Extent Of Scar Research Articles

Retraction Note to: Postconditioning promotes the cardiac repair through balancing collagen degradation and synthesis after myocardial infarction in rats.

Postconditioning (Postcon) reduces infarct size. However, its role in modulation of cardiac repair after infarction is uncertain. This study tested the hypothesis that Postcon inhibits adverse cardiac repair by reducing degradation of extracellular matrix (ECM) and synthesis of collagens via modulating matrix metalloproteinase (MMP) activity and transforming growth factor (TGF) β1/Smad signaling pathway. Sprague–Dawley rats were subjected to 45 min ischemia followed by 3 h, 7 or 42 days of reperfusion, respectively. In acute studies, four cycles of 10/10 s Postcon significantly reduced infarct size, which was blocked by administration of a mitochondrial KATP channel blocker, 5-hydroxydecanoate (5-HD) at reperfusion. In chronic studies, Postcon inhibited MMP activity and preserved ECM from degradation as evidenced by reduced extent of collagen-rich scar and increased mass of viable myocardium. Along with a reduction in collagen synthesis and fibrosis, Postcon significantly down-regulated expression of TGFβ1 and phospho-Smad2/3, and up-regulated Smad7 as compared to the control, consistent with a reduction in the population of α-smooth muscle actin expressing myofibroblasts within the infarcted myocardium. At 42 days of reperfusion, echocardiography showed significant improvements in left ventricular end-diastolic volume and ejection fraction. The wall thickness of the infarcted middle anterior septum in the Postcon was also significantly greater than that in the control. The beneficial effects of Postcon on cardiac repair were comparable to preconditioning and still evident after a blockade with 5-HD. These data suggest that Postcon is effective to promote cardiac repair and preserve cardiac function; protection is potentially mediated by inhibiting ECM degradation and collagen synthesis.

Anti-inflammatory cytokine TSG-6 inhibits hypertrophic scar formation in a rabbit ear model

Hypertrophic scars are characterized by excessive fibrosis and extracellular matrix (ECM) deposition and can be functionally and cosmetically problematic; however, there are few satisfactory treatments for controlling hypertrophic scars. The inflammatory cells and cytokines involved in excessive inflammation during wound healing facilitate fibroblast proliferation and collagen deposition, leading to pathologic scar formation. TSG-6 exhibits anti-inflammatory activity. This study examined the effect of recombinant TSG-6 on inflammation in hypertrophic scars using a rabbit ear model. Six 7-mm, full-thickness, circular wounds were made on the ears of 12 rabbits. TSG-6 and PBS were intradermally injected into the right and left ear wounds, respectively. The methods of TEM and TUNEL were used to detect fibroblast apoptosis. The expressions of inflammatory factors: IL-1β, IL-6 and TNF-α, were detected by immunohistochemistry and real time polymerase chain reaction. Collagen I and III expression detected by immunohistochemistry and Masson׳s trichrome staining and SEI (scar elevation index) was used to evaluate the extent of scarring. TSG-6 injection mitigated the formation of a hypertrophic scar in the rabbit ear. TSG-6-treated wounds exhibited decreased inflammation compared with the control group, as evidenced by the lower levels of IL-1β, IL-6, TNF-α and MPO. The SEI and the synthesis of collagens I and III were significantly decreased in the TSG-6-treated scars compared with control scars. The apoptosis rate was higher in the TSG-6-treated scars. TSG-6 exhibited anti-inflammatory effects during the wound healing process and cicatrization and significantly diminished hypertrophic scar formation in a rabbit ear model.

Magnetic resonance estimates of the extent and heterogeneity of scar tissue in ICD patients with ischemic cardiomyopathy predict ventricular arrhythmia.

