Noninvasive measurements of transmural myocardial metabolites using 3-D 31P NMR spectroscopy

A completely noninvasive three-dimensional (3-D) static magnetic field magnitude spatially localized 31P spectroscopy technique has been developed and applied to study the in vivo canine myocardium at 9.4 T. The technique incorporates both Fourier series windows and selective Fourier transform methods utilizing all three orthogonal gradients for 3-D phase encoding. The number of data acquisitions for each phase-encoding step was weighted according to the Fourier coefficients to define cylindrical voxels. Spatially localized 31P spectra can be generated for voxels of desired location within the field of view as a postprocessing step. The quality of localization was first demonstrated by using a three-compartment phantom. The technique was then applied to in vivo canine models and yielded 31P cardiac spectra with an excellent signal-to-noise ratio. The in vivo validation experiments, using an implanted 2-phosphoenolpyruvate-containing marker, demonstrated that the technique is capable of measuring at least two transmural layers of left ventricular myocardium representing the subepicardium and subendocardium.

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β-blockade abolishes the augmented cardiac tPA release induced by transactivation of heterodimerised bradykinin receptor-2 and β2-adrenergic receptor in vivo

Thrombosis and Haemostasis ◽

10.1160/th14-01-0059 ◽

2014 ◽

Vol 112 (11) ◽

pp. 951-959 ◽

Cited By ~ 1

Author(s):

Morten Eriksen ◽

Arnfinn Ilebekk ◽

Alessandro Cataliotti ◽

Cathrine Rein Carlson ◽

Torstein Lyberg ◽

...

Keyword(s):

Adrenergic Receptor ◽

Sympathetic Nerves ◽

Ventricular Myocardium ◽

Left Ventricular ◽

Left Ventricular Myocardium ◽

Adrenergic Stimulation ◽

Β2 Adrenergic Receptor ◽

Β Blocker

SummaryBradykinin (BK) receptor-2 (B2R) and β2-adrenergic receptor (β2AR) have been shown to form heterodimers in vitro. However, in vivo proofs of the functional effects of B2R-β2AR heterodimerisation are missing. Both BK and adrenergic stimulation are known inducers of tPA release. Our goal was to demonstrate the existence of B2R-β2AR heterodimerisation in myocardium and to define its functional effect on cardiac release of tPA in vivo. We further investigated the effects of a non-selective β-blocker on this receptor interplay. To investigate functional effects of B2R-β2AR heterodimerisation (i. e. BK transactivation of β2AR) in vivo, we induced serial electrical stimulation of cardiac sympathetic nerves (SS) in normal pigs that underwent concomitant BK infusion. Both SS and BK alone induced increases in cardiac tPA release. Importantly, despite B2R desensitisation, simultaneous BK infusion and SS (BK+SS) was characterised by 2.3 ± 0.3-fold enhanced tPA release compared to SS alone. When β-blockade (propranolol) was introduced prior to BK+SS, tPA release was inhibited. A persistent B2R-β2AR heterodimer was confirmed in BK-stimulated and nonstimulated left ventricular myocardium by immunoprecipitation studies and under non-reducing gel conditions. All together, these results strongly suggest BK transactivation of β2AR leading to enhanced β2AR-mediated release of tPA. Importantly, non-selective β-blockade inhibits both SS-induced release of tPA and the functional effects of B2R-β2AR heterodimerisation in vivo, which may have important clinical implications.

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Quantitative Assessment of Myocardial Ischemia in Multi-Vessel Coronary Artery Disease by Multimodal Stress Echocardiography with Semi-Supine Bicycle Ergometry

Rational Pharmacotherapy in Cardiology ◽

10.20996/1819-6446-2019-15-6-813-819 ◽

2020 ◽

Vol 15 (6) ◽

pp. 813-819

Author(s):

S. N. Koretskiy ◽

O. M. Drapkina ◽

F. B. Shukurov ◽

D. K. Vasiliev

Keyword(s):

