Cardiac output estimation using ballistocardiography: a feasibility study in healthy subjects.

There is no reliable automated non-invasive solution for monitoring circulation and guiding treatment in prehospital emergency medicine. Cardiac output (CO) monitoring might provide a solution, but CO monitors are not feasible/practical in the prehospital setting. Non-invasive ballistocardiography (BCG) measures heart contractility and tracks CO changes. This study analyzed the feasibility of estimating CO using morphological features extracted from BCG signals. In 20 healthy subjects ECG, carotid/abdominal BCG, and invasive arterial blood pressure based CO were recorded. BCG signals were adaptively processed to isolate the circulatory component from carotid (CCc) and abdominal (CCa) BCG. Then, 66 features were computed on a beat-to-beat basis to characterize amplitude/duration/area/length of the fluctuation in CCc and CCa. Subjects' data were split into development set (75%) to select the best feature subset with which to build a machine learning model to estimate CO and validation set (25%) to evaluate model's performance. The model showed a mean absolute error, percentage error and 95% limits of agreement of 0.83 L/min, 30.2% and - 2.18-1.89 L/min respectively in the validation set. BCG showed potential to reliably estimate/track CO. This method is a promising first step towards an automated, non-invasive and reliable CO estimator that may be tested in prehospital emergencies.

Cardiovascular phenotype of long-term anabolic-androgenic steroid abusers compared with strength-trained athletes.

INTRODUCTION: Abuse of anabolic-androgenic steroids (AAS) has been linked to a variety of different cardiovascular (CV) side effects, but still the clinical effects of AAS abuse on CV risk are not clear. The aim of this study was to assess the CV phenotype of a large cohort of men with long-term AAS use compared with strength-trained athletes without AAS use. METHODS: Fifty one strength-trained men with ≥3 years of AAS use was compared with twenty one strength-trained competing athletes. We verified substance abuse and non-abuse by blood and urine analyses. The participants underwent comprehensive CV evaluation including laboratory analyses, 12-lead ECG with measurement of QT dispersion, exercise ECG, 24 h ECG with analyses of heart rate variability, signal averaged ECG, basic transthoracic echocardiography, and coronary computed tomography angiography (CCTA). RESULTS: Hemoglobin levels and hematocrit were higher among the AAS users compared with non-users (16.8 vs. 15.0 g/dl, and 0.50% vs. 0.44%, respectively, both p < 0.01) and HDL cholesterol significantly lower (0.69 vs. 1.25 mmol/L, p < 0.01). Maximal exercise capacity was 270 and 280 W in the AAS and the non-user group, respectively (p = 0.04). Echocardiography showed thicker intraventricular septum and left ventricular (LV) posterior wall among AAS users (p < 0.01 for both), while LV ejection fraction was lower (50 vs. 54%, p = 0.02). Seven AAS users (17%) had evidence of coronary artery disease on CCTA. There were no differences in ECG measures between the groups. CONCLUSIONS: A divergent CV phenotype dominated by increased CV risk, accelerated coronary artery disease, and concentric myocardial hypertrophy was revealed among the AAS users.

Cardiovascular rEmodelling in living kidNey donorS with reduced glomerular filtration rate: rationale and design of the CENS study.