The majority of patients receiving implantable cardioverter-defibrillator (ICD) implantation under current guidelines never develop sustained ventricular arrhythmia; therefore, better markers of risk for sustained ventricular tachycardia and/or ventricular fibrillation are needed. The purpose of this study was to identify cardiac magnetic resonance arrhythmic risk predictors of ischemic cardiomyopathy before ICD implantation. Forty-three subjects (mean age, 64.5 ± 11.9 years) with previous myocardial infarction who were referred for ICD implantation were evaluated by cardiac magnetic resonance imaging (MRI). The MRI protocol included left ventricular functional parameter assessment using steady-state free precession and late gadolinium enhancement MRI using inversion recovery fast gradient echo. Left ventricular functional parameters were measured using cardiac magnetic resonance software. Subjects were followed up for 6-46 months, and the events of appropriate ICD treatments (shocks and antitachycardia pacing) were recorded. Twenty-eight patients experienced 46 spontaneous episodes during a median follow-up duration of 30 months. The total myocardial infarct (MI) size (18.05 ± 11.44 g vs 38.83 ± 19.87 g; P = .0006), MI core (11.63 ± 7.14 g vs 24.12 ± 12.73 g; P = .0002), and infarct gray zone (6.43 ± 4.64 g vs 14.71 ± 7.65 g; P = .0004) were significantly larger in subjects who received appropriate ICD therapy than in those who did not experience an episode of ventricular tachycardia and/or ventricular fibrillation. Multivariate regression analyses for the infarct gray zone and MI core adjusted for New York Heart Association class, diabetes, and etiology (primary or secondary prevention) revealed that the gray zone and MI core were predictors of appropriate ICD therapies (P = .0018 and P = .007, respectively). The extent of MI scar may predict which patients would benefit most from ICD implantation.

Can GDF-15 be Used to Assess ventricular recovery following Left Ventricular Assist Device Therapy?

With the rising incidence of end stage heart failure and the stagnating pool of donors, left ventricular assist device (LVAD) therapy has emerged as a bridge to recovery/transplant or as destination therapy. However, the number of patients who actually undergo device explant as a result of ventricular recovery happens to be highly variable at the present time [1,2]. Ventricular recovery is a complex phenomenon influenced by several factors such as the etiology/duration of heart failure, extent of scarring and fibrosis of the myocardium at the time of implantation and adjunct medical management protocol tailored for recovery immediately post device implantation.

Neurosurgery concepts: Key perspectives on dendritic cell vaccines, metastatic tumor treatment, and radiosurgery.

Background:This is a laboratory study to investigate the effect of adding brain-derived-neurotrophic factor (BDNF) in a poly (N-isopropylacrylamide-g-poly (ethylene glycol) scaffold and its effect on spinal cord injury in a rat model.Methods:This is a laboratory investigation of a spinal cord injury in a rat model. A dorsolateral funiculotomy was used to disrupt the dorsolateral funiculus and rubrospinal tract. Animals were then injected with either the scaffold polymer or scaffold polymer with BDNF. Postoperatively, motor functions were assessed with single pellet reach to grasp task, stair case reaching task and cylinder task. Histological study was also performed to look at extent of glial scar and axonal growth.Results:Animals received BDNF containing polymer had an increased recovery rate of fine motor function of forelimb, as assessed by stair case reaching task and single pellet reach to grasp task compared with control animals that received the polymer only. There is no significant difference in the glial scar formation. BDNF treated animals also had increased axon growth including increase in the number and length of the rubrospinal tract axons.Conclusion:BDNF delivered via a scaffold polymer results in increased recovery rate in forelimb motor function in an experimental model of spinal cord injury, possibly through a promotion of growth of axons of the rubrospinal tract.

The Localization and Characterization of Ischemic Scars in relation to the Infarct Related Coronary Artery Assessed by Cardiac Magnetic Resonance and a Novel Automatic Postprocessing Method.

Aims. The correspondence between the localization and morphology of ischemic scars and the infarct related artery (IRA) by use of cardiac magnetic resonance imaging and a novel automatic postprocessing method. Methods and Results. Thirty-four patients with one-year-old single IRA myocardial infarction were examined. Endocardium, epicardium, and the point where right and left ventricles are coinciding were manually marked. All measurements were automatically assessed by the method. The following are results with manual assessments of scar properties in parenthesis: mean scar size (FWHM criterion): 7.8 ± 5.5 as %LV (17.4 ± 8.6%); mean endocardial extent of infarction: 44 ± 26° (124 ± 47°); mean endocardial extent of infarction as %LV circumference: 9.7 ± 7.0% (34.6 ± 13.0%); and mean transmurality: 52 ± 20% of LV wall thickness (77 ± 23%). Scars located in segments 1, 2, 7, 8, 13, and 14 by use of the automatic method were 96–100% specific for LAD occlusion. The highest specificities of RCA and LCX occlusions were segment 4 with 93% and segment 6 with 64%, respectively. The scar localization assessed automatically or manually was without major differences. Conclusion. The automatic method is applicable and able to assess localization, size, transmurality, and endocardial extent of ischemic scars.

