Influence of site of regional ischemia on LV cavity shape change in dogs

1988 ◽  
Vol 254 (3) ◽  
pp. H547-H557 ◽  
Author(s):  
P. Marino ◽  
D. Kass ◽  
J. Lima ◽  
W. L. Maughan ◽  
W. Graves ◽  
...  
Keyword(s):  
Shape Change ◽  
Left Ventricular ◽  
Acute Ischemia ◽  
Short Axis ◽  
Cavity Shape ◽  
Specific Geometry ◽  
Specific Shape ◽  
Fourier Spectra ◽  
Shape Deformations ◽  
Regional Inhomogeneity

We assessed whether altering the location of acute ischemia produced differing and consistent changes in cavity shape in the canine left ventricle. Twenty anesthetized open-chest dogs underwent transient occlusion of the left anterior descending (LAD) or circumflex (Circ) artery, and cavity shape change was recorded in two-dimensional short-axis echocardiograms. The extent of injury was assessed by radiolabeled microspheres. Shape was analyzed by converting digitized endocardial contours into polar form and expressing the result as a Fourier series. Series terms reflected specific shape deformations, i.e., 2nd term would equal "elongation," 3rd term would equal "triangular." During LAD occlusions, 32.5 +/- 3.0% of the ventricle was hypoperfused compared with 29.8 +/- 2.9% during Circ occlusions (NS). Normal ventricular shape became more circular during ejection indicated by a reduction in the power in nearly all of the Fourier spectra components. During Circ occlusion, the chamber became more elongated, seen in a 63 +/- 16% rise in the 2nd component, and overall shape significantly less circular at end systole than at end diastole. LAD occlusion produced an entirely different pattern, one with no significant elongation but the development of a more triangular shape (86 +/- 27% rise in the 3rd term) by end systole. We conclude that there are characteristic and contrasting shape deformations in LV short-axis contours that depend on the site of ischemic injury. These changes may relate to site-specific geometry and loading, and they point to potential limitations of left ventricular models that do not account for regional inhomogeneity.

An approach for comparative quantification of myocardial blood flow (0-15-H2O-PET), perfusion (Tc-99m-tetrofosmin-SPECT), and metabolism (F 18-FDG-PET)

2001 ◽  
Vol 40 (05) ◽  
pp. 164-171 ◽  
Author(s):  
B. Nowak ◽  
H.-J. Kaiser ◽  
S. Block ◽  
K.-C. Koch ◽  
J. vom Dahl ◽  
...  
Keyword(s):  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Fdg Pet ◽  
Model Fitting ◽  
Compartment Model ◽  
Left Ventricular ◽  
Short Axis ◽  
New Approach ◽  
Single Compartment Model ◽  
Tissue Fraction

Summary Aim: In the present study a new approach has been developed for comparative quantification of absolute myocardial blood flow (MBF), myocardial perfusion, and myocardial metabolism in short-axis slices. Methods: 42 patients with severe CAD, referred for myocardial viability diagnostics, were studied consecutively with 0-15-H2O PET (H2O-PET) (twice), Tc-99m-Tetrofosmin 5PECT (TT-SPECT) and F-18-FDG PET (FDG-PET). All dato sets were reconstructed using attenuation correction and reoriented into short axis slices. Each heart was divided into three representative slices (base, rnidventricular, apex) and 18 ROIs were defined on the FDG PET images and transferred to the corresponding H2O-PET and TT-SPECT slices. TT-SPECT and FDG-PET data were normalized to the ROI showing maximum perfusion. MBF was calculated for all left-ventricular ROIs using a single-compartment-model fitting the dynamic H2O-PET studies. Microsphere equivalent MBF (MBF_micr) was calculated by multiplying MBF and tissue-fraction, a parameter which was obtained by fitting the dynamic H2O-PET studies. To reduce influence of viability only well perfused areas (>70% TT-SPECT) were used for comparative quantification. Results: First and second mean global MBF values were 0.85 ml × min-1 × g-1 and 0.84 ml × min-1 × g1, respectively, with a repeatability coefficient of 0.30 ml ÷ min-1 × gl. After sectorization mean MBF_micr was between 0.58 ml × min1 ÷ ml"1 and 0.68 ml × min-1 × ml"1 in well perfused areas. Corresponding TT-SPECT values ranged from 83 % to 91 %, and FDG-PET values from 91 % to 103%. All procedures yielded higher values for the lateral than the septal regions. Conclusion: Comparative quantification of MBF, MBF_micr, TT-SPECT perfusion and FDG-PET metabolism can be done with the introduced method in short axis slices. The obtained values agree well with experimentally validated values of MBF and MBF_micr.