Purpose: Until recently, it has been believed that donating a kidney not represents any risk for development of cardiovascular disease. However, a recent Norwegian epidemiological study suggests that kidney donors have an increased long-term risk of cardiovascular mortality. The pathophysiological mechanisms linking reduced kidney function to cardiovascular disease are not known. Living kidney donors are screened for cardiovascular morbidity before unilateral nephrectomy, and are left with mildly reduced glomerular filtration rate (GFR) after donation. Therefore, they represent an unique model for investigating the pathogenesis linking reduced GFR to cardiovascular disease and cardiovascular remodelling. We present the study design of Cardiovascular rEmodelling in living kidNey donorS with reduced glomerular filtration rate (CENS), which is an investigator-initiated prospective observational study on living kidney donors. The hypothesis is that living kidney donors develop cardiovascular remodelling due to a reduction of GFR.Materials and methods: 60 living kidney donors and 60 age and sex matched healthy controls will be recruited. The controls will be evaluated to fulfil the Norwegian transplantation protocol for living kidney donors. Investigations will be performed at baseline and after 1, 3, 6 and 10 years in both groups. The investigations include cardiac magnetic resonance imaging, echocardiography, bone density scan, flow mediated dilatation, laser Doppler flowmetry, nailfold capillaroscopy, office blood pressure, 24-h ambulatory blood pressure, heart rate variability and investigation of microbiota and biomarkers for inflammation, cardiovascular risk and the calcium-phosphate metabolism.Conclusions: The present study seeks to provide new insight in the pathophysiological mechanisms linking reduced kidney function to cardiovascular disease. In addition, we aim to enlighten predictors of adverse cardiovascular outcome in living kidney donors. The study is registered at Clinical-Trials.gov (identifier: NCT03729557).

Catheter-based left atrial appendage closure. / Kateterbasert lukking av venstre atriums aurikkel.

BAKGRUNN: Atrieflimmer er en vanlig tilstand i befolkningen og gir økt risiko for hjerneslag. Antikoagulasjonsbehandling er effektivt for å forebygge tromboembolisme ved atrieflimmer, men av ulike grunner blir mange atrieflimmerpasienter med indikasjon for antikoagulasjonsbehandling ikke behandlet. Kateterbasert lukking av venstre atriums aurikkel er en ny metode for å forebygge hjerneslag ved atrieflimmer. MATERIALE OG METODE: I perioden september 2014-april 2016 gjennomgikk 27 pasienter med atrieflimmer og høy risiko for hjerneslag forsøk på kateterbasert lukking av venstre atriums aurikkel ved Oslo universitetssykehus. Antikoagulasjonsbehandling var vurdert som kontraindisert hos 26 av pasientene. Vi presenterer resultater fra prosedyre, ekkokardiografikontroller og kliniske hendelser i oppfølgingsperioden på ett år. RESULTATER: Aurikkelplugg ble vellykket implantert hos 26 pasienter. To pasienter fikk komplikasjoner i forbindelse med prosedyren: En fikk hjerneslag og en fikk transfusjonskrevende lyskeblødning. En pasient fikk hjertetamponade fem måneder etter prosedyren. En pasient som grunnet anatomisk vanskelige forhold ikke fikk implantert aurikkelplugg, døde av hjerneslag i oppfølgingsperioden. Tre pasienter hadde klinisk transitorisk iskemisk anfall (TIA). Det var ingen forekomst av intrakranial eller gastrointestinal blødning. FORTOLKNING: Kateterbasert lukking av venstre atriums aurikkel er gjennomførbart, men innebærer risiko for komplikasjoner og bør forbeholdes pasienter med høy risiko for hjerneslag og kontraindikasjon mot antikoagulasjonsbehandling.

Systolic mitral annulus velocity is a sensitive index for changes in left ventricular systolic function during inotropic therapy in patients with acute heart failure.

BACKGROUND: Echocardiography is recommended for assessment of left ventricular systolic function in patients with acute heart failure but few randomised trials have validated techniques like tissue Doppler (TDI) and speckle tracking (STE) in patients with acute heart failure following ST-elevation myocardial infarction. METHODS: This was a substudy from the LEAF (LEvosimendan in Acute heart Failure following myocardial infarction) trial (NCT00324766 ), which randomised 61 patients developing acute heart failure, including cardiogenic shock, within 48 hours after ST-elevation myocardial infarction, double-blind to a 25-hour infusion of levosimendan or placebo. TDI-derived systolic mitral annulus velocity (S'), STE-derived global longitudinal strain (Sl) and strain rate (SRl) were measured at baseline, day 1, day 5 and after 42 days. RESULTS: Datasets rejected for analyses were 2% (TDI) and 17% (STE). S' increased by 23% in the levosimendan group versus 8% in the placebo group from baseline to day 1 ( p= 0.011) and by 30% vs. 3% from baseline to day 5 ( p <0.0005). Significant, but less pronounced, improvements in global Sl ( p = 0.025 and p = 0.032) and in global SRl ( p = 0.046 and p = 0.001) in favour of levosimendan were also present. CONCLUSION: S' by TDI and STE-derived Sl and SRl were sensitive indices for changes in left ventricular systolic function related to treatment with levosimendan. However, S' by TDI was more feasible and sensitive and might be preferred for assessment of changes in left ventricular systolic function in critically ill patients with acute heart failure receiving inotropic therapy.