Labeling galectin-3 for the assessment of myocardial infarction in rats.

BackgroundGalectin-3 is a ß-galactoside-binding lectin expressed in most of tissues in normal conditions and overexpressed in myocardium from early stages of heart failure (HF). It is an established biomarker associated with extracellular matrix (ECM) turnover during myocardial remodeling. The aim of this study is to test the ability of 123I-galectin-3 (IG3) to assess cardiac remodeling in a model of myocardial infarction (MI) using imaging techniques.MethodsRecombinant galectin-3 was labeled with iodine-123 and in vitro binding assays were conducted to test 123I-galectin-3 ability to bind to ECM targets. For in vivo studies, a rat model of induced-MI was used. Animals were subjected to magnetic resonance and micro-SPETC/micro-CT imaging two (2 W-MI) or four (4 W-MI) weeks after MI. Sham rats were used as controls. Pharmacokinetic, biodistribution, and histological studies were also performed after intravenous administration of IG3.ResultsIn vitro studies revealed that IG3 shows higher binding affinity (measured as counts per minute, cpm) (p < 0.05) to laminin (2.45 ± 1.67 cpm), fibronectin (4.72 ± 1.95 cpm), and collagen type I (1.88 ± 0.53 cpm) compared to bovine serum albumin (BSA) (0.88 ± 0.31 cpm). Myocardial quantitative IG3 uptake (%ID/g) was higher (p < 0.01) in the infarct of 2 W-MI rats (0.15 ± 0.04%) compared to control (0.05 ± 0.03%). IG3 infarct uptake correlates with the extent of scar (rs = 1, p = 0.017). Total collagen deposition in the infarct (percentage area) was higher (p < 0.0001) at 2 W-MI (24.2 ± 5.1%) and 4 W-MI (30.4 ± 7.5%) compared to control (1.9 ± 1.1%). However, thick collagen content in the infarct (square micrometer stained) was higher at 4 W-MI (20.5 ± 11.2 μm2) compared to control (4.7 ± 2.0 μm2, p < 0.001) and 2 W-MI (10.6 ± 5.1 μm2, p < 0.05).ConclusionsThis study shows, although preliminary, enough data to consider IG3 as a potential contrast agent for imaging of myocardial interstitial changes in rats after MI. Labeling strategies need to be sought to improve in vivo IG3 imaging, and if proven, galectin-3 might be used as an imaging tool for the assessment and treatment of MI patients.

Endogenous assessment of chronic myocardial infarction with T(1ρ)-mapping in patients.

BackgroundDetection of cardiac fibrosis based on endogenous magnetic resonance (MR) characteristics of the myocardium would yield a measurement that can provide quantitative information, is independent of contrast agent concentration, renal function and timing. In ex vivo myocardial infarction (MI) tissue, it has been shown that a significantly higher T1ρ is found in the MI region, and studies in animal models of chronic MI showed the first in vivo evidence for the ability to detect myocardial fibrosis with native T1ρ-mapping. In this study we aimed to translate and validate T1ρ-mapping for endogenous detection of chronic MI in patients.MethodsWe first performed a study in a porcine animal model of chronic MI to validate the implementation of T1ρ-mapping on a clinical cardiovascular MR scanner and studied the correlation with histology. Subsequently a clinical protocol was developed, to assess the feasibility of scar tissue detection with native T1ρ-mapping in patients (n = 21) with chronic MI, and correlated with gold standard late gadolinium enhancement (LGE) CMR. Four T1ρ-weighted images were acquired using a spin-lock preparation pulse with varying duration (0, 13, 27, 45 ms) and an amplitude of 750 Hz, and a T1ρ-map was calculated. The resulting T1ρ-maps and LGE images were scored qualitatively for the presence and extent of myocardial scarring using the 17-segment AHA model.ResultsIn the animal model (n = 9) a significantly higher T1ρ relaxation time was found in the infarct region (61 ± 11 ms), compared to healthy remote myocardium (36 ± 4 ms) . In patients a higher T1ρ relaxation time (79 ± 11 ms) was found in the infarct region than in remote myocardium (54 ± 6 ms). Overlap in the scoring of scar tissue on LGE images and T1ρ-maps was 74%.ConclusionWe have shown the feasibility of native T1ρ-mapping for detection of infarct area in patients with a chronic myocardial infarction. In the near future, improvements on the T1ρ -mapping sequence could provide a higher sensitivity and specificity. This endogenous method could be an alternative for LGE imaging, and provide additional quantitative information on myocardial tissue characteristics.

