Redistribution Of Blood Flow Research Articles

The effects of cardiac stenting on the organ of vision in patients with chronic ischemic optic neuropathy

Purpose. To evaluate the effect of coronary artery stenting on the functional state of organ of vision in patients with chronic ischemic optic neuropathy (CION). Material and methods. 33 patients (53 eyes) diagnosed with CION aged 51 to 85 years, average 66.78±1.54 years, who underwent stenting of the coronary arteries. Results. Stenting of the coronary arteries did not affect on BCVA parameters, the percentage of pupil contraction increased from 9.57±0.49 to 9.74±0.46 ms (p<0.05), the recovery of the sympathetic phase of the pupil’s reaction to light accelerated from 83.79±0.44 to 83.56±0.43 ms (p<0.05), a decrease in IACG was recorded from 13.39±4.67 to 7.01±0.56 mm Hg. Art./ mm3 (p<0.05), negative dynamics of CFSM in green color from 33.5±0.8 to 33.06±0.73 after 1 month and to 33.17±0.75 after 3 months from initial values, deterioration of static perimetry after 3 months from 94.60±0.97 to 93.17±1.88 (p<0.05), narrowing of kinetic perimetry to green stimulus after 1 month from 267.48±13.96 up to 267.48±13.96 gr. (p<0.05). Conclusion. In the subjects, cardiac symptoms predominated rather than visual ones. In patients who underwent stenting of the coronary arteries, BCVA did not change and remained at the same level throughout the entire observation period; according to ultrasonography of the orbital vessels, there was an insignificant redistribution of blood flow in the ophthalmic artery basin; IACG significantly decreased by 2 times after 1 month (p<0.05), the indicator of CFSM for green color worsened in long-term follow-up (p<0.05), negative dynamics were recorded according to the program of static perimetry and kinetic perimetry for green color 1 later (p<0.05). Revascularization of the coronary arteries affects the restoration of the sympathetic phase of the pupil’s response to light and the force of pupil contraction (p<0.05). Key words:: chronic ischemic optic neuropathy, the cardiovascular system, cardiac stenting, optic nerve

Clinical Characteristics of Immediate Contralateral Ischemia Subsequent to Revascularization for Moyamoya Disease

Moyamoya disease is a bilateral steno-occlusive disease involving the cerebral vasculature. While some patients are affected by procedure-related ipsilateral ischemia, ischemic complications contralateral to the revascularization are rarely observed. We retrospectively investigated 135 hemispheres (103 patients) that underwent revascularization in our institution between April 2006 and September 2022. Revascularization surgery comprised single superficial temporal artery-middle cerebral artery anastomosis and encephalo-myo-synangiosis. Certain patients aged under 10years underwent indirect revascularization. Bilateral revascularization was performed with an interval of >3months. Medical records and neuroimages were reviewed, and patients with contralateral ischemic complications were identified. Some cases underwent genetic analysis. The mean age was 34.5 (range: 5-71) years, and 95 cases (70.4%) were in women. Of the 102 cases examined for the RNF213 c.14429G > A (p.Arg4810Lys) variant, 33 (32.4%) and 69 (67.6%) showed the GG and GA genotype, respectively. Three cases (2.2%, all female, age range 44-71years) were complicated with contralateral infarction. The infarcted area distributions of the 2 cases with RNF213 c.14429G > A variant were patchy and peripheral. Theother case showed on magnetic resonance imaging (MRI) angiography total occlusion of the internal carotidartery where patency had been confirmed preoperatively. Contralateral ischemia after revascularization occurred in 2.2% of cases. We classified them into peripheral and central types: peripheral type, an infarction owing to hemodynamic insufficiency or intracranial blood flow redistribution; central type, total occlusion of the contralateral internal carotid artery. Intensive preoperative management can minimize the risk of peripheral types, and neurosurgeons should beware of severe central types.

Hypoxia sensing in the body: An update on the peripheral and central mechanisms.