Drug-Eluting or Bare-Metal Stents for Coronary Artery Disease.

BACKGROUND: Limited data are available on the long-term effects of contemporary drug-eluting stents versus contemporary bare-metal stents on rates of death, myocardial infarction, repeat revascularization, and stent thrombosis and on quality of life. METHODS: We randomly assigned 9013 patients who had stable or unstable coronary artery disease to undergo percutaneous coronary intervention (PCI) with the implantation of either contemporary drug-eluting stents or bare-metal stents. In the group receiving drug-eluting stents, 96% of the patients received either everolimus- or zotarolimus-eluting stents. The primary outcome was a composite of death from any cause and nonfatal spontaneous myocardial infarction after a median of 5 years of follow-up. Secondary outcomes included repeat revascularization, stent thrombosis, and quality of life. RESULTS: At 6 years, the rates of the primary outcome were 16.6% in the group receiving drug-eluting stents and 17.1% in the group receiving bare-metal stents (hazard ratio, 0.98; 95% confidence interval [CI], 0.88 to 1.09; P=0.66). There were no significant between-group differences in the components of the primary outcome. The 6-year rates of any repeat revascularization were 16.5% in the group receiving drug-eluting stents and 19.8% in the group receiving bare-metal stents (hazard ratio, 0.76; 95% CI, 0.69 to 0.85; P<0.001); the rates of definite stent thrombosis were 0.8% and 1.2%, respectively (P=0.0498). Quality-of-life measures did not differ significantly between the two groups. CONCLUSIONS: In patients undergoing PCI, there were no significant differences between those receiving drug-eluting stents and those receiving bare-metal stents in the composite outcome of death from any cause and nonfatal spontaneous myocardial infarction. Rates of repeat revascularization were lower in the group receiving drug-eluting stents. (Funded by the Norwegian Research Council and others; NORSTENT ClinicalTrials.gov number, NCT00811772 .).

Association of interleukin 8 and myocardial recovery in patients with ST-elevation myocardial infarction complicated by acute heart failure.

BACKGROUND: No data from controlled trials exists regarding the inflammatory response in patients with de novo heart failure (HF) complicating ST-elevation myocardial infarction (STEMI) and a possible role in the recovery of contractile function. We therefore explored the time course and possible associations between levels of inflammatory markers and recovery of impaired left ventricular function as well as levosimendan treatment in STEMI patients in a substudy of the LEvosimendan in Acute heart Failure following myocardial infarction (LEAF) trial. METHODS: A total of 61 patients developing HF within 48 hours after a primary PCI-treated STEMI were randomised double-blind to a 25 hours infusion of levosimendan or placebo. Levels of IL-6, CRP, sIL-6R, sgp130, MCP-1, IL-8, MMP-9, sICAM-1, sVCAM-1 and TNF-α were measured at inclusion (median 22 h, interquartile range (IQR) 14, 29 after PCI), on day 1, day 2, day 5 and 6 weeks. Improvement in left ventricular function was evaluated as change in wall motion score index (WMSI) by echocardiography. RESULTS: Only circulating levels of IL-8 at inclusion were associated with change in WMSI from baseline to 6 weeks, r = ÷ 0.41 (p = 0.002). No association, however, was found between IL-8 and WMSI at inclusion or peak troponin T. Furthermore, there was a significant difference in change in WMSI from inclusion to 6 weeks between patients with IL-8 levels below, compared to above median value, ÷ 0.44 (IQR ÷ 0.57, ÷ 0.19) vs. ÷ 0.07 (IQR ÷ 0.27, 0.07), respectively (p < 0.0001). Levosimendan did not affect the levels of inflammary markers compared to control. CONCLUSION: High levels of IL-8 in STEMI patients complicated with HF were associated with less improvement in left ventricular function during the first 6 weeks after PCI, suggesting a possible role of IL-8 in the reperfusion-related injury of post-ischemic myocardium. Further studies are needed to confirm this hypothesis. TRIAL REGISTRATION: ClinicalTrials.gov NCT00324766.

