| 1. |
- Axelsson, Jimmy, et al.
(författare)
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Ejection fraction in left bundle branch block is disproportionately reduced in relation to amount of myocardial scar
- 2018
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Ingår i: Journal of Electrocardiology. - : Elsevier BV. - 0022-0736 .- 1532-8430. ; 51:6, s. 1071-1076
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: The relationship between left ventricular (LV) ejection fraction (EF) and LV myocardial scar can identify potentially reversible causes of LV dysfunction. Left bundle branch block (LBBB) alters the electrical and mechanical activation of the LV. We hypothesized that the relationship between LVEF and scar extent is different in LBBB compared to controls. Methods: We compared the relationship between LVEF and scar burden between patients with LBBB and scar (n = 83), and patients with chronic ischemic heart disease and scar but no electrocardiographic conduction abnormality (controls, n = 90), who had undergone cardiovascular magnetic resonance (CMR) imaging at one of three centers. LVEF (%) was measured in CMR cine images. Scar burden was quantified by CMR late gadolinium enhancement (LGE) and expressed as % of LV mass (%LVM). Maximum possible LVEF (LVEFmax) was defined as the function describing the hypotenuse in the LVEF versus myocardial scar extent scatter plot. Dysfunction index was defined as LVEFmax derived from the control cohort minus the measured LVEF. Results: Compared to controls with scar, LBBB with scar had a lower LVEF (median [interquartile range] 27 [19–38] vs 36 [25–50] %, p < 0.001), smaller scar (4 [1–9] vs 11 [6–20] %LVM, p < 0.001), and greater dysfunction index (39 [30–52] vs 21 [12–35] % points, p < 0.001). Conclusions: Among LBBB patients referred for CMR, LVEF is disproportionately reduced in relation to the amount of scar. Dyssynchrony in LBBB may thus impair compensation for loss of contractile myocardium.
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| 2. |
- Berg, Jonathan, et al.
(författare)
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Mild hypothermia attenuates ischemia/reperfusion injury - insights from serial non-invasive pressure-volume loops
- 2023
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Ingår i: Cardiovascular Research. - : Oxford University Press (OUP). - 1755-3245 .- 0008-6363. ; 119:12, s. 2230-2243
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Mild hypothermia, 32-35°C, reduces infarct size in experimental studies, potentially mediating reperfusion injuries, but human trials have been ambiguous. To elucidate the cardioprotective mechanisms of mild hypothermia, we analyzed cardiac performance in a porcine model of ischemia/reperfusion, with serial cardiovascular magnetic resonance (CMR) imaging throughout one week using non-invasive pressure-volume loops.METHODS AND RESULTS: Normothermia and Hypothermia groups sessions (n=7+7 pigs, nonrandom allocation) were imaged with CMR at baseline and subjected to 40 minutes of normothermic ischemia by catheter intervention. Thereafter, the Hypothermia group was rapidly cooled (mean 34.5°C) for 5 minutes before reperfusion. Additional CMR sessions at two hours, 24 hours, and seven days acquired ventricular volumes and ischemic injuries (unblinded analysis).Stroke volume (-24%; p=0.029; Friedmans test) and ejection fraction (-20%; p=0.068) were notably reduced at 24h in the Normothermia group compared to baseline. In contrast, the decreases were ameliorated in the Hypothermia group (stroke volume: -6%; p=0.77; ejection fraction: -6%; p=0.13). Mean arterial pressure remained stable in Normothermic animals (-3%, p=0.77) but dropped two hours post-reperfusion in hypothermic animals (-18%, p=0.007). Both groups experienced a decrease and partial recovery pattern for PV loop-derived variables over one week, but the adverse effects tended attenuated in the Hypothermia group. Infarct sizes were 10±8% in Hypothermic and 15±8% in Normothermic animals (p=0.32). Analysis of covariance at 24 hours indicated that hypothermia has cardioprotective properties incremental to reducing infarct size, such as higher external power (p=0.061) and lower arterial elastance (p=0.015).CONCLUSION: Using non-invasive pressure-volume loops by CMR, we observed that mild hypothermia at reperfusion alleviates the heart's work after ischemia/reperfusion injuries during the first week and preserves short-term cardiac performance. This hypothesis-generating study suggests hypothermia to have cardioprotective properties, incremental to reducing infarct size. The primary cardioprotective mechanism was likely an afterload reduction acutely unloading the left ventricle.