Stress Echocardiography ◽

Peak Load ◽

Three Dimensional ◽

Ventricular Myocardium ◽

Cardiovascular Complications ◽

Artery Occlusion ◽

Left Ventricular ◽

Myocardial Imaging ◽

Left Ventricular Myocardium ◽

Bicycle Ergometry

Stress echocardiography is a modern widely used method of noninvasive diagnosis of coronary heart disease and stratification of the risk of cardiovascular complications. In addition, exercise echocardiography is an important tool to clarify the localization of ischemia and establish a symptomassociated artery for management of patient with known coronary angiography data. This is especially important in multivessel lesions, the presence of an occluded artery or borderline stenosis. Currently, various stress agents are used for stress echocardiography in clinical practice: pharmacological drugs (dobutamine or adenosine), transesophageal or endocardial pacing, treadmill, semi-supine bicycle. To detect signs of ischemia usually used only visual estimation of local contractility in the two-dimensional gray-scale mode. Modern modes of myocardial imaging, such as speckletracking echocardiography or three-dimensional visualization, are practically not used. In the presented clinical case, the possibility of combining standard and modern imaging modes to clarify the localization and quantification of ischemia in multivessel coronary lesions, including chronic artery occlusion, is shown. As a stress agent, a semi-supine bicycle was chosen, the use of which allowed to obtain a qualitative image of the left ventricular myocardium at rest and at peak load, suitable for assessing deformation and threedimensional visualization. Evaluation of left ventricular myocardial deformation by speckle-tracking echocardiography was more accurate than standard diagnosis in detecting signs of ischemia in a patient with multivessel lesions. Three-dimensional imaging was inferior in sensitivity to speckletracking stress echocardiography and, at present, seems to have more research value.

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Automated three-dimensional tracking of the left ventricular myocardium in time-resolved and dose-modulated cardiac CT images using deformable image registration

Journal of Cardiovascular Computed Tomography ◽

10.1016/j.jcct.2018.01.005 ◽

2018 ◽

Vol 12 (2) ◽

pp. 139-148 ◽

Cited By ~ 5

Author(s):

Vikas Gupta ◽

Jonas Lantz ◽

Lilian Henriksson ◽

Jan Engvall ◽

Matts Karlsson ◽

...

Keyword(s):

Image Registration ◽

Cardiac Ct ◽

Three Dimensional ◽

Deformable Image Registration ◽

Ventricular Myocardium ◽

Ct Images ◽

Left Ventricular ◽

Left Ventricular Myocardium ◽

Time Resolved

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Laminar fiber architecture and three-dimensional systolic mechanics in canine ventricular myocardium

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1999.276.2.h595 ◽

1999 ◽

Vol 276 (2) ◽

pp. H595-H607 ◽

Cited By ~ 100

Author(s):

Kevin D. Costa ◽

Yasuo Takayama ◽

Andrew D. McCulloch ◽

James W. Covell

Keyword(s):

Three Dimensional ◽

Ventricular Myocardium ◽

Left Ventricular ◽

Wall Thickening ◽

Left Ventricular Myocardium ◽

Fiber Architecture ◽

Left Ventricular Free Wall ◽

Ventricular Mechanics ◽

Interlaminar Shear ◽

Canine Ventricular Myocardium

Previous studies suggest that the laminar architecture of left ventricular myocardium may be critical for normal ventricular mechanics. However, systolic three-dimensional deformation of the laminae has never been measured. Therefore, end-systolic finite strains relative to end diastole, from biplane radiography of transmural markers near the apex and base of the anesthetized open-chest canine anterior left ventricular free wall ( n = 6), were referred to three-dimensional laminar microstructural axes reconstructed from histology. Whereas fiber shortening was uniform [−0.07 ± 0.04 (SD)], radial wall thickening increased from base (0.10 ± 0.09) to apex (0.14 ± 0.13). Extension of the laminae transverse to the muscle fibers also increased from base (0.08 ± 0.07) to apex (0.11 ± 0.08), and interlaminar shear changed sign [0.05 ± 0.07 (base) and −0.07 ± 0.09 (apex)], reflecting variations in laminar architecture. Nevertheless, the apex and base were similar in that at each site laminar extension and shear contributed ∼60 and 40%, respectively, of mean transmural thickening. Kinematic considerations suggest that these dual wall-thickening mechanisms may have distinct ultrastructural origins.

