Acute Blood Pressure Elevation Research Articles

Caffeine intake and cardiometabolic risk factors in adolescents in the United States.

In adults, caffeine has protective effects against kidney dysfunction and type 2 diabetes mellitus (T2DM) but increases the risk of acute blood pressure (BP) elevation and dyslipidemia. These relationships are unclear in adolescents. This study aimed to determine the association between caffeine intake and markers of childhood cardiometabolic risk, hypothesizing that higher caffeine intake would be associated with elevated BP and dyslipidemia but improved kidney function and insulin sensitivity. Adolescents ages 13-17 who participated in the National Health and Nutritional Examination Survey (NHANES) from 2011 to 2018 and completed 24-h dietary recalls were included. Logistic and linear regression models were used to analyze cross-sectional associations between caffeine and cardiometabolic risk factors. The mean participant age was 15.0 years, with a sex distribution of 49.9% male and 50.1% female. In fully adjusted regression models, higher caffeine intake was not associated with any changes in BP (OR = 0.78, 95%CI [0.52,1.16], p = 0.21), dyslipidemia (OR = 0.91, 95%CI [0.65,1.27], p = 0.57), glomerular hyperfiltration (OR = 1.01, 95%CI [0.60,1.71], p = 0.96), albuminuria (OR = 0.94, 95%CI [0.45,1.98], p = 0.87), or insulin resistance (OR = 1.15, 95%CI [0.85,1.56], p = 0.36). Contrary to its cardiometabolic effects in adults, caffeine intake was not associated with an increased or reduced risk of kidney dysfunction, T2DM, hypertension, or dyslipidemia in adolescents. Although the effects of caffeine intake on cardiometabolic risk have been well defined in adults, data exploring its impact on adolescent cardiovascular and metabolic function is limited. The goal of this study was to understand the relationship between caffeine intake and markers of childhood cardiometabolic risk. Unlike its established effects in adults, caffeine consumption showed no association with markers of cardiometabolic disease, such as kidney dysfunction, type 2 diabetes mellitus, blood pressure, dyslipidemia, or hyperuricemia in adolescents. These findings offer novel insight into the effects of caffeine on cardiometabolic function in adolescents, which may guide clinical recommendations for at-risk patients.

Redefining postoperative hypertension management in carotid surgery: a comprehensive analysis of blood pressure homeostasis and hyperperfusion syndrome in unilateral vs. bilateral carotid surgeries and implications for clinical practice.

This study evaluates the implications of blood pressure homeostasis in bilateral vs. unilateral carotid surgeries, focusing on the incidence of postoperative hypertension, hyperperfusion syndrome, and stroke as primary outcomes. It further delves into the secondary outcomes encompassing major adverse cardiovascular events and all-cause mortality. Spanning two decades (2002-2023), this comprehensive retrospective research encompasses 15,369 carotid referrals, out of which 1,230 underwent carotid interventions. A subset of 690 patients received open carotid procedures, with a 10-year follow-up, comprising 599 unilateral and 91 bilateral surgeries. The Society for Vascular Surgery Carotid Reporting Standards underpin our methodological approach for data collection. Both univariate and multivariate analyses were utilized to identify factors associated with postoperative hypertension using the Statistical Package for the Social Sciences (SPSS) Version 22 (SPSS®, IBM® Corp., Armonk, N.Y., USA). A marked acute elevation in blood pressure was observed in patients undergoing both unilateral and bilateral carotid surgeries (p < 0.001). Smoking (OR: 1.183, p = 0.007), hyperfibrinogenemia (OR: 0.834, p = 0.004), emergency admission (OR: 1.192, p = 0.005), severe ipsilateral carotid stenosis (OR: 1.501, p = 0.022), and prior ipsilateral interventions (OR: 1.722, p = 0.003) emerged as significant factors that correlates with postoperative hypertension in unilateral surgeries. Conversely, in bilateral procedures, gender, emergency admissions (p = 0.012), and plaque morphology (p = 0.035) significantly influenced postoperative hypertension. Notably, 2.2% of bilateral surgery patients developed hyperperfusion syndrome, culminating in hemorrhagic stroke within 30 days. Intriguingly, postoperative stage II hypertension was identified as an independent predictor of neurological deficits post-secondary procedure in bilateral CEA cases (p = 0.004), attributable to hyperperfusion syndrome. However, it did not independently predict myocardial infarction or mortality outcomes. The overall 30-day stroke rate stood at 0.90%. Lowest incidence of post operative hypertension or any complications were observed in eversion carotid endartrertomy. The study identifies postoperative hypertension as a crucial independent predictor of perioperative stroke following bilateral carotid surgery. Moreover, the study elucidates the significant impact of bilateral CEA on the development of post-operative hyperperfusion syndrome or stroke, as compared to unilateral CEA. Currently almost 90% of our carotid practice is eversion carotid endartrerectomy.