Abstract 19159: Assessment of Myocardial Viability After Acute Myocardial Infarction: A Head-to-head Comparison of the Perfusable Tissue Index by PET and Delayed Contrast-enhanced CMR

Introduction: Early recognition of viable myocardium is of great clinical importance after acute myocardial infarction (AMI). Delayed contrast-enhanced magnetic resonance imaging (DCE-CMR) has been validated extensively for the detection of viability. An alternative method for detecting viability is the perfusable tissue index (PTI), a positron emission tomography (PET) derived parameter, which is inversely related to the extent of myocardial scar (nonperfusable tissue). Aims: To investigate the predictive value of PTI on recovery of LV function after percutaneous coronary intervention (PCI) for AMI. Methods: Twenty-six patients with AMI successfully treated by PCI were included. Subjects were examined one week and three months after AMI with [15O]H2O PET and DCE-CMR to assess PTI, regional function and scar. Viability was defined as recovery of systolic wall thickening (SWT) ≥ 3.0 mm at follow-up. Results: A total of 396 segments were available for serial analysis. At baseline, 166 segments were dysfunctional, of which 125 (75%) exhibited significant DCE and were located in the myocardial territory supplied by the culprit-artery. Fourty-nine of these dysfunctional segments showed full recovery during follow-up (viable), whereas 76 segments remained dysfunctional (nonviable). Baseline PTI of viable segments was 0.94 ± 0.07 and was significantly higher compared to nonviable segments (0.80 ± 0.11, p = 0.01). The optimal cut-off value for the PTI was 0.85 with a sensitivity of 92% and specificity of 71%, and an area under the curve (AUC) of 0.88. In comparison, a cut-off value of 40% for the extent of DCE resulted in a sensitivity of 75% and a specificity of 65%, and an AUC of 0.75 (p = 0.02 vs PTI). Conclusions: This study shows that assessment of myocardial viability shortly after reperfused AMI is feasible with PET, and that the PTI is a good prognostic indicator for recovery of contractile function when compared to DCE-CMR.

Abstract 12941: Disease Progression in Patients With Arrhythmogenic Right Ventricular Cardiomyopathy and Ventricular Tachycardia: A Longitudinal Study With Unipolar Voltage Mapping

Introduction: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is believed to result in progressive fibrofatty replacement of the RV myocardium with development of multiple ventricular tachycardia (VT) circuits. Endocardial unipolar voltage mapping has been shown to reliably identify epicardial and endocardial (epi-endo) scar in ARVC. Hypothesis: We studied the prevalence and mechanisms of disease progression in patients with ARVC and VT through longitudinal unipolar voltage mapping studies. Methods: Eighteen consecutive patients (age 38±14 years) who fulfilled the revised Task Force criteria for ARVC underwent two detailed sinus rhythm endocardial unipolar voltage maps (mean 348±118 points) performed a median of 36 months apart (interquartile range 21 to 36 months, minimum 9 months) as part of VT ablation procedures. Epi-endo scar was defined using established unipolar voltage cutoff (5.5 mV). The extent of RV scar and total RV volume was measured by a dedicated software. A &gt;5% increase in RV scar area or volume over follow-up was considered significant. Results: At baseline, all patients had evidence of epi-endo RV scar (mean 141±82 cm 2 ; 56±27% of the RV surface area). After a mean follow-up of 49±36 months, no significant progression of unipolar voltage scar was observed (mean 159±83 cm 2 , P=0.14; 63±27% of the RV surface area, P=0.07). Specifically, only 3 (17%) patients presented with progression of the RV scar &gt;5%. The RV volumes increased during follow-up (from 206±74 mL to 258±77 mL, P=0.0003), with the majority of patients (15/18, 83%) having a significant increase in the RV volume (mean increase = 38.9%). Only 3 (17%) patients had no change in both RV scar size and volume over time. Conclusions: In patients with ARVC and VT, progressive RV dilatation is almost uniformly observed, while rapid epi-endo scar progression is rare. These findings suggest that aggressive epi-endocardial substrate ablation should provide long-term VT control, and further research is needed to identify the mechanism(s) for and to prevent ongoing RV dilatation in these patients.