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Immuno-Enzyme Histochemistry of Creatine Phosphokinase

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s042482010007967x ◽

1977 ◽

Vol 35 ◽

pp. 446-447

Author(s):

N. Baba ◽

E.T. Poe ◽

J. Scillian ◽

T. Myser

Keyword(s):

Creatine Phosphokinase ◽

Ventricular Myocardium ◽

Left Ventricular ◽

Left Ventricular Myocardium ◽

Rabbit Muscle ◽

Cytoplasmic Staining ◽

Heart Muscle Cells ◽

Diffuse Cytoplasmic Staining ◽

Strong Staining

With a commercially available rabbit muscle (MM) type isoenzyme of the creatine phosphokinase (CPK) (Worthington Biochemical), anti-CPK antibody was produced in chicken and goat (Figure 1). Fab' fragments of the chicken and goat IgG were isolated and conjugated with a commercially available horseradish peroxidase (HRP) according to the Nakane method (J. Histochem. Cytochem,, 22:1084, 1974).Rabbit hearts were perfused in vivo with freshly prepared 2% paraformaldehyde solution, and the left ventricular myocardium was fixed for 30 minutes. Forty-micrometer-thick frozen sections of the myocardium were incubated with the Fab'-HRP conjugate overnight at 4°C. After a thorough rinse, the sections were stained for the peroxidase reaction.In an electron microscope, diffuse cytoplasmic staining of the heart muscle cells was noted, indicating the diffuse cytosol distribution of CPK (Figure 2). In addition, there was strong staining of the intermembranous and intracristal space of the mitochondria as well as the M-lines of the myofibrils (Figures 3 and 4).

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Fully automatic segmentation of left ventricular myocardium in real-time three-dimensional echocardiography

10.1117/12.654050 ◽

2006 ◽

Cited By ~ 9

Author(s):

Vivek Walimbe ◽

Vladimir Zagrodsky ◽

Raj Shekhar

Keyword(s):

Real Time ◽

Automatic Segmentation ◽

Three Dimensional ◽

Ventricular Myocardium ◽

Left Ventricular ◽

Left Ventricular Myocardium ◽

Fully Automatic ◽

Dimensional Echocardiography ◽

Three Dimensional Echocardiography

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In vivo detection of endogenous acetylcholine release in cat ventricles

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.266.3.h854 ◽

1994 ◽

Vol 266 (3) ◽

pp. H854-H860 ◽

Cited By ~ 13

Author(s):

T. Akiyama ◽

T. Yamazaki ◽

I. Ninomiya

Keyword(s):

Nerve Stimulation ◽

Ventricular Myocardium ◽

Left Ventricular ◽

Vagal Nerve ◽

Vagal Nerve Stimulation ◽

Left Ventricular Myocardium ◽

Ach Release ◽

Vagal Nerves ◽

Dialysis Technique

To detect and monitor endogenous acetylcholine (ACh) release in the in vivo heart, we applied a dialysis technique to the hearts of anesthetized cats. Dialysis probes were implanted in the left ventricular myocardium and were perfused with Krebs-Henseleit solution containing Eserine (10(-4) M) at 3 microliters/min. Dialysate ACh concentration was measured with high-performance liquid chromatography. In four cats, the response to vagal stimulation was studied. Electrical stimulation of efferent vagal nerves (10 Hz) significantly increased dialysate ACh concentration from 596 +/- 118 (control) to 12,210 +/- 1,661 pM. After stimulation, dialysate ACh concentration significantly decreased to 382 +/- 80 pM below control. The influence of ganglionic blocker was determined in six cats. Control vagal nerve stimulation (10 Hz) increased dialysate ACh concentration from 582 +/- 136 to 9,102 +/- 754 pM. Local perfusion of hexamethonium (10(-4) M) did not affect this nerve stimulation-induced ACh increase (8,611 +/- 1,189 pM), and intravenous administration of hexamethonium (20 mg/kg) prevented this increase (340 +/- 88 pM). We examined the response to vagal nerve stimulation at different frequencies in three cats. Vagal nerve stimulation increased dialysate ACh concentration from a control of 588 +/- 211 to 1,227 +/- 195 pM at 2 Hz, 3,946 +/- 1,059 pM at 5 Hz, and 9,366 +/- 1,873 pM at 10 Hz. Dialysate ACh concentration reflects ACh release from postganglionic vagal nerves innervating the left ventricular myocardium; the dialysis technique permits estimation of relative changes in efferent cardiac vagal nerve activity.

