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Sökning: WFRF:(Heiberg Einar)

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1.
  • Allencherril, Joseph, et al. (författare)
  • Appropriateness of anteroseptal myocardial infarction nomenclature evaluated by late gadolinium enhancement cardiovascular magnetic resonance imaging
  • 2018
  • Ingår i: Journal of Electrocardiology. - : Elsevier BV. - 0022-0736. ; 51:2, s. 218-223
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: In traditional literature, it appears that "anteroseptal" MIs with Q waves in V1-V3 involve basal anteroseptal segments although studies have questioned this belief. Methods: We studied patients with first acute anterior Q-wave (>. 30. ms) MI. All underwent late gadolinium enhancement (LGE) cardiac magnetic resonance imaging (MRI). Results: Those with Q waves in V1-V2 (n = 7) evidenced LGE >. 50% in 0%, 43%, 43%, 57%, and 29% of the basal anteroseptal, mid anteroseptal, apical anterior, apical septal segments, and apex, respectively. Patients with Q waves in V1-V3 (n = 14), evidenced involvement was 14%, 43%, 43%, 50%, and 7% of the same respective segments. In those with extensive anterior Q waves (n = 7), involvement was 0%, 71%, 57%, 86%, and 86%. Conclusions: Q-wave MI in V1-V2/V3 primarily involves mid- and apical anterior and anteroseptal segments rather than basal segments. Data do not support existence of isolated basal anteroseptal or septal infarction. "Anteroapical infarction" is a more appropriate term than "anteroseptal infarction.".
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2.
  • Allencherril, Joseph, et al. (författare)
  • Correlation of anteroseptal ST elevation with myocardial infarction territories through cardiovascular magnetic resonance imaging
  • 2018
  • Ingår i: Journal of Electrocardiology. - : Elsevier BV. - 0022-0736. ; 51:4, s. 563-568
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Anteroseptal ST elevation myocardial infarction (STEMI) is traditionally defined on the electrocardiogram (ECG) by ST elevation (STE) in leads V1-V3, with or without involvement of lead V4. It is commonly taught that such infarcts affect the basal anteroseptal myocardial segment. While there are suggestions in the literature that Q waves limited to V1-V4 represent predominantly apical infarction, none have evaluated anteroseptal ST elevation territories. We compared the distribution of the myocardium at risk (MaR) in STEMI patients presenting with STE limited to V1-V4 and those with more extensive STE (V1-V6). Methods: We identified patients in the MITOCARE study presenting with a first acute STEMI and new STE in at least two contiguous anterior leads from V1 to V6. Patients underwent cardiac magnetic resonance (CMR) imaging three to five days after acute infarction. Results: Thirty-two patients met inclusion criteria. In patients with STE in V1-V4 (n = 20), myocardium at risk (MaR) > 50% was seen in 0%, 85%, 75%, 100%, and 90% in the basal anteroseptal, mid anteroseptal, apical anterior, apical septal segments, and apex, respectively. The group with STE in V1-V6 (n = 12), MaR > 50% was seen in 8%, 83%, 83%, 92%, and 83% of the same segments. Conclusions: Patients with acute STEMI and STE in leads V1-V4, exhibit MaR in predominantly apical territories and rarely in the basal anteroseptum. We found no evidence to support existence of isolated basal anteroseptal or septal STEMI. “Anteroapical” infarction is a more precise description than “anteroseptal” infarction for acute STEMI patients exhibiting STE in V1-V4.
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3.
  • Arvidsson, Per M., et al. (författare)
  • Hemodynamic forces using four-dimensional flow MRI : An independent biomarker of cardiac function in heart failure with left ventricular dyssynchrony?
  • 2018
  • Ingår i: American Journal of Physiology - Heart and Circulatory Physiology. - : American Physiological Society. - 0363-6135 .- 1522-1539. ; 315:6, s. 1627-1639
  • Tidskriftsartikel (refereegranskat)abstract
    • Patients with heart failure with left ventricular (LV) dyssynchrony often do not respond to cardiac resynchronization therapy (CRT), indicating that the pathophysiology is insufficiently understood. Intracardiac hemodynamic forces computed from four-dimensional (4-D) flow MRI have been proposed as a new measure of cardiac function. We therefore aimed to investigate how hemodynamic forces are altered in LV dyssynchrony. Thirty-one patients with heart failure and LV dyssynchrony and 39 control subjects underwent cardiac MRI with the acquisition of 4-D flow. Hemodynamic forces were computed using Navier-Stokes equations and integrated over the manually delineated LV volume. The ratio between transverse (lateral-septal and inferior-anterior) and longitudinal (apical-basal) forces was calculated for systole and diastole separately and compared with QRS duration, aortic valve opening delay, global longitudinal strain, and ejection fraction (EF). Patients exhibited hemodynamic force patterns that were significantly altered compared with control subjects, including loss of longitudinal forces in diastole (force ratio, control subjects vs. patients: 0.32 vs. 0.90, P < 0.0001) and increased transverse force magnitudes. The systolic force ratio was correlated with global longitudinal strain and EF (P < 0.01). The diastolic force ratio separated patients from control subjects (area under the curve: 0.98, P < 0.0001) but was not correlated to other dyssynchrony measures (P > 0.05 for all). Hemodynamic forces by 4-D flow represent a new approach to the quantification of LV dyssynchrony. Diastolic force patterns separate healthy from diseased ventricles. Different force patterns in patients indicate the possible use of force analysis for risk stratification and CRT implantation guidance. NEW & NOTEWORTHY In this report, we demonstrate that patients with heart failure with left ventricular dyssynchrony exhibit significantly altered hemodynamic forces compared with normal. Force patterns in patients mechanistically reflect left ventricular dysfunction on the organ level, largely independent of traditional dyssynchrony measures. Force analysis may help clinical decision making and could potentially be used to improve therapy outcomes.
