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OBJECTIVES: Quality and safety of emergency care is critical. Patients rely on emergency medicine (EM) for accessible, timely and high-quality care in addition to providing a 'safety-net' function. Demand is increasing, creating resource challenges in all settings. Where EM is well established, this is recognised through the implementation of quality standards and staff training for patient safety. In settings where EM is developing, immense system and patient pressures exist, thereby necessitating the availability of tiered standards appropriate to the local context. METHODS: The original quality framework arose from expert consensus at the International Federation of Emergency Medicine (IFEM) Symposium for Quality and Safety in Emergency Care (UK, 2011). The IFEM Quality and Safety Special Interest Group members have subsequently refined it to achieve a consensus in 2018. RESULTS: Patients should expect EDs to provide effective acute care. To do this, trained emergency personnel should make patient-centred, timely and expert decisions to provide care, supported by systems, processes, diagnostics, appropriate equipment and facilities. Enablers to high-quality care include appropriate staff, access to care (including financial), coordinated emergency care through the whole patient journey and monitoring of outcomes. Crowding directly impacts on patient quality of care, morbidity and mortality. Quality indicators should be pragmatic, measurable and prioritised as components of an improvement strategy which should be developed, tailored and implemented in each setting. CONCLUSION: EDs globally have a remit to deliver the best care possible. IFEM has defined and updated an international consensus framework for quality and safety.

BACKGROUND: In 2013, Danish policy-makers on a nationwide level decided to set up a national quality of care database for hospital-based emergency care in Denmark including the selection of quality indicators. The aim of the study was to describe the Delphi process that contributed to the selection of quality indicators for a new national database of hospital-based emergency care in Denmark. METHODS: The process comprised a literature review followed by a modified-Delphi survey process, involving a panel of 54 experts (senior clinicians, researchers and administrators from the emergency area and collaborating specialties). Based on the literature review, we identified 43 potential indicators, of which eight were time-critical conditions. We then consulted the Expert panel in two consecutive rounds. The Expert panel was asked to what extent each indicator would be a good measure of hospital-based emergency care in Denmark. In each round, the Expert panel participants scored each indicator on a Likert scale ranging from one (=disagree completely) through to six (=agree completely). Consensus for a quality indicator was reached if the median was greater than or equal to five (=agree). The Delphi process was followed by final selection by the steering group for the new database. RESULTS: Following round two of the Expert panel, consensus was reached on 32 quality indicators, including three time-critical conditions. Subsequently, the database steering group chose a set of nine quality indicators for the initial version of the national database for hospital-based emergency care. CONCLUSIONS: The two-round modified Delphi process contributed to the selection of an initial set of nine quality indicators for a new a national database for hospital-based emergency care in Denmark. Final selection was made by the database steering group informed by the Delphi process.

Background: Asymmetric dimethylarginine (ADMA), an endogenous methylated amino acid, has been identified as a competitive inhibitor of nitric oxide synthase (NOS). Elevated ADMA levels have been demonstrated in cardiovascular disorders and many studies have reported an inverse correlation between ADMA and endothelial function. The majority of ADMA is metabolized by dimethylarginine dimethylaminohydrolases (DDAH-1 and DDAH-2). Our aim was to study the genetic variation in the DDAH-1 gene in relation to ADMA levels and endothelial function. Methods: A total of 959 individuals, aged 70, from the community based Prospective Study of the Vasculature in Uppsala Seniors (PIVUS) study were included. Plasma concentrations of ADMA were measured by high performance liquid chromatography. Endothelial function was evaluated with both the invasive forearm technique (measuring endothelial dependent vasodilation in resistance arteries) and with brachial artery ultrasound (measuring flow mediated dilation in a conduit artery). Forty common single nucleotide polymorphisms (SNPs) in the DDAH-1 gene were analyzed. Results: There were significant associations between DDAH-1 genotype and ADMA levels in 20 of the 40 selected SNPs. However, no associations were seen between DDAH-1 genotype and endothelial function. Conclusion: These results indicate that genetic variation in the DDAH-1 gene has an impact on ADMA concentration in plasma. However, it does not seem to have a major influence on endothelial function.

Treatment with angiotensin II receptor blockers is associated with lower risk for the development of type 2 diabetes mellitus compared with thiazide diuretics. The Mechanisms for the Diabetes Preventing Effect of Candesartan Study addressed insulin action and secretion and body fat distribution after treatment with candesartan, hydrochlorothiazide, and placebo. Twenty-six nondiabetic, abdominally obese, hypertensive patients were included in a multicenter 3-way crossover trial, and 22 completers (by predefined criteria; 10 men and 12 women) were included in the analyses. They underwent 12-week treatment periods with candesartan (C; 16 to 32 mg), hydrochlorothiazide (H; 25 to 50 mg), and placebo (P), respectively, and the treatment order was randomly assigned and double blinded. Intravenous glucose tolerance tests and euglycemic hyperinsulinemic (56 mU/m(2) per minute) clamps were performed. Intrahepatic and intramyocellular and extramyocellular lipid content and subcutaneous and visceral abdominal adipose tissue were measured using proton magnetic resonance spectroscopy and MRI. Insulin sensitivity (M-value) was reduced following H versus C and P (6.07+/-2.05, 6.63+/-2.04, and 6.90+/-2.10 mg/kg of body weight per minute, mean+/-SD; P Udgivelsesdato: 2008/12

