Control Of Arterial Blood Pressure Research Articles

Fluid Resuscitation for Refractory Hypotension.

Hypotension is a common occurrence, especially in anesthetized patients and in critical patients suffering from hypovolemia due to shock and sepsis. Hypotension can also occur in normovolemic animals, anesthetized or conscious, under conditions of vasodilation or decreased cardiac function. The main consequence of hypotension is decreased organ perfusion and tissue injury/dysfunction. In the human literature there is no consensus on what is the threshold value for hypotension, and ranges from < 80 to < 100 mmHg for systolic blood pressure and from < 50 to < 70 mmHg for mean arterial blood pressure have been referenced for intraoperative hypotension. In veterinary medicine, similar values are referenced, despite marked differences in normal arterial blood pressure between species and with respect to humans. Therapeutic intervention involves fluid therapy to normalize volemia and use of sympathomimetics to enhance cardiac function and regulate peripheral vascular resistance. Despite these therapeutic measures, there is a subset of patients that are seemingly refractory and exhibit persistent hypotension. This review covers the physiological aspects that govern arterial blood pressure control and blood flow to tissues/organs, the pathophysiological mechanisms involved in hypotension and refractory hypotension, and therapeutic considerations and expectations that include proper interpretation of cardiovascular parameters, fluid recommendations and therapy rates, use of sympathomimetics and vasopressors, and newer approaches derived from the human literature.

The role of baseline and post-treatment frontal QRS-T angle for detecting arterial blood pressure control

ABSTRACT Objectives: In this study, we aimed to investigate the value of the frontal QRS-T angle (f(QRS-T)) in determining blood pressure control among newly diagnosed hypertensive patients with no left ventricular hypertrophy. Methods: Fifty patients with newly diagnosed hypertension were included in this single-center study. The patients were examined with 12-lead ECGs and 24-hour ambulatory blood pressure monitoring (24 h-ABPM) before and 1 month after antihypertensive treatment. Results: Baseline and post-treatment f(QRS-T) angle values were observed to be similar (38.0 [0.0–174.0] and 37.0 [1.0–139.0], respectively; p = .827). The values of QT minimum (p = .006), QTc mean (p = .030), Tp-e (p = .027), and JTc (p = .010) significantly decreased after control of blood pressure. Conclusions: The f(QRS-T) angle, which can be easily calculated on the ECG, is not a useful tool to determine hypertension control at early stage in newly diagnosed hypertensive patients.

Novel Pannexin-1-Coupled Signaling Cascade Involved in the Control of Endothelial Cell Function and NO-Dependent Relaxation.

Deletion of pannexin-1 (Panx-1) leads not only to a reduction in endothelium-derived hyperpolarization but also to an increase in NO-mediated vasodilation. Therefore, we evaluated the participation of Panx-1-formed channels in the control of membrane potential and [Ca2+]i of endothelial cells. Changes in NO-mediated vasodilation, membrane potential, superoxide anion (O2·–) formation, and endothelial cell [Ca2+]i were analyzed in rat isolated mesenteric arterial beds and primary cultures of mesenteric endothelial cells. Inhibition of Panx-1 channels with probenecid (1 mM) or the Panx-1 blocking peptide 10Panx (60 μM) evoked an increase in the ACh (100 nM)-induced vasodilation of KCl-contracted mesenteries and in the phosphorylation level of endothelial NO synthase (eNOS) at serine 1177 (P-eNOSS1177) and Akt at serine 473 (P-AktS473). In addition, probenecid or 10Panx application activated a rapid, tetrodotoxin (TTX, 300 nM)-sensitive, membrane potential depolarization and [Ca2+]i increase in endothelial cells. Interestingly, the endothelial cell depolarization was converted into a transient spike after removing Ca2+ ions from the buffer solution and in the presence of 100 μM mibefradil or 10 μM Ni2+. As expected, Ni2+ also abolished the increment in [Ca2+]i. Expression of Nav1.2, Nav1.6, and Cav3.2 isoforms of voltage-dependent Na+ and Ca2+ channels was confirmed by immunocytochemistry. Furthermore, the Panx-1 channel blockade was associated with an increase in O2·– production. Treatment with 10 μM TEMPOL or 100 μM apocynin prevented the increase in O2·– formation, ACh-induced vasodilation, P-eNOSS1177, and P-AktS473 observed in response to Panx-1 inhibition. These findings indicate that the Panx-1 channel blockade triggers a novel complex signaling pathway initiated by the sequential activation of TTX-sensitive Nav channels and Cav3.2 channels, leading to an increase in NO-mediated vasodilation through a NADPH oxidase-dependent P-eNOSS1177, which suggests that Panx-1 may be involved in the endothelium-dependent control of arterial blood pressure.