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4.
  • Arvidsson, Per Martin, et al. (författare)
  • Kinetic energy of left ventricular blood flow across heart failure phenotypes and in subclinical diastolic dysfunction
  • 2022
  • Ingår i: Journal of Applied Physiology. - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 133:3, s. 697-709
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Kinetic energy (KE) of intracardiac blood flow reflects myocardial work spent on accelerating blood and provides a mechanistic window into diastolic filling dynamics. Diastolic dysfunction may represent an early stage in the development of heart failure (HF). Here we evaluated the hemodynamic effects of impaired diastolic function in subjects with and without HF, testing the hypothesis that left ventricular KE differs between controls, subjects with subclinical diastolic dysfunction (SDD), and HF patients.METHODS: We studied 77 subjects (16 controls, 20 subjects with SDD, 16 HFpEF, 9 HFmrEF, and 16 HFrEF patients, age- and sex-matched at the group level). Cardiac magnetic resonance at 1.5T included intracardiac 4D flow and cine imaging. Left ventricular KE was calculated as 0.5*m*v 2. RESULTS: Systolic KE was similar between groups (p>0.4), also after indexing to stroke volume (p=0.25), and was primarily driven by ventricular emptying rate (p<0.0001, R 2=0.52). Diastolic KE was higher in heart failure patients than controls (p<0.05) but similar between SDD and HFpEF (p>0.18), correlating with inflow conditions (E-wave velocity, p<0.0001, R 2=0.24) and end-diastolic volume (p=0.0003, R 2=0.17) but not with average e' (p=0.07). CONCLUSIONS: Diastolic KE differs between controls and heart failure, suggesting more work is spent filling the failing ventricle, while systolic KE does not differentiate between well-matched groups with normal ejection fraction even in the presence of relaxation abnormalities and heart failure. Mechanistically, KE reflects the acceleration imparted on the blood and is driven by variations in ventricular emptying and filling rates, volumes, and heart rate, regardless of underlying pathology.
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5.
  • Arvidsson, Per Martin, et al. (författare)
  • Kinetic energy of left ventricular blood flow across heart failure phenotypes and in subclinical diastolic dysfunction.
  • 2022
  • Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 1522-1601.
  • Tidskriftsartikel (refereegranskat)abstract
    • Kinetic energy (KE) of intracardiac blood flow reflects myocardial work spent on accelerating blood and provides a mechanistic window into diastolic filling dynamics. Diastolic dysfunction may represent an early stage in the development of heart failure (HF). Here we evaluated the hemodynamic effects of impaired diastolic function in subjects with and without HF, testing the hypothesis that left ventricular KE differs between controls, subjects with subclinical diastolic dysfunction (SDD), and HF patients.We studied 77 subjects (16 controls, 20 subjects with SDD, 16 HFpEF, 9 HFmrEF, and 16 HFrEF patients, age- and sex-matched at the group level). Cardiac magnetic resonance at 1.5T included intracardiac 4D flow and cine imaging. Left ventricular KE was calculated as 0.5*m*v2.Systolic KE was similar between groups (p>0.4), also after indexing to stroke volume (p=0.25), and was primarily driven by ventricular emptying rate (p<0.0001, R2=0.52). Diastolic KE was higher in heart failure patients than controls (p<0.05) but similar between SDD and HFpEF (p>0.18), correlating with inflow conditions (E-wave velocity, p<0.0001, R2=0.24) and end-diastolic volume (p=0.0003, R2=0.17) but not with average e' (p=0.07).Diastolic KE differs between controls and heart failure, suggesting more work is spent filling the failing ventricle, while systolic KE does not differentiate between well-matched groups with normal ejection fraction even in the presence of relaxation abnormalities and heart failure. Mechanistically, KE reflects the acceleration imparted on the blood and is driven by variations in ventricular emptying and filling rates, volumes, and heart rate, regardless of underlying pathology.
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6.