BACKGROUND: Studies suggest that endothelin-1 contributes to the pathogenesis of hypertension. A G5665T gene polymorphism of preproendothelin-1 has been shown to be associated with higher blood pressure in overweight patients. No study has yet determined the effect of this polymorphism on the change in blood pressure during antihypertensive treatment. HYPOTHESIS: This study aimed to determine this effect in hypertensive patients with left ventricular (LV) hypertrophy during antihypertensive treatment with either irbesartan or atenolol. METHODS: We determined the preproendothelin-1 genotype using minisequencing in 102 patients with essential hypertension and LV hypertrophy verified by echocardiography, randomized in a double-blind fashion to treatment with either the AT1-receptor antagonist irbesartan or the beta1-adrenoceptor antagonist atenolol. RESULTS: The change in systolic blood pressure (SBP) after 12 weeks of treatment was related to the preproendothelin-1 genotype in men; after adjustment for potential covariates (age, blood pressure, and LV mass index at study entry, dose of irbesartan/atenolol, and type of treatment), those carrying the T-allele responded on average with a more than two-fold greater reduction than those with the G/G genotype (-21.9 mmHg [13.9] vs. -8.9 [2.3], p = 0.007). No significant differences in blood pressure change between G/G and carriers of the T-allele were seen among women. CONCLUSIONS: Our finding suggests a gender-specific relationship between the G5665T preproendothelin-1 polymorphism and change in SBP in response to antihypertensive treatment with irbesartan or atenolol, suggesting the endothelin pathway to be a common mechanism included in the hypertensive action of the drugs.

Background: Studies suggest that the Ser49Gly and Arg389Gly polymorphisms in the β1-adrenergic receptor might be of functional importance for the cardiovascular system. Both have been associated with altered receptor activity in vitro, and with hypertension and cardiac failure in vivo. Hypothesis: The aim of this study was to test whether these polymorphisms were associated with the change in heart rate or blood pressure in patients with essential hypertension and left ventricular (LV) hypertrophy treated with the β1-adrenergic receptor blocker atenolol. Methods: Blood pressure and heart rate were measured in 101 hypertensive patients with echocardiographically verified LV hypertrophy, randomized in a double-blind study to treatment with either the β1-adrenergic receptor blocker atenolol or the angiotensin II type I receptor antagonist irbesartan. Changes in blood pressure and heart rate were evaluated after 12 weeks. Beta1-adrenergic receptor genotyping was performed using polymerase chain reaction and restriction fragment length polymorphism. Results: We found no significant associations between the changes in the measured variables and either of the two polymorphisms. However, carriers of the 49Gly allele showed a tendency toward a greater reduction in heart rate compared with patients with the Ser/Ser49 genotype (p = 0.06). Conclusions: The Ser49Gly and Arg389Gly β1-adrenergic receptor polymorphisms do not seem to exert a major effect on the changes in heart rate and blood pressure during 12 weeks of treatment with atenolol in patients with essential hypertension and LV hypertrophy.

Objective: Hypertension is associated with a number of adverse morphologic and functional changes in the cardiovascular system, including left ventricular (LV) hypertrophy. Studies have demonstrated that bradykinin, through the B2 bradykinin receptor (B2BKR), mediates important cardiovascular effects that may protect against LV hypertrophy. Recently, a +9/-9 exon 1 polymorphism of the B2BKR was shown to be strongly associated with LV growth response among normotensive males undergoing physical training. We aimed to clarify whether the processes found in exercise-induced LV growth in normotensive people also occur in pathological LV hypertrophy. Design and methods: We determined the B2BKR genotype of 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, included in a double-blind study to receive treatment for 48 weeks with either the angiotensin II type 1 (AT1) receptor antagonist irbesartan or the ▀1 -adrenoceptor antagonist atenolol. Results: B2BKR +9/+9 genotypes responded poorly in LV mass regression, independent of blood pressure reduction or treatment, as compared to the other genotypes (adjusted mean change in LV mass index = -10.0 ▒ 4.6 versus -21.6 ▒ 2.2 g/m2, P = 0.03). Conclusions: Our results suggest an impact of the B2BKR polymorphism on LV mass regression during antihypertensive treatment. ⌐ 2003 Lippincott Williams & Wilkins.

