Signs Of End-organ Damage Research Articles

Emergency Department Blood Pressure Treatment and Outcomes in Adults Presenting with Severe Hypertension.

Patients who present to the emergency department (ED) with severe hypertension defined as a systolic blood pressure (SBP) ≥180 millimeters of mercury (mm Hg) or diastolic (DBP) ≥120 (mm Hg) without evidence of acute end-organ damage are often deemed high risk and treated acutely in the ED. However, there is a dearth of evidence from large studies with long-term follow-up for the assessment of major adverse cardiovascular events (MACE). We conducted the largest study to date of patients presenting with severe hypertension to identify predictors of MACE and examine whether blood pressure at discharge is associated with heightened risk. We enrolled ED patients with a SBP of 180-220mm Hg but without signs of end-organ damage and followed them for one year. The primary outcome was MACE within one year of discharge. Secondarily, we performed a propensity-matched analysis to test whether SBP ≤160mm Hg at discharge was associated with reduced MACE at 30 days. A total of 12,044 patients were enrolled. The prevalence of MACE within one year was 1,865 (15.5%). Older age, male gender, history of cardiovascular disease, cerebrovascular disease, diabetes, smoking, presentation with chest pain, altered mental status, dyspnea, treatment with intravenous and oral hydralazine, and oral metoprolol were independent predictors for one-year MACE. Additionally, discharge with an SBP ≤160mm Hg was not associated with 30-day MACE-free survival after propensity matching (hazard ratio 0.99, 95% confidence interval 0.78-1.25, P = 0.92). One-year MACE was relatively common in our cohort of ED patients with severe hypertension without acute end-organ damage. However, discharge blood pressure was not associated with 30-day or one-year MACE, suggesting that BP reduction in and of itself is not beneficial in such patients.

Association of routine hematological parameters with the development of monoclonal gammopathies: a case-control study of 134,740 patients

The diagnosis of multiple myeloma requires detection of paraproteinemia and confirmation of monoclonal bone marrow infiltration, along with signs of end-organ damage. Despite the increasing prevalence, serum paraproteinemia is not routinely measured. We examined the relationship between alterations in routine hematological parameters and the development of paraproteinemia in a case-control study. Data was retrieved from a laboratory database in the capital region of Denmark between 01/01/2012 and 31/12/2022. Patients were included if they had a test for paraproteinemia (n = 134,740) and at least one prior hematological parameter (white blood cells, hemoglobin and platelet count) with a minimum follow-up of 1 year.Between 96,999 and 103,590 patients were included in each of the three hematological groups. We found white blood cell count and the presence of paraproteinemia followed an inverse J-shaped curve, with the highest presence below 3 × 109/L and above > 9 × 109/L. The adjusted OR below and above the nadir of 4 × 109/L was 1.61 (95% CI 1.25; 2.08, p < 0.0001) and 1.03 (95% CI 1.03; 1.04, p < 0.0001). Hemoglobin levels were inversely associated the presence of paraproteinemia, with the highest association below 6 mmol/L with an OR of 1.30 (95% CI 1.28; 1.32, p < 0.0001) adjusted for age and gender. Platelet count followed a U-shaped curve with the highest association at < 100 × 109/L. The adjusted OR below and above the nadir of 250 × 109/L was 1.13 (95% CI 1.10; 1.17, p < 0.0001) and 1.10 (95% CI 1.08; 1.12, p < 0.0001) respectively. In conclusion, all three parameters showed significant association with later paraproteinemia.

Missed Opportunities to Diagnose and Treat Asymptomatic Hypertension in Emergency Departments in the United States, 2016-2019

BackgroundFewer than one-half of U.S. adults with hypertension (HTN) have it controlled and one-third are unaware of their condition. The emergency department (ED) represents a setting to improve HTN control by increasing awareness of asymptomatic hypertension (aHTN) according to the 2013 American College of Emergency Physicians asymptomatic elevated blood pressure clinical policy. ObjectiveThe aim of the study was to estimate the prevalence and management of aHTN in U.S. EDs. MethodsWe examined the 2016–2019 National Hospital Ambulatory Medical Care Surveys to provide a more valid estimate of aHTN visits in U.S. EDs. aHTN is defined as adult patients with blood pressure ≥ 160/100 mm Hg at triage and discharge without trauma or signs of end organ damage. We then stratified aHTN into a 160–179/100–109 mm Hg subgroup and > 180/110 mm Hg subgroup and examined diagnosis and treatment outcomes. ResultsApproximately 5.9% of total visits between 2016 and 2019 met the definition for aHTN and 74% of patients were discharged home, representing an estimated 26.5 million visits. Among those discharged home, emergency physicians diagnosed 13% (95% CI 10.6–15.8%) and treated aHTN in 3.9% (95% CI 2.8–5.5%) of patients in the higher aHTN subgroup. In the lower aHTN subgroup, diagnosis and treatment decreased to 3.1% (95% CI 2.4–4.1%) and 1.2% (95% CI 0.7–2.0%), respectively. ConclusionsMillions of ED patients found to have aHTN are discharged home without diagnosis or treatment. Although management practices follow clinical policy to delay treatment of aHTN, there are missed opportunities to diagnosis aHTN.