Automatic localization of the left ventricular blood pool centroid in short axis cardiac cine MR images

2017 ◽  
Vol 56 (6) ◽  
pp. 1053-1062 ◽  
Author(s):  
Li Kuo Tan ◽  
Yih Miin Liew ◽  
Einly Lim ◽  
Yang Faridah Abdul Aziz ◽  
Kok Han Chee ◽  
...  
Keyword(s):  
Blood Pool ◽  
Left Ventricular ◽  
Short Axis ◽  
Mr Images ◽  
Cine Mr ◽  
Cardiac Cine ◽  
Automatic Localization

scholarly journals Endogenous T1ρ cardiovascular magnetic resonance in hypertrophic cardiomyopathy

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Elizabeth W. Thompson ◽  
Srikant Kamesh Iyer ◽  
Michael P. Solomon ◽  
Zhaohuan Li ◽  
Qiang Zhang ◽  
...  
Keyword(s):  
Cardiovascular Magnetic Resonance ◽  
Hypertrophic Cardiomyopathy ◽  
Magnetic Resonance ◽  
Extracellular Volume ◽  
Relaxation Times ◽  
Left Ventricular ◽  
Cardiomyocyte Hypertrophy ◽  
Short Axis ◽  
Spearman's Rho ◽  
Spearman’S Rho

Abstract Background Hypertrophic cardiomyopathy (HCM) is characterized by increased left ventricular wall thickness, cardiomyocyte hypertrophy, and fibrosis. Adverse cardiac risk characterization has been performed using late gadolinium enhancement (LGE), native T1, and extracellular volume (ECV). Relaxation time constants are affected by background field inhomogeneity. T1ρ utilizes a spin-lock pulse to decrease the effect of unwanted relaxation. The objective of this study was to study T1ρ as compared to T1, ECV, and LGE in HCM patients. Methods HCM patients were recruited as part of the Novel Markers of Prognosis in Hypertrophic Cardiomyopathy study, and healthy controls were matched for comparison. In addition to cardiac functional imaging, subjects underwent T1 and T1ρ cardiovascular magnetic resonance imaging at short-axis positions at 1.5T. Subjects received gadolinium and underwent LGE imaging 15–20 min after injection covering the entire heart. Corresponding basal and mid short axis LGE slices were selected for comparison with T1 and T1ρ. Full-width half-maximum thresholding was used to determine the percent enhancement area in each LGE-positive slice by LGE, T1, and T1ρ. Two clinicians independently reviewed LGE images for presence or absence of enhancement. If in agreement, the image was labeled positive (LGE + +) or negative (LGE −−); otherwise, the image was labeled equivocal (LGE + −). Results In 40 HCM patients and 10 controls, T1 percent enhancement area (Spearman’s rho = 0.61, p < 1e-5) and T1ρ percent enhancement area (Spearman’s rho = 0.48, p < 0.001e-3) correlated with LGE percent enhancement area. T1 and T1ρ percent enhancement areas were also correlated (Spearman’s rho = 0.28, p = 0.047). For both T1 and T1ρ, HCM patients demonstrated significantly longer relaxation times compared to controls in each LGE category (p < 0.001 for all). HCM patients also showed significantly higher ECV compared to controls in each LGE category (p < 0.01 for all), and LGE −− slices had lower ECV than LGE + + (p = 0.01). Conclusions Hyperenhancement areas as measured by T1ρ and LGE are moderately correlated. T1, T1ρ, and ECV were elevated in HCM patients compared to controls, irrespective of the presence of LGE. These findings warrant additional studies to investigate the prognostic utility of T1ρ imaging in the evaluation of HCM patients.