An adequate supply of O2 is essential for the maintenance of cellular activity. Systemic or local hypoxia can be experienced during decreased O2 availability or associated with diseases, or a combination of both. Exposure to hypoxia triggers adjustments in multiple physiological systems in the body to generate appropriate homeostatic responses. However, with significant reductions in the arterial partial pressure of O2, hypoxia can be life-threatening and cause maladaptive changes or cell damage and death. To mitigate the impact of limited O2 availability on cellular activity, O2 chemoreceptors rapidly detect and respond to reductions in the arterial partial pressure of O2, triggering orchestrated responses of increased ventilation and cardiac output, blood flow redistribution and metabolic adjustments. In mammals, the peripheral chemoreceptors of the carotid body are considered to be the main hypoxic sensors and the primary source of excitatory feedback driving respiratory, cardiovascular and autonomic responses. However, current evidence indicates that the CNS contains specialized brainstem and spinal cord regions that can also sense hypoxia and stimulate brain networks independently of the carotid body inputs. In this manuscript, we review the discoveries about the functioning of the O2 chemoreceptors and their contribution to the monitoring of O2 levels in the blood and brain parenchyma and mounting cardiorespiratory responses to maintain O2 homeostasis. We also discuss the implications of the chemoreflex-related mechanisms in paediatric and adult pathologies.

Morphological changes in the abdominal organs after left gastric artery embolization in an experiment

Objective – to experimentally evaluate the morphological changes of internal organs (liver, spleen, duodenum, pancreas) after embolization of gastric arteries.Material and methods. To conduct the experiment, 10 Vietnamese pigs aged 4-5 months, female, were selected and fed a high-fat diet for 2 months to simulate obesity. Aorta contrast and celiacography with "Vazipak" solution (5-10 ml per injection) were performed on animals under general anesthesia. Superselective bariatric embolization of the left gastric artery was performed with a 3F microcatheter. After 3 weeks, a morphological (hematoxylin-eosin staining) examination of such organs as liver, duodenum, spleen, pancreas was performed. Photofixation of the histopreparations of the relevant organs was carried out using a trinocular microscope of laboratory class Nikon Eclipse Ci-E with 10x, 20x and 40x plan achromat objectives.Results. In general, no macroscopic signs of ischemia of adjacent organs were noted against the background of the performed selective embolization of the left gastric artery. Blood filling of the liver was uneven, the perisinusoidal spaces were expanded, which indicated its edema. In the duodenum, reactive disturbances of microcirculation were manifested by expansion and congestion of venous vessels and blood stasis. Microscopic changes in the spleen were characterized by congestion of the sinusoids, while the vessels of the pancreas were unevenly filled with blood, and at the same time, venous congestion prevailed.Conclusion. Microcirculation disorders, dystrophic changes, and signs of a shock reaction, which can be considered transient, occur in the examined organs after embolization of the gastric arteries. These data indicate the safety of performing selective embolization of gastric arteries and the absence of signs of critical redistribution of blood flow or ischemia "robbing".

Abstract 15953: Stressed Into a STEMI

Introduction: Chest pain is the second most common presenting symptom in the emergency department (ED). 5.1% of all presentations with chest pain are acute coronary syndrome (ACS). ACS includes ST-segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and unstable angina (UA). We present a case of UA that progressed to STEMI after a regadenoson stress test. Case: A 55 years old male with 30 pack-year smoking history presented to the ED with sudden onset, sharp, left-sided chest pain associated with diaphoresis that lasted a few minutes. EKG showed sinus rhythm with premature ventricular complexes without ischemic changes. High sensitivity troponin at 0, 1, and 3 hours were within normal limits. While he was undergoing a radionucleotide stress test, he reported severe chest pain immediately after the regadenoson injection. Bedside telemetry showed ST elevation in inferior leads. EKG was consistent with 1mm ST-elevation in leads II, III, and aVF. He underwent an emergent coronary angiogram which revealed 100% occlusion in the mid-right coronary artery (RCA) and 80% in the second marginal distribution. He received a drug-eluting stent to RCA with the resolution of his chest pain. Discussion: Rupture or erosion of atherosclerotic plaque exposes the underlying thrombogenic core which can lead to occlusion of the coronary artery. A partial occlusion due to an unstable plaque can lead to UA or NSTEMI. STEMI results from complete occlusion of the coronary circulation. In our case, the patient presented with unstable angina however undergoing a stress test triggered him to STEMI. The administration of regadenoson led to coronary vasodilation, resulting in the redistribution of coronary blood flow away from the nearly occluded RCA but what led to plaque rupture at the same time leading to a STEMI is unclear. Conclusions: A regadenson stress test can trigger STEMI in patients with unstable angina however the mechanism is unclear

