| 61. |
- Lindholm, Daniel, et al.
(författare)
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Combined association of key risk factors on ischaemic outcomes and bleeding in patients with myocardial infarction
- 2019
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Ingår i: Heart. - : BMJ PUBLISHING GROUP. - 1355-6037 .- 1468-201X. ; 105:15, s. 1175-1181
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Tidskriftsartikel (refereegranskat)abstract
- Objective: In patients with myocardial infarction (MI), risk factors for bleeding and ischaemic events tend to overlap, but the combined effects of these factors have scarcely been studied in contemporary real-world settings. We aimed to assess the combined associations of established risk factors using nationwide registries.Methods: Using the Swedish Web-system for Enhancement and Development of Evidence-based care in Heart disease Evaluated According to Recommended Therapies registry, patients with invasively managed MI in 2006-2014 were included. Six factors were assessed in relation to cardiovascular death (CVD)/MI/stroke, and major bleeding: age >= 65, chronic kidney disease, diabetes, multivessel disease, prior bleeding and prior MI.Results: We studied 100 879 patients, of whom 20 831 (20.6%) experienced CVD/MI/stroke and 5939 (5.9%) major bleeding, during 3.6 years median follow-up. In adjusted Cox models, all factors were associated with CVD/MI/stroke, and all but prior MI were associated with major bleeding. The majority (53.5%) had >= 2 risk factors. With each added risk factor, there was a marked but gradual increase in incidence of the CVD/MI/stroke. This was seen also for major bleeding, but to a lesser extent, largely driven by prior bleeding as the strongest risk factor.Conclusions: The majority of patients with MI had two or more established risk factors. Increasing number of risk factors was associated with higher rate of ischaemic events. When excluding patients with prior major bleeding, bleeding incidence rate increased only minimally with increasing number of risk factors. The high ischaemic risk in those with multiple risk factors highlights an unmet need for additional preventive measures.
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| 62. |
- Mills, Nicholas L, et al.
(författare)
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Diesel exhaust inhalation does not affect heart rhythm or heart rate variability
- 2011
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Ingår i: Heart. - : BMJ. - 1355-6037 .- 1468-201X. ; 97:7, s. 544-550
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Tidskriftsartikel (refereegranskat)abstract
- 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 h to dilute diesel exhaust (particle concentration 300 μg/m(3)) or filtered air.Main outcome measures Heart rhythm and heart rate variability were monitored during and for 24 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.
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| 63. |
- Minners, Jan, et al.
(författare)
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Adjusting parameters of aortic valve stenosis severity by body size
- 2014
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Ingår i: Heart. - : BMJ. - 1355-6037 .- 1468-201X. ; 100:13, s. 1024-1030
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Tidskriftsartikel (refereegranskat)abstract
- Background Adjustment of cardiac dimensions by measures of body size appears intuitively convincing and in patients with aortic stenosis, aortic valve area (AVA) is commonly adjusted by body surface area (BSA). However, there is little evidence to support such an approach. Objective To identify the adequate measure of body size for the adjustment of aortic stenosis severity. Methods Parameters of aortic stenosis severity (jet velocity, mean pressure gradient (MPG) and AVA) and measures of body size (height, weight, BSA and body mass index (BMI)) were analysed in 2843 consecutive patients with aortic stenosis (jet velocity >= 2.5 m/s) and related to outcomes in a second cohort of 1525 patients from the Simvastatin/Ezetimibe in Aortic Stenosis (SEAS) study. Results Whereas jet velocity and MPG were independent of body size, AVA was significantly correlated with height, weight, BSA and BMI (Pearson correlation coefficient (r) 0.319, 0.281, 0.317 and 0.126, respectively, all p<0.001) to the effect that larger patients presented with larger AVA (less severe stenosis). Of the anthropometric measures used for linear adjustment, BSA was most effective in eliminating the correlation between AVA and body size (r=0.007), rivalled only by allometric (non-linear) models, findings that are confirmed in 1525 prospectively followed patients from the SEAS study. Predictive accuracy for aortic valve events and cardiovascular death during 46 months of follow-up was unchanged by adjusting AVA, regardless of measure of body size (area under the receiver operating curve for AVA 0.72 (CI 0.58 to 0.87) versus, for example, AVA/BSA 0.75 (CI 0.61 to 0.88), p=0.22). Conclusions In the assessment of aortic stenosis, linear adjustment of AVA by BSA improves comparability between patients with diverging body size without, however, increasing the predictive accuracy for clinical events in a population with mild to moderate stenosis.
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| 64. |
- Nestelberger, Thomas, et al.