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Quantified growth of the human embryonic heart

Biology Open ◽

10.1242/bio.057059 ◽

2021 ◽

Vol 10 (2) ◽

pp. bio057059 ◽

Cited By ~ 1

Author(s):

Jaeike W. Faber ◽

Jaco Hagoort ◽

Antoon F. M. Moorman ◽

Vincent M. Christoffels ◽

Bjarke Jensen

Keyword(s):

Heart Development ◽

Three Dimensional ◽

Ventricular Myocardium ◽

Left Ventricular ◽

Embryonic Heart ◽

Growth Patterns ◽

Right Atrial ◽

Left Ventricular Myocardium ◽

Atrioventricular Canal ◽

The Right

ABSTRACTThe size and growth patterns of the components of the human embryonic heart have remained largely undefined. To provide these data, three-dimensional heart models were generated from immunohistochemically stained sections of ten human embryonic hearts ranging from Carnegie stage 10 to 23. Fifty-eight key structures were annotated and volumetrically assessed. Sizes of the septal foramina and atrioventricular canal opening were also measured. The heart grows exponentially throughout embryonic development. There was consistently less left than right atrial myocardium, and less right than left ventricular myocardium. We observed a later onset of trabeculation in the left atrium compared to the right. Morphometry showed that the rightward expansion of the atrioventricular canal starts in week 5. The septal foramina are less than 0.1 mm2 and are, therefore, much smaller than postnatal septal defects. This chronological, graphical atlas of the growth patterns of cardiac components in the human embryo provides quantified references for normal heart development. Thereby, this atlas may support early detection of cardiac malformations in the foetus.This article has an associated First Person interview with the first author of the paper.

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Impact of acute and enduring volume overload on mechanotransduction and cytoskeletal integrity of canine left ventricular myocardium

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00392.2006 ◽

2007 ◽

Vol 292 (5) ◽

pp. H2324-H2332 ◽

Cited By ~ 14

Author(s):

Dirk W. Donker ◽

Jos G. Maessen ◽

Fons Verheyen ◽

Frans C. Ramaekers ◽

Roel L. H. M. G. Spätjens ◽

...

Keyword(s):

Protein Expression ◽

Volume Overload ◽

Ventricular Myocardium ◽

Left Ventricular ◽

Left Ventricular Myocardium ◽

Mechanical Stimuli ◽

Hypertrophic Growth ◽

Lim Protein ◽

Ventricular Mechanics

It is poorly understood how mechanical stimuli influence in vivo myocardial remodeling during chronic hemodynamic overload. Combined quantitation of ventricular mechanics and expression of key proteins involved in mechanotransduction can improve fundamental understanding. Adult anesthetized dogs ( n = 20) were studied at sinus rhythm (SR) and 0, 3, 10, and 35 days of complete atrioventricular block (AVB). Serial left ventricular (LV) myofiber mechanics were measured. Repeated LV biopsies were analyzed for mRNA and/or protein expression of β1D-integrin, melusin, Akt, GSK3β, muscle LIM protein (MLP), four-and-a-half LIM protein 2 (fhl2), desmin, and calpain. Upon AVB, increased ejection strain (0.29 ± 0.01 vs. 0.13 ± 0.02, SR) and end-diastolic stress (4.8 ± 1.1 vs. 2.7 ± 0.4 kPa) dominated mechanical changes. Brain natriuretic peptide plasma levels were correspondingly high (33 ± 4 vs. 19 ± 1 pg/ml, SR). β1D-Integrin protein expression increased chronically after AVB. Melusin was temporarily overexpressed (+33 ± 9%, 3 days AVB vs. SR), followed by elevated ratios of phosphorylated (P)-Akt to Akt and P-GSK3β to GSK3β (+26 ± 6% and +30 ± 8% at 10 days AVB vs. SR). These changes corresponded to peak hypertrophic growth at 3 to 10 days. MLP increased gradually to maxima at chronic AVB (+36 ± 7%). In contrast, fhl2 (−22 ± 3%, 3 days) and desmin (−30 ± 9%, 10 days AVB) transiently declined but recovered at chronic AVB. Calpain protein expression remained unaltered. In conclusion, volume overload after AVB causes a transient compromise of cytoskeletal integrity based, at least partly, on transcriptional downregulation. Subsequent cytoskeletal reorganization coincides with the upregulation of melusin, P-Akt, P-GSK3β, and MLP, indicating a strong drive to compensated hypertrophy.

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