Age-related alterations in the cardiovascular responses to acute exercise in males and females: role of the exercise pressor reflex.

Autonomic adjustments of the cardiovascular system are critical for initiating and sustaining exercise by facilitating the redistribution of blood flow and oxygen delivery to meet the metabolic demands of the active skeletal muscle. Afferent feedback from active skeletal muscles evokes reflex increases in sympathetic nerve activity and blood pressure (BP) (i.e., exercise pressor reflex) and contributes importantly to these primary neurovascular adjustments to exercise. When altered, this reflex contributes significantly to the exaggerated sympathetic and BP response to exercise observed in many cardiovascular-related diseases, highlighting the importance of examining the reflex and its underlying mechanism(s). A leading risk factor for the pathogenesis of cardiovascular disease in both males and females is aging. Although regular exercise is an effective strategy for mitigating the health burden of aging, older adults face a greater risk of experiencing an exaggerated cardiovascular response to exercise. However, the role of aging in mediating the exercise pressor reflex remains highly controversial, as conflicting findings have been reported. This review aims to provide a brief overview of the current understanding of the influence of aging on cardiovascular responses to exercise, focusing on the role of the exercise pressor reflex and proposing future directions for research. We reason that this review will serve as a resource for health professionals and researchers to stimulate a renewed interest in this critical area.

Réducteur de sinus coronaire : revue de littérature et enjeux autour du registre France Reducer

Coronary sinus Reducer implantation is a percutaneous technique used to treat patients suffering from refractory angina pectoris. The device narrows the coronary sinus, increases the back pressure in the myocardial venous system and forces redistribution of coronary blood flow from less ischemic subepicardium to the more ischemic subendocardium. Multiple clinical studies had proven its efficacy to alleviate myocardial ischemia and related symptoms, and to improve the quality of life of patients with refractory symptomatic chronic coronary artery disease for whom coronary revascularization is deemed unsuitable. This literature review aims to expose the device design, its mechanisms of action, and the clinical data supporting its use.Since November 2021 Reducer's reimbursement has been granted in France by the national health authority. It is the first device to be approved under a newly established reimbursement approval process. A transitional coverage is provided with opportunities for renewal before applying for full-time reimbursement. To fulfill the requirements of the National Commission for Evaluation of Medical Devices and Health Technologies, the French Society of Cardiology has been creating the France Reducer registry. This clinical registry has been collecting data from patients undergoing coronary sinus Reducer implantation regarding their clinical situation, periprocedural information, and one-year follow-up. It is crucial for the future of this emerging therapeutic option in France. To date, 215 patients from 28 centers have been included between June 2022 and September 2023.