(författare)
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Diagnosis of acute myocardial infarction in the presence of left bundle branch block
- 2019
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Ingår i: Heart. - : BMJ PUBLISHING GROUP. - 1355-6037 .- 1468-201X. ; 105:20, s. 1559-1567
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Patients with suspected acute myocardial infarction (AMI) in the setting of left bundle branch block (LBBB) present an important diagnostic and therapeutic challenge to the clinician.Methods: We prospectively evaluated the incidence of AMI and diagnostic performance of specific ECG and high-sensitivity cardiac troponin (hs-cTn) criteria in patients presenting with chest discomfort to 26 emergency departments in three international, prospective, diagnostic studies. The final diagnosis of AMI was centrally adjudicated by two independent cardiologists according to the universal definition of myocardial infarction.Results: Among 8830 patients, LBBB was present in 247 (2.8%). AMI was the final diagnosis in 30% of patients with LBBB, with similar incidence in those with known LBBB versus those with presumably new LBBB (29% vs 35%, p=0.42). ECG criteria had low sensitivity (1%-12%) but high specificity (95%-100%) for AMI. The diagnostic accuracy as quantified by the receiver operating characteristics (ROC) curve of hs-cTnT and hs-cTnI concentrations at presentation (area under the ROC curve (AUC) 0.91, 95%CI 0.85 to 0.96 and AUC 0.89, 95%CI 0.83 to 0.95), as well as that of their 0/1-hour and 0/2-hour changes, was very high. A diagnostic algorithm combining ECG criteria with hs-cTnT/I concentrations and their absolute changes at 1hour or 2hours derived in cohort 1 (45 of 45(100%) patients with AMI correctly identified) showed high efficacy and accuracy when externally validated in cohorts 2 and 3 (28 of 29 patients, 97%).Conclusion: Most patients presenting with suspected AMI and LBBB will be found to have diagnoses other than AMI. Combining ECG criteria with hs-cTnT/I testing at 0/1 hour or 0/2hours allows early and accurate diagnosis of AMI in LBBB.
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| 65. |
- Nielsen, Jens Cosedis, et al.
(författare)
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Long-term efficacy of catheter ablation as first-line therapy for paroxysmal atrial fibrillation : 5-year outcome in a randomised clinical trial.
- 2017
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Ingår i: Heart. - : BMJ Publishing Group Ltd. - 1355-6037 .- 1468-201X. ; 103:5, s. 368-376
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: The Medical ANtiarrhythmic Treatment or Radiofrequency Ablation in Paroxysmal Atrial Fibrillation (MANTRA-PAF) trial compared radiofrequency catheter ablation (RFA) with antiarrhythmic drug therapy (AAD) as first-line treatment for paroxysmal atrial fibrillation (AF). Endpoint of ablation was elimination of electrical activity inside pulmonary veins. We present the results of the 5-year follow-up.METHODS: This pre-specified 5-year follow-up included assessment of any AF and symptomatic AF burden by one 7-day Holter recording and quality of life (QoL) assessment, using SF-36 questionnaire physical and mental component scores. Analysis was intention-to-treat. Imputation was used to compensate for missing Holter data.RESULTS: 245 of 294 patients (83%) randomised to RFA (n=125) or AAD (n=120) attended the 5-year follow-up, 227 with Holter recording. Use of class I or III AAD was more frequent in AAD group (N=61 vs 13, p<0.001). More patients in the RFA group were free from AF (126/146 (86%) vs 105/148 (71%), p=0.001, relative risk (RR) 0.82; 95% CI 0.73 to 0.93) and symptomatic AF (137/146 (94%) vs 126/148 (85%), p=0.015, χ(2) test, RR 0.91; 95% CI 0.84 to 0.98) in 7-day Holter recording. AF burden was significantly lower in the RFA group (any AF: p=0.003; symptomatic AF: p=0.02). QoL scores did not differ between randomisation groups. QoL scores remained improved from baseline (both components p<0.001), and did not differ from 2-year scores.CONCLUSIONS: At 5 years, the occurrence and burden of any AF and symptomatic AF were significantly lower in the RFA group than in the AAD group. Improved QoL scores observed after 2 years persisted after 5 years without between-group differences.TRIAL REGISTRATION NUMBER: NCT00133211; Results.
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| 66. |
- Nilsson, Lennart, et al.
