Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where Marcus Carlsson is active.

Publication


Featured researches published by Marcus Carlsson.


computing in cardiology conference | 2005

Time resolved three-dimensional automated segmentation of the left ventricle

Einar Heiberg; L Wigstrom; Marcus Carlsson; Matts Karlsson

This paper describes a robust approach for multimodality segmentation of the cardiac left ventricle. The method is based on the concept of deformable models, but extended with an enhanced and fast edge detection scheme that includes temporal information, and anatomical a priori information. The algorithm is implemented with a fast numeric scheme for solving energy minimization, and efficient filter nets for fast edge detection. This allows clinically applicable time for a whole time resolved 3D cardiac data set to be achieved on a standard desktop computer. The algorithm is validated on images acquired using MRI gradient echo, MRI (SSFP) images, and Cardiac CT The complete algorithm is implemented into a software package freely available for non commercial research at http://segment.heiberg.se


American Journal of Physiology-heart and Circulatory Physiology | 2008

Quantitative MR measurements of regional and global left ventricular function and strain after intramyocardial transfer of VM202 into infarcted swine myocardium

Marcus Carlsson; Nael F. Osman; Philip C. Ursell; Alastair J. Martin; Maythem Saeed

Previous studies have shown the beneficial effects of the hepatocyte growth factor (HGF) gene on myocardial perfusion and infarction size but not on the regional strain in relationship to global left ventricular function. A noninvasive magnetic resonance (MR) study was performed to determine the effect of a new HGF gene, VM202, expressing two isoforms of HGF, on regional and global left ventricular function. Pigs (8/group) were divided into three groups: 1) controls without infarction; 2) reperfused, infarcted controls; and 3) infarcted, treated (1 h after reperfusion) with VM202 injected at eight sites. Cine, tagging, and delayed enhancement MR images were acquired at 3 and 50 +/- 3 days after infarction. At 50 days, ejection fraction in infarcted, treated animals increased (38 +/- 1% to 47 +/- 2%, P < 0.01) to the level of controls without infarction (52 +/- 1%, P = 0.16) but decreased in infarcted controls (41 +/- 1% to 37 +/- 1%, P < 0.05). Two-dimensional strain improved in remote, peri-infarcted, and infarcted myocardium. Furthermore, the infarction size was smaller in infarcted, treated animals (7.0 +/- 0.5%) compared with infarcted controls (13.2 +/- 1.6%, P < 0.05). Histopathology showed a lack of hypertrophy in myocytes in peri-infarcted and remote myocardium and the formation of islands/peninsulas of myocytes in infarcted, treated animals but not in infarcted controls. In conclusion, the plasmid HGF gene caused a near complete recovery of ejection fraction and improved the radial and circumferential strain of remote, peri-infarcted, and infarcted regions within 50 days. These beneficial effects may be explained by the combined effects of a speedy and significant infarct resorption and island/peninsulas of hypertrophied myocytes within the infarcted territory but not by compensatory hypertrophy. The combined use of cine and tagging MR imaging provides valuable information on the efficacy of gene therapy.


Radiology | 2009

Myocardial Microinfarction after Coronary Microembolization in Swine: MR Imaging Characterization

Marcus Carlsson; Mark W. Wilson; Alastair J. Martin; Maythem Saeed

PURPOSEnTo use first-pass perfusion and delayed-enhanced (DE) magnetic resonance (MR) imaging for the detection of the early effects of coronary microembolization on myocardial perfusion and viability.nnnMATERIALS AND METHODSnApproval was obtained from the institutional committee on animal research. A hybrid x-ray and MR imaging system was used to guide the endovascular catheter and quantify the left anterior descending coronary artery (LAD) perfusion territory before microembolization and ischemic myocardium and microinfarction after microembolization. The embolic agent was selectively delivered in the LAD in six pigs. First-pass perfusion MR imaging was performed 1 hour and 1 week after microembolization. Microinfarction was measured on DE MR images in beating and nonbeating hearts (high-spatial-resolution sequence) by using extracellular and blood pool MR contrast media and after death. The Wilcoxon signed rank test and correlation analysis were used.nnnRESULTSnThe LAD perfusion territory was 35% of left ventricular (LV) mass +/- 2 (standard error of the mean). Microembolization caused perfusion deficit in 15.7% of LV mass +/- 2.6 compared with that of LAD territory (P = .03). At 1 week, perfusion parameters improved and the extent of hypoperfused territory declined (4.6% of LV mass +/- 1.4, P = .03). Microinfarction size expanded from 1.4% of LV mass +/- 0.2 at 1 hour to 7.5% of LV mass +/- 1.2 at 1 week. In nonbeating hearts and at triphenyltetrazolium chloride staining at 1 week, microinfarction size was 7.6% of LV mass +/- 1.4 and 7.2% of LV mass +/- 1.5, respectively. There was no correlation between the ejection fraction and the extents of microinfarction or hypoperfused territory. Histopathologic findings confirmed the presence of patchy microinfarction.nnnCONCLUSIONnCoronary microembolization caused persistent decline in myocardial perfusion at first-pass perfusion imaging. DE MR imaging has the potential to help reliably quantify subacute microinfarction. The magnitude of LV dysfunction is not related to the extents of microinfarction or hypoperfused territory.