PENERAPAN CATATAN AKTIFITAS FISIK, DIET, ISTIRAHAT & KELOLA STRESS PADA IBU RUMAH TANGGA DI RT.2 RW.4 GAYUNGAN, SURABAYA

Introduction & Aim: This PPM activity is motivated by the high incidence of non-communicable diseases such as cardiovascular disease. The epidemiological transition of this disease describes a tendency towards degenerative diseases which is determined by people's behavior. Based on a survey conducted in RT 2 RW 4, Gayungan, Surabaya City, most of the residents suffer from high blood pressure. High blood pressure is a type of cardiovascular disease. The aim of this activity is to provide education on healthy lifestyles to avoid the risk of contracting CHD to residents. Method of Activity: This community service is carried out by providing education about cardiovascular disease and its prevention. At the end of the education, being given a notebook of daily activities can be a motivation to continue to behave in a healthy way to manage stress. Results: This activity was carried out on Jl. Dukuh Menanggal RT 2 RW 4 Gayungan sub-district, Surabaya City. Education is provided through PowerPoint media, leaflets, and daily recording sheets to improve healthy living and manage stress. After being given counseling, the level of knowledge of residents increased. To be able to implement what they have learned, residents are provided with personal notes as a reminder to live healthily. Discussion: survey results show that the majority of residents still lack regular physical activity. Cardiovascular disease is prone to attack people who lack physical activity. Physical exercise and sports activities will increase cardiac output, redistribution of blood flow, and reduce cholesterol and blood fat levels. Eating foods with balanced nutrition, as well as fruit and vegetables can provide additional vitamins, antioxidants, and fiber that the body needs. Conclusion living a healthy lifestyle with regular physical activity and eating more fruit and vegetables can avoid degenerative diseases.

The role of leptomeningeal collaterals in redistributing blood flow during stroke.

Leptomeningeal collaterals (LMCs) connect the main cerebral arteries and provide alternative pathways for blood flow during ischaemic stroke. This is beneficial for reducing infarct size and reperfusion success after treatment. However, a better understanding of how LMCs affect blood flow distribution is indispensable to improve therapeutic strategies. Here, we present a novel in silico approach that incorporates case-specific in vivo data into a computational model to simulate blood flow in large semi-realistic microvascular networks from two different mouse strains, characterised by having many and almost no LMCs between middle and anterior cerebral artery (MCA, ACA) territories. This framework is unique because our simulations are directly aligned with in vivo data. Moreover, it allows us to analyse perfusion characteristics quantitatively across all vessel types and for networks with no, few and many LMCs. We show that the occlusion of the MCA directly caused a redistribution of blood that was characterised by increased flow in LMCs. Interestingly, the improved perfusion of MCA-sided microvessels after dilating LMCs came at the cost of a reduced blood supply in other brain areas. This effect was enhanced in regions close to the watershed line and when the number of LMCs was increased. Additional dilations of surface and penetrating arteries after stroke improved perfusion across the entire vasculature and partially recovered flow in the obstructed region, especially in networks with many LMCs, which further underlines the role of LMCs during stroke.

Cardiovascular decline in offspring during the perinatal period in an ovine model of fetal growth restriction.

Fetal growth restriction (FGR) increases the risk cardiovascular disease (CVD) in adulthood. Placental insufficiency and subsequent chronic fetal hypoxemia are causal factors for FGR, leading to a redistribution of blood flow that prioritizes vital organs. Subclinical signs of cardiovascular dysfunction are evident in growth-restricted neonates; however, the mechanisms programming for CVD in adulthood remain unknown. This study aimed to determine the potential mechanisms underlying structural and functional changes within the heart and essential (carotid) and nonessential (femoral) vascular beds in growth-restricted lambs. Placental insufficiency was surgically induced in ewes at 89 days gestational age (dGA, term = 148dGA). Three age groups were investigated: fetal (126dGA), newborn (24 h after preterm birth), and 4-wk-old lambs. In vivo and histological assessments of cardiovascular indices were undertaken. Resistance femoral artery function was assessed via in vitro wire myography and blockade of key vasoactive pathways including nitric oxide, prostanoids, and endothelium-dependent hyperpolarization. All lambs were normotensive throughout the first 4 wk of life. Overall, the FGR cohort had more globular hearts compared with controls (P = 0.0374). A progressive decline in endothelium-dependent vasodilation was demonstrated in FGR lambs compared with controls. Further investigation revealed that impairment of the prostanoid pathway may drive this reduction in vasodilatory capacity. Clinical indicators of CVD were not observed in our FGR lambs. However, subclinical signs of cardiovascular dysfunction were present in our FGR offspring. This study provides insight into potential mechanisms, such as the prostanoid pathway, that may warrant therapeutic interventions to improve cardiovascular development in growth-restricted newborns.NEW & NOTEWORTHY Our findings provide novel insight into the potential mechanisms that program for cardiovascular dysfunction in growth-restricted neonates as our growth-restricted lambs exhibited a progressive decline in endothelium-dependent vasodilation in the femoral artery between birth and 4 wk of age. Subsequent analyses indicated that this reduction in vasodilatory capacity is likely to be mediated by the prostanoid pathway and prostanoids could be a potential target for therapeutic interventions for fetal growth restriction (FGR).

