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  • 1.
    Gonzalez Garcia, Manuel Cruz
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    The role of leptin in endothelial dysfunction and cardiovascular disease2013Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    Objective:  Obesity has become the leading cause of mortality worldwide; however, the fundamental pathophysiology underlying this association remains unclear. The discovery of adipokines, i.e., cytokines produced by adipose cells (adipocytes), revealed that adipose tissue is a highly endocrine organ, thus opening new lines of investigation. The prototypical adipokine leptin increases in obesity, and leptin receptors are found in vascular cells. However, results are contradictory regarding the role of leptin in vascular and endothelial functions. Leptin has been shown to elicit vasodilatation, but has also been linked with atherosclerotic and thrombotic disease. The main aim of the present thesis was to study the association of circulating levels of leptin with markers of endothelial function, and to analyze the effects of leptin infusion in vivo  on vasomotor function and endogenous fibrinolysis.

    Material:  Four associative studies and two interventional studies were conducted. The former included DISARM (studies 1 and 2), the PIVUS study (study 3), and the Scottish post-infarction study (study 4). The DISARM studies and study 4, respectively, recruited 20 men and 83 men and women with stable ischemic heart disease. Study 3 included a random sample of 1016 subjects (54% women, 70 years old) living in the community of Uppsala, Sweden. For the interventional studies (studies 5 and 6), 10 healthy men were recruited for each study.

    Methods:  In all studies, endothelial function was estimated based on forearm blood flow (FBF) as measured by strain-gauge venous occlusion plethysmography, at rest or during infusion of vasodilators. In study 3, additional measurement techniques were used, such as brachial ultrasound flow-mediated dilation (FMD) and the aortic augmentation index (AoAIx) by tonometry in the radial artery. Fibrinolytic status was estimated based on basal and stimulated levels of tissue plasminogen activator antigen (t-PA), and by assessment of the endothelial release of t-PA (net t-PA release). Plasma leptin levels were measured by radioimmunoassay. In the associative studies, endothelial function and fibrinolytic status were related to circulating plasma leptin levels. In the experimental studies, exogenous leptin was administered in the brachial artery and endothelial function was assessed by strain-gauge plethysmography

    Results:  In elderly men and women, leptin was independently associated with decreased endothelial-dependent and -independent vasodilatation, reflecting disturbed endothelial function in resistance vessels. This association was attenuated after adjustment for BMI, and when analyzed among subjects with high plasma leptin levels. FMD (a measure of endothelial function in conduit vessels) was not associated with leptin. Exogenous leptin infusion did not alter vasomotor tone, but the endothelium-dependent and -independent vasodilatation was impaired during concomitant infusion of leptin and vasodilators. Infused leptin in the forearm did not affect blood pressure or pulse rate. Chronic hyperleptinemia, but not acutely induced hyperleptinemia, was associated with release of endothelial tissue plasminogen activator (net t-PA).

    Conclusions:  In humans, leptin was associated with impaired vasodilatation. However, this relationship was blunted after adjustment for BMI, suggesting that leptin could be the mediator between obesity and impaired vascular function. Furthermore, the observed lack of association in hyperleptinemic subjects may reflect a state of leptin resistance. The experimental result showing attenuated vascular reactivity following leptin infusion is in accordance with the results of the associative studies. The augmented net t-PA release in patients with chronic hyperleptinemia may indicate a state of “vascular activation,” which was not observed in healthy endothelium during a short period of leptin infusion. This thesis addresses several controversial issues regarding the action of leptin on vascular tissue in humans. The final results indicate that the in vivo action of leptin on vascularity is complex and mediated by several mechanisms. Our findings suggest that leptin is an important mediator between obesity and endothelial dysfunction, and should stimulate further investigation of this matter.