Abstract 300: Alda-1 Attenuates Acute Ischemia-reperfusion Mediated Cardiac Damage in Aldehyde Dehydrogenase 2 Mutant Diabetic Mice

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Guodong Pan
Keyword(s):  
Aldehyde Dehydrogenase ◽  
Ischemia Reperfusion ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Acute Ischemia ◽  
Protective Effects ◽  
Diabetic Mice ◽  
Aldehyde Dehydrogenase 2 ◽  
Cardiac Damage ◽  
Western Blots

Aldehyde dehydrogenase 2 (ALDH2), a mitochondrial enzyme in heart, can remove 4-hydroxy-2-nonenal (4-HNE), a toxic by-products of oxidative stress induced by diabetes and ischemia-reperfusion (I/R) injury. A common inactivating mutation of ALDH2 (termed ALDH2*2) was found in 8% of the world’s population, which causes lower ALDH2 activity in mutation carriers. We hypothesized that Alda-1, the only known activator of both ALDH2 and ALDH2*2 mutation, is able to protect heart from I/R injury in diabetic mice with/without ALDH2*2 mutation. Adult male ALDH2*2 mutant and C57B6 wild-type (WT) mice at 3-4 months of age were made hyperglycemic with streptozotocin injection (150 mg/kg. i.p.). Three weeks after injection, Alzet osmotic pumps were implanted subcutaneously to deliver Alda-1 (10 mg/kg) or vehicle. Mice were sacrificed after one day of pump implantation. Hearts were isolated and subjected to 30-minute ischemic followed by 90-minute reperfusion in a Langendorff apparatus. The basal myocardial ALDH2 activity in diabetic ALDH2*2 mutant was significantly lower than in diabetic WT mice (0.50±0.23 vs 0.83±0.08 mmol/min/μg, -39.8%, p<0.05). Alda-1 significantly increased myocardial ALDH2 activity in both ALDH2*2 (1.17±0.38 mmol/min/μg, +134.0%, p<0.05) and WT (1.46±0.40 mmol/min/μg, +75.9%, p<0.05) diabetic mice. Compared with vehicle, Alda-1 significantly improved left ventricular pressure (LVP), and decreased infarcted areas (IA) both in ALDH2*2 (LVP: 4.30±2.03 vs 15.77±8.99 mmHg, +266.7%, p<0.05; IA: 75.17%±9.49 vs 40.46%±7.20, -46.2%, p<0.05) and WT (LVP: 14.22±7.92 vs 21.96±4.32 mmHg, +54.4%, p<0.05; IA: 42.44%±8.60 vs 28.61%±8.55, -32.6%, p<0.05) subjected to I/R injury. Western-blots showed that Alda-1 decreased levels of 4-HNE protein adducts, and increased levels of mitochondrial complex V in both ALDH2*2 and WT mice. Our data suggest that one-day Alda-1 treatment can confer cardio-protective effects against I/R injury in ALDH2*2 diabetic mice possibly accelerating the detoxification of toxic 4-HNE and thereby protecting mitochondria.

Resetting of regional preload due to ventricular shape change alters diastolic and systolic performance

1993 ◽  
Vol 265 (5) ◽  
pp. H1629-H1637 ◽  
Author(s):  
S. Yamaguchi ◽  
Y. Tamada ◽  
H. Miyawaki ◽  
Y. Niida ◽  
A. Fukui ◽  
...  
Keyword(s):  
Shape Change ◽  
Interventricular Septum ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Chamber Pressure ◽  
Right Ventricular Free Wall ◽  
Active Length ◽  
Wall Area ◽  
Ventricular Interaction ◽  
Regional Area