Glomerular microcirculation: Implications for diabetes, preeclampsia, and kidney injury.

This review outlines the features of tandem regulation of glomerular microcirculation by autoregulatory mechanisms and intraglomerular redistribution of blood flow. Multiple points of cooperation exist between autoregulatory and distributional mechanisms. Mutual interactions between myogenic and tubuloglomerular feedback (TGF) mechanisms regulating the inflow are briefly discussed. In addition to this, TGF operation involving purinergic, autocoid, and NO signaling affects, however, not only afferent arteriolar tone, but mesangial cell tone as well. The latter reversibly reconfigures the distribution of blood flow between the shorter and longer pathways in the glomerular tuft. I advance a hypothesis that blood flow in these pathways spontaneously alternates, and mesangial cell tonicity serves as a rheostatic shift between them. Furthermore, humoral messengers from macula densa cells, themselves dependent on myogenic mechanisms, fine-tune the secretion of renin and, subsequently, the local, intrarenal generation of angiotensin II, which, in turn, provides additional vasomotor signaling to glomerular capillaries through changing the tone of mesangial cells. This complex regulatory network may partially explain the phenomenon of renal functional reserve, as well as suggest implications for changes in renal function during pregnancy, early diabetes mellitus, and acute kidney injury.

Novel concepts in the management of angina in coronary artery disease.

Coronary artery disease remains a condition with high prevalence and detrimental effects on the quality of life of affected individuals. Its most frequent manifestation, stable angina pectoris, may be challenging to manage despite the available antianginal pharmacotherapy and adequate risk factor control, especially in subjects not amenable to revascularization. In the direction of refractory angina pectoris, several approaches have been developed over the years with varying degrees of success. Among the most recognized techniques in managing angina is enhanced external counterpulsation, which utilizes mechanical compression of the lower extremities to increase blood flow to the heart. Moving to coronary sinus reduction, it leads to an increase in coronary sinus backward pressure, ultimately augmenting myocardial blood flow redistribution to ischemic regions and ameliorating chronic angina. Clinical trial results of the above-mentioned techniques have been encouraging but are based on small sample sizes to justify their widespread application. Other interventional approaches, such as transmyocardial laser revascularization, extracorporeal shockwave myocardial revascularization, and spinal cord stimulation, have been met with either controversial or negative results, and their use is not recommended. Lastly, angiogenic therapy with targeted intramyocardial vascular endothelial growth factor injection or CD34+ cell therapy may be beneficial and warrants further investigation. In this review, we summarize the current knowledge in the field of angina management, highlighting the potential and the gaps in the existing evidence that ought to be addressed in future larger-scale, randomized studies before these techniques can be safely adapted in the clinical practice of patients with refractory angina pectoris.

Magnetic Resonance Imaging of Lung Perfusion.