Journal of Electrocardiology | 2008

Magnetic resonance imaging as a potential gold standard for infarct quantification.

Marcus Carlsson; Håkan Arheden; Charles B. Higgins; Maythem Saeed

Accurate diagnosis, characterization, and quantification of myocardial infarction (MI) is essential to assess the impact of therapy and to aid in predicting prognosis of patients with ischemic heart disease. Delayed contrast-enhanced magnetic resonance (DE-MR) imaging has the potential of being the gold standard for quantification of MI. It has also been useful in correlating electrocardiography abnormalities with the location and transmurality of infarction. The focus of this review is to address the strengths and limitations of DE-MR imaging in the detection and quantification of MI for clinicians and investigators in the field of electrocardiology. The biological rationale and technical background for detecting MI by DE-MR imaging were reviewed as well as the different approaches for quantification of the DE-MR images, exemplified by patient cases.


Magnetic Resonance in Medicine | 2009

Magnetic resonance imaging quantification of left ventricular dysfunction following coronary microembolization.

Marcus Carlsson; Alastair J. Martin; Philip C. Ursell; David Saloner; Maythem Saeed

Microembolization is common after coronary interventions, and therefore this MRI study aimed to quantify the effect of coronary microembolization on left ventricular (LV) function. The left anterior descending artery (LAD) was selectively catheterized in an XMR suite (Philips Medical Systems, Best, The Netherlands) in eight pigs to deliver MR contrast media to measure the LAD territory using first‐pass perfusion and for intracoronary delivery of the embolic agent. Cine, tagged, and delayed contrast‐enhanced MRI (DCE‐MRI) was performed to assess LV volumes, ejection fraction, radial and circumferential strain, and viability at baseline, 1 h, and 1 week after microembolization. Histopathology and histochemical staining were used to characterize and measure the extent of microinfarction. The LAD territory was 35% ± 2% LV mass. Patchy microinfarction on DCE‐MRI at 1 week was 22.0% ± 3.6% LAD territory (7.5% LV mass). Microembolization caused persistent decline in ejection fraction (baseline = 49% ± 1%, 1 h = 29% ± 1%, P = 0.02 and 1 week = 36% ± 1%, P = 0.03) and increased end‐diastolic (79.6 ± 3.9 ml, 85.5 ± 4.5 ml, P = 0.03 and 92.4 ± 6.2 ml, P = 0.06, respectively) and end‐systolic (40.8 ± 2.1 ml, 60.2 ± 3.4 ml, P = 0.02 and 59.3 ± 4.8 ml, P = 0.03, respectively) volumes. The microembolized territory was manifested as dysfunctional regions for 1 week on cine and tagged MRI. Histopathology revealed occlusive microemboli surrounded by necrotic tissue undergoing repair. Microinfarction was visualized after coronary microembolization and caused LV dysfunction disproportionate to the size of myocardial damage. It also changed LV geometry and decreased radial and circumferential strain over the course of 1 week. Magn Reson Med, 2009.


Journal of Magnetic Resonance Imaging | 2009

Persistent decline in longitudinal and radial strain after coronary microembolization detected on velocity encoded phase contrast magnetic resonance imaging

Demetrius L. Dicks; Marcus Carlsson; Einar Heiberg; Alastair J. Martin; David Saloner; Håkan Arheden; Maythem Saeed

To use velocity‐encoded phase contrast (PC) MRI in assessing the effect of coronary microembolization on longitudinal and radial myocardial strain.


Academic Radiology | 2008

Intracoronary Injection of Contrast Media Maps the Territory of the Coronary Artery: An MRI Technique for Assessing the Effects of Locally Delivered Angiogenic Therapies

Marcus Carlsson; Maythem Saeed

RATIONALE AND OBJECTIVESnThe effects of locally delivered angiogenic factors or stem cells on the coronary artery perfusion territory are not well defined. Therefore, the aim of this study was to determine the ability of the selective injection of magnetic resonance contrast media (MR-CM) to map and quantify the territories of the major coronary arteries.nnnMATERIALS AND METHODSnSelective coronary catheterization (n = 16 pigs) was performed under x-ray and magnetic resonance imaging (MRI) fluoroscopy in an x-ray and magnetic resonance suite. Catheters were placed in the left anterior descending (LAD), circumflex, or right coronary artery. The coronary perfusion territories were mapped by the intracoronary injection of MR-CM using first-pass perfusion (FPP) and early contrast-enhanced (CE) MRI. Cine MRI was used to quantify left ventricular (LV) mass. In 12 animals, the LAD coronary artery was occluded by microspheres to create infarctions. Infarct size was measured on delayed enhanced (DE) MRI after the intravenous injection of MR-CM.nnnRESULTSnX-ray and magnetic resonance fluoroscopy were successfully used to catheterize the coronary arteries. The perfusion territories of the coronary arteries were defined as hyperenhanced regions on FPP and CE MRI. The LAD coronary artery territory was 33.7 +/- 2.2% of LV mass on FPP MRI and 33.0 +/- 2.3% on CE MRI (P = .63). Bland-Altman analysis showed close agreement between the two methods (0.7 +/- 5.0%). DE MRI demonstrated the infarcted myocardium as hyperenhanced subregions of the perfusion territory (7.5 +/- 1.2% of LV mass).nnnCONCLUSIONSnInterventional cardiac x-ray and magnetic resonance fluoroscopy can be used to map and quantify the perfusion territory of each coronary artery. This experimental method can be used before and after the local delivery of angiogenic factors and stem cell therapy to determine their efficacy.