Abstract P203: Microvascular Imaging As Early Predictor For Cardiac Dysfunction After Preeclampsia

Preeclampsia (PE), the most common pregnancy disease, is the main cause for maternal and fetal mortality and morbidity worldwide. The disease is characterized by a sudden increase in blood pressure in combination with signs of end organ damage, e.g. proteinuria and the underlying mechanisms are poorly understood. Immune dysregulation and endothelial dysfunction are important pathomechanisms leading to PE, we hypothesize that anti-angiogenesis and dysregulation of microvascular perfusion postpartum lead to the increased cardiovascular risk in later life. In addition, we will test if the examination of retinal vessels can be used as a diagnostic window for early risk prediction of cardiovascular alterations. In a well-established transgenic rat model for PE, we performed speckle tracking echocardiography, immunostaining, RNA sequencing and small vessel imaging by micro-computed tomography of the heart and the eyes in former preeclamptic rats (PEpp) and healthy controls (WTpp). A reduction of cardiac vessels (AUC 0-200 μm: WTpp 77.19±4.64 vs. PEpp 62.59±2.72) in combination with an increase of small vessels in the retina (AUC 0-50 μm: WTpp 52.89±1.47 vs. PEpp 59.54±1.09) is shown postpartum. Data from echocardiography (Global longitudinal strain: WTpp -22.03±2.47 % vs. PEpp -14.50±1.80 %) and histological staining (CD31: WTpp 292.7±30.9 per fov vs. PEpp 219.0±10.5 per fov) support the hypothesis of persistent cardiovascular alterations after PE. Performing RNAseq, 65 genes were found to be permanently altered in the left ventricle of the heart of preeclamptic rats compared to 4 genes in controls. In the retinal tissue, 39 genes in PEpp and no genes in WTpp were identified postpartum compared to never pregnant animals (adjusted p-value &lt; 0.05,

Managing severe hypertension in children.

Severe childhood hypertension is uncommon and frequently not recognised and is best defined as a systolic blood pressure (SBP) above the stage 2 threshold of the 95th centile + 12mmHg. If no signs of end-organ damage are present, this is urgent hypertension which can be managed by the slow introduction of oral or sublingual medication, but if signs are present, the child has emergency hypertension (or hypertensive encephalopathy if they include irritability, visual impairment, fits, coma, or facial palsy), and treatment must be started promptly to prevent progression to permanent neurological damage or death. However, detailed evidence from case series shows that the SBP must be lowered in a controlled manner over about 2days by infusing short-acting intravenous hypotensive agents, with saline boluses ready in case of overshoot, unless the child had documented normotension within the last day. This is because sustained hypertension may increase pressure thresholds of cerebrovascular autoregulation which take time to reverse. A recent PICU study that suggested otherwise was significantly flawed. The target is to reduce the admission SBP by its excess, to just above the 95th centile, in three equal steps lasting about ≥ 6h, 12h, and finally ≥ 24h, before introducing oral therapy. Few of the current clinical guidelines are comprehensive, and some advise reducing the SBP by a fixed percentage, which may be dangerous and has no evidence base. This review suggests criteria for future guidelines and argues that these should be evaluated by establishing prospective national or international databases.

Abstract P322: 2-year Morbidity And Mortality Due To Hypertensive Crisis In A Predominantly African American Population