"Lung perfusion" in the context of imaging conventionally refers to the delivery of blood to the pulmonary capillary bed through the pulmonary arteries originating from the right ventricle required for oxygenation. The most important physiological mechanism in the context of imaging is the so-called hypoxic pulmonary vasoconstriction (HPV, also known as "Euler-Liljestrand-Reflex"), which couples lung perfusion to lung ventilation. In obstructive airway diseases such as asthma, chronic-obstructive pulmonary disease (COPD), cystic fibrosis (CF), and asthma, HPV downregulates pulmonary perfusion in order to redistribute blood flow to functional lung areas in order to conserve optimal oxygenation. Imaging of lung perfusion can be seen as a reflection of lung ventilation in obstructive airway diseases. Other conditions that primarily affect lung perfusion are pulmonary vascular diseases, pulmonary hypertension, or (chronic) pulmonary embolism, which also lead to inhomogeneity in pulmonary capillary blood distribution. Several magnetic resonance imaging (MRI) techniques either dependent on exogenous contrast materials, exploiting periodical lung signal variations with cardiac action, or relying on intrinsic lung voxel attributes have been demonstrated to visualize lung perfusion. Additional post-processing may add temporal information and provide quantitative information related to blood flow. The most widely used and robust technique, dynamic-contrast enhanced MRI, is available in clinical routine assessment of COPD, CF, and pulmonary vascular disease. Non-contrast techniques are important research tools currently requiring clinical validation and cross-correlation in the absence of a viable standard of reference. First data on many of these techniques in the context of observational studies assessing therapy effects have just become available. LEVEL OF EVIDENCE: 5 TECHNICAL EFFICACY: Stage 5.

The effects of water temperature on cerebral blood flow during aquatic exercise

PurposeRecent studies suggest that episodic increases in cerebral blood flow (CBF) may contribute to the improvement in brain health associated with exercise training. Optimising CBF during exercise may enhance this benefit. Water immersion in ~ 30–32 °C augments CBF at rest and during exercise; however, the impact of water temperature on the CBF response has not been investigated. We hypothesised that cycle ergometry in water would increase CBF compared to land-based exercise, and that warm water would attenuate the CBF benefits.MethodsEleven young heathy participants (nine males; 23.8 ± 3.1 yrs) completed 30 min of resistance-matched cycle exercise in three separate conditions; non-immersion (Land), 32 °C and 38 °C water immersion up to the level of the waist. Middle cerebral artery velocity (MCAv), blood pressure, and respiratory measures were assessed throughout the exercise bouts.ResultsCore temperature was significantly higher in the 38 °C immersion than 32 °C (+ 0.84 ± 0.24 vs + 0.04 ± 0.16, P < 0.001), whilst mean arterial pressure was lower during 38 °C exercise compared to Land (84 ± 8 vs 100 ± 14 mmHg, P < 0.001) and 32 °C (92 ± 9, P = 0.03). MCAv was higher in 32 °C immersion compared to the Land and 38 °C conditions throughout the exercise bout (68 ± 10 vs 64 ± 11 vs 62 ± 12 cm/s, P = 0.03 and P = 0.02, respectively).ConclusionOur findings suggest that cycle exercise in warm water attenuates the beneficial impact of water immersion on CBF velocity due to redistribution of blood flow to subserve thermoregulatory demand. Our findings suggest that, whilst water-based exercise can have beneficial effects on cerebrovascular function, water temperature is a key determinant of this benefit.

The Role of PRRC2B in Cerebral Vascular Remodeling Under Acute Hypoxia in Mice.

High altitude exposure leads to various cognitive impairments. The cerebral vasculature system plays an integral role in hypoxia-induced cognitive defects by reducing oxygen and nutrition supply to the brain. RNA N6-methyladenosine (m6A) is susceptible to modification and regulates gene expression in response to environmental changes, including hypoxia. However, the biological significance of m6A in endothelial cell performance under hypoxic conditions is unknown. Using m6A-seq, RNA immunoprcipitation-seq, and transcriptomic co-analysis, the molecular mechanism of vascular system remodeling under acute hypoxia is investigated. A novel m6A reader protein, proline-rich coiled-coil 2B (PRRC2B), exists in endothelial cells. PRRC2B knockdown promoted hypoxia-induced endothelial cell migration by regulating alternative splicing of the alpha 1 chain of collagen type XII in an m6A-dependent manner and the decay of matrix metallopeptidase domain 14 and ADAM metallopeptidase domain 19 mRNA in an m6A-independent manner. In addition, conditional knockout of PRRC2B in endothelial cells promotes hypoxia-induced vascular remodeling and cerebral blood flow redistribution, thus alleviating hypoxia-induced cognitive decline. Therefore, PRRC2B is integral in the hypoxia-induced vascular remodeling process as a novel RNA-binding protein. These findings provide a new potential therapeutic target for hypoxia-induced cognitive decline.