Connexin Signaling in the Juxtaglomerular Apparatus (JGA) of Developing, Postnatal Healthy and Nephrotic Human Kidneys.

Our study analyzed the expression pattern of different connexins (Cxs) and renin positive cells in the juxtaglomerular apparatus (JGA) of developing, postnatal healthy human kidneys and in nephrotic syndrome of the Finnish type (CNF), by using double immunofluorescence, electron microscopy and statistical measuring. The JGA contained several cell types connected by Cxs, and consisting of macula densa, extraglomerular mesangium (EM) and juxtaglomerular cells (JC), which release renin involved in renin-angiotensin- aldosteron system (RAS) of arterial blood pressure control. During JGA development, strong Cx40 expression gradually decreased, while expression of Cx37, Cx43 and Cx45 increased, postnatally showing more equalized expression patterning. In parallel, initially dispersed renin cells localized to JGA, and greatly increased expression in postnatal kidneys. In CNF kidneys, increased levels of Cx43, Cx37 and Cx45 co-localized with accumulations of renin cells in JGA. Additionally, they reappeared in extraglomerular mesangial cells, indicating association between return to embryonic Cxs patterning and pathologically changed kidney tissue. Based on the described Cxs and renin expression patterning, we suggest involvement of Cx40 primarily in the formation of JGA in developing kidneys, while Cx37, Cx43 and Cx45 might participate in JGA signal transfer important for postnatal maintenance of kidney function and blood pressure control.

Protocolo diagnóstico y terapéutico de la nefropatía diabética

Diabetic nephropathy (DN) is a common disorder in diabetic patients associated with increased cardiovascular risk. The diagnosis is fundamentally clinical, based on a persistent reduction of the estimated glomerular filtration rate (eGFR) (using CKD-EPI equation and/or proteinuria [albumin/creatinine ratio in urine]). Other tests are required in atypical presentation, including kidney biopsy for selected cases. Staging and follow-up is based on albuminuria values and eGFR. Management includes general treatment, glycemic control (glycosylated hemoglobin [HbA1c] levels<7%) and the control of arterial blood pressure (< 130/80mmHg). Nephroprotective drugs like renin-angiotensin-aldosterone blockers (ACEI and ARA II), sodium–glucose co-transporter type 2 (SGLT2) and glucagon-like peptide-1 receptor agonists (GLP1), which improve renal prognosis and preventing cardiovascular events.