O250: Blood Pressure Homeostasis and Hyper-perfusion Syndrome Following Carotid Surgeries

Abstract Objectives We aim to compare blood pressure homeostasis in patients undergoing bilateral versus unilateral carotid surgeries. Our primary endpoints are the incidence of postoperative hypertension and hyperperfusion syndrome (HPS). Secondary endpoints are major adverse cardiovascular events and all-cause mortality. Methods All patients undergoing carotid endarterectomy (CEA) from 2003 to 2022 were reviewed. We performed 1230 carotid interventions, of which 690 procedures had ten years of follow-up. Results Both the unilateral (512) and bilateral (91) carotid interventions caused a significant acute elevation in blood pressure (p&amp;lt;0.001). In unilateral carotid interventions, the mean SBP was 137 ± 19.90 mmHg preoperatively and 152 ± 25.80 postoperatively (p&amp;lt;0.001). Smoking (p=0.007), hyperfibrinogenemia (p=0.004), emergency admission (p=0.005), ipsilateral carotid stenosis &amp;gt;90% (p=0.022), and previous ipsilateral carotid intervention (p=0.003) were significantly associated with the development of postoperative hypertension. No incidence of HPS occurred in the unilateral group. In bilateral carotid interventions, the mean SBP was 138 ± 20.50 mmHg preoperatively and 159 ± 24.60 mmHg postoperatively (p&amp;lt;0.001). Emergency admission (p=0.012) and plaque morphology (p=0.035) were significantly associated with postoperative hypertension. Three patients with bilateral carotid interventions had HPS (3.3%) and developed hemorrhagic stroke within 30 days. Multivariate analysis found postoperative stage II hypertension following bilateral carotid procedures to be an independent predictor of stroke (p=0.004). However, postoperative hypertension was not an independent predictor of myocardial infarction (p=0.475) and mortality (p=0.608). Conclusion Significant acute elevation in blood pressure occurred following carotid surgeries. We observed HPS post bilateral carotid interventions, with postoperative hypertension being an independent predictor of peri-operative stroke.

Chronic renal failure as predictive factor for acute elevation of systolic blood pressure after fluorescein angiography in patients with retinal diseases

PurposeTo investigate the influence of fluorescein angiography (FA) on blood pressure (BP) in patients with retinal diseases, and analyze the predictive factors for acute elevation of systolic BP after FA. Designand Methods: A prospective study was conducted with 636 patients undergoing FA between April 2021 and October 2021. BP and pulse were measured in each patient before and 20 min after FA. The baseline characteristics of patients who developed an acute elevation in systolic BP (>10 mmHg) were compared with those of the remaining patients to detect factors that may predict this acute elevation. ResultsOverall, mean systolic BP changed from 142 ± 17 mmHg to 140 ± 20 mmHg after 20 min (p = 0.1). Mean diastolic BP changed from 79 ± 15 mmHg to 78 ± 13 mmHg after 20 min (p = 0.45). Mean pulse rate changed from 73 ± 14 bpm to 70 ± 12 bpm after 20 min (p = 0.001). 103 patients (16 %) had acute elevation of systolic BP (>10 mmHg). Mean systolic BP changed from 143 ± 17 mmHg to 162 ± 19 mmHg after 20 min in this group (p = 0.001). Patients in this group were significantly older compared to the rest (73 ± 12 vs 67 ± 15, p = 0.001). The rate of chronic renal failure was significantly higher in this group compared to the rest of the patients (42/7.8 % vs 15/14.6 %, p = 0.01). ConclusionsThis study demonstrated that fluorescein angiography is a relatively safe procedure with regards to blood pressure changes. However, chronic renal failure could be considered as predictive factor for acute elevation of systolic blood pressure after this procedure.