(författare)
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Early measurements of plasma matrix metalloproteinase-2 predict infarct size and ventricular dysfunction in ST-elevation myocardial infarction
- 2012
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Ingår i: Heart. - : BMJ Publishing Group. - 1355-6037 .- 1468-201X. ; 98:1, s. 31-36
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Tidskriftsartikel (refereegranskat)abstract
- Background Immediate reopening of the acutely occluded infarct-related artery via primary PCI is the preferred treatment in ST-elevation myocardial infarction (STEMI). However, the sudden reinitiation of blood flow can lead to a local acute inflammatory response with further endothelial and myocardial damage, so-called reperfusion injury. The activation of matrix metalloproteinases (MMPs) is suggested to be a key event in this process. Objectives To investigate circulating MMPs, tissue inhibitors of metalloproteinases (TIMPs) and myeloperoxidase (MPO) in relation to infarct size, left ventricular dysfunction and remodelling in a STEMI population undergoing PCI. Methods 58 Patients with STEMI undergoing primary PCI were included. Blood samples were collected at baseline before PCI and at 12, 24 and 48 h for later analysis of MMPs, TIMPs and MPO by ELISA. Infarct size, left ventricular (LV) dysfunction and remodelling were assessed by cardiac MRI at 5 days and 4 month after STEMI. Results Plasma MMP-2 at 0 and 12 h showed a consistent and significant correlation with infarct size and LV dysfunction measured both at 5 days and at 4 months and correlated well with troponin I measurements. For TIMP-1 and TIMP-2 some support was found for associations with infarct size and LV dysfunction, but these were not as consistent as for MMP-2. MMP-8, MMP-9 and MPO did not overall correlate with measures of infarct size, LV dysfunction or remodelling. Conclusions In patients with STEMI, circulating levels of MMP-2, measured early and even before reperfusion therapy, are strongly associated with infarct size and LV dysfunction. This provides further evidence for the role of MMP-2 in ischaemia-reperfusion injury.
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| 67. |
- Oldgren, Jonas, et al.
(författare)
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Fibrinolytic therapy and bleeding complications: risk predictors from RIKS-HIA
- 2010
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Ingår i: HEART. - : BMJ Publishing Group; 1999. - 1355-6037 .- 1468-201X. ; 96:18, s. 1451-1457
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Tidskriftsartikel (refereegranskat)abstract
- Background Fibrinolytic treatment for ST-elevation myocardial infarction is associated with increased bleeding risk but is still widely used world wide, mainly because of limited access to primary PCI. Objective To analyse contemporary fibrinolytic treatment patterns, in-hospital bleeding risk and prognosis during 2001 to 2006 in unselected Swedish patients. Methods and results The RIKS-HIA registry covers almost all Swedish patients treated for acute coronary syndromes. Major in-hospital bleeding was defined as lethal or intracranial bleeding or bleeding requiring surgery or blood transfusion. Survival status of the 15 373 patients was obtained from the National Cause of Death Register. The number of patients receiving fibrinolysis as reperfusion therapy decreased from 4336 patients in 2001 to 733 in 2006. Cases of major in-hospital bleeding increased from 1.2% (including 0.7% lethal or intracranial) in 2001 to 4.0% (1.1%) in 2006, pandlt;0.001. Higher age, female gender, hypertension, kidney failure, clopidogrel treatment before admission, pre-hospital administration of fibrinolysis and fibrin-specific fibrinolytic agents were identified as predictors for bleeding. Major in-hospital bleeding was the strongest predictor of adverse prognosis with a more than threefold increase in 1-year mortality. Conclusion During 2001 to 2006 the use of fibrinolytic treatment markedly decreased while the incidence of major bleeding complications more than doubled. The latter might in part be explained by increasing use concomitant antiplatelet therapy, pre-hospital treatment and fibrin-specific fibrinolytic agents. Future close monitoring of bleeding complications is warranted, especially when considering the increased use of various combinations of antithrombotic drugs in conjunction with fibrinolysis and the great impact of bleeding on long-term mortality.
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| 68. |
- Olsson, Christian, et al.
(författare)
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Family history, comorbidity and risk of thoracic aortic disease : a population-based case-control study
- 2013
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Ingår i: Heart. - : BMJ. - 1355-6037 .- 1468-201X. ; 99:14, s. 1030-1033
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE:To examine the risk of thoracic aortic disease (TAD) when one or more first-degree relatives are affected, and to relate the risk of family history to the risk of other cardiopulmonary comorbidity.DESIGN:Population-based, matched, case-control study.SETTING:Registry-based investigation. PATIENTS: All cases, nationwide, of TAD diagnosed 2001-2005 in individuals born 1932 or later (n=2436) were identified, and a random control-group (n=12 152) matched for age, sex and geography was generated. First-degree relatives were identified in the Multigeneration Registry. Family history of TAD was assessed by cross-linking nationwide health registries.INTERVENTIONS:None.RESULTS:Family history was present in 108 cases (4.4%), compared with 93 (0.77%) controls (p<0.0001). The risk of TAD increased with number of affected relatives: OR 5.8 (95% CI 4.3 to 7.7) vs OR 20 (2.2 to 179) with one versus two or more affected relatives. The relative risk of TAD was highest in the youngest (≤49 years) age group and slightly more pronounced in women than in men (OR 7.2 (4.2 to 12) vs OR 5.5 (3.9 to 7.7)). Among cardiopulmonary comorbidities, heart failure conferred the highest relative risk, OR 6.3 (4.1 to 9.8).CONCLUSIONS:Family history confers a significantly increased (sixfold to 20-fold) relative risk of TAD. The effect is more pronounced in women and in younger subjects, and is not conveyed by cardiopulmonary comorbidity. Knowledge of family history is important to counselling, treatment indications, surveillance and screening protocols.
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| 69. |
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