The diastolic and systolic pressure of one ventricle is increased by an increase in volume and/or pressure of the opposite ventricle; however, a mechanism for the ventricular interaction remains unclear. We hypothesized that the shape change of one ventricle elicited by the opposite ventricle would lead to resetting of the regional length, which may explain the ventricular interaction. We used 15 cross-circulated isovolumically contracting canine hearts in which both ventricular volumes were independently controlled. Diastolic regional segment area was calculated by multiplying circumferential and longitudinal lengths on right ventricular free wall (RVFW; n = 6), interventricular septum (IVS; n = 11), and left ventricular (LV) FW (n = 12). The regional area at relatively small volumes of both ventricles were expressed as 100%. With constant RV volume, increasing LV from 7 to 19 ml increased RV diastolic and systolic pressures by 2.7 and 5.5 mmHg, respectively. Conversely, increasing RV volume increased LV diastolic and systolic pressures by 2.3 and 7.5 mmHg, respectively. Increasing LV volume increased RVFW regional area from 121.0 to 124.6% (P < 0.01) and increased IVS regional area from 103.3 to 108.7% (P < 0.01), whereas the RV volume was held constant. Increasing RV volume also increased LVFW and IVS regional areas from 109.9 to 111.6% (P < 0.01) and from 106.8 to 108.9% (P < 0.05), respectively. Ventricular shape change elicited by ventricular interaction will increase the regional wall area, even though the volume of the chamber is unchanged. The increase in the regional area alters the position of the tissue on its resting and active length-tension relations and, thus, leads to enhancement of the chamber pressure.

Influence of posture on left ventricular long- and short-axis shortening

2002 ◽  
Vol 283 (4) ◽  
pp. H1302-H1306 ◽  
Author(s):  
Patrik Sundblad ◽  
Bengt Wranne
Keyword(s):  
Supine Position ◽  
Healthy Subjects ◽  
Mitral Annulus ◽  
Left Ventricular ◽  
Upright Position ◽  
Lateral Part ◽  
Short Axis ◽  
Spherical Form ◽  
End Diastolic Volume ◽  
Axis Length

End-diastolic volume and left ventricular stroke volume are increased in the supine compared with upright position, but the contribution of long-axis (LAS) and short-axis shortening (SAS) to these changes with change in posture has not been established. We examined long- and short-axis motion and dimensions with echocardiography in 10 healthy subjects in the upright and supine position. Long-axis length at end diastole was almost identical, whereas the diastolic short-axis diameter was increased in the supine position. At end systole, there was a decreased long-axis length and increased short-axis length in the supine vs. upright position. Both LAS and SAS were enhanced in supine vs. upright positions [LAS: 9.3 ± 2.2 vs. 15.1 ± 3.1 mm ( P < 0.001); SAS: 12.7 ± 3.2 vs. 16.3 ± 2.8 mm ( P < 0.001)], presumably via Starling mechanisms. LAS increased more in the lateral part of the mitral annulus than in the septal part [7.7 ± 2.6 vs. 4.0 ± 2.8 mm ( P < 0.006)], which implies that the more spherical form, in the supine position, induces more stretch at the lateral free wall than in the ventricular septum. These findings support the notion that Starling mechanisms affect systolic LAS.

Role of endogenous testosterone in myocardial proinflammatory and proapoptotic signaling after acute ischemia-reperfusion

2005 ◽  
Vol 288 (1) ◽  
pp. H221-H226 ◽  
Author(s):  
Meijing Wang ◽  
Ben M. Tsai ◽  
Ajay Kher ◽  
Lauren B. Baker ◽  
G. Mathenge Wairiuko ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Functional Recovery ◽  
Caspase 3 ◽  
Diastolic Pressure ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Acute Ischemia ◽  
Caspase 1 ◽  
Tnf Α