Abstract P378: Expression Of Micro-rna 221, 222 And 223 In Individuals Suffering From Ischemic Stroke Due To Hypertensive Emergency

Hypertensive crisis can account for damage on target organs characterizing hypertensive emergencies (HE). Ischemic Stroke (IS) is among these injuries. Expression of microRNAs (miRNAs) is considered the possible factors related to HE. This study evaluated the association of expression of miRNAs 221, 222 and 223 in patients suffering ischemic stroke due to HE. Material and Methods Thirty and four patients with IS due to hypertensive emergency (IS-HE), 33 individuals with IS without HE (IS), 31 controlled hypertensive (CHT) and 33 normotensive (NT) individuals were studied. The expression of miRNAs 221, 222 and 223 was performed by RT-q PCR (real-time quantitative polymerase chain reaction). Results Systolic and diastolic blood pressure were significantly higher in the IS-HE compared to IS, CHT and NT groups (162/99 mmHg vs 140/87, 128/69 and 129/82 mmHg, respectively; p &lt;0.05). The miRNA-221 expression was higher in the IS-HE group compared to the IS, CHT and NT groups (4.23 vs 2.44, 1.35 and 1.05, respectively; p&lt;0.0001). There was overexpression of miRNA-223 in the IS-HE and IS groups compared to CHT and NT groups (1.56 and 1.73 vs 0.13 and 0.66; p &lt; 0.001). For miRNA-222 there was overexpression in the IS-HE, IS, and NT groups compared to the CHT group (P&lt;0.0001 for all). Conclusions This study provides evidence of the miRNAs participation in the pathophysiology of ischemic stroke due hypertensive emergency, thus assuring that the increased expression of miR-221 and miR-223 determines a greater chance of the individual presenting IS due HE. The miRNAs 221 and 223 are related to endothelial damage; thus, their overexpression shows the participation of endothelial dysfunction in cases of acute blood pressure elevation.

A Systematic Review and Meta-analysis of the Clinical and Epidemiological Characteristics of Patients with Hypertensive Emergencies: Implication for Risk Stratification.

Acute severe elevation of blood pressure (BP) is a common clinical event, that can present as hypertensive emergency (HTNE) and hypertensive urgency (HTNU). HTNE results in life-threatening target organ damage, including myocardial infarction, pulmonary edema, stroke, and acute kidney injury. It is associated with high utilization of healthcare and increased cost. HTNU is high BP without acute serious complications. The purpose of this review was to examine the clinical-epidemiological characteristics of patients with HTNE and propose a risk stratification framework to differentiate between the two conditions, since prognosis, setting of therapy and treatment is vastly different. Systematic review. Fourteen full-text studies were included in this review. In comparison with HTNU, patients with HTNE had higher mean systolic (mean difference 2.413, 95% CI 0.477, 4.350) and diastolic BP (mean difference 2.043, 95% CI 0.624, 3.461). HTNE were more prevalent in men (OR 1.390, 95% CI 1.207, 1.601), older adults (mean difference 5.282, 95% CI 3.229, 7.335) and those with diabetes (OR 1.723, 95% CI 1.485, 2.000). Non-adherence to BP medications (OR 0.939, 95% CI 0.647, 1.363) and unawareness of hypertension diagnosis (OR 0.807, 95% CI 0.564, 1.154) did not elevate the risk of HTNE. Systolic and diastolic BP are marginally higher in patients with HTNE. Given that these differences are not clinically significant, other epidemiological and medical characteristics (older age, male sex, cardiometabolic comorbidities) as well as patient's presentation should be considered to differentiate between HTNU and HTNE.

