lower values than the control group, both in systolic and diastolic pressure. The systolic pressure of the control group showed an average of 116.5 ± 7.9 mmHg and 117.4 ± 8.9 mmHg and the treatment group showed an average of 113.6 ± 7.9 mmHg and 111.8 ± 10.0 mmHg (pretreatment and posttreatment respectively). Tonometry: the values obtained using the TONOVET Plus® (19 ± 3 mmHg) are on average higher than the values obtained using the TONO-PEN VET® (17 ± 3 mmHg). It was possible to demonstrate the relationship between systemic blood pressure and intraocular pressure in New Zealand white rabbits. Rebound tonometry showed less variability in results than applanation tonometry. This study confirmed that both tonometers are reliable for measuring IOP in rabbits.

Association of serum uric acid with systemic blood pressure – A Cross Sectional study.

Objective: To determine association of Serum Uric Acid levels (SUA) in subjects suffering Systemic Blood Pressure and to determine its association with systolic and diastolic blood pressure. Study Design: Cross Sectional Study. Setting: Department of Faculty of Medicine and Allied Medical Sciences, Isra University, Hyderabad, Sindh, Pakistan. Period: January 2018 to September 2019. Material & Methods: 150 diagnosed cases of systemic hypertension and 150 controls were selected though non-probability purposive sampling according to inclusion and exclusion criteria. 2 ml venous blood was taken, centrifuged and sera were used for uric acid. Data was saved in a pre- structured Performa. Statistical software (SPSS v 21.0, IBM, Incorporation, USA) of data variables was analyzed at 95% CI (P ≤ 0.05). Results: Serum uric acid in controls was 2.93±0.72 compared to cases 4.25±1.44 mg/dl (P=0.0001). Hyperuricemia was observed in 58 (38.6%) cases compared to 23 (15.3%) controls. Uric acid shows strong positive association with Systolic BP (r= 0.52*, p=0.0001) and Diastolic BP (r= 0.46**, p=0.0001). Conclusion: We found hyperuricemia in 58 (38.6%) of systemic hypertension cases. Systolic and Diastolic Blood pressure show positive association with uric acid.

Retinal Microvascular Reactivity in Chronic Cigarette Smokers and Non-smokers: An Observational Cross-Sectional Study

Purpose: To evaluate the changes in the retinal microvasculature and its reactivity in chronic cigarette smokers.Methods: Thirty-four male chronic cigarette smokers and 18 male non-smokers were enrolled. Optical coherence tomography angiography was used to measure the perfused retinal vessel densities (PVDs) of the peripapillary and parafoveal areas at baseline and during phase IV of the Valsalva maneuver (VM-IV). Systemic blood pressure and intraocular pressure were also measured.Results: The baseline PVD in the peripapillary area of the smokers was significantly lower than the non-smokers (59.56 ± 2.26% vs. 61.67 ± 3.58%, respectively; P = 0.005). However, there was no significant difference in the foveal avascular zone or parafoveal PVD between the two groups. During VM-IV, the peripapillary PVD of the smokers decreased by 1.13 ± 3.50%, which was significantly less than that of the non-smokers (−3.83 ± 4.26%, P < 0.05). Similarly, the parafoveal PVD of the smokers decreased by 5.49 ± 9.70%, which was significantly less than the percentage change of the non-smokers (−13.01 ± 8.39%, P < 0.05). There was no significant difference in the percentage change in systemic blood pressure parameters between the two groups.Conclusion: The retinal microvasculature and its reactivity were impaired in chronic smokers compared with non-smokers. The extent of impairment differed among different regions of the fundus.

Neflamapimod Induces Vasodilation in Resistance Mesenteric Arteries by Inhibiting p38 Mitogen-Activated Protein Kinase Alpha (MAPKα) and Heat-Shock Protein 27 (Hsp27) Phosphorylation

Neflamapimod, a selective inhibitor of p38 MAPKα, is under clinical investigation for its efficacy in Alzheimer’s disease (AD) and dementia with Lewy Bodies (DLB). Here, we investigated if neflamapimod-mediated acute inhibition of p38 MAPKα could induce vasodilation in resistance-size rat mesenteric arteries. Our pressure myography data demonstrated that neflamapimod produced a dose-dependent vasodilation in mesenteric arteries. Our Western blotting data revealed that acute neflamapimod treatment significantly reduced the phosphorylation of p38 MAPKα and its downstream target heat-shock protein 27 (Hsp27) that is involved in cytoskeletal reorganization and smooth muscle contraction. Likewise, non-selective inhibition of p38 MAPK by SB203580 attenuated p38 MAPKα and Hsp27 phosphorylation, and induced vasodilation. Endothelium denudation or pharmacological inhibition of endothelium-derived vasodilators such as nitric oxide (NO) and prostacyclin (PGI2) had no effect on such vasodilation. Neflamapimod-evoked vasorelaxation remained unaltered by the inhibition of smooth muscle cell K+ channels. Altogether, our data for the first time demonstrates that in resistance mesenteric arteries, neflamapimod inhibits p38 MAPKα and phosphorylation of its downstream actin-associated protein Hsp27, leading to vasodilation. This novel finding may be clinically significant and is likely to improve systemic blood pressure and cognitive deficits in AD and DLB patients for which neflamapimod is being investigated.