RETRACTED: Dual ACE-inhibition and angiotensin II AT1 receptor antagonism with curcumin attenuate maladaptive cardiac repair and improve ventricular systolic function after myocardial infarctionin rat heart

Curcumin has been shown to improve cardiac function by reducing degradation of extracellular matrix and inhibiting synthesis of collagen after ischemia. This study tested the hypothesis that attenuation of maladaptive cardiac repair with curcumin is associated with a dual ACE-inhibition and angiotensin II AT1 receptor antagonism after myocardial infarction. Sprague-Dawley rats were subjected to 45min ischemia followed by 7 and 42 days of reperfusion, respectively. Curcumin was fed orally at a dose of 150mg/kg/day only during reperfusion. Relative to the control animals, dietary treatment with curcumin significantly reduced levels of ACE and AT1 receptor protein as determined by Western blot assay, coincident with less locally-expressed ACE and AT1 receptor in myocardium and coronary vessels as identified by immunohistochemistry. Along with this inhibition, curcumin significantly increased protein level of AT2 receptor and its expression compared with the control. As evidenced by less collagen deposition in fibrotic myocardium, curcumin also reduced the extent of collagen-rich scar and increased mass of viable myocardium detected by Masson׳s trichrome staining. Echocardiography showed that the wall thickness of the infarcted anterior septum in the curcumin group was significantly greater than that in the control group. Cardiac contractile function was improved in the curcumin treated animals as measured by fraction shortening and ejection fraction. In cultured cardiac muscle cells, curcumin inhibited oxidant-induced AT1 receptor expression and promoted cell survival. These results suggest that curcumin attenuates maladaptive cardiac repair and enhances cardiac function, primarily mediated by a dual ACE-inhibition and AT1 receptor antagonism after myocardial infarction.

Structural contributions to fibrillatory rotors in a patient-derived computational model of the atria.

The aim of this study was to investigate structural contributions to the maintenance of rotors in human atrial fibrillation (AF) and possible mechanisms of termination. A three-dimensional human biatrial finite element model based on patient-derived computed tomography and arrhythmia observed at electrophysiology study was used to study AF. With normal physiological electrical conductivity and effective refractory periods (ERPs), wave break failed to sustain reentrant activity or electrical rotors. With depressed excitability, decreased conduction anisotropy, and shorter ERP characteristic of AF, reentrant rotors were readily maintained. Rotors were transiently or permanently trapped by fibre discontinuities on the lateral wall of the right atrium near the tricuspid valve orifice and adjacent to the crista terminalis, both known sites of right atrial arrhythmias. Modelling inexcitable regions near the rotor tip to simulate fibrosis anchored the rotors, converting the arrhythmia to macro-reentry. Accordingly, increasing the spatial core of inexcitable tissue decreased the frequency of rotation, widened the excitable gap, and enabled an external wave to impinge on the rotor core and displace the source. These model findings highlight the importance of structural features in rotor dynamics and suggest that regions of fibrosis may anchor fibrillatory rotors. Increasing extent of fibrosis and scar may eventually convert fibrillation to excitable gap reentry. Such macro-reentry can then be eliminated by extending the obstacle or by external stimuli that penetrate the excitable gap.