EXPRESSION OF MICRO-RNA 221 AND 223 IN ISCHEMIC STROKE DUE HYPERTENSIVE EMERGENCY

Objective: Hypertensive crisis can account for damage on target organs characterizing hypertensive emergencies (HE). Ischemic Stroke (IS) is among these injuries. Expression of microRNAs (miRNAs) is considered the possible factors related to HE. This study evaluated the association of expression of miRNAs 221 and 223 in patients suffering ischemic stroke due to HE. Design and method: Thirty and four patients with IS due to hypertensive emergency (IS-HE), 33 individuals with IS without HE (IS), 31 controlled hypertensive (CHT) and 33 normotensive (NT) individuals were studied. The expression of miRNAs 221 and 223 was performed by RT-q PCR (real-time quantitative polymerase chain reaction). Results: Systolic and diastolic blood pressure were significantly higher in the IS-HE compared to IS, CHT and NT groups (162/99 mmHg vs 140/87, 128/69 and 129/82 mmHg, respectively; p &lt;0.05). The miRNA-221 expression was higher in the IS-HE group compared to the IS, CHT and NT groups (4.23 vs 2.44, 1.35 and 1.05, respectively; p&lt;0.0001). There was overexpression of miR-223 in the IS-HE and IS groups compared to CHT and NT groups (1.56 and 1.73 vs 0.13 and 0.66; p &lt; 0.001). Conclusions: This study provides evidence of the miRNAs participation in the pathophysiology of ischemic stroke due hypertensive emergency, thus assuring that the increased expression of miR-221 and miR-223 determines a greater chance of the individual presenting IS due HE. The miRNAs 221 and 223 are related to endothelial damage; thus, their overexpression shows the participation of endothelial dysfunction in cases of acute blood pressure elevation. FAPESP 2016/08203-6.

Sudden gamer death: non-violent death cases linked to playing video games

Background and aimsInternet gaming disorder (IGD) is an emerging problem. Rarely, media reports about people, who have died during playing video games, but thus far no systematic, scientific study is available about the topic. We investigated such cases, looking for common characteristics, connection between gaming and death, and the possible reasons leading to death.MethodsCases were collected through internet search with general keywords, with ones specific to identified cases, and by working along cross references.Results24 cases were found: one from 1982, the others between 2002 and 2021. Twenty-three of the victims were male, age ranged from 11 to 40 years. More than half of the cases originated from Southeast Asia, and 12 deaths happened in internet cafes. Gamers played action-rich multiplayer games. In 18 cases the gaming session before death was extremely long (around a day or even several days) with minimal rest. The cause of death was pulmonary embolism in 5 cases, cerebral hemorrhage in 2 cases, most of the rest was presumably due to fatal cardiac arrhythmia.DiscussionLong sedentary position and dehydration may precipitate thromboembolism, acute blood pressure elevation during gaming may promote cerebral hemorrhage, and several factors (including acute and chronic sleep deprivation, exhaustion, stress) can lead to acute autonomic dysfunction and fatal arrhythmia.ConclusionIncidence of non-violent death cases linked to playing video games is presumably very low. It mostly occurs in young males and it is often characterized by extremely long gaming time.

Blood pressure elevations in hospital.

Long-term hypertension control in the community significantly reduces cardiovascular risk. However, the benefit of controlling acute elevations of blood pressure in hospitalised patients is unclear. In-hospital elevations of blood pressure are relatively common and might not reflect poorly controlled blood pressure before admission. The measurement of blood pressure in hospital patients significantly differs from the best practice recommended for primary care and outpatients. Recent observational studies suggest that the pharmacological treatment of acute, asymptomatic, in-hospital elevations of blood pressure may have no benefit. However, it may increase the risk of in-hospital and post-discharge complications. Pending the development of robust inpatient measurement protocols, acute blood pressure elevations in hospitalised patients should not routinely require antihypertensive treatment in the absence of symptoms or acute end-organ damage. Rather, such elevations should facilitate follow-up of blood pressure and other cardiovascular risk factors after discharge.