Levosimendan in acute heart failure following primary percutaneous coronary intervention-treated acute ST-elevation myocardial infarction. Results from the LEAF trial: a randomized, placebo-controlled study.

AIMS: The calcium sensitizer levosimendan may counteract stunning after reperfusion of ischaemic myocardium, but no randomized placebo-controlled trials exist regarding its use in PCI-treated ST-segment elevation infarction (STEMI). We evaluated the efficacy and safety of levosimendan in patients with a primary PCI-treated STEMI complicated by symptomatic heart failure (HF). METHODS AND RESULTS: A total of 61 patients developing clinical signs of HF within 48 h after a primary PCI-treated STEMI (including cardiogenic shock) were randomized double-blind to a 25 h infusion of levosimendan or placebo. The primary endpoint was change in wall motion score index (WMSI) from baseline to day 5 measured by echocardiography. There was a significantly larger improvement in WMSI from baseline to day 5 in the levosimendan group compared with placebo (from 1.94 ± 0.20 to 1.66 ± 0.31 vs. 1.99 ± 0.22 to 1.83 ± 0.26, respectively, P = 0.031). There were significantly more episodes of hypotension during study drug infusion in the levosimendan group (67% vs. 36%, P = 0.029), but no significant difference in blood pressure at the end of infusion or in use of vasopressors. No significant between-group differences in changes in NT-proBNP levels, clinical composite score, frequency of atrial fibrillation or ventricular arrhythmia, infarct size at 6 weeks, or new clinical events up to 6 months were found. One and four patients died in the levosimendan and placebo group, respectively. CONCLUSIONS: Levosimendan treatment improved contractility in post-ischaemic myocardium in patients with PCI-treated STEMI complicated by HF. The treatment was well tolerated, without any increase in arrhythmias.

Assessment of left ventricular function in ST-elevation myocardial infarction by global longitudinal strain: a comparison with ejection fraction, infarct size, and wall motion score index measured by non-invasive imaging modalities.

AIMS: We aimed to compare two-dimensional global longitudinal strain (GS) with different non-invasive imaging modalities for the assessment of left ventricular function in an ST-elevation myocardial infarction population. METHODS AND RESULTS: GS was compared with ejection fraction (EF) determined by magnetic resonance imaging (MRI), standard echocardiography (echo), contrast echo, and electrocardiography-gated single-photon emission computed tomography (SPECT), as well as with MRI-determined relative infarct size and echo-determined wall motion score index (WMSI), in 163 patients participating in the NORwegian Study on District Treatment of ST-Elevation Myocardial Infarction (NORDISTEMI). The linear relation between GS and standard echo (r(2)= 0.43, P <0.001), contrast echo (r(2)= 0.38, P <0.001), and SPECT-determined EF (r(2)= 0.52, P <0.001) was almost identical as that between GS and the gold standard MRI-determined EF (r(2)= 0.47, P <0.001). GS was best associated with WMSI by echo (r(2)= 0.55, P <0.001), while the associations between GS and relative infarct size were weaker (r = 0.43, P <0.001). Receiver operator characteristics curves, used to analyse the ability of GS to discriminate low EF (≤ 40%) measured by the four different modalities, large myocardial infarction (MI ≥ 15.7%), and high WMSI (≥ 1.5), were significant for all. GS was shown to be the best predictor of low EF measured by MRI [area under the curve (AUC) 0.965], while the lowest AUC was found between GS and large MI (0.814). CONCLUSION: Global strain is associated well with EF measured by all modalities. Global strain was found to be the best predictor of low EF measured by the gold standard MRI. Since global strain is an inexpensive test, these data may be of health economic interest.