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| 3. |
- Berg, Jonathan, et al.
(författare)
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Ventricular longitudinal function by cardiovascular magnetic resonance predicts cardiovascular morbidity in HFrEF patients
- 2022
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Ingår i: ESC Heart Failure. - : Wiley. - 2055-5822. ; 9:4, s. 2313-2324
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Tidskriftsartikel (refereegranskat)abstract
- Aims: Ventricular longitudinal function measured as basal-apical atrioventricular plane displacement (AVPD) or global longitudinal strain (GLS) is a potent predictor of mortality and could potentially be a predictor of heart failure-associated morbidity. We hypothesized that low AVPD and GLS are associated with the combined endpoint of cardiovascular mortality and heart failure-associated morbidity. Methods and results: Two hundred eighty-seven patients (age 62 ± 12 years, 78% male) with heart failure with reduced (≤40%) ejection fraction (HFrEF) referred to a cardiovascular magnetic resonance exam were included. Ventricular longitudinal function, ventricular volume, and myocardial fibrosis or infarction were analysed from cine and late gadolinium enhancement images. National registries provided data on causes of cardiovascular hospitalizations and cardiovascular mortality for the combined endpoint. Time-to-event analysis capable of including reoccurring events was employed with a 5-year follow-up. HFrEF patients had EF 26.5 ± 8.0%, AVPD 7.8 ± 2.4 mm, and GLS −7.5 ± 3.0%. In contrast, ventricular longitudinal function was approximately twice as large in an age-matched control group (AVPD 15.3 ± 1.6 mm; GLS −20.6 ± 2.0%; P < 0.001 for both). There were 578 events in total, and the majority were HF hospitalizations (n = 418). Other major events were revascularizations (n = 64), cardiovascular deaths (n = 40), and myocardial infarctions (n = 21). One hundred fifty-five (54%) patients experienced at least one event (mean 2.0, range 0–64). Of these patients, 119 (71%) had three events or fewer, and the first three events comprised 51% of all events (295 events). Patients in the bottom AVPD or GLS tertile (<6.8 mm or >−6.1%) overall experienced more than 3 times as many events as the top tertile (>8.8 mm or <−8.4%; P < 0.001). Patients in this tertile also faced more cardiovascular deaths (P < 0.05), HF hospitalizations (P = 0.001), myocardial infarctions (only GLS: P = 0.032), and accumulated longer in-hospital length-of-stay overall (AVPD 20.9 vs. 9.1 days; GLS 22.4 vs. 6.5 days; P = 0.001 for both), and from HF hospitalizations (AVPD 19.3 vs. 8.3 days; GLS 19.3 vs. 5.4 days; P = 0.001 for both). In multivariate analysis adjusted for significant covariates, AVPD and GLS remained independent predictors of events (hazard ratio 1.12 per-mm-decrease and 1.13 per-%-increase) alongside hyponatremia (<135 mmol/L), aetiology of HF, and LV end-diastolic volume index. Conclusions: Low ventricular longitudinal function is associated with an increase in number of events as well as longer in-hospital stay from cardiovascular causes. In addition, AVPD and GLS have independent prognostic value for cardiovascular mortality and morbidity in HFrEF patients.
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| 4. |
- Carlsson, Marcus, et al.
(författare)
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Coronary microembolization causes long-term detrimental effects on regional left ventricular function.