Voriconazole Associated Hypertension: A Case Report

Objective: The study report a case of a young female with candida tropicalis and candida krusei infection who developed severe hypertension after she had repeated received voriconazole for few days.&#x0D; Case Presentation: A 23-year-old female was admitted to hospital because of recurrent urinary tract infection. She underwent horseshoe nephrectomy, extracorporeal lithotripsy treatment and double J-tube placement in the past 5 years. After multiple surgeries, she developed recurring fungal urinary tract infections and underwent anti-infective treatment. Twenty days ago, the patient developed chills, fever, dizziness, fatigue, urinary tract irritation signs and bilateral low back pain. Urine culture suggests Candida croco (resistant to fluconazole). After taking antifungal therapy with voriconazole 300 mg q12h, the patient experienced an unexplained increased blood pressure and transient loss of consciousness.&#x0D; The patient began to experience an increase in blood pressure (140-160/90-100 mmHg) on the second day of voriconazole treatment. After 5 days of taking voriconazole, the patient developed fatigue, dizziness and blurred vision with persistent hypertension (150/100 mmHg), and temporary loss of consciousness and syncope on day8, when blood pressure was measured at 175/95 mmHg.&#x0D; Conclusion: This case illustrates that acute blood pressure elevation may manifest in patients taking normal doses of voriconazole, which deserves the attention of clinicians.

High-dose nitroglycerin infusion description of safety and efficacy in sympathetic crashing acute pulmonary edema: The HI-DOSE SCAPE study

BackgroundSympathetic crashing acute pulmonary edema (SCAPE) is a medical emergency in which severe, acute elevation in blood pressure results in acute heart failure and fluid accumulation in the lungs. Without prompt recognition and treatment, the condition often progresses rapidly to respiratory failure necessitating intubation and intensive care unit (ICU) admission. In addition to non-invasive positive pressure ventilation (NIPPV), high-dose nitroglycerin (HDN) has become a mainstay of treatment; however, an optimal dosing strategy has not been established. ObjectiveThe purpose of this study was to describe the characteristics and outcomes of patients who received an HDN infusion (≥ 100 μg/min) for the management of SCAPE in the Emergency Department (ED) of a large urban academic medical center. Outcomes were also analyzed to determine predictors of safety and efficacy including use of adjunct medication therapies. ResultsThere were 67 adult patients who received HDN infusion for SCAPE from January 1, 2018 to December 31, 2018. The median (IQR) systolic blood pressure (SBP) on initiation of HDN infusion was 211 (192–233) mmHg. Patients were 63% male, 84% black, 51% had a history of heart failure (HF), and 36% had end-stage renal disease (ESRD). IV nitroglycerin (NTG) was initiated at a median (IQR) dose of 100 (100−200) mcg/min with median (IQR) peak rate in the first hour of 200 (127.5–200) mcg/min and an absolute maximum observed rate of 400 μg/min overall. 73% of patients received NIPPV, 48% sublingual (SL) or IV bolus nitroglycerin before HDN infusion, 58% loop diuretic, and 34% angiotensin-converting enzyme inhibitor (ACEI) or angiotensin II receptor blocker (ARB). Rates of ICU admission, intubation, acute kidney injury (AKI) at 48 h, and hypotension were 37%, 21%, 13%, and 4% respectively. ConclusionThis is the largest to date study describing the use of an HDN infusion (≥100 μg/min) strategy for the management of SCAPE. HDN infusion may be a safe alternative strategy to intermittent bolus HDN.

Hypertensive Emergency In UMOD-Related Autosomal Dominant Tubulointerstitial Kidney Disease

Hypertensive emergency is characterized by an acute elevation in blood pressure with evidence of impending or progressive acute target organ damage. Management relies mainly on intravenous medications guided by the type of target-organ damage, but there is considerable variability in practice regarding the choice of medications and optimal therapy. Such variables include the choice of agent and the blood pressure goal, but also underlying medical conditions. We report a case of hypertensive emergency in a 39-year-old-male with a rare genetic condition, UMOD-related autosomal dominant tubulointerstitial kidney disease which gave rise to adolescent gout, worsening kidney function over decades and treatment-resistant hypertension.