  • Arvidsson, Per M., et al. (författare)
  • Left and right ventricular hemodynamic forces in healthy volunteers and elite athletes assessed with 4D flow magnetic resonance imaging
  • 2017
  • Ingår i: American Journal of Physiology - Heart and Circulatory Physiology. - : American Physiological Society. - 0363-6135 .- 1522-1539. ; 312:2, s. 314-328
  • Tidskriftsartikel (refereegranskat)abstract
    • Intracardiac blood flow is driven by hemodynamic forces that are exchanged between the blood and myocardium. Previous studies have been limited to 2D measurements or investigated only left ventricular (LV) forces. Right ventricular (RV) forces and their mechanistic contribution to asymmetric redirection of flow in the RV have not been measured. We therefore aimed to quantify 3D hemodynamic forces in both ventricles in a cohort of healthy subjects, using magnetic resonance imaging 4D flow measurements. Twenty five controls, 14 elite endurance athletes, and 2 patients with LV dyssynchrony were included. 4D flow data were used as input for the Navier-Stokes equations to compute hemodynamic forces over the entire cardiac cycle. Hemodynamic forces were found in a qualitatively consistent pattern in all healthy subjects, with variations in amplitude. LV forces were mainly aligned along the apical-basal longitudinal axis, with an additional component aimed toward the aortic valve during systole. Conversely, RV forces were found in both longitudinal and short-axis planes, with a systolic force component driving a slingshot-like acceleration that explains the mechanism behind the redirection of blood flow toward the pulmonary valve. No differences were found between controls and athletes when indexing forces to ventricular volumes, indicating that cardiac force expenditures are tuned to accelerate blood similarly in small and large hearts. Patients’ forces differed from controls in both timing and amplitude. Normal cardiac pumping is associated with specific force patterns for both ventricles, and deviation from these forces may be a sensitive marker of ventricular dysfunction. Reference values are provided for future studies. New & Noteworthy Biventricular hemodynamic forces were quantified for the first time in healthy controls and elite athletes (n = 39). Hemodynamic forces constitute a slingshot-like mechanism in the right ventricle, redirecting blood flow toward the pulmonary circulation. Force patterns were similar between healthy subjects and athletes, indicating potential utility as a cardiac function biomarker.
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7.
  • Arvidsson, Per Martin, et al. (författare)
  • Quantification of left and right atrial kinetic energy using four-dimensional intracardiac magnetic resonance imaging flow measurements.
  • 2013
  • Ingår i: Journal of Applied Physiology. - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 114:10, s. 1472-1481
  • Tidskriftsartikel (refereegranskat)abstract
    • Kinetic energy (KE) of atrial blood has been postulated as a possible contributor to ventricular filling. Therefore, we aimed to quantify the left and right atrial blood KE using cardiac magnetic resonance (CMR). Fifteen healthy volunteers underwent CMR at 3T, including a four-dimensional phase contrast flow sequence. Mean left atrial (LA) KE was lower than right atrial (RA) KE (1.1±0.1 mJ vs 1.7±0.1 mJ, P<0.01). Three KE peaks were seen in both atria; one in ventricular systole, one during early ventricular diastole, and one during atrial contraction. The systolic LA peak was significantly smaller than the RA peak (P<0.001), and the early diastolic LA peak was larger than the RA peak (P<0.05). Rotational flow contained 46 ± 7% of total KE, and conserved energy better than non-rotational flow did. The KE increase in early diastole was higher in the LA (P<0.001). Systolic KE correlated with the combination of atrial volume and systolic velocity of the atrioventricular plane displacement (R2=0.57 for LA and R2=0.64 for RA). Early diastolic KE of the LA correlated with LV mass (R2=0.28), however no such correlation was found in the right heart. This suggests that LA KE increases during early ventricular diastole due to LV elastic recoil, indicating that LV filling is dependent on diastolic suction. RV relaxation does not seem to contribute to atrial KE. Instead, atrial KE generated during ventricular systole may be conserved in a hydraulic "flywheel" and transferred to the RV through helical flow, which may contribute to RV filling.
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8.
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9.
  • Arvidsson, Per, et al. (författare)
  • Vortex ring behavior provides the epigenetic blueprint for the human heart.
  • 2016
  • Ingår i: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 6
  • Tidskriftsartikel (refereegranskat)abstract
    • The laws of fluid dynamics govern vortex ring formation and precede cardiac development by billions of years, suggesting that diastolic vortex ring formation is instrumental in defining the shape of the heart. Using novel and validated magnetic resonance imaging measurements, we show that the healthy left ventricle moves in tandem with the expanding vortex ring, indicating that cardiac form and function is epigenetically optimized to accommodate vortex ring formation for volume pumping. Healthy hearts demonstrate a strong coupling between vortex and cardiac volumes (R(2) = 0.83), but this optimized phenotype is lost in heart failure, suggesting restoration of normal vortex ring dynamics as a new, and possibly important consideration for individualized heart failure treatment. Vortex ring volume was unrelated to early rapid filling (E-wave) velocity in patients and controls. Characteristics of vortex-wall interaction provide unique physiologic and mechanistic information about cardiac diastolic function that may be applied to guide the design and implantation of prosthetic valves, and have potential clinical utility as therapeutic targets for tailored medicine or measures of cardiac health.
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10.
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