Title: 2-Year Morbidity and Mortality due to Hypertensive Crisis in a Predominantly African American Population Hypertensive crisis (HTNC) is a complication of Hypertension with a prevalence of 1-2%. HTNC is defined by a sudden and unpredictable increase in systolic blood pressure of ≥180 mmHg or diastolic blood pressure of ≥120 mmHg. HTNC may present as hypertensive urgency (HTNU) if asymptomatic, or hypertensive emergency (HTNE) if there are signs of end organ damage (EOD) eg: stroke (CVA), congestive heart failure (CHF), acute kidney injury (AKI), acute myocardial infarction (AMI) and death. A 2y retrospective cohort study of 1100 participants: 550 cases and 550 hypertensive controls BP &gt;140/90) but &lt; 200/120, matched for race, sex, and age, was conducted to determine the incidence of EOD, and the 2year mortality. The population was: Blacks 481/550 (87.4%), White 18/550 (3.3%), Asian 2/550 (0.4%) and other 49 /550 (8.9%). The mean SBP for cases was SBP 209.7 (SD=23.1), controls 147.8(SD=22.8) p=0.239; DBP cases 115.5 (SD=22.4), controls 84.2 (SD=14.1) p&lt;.001. The incidence of new EOD for CHF: HTNE=39/440 (9.8%), HTNU=8/150 (5.3%), controls=6/550 (1.1%), p&lt;.001; AKI HTNE=27/400 (6.8%), HTNU=5/150 (6.7 %), controls=17/550 (3.1%) p&lt;0.001; AMI HTNE=6.5% and HTNU=2.7% controls=6/550 (1.1%) p&lt;.001. There was no significant difference in the incidence of hemorrhagic and ischemic CVA, but the trend was higher in HTNE and HTNC for ischemic CVA: HTNE=4/400 (1%), HTNU=1/150 (0.7%), controls=(0.2%) p=.234. The 2y mortality for HTNE=82/400 (20.5%), HTNU=16/150 (10.6%), controls= 36/550 (6.5 %). The odds of dying was 3.5 times greater in the HTNU (OR 3.5, 95% CI 1.78-6.98), p&lt;.001) and 4.3 times in the HTNE population (OR 4.3, 95% CI 2.65-7.01), p&lt;.001). The study reveals a high morbidity and mortality associated with hypertensive crisis, with 1/5 of the population of HTNE dying in two years, mostly from related cardiovascular disease and renal failure.

Post-COVID-19 patient with overlapping features between Multisystem inflammatory syndrome in children (MIS-C) and Secondary hemophagocytic lymphohistiocytosis (SHLH): A Rare Case Report

Multisystem inflammatory syndrome in children (MIS-C) is a potentially life-threatening consequence of coronavirus disease (COVID-19) infection characterized by hyperinflammatory state, leading to multi-organ damage that often requires hospitalization. Though the precise underlying etiopathogenesis of MIS-C is not completely comprehended, the correlation between MIS-C and COVID-19 infection implies a delayed immune response dysregulation in the post-COVID-19 infection setting. MIS-C patients may have a wide spectrum of manifestations including fever, elevated inflammatory parameters and signs of end organ damage including myocarditis, cardiac disfunction, gastrointestinal manifestations, respiratory impairment, acute kidney injury, and/or hematologic, dermatologic and/or neurological involvement. Although MIS-C may overlap with other well understood hyperinflammatory conditions such as secondary hemophagocytic lymphohistiocytosis (SHLH) in several Clinical features and laboratory findings, striking manifestations including Gastrointestinal and cardiac ones make the direction of the diagnostic compass geared more towards MIS-C which are unusual components of disease process in SHLH. Besides that, MIS-C can be distinguished from SHLH in the amplitude and severity of hyperinflammation, which are more pronounced in SHLH. Because of the overlap, diagnosis of MIS-C requires a high clinical index as prompt recognition and early intervention have favorable prognostic outcomes. We herein report a 5-year-old male child patient who presented with overlapping features between MIS-C and SHLH in a post-COVID-19 setting.

Preeclampsia and Gestational Hypertension: Biochemical and Antioxidant Features in Vitro Might Help Understand Different Outcomes.

Gestational hypertension (GH) is characterized by increased blood pressure after the 20th gestational week; the presence of proteinuria and/or signs of end-organ damage indicate preeclampsia (PE). Heme oxygenase-1 (HO-1) is an antioxidant enzyme with an important role in maintaining endothelial function, and induction of HO-1 by certain molecules shows potential in attenuating the condition's effects over endothelial tissue. HO-1 production can also be stimulated by potassium iodide (KI). Therefore, we evaluated the effects of KI over HO-1 expression in human umbilical vein endothelial cells (HUVECs) incubated with plasma from women diagnosed with GH or PE. Human umbilical vein endothelial cells were incubated with a pool of plasma of healthy pregnant women (n = 12), pregnant women diagnosed with GH (n = 10) or preeclamptic women (n = 11) with or without the addition of KI for 24 hours to evaluate its effect on this enzyme expression. Analysis of variance was performed followed by Dunnet's test for multiple comparisons between groups only or between groups with addition of KI (p ≤ 0.05). KI solution (1,000 µM) reduced HO-1 in the gestational hypertension group (p = 0.0018) and cytotoxicity in the preeclamptic group (p = 0.0143); treatment with KI reduced plasma cytotoxicity but did not affect the preeclamptic group's HO-1 expression. Our findings suggest that KI alleviates oxidative stress leading to decreased HO-1 expression; plasma from preeclamptic women did not induce the enzyme's expression in HUVECs, and we hypothesize that this is possibly due to inhibitory post-transcriptional mechanisms in response to overexpression of this enzyme during early pregnancy.