  • 2.
    Gonzalez Garcia, Manuel
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine. Australian eHealth Research Centre, CSIRO, Brisbane, QLD, Australia; Heart Centre, University Hospital of Umeå.
    Fatehi, Farhad
    Bashi, Nazli
    Varnfield, Marlien
    Iyngkaran, Pupalan
    Driscoll, Andrea
    Neil, Christopher
    Hare, David L.
    Oldenburg, Brian
    A Review of Randomized Controlled Trials Utilizing Telemedicine for Improving Heart Failure Readmission: Can a Realist Approach Bridge the Translational Divide?2019In: Clinical Medicine Insights: Cardiology, ISSN 1179-5468, E-ISSN 1179-5468, Vol. 13Article, review/survey (Refereed)
    Abstract [en]

    Background: Telemedicine and digital health technologies hold great promise for improving clinical care of heart failure. However, inconsistent and contradictory findings from randomized controlled trials have so far discouraged widespread adoption of digital health in routine clinical practice. We undertook this review study to summarize the study outcomes of the use of exploring the evidence for telemedicine in the clinical care of patients with heart failure and readmissions.

    Methods: We inspected the references of guidelines and searched PubMed for randomized controlled trials published over the past 10 years on the use of telemedicine for reducing readmission in heart failure. We utilized a modified realist review approach to identify the underlying contextual mechanisms for the intervention(s) in each randomized controlled trial, evaluating outcomes of the intervention and understanding how and under what conditions they worked. To provide uniformity, all extracted data were synthesized using adapted domains from the taxonomy for disease management created by the Disease Management Taxonomy Writing Group.

    Results: A total of 12 papers were eligible, 6 of them supporting and 6 others undermining the use of telemedicine for improving heart failure readmission. In general terms, those studies not supporting the use of telemedicine were multicentre, publicly funded, with large amount of participants, and long duration. The patients had also better rates of treatment with angiotensin-converting enzyme inhibitors/angiotensin II receptor blocker and beta-blockers, and telemonitoring and automatic transmission of vital signs were less utilized, in comparison with the studies in which telemedicine use was supported. The analysis of the environment, intensity, content of interventions, method of communication, quality of the underlying model of care and the ability, capability, and interest from health workers can help us to envisage probabilities of success of telemedicine use.

    Conclusions: A realist lens may aid to understand whom and in which circumstances the use of telemedicine can add any substantial value to traditional models of care. Wider outcome criteria beyond major adverse cardiovascular events, for example, cost efficacy, should also be considered as appropriate for effecting guidelines on care delivery when robust prognostic therapeutics already exist.

  • 3.
    Gonzalez, Manuel Cruz
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Robinson, Simon
    Mills, Nicholas L
    Eriksson, Marie
    Umeå University, Faculty of Social Sciences, Umeå School of Business and Economics (USBE), Statistics.
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Newby, David E
    Olsson, Tommy
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Hyperleptinemia is associated with altered endothelial functionManuscript (preprint) (Other academic)
    Abstract [en]

    Introduction The adipocyte-derived hormone leptin has been associated with increased risk of cardiovascular disease but the underlying mechanisms are unclear. Leptin effects on vascular endothelium may be a key mediator although contradictory results have been presented. We aimed to explore the effects of leptin on endothelial vasomotor and fibrinolytic function in healthy volunteers and patients with coronary heart disease.

    Methods and Results The vascular effects of leptin were assessed using venous occlusion plethysmography in healthy volunteers (n=17) and in patients with stable coronary heart disease (CHD) (n=83). In healthy male volunteers, intra-arterial infusion of recombinant human leptin (80, 800 and 8,000 ng/min; n=10) did not affect forearm blood flow or plasma tissue plasminogen activator (tPA) or plasminogen activator inhibitor type 1 (PAI-1) concentrations (all P>0.05).  However, during concomitant co-infusion with leptin (800 ng/min; n=10), induced vasodilatation was reduced (P=0.001), and tPA activity increased (P=0.002). In line with this, patients with coronary heart disease included in the highest tertile of plasma leptin concentrations had reduced substance P-induced vasodilatation (P<0.001), and increased tPA antigen and activity release (p<0.001 and p=0.03 respectively) compared to those in the lowest tertile.