P1009RENAL OUTCOMES IN DIABETIC KIDNEY PATIENTS TREATED WITH GLP1 AGONIST RECEPTORS VS SGLT2 INHIBITORS

Abstract Background and Aims End stage renal disease of diabetic cause is an increasing issue worldwide. Both GLP1 antagonist receptors (GLP1ar) and the sodium-glucose co-transporter 2 inhibitors (SGLT2i) have shown promising results in preventing or ameliorating the progression of renal disease, however there is no data comparing the effect of both drugs on renal outcomes. Method Here we present the result of a retrospective study analyzing the main renal outcomes of 98 T2DM patients treated with GLP1ar (25% dulaglutide, 25% liraglutide, 50% semaglutide) or SLGT2 (46.9% dapagliflozin, 21% empagliflozin, 32.1% canagliflozin). All participants were on ACEi/ARB on maximally tolerated dose and patients that have been on both treatments at any time during observation period were excluded. Mean follow-up was 1,9 years, (SD 1,1). Results Main descriptive data are shown on the table: in summary, patients on SGLT2i had higher eGFR (64,7 SD 22,7 vs 43,7 SD 13,5) ml/min/1,73m2 (p&amp;lt;0.001), lower BMI (30,2 SD 4,8 vs 35,0 SD 4,0 p&amp;lt;0,001) and were more frequently free from previous cardiovascular events (60% vs 29,4%, p 0,02)Incident kidney disease defined as drop of eGFR below 60 ml/min/1,73m2 and/or new onset albuminuria occurred on 18 (39,1%) and 7 (87,5%) of patients on SGLT2i and GLP1ar respectively (p 0,01), however, nor SGLT2i or GLP1ar treated patients suffered significant decrease on eGFR along the study period (2.5% change in eGFR-SGLT2i and 5% in GLP1ar). We found no significant differences on arterial blood pressure or glycemic control along the study period and BMI decrease was only significative on GLP1ar patients (-7,7%, p&amp;lt;0.001)6,7% and 15,8% of patients treated with GLP1ar and SGLT2i respectively suffered one CV event along the follow-up period (p ns) with 6,7% deaths on both groups (0.03 death/patient-year). Adverse events were similar on both groups though discontinuation rate was higher on SGLT2i (16,7% gastrointestinal intolerance, 58% “others”) Conclusion We conclude that both GLP1ar and SGLT2i prevent progression of kidney disease in T2DM patients. Though GLP1ar patients showed higher rates of incident kidney disease, when initiated on already decreased GFR this treatment achieved similar results to SGLT2i in preventing progression of kidney disease even in high cardiovascular risk patients.

Reduced sympathetic baroreflex sensitivity in individuals with multiple sclerosis during the Valsalva maneuver

Multiple sclerosis (MS) is a neurodegenerative autoimmune disease characterized by demyelination in central nervous system leading to potential impairments in the autonomic control of cardiovascular function. We have previously demonstrated individuals with MS exhibit a diminished ability to increase blood pressure in response to a simulated hypotensive stimulus (carotid neck pressure) compared with healthy controls likely due to impaired sympathetic modulation of the vasculature. The aim of the current investigation was to test the hypothesis that individuals with MS have a blunted muscle sympathetic nerve response (MSNA) to drops in arterial blood pressure induced via a Valsalva maneuver compared to matched healthy controls. Four patients with relapsing‐remitting MS (2 females/2 males, EDSS &lt; 4) and 4 sex‐, age‐ and mass‐matched healthy controls were instrumented for MSNA (peroneal nerve), arterial blood pressure (Finometer), and heart rate. Participants performed a Valsalva maneuver (VM) at 40 mmHg for a 15 s after a normal inspiration. Sympathetic baroreflex function was assessed by relating all sympathetic burst occurring during the 15 s straining period of the VM to the maximum fall in DBP measured from highest values (Phase I) to the nadir prior to the end of the VM (Phase III). Drops in diastolic pressure during the Valsalva were similar between groups (MS: −31 ± 10 mmHg: CON: −25 ± 15 mmHg; P = 0.30). Individuals with MS produced less total MSNA bursts during the 15 s VM compared to healthy controls (MS: 8.3 ± 4.1 bursts/15 s; CON: 15.0 ± 4.1 bursts/15 s; P = 0.003). Sympathetic baroreflex sensitivity was reduced in individuals with MS (MS: −0.32 ± 0.25 bursts/15 s/mmHg) vs. CON: −0.77 ± 0.43 bursts/15 s/mmHg; P = 0.048). Individuals with MS have a reduced ability to increase MSNA in response to decreases in blood pressure during the VM confirming previous speculations of abnormal sympathetic baroreflex control of arterial blood pressure in this clinical population.Support or Funding InformationNIH R15HL117224; National MS Society RG4696A3

Astrocytes monitor cerebral perfusion and control systemic circulation to maintain brain blood flow