Comparison of the effectiveness of captopril and olmesartan in hypertensive patients

Purpose: Hypertensive conditions are situations that require immediate intervention in emergency services. Captopril is one of the most commonly used drugs in patients presenting to emergency departments with high blood pressure. In this study; we aimed to find an answer to the question of whether orally administered olmesartan could be an alternative to captopril in urgent hypertensive situations. Material and Method: In this study, blood pressure measurements were made after a 5-minute rest period in patients who presented to the emergency department of our hospital with the diagnosis of hypertension. Patients with a blood pressure of 180/100 mmHg and above and no signs of end-organ damage were followed up. Forty patients were given sublingual captopril 25 mg, and the other 40 patients were given 40 mg of olmesartan, and they were allowed to swallow the drug with some water. Afterward, the patients were followed for 3 hours (with blood pressure and pulse measurements), and their blood pressure was measured and recorded at five-minute intervals. Results: The mean age of the patients receiving captopril was 60.70±11.43 years, and the mean age of the patients receiving olmesartan was 57.02±13.86 years. Of the patients receiving captopril, 19 (57.5%) were male, 21 (52.5%) were female, 17 (42.5%) of the patients receiving olmesartan were male and 23 (57.5%) were female. In this study, patients treated with captopril and olmesartan were monitored for 3 hours and the differences between them in pulse and blood pressure measurements were evaluated. When the systolic blood pressures were compared, the difference at the tenth minute was significant, but the difference between the other minutes was not significant. Differences in diastolic blood pressure and heart rate were not significant. Conclusion: Oral administration of olmesartan in emergency hypertensive patients may be an alternative to captopril due to its effectiveness in reducing mortality and morbidity.

Dietary protein source contributes to the risk of developing maternal syndrome in the Dahl salt-sensitive rat.

Preeclampsia (PE) is a disorder of pregnancy, which is categorized by hypertension and proteinuria or signs of end-organ damage. Though PE is the leading cause of maternal and fetal morbidity and mortality, the mechanisms leading to PE remain unclear. The present study examined the contribution of dietary protein source (casein versus wheat gluten) to the risk of developing maternal syndrome utilizing two colonies of Dahl salt-sensitive (SS/JrHsdMcwi) rats. While the only difference between the colonies is the diet, the colonies exhibit profound differences in the pregnancy phenotypes. The SS rats maintained on the wheat gluten (SSWG) chow are protected from developing maternal syndrome; however, approximately half of the SS rats fed a casein-based diet (SSC) exhibit maternal syndrome. Those SSC rats that develop pregnancy-specific increases in blood pressure and proteinuria have no observable differences in renal or placental immune profiles compared to the protected SS rats. A gene profile array of placental tissue revealed a downregulation in Nos3 and Cyp26a1 in the SSC rats that develop maternal syndrome accompanied with increases in uterine artery resistance index suggesting the source of this phenotype could be linked to inadequate remodeling within the placenta. Investigations into the effects of multiple pregnancies on maternal health replicated similar findings. The SSC colony displayed an exacerbation in proteinuria, renal hypertrophy and renal immune cell infiltration associated with an increased mortality rate while the SSWG colony were protected highlighting how dietary protein source could have beneficial effects in PE.

Treatment and Outcomes of Inpatient Hypertension Among Adults With Noncardiac Admissions