    Conclusions Although leptin does not directly affect basal vascular function, acute local and chronic systemic hyperleptinemia are associated with altered endothelial function in healthy volunteers and patients with coronary heart disease respectively. These results support hyperleptinemia as a link between obesity and cardiovascular disease.

  • 4.
    Gonzalez, Manuel
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Lind, Lars
    Uppsala Univ, Dept Med, Uppsala, Sweden.
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Leptin and endothelial function in the elderly: the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) study2013In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 228, no 2, p. 485-490Article in journal (Refereed)
    Abstract [en]

    Background: Leptin levels are elevated in obese humans. Several studies have shown an association between hyperleptinemia and development of atherosclerosis and cardiovascular disease (CVD), but the relationship between leptin and vascular function remains unclear.

    Aim: To evaluate associations between circulating plasma leptin and measures of vascular function in a large sample of elderly individuals from the community.

    Methods: This cross-sectional study included 1016 subjects aged 70 (50% women) from the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS). The invasive technique forearm plethysmography with intra-arterial infusions of acetylcholine and sodium nitroprusside was used for estimation of endothelial dependent vasodilatation (EDV) and endothelial independent vasodilatation (EIDV), respectively, in resistance arteries, and the non-invasive technique ultrasound assessed flow mediated vasodilation (FMD) in conduit arteries. The aortic augmentation index (AoAI), a surrogate measure of arterial stiffness, was evaluated by pulse wave analysis. Associations of vascular function, arterial stiffness and blood pressure with leptin were explored.

    Results: In sex-adjusted models, high levels of leptin were inversely associated with EDV and EIDV. These associations remained after stratification for sex, traditional risk factors of CVD and insulin resistance, but were attenuated after taking a measure of obesity (body mass index) into account. In addition, leptin associated with arterial stiffness and systolic and diastolic blood pressure.

    Conclusion: Hyperleptinemia associated inversely with vasodilatation in resistance arteries. Furthermore, hyperleptinemia associated with arterial stiffness and hypertension. These associations were attenuated after adjusting for body mass index suggesting that leptin may be the mediator between obesity and impaired vascular function. (C) 2013 Elsevier Ireland Ltd. All rights reserved.

  • 5.
    Gonzalez, Manuel
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology. Commonwealth Scientific Research and Industrial Organisation (CSIRO), Brisbane, Australia.
    Sjölin, Ingela
    Bäck, Maria
    Ögmundsdottir Michelsen, Halldora
    Tanha, Tina
    Sandberg, Camilla
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology. Umeå University, Faculty of Medicine, Department of Community Medicine and Rehabilitation, Physiotherapy.
    Schiopu, Alexandru
    Leosdottir, Margret
    Effect of a lifestyle-focused electronic patient support application for improving risk factor management, self-rated health, and prognosis in post-myocardial infarction patients: study protocol for a multi-center randomized controlled trial2019In: Trials, ISSN 1745-6215, E-ISSN 1745-6215, Vol. 20, article id 76Article in journal (Refereed)
    Abstract [en]

    Background: Cardiac rehabilitation (CR) programs addressing risk factor management, educational interventions, and exercise contribute to reduce mortality after myocardial infarction (MI). However, the fulfillment of guideline-recommended CR targets is currently unsatisfactory. eHealth, i.e., the use of electronic communication for healthcare, including the use of mobile smartphone applications combined with different sensors and interactive computerized programs, offers a new array of possibilities to provide clinical care. The present study aims to assess the efficacy of a web-based application (app) designed to support persons in adhering to lifestyle advice and medication as a complement to traditional CR programs for improvement of risk factors and clinical outcomes in patients with MI compared with usual care.

