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Fludrocortisone Is Associated With a Higher Risk of All-Cause Hospitalizations Compared With Midodrine in Patients With Orthostatic Hypotension.
Grijalva CG, Biaggioni I, Griffin MR, Shibao CA
(2017) J Am Heart Assoc 6:
MeSH Terms: Adrenergic alpha-1 Receptor Agonists, Aged, Blood Pressure, Databases, Factual, Female, Fludrocortisone, Heart Failure, Hospitalization, Humans, Hypotension, Orthostatic, Incidence, Logistic Models, Male, Medicaid, Middle Aged, Midodrine, Multivariate Analysis, Prevalence, Propensity Score, Retrospective Studies, Risk Factors, Tennessee, Time Factors, Treatment Outcome, United States, Vasoconstrictor Agents
Show Abstract · Added July 27, 2018
BACKGROUND - Orthostatic hypotension causes ≈80 000 hospitalizations per year in the United States. Treatments for orthostatic hypotension include fludrocortisone, a mineralocorticoid analog that promotes sodium reabsorption; and midodrine, an α-1 adrenergic agonist that is a direct vasoconstrictor. Although both medications are used to treat orthostatic hypotension, few studies have compared their relative safety.
METHODS AND RESULTS - We compared incidence rates of hospitalizations for all causes, and for congestive heart failure between users of fludrocortisone and users of midodrine in a retrospective cohort study of Tennessee Medicaid adult enrollees (1995-2009). Adjusted incidence rate ratios were calculated using negative binomial regression models. Subgroup analyses based on history of congestive heart failure were conducted. We studied 1324 patients initiating fludrocortisone and 797 patients initiating midodrine. Compared with fludrocortisone users, midodrine users had higher prevalence of cardiovascular conditions. Incidence rates of all-cause hospitalizations for fludrocortisone and midodrine users were 1489 and 1330 per 1000 person-years, respectively (adjusted incidence-rate ratio 1.20, 95% confidence interval, 1.02-1.40). The respective rates of heart failure-related hospitalization were 76 and 84 per 1000 person-years (adjusted incidence-rate ratio: 1.33, 95% confidence interval, 0.79-2.56). Among patients with a history of congestive heart failure, the rates of all-cause hospitalization for fludrocortisone and midodrine were 2448 and 1820 per 1000 person-years (adjusted incidence-rate ratio: 1.42, 95% confidence interval, 1.07-1.90), and the respective rates of heart failure exacerbation-related hospitalizations were 297 and 263 per 1000 person-years (adjusted incidence-rate ratio: 1.48, 95% confidence interval, 0.69-3.16).
CONCLUSIONS - Compared with users of midodrine, users of fludrocortisone had higher rates of all-cause hospitalizations, especially among patients with congestive heart failure.
© 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.
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Efficacy of Servo-Controlled Splanchnic Venous Compression in the Treatment of Orthostatic Hypotension: A Randomized Comparison With Midodrine.
Okamoto LE, Diedrich A, Baudenbacher FJ, Harder R, Whitfield JS, Iqbal F, Gamboa A, Shibao CA, Black BK, Raj SR, Robertson D, Biaggioni I
(2016) Hypertension 68: 418-26
MeSH Terms: Aged, Autonomic Nervous System, Blood Pressure, Blood Pressure Determination, Female, Humans, Hypotension, Orthostatic, Intermittent Pneumatic Compression Devices, Male, Midodrine, Monitoring, Physiologic, Splanchnic Circulation, Treatment Outcome, Vasoconstrictor Agents
Show Abstract · Added October 14, 2016
UNLABELLED - Splanchnic venous pooling is a major hemodynamic determinant of orthostatic hypotension, but is not specifically targeted by pressor agents, the mainstay of treatment. We developed an automated inflatable abdominal binder that provides sustained servo-controlled venous compression (40 mm Hg) and can be activated only on standing. We tested the efficacy of this device against placebo and compared it to midodrine in 19 autonomic failure patients randomized to receive either placebo, midodrine (2.5-10 mg), or placebo combined with binder on separate days in a single-blind, crossover study. Systolic blood pressure (SBP) was measured seated and standing before and 1-hour post medication; the binder was inflated immediately before standing. Only midodrine increased seated SBP (31±5 versus 9±4 placebo and 7±5 binder, P=0.003), whereas orthostatic tolerance (defined as area under the curve of upright SBP [AUCSBP]) improved similarly with binder and midodrine (AUCSBP, 195±35 and 197±41 versus 19±38 mm Hg×minute for placebo; P=0.003). Orthostatic symptom burden decreased with the binder (from 21.9±3.6 to 16.3±3.1, P=0.032) and midodrine (from 25.6±3.4 to 14.2±3.3, P<0.001), but not with placebo (from 19.6±3.5 to 20.1±3.3, P=0.756). We also compared the combination of midodrine and binder with midodrine alone. The combination produced a greater increase in orthostatic tolerance (AUCSBP, 326±65 versus 140±53 mm Hg×minute for midodrine alone; P=0.028, n=21) and decreased orthostatic symptoms (from 21.8±3.2 to 12.9±2.9, P<0.001). In conclusion, servo-controlled abdominal venous compression with an automated inflatable binder is as effective as midodrine, the standard of care, in the management of orthostatic hypotension. Combining both therapies produces greater improvement in orthostatic tolerance.