Amino-terminal pro-B-type natriuretic peptide (NT-proBNP) levels 3 months after myocardial infarction are more strongly associated with magnetic resonance-determined ejection fraction than NTproBNP levels in the acute phase.

BACKGROUND: The relationship between levels of amino-terminal pro-B-type natriuretic peptide (NT-proBNP) and left ventricular function determined by magnetic resonance imaging (MRI) in ST-segment-elevation myocardial infarction (STEMI) is largely unknown. METHODS AND RESULTS: This was a substudy of the Norwegian Study on District Treatment of STEMI, in which patients received thrombolysis followed by early or late invasive strategy. NT-proBNP was measured at 3 days and 3 months after the myocardial infarction, and magnetic resonance imaging was performed after 3 months (n = 160). Log NT-proBNP levels at both time points were significantly associated with ejection fraction (EF) (r(2) values 0.25 and 0.42, respectively) as well as infarct size (r(2) values 0.38 and 0.47, respectively; P < .0001 for all, adjusted for confounders). Furthermore, receiver operating characteristic (ROC) curves used to analyze the ability of NT-proBNP to discriminate long-term low EF (≤40%) and large infarct size (≥15.7%), were significant at both time points (P < .001 for all). Pairwise comparison of the ROC curves showed a significantly better performance of NT-proBNP at 3 months compared with 3 days for discrimination of low EF (P = .023). CONCLUSION: Repeated measurements of NT-proBNP in STEMI patients showed that NT-proBNP levels at 3 months were more strongly associated with long-term EF and infarct size than NT-pro BNP levels after 3 days. Our data suggest that measurement of NT-proBNP 3 months after myocardial infarction is a better indicator of left ventricular function compared with NT-proBNP in the acute phase.

Echocardiographic demonstration of improved myocardial function early after coronary artery bypass graft surgery.

The time course of recovery of left ventricular (LV) function after coronary artery bypass grafting (CABG) surgery is largely unknown. We aimed to test the hypothesis that LV function improves shortly after CABG by using echocardiography to elucidate myocardial contractility before and after CABG, and to determine the segmental distribution of viable myocardium. We prospectively studied 42 patients undergoing elective isolated CABG. No selection was done regarding preoperative LV ejection fraction. All patients underwent serial transthoracic two-dimensional echocardiography preoperatively, and at two to four days and six to seven weeks postoperatively. Regional wall motion was evaluated at each examination, and wall motion score index (WMSI) was calculated to assess recovery of contractile function. WMSI improved by surgery (P=0.005), stepwise from preoperatively to two to four days postoperatively (P=0.05) and borderline significantly between the two postoperative examinations (P=0.06). One hundred and one (15%) of 670 segments had abnormal contraction preoperatively; of which 69 were hypokinetic and 32 were akinetic. At six to seven weeks postoperatively a normalization of function was found in 35 (51%) hypokinetic and four (13%) akinetic segments. Our data suggest that CABG improves myocardial contractility within the first days postoperatively. Echocardiographic determination of wall motion is a useful tool to observe LV function.

Frequency of left ventricular thrombus in patients with anterior wall acute myocardial infarction treated with percutaneous coronary intervention and dual antiplatelet therapy.