Despite high prevalence of elevated blood pressure (BP) among medical inpatients, BP management guidelines are lacking for this population. The outcomes associated with intensifying BP treatment in the hospital are poorly studied. To characterize clinician response to BP in the hospital and at discharge and to compare short- and long-term outcomes associated with antihypertensive treatment intensification. This cohort study took place from January 1 to December 31, 2017, with 1 year of follow-up at 10 hospitals within the Cleveland Clinic Hospitals health care system. All adults admitted to a medicine service in 2017 were evaluated for inclusion. Patients with cardiovascular diagnoses were excluded. Demographic and BP characteristics were used for propensity matching. Acute hypertension treatment, defined as administration of an intravenous antihypertensive medication or a new class of an oral antihypertensive treatment. The association between acute hypertension treatment and subsequent inpatient acute kidney injury, myocardial injury, and stroke was measured. Postdischarge outcomes included stroke and myocardial infarction within 30 days and BP control up to 1 year. Among 22 834 adults hospitalized for noncardiovascular diagnoses (mean [SD] age, 65.6 [17.9] years; 12 993 women [56.9%]; 15 963 White patients [69.9%]), 17 821 (78%) had at least 1 hypertensive BP recorded during their admission. Of these patients, 5904 (33.1%) were treated. A total of 8692 of 106 097 cases (8.2%) of hypertensive systolic BPs were treated; of these, 5747 (66%) were treated with oral medications. In a propensity-matched sample controlling for patient and BP characteristics, treated patients had higher rates of subsequent acute kidney injury (466 of 4520 [10.3%] vs 357 of 4520 [7.9%]; P < .001) and myocardial injury (53 of 4520 [1.2%] vs 26 of 4520 [0.6%]; P = .003). There was no BP interval in which treated patients had better outcomes than untreated patients. A total of 1645 of 17 821 patients (9%) with hypertension were discharged with an intensified antihypertensive regimen. Medication intensification at discharge was not associated with better BP control in the following year. In this cohort study, hypertension was common among medical inpatients, but antihypertensive treatment intensification was not. Intensification of therapy without signs of end-organ damage was associated with worse outcomes.

SAT-504 Delayed Hypersensitivity to Levothyroxine, and Oral Desensitization

Introduction- Hypothyroidism is a common endocrine disorder, affecting about 4.6 percent of the U.S. population aged 12 and older. The most common treatment is synthetic thyroxine hormone supplementation-levothyroxine, starting at 1.6 mcg/kg.Hypersensitivity reactions to levothyroxine are rare. Two cases have been published of successful oral desensitization, for suspected IgE mediated reactions. There are no published protocols describing induction of drug tolerance to immunologic, non-IgE mediated reaction to levothyroxine. The objective of this case report is to describe a novel outpatient protocol, for oral desensitization to levothyroxine, in the setting of a delayed immunologic (non-IgE mediated) reaction.Case report- A 66 year old male with history of hypothyroidism, diagnosed in 2010 presented to outpatient endocrinology. Between 2010 and 2019, the patient was on multiple brands and formulations of levothyroxine. He noticed an itchy, raised rash on abdomen, chest and arms, within a few months after starting each of the above. No mucosal involvement or signs of end organ damage were noted. The rash was deemed a type IV delayed hypersensitivity reaction, based on history and histological findings on biopsy. The patient reported clearance of the rash when he was off any form of thyroid supplementation, and reappearance of the rash when he re-trialed it. The patient had normal thyroid stimulating hormone (TSH) levels while he was on supplementation despite the rash. The patient’s TSH after discontinuing treatment was 104 (uIU/mL) and free thyroxine (T4) was 0.13 ng/dl (0.9–1.7). All components of previous brands of levothyroxine were compared and no common ingredient was thought to be contributing to hypersensitivity reactions. Subsequently, an oral desensitization protocol was initiated at 0.075 mcg daily with weekly increase in doses over seven weeks to reach a target dose of 75 mcg.Discussion- The patient was tried on different brands of levothyroxine and dessicated thyroid hormone. He consistently developed a type IV hypersensitivity reaction within a few months after starting them. The patient had uncontrolled TSH levels after discontinuing the treatment and was at risk of complications of untreated hypothyroidism. This necessitated the need for desensitization. There have been previous case reports of oral or IV desensitization, in suspected IgE mediated reactions, but we describe the first case of induction of levothyroxine tolerance in an immunologic non-IgE mediated reaction. Subsequently, the patient tolerated a therapeutic dose of levothyroxine, with no appearance of rash or itching, for almost 6 months. This case report describes a novel approach to levothyroxine desensitization over a period of seven weeks in an outpatient setting in response to a delayed type hypersensitivity reaction.

Unusual Case of Acute Pulmonary Edema as a Manifestation of Postpartum Preeclampsia: A Case Report