CLINICAL TRIAL REGISTRATION - URL: https://www.clinicaltrials.gov. Unique identifier: NCT00223691.
© 2016 American Heart Association, Inc.
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14 MeSH Terms
Procalcitonin as an Early Marker of the Need for Invasive Respiratory or Vasopressor Support in Adults With Community-Acquired Pneumonia.
Self WH, Grijalva CG, Williams DJ, Woodworth A, Balk RA, Fakhran S, Zhu Y, Courtney DM, Chappell J, Anderson EJ, Qi C, Waterer GW, Trabue C, Bramley AM, Jain S, Edwards KM, Wunderink RG
(2016) Chest 150: 819-828
MeSH Terms: Aged, Biomarkers, Calcitonin, Cohort Studies, Community-Acquired Infections, Critical Care, Female, Humans, Logistic Models, Male, Middle Aged, Pneumonia, Prognosis, Prospective Studies, Respiration, Artificial, Respiratory Insufficiency, Risk Assessment, Severity of Illness Index, Shock, Septic, Vasoconstrictor Agents
Show Abstract · Added July 27, 2018
BACKGROUND - Predicting the need for intensive care among adults with community-acquired pneumonia (CAP) remains challenging.
METHODS - Using a multicenter prospective cohort study of adults hospitalized with CAP, we evaluated the association of serum procalcitonin (PCT) concentration at hospital presentation with the need for invasive respiratory or vasopressor support (IRVS), or both, within 72 h. Logistic regression was used to model this association, with results reported as the estimated risk of IRVS for a given PCT concentration. We also assessed whether the addition of PCT changed the performance of established pneumonia severity scores, including the pneumonia severity index and the American Thoracic Society minor criteria, for prediction of IRVS.
RESULTS - Of 1,770 enrolled patients, 115 required IRVS (6.5%). Using the logistic regression model, PCT concentration had a strong association with IRVS risk. Undetectable PCT (< 0.05 ng/mL) was associated with a 4% (95% CI, 3.1%-5.1%) risk of IRVS. For concentrations < 10 ng/mL, PCT had an approximate linear association with IRVS risk: for each 1 ng/mL increase in PCT, there was a 1% to 2% absolute increase in the risk of IRVS. With a PCT concentration of 10 ng/mL, the risk of IRVS was 22.4% (95% CI, 16.3%-30.1%) and remained relatively constant for all concentrations > 10 ng/mL. When added to each pneumonia severity score, PCT contributed significant additional risk information for the prediction of IRVS.
CONCLUSIONS - Serum PCT concentration was strongly associated with the risk of requiring IRVS among adults hospitalized with CAP and is potentially useful for guiding decisions about ICU admission.
Copyright © 2016 American College of Chest Physicians. All rights reserved.
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Sepsis: Protocolized care for critically ill patients with AKI.
Sileshi B, Shaw A
(2015) Nat Rev Nephrol 11: 10-1
MeSH Terms: Erythrocyte Transfusion, Female, Fluid Therapy, Hemoglobins, Humans, Male, Shock, Septic, Vasoconstrictor Agents
Added October 20, 2015
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Efficacy of paracetamol on patent ductus arteriosus closure may be dose dependent: evidence from human and murine studies.