Inflammatory cytokines are associated to lower glomerular filtration rate in patients with hypertensive crisis.

IntroductionHypertension and kidney function are closely related. However, there are few studies on renal function during acute elevation of blood pressure (BP), denominated hypertensive crisis (HC).ObjectivesTo evaluate the relationship between renal function and inflammatory cytokines in HC, subdivided into hypertensive urgency (HUrg) and emergency (HEmerg).Materials and methodsThis cross-sectional study was carried out in 74 normotensive (NT) and 74 controlled hypertensive individuals (ContrHT) followed up in outpatient care. Additionally, 78 subjects with hypertensive emergency (HEmerg) and 50 in hypertensive urgency (HUrg), attended in emergency room, were also evaluated. Hypertensive crisis was classified into HEmerg, defined by systolic blood pressure (BP) ≥ 180 mmHg and/or diastolic BP ≥ 120 mmHg in presence of target-organ damage (TOD), and HypUrg, clinical situation with BP elevation without TOD. The glomerular filtration rate (eGFR) was estimated, and cytokine levels were measured. Statistical analysis was performed using the Kruskal-Wallis or Mann-Whitney test and Spearman’s correlation, with significant differences p-value < 0.05.ResultsThe median age was 53.5 years in the NT group (52 female), 61 years in the ContrHT group (52 female), and 62.5 years in the HC group (63 female) (p-value < 0.0001). The median BP was 118.5/75 mmHg for NT, 113.5/71 for ContrHT, and 198.5/120 mmHg for HC, respectively (p-value < 0.0001 among groups). BP and heart rate levels were significantly higher in the HC group compared to the NT and ContrHT groups (P < 0.001 for all). The eGFR was significantly lower in HC group compared to the NT and ContrHT groups. The cytokine levels were higher in the HEmerg and HUrg groups compared to ContrHT group (P < 0.0001, except for IL-1β in HUrg vs. ContrHT), without difference between the acute elevation of BP groups. Thus, all cytokines were significantly elevated in patients with HC compared to the control groups (NT and ContrHT). There was a negative correlation between eGFR and the cytokines (IL-1β, IL-6, IL-8, IL-10, and TNF-α) in the HC group.ConclusionElevated inflammatory cytokines are associated with reduced eGFR in individuals with HC compared to control groups, suggesting that the inflammatory process participates in the pathogenesis of acute elevations of BP.

YAP mediates compensatory cardiac hypertrophy through aerobic glycolysis in response to pressure overload.

The heart utilizes multiple adaptive mechanisms to maintain pump function. Compensatory cardiac hypertrophy reduces wall stress and oxygen consumption, thereby protecting the heart against acute blood pressure elevation. The nuclear effector of the Hippo pathway, Yes-associated protein 1 (YAP), is activated and mediates compensatory cardiac hypertrophy in response to acute pressure overload (PO). In this study, YAP promoted glycolysis by upregulating glucose transporter 1 (GLUT1), which in turn caused accumulation of intermediates and metabolites of the glycolytic, auxiliary, and anaplerotic pathways during acute PO. Cardiac hypertrophy was inhibited and heart failure was exacerbated in mice with YAP haploinsufficiency in the presence of acute PO. However, normalization of GLUT1 rescued the detrimental phenotype. PO induced the accumulation of glycolytic metabolites, including l-serine, l-aspartate, and malate, in a YAP-dependent manner, thereby promoting cardiac hypertrophy. YAP upregulated the GLUT1 gene through interaction with TEA domain family member 1 (TEAD1) and HIF-1α in cardiomyocytes. Thus, YAP induces compensatory cardiac hypertrophy through activation of the Warburg effect.