Astrocytes provide neurons with essential metabolic and structural support, modulate neuronal circuit activity and may also function as versatile surveyors of brain milieu, tuned to sense conditions of potential metabolic insufficiency. Here we show that astrocytes detect falling cerebral perfusion pressure and activate CNS autonomic sympathetic control circuits to increase systemic arterial blood pressure and heart rate with the purpose of maintaining brain blood flow and oxygen delivery. Studies conducted in experimental animals (laboratory rats) show that astrocytes respond to acute decreases in brain perfusion with elevations in intracellular [Ca2+]. Blockade of Ca2+-dependent signaling mechanisms in populations of astrocytes that reside alongside CNS sympathetic control circuits prevents compensatory increases in sympathetic nerve activity, heart rate and arterial blood pressure induced by reductions in cerebral perfusion. These data suggest that astrocytes function as intracranial baroreceptors and play an important role in homeostatic control of arterial blood pressure and brain blood flow.

An optimal interval type-2 fuzzy logic control based closed-loop drug administration to regulate the mean arterial blood pressure

Background and ObjectiveThe main aim of this work is to present an optimal and robust controller design in order to improve the drug infusion to the automatic control of mean arterial blood pressure in conditions like critically-ill or post-operative or anaesthesia administration. The physiological systems also have uncertainty issues such as parameter variations with time or external disturbances and noise. Therefore, a controlled drug administration is necessary to regulate the mean arterial blood pressure of a person during surgery/observation. Over the years, the proportional-integral-derivative (PID) controller is the most commonly used controller in industries due to its easy structure and simplicity. However, this controller does not meet the desired performance with the complex and uncertain plants. Therefore, a robust controller is required to regulate the physiological variables that are uncertain in nature and can affect the human life. MethodsIn this work, a hybrid control scheme consisting of an interval type-2-fuzzy logic controller which acts as pre-compensator to the traditional PID controller is presented, to regulate the mean arterial blood pressure of a patient by administering the drug sodium nitroprusside in a controlled manner. An effective and well-established nature-inspired optimization technique namely cuckoo search algorithm is employed for obtaining the optimal parameters for the presented scheme. ResultsSimulation results are presented to show the effectiveness and robustness of proposed interval type-2-fuzzy logic controller based PID controller scheme, for maintaining the mean arterial pressure to 100 mmHg within considerable limit through SNP infusion. The results are further compared with other two controllers namely type-1 fuzzy logic based PID and traditional PID controllers for the parameter variations and external noise. ConclusionIn this study, the proposed interval type-2-fuzzy logic controller pre-compensator based PID controller provides an effective control than traditional type-1 fuzzy logic based control scheme and PID controller in terms of overshoot, settling-time and error which are the prime performance objectives of the closed-loop controlled drug delivery of human blood pressure. The presented study provides a firm base for initial design considerations for development of a low-cost closed-loop drug delivery system for blood pressure regulation.

Cardiac complications in children with chronic renal: Prevalence of risk factors

Cardiovascular complications are the leading cause of death and morbidity in chronic hemodialysis patients. The purpose of this study was to identify the factors associated with major cardiovascular events in hemodialysis children. Bi-centric study was carried out during in 2016 into two hemodialysis departments. We included hemodialysis children for more than one year. Fifty-two patients were included, sex ratio M/F: 1.3, average age: 10.7 years-old (3–16). The dialysis duration was 72.5 ± 1.6 months. Cardiac risk factors were evaluated: the hemoglobin blood concentration was < 10 g/dl in 31 patients; 6 children had hemoglobin level < 7 g/dl. Diastolic systolic hypertension was noted in 65% of patients, 5% of children presented HT grade 3, and 41.95% of patients had arteriovenous fistulas. Clinical and biological secondary hyperparathyroidism was diagnosed in 21.06% of patients. An acute pulmonary edema (APO) occurred in 45% of patients and pericarditis in 10%. Overall heart failure (1.20%), and arrhythmias (11.90%) were also retrieved. Echocardiography allowed to identify 21% of patients with pulmonary arterial hypertension (PAH); 86% of patients evidenced left ventricular hypertrophy and 50% a dilation of the left ventricle. PAH and LV dilatation were the most frequent morphological abnormalities. Posterior pericardial detachment was found in a proportion of 11.04%. Mitral and tricuspid valves abnormalities were noted in 31 patients. Three patients died during the study (hemorrhagic stroke in 2 patients, and overall heart failure in 1 patient), after an average duration of hemodialysis treatment of 2.5 years. Multivariate analysis allowed to show that severe arterial hypertension (RR = 12.15 [3.2–34.1]) and left ventricular systolic dysfunction (RR = 2.5 [1.02–08.3]) were major risk factors for mortality. Cardiovascular complications are almost constant in hemodialysis children with chronic renal failure strongly related with left ventricular hypertrophy and arterial hypertension. The high risk of mortality related to these cardiac complications makes it essential to have good control of arterial blood pressure and especially a good observance of treatment and regimen in hemodialysis children.