- 2011
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Ingår i: Scandinavian cardiovascular journal : SCJ. - : Informa UK Limited. - 1651-2006 .- 1401-7431. ; 45, s. 205-214
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Tidskriftsartikel (refereegranskat)abstract
- Abstract Objectives. To investigate whether coronary microemboli have long-term effects on left ventricular (LV) function in an experimental model. Furthermore, to determine if first-pass perfusion and late gadolinium enhancement (LGE) patterns differs between small- and large-sized microemboli. Design. Six pigs underwent left anterior descending (LAD)-coronary microembolization with small-sized (40-120 μm, n∼250 000) microemboli using a combined x-ray and MRI-system. MR-images before, one hour after and 7-8 weeks after microembolization were obtained. Results were compared to MRI obtained by large-sized (100-300 μm, n∼7200) microemboli. Results. Cine MRI showed an acute drop in ejection fraction (from 49.5 ± 2.6% to 32.5 ± 2.8) that substantially recovered at 7-8 weeks (47.5 ± 3.2%). Regional LV-function assessed as circumferential, longitudinal and radial strain declined in both microinfarcts and remote regions followed by partial recovery at 7-8 weeks. The decline in LV function and the severe perfusion deficit from the small microemboli was similar to the large microemboli at one hour. There was a significant recovery in perfusion at 7-8 weeks in the microinfarcts. LGE demonstrated the microinfarcts at 7-8 weeks but not at one hour and the microinfarcts were confirmed by histopathology. Conclusion. Microembolization causes long-term, regional LV dysfunction and this study confirmed the need of a comprehensive MRI-protocol for the detection of microinfarcts. These findings suggest that even small microemboli (40-120 μm in diameter), which may escape the distal protective devices influence cardiac function.
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| 5. |
- Chaudhry, Uzma, et al.
(författare)
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Evaluation of the ECG based Selvester scoring method to estimate myocardial scar burden and predict clinical outcome in patients with left bundle branch block, with comparison to late gadolinium enhancement CMR imaging
- 2017
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Ingår i: Annals of Noninvasive Electrocardiology. - : Wiley. - 1082-720X. ; 22:5
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Tidskriftsartikel (refereegranskat)abstract
- Background: Myocardial scar burden quantification is an emerging clinical parameter for risk stratification of sudden cardiac death and prediction of ventricular arrhythmias in patients with left ventricular dysfunction. We investigated the relationships among semiautomated Selvester score burden and late gadolinium enhancement-cardiovascular magnetic resonance (LGE-CMR) assessed scar burden and clinical outcome in patients with underlying heart failure, left bundle branch block (LBBB) and implantable cardioverter-defibrillator (ICD) treatment. Methods: Selvester QRS scoring was performed on all subjects with ischemic and nonischemic dilated cardiomyopathy at Skåne University Hospital Lund (2002-2013) who had undergone LGE-CMR and 12-lead ECG with strict LBBB pre-ICD implantation. Results: Sixty patients were included; 57% nonischemic dilated cardiomyopathy and 43% ischemic cardiomyopathy with mean left ventricular ejection fraction of 27.6% ± 11.7. All patients had scar by Selvester scoring. Sixty-two percent had scar by LGE-CMR (n = 37). The Spearman correlation coefficient for LGE-CMR and Selvester score derived scar was r = .35 (p = .007). In scar negative LGE-CMR, there was evidence of scar by Selvester scoring in all patients (range 3%-33%, median 15%). Fourteen patients (23%) had an event during the follow-up period; 11 (18%) deaths and six adequate therapies (10%). There was a moderate trend indicating that presence of scar increased the risk of clinical endpoints in the LGE-CMR analysis (p = .045). Conclusion: There is a modest correlation between LGE-CMR and Selvester scoring verified myocardial scar. CMR based scar burden is correlated to clinical outcome, but Selvester scoring is not. The Selvester scoring algorithm needs to be further refined in order to be clinically relevant and reliable for detailed scar evaluation in patients with LBBB.
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| 6. |
- Engblom, Henrik, et al.