    Methods/design: An open-label multi-center randomized controlled trial is being conducted at different CR centers from three Swedish University Hospitals. The aim is to include 150 patients with MI < 75 years of age who are confident smartphone and/or Internet users. In addition to participation in CR programs according to the usual routine at each center, patients randomized to the intervention arm will receive access to the web-based app. A CR nurse reviews the patients’ self-reported data twice weekly through a medical interface at the clinic. The primary outcome of the study will be change in submaximal exercise capacity (in watts) between 2 and 4 weeks after discharge and when the patient has completed his/her exercise program at the CR center, usually around 3–6 months post-discharge. Secondary outcomes include changes in self-reported physical activity, objectively assessed physical activity by accelerometry, self-rated health, dietary, and smoking habits, body mass index, blood pressure, blood lipids, and glucose/HbA1c levels between inclusion and follow-up visits during the first year post-MI. Additionally, we will assess uptake and adherence to the application, the number of CR staff contacts, and the incidence of cardiovascular events at 1 and 3 years after the MI. Patient recruitment started in 2016, and the first study results are expected in the beginning of 2019.

    Discussion: The present study will add evidence to whether electronic communication can be used to improve traditional CR programs for patients after MI.

  • 6.
    Henein, Mark
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Gonzalez, Manuel
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Tossavainen, Erik
    Henein, Michael Y
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Lindqvist, Per
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Left atrial strain rate using speckle tracking echocardiography during atrial systole in estimation of pulmonary capillary wedge pressure: a simultaneous echocardiography and cardiac catheterization studyArticle in journal (Other academic)
  • 7.
    Henein, Mark
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Tossavainen, Erik
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Grönlund, Christer
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Radiation Physics.
    Gonzalez, Manuel
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Lindqvist, Per
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Clinical Physiology. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Left atrial strain rate estimates PCWP2013In: International cardiovascular forum, ISSN 2409-3424, no 1, p. 25-30Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: Raised left atrial (LA) pressure is a common pathway for many pathologies and is known for its complications. It has a direct effect on LA cavity size and potentially also its function. We hypothesized that raised LA pressure, as shown by pulmonary capillary wedge pressure (PCWP), correlates with severity of global LA deformation abnormalities during atrial systole (LASRa). DESIGN AND PATIENTS: We prospectively studied 46 consecutive patients, mean age 61 ±13 years, 17 males, of various etiologies who underwent right heart catheterization and simultaneous Doppler echocardiography using spectral, tissue Doppler and speckle tracking echocardiography techniques for assessing LA structure and function. RESULTS: PCWP correlated with direct measurements of LA structure and function: LA volume (r= 0.43, p<0.01) and LASRa (r=0.79, p<0.001). PCWP correlated also with other indirect measures of LA pressure such as E/A (r=0.65, p<0.001), E wave deceleration time (r=0.54, p<0.001), E/e’ (r=0.49, p<0.001) and LA systolic filling fraction (r=0.52, p<0.001). However, LASRa together with LA systolic filling fraction, had the highest areas under the curve (0.83 and 0.87, respectively) for identifying patients with PCWP > 15 mmHg. CONCLUSION: PCWP correlates with LA deformation rate during atrial systole and to a higher extent than conventional Doppler measures of raised LA pressures. These findings should have significant clinical implications in correctly identifying breathless patients due to raised LA pressure.

  • 8.
    Henein, Michael Y
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Grönlund, Christer
    Umeå University, Faculty of Medicine, Department of Radiation Sciences.
    Tossavainen, Erik
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Gonzalez, Manuel
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Section of Medicine.
    Lindqvist, Per
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Clinical Physiology.
    Right and left heart dysfunction predict mortality in pulmonary hypertension2017In: Clinical Physiology and Functional Imaging, ISSN 1475-0961, E-ISSN 1475-097X, Vol. 37, no 1, p. 45-51Article in journal (Refereed)
    Abstract [en]