Multi-Model Adaptive Predictive Control System for Automated Regulation of Mean Blood Pressure

After cardiac surgery operation, severe complications may occur in patients due to hypertension. To decrease the chances of complication it is necessary to reduce elevated mean arterial pressure (MAP) as soon as possible. Continuous infusion of vasodilator drugs, such as sodium nitroprusside (Nipride), it is used to reduce MAP quickly in most patients. For maintaining the desired blood pressure, a constant monitoring of arterial blood pressure is required and a frequently adjust on drug infusion rate. The manual control of arterial blood pressure by clinical professionals it is very demanding and time consuming, usually leading to a poor control quality of the hypertension. The objective of the study is to develop an automated control procedure of mean arterial pressure (MAP), during acute hypotension, for any patient, without changing the controller. So, a multi-model adaptive predictive methodology was developed and, for each model, a Predictive Controller can be a priori designed (MMSPGPC). In this paper, a sensitivity analysis was performed and the simulation results showed the importance of weighting factor (φ), which controls the initial drug infusion rate, to prevent hypotension and thus preserve patient's health. Simulation results, for 51 different patients, showed that the MMSPGPC provides a fast control with mean settling time of 04:46 min, undershoots less than 10 mmHg and steady-state error less than ± 5 % from the MAP setpoint.

The Effect of Different Doses of Isoflurane on Hemodynamic Changes and Bleeding in Patients Undergoing Endoscopic Sinus Surgery under General Anesthesia.

BackgroundNowadays, endoscopic sinus surgery is one of the most common surgeries in the field of ear, nose, and throat. This surgery has always been followed by bleeding and can cause hemodynamic disorders due to the direct effect of the endoscopic sinus surgery.ObjectivesThis study aimed to investigate the hemodynamic changes with different doses of isoflurane during endoscopic sinus surgery.MethodsIn a randomized clinical trial, 90 patients were selected based on ASA class I and II, and divided into three groups of 30 people. The method of anesthesia induction in groups was alike. After induction anesthesia, isoflurane with percentages of 1%, 1.2%, and 1.5% was used in the groups of 1, 2, and 3, respectively and remifentanil was fixed and used in the groups in a dose of 0.1 g/kg/min during the surgery.ResultsThere was a significant difference in changes in mean of arterial pressure (MAP) after induction in the 3 groups (P < 0.001) that the reduction in mean of arterial pressure between 1 and 3 groups and between 2 and 3 groups were significantly different. There was a significant difference in heart rate per 30, 45, and 60 minutes between 1 and 2 groups (P < 0.001). ConclusionsIsoflurane percentages of 1.5% versus 1.2% and 1% affected generally a considerable reduction rate of 1% in bleeding and better control of mean arterial blood pressure. In addition, the mean heart rate in several minutes in group 2 with 1.2% isoflurane was less than other groups.

Perioperative Quality Initiative consensus statement on the physiology of arterial blood pressure control in perioperative medicine