The aim of the present study was to investigate the prevalence of left ventricular (LV) thrombus formation and important determinants in patients with acute ST elevation myocardial infarction localized to the anterior wall treated with percutaneous coronary intervention (PCI) and dual-antiplatelet therapy. One hundred selected patients with ST elevation myocardial infarctions revascularized with PCI in the left anterior descending coronary artery were included. The patients participated in the Autologous Stem Cell Transplantation in Acute Myocardial Infarction (ASTAMI) trial. All were treated with aspirin 75 mg/day and clopidogrel 75 mg/day and underwent serial echocardiography and magnetic resonance imaging during the first 3 months after PCI. After 4 to 5 days, the ejection fraction and infarct size in percentage of the left anterior descending coronary artery area were assessed using single photon-emission computed tomography in addition to the ejection fraction by echocardiography. LV thrombi were detected in 15 patients during the first 3 months, 2/3 of them within the first week. No differences in baseline characteristics between the groups with and without LV thrombi were shown. However, in the thrombus group, significantly higher peak creatine kinase levels (6,128 vs 2,197 U/L, p <0.01), larger infarct sizes (82.5% vs 63.8%, p <0.01), and lower ejection fractions on single photon-emission computed tomography (35.5% vs 40.0%, p = 0.03) and on echocardiography (43.0% vs 46.0%, p = 0.03) were found compared to patients without LV thrombi. In conclusion, LV thrombus formation is a frequent finding in patients with anterior wall ST elevation myocardial infarction treated acutely with PCI and dual-antiplatelet therapy and should be assessed by echocardiography within the first week.

Left ventricular function in acute myocardial infarction treated with thrombolysis followed by early versus late invasive strategy.

BACKGROUND: Thrombolysis remains the treatment of choice in acute ST-segment elevation myocardial infarction (STEMI) when primary percutaneous coronary intervention (PCI) cannot be performed within 90 to 120 minutes. The optimal treatment after thrombolysis is still debated, but several studies have shown improved clinical outcomes with early transfer for PCI. The aim of this study was to investigate whether an early invasive strategy after thrombolysis preserved left ventricular function better than a late invasive strategy. METHODS: This was a substudy of the NORwegian study on DIstrict treatment of ST-Elevation Myocardial Infarction. Patients with STEMI of <6 hours of duration and >90 minutes of expected transfer delays to PCI were treated with aspirin, tenecteplase, enoxaparin, and clopidogrel and randomized to early or late invasive strategy (N = 266). Left ventricular volumes and ejection fraction were assessed by single-photon emission computed tomography, echocardiography, and magnetic resonance imaging 3 months after the index infarction. RESULTS: Noninvasive imaging was completed in 241 patients (91%). Median end-diastolic and end-systolic volumes after 3 months did not differ between groups. Median ejection fraction was well preserved and also without differences: 63% (interquartile range 51-70) in the early invasive versus 65% (interquartile range 55-71) in the late invasive group when assessed by single-photon emission computed tomography (P = .30), 55% versus 55% when assessed by echocardiography (P = .88), and 57% versus 57% when assessed by magnetic resonance imaging (P = .99). CONCLUSION: In this group of STEMI patients treated with thrombolysis, no difference in left ventricular function after 3 months was found between patients treated with early versus late invasive strategy.

Assessment of left ventricular function with magnetic resonance imaging vs. echocardiography, contrast echocardiography, and single-photon emission computed tomography in patients with recent ST-elevation myocardial infarction.

AIMS: Magnetic resonance imaging (MRI) is often considered to be the gold standard in measuring left ventricular function and volumes. The aim of this study was to assess the agreements between standard echocardiography (standard echo), contrast echocardiography (contrast echo), single-photon emission computed tomography (SPECT), and MRI in the determination of left ventricular ejection fraction (EF) and end-diastolic volumes (EDV) in patients treated for acute ST-elevation myocardial infarction (STEMI). METHODS AND RESULTS: Standard echo, contrast echo, SPECT and MRI were performed on the same day, 3 months after STEMI in 150 patients participating in the NORwegian Study on District Treatment of ST-Elevation Myocardial Infarction (NORDISTEMI). Bland-Altman analysis of EF measured by all four imaging modalities showed generally low mean differences but wide limits of agreement. The mean EDV difference, however, was consistently higher when MRI was compared with standard echo (54.9 mL), contrast echo (41.7 mL) and SPECT (54.6 mL), and the limits of agreement were wider. The mean EDV differences between contrast echo vs. standard echo, SPECT vs. standard echo and contrast echo vs. SPECT were small. CONCLUSION: Our data suggest that all four imaging modalities measured EF closely similar after STEMI as demonstrated by a very small bias. The limits of agreement were however wide. EDV measured by MRI was consistently higher when compared with the other methods which may be caused by different tracing-methods and imaging principles. As echocardiography is preferable from a cost-benefit point of view, further analysis would be needed to clarify the nature of such differences.