    In pulmonary hypertension (PH), the right heart dysfunction is a strong predictor of adverse clinical outcome, while the role of the left heart is not fully determined. The aim of this study was to identify predictors of mortality in precapillary PH including measures of both right and left heart function. We studied 34 patients (mean age 64 ± 13, range 31-82 years, 24 females) with precapillary PH, all of whom underwent detailed Doppler echocardiographic examination of the right and left heart function using conventional and speckle-tracking echocardiography. Patients were followed up for up to 8 years (mean 4·2 ± 1·9 years). At follow-up, 16 patients survived. Left ventricular (LV) filling time (P = 0·007), pulmonary artery acceleration time (P = 0·009), right atrial pressure (RAP) (P<0·001) and tricuspid regurgitation (TR) severity (P = 0·007) were worse in the deceased group. RV global longitudinal strain (GLS) (P = 0·001), RAP (P≤0·001), LV filling time (P<0·001) and TR severity (P<0·001) were the most accurate predictors, having the largest AUC (>0·65) and carried the highest risk for mortality (P<0·001 for all). The strongest predictors of mortality in precapillary PH indirectly reflect both left and right heart dysfunction including atrial structure and function disturbances. While an interaction pattern is observed, it needs to be confirmed in a larger cohort.

  • 9. Lindqvist, G
    et al.
    Grönlund, Christer
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Radiation Physics.
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Gonzalez, Manuel
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Henein, Michael Y
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Tossavainen, Erik
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Biventricular dysfunction and their consequences predict mortality in pulmonary arterial hypertension2014In: European Heart Journal, ISSN 0195-668X, E-ISSN 1522-9645, Vol. 35, no Supplement 1, Meeting abstract P492, p. 78-78Article in journal (Other academic)
  • 10.
    Lindqvist, Per
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Gonzalez, Manuel Garcia
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Tossavainen, Erik
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Henein, Michael Y
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Echocardiography based estimation of pulmonary vascular resistance in patients with pulmonary hypertension: a simultaneous Doppler echocardiography and cardiac catheterization study2011In: European Journal of Echocardiography, ISSN 1525-2167, E-ISSN 1532-2114, Vol. 12, no 12, p. 961-966Article in journal (Refereed)
    Abstract [en]

    Aims: Pulmonary vascular resistance (PVR) is an important measurement for the diagnosis of patients with pulmonary hypertension (PH) but needs accurate determination of mean pulmonary artery pressure (PAMP). We aimed to test the accuracy of a Doppler-derived measurement of PVR, using the conventional invasive equation in patients with PH.

    Methods and results: We investigated 30 patients undergoing right heart catheterization (RHC), mean age 62 ± 13 years, 21 females, with different diseases; idiopathic pulmonary arterial hypertension (PAH) (n= 5), associated PAH (n= 16), chronic thromboembolic PH (n= 6), interstitial lung disease (n= 2), and after closure of an atrial septal defect (n= 1). Patients with impaired left ventricular systolic function (EF < 50%) or elevated pulmonary capillary wedge pressure (PCWP >15 mmHg on RHC) were excluded. We used the formula: PAMP = PASPecho × 0.61 + 2 mmHg, where PASPecho is the peak tricuspid regurgitation pressure drop + 10 or 7 mmHg. Pulmonary vascular resistance was then calculated as PAMPecho− PCWP/cardiac output. Pulmonary capillary wedge pressure was estimated at 10 mmHg in all cases. The Doppler-derived estimation of PVRecho was achievable in 90% of patients, in whom accurate calculation of PAMP was obtainable. Pulmonary vascular resistance echo individual values strongly correlated with those from RHC (r= 0.85, P< 0.001 and r= 0.87, P< 0.001 for the two estimated values for right atrial pressure, respectively). The regression equation using this formula was PVRrhc = 0.95 × PVRecho− 0.29, and the regression line was close to identity. The Bland–Altman plot showed a good agreement between PVRecho and PVRrhc values, with a mean difference of −0.66 ± 2.1 Wood unit.

    Conclusion: The proposed Doppler-derived formula for estimating PVR based on the conventionally used invasive equation strongly correlates with invasive gold standard measures.