ODONTECTOMY MANAGEMENT WITH LOCAL ANESTHESIA IN PATIENT WITH OPEN-ANGLE GLAUCOMA

Background: Glaucoma is characterized by optic neuropathy with increased intraocular pressure. The high prevalence of impaction causes some glaucoma patients to require odontectomy. There are no contraindications to odontectomy in glaucoma patients, but special preparation is needed to prevent recurrence during the procedure. Glaucoma recurrence is precipitated by increased intraocular pressure which correlates with elevated systemic blood pressure with increased intraocular pressure and corticosteroid use. Therefore, dentists must be vigilant in choosing an atraumatic odontectomy procedure, anesthetic dose and techniques, as well as administering the type and dose of analgesics. Objective: This paper reports a case of mandibular third molar odontectomy with local anesthesia in a patient with open-angle glaucoma, which is a rare case and in this case there is a high risk of complications. Case: A 26-year-old male patient complained of pain in the left back gum when chewing. Orthopantomographic radiographic examination showed impacted 38. The patient has been diagnosed with open-angle glaucoma for 5 years. An odontectomy was performed under local anesthesia. Durante surgery, bleeding is minimal and does not cause recurrence of glaucoma. Postoperative evaluation gave good results, minimal complications, and no recurrence of glaucoma.Conclusion: Odontontectomy with local anesthesia in glaucoma patients requires special preparation in the form of atraumatic surgical procedures and perioperative pharmacotherapy management in the form of pre-emptive analgesia, selection of a maximum of two ampoules of lidocaine and epinephrine 1:80,000 with the mandibular block anesthetic technique, and using multimodal analgesia in combination with NSAIDs without corticosteroids. Keywords: Complications, Glaucoma, Odontectomy

Effects of Regular Long-Term Circuit Training (Once per Week) on Cardiorespiratory Fitness in Previously Sedentary Adults

The purpose of the study was (1) to investigate the effects of regular long-term circuit training (once per week) on cardiorespiratory fitness (CRF) in sedentary adults and (2) to compare training progress with the effects of continued exercise participation by regularly active age-matched individuals. Ten sedentary, middle-aged (51 ± 6 years) individuals (sedentary group, SG) of both sexes performed 32 weeks (1 training session/week) of supervised circuit training and 10 weeks of self-managed training. Effects were compared to an age-matched group (51 ± 8 years; n = 10) of regularly active individuals (active group, AG). CRF (expressed as peak oxygen uptake: VO2peak; peak power output: PPO) and systemic blood pressure (BP) during the incremental test were measured at the start and after the training intervention. CRF decreased significantly within the AG (VO2peak: 43.1 ± 7.3 vs. 40.3 ± 6.5 mL/min/kg, p < 0.05; PPO: 3.3 ± 0.6 vs. 3.1 ± 0.6; p < 0.05) but was maintained in the SG. In addition, significant improvements in restoration of the oxygen level in leg muscles after exercise and reduced systolic BP (180 ± 14 vs. 170 ± 17 mmHg, p = 0.01) at submaximal exercise were found within the SG. However, differences in changes from pre to post did not reach significance between groups. In contrast to the regularly active individuals, circuit training once per week over 32 weeks prevented the aging-related decline of CRF in previously sedentary subjects and reduced systolic BP during submaximal exercise, indicating improved exercise tolerance.

A plasma membrane-localized polycystin-1/polycystin-2 complex in endothelial cells elicits vasodilation

Polycystin-1 (PC-1, PKD1), a receptor-like protein expressed by the Pkd1 gene, is present in a wide variety of cell types, but its cellular location, signaling mechanisms and physiological functions are poorly understood. Here, by studying tamoxifen-inducible, endothelial cell (EC)-specific Pkd1 knockout (Pkd1 ecKO) mice, we show that flow activates PC-1-mediated, Ca2+-dependent cation currents in ECs. EC-specific PC-1 knockout attenuates flow-mediated arterial hyperpolarization and vasodilation. PC-1-dependent vasodilation occurs over the entire functional shear stress range and primarily via the activation of nitric oxide synthase (NOS), with a smaller contribution from small-conductance Ca2+-activated K+ (SK) channels. EC-specific PC-1 knockout increases systemic blood pressure without altering kidney anatomy. PC-1 coimmunoprecipitates with polycystin-2 (PC-2, PKD2), a TRP polycystin channel, and clusters of both proteins locate in nanoscale proximity in the EC plasma membrane. Knockout of either PC-1 or PC-2 (Pkd2 ecKO mice) abolishes surface clusters of both PC-1 and PC-2 in ECs. Single knockout of PC-1 or PC-2 or double knockout of PC-1 and PC-2 (Pkd1/Pkd2 ecKO mice) similarly attenuates flow-mediated vasodilation. Flow stimulates non-selective cation currents in ECs that are similarly inhibited by either PC-1 or PC-2 knockout or by interference peptides corresponding to the C-terminus coiled-coil domains present in PC-1 or PC-2. In summary, we show that PC-1 regulates arterial contractility and demonstrate that this occurs through the formation of an interdependent signaling complex with PC-2 in endothelial cells. Flow stimulates PC-1/PC-2 clusters in the EC plasma membrane, leading to Ca2+ influx, NOS and SK channel activation, vasodilation and a reduction in blood pressure.