El-Khuffash A, Jain A, Corcoran D, Shah PS, Hooper CW, Brown N, Poole SD, Shelton EL, Milne GL, Reese J, McNamara PJ
(2014) Pediatr Res 76: 238-44
MeSH Terms: Acetaminophen, Administration, Intravenous, Administration, Oral, Animals, Blood Pressure, Cyclooxygenase Inhibitors, Dose-Response Relationship, Drug, Drug Administration Schedule, Ductus Arteriosus, Ductus Arteriosus, Patent, Humans, Indomethacin, Infant, Newborn, Ligation, Prostaglandin Antagonists, Retrospective Studies, Time Factors, Treatment Outcome, Vasoconstriction, Vasoconstrictor Agents
Show Abstract · Added April 9, 2015
BACKGROUND - We evaluated the clinical effectiveness of variable courses of paracetamol on patent ductus arteriosus (PDA) closure and examined its effect on the in vitro term and preterm murine ductus arteriosus (DA).
METHODS - Neonates received one of the following three paracetamol regimens: short course of oral paracetamol (SCOP), long course of oral paracetamol (LCOP), and intravenous paracetamol (IVP) for 2-6 d. Pressure myography was used to examine changes in vasomotor tone of the preterm and term mouse DA in response to paracetamol or indomethacin. Their effect on prostaglandin synthesis by DA explants was measured by mass spectroscopy.
RESULTS - Twenty-one preterm infants were included. No changes in PDA hemodynamics were seen in SCOP infants (n = 5). The PDA became less significant and eventually closed in six LCOP infants (n = 7). PDA closure was achieved in eight IVP infants (n = 9). On pressure myograph, paracetamol induced a concentration-dependent constriction of the term mouse DA, up to 30% of baseline (P < 0.01), but required >1 µmol/l. Indomethacin induced greater DA constriction and suppression of prostaglandin synthesis (P < 0.05).
CONCLUSION - The clinical efficacy of paracetamol on PDA closure may depend on the duration of treatment and the mode of administration. Paracetamol is less potent than indomethacin for constriction of the mouse DA in vitro.
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Inflammation and mechanical stretch promote aortic stiffening in hypertension through activation of p38 mitogen-activated protein kinase.
Wu J, Thabet SR, Kirabo A, Trott DW, Saleh MA, Xiao L, Madhur MS, Chen W, Harrison DG
(2014) Circ Res 114: 616-25
MeSH Terms: Adoptive Transfer, Angiotensin II, Animals, Aortic Diseases, CD4 Antigens, CD8 Antigens, Cells, Cultured, Collagen, Disease Models, Animal, Elastin, Fibroblasts, Homeodomain Proteins, Hypertension, Inflammation, Interleukin-17, Male, Mice, Mice, Knockout, Stress, Mechanical, T-Lymphocytes, Vascular Stiffness, Vasculitis, Vasoconstrictor Agents, p38 Mitogen-Activated Protein Kinases
Show Abstract · Added July 21, 2014
RATIONALE - Aortic stiffening commonly occurs in hypertension and further elevates systolic pressure. Hypertension is also associated with vascular inflammation and increased mechanical stretch. The interplay between inflammation, mechanical stretch, and aortic stiffening in hypertension remains undefined.
OBJECTIVE - Our aim was to determine the role of inflammation and mechanical stretch in aortic stiffening.
METHODS AND RESULTS - Chronic angiotensin II infusion caused marked aortic adventitial collagen deposition, as quantified by Masson trichrome blue staining and biochemically by hydroxyproline content, in wild-type but not in recombination activating gene-1-deficient mice. Aortic compliance, defined by ex vivo measurements of stress-strain curves, was reduced by chronic angiotensin II infusion in wild-type mice (P<0.01) but not in recombination activating gene-1-deficient mice (P<0.05). Adoptive transfer of T-cells to recombination activating gene-1-deficient mice restored aortic collagen deposition and stiffness to values observed in wild-type mice. Mice lacking the T-cell-derived cytokine interleukin 17a were also protected against aortic stiffening. In additional studies, we found that blood pressure normalization by treatment with hydralazine and hydrochlorothiazide prevented angiotensin II-induced vascular T-cell infiltration, aortic stiffening, and collagen deposition. Finally, we found that mechanical stretch induces the expression of collagen 1α1, 3α1, and 5a1 in cultured aortic fibroblasts in a p38 mitogen-activated protein kinase-dependent fashion, and that inhibition of p38 prevented angiotensin II-induced aortic stiffening in vivo. Interleukin 17a also induced collagen 3a1 expression via the activation of p38 mitogen-activated protein kinase.