Background: Hypertensive disease of pregnancy remains a leading cause of maternal morbidity and mortality. Four subcategories of hypertensive disorders of pregnancy are recognized by the international society for the study of hypertension in pregnancy: chronic hypertension; gestational hypertension, pre-eclampsia, & white coat hypertension. Pre-eclampsia is defined as systolic BP ≥ 140 mmHg or diastolic BP ≥ 90 on two occasions at least 4 hours apart after 20 weeks of gestation with accompanying signs of end organ damage in a woman with previously normal blood pressure. The majority of cases present ante-partum or immediately post-partum. I review the case of a woman diagnosed with pre-eclampsia at 2 weeks post-partum. Case presentation: A 38-year-old woman presented with increasing dyspnea, orthopnea, intermittent palpitations, and central chest pain 2 weeks after an uncomplicated vaginal delivery. On arrival, she was hypertensive at 168/117, spO2 of 100% on BiPAP. Exam was notable for diffuse rales, a regular rhythm, no JVD, and 1+ peripheral edema. Urine was positive for hemoglobin and protein and the liver panel revealed transaminitis (AST=50 ALT=53), Chest X-ray demonstrated increased pulmonary vasculature congestion, confirmed on CT angiography which was negative for venous thromboembolism. Echocardiography found a preserved ejection fraction without diastolic dysfunction or valvular abnormalities. She was managed with a nitroglycerin infusion and parenteral diuresis with resolution of her pulmonary edema. Conclusion: Pre-eclampsia affects 4-9% of all pregnancies and confers a high risk for both fetal and maternal morbidity and mortality. The definitive treatment for preeclampsia is delivery of fetus and placenta but there is limited information to guide the management of post-partum pre-eclampsia. It has been hypothesized that activation of maternal platelets in the placental bed play a role in preeclampsia through activation of inflammasomes such as sFlt-1. Yes, further research is needed to explore the benefit of suppressing these inflammasomes. Although peri-partum cardiomyopathy and venous thromboembolism usually come to mind in women with cardio-pulmonary complaints post-partum. In the appropriate setting, post-partum pre-eclampsia should also be entertained in the differential.

The exaggerated natriuresis of essential hypertension occurs independently of changes in renal medullary blood flow.

In patients with essential hypertension, abnormal renal sodium handling includes exaggerated natriuresis in response to extracellular volume expansion. We tested the hypothesis that exaggerated natriuresis is associated with increases in medullary and/or cortical renal blood flow. Patients with mild essential hypertension, but no signs of end organ damage, and control subjects were studied after 4days of dietary standardization (<60mmol Na+ day-1 ) preceded in patients by a 14-day drug washout period. On the study day, subjects received a 4-hour intravenous volume expansion with saline (2.1% of body mass). Renal medullary and cortical blood flows were measured by PET scanning using H215 O as tracer; anatomical regions of interest were defined by contrast-enhanced CT scanning. In patients, arterial blood pressure increased during volume expansion (107±2-114±3mmHg, P<0.05) in contrast to the control group (92±2-92±2mmHg). Renal sodium excretion increased more in patients than in controls (+133±31µmolmin-1 vs +61±14µmolmin-1 , respectively, P<0.05) confirming exaggerated natriuresis. During volume expansion, renal medullary blood flow did not change significantly in patients (2.8±0.4-2.5±0.5mL (g tissue)-1 min-1 ) or in controls (3.2±0.3-3.1±0.2mL (g tissue)-1 min-1 ). In control subjects, renal cortical blood flow fell during volume expansion (4.1±0.3-3.7±0.2mL (g tissue)-1 min-1 , P<0.05) in contrast to patients in which deviations remained insignificant. Exaggerated natriuresis, a hallmark of essential hypertension, is not mediated by increases in regional, renal blood flow.

136 - Baseline Chronic Kidney Disease Predicts In-Hospital and Long-Term Mortality in Cardiogenic Shock

Background: Despite advances in care, mortality in cardiogenic shock (CS) remains high. Further, there is limited data to stratify patients in CS based on patient characteristics. Methods: Patients admitted to the University of Virginia Coronary Care Unit from 2011 to 2013 were retrospectively analyzed to identify patients with CS as defined by sustained hypotension, reduced cardiac index <2.2 L/min/m2, and elevated pulmonary capillary wedge pressure >15 mmHg. Patients with primary cardiac pathology, pressor requirement, and signs of end-organ damage were also included. Using multivariable logistic regression, baseline patient characteristics and admission data including age, sex, presence of CS on admission, and co-morbidities prior to admission (congestive heart failure, coronary artery disease, diabetes mellitus, chronic kidney disease (CKD), chronic obstructive pulmonary disease, peripheral vascular disease) were evaluated for association with our primary outcome, in-hospital mortality. Three-year survival was assessed with Cox proportional hazards regression. Results: 248 patients were identified with CS and overall in-hospital mortality was 46%. Of all characteristics evaluated, only CKD (OR 3.13, 95% CI 1.72–5.68, P < .0002) was significantly associated with mortality. With adjustment for number of vasopressors/inotropes used, the association of CKD remained significant (OR 2.74, 95% CI 1.43–5.27, P = .0025). CKD was more strongly associated with mortality in CS secondary to acute coronary syndrome (ACS) (n = 93; OR 8.98, 95% CI 2.33–34.61, P = .0014) than in CS secondary to decompensated heart failure (n = 100; OR 2.82, 95% CI 0.93–8.58, P = .068). Patients with CKD also demonstrated lower three-year survival (HR 1.56 for mortality, 95% CI 1.15–2.12, P = .004, Fig. 1). Conclusions: This data demonstrates that the presence of CKD prior to admission is a strong, independent predictor of in-hospital and long-term mortality in CS, particularly in CS due to ACS, while no other factors showed predictive utility. Further investigation is warranted as predictive factors in CS could prove useful in risk stratification, patient counseling, and early therapeutic interventions.