BackgroundPerioperative arterial blood pressure management is a physiologically complex challenge influenced by multiple factors. MethodsA multidisciplinary, international working subgroup of the Third Perioperative Quality Initiative (POQI) consensus meeting reviewed the (patho)physiology and measurement of arterial pressure as applied to perioperative medicine. We addressed predefined questions by undertaking a modified Delphi analysis, in which primary clinical research and review articles were identified using MEDLINE. Strength of recommendations, where applicable, were graded by National Institute for Health and Care Excellence (NICE) guidelines. ResultsMultiple physiological factors contribute to the perioperative physiological importance of arterial pressure: (i) arterial pressure is the input pressure to organ blood flow, but is not the sole determinant of perfusion pressure; (ii) blood flow is often independent of changes in perfusion pressure because of autoregulatory changes in vascular resistance; (iii) microvascular dysfunction uncouples microvascular blood flow from arterial pressure (haemodynamic incoherence). From a practical clinical perspective, we identified that: (i) ambulatory measurement is the optimal method to establish baseline arterial pressure; (ii) automated and invasive arterial pressure measurements have inherent physiological and technical limitations; (iii) individualised arterial pressure targets may change over time, especially in the perioperative period. There remains a need for research in non-invasive, continuous arterial pressure measurements, macro- and micro-circulatory control, regional perfusion pressure measurement, and the development of sensitive, specific, and continuous measures of cellular function to evaluate blood pressure management in a physiologically coherent manner. ConclusionThe multivariable, complex physiology contributing to dynamic changes in perioperative arterial pressure may be underappreciated clinically. The frequently unrecognised dissociation between arterial pressure, organ blood flow, and microvascular and cellular function requires further research to develop a more refined, contextualised clinical approach to this routine perioperative measurement.

Posterior reversible encephalopathy syndrome secondary to preeclampsia-a case report

In this article, we aimed to present a 29 year-old preeclampsia patient with sudden loss of vision in both eyes after cesarean section. In her ophthalmoscopic examination her visual acuity was at the level of light perception on both of eyes. The anterior segment examination of the patient was normal with normal eye movement in all directions. The fundus had a tilted disc, which was evident on the left. Emergency orbital, cranial MRI, carotid Doppler were requested with arterial blood pressure control of the patient. Close follow-up was recommended. Patient was diagnosed as posterior reversible encephalopathy syndrome with cortical visual loss due to vasogenic edema according to diffusion MRI result. PatientÂ’s visual acuity was 10/10 on the right side and 16/100 on the left side after 3 days with control of arterial blood pressure.

The cervicofacial lift under pure local anaesthesia diminishes the incidence of post-operative haematoma

The cervicofacial lift is a frequently performed procedure in plastic surgery. It is the reference technique for facial rejuvenation and restoration of the oval form of the face and it is essential to treat excess skin. One of the most frequent complications of this procedure is the formation of haematomas. The aim of this article is to analyse the incidence of bleeding in the standard cervicofacial lift carried out under pure local anaesthesia. The entire operation, including liposuction and tightening of the SMAS, can be done under local anaesthesia. A total of 1500 patients, who have undergone cervicofacial lift under pure local anaesthesia between November 1995 and January 2016, were included in the study. The incidence of early bleeding (in the first 15 days following the operation) was recorded and analysed. Pre- intra- and post-operative monitoring of the arterial blood pressure revealed stable pressure in the peri‑operative period. The mean difference in blood pressure when comparing the intra-operative to the post-operative periods was 7 mmHg for the systolic BP [range from 3 to 25] and 4 mmHg [range from 2 to 12] for the diastolic BP, with lower mean values in the post-operative period. We identified nine bleeding events in 1500 patients (0.6%). The cervicofacial lift under pure local anaesthesia does not radically modify the surgical technique. It allows better control of arterial blood pressure of patients throughout the surgical procedure and avoids fluctuations in blood pressure, which is one of the main causes of bleeding and haematoma formation. The infiltration of xylocaine adrenaline combined with the absence of hypotensive general anaesthesia diminishes the incidence of haematoma and ensures an early return home for the patients.