Gender differences in management and outcome of acute myocardial infarctions treated in 2006-2007.

OBJECTIVES: Women with acute myocardial infarction (AMI) previously received less invasive evaluation and experienced higher mortality than men. After improvements in AMI care it is unclear whether gender differences still exist in management and outcome of AMI. METHODS: All patients admitted to Ullevål University Hospital for AMI during 2006 and 2007 were included in this cohort study. Predefined data were recorded during the hospital stay, and the survival status of the patients was ascertained on June 30, 2008. RESULTS: A total of 931 women and 2,174 men were included. No gender differences were observed in treatment delay or age-adjusted odds ratio (OR) of invasive evaluation in ST-elevation myocardial infarction (STEMI). In non-ST-elevation myocardial infarction (NSTEMI), women were less likely than men to undergo coronary angiography (adjusted OR 0.72, 95% CI 0.53-0.99, p = 0.044) and percutaneous coronary intervention (adjusted OR 0.60, 95% CI 0.47-0.76, p = 0.0001). Age-adjusted in-hospital mortality and long-term survival were similar between men and women. CONCLUSIONS: Women with STEMI experienced similar treatment delays and odds of invasive evaluation as men. However, gender differences in invasive evaluation were still observed in NSTEMI patients. No sex differences were observed in age-adjusted early and long-term mortality.

[Musculoskeletal pain in ultrasound operators]. / Muskel- og skjelettplager hos ultralydoperatører.

BACKGROUND: Ultrasound-based techniques are frequently used in cardiology, gynecology and radiology. Work-related symptoms are reported for ultrasound operators, but controlled studies have not been published. We wanted to map symptoms and clinical diagnoses in ultrasound operators, compare them to matched controls and evaluate a possible relation between symptoms and exposure. MATERIAL AND METHODS: All ultrasound operators working at Rikshospitalet and Ullevaal University hospitals and matched controls who had other work at the hospitals were invited to participate. They answered questions about pain, well-being at the workplace, physical activity, smoking and validated function scores for the back (Oswestry Disability Index-ODI), shoulder and arm (Quick-DASH), and health- related quality of life (EQ-5D and EQ-VAS, as well as exposure time for ultrasound examinations. All participants underwent a blinded, systematic clinical examination. RESULTS: 81 persons participated (43 women, 38 men); 44 operators and 37 controls. The ultrasound operators reported significantly more work-related pain from the wrist, elbow and shoulder and scored significantly worse on Quick-DASH (difference 6.1 [95 % CI 2.0 to 10.2, p < 0.001) and health-related function (EQ-5D). There was no difference in health-related quality of life (EQ-VAS) or back function (ODI). The number of persons with one or more clinical diagnosis was significantly higher for ultrasound operators (26/44 [59 %]) than controls (7/37 [19 %]), odds ratio 5.2; 95 % CI 2,0 to 14.0, p < 0.001. For subacromial pain the numbers were 11/44 (25 %) and 2/37 (5 %), odds ratio 5,8; CI 1.2 to 28.3, p = 0.034. For the ultrasound operators there was a significant association between exposure > 1000 min/week and Quick-DASH, subacromial pain and lateral epicondylagia. INTERPRETATION: Ultrasound operators reported significantly more shoulder and arm complaints and clinical diagnosis than controls.

Cardiac-restricted expression of the carboxyl-terminal fragment of GRK3 Uncovers Distinct Functions of GRK3 in regulation of cardiac contractility and growth: GRK3 controls cardiac alpha1-adrenergic receptor responsiveness.