We aimed to develop a microarray genotyping system for multiplex analysis of a panel of single nucleotide polymorphisms (SNPs) in genes encoding proteins involved in blood pressure regulation, and to apply this system in a pilot study demonstrating its feasibility in the pharmacogenetics of hypertension. A panel of 74 SNPs in 25 genes involved in blood pressure regulation was selected from the SNP databases, and genotyped in DNA samples of 97 hypertensive patients. The patients had been randomized to double-blind treatment with either the angiotensin II type 1 receptor blocker irbesartan or the ▀1-adrenergic receptor blocker atenolol. Genotyping was performed using a microarray based DNA polymerase assisted 'minisequencing' single nucleotrde primer extension assay with fluorescence detection. The observed genotypes were related to the blood pressure reduction using stepwise multiple regression analysis. The allele frequencies of the selected SNPs were determined in the Swedish population. The established microarray-based genotyping system was validated and allowed unequivocal multiplex genotyping of the panel of 74 SNPs in every patient. Almost 7200 SNP genotypes were generated in thestudy. Profiles of four or five SNP-genotypes that may be useful as predictors of blood pressure reduction after antihypertensive treatment were identified. Our results highlight the potential of microarray-based technology for SNP genotyping in pharmacogenetics. Pharrnacogenetics 13:7-17 ⌐ 2003 Lippincott Williams & Wilkins.

Background: Adipocyte-derived leucine aminopeptidase (ALAP) is a recently identified member of the M1 family of zinc-metallopeptidases and is thought to play a role in blood pressure control through inactivation of angiotensin II and/or generation of bradykinin. The enzyme seems to be particularly abundant in the heart. Recently, the Arg528-encoding allele of the ALAP gene was shown to be associated with essential hypertension. Methods: We evaluated the influence of this polymorphism on the change in left ventricular mass index in 90 patients with essential hypertension and echocardiographically diagnosed left ventricular hypertrophy, randomised in a double-blind study to receive treatment with either the angiotensin II type I receptor antagonist irbesartan or the beta1-adrenoceptor blocker atenolol for 48 weeks. Genyotyping was performed using minisequencing. Results: After adjustment for potential covariates (blood pressure and left ventricular mass index at baseline, blood pressure change, age, sex, dose and added antihypertensive treatment), there was a marked difference between the Arg/Arg and Lys/Arg genotypes in patients treated with irbesartan, those with the Arg/Arg genotype responded on average with an almost two-fold greater regression of left ventricular mass index than patients with the Lys/Arg genotype (-30.1 g/m2 [3.6] vs - 16.7 [4.5], p = 0.03). Conclusions: The ALAP genotype seems to determine the degree of regression of left ventricular hypertrophy during antihypertensive treatment with the angiotensin II type I receptor antagonist irbesartan in patients with essential hypertension and left ventricular hypertrophy. This is the first report of a role for ALAP/aminopeptidases in left ventricular mass regulation, and suggests a new potential target for antihypertensive drugs.

Background: Our aim was to determine whether the aldosterone synthase (CYP11B2) -344 C/T polymorphism was associated with the blood pressure (BP)-lowering response to antihypertensive treatment. Methods: Patients with mild-to-moderate primary hypertension and left ventricular hypertrophy were randomized in a double-blind study to receive treatment with either the angiotensin II type 1 (AT1) receptor antagonist irbesartan (n = 43), or the ß1-adrenergic receptor blocker atenolol (n = 43). The aldosterone synthase (CYP11B2) -344 C/T polymorphism was analyzed using solid-phase minisequencing and related to BP reduction after 3 months treatment. Serum aldosterone levels were measured. Results: After 3 months treatment the mean reductions in BP were similar for both treatment groups. When assessing the systolic BP reduction in the irbesartan group, patients with the TT variant had a more pronounced reduction (-21 ± 19 SD mm Hg, n = 17) than both the TC (-14 ± 18 mm Hg, n = 18) and CC (0 ± 17 mm Hg, n = 8) genotypes (P = .04). There was no association between this polymorphism and the diastolic BP response. The -344 C/T polymorphism was not associated with the BP response to atenolol. Nor was it related to the baseline serum aldosterone level. Conclusions: The aldosterone synthase -344 C/T polymorphism was related to the BP-lowering response in hypertensive patients treated with the AT1-receptor antagonist irbesartan. © 2002 American Journal of Hypertension, Ltd.

Objectives To determine whether polymorphisms in the renin-angiotensin system can predict blood pressure-lowering response to antihypertensive treatment, more specifically, in response to treatment with irbesartan or atenolol. Design and methods Eighty-six patients with hypertension were randomized to double-blind treatment with either the angiotensin II type 1 receptor antagonist irbesartan or the ß1 adrenergic receptor blocker atenolol and followed for 3 months. We analysed angiotensinogen T174M and M235T, angiotensin converting enzyme (ACE) I/D and angiotensin II type 1 receptor A1166C polymorphisms and related them to blood pressure reduction. Results The mean reductions in blood pressure were similar for both treatments. In the irbesartan group, individuals homozygous for the ACE gene I allele showed a greater reduction in diastolic blood pressure, exceeding those with the D allele (-18±11 SD versus -7±10 mmHg, P=0.0096). This was not the case during treatment with atenolol, and the interaction term between type of treatment and ACE II genotype was significant (P=0.0176). The angiotensinogen and angiotensin II type 1 receptor polymorhisms were not related to the response to treatment Conclusions ACE genotyping predicted the blood pressure-lowering response to antihypertensive treatment with irbesartan but not atenolol. Thus, specific genotypes might predict the response to specific antihypertensive treatment. © 2001 Lippincott Williams & Wilkins.