CONCLUSIONS - Our data define a pathway in which inflammation and mechanical stretch lead to vascular inflammation that promotes collagen deposition. The resultant increase in aortic stiffness likely further worsens systolic hypertension and its attendant end-organ damage.
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Human interventions to characterize novel relationships between the renin-angiotensin-aldosterone system and parathyroid hormone.
Brown JM, Williams JS, Luther JM, Garg R, Garza AE, Pojoga LH, Ruan DT, Williams GH, Adler GK, Vaidya A
(2014) Hypertension 63: 273-80
MeSH Terms: Adult, Aldosterone, Angiotensin II, Antihypertensive Agents, Captopril, Diuretics, Dose-Response Relationship, Drug, Female, Humans, Hyperaldosteronism, Hypertension, Male, Middle Aged, Parathyroid Glands, Parathyroid Hormone, Renin-Angiotensin System, Spironolactone, Vasoconstrictor Agents, Vitamin D
Show Abstract · Added October 27, 2014
Observational studies in primary hyperaldosteronism suggest a positive relationship between aldosterone and parathyroid hormone (PTH); however, interventions to better characterize the physiological relationship between the renin-angiotensin-aldosterone system (RAAS) and PTH are needed. We evaluated the effect of individual RAAS components on PTH using 4 interventions in humans without primary hyperaldosteronism. PTH was measured before and after study (1) low-dose angiotensin II (Ang II) infusion (1 ng/kg per minute) and captopril administration (25 mg×1); study (2) high-dose Ang II infusion (3 ng/kg per minute); study (3) blinded crossover randomization to aldosterone infusion (0.7 µg/kg per hour) and vehicle; and study (4) blinded randomization to spironolactone (50 mg/daily) or placebo for 6 weeks. Infusion of Ang II at 1 ng/kg per minute acutely increased aldosterone (+148%) and PTH (+10.3%), whereas Ang II at 3 ng/kg per minute induced larger incremental changes in aldosterone (+241%) and PTH (+36%; P<0.01). Captopril acutely decreased aldosterone (-12%) and PTH (-9.7%; P<0.01). In contrast, aldosterone infusion robustly raised serum aldosterone (+892%) without modifying PTH. However, spironolactone therapy during 6 weeks modestly lowered PTH when compared with placebo (P<0.05). In vitro studies revealed the presence of Ang II type I and mineralocorticoid receptor mRNA and protein expression in normal and adenomatous human parathyroid tissues. We observed novel pleiotropic relationships between RAAS components and the regulation of PTH in individuals without primary hyperaldosteronism: the acute modulation of PTH by the RAAS seems to be mediated by Ang II, whereas the long-term influence of the RAAS on PTH may involve aldosterone. Future studies to evaluate the impact of RAAS inhibitors in treating PTH-mediated disorders are warranted.
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Episodic monoplane transesophageal echocardiography impacts postoperative management of the cardiac surgery patient.
Maltais S, Costello WT, Billings FT, Bick JS, Byrne JG, Ahmad RM, Wagner CE
(2013) J Cardiothorac Vasc Anesth 27: 665-9
MeSH Terms: APACHE, Cardiac Surgical Procedures, Cardiac Tamponade, Critical Care, Critical Illness, Echocardiography, Transesophageal, Fluid Therapy, Hemodynamics, Humans, Hypovolemia, Pericardial Effusion, Postoperative Care, Prospective Studies, Vasoconstrictor Agents, Ventricular Dysfunction, Right
Show Abstract · Added January 20, 2015
OBJECTIVE - A new slender, flexible, and miniaturized disposable monoplane transesophageal TEE probe has been approved for episodic hemodynamic transesophageal echocardiographic monitoring. The authors hypothesized that episodic monoplane TEE with a limited examination would help guide the postoperative management of high-risk cardiac surgery patients.