G protein-coupled receptor kinase-2 and -3 (GRK2 and GRK3) in cardiac myocytes catalyze phosphorylation and desensitization of different G protein-coupled receptors through specificity controlled by their carboxyl-terminal pleckstrin homology domain. Although GRK2 has been extensively investigated, the function of cardiac GRK3 remains unknown. Thus, in this study cardiac function of GRK3 was investigated in transgenic (Tg) mice with cardiac-restricted expression of a competitive inhibitor of GRK3, i.e. the carboxyl-terminal plasma membrane targeting domain of GRK3 (GRK3ct). Cardiac myocytes from Tg-GRK3ct mice displayed significantly enhanced agonist-stimulated alpha(1)-adrenergic receptor-mediated activation of ERK1/2 versus cardiac myocytes from nontransgenic littermate control (NLC) mice consistent with inhibition of GRK3. Tg-GRK3ct mice did not display alterations of cardiac mass or left ventricular dimensions compared with NLC mice. Tail-cuff plethysmography of 3- and 9-month-old mice revealed elevated systolic blood pressure in Tg-GRK3ct mice versus control mice (3-month-old mice, 136.8 +/- 3.6 versus 118.3 +/- 4.7 mm Hg, p < 0.001), an observation confirmed by radiotelemetric recording of blood pressure of conscious, unrestrained mice. Simultaneous recording of left ventricular pressure and volume in vivo by miniaturized conductance micromanometry revealed increased systolic performance with significantly higher stroke volume and stroke work in Tg-GRK3ct mice than in NLC mice. This phenotype was corroborated in electrically paced ex vivo perfused working hearts. However, analysis of left ventricular function ex vivo as a function of increasing filling pressure disclosed significantly reduced (dP/dt)(min) and prolonged time constant of relaxation (tau) in Tg-GRK3ct hearts at elevated supraphysiological filling pressure compared with control hearts. Thus, inhibition of GRK3 apparently reduces tolerance to elevation of preload. In conclusion, inhibition of cardiac GRK3 causes hypertension because of hyperkinetic myocardium and increased cardiac output relying at least partially on cardiac myocyte alpha(1)-adrenergic receptor hyper-responsiveness. The reduced tolerance to elevation of preload may cause impaired ability to withstand pathophysiological mechanisms of heart failure.

From treatment to organ damage; a 5-year follow-up study of ambulatory blood pressure in essential hypertension. Diversity between development of left ventricular hypertrophy and urinary albumin excretion.

This study aimed to assess blood pressure (BP) profile, BP control, left ventricular hypertrophy (LVH) and albumin/creatinine ratio (ACR) in urine after 5 years of antihypertensive treatment in subjects with newly diagnosed essential hypertension. Fifty-four subjects were included and prescribed calcium-channel blocker in monotherapy during an 8-week period, and later 46 subjects (34 men, 12 women, 53.1+/-8.6 years) attended a 5-year follow-up visit at the hypertension clinic. They underwent 24-h ambulatory BP monitoring (ABPM), ECG and ACR at baseline and after 5 years. Echocardiography performed after 5 years revealed LVH in 54% of the subjects, while there was no change in Cornell product, an ECG criterion for LVH. BP control assessed by office BP was 33%, and only 20% using 24-h ABP. Night-time fall in BP was significantly attenuated from 13.2+/-5.9% to 10.7+/-6.0%, p = 0.01 for systolic BP and from 13.3+/-6.9% to 9.8+/-6.8%, p = 0.004 for diastolic BP. The number of dippers decreased after 5 years, but this did not reach statistical significance. In contrast to the lack of change in Cornell product, there was a significant decrease in ACR, and 93% of the subjects had ACR<1.5 mg/mmol after 5 years compared with 57% at baseline (p<0.001). Thus, ABPM should be encouraged in the follow-up of all hypertensive subjects as it reveals better inadequate BP control than office BP and gives information about night-time fall, as this may explain the high prevalence of LVH. The diversity in development of LVH and ACR during antihypertensive treatment needs to be verified.