Consideration of hypertensive retinopathy as an important end-organ damage in patients with hypertension.

Longstanding and therapy-resistant hypertension may cause cerebral, renal, cardiac and retinal end-organ damage (EOD). Retinal hypertensive abnormalities are correlated with an increased risk of cardiovascular (CV) disease in general but are not included in CV risk assessment tools. Research into prevalence and determinants of retinal organ damage, such as hypertensive retinopathy (HR), is scarce. We evaluated the prevalence of HR and the association with other signs of EOD in patients with hypertension. A retrospective observational study was performed in all hypertensive patients referred by a general practitioner to the hypertension clinic at the Diakonessenhuis, Utrecht and Zeist, the Netherlands between 2011 and 2013. A screening of risk factors, albuminuria, left-ventricular hypertrophy (LVH) and retinal fundoscopy was performed. In all, 44% (123/280) of patients referred to the clinic were diagnosed with HR, while 15 and 11% were diagnosed with LVH and microalbuminuria, respectively. Patients with isolated HR consisted of 31% of all patients. When HR was added as a form of EOD, the percentage of patients with a treatment indication increased from 3 to 14%. Patients who were already on treatment goal exhibited a high prevalence of HR (28%), warranting treatment intensification. HR is prevalent in a third of hypertensive patients referred to our clinic, and isolated HR accounts for the majority of (end-) organ damages. Fundoscopy in the evaluation of hypertension might improve the indication for therapy. Furthermore, diagnosing HR could be helpful in selecting patients with hypertension on treatment goal in need of more aggressive treatment.

Association of Medical Comorbidities, Surgical Outcomes, and Failure to Rescue: An Analysis of the Rhode Island Hospital NSQIP Database

Failure to rescue (FTR) is a key metric of perioperative morbidity and mortality. We review perioperative medical comorbidities (MCMs) to determine what factors are associated with complications and rates of FTR. A retrospective review of a NSQIP database including general, vascular, and surgical subspecialty patients from a tertiary referral center between March 2008 and March 2013 was performed. Demographics, MCMs, complications, 30-day mortality, and risk of FTR associated with specific complications and MCM were evaluated. A total of 7,763 patients were included; 52.6% had MCMs and 14% (n = 1,099) experienced a complication. Patients with complications were older (64.9 vs 55 years; p < 0.001), more likely male (54% vs 44%; p < 0.001), and had more MCMs per patient (1.6 vs 1.4; p < 0.001). Complications were also associated with renal failure (odds ratio [OR] = 1.4; 95% CI, 1.0-2.0), steroid use (OR = 1.9; 95% CI, 1.4-2.5), CHF (OR = 2.5; 95% CI, 1.2-5.1), and ascites (OR = 9.1; 95% CI, 3.7-21.7), but not diabetes, hypertension, or COPD. There were 117 (11%) deaths among patients with complications. Adjusting for age, sex, American Society of Anesthesiologists class, and number of comorbidities, FTR was associated with postoperative respiratory failure, sepsis, and renal failure, as well as comorbid CHF, renal failure, ascites, and disseminated cancer. Specific comorbidities are associated with higher rates of complications and FTR. Preoperative CHF, renal failure, and ascites, which were associated with FTR, can reflect a physiologic inability to tolerate complication-induced fluid shifts. Postoperative mortality was associated with signs of end organ damage, including sepsis, respiratory failure, and renal failure. Earlier recognition of these complications in at-risk patients should improve rates of FTR.