(författare)
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A new automatic algorithm for quantification of myocardial infarction imaged by late gadolinium enhancement cardiovascular magnetic resonance : Experimental validation and comparison to expert delineations in multi-center, multi-vendor patient data
- 2016
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Ingår i: Journal of Cardiovascular Magnetic Resonance. - : Springer Science and Business Media LLC. - 1097-6647 .- 1532-429X. ; 18:1
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Tidskriftsartikel (refereegranskat)abstract
- Background: Late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR) using magnitude inversion recovery (IR) or phase sensitive inversion recovery (PSIR) has become clinical standard for assessment of myocardial infarction (MI). However, there is no clinical standard for quantification of MI even though multiple methods have been proposed. Simple thresholds have yielded varying results and advanced algorithms have only been validated in single center studies. Therefore, the aim of this study was to develop an automatic algorithm for MI quantification in IR and PSIR LGE images and to validate the new algorithm experimentally and compare it to expert delineations in multi-center, multi-vendor patient data. Methods: The new automatic algorithm, EWA (Expectation Maximization, weighted intensity, a priori information), was implemented using an intensity threshold by Expectation Maximization (EM) and a weighted summation to account for partial volume effects. The EWA algorithm was validated in-vivo against triphenyltetrazolium-chloride (TTC) staining (n = 7 pigs with paired IR and PSIR images) and against ex-vivo high resolution T1-weighted images (n = 23 IR and n = 13 PSIR images). The EWA algorithm was also compared to expert delineation in 124 patients from multi-center, multi-vendor clinical trials 2-6 days following first time ST-elevation myocardial infarction (STEMI) treated with percutaneous coronary intervention (PCI) (n = 124 IR and n = 49 PSIR images). Results: Infarct size by the EWA algorithm in vivo in pigs showed a bias to ex-vivo TTC of -1 ± 4%LVM (R = 0.84) in IR and -2 ± 3%LVM (R = 0.92) in PSIR images and a bias to ex-vivo T1-weighted images of 0 ± 4%LVM (R = 0.94) in IR and 0 ± 5%LVM (R = 0.79) in PSIR images. In multi-center patient studies, infarct size by the EWA algorithm showed a bias to expert delineation of -2 ± 6 %LVM (R = 0.81) in IR images (n = 124) and 0 ± 5%LVM (R = 0.89) in PSIR images (n = 49). Conclusions: The EWA algorithm was validated experimentally and in patient data with a low bias in both IR and PSIR LGE images. Thus, the use of EM and a weighted intensity as in the EWA algorithm, may serve as a clinical standard for the quantification of myocardial infarction in LGE CMR images. Clinical trial registration: CHILL-MI: NCT01379261. MITOCARE: NCT01374321.
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| 7. |
- Engblom, Henrik, et al.
(författare)
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Importance of standardizing timing of hematocrit measurement when using cardiovascular magnetic resonance to calculate myocardial extracellular volume (ECV) based on pre- and post-contrast T1 mapping
- 2018
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Ingår i: Journal of Cardiovascular Magnetic Resonance. - : Springer Science and Business Media LLC. - 1097-6647 .- 1532-429X. ; 20:1
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Tidskriftsartikel (refereegranskat)abstract
- Background: Cardiovascular magnetic resonance (CMR) can be used to calculate myocardial extracellular volume fraction (ECV) by relating the longitudinal relaxation rate in blood and myocardium before and after contrast-injection to hematocrit (Hct) in blood. Hematocrit is known to vary with body posture, which could affect the calculations of ECV. The aim of this study was to test the hypothesis that there is a significant increase in calculated ECV values if the Hct is sampled after the CMR examination in supine position compared to when the patient arrives at the MR department. Methods: Forty-three consecutive patients including various pathologies as well as normal findings were included in the study. Venous blood samples were drawn upon arrival to the MR department and directly after the examination with the patient remaining in supine position. A Modified Look-Locker Inversion recovery (MOLLI) protocol was used to acquire mid-ventricular short-axis images before and after contrast injection from which motion-corrected T1 maps were derived and ECV was calculated. Results: Hematocrit decreased from 44.0 ± 3.7% before to 40.6 ± 4.0% after the CMR examination (p < 0.001). This resulted in a change in calculated ECV from 24.7 ± 3.8% before to 26.2 ± 4.2% after the CMR examination (p < 0.001). All patients decreased in Hct after the CMR examination compared to before except for two patients whose Hct remained the same. Conclusion: Variability in CMR-derived myocardial ECV can be reduced by standardizing the timing of Hct measurement relative to the CMR examination. Thus, a standardized acquisition of blood sample for Hct after the CMR examination, when the patient is still in supine position, would increase the precision of ECV measurements.
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| 8. |
- Fernlund, Eva I., et al.