I-123 mIBG and Tc-99m myocardial SPECT imaging to predict inducibility of ventricular arrhythmia on electrophysiology testing: A retrospective analysis

ObjectivesThe purpose of this study is to assess mIBG uptake in scar border zone and its relation with ventricular arrhythmia (VA) inducibility on electrophysiology (EP) testing using I-123 mIBG SPECT and resting Tc-99m SPECT myocardial perfusion imaging (MPI). MethodsForty-seven patients from a previous clinical trial were retrospectively analyzed. These patients underwent I-123 mIBG and resting Tc-99m tetrofosmin SPECT, and EP testing. Twenty-eight patients were positive (EP+) and 19 patients were negative (EP−) for inducibility of sustained (>30 seconds) VA on EP testing. MPI scar extent, border zone extent, and mIBG uptake in border zone were used to predict VA inducibility on EP testing, respectively. ResultsThere was no significant difference in scar extent between the EP+ and EP− groups. The EP+ group had significantly larger border zone and lower mIBG uptake ratio in the border zone than the EP− group. Receiver operating characteristic (ROC) curve analysis showed that the prediction accuracy for border zone extent (area under ROC = 0.75) was better than scar extent (area under ROC = 0.66). The prediction accuracy was further improved (area under ROC = 0.78), when assessing mIBG uptake in the border zone. ConclusionA new tool has been developed to measure scar and border zone and to assess mIBG uptake in scar and border zone from combined I-123 MIBG SPECT and resting Tc-99m SPECT MPI. The mIBG uptake in the border zone predicted VA inducibility on EP testing with a promising accuracy.

TCT-290 Assessment Of Myocardial Viability After Acute Myocardial Infarction: A Head-To-Head Comparison Of The Perfusable Tissue Index By PET And Delayed Contrast-Enhanced CMR

Introduction: Early recognition of viable myocardium is of great clinical importance after acute myocardial infarction (AMI). Delayed contrast-enhanced magnetic resonance imaging (DCE-CMR) has been validated extensively for the detection of viability. An alternative method for detecting viability is the perfusable tissue index (PTI), a positron emission tomography (PET) derived parameter, which is inversely related to the extent of myocardial scar (nonperfusable tissue). Aims: To investigate the predictive value of PTI on recovery of LV function after percutaneous coronary intervention (PCI) for AMI. Methods: Twenty-six patients with AMI successfully treated by PCI were included. Subjects were examined one week and three months after AMI with [15O]H2O PET and DCE-CMR to assess PTI, regional function and scar. Viability was defined as recovery of systolic wall thickening (SWT) ≥ 3.0 mm at follow-up. Results: A total of 396 segments were available for serial analysis. At baseline, 166 segments were dysfunct...

Evaluation of left ventricle diastolic dysfunction in ischemic heart disease by CMR: Correlation with echocardiography and myocardial scarring

ObjectiveTo detect the value of cardiac MR imaging in assessment of left ventricle diastolic function in patients with ischemic heart disease compared to echocardiography and to correlate the degree of dysfunction to the extent of myocardial scarring. Patients and methodsWe examined 40 patients with known coronary artery disease. Mean patient’s age was 48±10. All patients were subjected to 2D echocardiography and CMR including transmitral flow and left atrial planimetry. The degree of diastolic dysfunction was detected and correlated with the echocardiographic results and the extent of myocardial scarring. ResultsOn CMR, 35% of the cases had grade I diastolic dysfunction, 35% showed grade II, 15% had grade III while 15% showed normal diastolic function. CMR showed 94.12% sensitivity, 100% specificity and 95% accuracy. Excellent agreement with echocardiography was detected (Kappa coefficient 0.931). There was a significant correlation between the degree of diastolic dysfunction and the extent of myocardial scarring with Spearman’s correlation coefficient of 0.492 and p=0.028. ConclusionCMR has comparative results to echocardiography in assessment of diastolic dysfunction. We found a significant correlation between the degree of diastolic dysfunction and the extent of myocardial scarring.

High sensitivity of late gadolinium enhancement for predicting microscopic myocardial scarring in biopsied specimens in hypertrophic cardiomyopathy.