Hypertensive eye disease

Hypertensive eye disease includes a spectrum of pathological changes, the most well known being hypertensive retinopathy. Other commonly involved parts of the eye in hypertension include the choroid and optic nerve, sometimes referred to as hypertensive choroidopathy and hypertensive optic neuropathy. Together, hypertensive eye disease develops in response to acute and/or chronic elevation of blood pressure. Major advances in research over the past three decades have greatly enhanced our understanding of the epidemiology, systemic associations and clinical implications of hypertensive eye disease, particularly hypertensive retinopathy. Traditionally diagnosed via a clinical funduscopic examination, but increasingly documented on digital retinal fundus photographs, hypertensive retinopathy has long been considered a marker of systemic target organ damage (for example, kidney disease) elsewhere in the body. Epidemiological studies indicate that hypertensive retinopathy signs are commonly seen in the general adult population, are associated with subclinical measures of vascular disease and predict risk of incident clinical cardiovascular events. New technologies, including development of non-invasive optical coherence tomography angiography, artificial intelligence and mobile ocular imaging instruments, have allowed further assessment and understanding of the ocular manifestations of hypertension and increase the potential that ocular imaging could be used for hypertension management and cardiovascular risk stratification.

Hypertension after COVID-19 vaccination

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) rapidly spread across the world, killing more than 4 million individuals globally, with 240 million individuals being confirmed by laboratory tests. Among different therapeutic strategies to prevent SARS-CoV-2 infection, vaccines are the most promising approach for curbing the pandemic. They elicit an immune neutralizing response and thus offer protection against coronavirus disease 2019 (COVID-19). However, some questions regarding the safety of COVID-19 vaccines have been raised and based on sparse reports of severe systemic reactions after vaccination. Among these, evidences on the potential effect of vaccination on the acute rise in blood pressure have been recently accrued. Approved vaccines in Europe increase the endogenous synthesis of SARS-CoV-2 Spike proteins from a variety of cells. Once synthetized in the cells reached by the vaccine, the Spike proteins first assemble in the cytoplasm and then migrate to the cell surface to protrude with a native-like conformation. Spike proteins are recognized by the immune system which rapidly develops an immune response. Furthermore, the Spike proteins assembled in the cells which are eventually destroyed by the immune response circulate in the blood as free-floating forms. Free-floating Spike proteins may interact with angiotensin-converting enzyme 2 (ACE2) receptors leading to internalization, degradation, and dysregulation of the catalytic activities of these receptors. The consequent loss of ACE2 receptor activity leads to a rapid drop in the generation of angiotensin1,7 resulting from inactivation of angiotensin II. The imbalance between angiotensin II (overactivity) and of angiotensin1,7 (deficiency) might play a role in the genesis of acute elevation in blood pressure.

Pharmacotherapy for hypertensive urgency and emergency in COVID-19 patients

ABSTRACT Introduction Hypertension is a common chronic disorder in patients hospitalized for coronavirus disease 2019 (COVID-19). Furthermore, an exaggerated cardiovascular response with persistently raised blood pressure during hospitalization seems independently associated with in-hospital all-cause mortality, intensive care unit admission and heart failure. However, the real burden of elevated blood pressure during the acute phase of COVID-19 remains undefined. Areas covered The authors review the available evidence on the pharmacotherapy for the treatment of acute elevations in blood pressure (including hypertensive urgency and emergency) in COVID-19 patients. Expert opinion Acute elevations in blood pressure and unstable in-hospital blood pressure may be associated with organ damage and worse outcome in patients with COVID-19. In this setting, hypertensive emergencies require immediate reduction in blood pressure through intravenous treatment according to specific features and goals. Conversely, hypertensive urgencies usually require solely oral treatment. Diuretics, beta-blockers, renin-angiotensin-aldosterone system inhibitors, and calcium channel blockers may be of benefit in treating COVID-19 patients with elevated blood pressure values.

CE: Hypertensive Emergencies: A Review.