DESIGN - The authors analyzed the initial consecutive observational experience with the miniaturized transesophageal echocardiography monitoring system (ClariTEE, ImaCor, Uniondale, New York).
SETTING - Single institution in a university setting.
PARTICIPANTS - Unstable cardiac surgery patients.
INTERVENTIONS - The authors assessed fluid responsiveness, echocardiographic data, and concordance among hemodynamic data.
MEASUREMENTS AND MAIN RESULTS - From June 2010 to February 2011, 21 unstable cardiac surgery patients with postoperative instability were identified. Two patients (10%) required reoperation for bleeding and tamponade physiology. Right ventricular dysfunction was diagnosed by episodic TEE monitoring in 7 patients (33%), while hypovolemia was documented in 12 patients (57%). Volume responsiveness was documented in 11 patients. In this observational study, discordance between hemodynamic monitoring and episodic TEE was qualitatively observed in 14 patients (66%).
CONCLUSION - The authors demonstrated the ability of episodic monoplane TEE to identify discordance between hemodynamic monitoring to better define clinical scenarios in unstable cardiac surgery patients. For these challenging patients, limited episodic TEE assessment has become a cornerstone of ICU care in this institution.
Copyright © 2013 Elsevier Inc. All rights reserved.
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Endoplasmic reticulum stress and hypertension - a new paradigm?
Hasty AH, Harrison DG
(2012) J Clin Invest 122: 3859-61
MeSH Terms: Angiotensin II, Animals, Brain, Endoplasmic Reticulum Stress, Hypertension, Vasoconstrictor Agents
Show Abstract · Added March 27, 2013
Hypertension occurs in approximately 30% of individuals in Western populations and is known to be a major cause of stroke, heart failure, and myocardial infarction. Despite this, the molecular etiology of hypertension remains poorly understood. In this issue of the JCI, Young et al. show that endoplasmic reticulum (ER) stress is an essential signaling event for angiotensin II-induced hypertension in cells of the central nervous system. This provides new insight into the molecular mechanisms that drive hypertension and suggests a potential target for future therapy.
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Impact of maternal dexamethasone on coronary PGE(2) production and prostaglandin-dependent coronary reactivity.
Roghair RD, Volk KA, Lamb FS, Segar JL
(2012) Am J Physiol Regul Integr Comp Physiol 303: R513-9
MeSH Terms: Angiotensin II, Animals, Cells, Cultured, Coronary Vessels, Cyclooxygenase Inhibitors, Dexamethasone, Dinoprostone, Female, Glucocorticoids, Indomethacin, Models, Animal, Muscle, Smooth, Vascular, Pregnancy, Prenatal Exposure Delayed Effects, Prostaglandins, Sheep, Vasoconstriction, Vasoconstrictor Agents, Vasodilation
Show Abstract · Added February 22, 2016
Intrauterine growth restriction is associated with increased fetal glucocorticoid exposure and an increased risk of adult coronary artery disease. Coronary arteries from sheep exposed to early gestation dexamethasone (Dex) have increased constriction to angiotensin II (ANG II). Prostaglandin E(2) (PGE(2)) helps maintain coronary dilation, but PGE(2) production is acutely decreased by Dex administration. We hypothesized early gestation Dex exposure impairs adult coronary PGE(2) production with subsequent increases in coronary reactivity. Dex was administered to ewes at 27-28 days gestation (term 145 days). Coronary reactivity was assessed by wire myography in offspring at 4 mo of age (N = 5 to 7). Coronary smooth muscle cells were cultured and prostaglandin production was measured after 90 min incubation with radiolabeled arachidonate. Coronary myocytes from Dex-exposed lambs had a significant decrease in PGE(2) production that was reversed with ANG II incubation. Dex-exposed coronary arteries had increased constriction to ANG II and attenuated dilatation to arachidonic acid, with the greatest difference seen after the endothelium was inactivated by rubbing. Preincubation with the cyclooxygenase (COX) inhibitor indomethacin altered control responses and recapitulated the heightened coronary tone seen following Dex exposure. We conclude that impaired coronary smooth muscle COX-mediated PGE(2) production contributes to the coronary dysfunction elicited by early gestation Dex. Programmed inhibition of vasodilatory prostanoid production may link an adverse intrauterine environment with adult coronary artery disease.
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19 MeSH Terms