Myocardial ischemia is the leading cause of death in both men and women; however, very little information exists regarding the effect of testosterone on the response of myocardium to acute ischemic injury. We hypothesized that testosterone may exert deleterious effects on myocardial inflammatory cytokine production, p38 MAPK activation, apoptotic signaling, and myocardial functional recovery after acute ischemia-reperfusion (I/R). To study this, isolated, perfused rat hearts (Langendorff) from adult males, castrated males, and males treated with a testosterone receptor blocker (flutamide) were subjected to 25 min of ischemia followed by 40 min of reperfusion. Myocardial contractile function (left ventricular developed pressure, left ventricular end-diastolic pressure, positive and negative first derivative of pressure) was continuously recorded. After reperfusion, hearts were analyzed for expression of tissue TNF-α, IL-1β, and IL-6 (ELISA) and activation of p38 MAPK, caspase-1, caspase-3, caspase-11, and Bcl-2 (Western blot). All indices of postischemic myocardial functional recovery were significantly higher in castrated males or flutamide-treated males compared with untreated males. After I/R, castrated male and flutamide-treated male hearts had decreased TNF-α, IL-1β, and IL-6; decreased activated p38 MAPK; decreased caspase-1, caspase-3, and caspase-11; and increased Bcl-2 expression compared with untreated males. These results show that blocking the testosterone receptor (flutamide) or depleting testosterone (castration) in normal males improves myocardial function after I/R. These effects may be attributed to the proinflammatory and/or the proapoptotic properties of endogenous testosterone. Further understanding may allow therapeutic manipulation of sex hormone signaling mechanisms in the treatment of acute I/R.

Automatic estimation of left atrial function from short axis CINE-MRI using machine learning

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Lourenco ◽  
E Kerfoot ◽  
C Dibblin ◽  
H Chubb ◽  
A Bharath ◽  
...  
Keyword(s):  
Machine Learning ◽  
Cardiac Cycle ◽  
Left Ventricular ◽  
Atrial Function ◽  
Cine Mri ◽  
Funding Source ◽  
Slice Thickness ◽  
Short Axis ◽  
Short Axis Cine ◽  
Entire Cardiac Cycle

Abstract Introduction The importance of atrial mechanical dysfunction in atrial and ventricular pathologies is becoming increasingly recognised. Although machine learning (ML) tools have the ability to automatically estimate atrial function, to date ML techniques have not been used to automatically estimate atrial volumes and functional parameters directly from short axis CINE MRI. Purpose We introduce a convolutional neural network (CNN) to automatically segment the left atria (LA) in CINE-MRI. As a demonstration of the clinical utility of this technique, we calculated LA and left ventricular (LV) ejection fractions automatically from CINE images. Methods Short axis CINE MRI stacks, covering both ventricles and atria, were obtained in a 1.5T Philips Ingenia scanner. A 2D bSSFP ECG-gated protocol was used (FA=60°, TE/TR=1.5/2.9 ms), typical FOV =385 x 310 x 150 mm3, acquisition matrix = 172 x 140, slice thickness = 10 mm, reconstructed with resolution 1.25 x 1.25 x 10 mm3, 30–50 cardiac phases. Images were collected from 37 AF patients in sinus rythm at the time of scan (31–72 years old, 75% male, 18 with paroxysmal AF (PAF), 19 with persistent AF (persAF)). To automatically segment the LA, we used a dedicated CNN that follows a U-Net architecture and was trained in 715 images of the LA, manually segmented by an expert. Data augmentation techniques that included noise addition and linear and non-linear image transforms were also used to increase the training dataset. Ventricular structures, including the LV blood pool, were automatically segmented in these images using a CNN previously trained for this task. Volumetric time plots of LA and LV volume were produced and used to automatically compute maximal and minimal volumes, from which LA and LV ejection fractions (EFs) were assessed. A Bland-Altman analysis compared these automatically computed LA volumes and LA EFs with clinical manual estimates from the same scanning session. Results The CNN achieved very good quality LA segmentations when compared to manual ones (Fig a,b): Dice coefficients (0.90±0.07), median contour distances (0.50±1.12mm) and Hausdorff distances (6.70±6.16mm). Bland-Altman analyses show very good agreement between automatic and manual LA volumes and EFs (Fig e). A moderate linear correlation between LA and LV EFs in AF patients was found (Fig d). The measured LA EF was higher for PAF (29±8%) than PersAF patients (21±11%), although non-significantly (t-test p-value: 0.10). Conclusions We present a reliable automatic method to perform LA segmentations from CINE MRI across the entire cardiac cycle. This approachs opens up the possibility of automatically calculating more sophisticated biomarkers of LA function which take into account information about LA volumes across the entire cardiac cycle, including biomarkers of LA booster pump function. Figure 1 Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): British Heart Foundation; EPSRC/Wellcome Centre for Medical Engineering

Sign in / Sign up

Export Citation Format

Share Document