Animal experimental study on the effects of different levels of amputation on cardiovascular system

Vascular injury resulting from lower limb amputation leads to the redistribution of blood flow and changes in vascular terminal resistance, which can affect the cardiovascular system. However, there was no clear understanding of how different amputation levels affect the cardiovascular system in animal experiments. Therefore, this study established two animal models of above-knee amputation (AKA) and below-knee amputation (BKA) to explore the effects of different amputation levels on the cardiovascular system through blood and histopathological examinations. The results showed that amputation caused pathological changes in the cardiovascular system of animals, including endothelial injury, inflammation, and angiosclerosis. The degree of cardiovascular injury was higher in the AKA group than in the BKA group. This study sheds light on the internal mechanisms of amputation's impact on the cardiovascular system. Based on the amputation level of patients, the findings recommend more comprehensive and targeted monitoring after surgery and necessary interventions to prevent cardiovascular diseases.

Echocardiographic assessment of brain sparing in small-for-gestational age infants and association with neonatal outcomes

Brain sparing is an adaptive phenomenon (redistribution of blood flow to the brain) observed in fetuses exposed to chronic hypoxia, who are at risk of intrauterine growth restriction. Here, we assessed the blood flow distribution during the early neonatal period (< 7 days of life) using echocardiography, and evaluated the impact of brain-sparing on postnatal course and neurodevelopmental outcomes. This retrospective study included 42 small-for-gestational age (SGA) infants [further classified into asymmetric SGA (a-SGA, n = 21) and symmetric SGA (s-SGA, n = 21) groups according to their birth head circumference percentiles], and 1: 2 matched appropriate-for-gestational age (AGA) infants (n = 84) admitted to the neonatal intensive care unit. Left ventricular (LV) stroke volume, LV cardiac output (LVCO), upper body blood flow (UBBF), and UBBF/LVCO ratio (%) were significantly higher in both a-SGA and s-SGA infants than in AGA infants. Both a-SGA and s-SGA groups consisted predominantly of infants with higher UBBF/LVCO (%). A UBBF/LVCO ≥ 58.2% (3rd interquartile range) was associated with a later need for rehabilitative therapy after discharge. In summary, brain-sparing effect may continue during the early postnatal life in SGA infants, and may be a promising marker to detect future adverse neurodevelopmental outcomes.

P321 NEOVASC REDUCER IMPLANTATION AS A USEFUL THERAPEUTIC CHANCE IN REFRACTORY ANGINA

Abstract Refractory angina is a clinical condition caused by myocardial ischemia inadequately controlled by medical therapy and coronary revascularization. Emblematic case of this condition concerns a 72–year–old man with chronic coronary syndrome (percutaneous transluminal coronary angioplasty [PTCA] + drug–eluting stent [DES] on the proximal portion of the left main coronary artery [LMCA] in 2009 and PTCA + 2 overlapping DES on the proximal portion of the right coronary artery [RCA] in 2017) who accessed in the emergency room for unstable angina. The patient‘s past medical history was positive for repeated hospitalizations for unstable angina: in particular, was registered an admission in 2019 with angiographic evidence of intermediate stenosis 30% at the mid–distal tract of LMCA and good distant outcome of previously implanted stents on LMCA and RCA, and a further admission in 2021 with coronary evidence overlapping the previous one. In both hospitalizations, medical therapy optimization was carried out by adding also 2nd–line drugs to the antianginal therapy with Bisoprolol 2.5 mg and Amlodipine 5 mg such as transdermal Nitroglycerin 15 mg, Ranolazine 750 mg bis in die, and subsequently Trimetazidine 20 mg ter in die during the first and second hospitalizations, respectively. In the context of this re–hospitalization, coronarography was repeated again with evidence of unchanged angiographic picture from the previous one (2021) and, in view of the refractoriness of the anginal symptoms, was placed an indication for Neovasc Reducer device implantation. This device creates a pressor gradient in the coronary sinus, determining a redistribution of blood flow from the subepicardial areas to the ischemic subendocardial areas. Therefore, by performing jugular venous access we engaged the coronary sinus with 6F diagnostic catheter then by mother and child technique we placed the 9F guide catheter advancing as distally as possible in the coronary sinus and finally we implanted the Neovasc Reducer device (4 atm for 60‘‘), obtaining a good final angiographic result. At 6–month follow–up, the patient experienced symptomatic improvement, in particular he improved by 2 Canadian Cardiovascular Society (CCS) angina classes. The Neovasc Reducer device, by improving quality of life and reducing the need for hospitalizations for unstable angina, is a viable therapeutic strategy in patients angina unresponsive to medical therapy and coronary revascularization.