While acute blood pressure elevations are commonly seen in the ED, not all require emergency treatment. True hypertensive emergencies are characterized by a rapid elevation in blood pressure to a level above 180/120 mmHg and are associated with acute target organ damage, which requires immediate hospitalization for close hemodynamic monitoring and IV pharmacotherapy. Recognizing the clinical signs and symptoms of hypertensive emergency, which may vary widely depending on the target organ involved, is critical. High blood pressure levels that produce no signs or symptoms of target organ damage may be treated without hospitalization through an increase in or reestablishment of previously prescribed oral antihypertensive medication. However, all patients presenting with blood pressure this high should undergo evaluation to confirm or rule out impending target organ damage, which differentiates hypertensive emergency from other hypertensive crises and is vital in facilitating appropriate emergency treatment. Drug therapy for hypertensive emergency is influenced by end-organ involvement, pharmacokinetics, potential adverse drug effects, and patient comorbidities. Frequent nursing intervention and close monitoring are crucial to recuperation. Here, the authors define the spectrum of uncontrolled hypertension; discuss the importance of distinguishing hypertensive emergencies from hypertensive urgencies; and describe the pathophysiology, clinical manifestations, and management of hypertensive emergencies.

Impact of Intravenous Antihypertensives on Outcomes Among Hospitalized Patients.

Many hospitalized patients with acute elevations in blood pressure (BP) are treated with intravenous (IV) antihypertensive medications without evidence of benefit. This study investigated the effects of IV as-needed (PRN) antihypertensives on BP, hospital length of stay, and mortality. We included hospitalized patients with an order for an IV PRN antihypertensive medication. We excluded patients with target organ damage. We performed multivariate analysis to assess whether the medication was independently associated with outcomes. 1,784 out of 5,680 patients (31%) had an administration of the PRN medication. Patients who received the medication had a longer hospital stay compared with patients with an order for the medication who did not receive it (4.9 ± 6.1 vs. 3.1 ± 4.1 days, P < 0.001). This remained statistically significant after adjusting for covariates. In-hospital mortality was higher in the group that received the medication (3.3% vs. 1.6%, P < 0.001), but this was not statistically significant on multivariate analysis. IV hydralazine caused the most significant reduction in BP and led to a shorter length of stay when compared with enalapril and labetalol. A total of 62% of patients received the medication for a systolic BP lower than 180 mm Hg. Treating hypertension in the in-patient setting remains complex. Rapid lowering of BP can cause harm to patients, and this study showed that antihypertensive medication increased hospital length of stay. Once assuring no target organ damage, a strategic approach should be to treat modifiable factors and gradually reduce BP.

RELATIONSHIPS BETWEEN CHOROIDAL THICKNESS AND 24 H PULSE PRESSURE IN HYPERTENSIVE PATIENTS

Objective: The choroid is a pure vascular structure and its thinning may reflect a microvascular damage, that may be the local expression of a more generalised vascular injury. Choroid may be easily damaged directly by acute and chronic severe elevation of blood pressure (BP). However, all the studies exploring the association of BP values with choroidal thickness yielded conflicting results. Our study was aimed to assess in hypertensive patients the relationships between choroidal thickness and “office” and 24-hour BP readings. Design and method: We enrolled 158 consecutive hypertensive subjects (age: 48 ± 13 years) attending our Hypertension Centre. All the patients underwent clinic BP measurements, 24-h ambulatory BP monitoring (ABPM) and morphological evaluation of the retino-choroidal district by SS-OCT. OCT measurements were performed according to the ETDRS protocol whose map divides the macula into 9 subfields. The circular grid is centred over the fovea and consists of 3 concentric rings,the inner and outer rings are further divided into quadrants: temporal, nasal, superior, and inferior. The retinal and choroidal thicknesses were automatically calculated by the OCT mapping software and only one eye of each subject was randomly selected for analysis and for sake of brevity we show only the data referring to the mean choroidal thickness. (MCT). Results: MCT (250 ± 62 m) showed significant correlations with: mean 24-h DBP (r = 0.18; p = 0.02) and diurnal (r = 0.21; p = 0.009), mean 24-h pulse pressure (PP) (r = - 0.30; p &lt; 0.001), of the day (r = - 0.19; p = 0.02) and of the night (r = - 0.25; p = 0.002). The correlation between the 24-hour PP and the SCM remains significant even after accounting for confounders in the multiple linear regression (r = - 0.18; p = 0.02). Conclusions: Our results, highlighting an inverse association between choroid thickness and 24-hour PP (possible index of arterial stiffness) seem to reinforce the hypothesis that choroidal thinning may be the expression of systemic vascular damage.