150. Uteroplacental acute atherosis, cardiovascular biomarkers and vasoactive hormones in pregnancy

Introduction Cardiovascular disease (CVD) is the leading cause of death for women. A history of hypertensive disorders of pregnancy increases the risk. Uteroplacental spiral arterial.acute atherosis is a pregnancy-specific lesion resembling early atherosclerosis, frequently found in preeclampsia. The renin-angiotensin-system (RAS) plays a role in atherosclerosis and is dysregulated in preeclampsia. RAS and natriuretic peptides are physiological opponents in the regulation of arterial blood pressure and intravascular volume control. We previously reported increased concentrations of the natriuretic hormone precursor midregional proatrial natriuretic peptide (MR-proANP) in preeclampsia and suggested a cardiac origin. Objective To assess whether uteroplacental acute atherosis correlates with cardiovascular biomarkers and vasoactive hormones in maternal circulation at delivery in preeclamptic and normotensive pregnancies. Methods Third trimester maternal blood samples were analyzed for renin, prorenin and MR-proANP [normotensive pregnancies n = 50, preeclampsia (PE) n = 71]. Decidua basalis tissue for acute atherosis diagnosis (immunohistochemistry) was available for 53 of these pregnancies (normotensives n = 25 and PE n = 28). Statistical analyses: Skewed data were log-transformed. Linear regression and Fisher’s Exact test were applied as appropriate. A p-value Results A negative correlation between renin and MR-proANP concentrations was confirmed for both study groups. The presence of acute atherosis was not associated with maternal levels of circulating renin, prorenin or MR-proANP. Presence of acute atherosis was neither associated with MR-proANP/renin ratio nor maternal renin in the lower 2 quartiles in combination with MR-proANP in the upper 2 quartiles (normotensives p = 1.0 and PE p = 0.7). Discussion This is the first report on RAS and vasoactive hormones in pregnancy in relation to uteroplacental acute atherosis. We find that maternal circulating biomarkers previously shown to indicate hemodynamic stress in preeclampsia are not increased in pregnancies with acute atherosis. Further studies exploring the longitudinal association between maternal circulating cardiovascular biomarkers and postpartum CVD surrogate markers are underway.

Curative Transvenous Embolization for Ruptured Brain Arteriovenous Malformations: A Single-Center Experience from China

To evaluate feasibility and safety of transvenous embolization for brain arteriovenous malformations (AVMs). Between November 2016 and August 2017, a transvenous endovascular embolization protocol was implemented at the Henan Provincial People's Hospital for consecutive patients with ruptured brain AVMs. Therapeutic decision making was based on Spetzler-Martin grade, brain AVM location, pattern of venous drainage, and angioarchitecture. Transvenous embolization was combined with transarterial support. Complete angiographic obliteration of the nidus was the objective of treatment. Among 10 patients with ruptured brain AVMs, 8 were male. Spetzler-Martin grades before transvenous embolization were IV in 3 patients, III in 5 patients, II in 1 patient, and I in 1 patient. Modified Rankin Scale score before the procedure was 0-2 for 6 of 10 patients. Five patients also had deep venous drainage. Arterial blood pressure control and venous pressure cooker technique were used in all 10 patients; 9 patients had immediate angiographic occlusion. Two patients had a ventricular hemorrhage, which did not cause any disability after medical treatment. Seven patients underwent angiography 3-5 months after the procedure, and complete obliteration of the nidus was confirmed. Median clinical follow-up for all 10 patients was 8 months (range, 3-12 months). Epilepsy occurred in 1 patient 3 months after the procedure, and modified Rankin Scale scores for all patients were ≤1. Transvenous embolization of brain AVMs is feasible and may improve cure rates. The safety and long-term effects need further validation.

Vascular and autonomic changes in adult cancer patients receiving anticancer chemotherapy.