Antihypertensive Effect of Aliskiren as Related to BMI in Young Female Egyptian with Metabolic Syndrome

Background : In view of the potential benefit of direct renin inhibition, this clinical research article was designed to assess blood pressure lowering to the target blood pressure in 100 young (18-25 years) Egyptian female patients with metabolic syndrome (MS) and with body mass index of ≥30 kg/m 2 treated with aliskiren in multiple primary care units of female and child health all around Egypt. Methods : At an initial visit, physicians assessed baseline blood pressure (BP), (HR), risk factors, signs of end organ damage and prior antihypertensive medication. Patients were prescribed aliskiren 40 mg/kg/day orally. Efficacy and tolerability were measured by assessing blood pressure, and side effects at a further visit after two months. Blood pressure target was defined according to the Seventh Report of the Joint National Committee on Prevention, Detection, evaluation and Treatment of High Blood Pressure (JNC7) that recommends a BP treatment goal of <130/80 mmHg for patients MS with diabetes mellitus (DM). Results : Mean sitting systolic blood pressure/mean sitting diastolic blood pressure was lowered equally effectively (systolic/diastolic, p=1.0/0.8) in patients with metabolic syndrome (-22.0± 15.8/-10.9 ±9.6mmHg). Side effects were reported in 1% of all cases, none of them was life threatening. Conclusion : Aliskiren administration for 2 months at a dose of 40 mg/kg/day orally was effective in young Egyptian female who were hypertensive with MS.

Clozapine induced eosinophilia: An often neglected important adverse effect.

Sir, Clozapine, though effective in resistant schizophrenia, needs extensive monitoring more than any drug in psychiatry. Initial concerns were mainly related to agranulocytosis, but in recent years the focus has been shifted to eosinophilia and its potentially fatal complications.[12] Eosinophilia, a nondose-dependent side-effect, is seen in around 1% of clozapine-treated patients. It occurs during 1st year of treatment, mostly in the initial 4 weeks.[134] It is considered as an allergic reaction with a transient course and spontaneous remission. However, in some cases, it may predict subsequent neutropenia, myocarditis, eosinophilic colitis, pancreatitis and toxic hepatitis.[34] The manufacturer of clozapine recommends to interrupt its use when absolute eosinophil count >4000/cu mm until the eosinophil count falls below 3000/cu mm.[5] However, if there are no signs of end-organ damage or inflammation, clozapine continuation or rechallenge with careful monitoring may be considered.[6] Hereby reporting a patient who developed eosinophilia with clozapine. Mr. K.B, a 45-year-old male, was admitted in November 2012 with diagnosis of schizophrenia undifferentiated. Due to inadequate response to other antipsychotics, he was put on clozapine. His leukocyte count prior to the initiation of clozapine was 10,300/cu mm with eosinophil count being 1%. However, on day 7 of initiation of clozapine, the total leukocyte count of the patient was found to be 12,300/cu mm (eosinophil count 27%). After ruling out other medical causes, eosinophilia was found to be clozapine-induced. Instead of discontinuing, clozapine was continued and escalated gradually with close monitoring of its complications. The eosinophil count started falling by the 2nd week to 22%, further reduced to 20% by 4th week and the patient got discharged. Clozapine induced eosinophilia, leukocytosis and thrombocytopenia are generally benign events that resolves on their own.[47] In the above case, the eosinophil count increased during the 1st week of clozapine treatment, thereafter started resolving gradually. Eosinophilia, though considered benign and transient, needs to be monitored in view of a possible association with life-threatening conditions like myocarditis and predictor of subsequent neutropenia. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

Metabolic syndrome in hypertensive patients: An unholy alliance

For many years, it has been recognized that hypertension tends to cluster with various anthropometric and metabolic abnormalities including abdominal obesity, elevated triglycerides, reduced high-density lipoprotein cholesterol, glucose intolerance, insulin resistance and hyperuricemia. This constellation of various conditions has been transformed from a pathophysiological concept to a clinical entity, which has been defined metabolic syndrome (MetS). The consequences of the MetS have been difficult to assess without commonly accepted criteria to diagnose it. For this reason, on 2009 the International Diabetes Federation, the American Heart Association and other scientific organizations proposed a unified MetS definition. The incidence of the MetS has been increasing worldwide in parallel with an increase in overweight and obesity. The epidemic proportion reached by the MetS represents a major public health challenge, because several lines of evidence showed that the MetS, even without type 2 diabetes, confers an increased risk of cardiovascular morbidity and mortality in different populations including also hypertensive patients. It is likely that the enhanced cardiovascular risk associated with MetS in patients with high blood pressure may be largely mediated through an increased prevalence of preclinical cardiovascular and renal changes, such as left ventricular hypertrophy, early carotid atherosclerosis, impaired aortic elasticity, hypertensive retinopathy and microalbuminuria. Indeed, many reports support this notion, showing that hypertensive patients with MetS exhibit, more often than those without it, these early signs of end organ damage, most of which are recognized as significant independent predictors of adverse cardiovascular outcomes.