BackgroundMyocardial scarring can be assessed by cardiac magnetic resonance imaging with late gadolinium enhancement and by endomyocardial biopsy. However, accuracy of late gadolinium enhancement for predicting microscopic myocardial scarring in biopsied specimens remains unknown in hypertrophic cardiomyopathy. We investigated whether late gadolinium enhancement in the whole heart reflects microscopic myocardial scarring in the small biopsied specimens in hypertrophic cardiomyopathy.Methods and ResultsTwenty-one consecutive patients with hypertrophic cardiomyopathy who were examined both by cardiac magnetic resonance imaging and by endomyocardial biopsy were retrospectively studied. The right interventricular septum was the target site for endomyocardial biopsy in all patients. Late gadolinium enhancement in the ventricular septum had an excellent sensitivity (100%) with a low specificity (40%) for predicting microscopic myocardial scarring in biopsied specimens. The sensitivity of late gadolinium enhancement in the whole heart remained 100% with a specificity of 27% for predicting microscopic myocardial scarring in biopsied specimens. Quantitative assessments of fibrosis revealed that the extent of late gadolinium enhancement in the whole heart was the only independent variable related to the microscopic collagen fraction in biopsied specimens (β = 0.59, 95% confident interval: 0.15 – 1.0, p = 0.012).ConclusionsAlthough there was a compromise in the specificity, the sensitivity of late gadolinium enhancement was excellent for prediction of microscopic myocardial scarring in hypertrophic cardiomyopathy. Moreover, the severity of late gadolinium enhancement was independently associated with the quantitative collagen fraction in biopsied specimens in hypertrophic cardiomyopathy. These findings indicate that late gadolinium enhancement can reflect both the presence and the extent of microscopic myocardial scarring in the small biopsied specimens in hypertrophic cardiomyopathy.

Left ventricular strain and its pattern estimated from cine CMR and validation with DENSE

Measurement of local strain provides insight into the biomechanical significance of viable myocardium. We attempted to estimate myocardial strain from cine cardiovascular magnetic resonance (CMR) images by using a b-spline deformable image registration method. Three healthy volunteers and 41 patients with either recent or chronic myocardial infarction (MI) were studied at 1.5 Tesla with both cine and DENSE CMR. Regional circumferential and radial left ventricular strains were estimated from cine and DENSE acquisitions. In all healthy volunteers, there was no difference for peak circumferential strain (− 0.18 ± 0.04 versus − 0.18 ± 0.03, p = 0.76) between cine and DENSE CMR, however peak radial strain was overestimated from cine (0.84 ± 0.37 versus 0.49 ± 0.2, p < 0.01). In the patient study, the peak strain patterns predicted by cine were similar to the patterns from DENSE, including the strain evolution related to recovery time and strain patterns related to MI scar extent. Furthermore, cine-derived strain disclosed different strain patterns in MI and non-MI regions, and regions with transmural and non-transmural MI as DENSE. Although there were large variations with radial strain measurements from cine CMR images, useful circumferential strain information can be obtained from routine clinical CMR imaging. Cine strain analysis has potential to improve the diagnostic yield from routine CMR imaging in clinical practice.

Combined identification of septal flash and absence of myocardial scar by cardiac magnetic resonance imaging improves prediction of response to cardiac resynchronization therapy

Septal flash (SF) describes early inward motion of the ventricular septum in patients with left bundle branch block (LBBB), and correction corresponds to increased response to cardiac resynchronization therapy (CRT). SF has traditionally been assessed by echocardiography. We sought to determine if cardiac magnetic resonance (CMR) imaging could identify SF and if the additional assessment of scar would improve the ability of CMR to predict CRT response. Fifty-two patients with LBBB and heart failure underwent prospective CMR scanning prior to CRT implantation. The presence of SF was assessed visually and by using endocardial contour-tracking software. Presence and extent of myocardial scar was assessed by delayed enhancement imaging during CMR. The association between SF, scar and reverse remodelling (RR) at 6 months was explored. RR rate to CRT at 6 months was 52%. CMR-derived SF was identified in 24 (46%) patients. RR was seen in more patients with SF than those without (88% vs 21%; P < 0.001). The absence of scar combined with the presence of SF had 96% specificity for predicting RR. In a multivariate regression model, the presence of SF was the only independent predictor of RR. SF can be assessed by CMR and predicts increased response to CRT. The additional value of CMR is the assessment of scar. The presence of SF with no scar is a highly specific predictor of CRT response.