Chemotherapy is associated with acute and long-term cardiotoxicity. To date, risk assessment has primarily focused on the heart; however, recent findings suggest that vascular and autonomic function may also be compromised. Whether this occurs during chemotherapy treatment remains unknown. Therefore, the present study evaluated carotid artery stiffness, cardiovagal baroreflex sensitivity (cBRS), and heart rate variability (HRV) in cancer patients currently being treated with adjuvant chemotherapy. Eleven current cancer patients receiving adjuvant chemotherapy and 11 matched (1:1) controls were studied. Carotid artery stiffness was assessed via two-dimensional ultrasonography. cBRS was assessed from the spontaneous changes in beat-to-beat time series of R-R interval and systolic blood pressure via the cross-correlation technique. HRV was assessed using the standard deviation of R-R intervals (SDNN) and low (LF) and high (HF) power frequencies. Carotid artery β-stiffness was significantly higher in the cancer patients compared with control participants (8.0 ± 0.8 vs. 6.3 ± 0.6 U, respectively; P = 0.02). cBRS was lower in the cancer patients compared with controls (4.3 ± 0.7 vs. 10.7 ± 1.9 ms/mmHg, respectively; P = 0.01), and all indices of HRV were lower in the cancer patients (SDNN, P = 0.02; LF, P = 0.01; HF, P = 0.02). There was no significant correlation between β-stiffness and cBRS ( P = 0.4). However, LF power was significantly correlated with cBRS (r = 0.66, P < 0.001). Compared with matched healthy controls, cancer patients undergoing chemotherapy demonstrated a significantly higher arterial stiffness and lower cBRS. The previously reported adverse effects of chemotherapy on the heart appear to also influence other aspects of cardiovascular health. NEW & NOTEWORTHY Patients treated with anticancer chemotherapy exhibit an impaired baroreflex control of arterial blood pressure and increased arterial stiffness. These findings hold significant value, in particular as part of a risk-stratification strategy in current cancer patients receiving chemotherapy. This is the first investigation, to our knowledge, to demonstrate an attenuated spontaneous baroreflex control of arterial blood pressure in cancer patients currently undergoing chemotherapy.

Intracranial Pressure Is a Determinant of Sympathetic Activity

Intracranial pressure (ICP) is the pressure within the cranium. ICP rise compresses brain vessels and reduces cerebral blood delivery. Massive ICP rise leads to cerebral ischemia, but it is also known to produce hypertension, bradycardia and respiratory irregularities due to a sympatho-adrenal mechanism termed Cushing response. One still unresolved question is whether the Cushing response is a non-synaptic acute brainstem ischemic mechanism or part of a larger physiological reflex for arterial blood pressure control and homeostasis regulation. We hypothesize that changes in ICP modulates sympathetic activity. Thus, modest ICP increase and decrease were achieved in mice and patients with respectively intra-ventricular and lumbar fluid infusion. Sympathetic activity was gauged directly by microneurography, recording renal sympathetic nerve activity in mice and muscle sympathetic nerve activity in patients, and gauged indirectly in both species by heart-rate variability analysis. In mice (n = 15), renal sympathetic activity increased from 29.9 ± 4.0 bursts.s−1 (baseline ICP 6.6 ± 0.7 mmHg) to 45.7 ± 6.4 bursts.s−1 (plateau ICP 38.6 ± 1.0 mmHg) and decreased to 34.8 ± 5.6 bursts.s−1 (post-infusion ICP 9.1 ± 0.8 mmHg). In patients (n = 10), muscle sympathetic activity increased from 51.2 ± 2.5 bursts.min−1 (baseline ICP 8.3 ± 1.0 mmHg) to 66.7 ± 2.9 bursts.min−1 (plateau ICP 25 ± 0.3 mmHg) and decreased to 58.8 ± 2.6 bursts.min−1 (post-infusion ICP 14.8 ± 0.9 mmHg). In patients 7 mmHg ICP rise significantly increases sympathetic activity by 17%. Heart-rate variability analysis demonstrated a significant vagal withdrawal during the ICP rise, in accordance with the microneurography findings. Mice and human results are alike. We demonstrate in animal and human that ICP is a reversible determinant of efferent sympathetic outflow, even at relatively low ICP levels. ICP is a biophysical stress related to the forces within the brain. But ICP has also to be considered as a physiological stressor, driving sympathetic activity. The results suggest a novel physiological ICP-mediated sympathetic modulation circuit and the existence of a possible intracranial (i.e., central) baroreflex. Modest ICP rise might participate to the pathophysiology of cardio-metabolic homeostasis imbalance with sympathetic over-activity, and to the pathogenesis of sympathetically-driven diseases.

Postpartum management of hypertensive disorders of pregnancy: a systematic review

ObjectivesHypertensive disorders of pregnancy (HDP) affect one in ten pregnancies and often persist postpartum when complications can occur. We aimed to determine the effectiveness and safety of pharmacological interventions, other...