  • 11.
    Mills, Nicholas L
    et al.
    Centre for Cardiovascular Science, Edinburgh University, Edinburgh, UK .
    Finlayson, Alexander E
    Centre for Cardiovascular Science, Edinburgh University, Edinburgh, UK .
    Gonzalez, Manuel C
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Törnqvist, Håkan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Barath, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Vink, Elen
    Centre for Cardiovascular Science, Edinburgh University, Edinburgh, UK .
    Goudie, Colin
    Centre for Cardiovascular Science, Edinburgh University, Edinburgh, UK .
    Langrish, Jeremy P
    Centre for Cardiovascular Science, Edinburgh University, Edinburgh, UK .
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Boon, Nicholas A
    ntre for Cardiovascular Science, Edinburgh University, Edinburgh, UK .
    Fox, Keith A A
    ntre for Cardiovascular Science, Edinburgh University, Edinburgh, UK .
    Donaldson, Ken
    ELEGI Colt Laboratory, Centre for Inflammation Research, Edinburgh University, Edinburgh, UK .
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Newby, David E
    Centre for Cardiovascular Science, Edinburgh University, Edinburgh, UK.
    Diesel exhaust inhalation does not affect heart rhythm or heart rate variability2011In: Heart, ISSN 1355-6037, E-ISSN 1468-201X, Vol. 97, no 7, p. 544-550Article in journal (Refereed)
    Abstract [en]

    Objective Exposure to air pollution is associated with increases in cardiovascular morbidity and mortality. This study was undertaken to determine the effect of diesel exhaust inhalation on heart rhythm and heart rate variability in healthy volunteers and patients with coronary heart disease.

    Design and setting Double-blind randomised crossover studies in a university teaching hospital.

    Patients 32 healthy non-smoking volunteers and 20 patients with prior myocardial infarction.

    Interventions All 52 subjects were exposed for 1&emsp14;h to dilute diesel exhaust (particle concentration 300&emsp14;μg/m(3)) or filtered air.

    Main outcome measures Heart rhythm and heart rate variability were monitored during and for 24&emsp14;h after the exposure using continuous ambulatory electrocardiography and assessed using standard time and frequency domain analysis.

    Results No significant arrhythmias occurred during or following exposures. Patients with coronary heart disease had reduced autonomic function in comparison to healthy volunteers, with reduced standard deviations of the NN interval (SDNN, p<0.001) and triangular index (p<0.001). Diesel exhaust did not affect heart rate variability compared with filtered air (p>0.05 for all) in healthy volunteers (SDNN 101±6 vs 91±6, triangular index 20±1 vs 21±1) or patients with coronary heart disease (SDNN 47±5 vs 38±4, triangular index 8±1 vs 7±1).

    Conclusions Brief exposure to dilute diesel exhaust does not alter heart rhythm or heart rate variability in healthy volunteers or well-treated patients with stable coronary heart disease. Autonomic dysfunction does not appear to be a dominant mechanism that can explain the observed excess in cardiovascular events following exposure to combustion-derived air pollution.

  • 12. Mills, Nicholas L
    et al.
    Robinson, Simon D
    Boon, Nicholas A
    Newby, David E
    Törnqvist, Håkan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Gonzalez, Manuel
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Darnley, Kareen
    MacNee, William
    Donaldson, Ken
    Response to letter regarding article "Diesel exhaust inhalation causes vascular dysfunction and impaired endogenous fibrinolysis"2006In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 113, no 24, article id e872Article in journal (Other academic)
  • 13. Mills, Nicholas L
    et al.
    Törnqvist, Håkan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Gonzalez, Manuel
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Vink, Elen
    Robinson, Simon D
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Boon, Nicholas A
    Donaldson, Ken
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Newby, David E
    Ischemic and thrombotic effects of dilute diesel-exhaust inhalation in men with coronary heart disease2007In: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 357, no 11, p. 1075-1082Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Exposure to air pollution from traffic is associated with adverse cardiovascular events. The mechanisms for this association are unknown. We conducted a controlled exposure to dilute diesel exhaust in patients with stable coronary heart disease to determine the direct effect of air pollution on myocardial, vascular, and fibrinolytic function.

    METHODS: In a double-blind, randomized, crossover study, 20 men with prior myocardial infarction were exposed, in two separate sessions, to dilute diesel exhaust (300 mug per cubic meter) or filtered air for 1 hour during periods of rest and moderate exercise in a controlled-exposure facility. During the exposure, myocardial ischemia was quantified by ST-segment analysis using continuous 12-lead electrocardiography. Six hours after exposure, vasomotor and fibrinolytic function were assessed by means of intraarterial agonist infusions.