Redistribution of blood flow during exercise is impaired in heart failure with preserved ejection fraction

Exercise intolerance is a cardinal symptom in heart failure with preserved ejection fraction (HFpEF). The underlying pathophysiological mechanisms of HFpEF and their influence on exercise intolerance remains poorly understood. This study investigated the role of re-distribution of blood flow in modulating the increase in hindlimb muscle blood flow during HFpEF.We proposed that exercise intolerance is partially contributed by an impaired ability to divert blood flow from peripheral organs such as the kidney during exercise. We utilised an ovine model of HFpEF in which hypertension was established in aged female sheep. We then examined the mean arterial pressure, heart rate, cardiac output, renal blood flow and hindlimb blood flow response to treadmill exercise in both groups of conscious animals.Animals with HFpEF had elevated left ventricular end diastolic pressures (13 ± 6 vs. 0 ± 1 mmHg, p&lt;0.05) as well as enlarged cardiomyocytes compared to normotensive controls. Exercise in the control animals led to increases in cardiac output and heart rate. These responses were significantly attenuated in HFpEF (increase of 4.5 ± 1 vs. 8 ± 1 L/min, p&lt;0.05) and heart rate (increase of 32 ± 3 vs. 41 ± 4 bpm, p&lt;0.05). In a separate group of instrumented animals, the increase in blood flow to the hindlimb vasculature was attenuated in the HFpEF animals compared to control animals (increase of 2 ± 1 vs. 4 ± 2 L/min, p&lt;0.05). There was a reduction in renal blood flow in the control animals (-150 ± 50 ml/min) and this change was reversed to an increase in the HFpEF animals (+50 ± 20 ml/min).Our results suggest that the exercise intolerance observed in our ovine model of HFpEF may in part be due to an impaired ability to regulate blood flow to the kidney and hindlimb muscles during exercise. RR gratefully acknowledges granting support from the Health Research Council of New Zealand, the University of Auckland Faculty Research Development Fund and the National Heart Foundation of New Zealand. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Endothelial-endothelial signaling as a mechanism for neurovascular coupling

The brain is an energetically expensive organ, consuming 20% of the body’s cardiac output at rest while only accounting for 2% of its mass. Unable to store long-term energy reserves, the brain rapidly redistributes blood flow to active regions in order to meet moment-to-moment changes in metabolic demand. This dynamic process, known as neurovascular coupling, is the basis of most non-invasive human imaging and plays a crucial role in maintaining brain health. However, despite its broad-ranging importance, the cellular mechanisms that underlie neurovascular coupling remain elusive. During neurovascular coupling, activity-evoked signals drive smooth muscle relaxation, resulting in arterial dilation and a robust increase in downstream capillary blood flow. These dilation events occur quickly – on the order of milliseconds – and spread rapidly through the arterial network to effectively recruit perfusion. Electrical signals propagated along the cerebrovascular endothelium are increasingly speculated to underpin this phenomenon, but this idea remains fundamentally untested. Here, we leverage a combination of mouse genetics, molecular biology techniques, and in vivo imaging in awake mice to evaluate the role of propagated electrical signals in the neurovascular coupling response. Our preliminary results indicate that brain endothelial cells are capable of electrical communication and establish a foundation to test the physiological significance of the signals they relay. R01 HL153261/HL/NHLBI NIH HHS/United States; HHMI/Howard Hughes Medical Institute/United States This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.