Atrial structure and function 5 years after successful ablation for persistent atrial fibrillation: an MRI study.

The atrial outcome after extensive ablation is unknown. We sought to quantify atrial structure and function years after successful ablation for persistent atrial fibrillation (PsAF). We studied after 80 ± 15 months 26 patients (54 ± 8 years, 1 woman) with PsAF successfully treated by ablation (2.2 ± 0.7 stepwise approach procedures, cumulative RF duration 126 ± 37 minutes). At follow-up atrial scar burden and atrial outflows were quantified using delayed-enhanced and velocity-encoded MRI, respectively. Cine imaging was used to quantify atrial conduit function (CF), active emptying fraction (AEF), expansion index (EI), and the inter-appendage mechanical activation delay. Patients underwent exercise testing at baseline and follow-up. LA and RA scar extent were 29 ± 6 and 4.3 ± 2.8%, respectively. LA and RA AEF were 10.0 ± 5.3 and 30 ± 8%. Mean inter-appendage delay was 83 ± 47 ms [42-217]. Complete LAA isolation was found in 3 patients. A wave was absent in 9/26 patients. LA scar extent related to the number of procedures (R = 0.58, P = 0.002) and total RF duration (R = 0.56, P = 0.003). Among follow-up characteristics, LA scar extent related to LAAEF (R = -0.73, P < 0.0001), LAEI (R = -0.64, P = 0.0003), A-wave peak (R = -0.72, P < 0.0001), and inter-appendage mechanical delay (R = 0.47, P = 0.02). At multivariable analysis, LA scar extent was independently related to LAAEF and LAEI. LAAEF and LA scar extent correlated with exercise capacity at follow-up (R = 0.44, P = 0.02, and R = -0.40; P = 0.04). LA contractility and compliance are markedly impaired years after successful PsAF ablation. LA dysfunction is closely related to scar burden.

Left ventricular function after recanalization of chronic total occlusion

Dear Editors, We read with great interest the article by Erdogan et al. that was recently published in Clinics (1). In this study, the authors evaluated the role of novel echocardiographic techniques in detecting left ventricular functional recovery after successful percutaneous coronary intervention to treat chronic total occlusion. Their study highlights the benefits of restoring blood flow in symptomatic patients and in patients with detectable ischemia in the territory of the occluded vessel. Although the authors did a great job of providing a broad review of echocardiographic data obtained from a considerable number of patients, there are certain missing points that we wish to emphasize. The authors concluded that the improvements in the strain parameters were more significant in patients with an ejection fraction ≥50% and less significant in patients with diabetes. However, they did not use a multivariate regression analysis to adjust for other potential confounders. If they had performed a regression analysis, the authors would have provided more useful information about the impact of percutaneous coronary intervention on different groups. Without an accurate statistical analysis, it is not possible to draw conclusions about the benefits of this treatment in subgroups such as diabetics or patients with a higher ejection fraction. In previous studies, the duration of the occlusion, collateral circulation, and previous myocardial infarction were found to be predictors of the restoration of systolic function after percutaneous intervention (2-5). None of these parameters was evaluated in this research. In a recent study, the influence of the recanalization of chronic total occlusion on left ventricular function was shown using three-dimensional echocardiography. In that study, left ventricular function improved in patients with rich collateral circulation, but no significant change was found in patients with a previous myocardial infarction. In another study, the recovery of left ventricular function was associated with the transmural extent of the myocardial scar, suggesting the impact of previous infarction (6). Given the heterogeneity of the occluded vessels in the study by Erdogan et al., it would have been valuable to provide additional regional wall motion analyses. In a study by Ermis et al., coronary intervention had a positive impact on both global and regional left ventricular function in patients with chronic coronary artery occlusion (7). In another study, which used magnetic resonance imaging, early and late improvements in regional myocardial function were observed in the territory of the occlusion (6). In conclusion, Erdogan et al. demonstrated the benefits of revascularization for left ventricular function in chronic total occlusion. However, a more detailed history of the patients, additional regional wall motion analyses, and a multivariate regression model would have provided valuable information about selecting appropriate patients for this procedure.