(författare)
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Serum biomarkers of early stages of hypertrophic cardiomyopathy in a young population
- 2015
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Ingår i: Journal of the American College of Cardiology. - 0735-1097. ; 65:10S, s. 787-787
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Konferensbidrag (refereegranskat)abstract
- Background: Hypertrophic cardiomyopathy (HCM) is the most common monogenic cardiac disorder and the leading cause of sudden cardiac death in the young. Although in a majority of HCM cases there are gene mutations coding for sarcomere proteins, the onset for the clinical consequences of these mutations are difficult to predict, as these mutations do not show any clear relationship to the degree of myocardial hypertrophy. Hence identification of early markers for this disease is important. The aim of this study was to investigate novel serum biomarkers reflecting myocardial remodeling, microfibrosis and coronary endotheliopathy in young presymtomatic HCM patients and in individuals at risk for developing HCM. Methods: Eighty-nine participants (18 HCM patients, 14 HCM-risk individuals, and 57 healthy controls) with median age of 15 (range 0-30) years underwent assessment with echocardiography and serum analysis for myostatin, cathepsin S, endostatin, type I collagen degradation marker (ICTP), matrix metalloproteinase (MMP) 9, vascular (VCAM) and intercellular adhesion molecules (ICAM). In some individuals, myocardial perfusion was measured both at rest and after adenosine via magnetic resonance. Results: Both cathepsin S and endostatin were increased in the HCM group (p0.3) and diastolic function, expressed as E/e' (p0.3). In the HCM-risk group, myostatin was decreased (p0.1). Conclusion: To the best of our knowledge, this is the first study to suggest early onset changes in biomarkers of myoblast regulation, endothelial function and matrix remodeling in young presymptomatic HCM patients and in HCM-risk individuals.
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| 9. |
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| 10. |
- Jablonowski, Robert
(författare)
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Assessment of myocardial viability using magnetic resonance imaging
- 2015
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Myocardial infarction (MI) following an acute coronary occlusion is a leading cause of morbidity and mortality. During revascularization, microemboli may complicate treatment and affect cardiac function. The long-term effects of microembolization are not fully elucidated. Following an MI it is important to accurately determine the size of the infarction, as it can be used for guidance in terms of prognosis. However, in the acute setting after an MI the infarct size may be overestimated due to the inclusion of a possible reversibly injured area around the infarction, the peri-infarction zone. In chronic MI and in non-ischemic cardiomyopathies, heterogeneous fibrotic areas have been proposed as substrate for arrhythmias which may cause sudden cardiac death (SCD). Quantification of these areas may provide better risk stratification than current guidelines. In young people and athletes the most common cause for SCD is hypertrophic cardiomyopathy (HCM), possibly due to areas of fibrosis causing fatal arrhythmias. However, the pathophysiological mechanism behind the development of fibrosis in HCM is still unclear. Magnetic resonance imaging (MRI) can be used to assess function, perfusion and viability using late gadolinium enhancement (LGE). Therefore, this thesis investigates how MRI can be used for diagnosis, prognosis and for understanding the pathophysiological mechanisms behind ischemic and non-ischemic cardiomyopathy. Study I showed that coronary microembolization causes long-term, regional left ventricular dysfunction and that even small microemboli, which may escape the distal protective devices, influence cardiac function. Study II demonstrated that infarct quantification with a 2D-PSIR and a 3D-IR sequence shows good agreement in patients, which allows for the sequences to be used interchangeably. Both these LGE-sequences optimized for in vivo-use yield an overestimation of infarct size ex vivo. Study III is an experimental study which showed that contrast-enhanced MRI overestimates myocardial infarct size compared to histopathology in the acute phase but not at seven days. This is associated with a significantly higher extracellular volume in the peri-infarction zone acutely compared to seven days later, possibly due to edema. Study IV showed that young patients with HCM had decreased perfusion in areas with hypertrophy and even lower perfusion in LGE positive, fibrotic myocardium. The stress-induced hypoperfused regions exceed regions with fibrosis indicating that hypoperfusion precede fibrosis and may be a more sensitive marker of diseased myocardium. Finally, Study V demonstrated that a heterogeneous LGE borderzone, quantified by two different algorithms, predicts appropriate ICD-therapy to a larger extent than ejection fraction, total, and core LGE size.
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