International Journal of Cardiology | 2010

Percutaneous transendocardial VEGF gene therapy: MRI guided delivery and characterization of 3D myocardial strain

Demetrius L. Dicks; David Saloner; Alastair J. Martin; Marcus Carlsson; Maythem Saeed

BACKGROUNDnPatients with myocardial infarcts have unfavorable left ventricular (LV) remodeling and devastating outcomes. This study was performed to determine whether VEGF-gene delivered transendocardially under MR-guidance improves LV three-dimensional (3D) strain (circumferential, longitudinal and radial), reduces infarct transmurality and increases vascular density in a canine model of permanent LAD coronary artery occlusion.nnnMETHODSnImaging was performed using a 1.5-T MR scanner. Three days after occlusion, a percutaneous catheter was advanced under MR-guidance into the LV chamber for transendocardial delivery of VEGF-gene therapy (n=6) or LacZ-gene as control (n=6) into infarcted and peri-infarcted myocardium. MRI was performed before (3xa0days) and after (50xa0days) the delivery of therapy using cine, tagged and delayed contrast enhancement. Histochemical and pathological stains were used to assess myocardial viability and vascular density, respectively.nnnRESULTSnTransendocardial delivery of VEGF-gene therapy and LacZ-gene under MRI guidance was successful in all animals. Significant improvement in 3D strain was observed within 50xa0days in treated animals. On the other hand, control animals demonstrated deterioration in regional strain over time. Significant reductions in infarct transmurality and increases in capillary and arteriole densities were also observed in VEGF-treated as compared to control animals.nnnCONCLUSIONnMR-guided transendocardial delivery of VEGF-gene improved myocardial strain and enhanced transmural infarct resorption. This minimally invasive technique may be useful for delivery of local therapies, designed to promote angiogenesis or myogenesis.


Contrast Media & Molecular Imaging | 2008

Identification of residual ischemia, infarction, and microvascular impairment in revascularized myocardial infarction using 64-slice MDCT.

Andre Furtado; Marcus Carlsson; Max Wintermark; Karen G. Ordovas; Maythem Saeed

This study aimed to assess the potential of 64-slice MDCT in characterizing revascularized infarcted myocardium at the cellular and microvascular levels. Pigs (n = 7) underwent 2 h left anterior descending coronary artery occlusion/reperfusion. In acute (2-4 h) and subacute (1 week) infarction, first-pass perfusion (FPP) (1 ml/kg of 300 mg/ml Omnipaque) was performed using a cine (rotation time 60 s/bpm) non-ECG gated sequence (mAS/kV = 100/120). Delayed contrast enhanced images (DE) (mAS/kV = 650/120) were acquired every 2 min for 10 min to determine the kinetics of Omnipaque and to define infarcted myocardium and microvascular impairment (representing microvascular obstruction and/or no- or low-reflow phenomenon). Maximum upslope, maximum attenuation and time to the peak were measured from FPP plots. 2,3,5-Triphenyltetrazolium-chloride (TTC) was used to define true infarction in the excised hearts. Hyperenhanced myocardium on DE was measured and compared with TTC. The contrast media caused minor beam hardening and X-ray scatter on FPP. The above-mentioned perfusion parameters significantly differed between remote and acute infarction. Infarcted myocardium showed two patterns of enhancement on DE, hyperenhanced rim representing the perfused infarction and hypoenhanced core representing a microvascular impaired region, with significantly different attenuation. The extent of infarction on DE-MDCT decreased over the course of 1 week and did not differ from TTC. Post-processed FPP semi-quantitative images showed a decline in myocardial blood volume and flow in acute revascularized infarction. In conclusion, modern MDCT has the potential to identify residual ischemia on FPP and microvascular impairment and infarction on DE images.


Scandinavian Cardiovascular Journal | 2011

Coronary microembolization causes long-term detrimental effects on regional left ventricular function.

Marcus Carlsson; Robert Jablonowski; Alastair J. Martin; Philip C. Ursell; Maythem Saeed

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.

Collaboration


Dive into the Marcus Carlsson's collaboration.

Top Co-Authors

Avatar

Maythem Saeed

University of California

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar

David Saloner

University of California

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Matts Karlsson

University of California

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Andre Furtado

University of California

View shared research outputs
Top Co-Authors

Avatar

Ann F. Bolger

University of California

View shared research outputs
Researchain Logo
Decentralizing Knowledge