    RESULTS: During both exposure sessions, the heart rate increased with exercise (P<0.001); the increase was similar during exposure to diesel exhaust and exposure to filtered air (P=0.67). Exercise-induced ST-segment depression was present in all patients, but there was a greater increase in the ischemic burden during exposure to diesel exhaust (-22+/-4 vs. -8+/-6 millivolt seconds, P<0.001). Exposure to diesel exhaust did not aggravate preexisting vasomotor dysfunction, but it did reduce the acute release of endothelial tissue plasminogen activator (P=0.009; 35% decrease in the area under the curve).

    CONCLUSIONS: Brief exposure to dilute diesel exhaust promotes myocardial ischemia and inhibits endogenous fibrinolytic capacity in men with stable coronary heart disease. Our findings point to ischemic and thrombotic mechanisms that may explain in part the observation that exposure to combustion-derived air pollution is associated with adverse cardiovascular events.

  • 14.
    Tossavainen, Erik
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Grönlund, Christer
    Umeå University, Faculty of Medicine, Department of Radiation Sciences.
    Gonzalez, Manuel
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Henein, Michael Y
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Lindqvist, Per
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology. Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Clinical Physiology.
    Pulmonary artery acceleration time in identifying pulmonary hypertension patients with raised pulmonary vascular resistance2013In: European Heart Journal Cardiovascular Imaging, ISSN 2047-2404, E-ISSN 2047-2412, Vol. 14, no 9, p. 890-897Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: In patients with pulmonary hypertension (PH), ascertaining raised vascular resistance as a cause is a clinical objective, for which various Doppler-based measurements have been proposed, but with modest accuracy. We hypothesize that pulmonary acceleration time (PAcT) and the ratio of PAcT/peak pulmonary artery systolic pressure (PASP) reflect better the extent of the vascular resistance, compared with other available methods, and can differentiate accurately between pre- and post-capillary PH.

    METHODS AND RESULTS: We investigated 56 patients (mean age 61 ± 13 years, 23 males) in a simultaneous echocardiography and right heart catheterization (RHC) study. Based on the RHC, pulmonary vascular resistance (PVR), and pulmonary capillary wedge pressure (PCWP), patients were divided into four groups: Group 1 = normal PVR [<3 WU (Wood units)] and PCWP (<12 mmHg), Group 2 = raised PVR but normal PCWP, Group 3 = raised PVR and PCWP; and Group 4 = normal PVR but raised PCWP. We used spectral Doppler to measure PAcT (corrected for heart rate) and to estimate PASP (peak tricuspid regurgitation pressure drop + estimated right atrial pressure of 7 mmHg). We also tested other available methods for assessing PVR. There were small age differences between patient groups but no age difference between Groups 2 and 4. PAcT and PAcT/PASP were both significantly (P = 0.008) reduced in Groups 2 and 3 compared with Groups 1 and 4. PAcT ≤90 had an 84% sensitivity and an 85% specificity in identifying patients with PVR ≥3 WU with a positive and a negative predictive value of 88% and 81%, respectively. The non-linear relationship between PVR and PAcT gave a quadratic r = 0.61, P < 0.001. ROC curve analysis showed PAcT having the best accuracy (83%) in detecting a PVR ≥3 WU.

    CONCLUSION: PAcT <90 ms can serve as a strong non-invasive predictor of PVR >3 WU, which could differentiate patients with pre- and post-capillary PH.

  • 15.
    Törnqvist, Håkan
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Mills, Nicholas L
    Gonzalez, Manuel
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Miller, Mark R
    Robinson, Simon D
    Megson, Ian L
    Macnee, William
    Donaldson, Ken
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Newby, David E
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Persistent endothelial dysfunction in humans after diesel exhaust inhalation.2007In: American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, E-ISSN 1535-4970, Vol. 176, no 4, p. 395-400Article in journal (Refereed)
1 - 15 of 15
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