Patterns Of Myocardial Fibrosis Research Articles

Subclinical myocardial fibrosis is almost ubiquitous in the hearts of older British persons: 'MyoFit46' cardiovascular sub-study of the NSHD

Abstract Background Unprecedented numbers are now surviving to older age, but little is known about the burden or pattern of myocardial fibrosis in the asymptomatic elderly population. Previous 1.5 Tesla (T) cardiovascular magnetic resonance (CMR) studies found a prevalence of unexpected infarct-pattern late gadolinium enhancement (LGE) of 17-20% above 75 years but less is known about non-infarct pattern scar in this group. We investigated the prevalence, patterns, and clinical predictors of left ventricular (LV) scar in a large asymptomatic older age cohort. Methods CMR with a single 3T magnet was performed on participants all born in the same week in March 1946, as part of the longest running continued surveillance birth cohort: the National Survey of Health and Development. LV short-axis stack LGE imaging was performed using a free-breathing motion-corrected balanced steady-state free precession sequence with phase-sensitive inversion-recovery. Two blinded observers independently recorded the prevalence, extent, and pattern of LGE per participant. Logistic regression was used to study the association between clinicodemographic parameters and LGE. Results 460 participants were prospectively recruited of which 406 completed CMR with LGE imaging (77.8 ± 0.1 years, 44% male). 341 (84%) demonstrated LGE affecting a mean of 2.1±1.2 myocardial segments per participant (Figure 1). The commonest pattern of LGE was inferior right ventricular insertion point (RVIP), observed in 66.9%. Other patterns included (Figure 2): Linear mid-wall (19.6%) of which 38% were located in the inferior/lateral walls; subepicardial (12.1%); subendocardial infarct-pattern (8.8%); patchy/diffuse (1.6%); embolic LGE (0.6%). Sub-analysis was performed comparing those without significant unexpected fibrosis (LGE–) vs those with focal fibrosis (LGE+, excluding RVIP and those participants with a known history of prior myocardial infarction). LGE+ participants were more likely to be female (71.7% vs 49.1%, p<0.001) or diabetic (11.3% vs 5.1%, p=0.05), had a higher body surface area (BSA, 1.9 vs 1.8 m2, p<0.001), weight (80.1 vs 72.8 kg, p<0.001), LV indexed end systolic volume (24.2 vs 20.4 ml/m2, p=0.001) and LV indexed mass (59.2 vs 55.4 g/m2, p<0.001), and a lower LV ejection fraction (67.9 vs 71.8%, p<0.001) In multivariable logistic regression: BSA, LV indexed mass, LV ejection fraction and diabetic status were independently associated with LGE+ status (odds ratios [95% confidence intervals]: 9.4 [0.7–3.8]; 1.0 [0.01–0.05]; 0.9 [-0.08--0.02]; and 2.5 [0.03–1.7] respectively, p<0.05). Conclusion Advanced PSIR MOCO LGE imaging at 3T reveals that the majority (84%) of asymptomatic British persons above the age of 75 harbour unexpected ‘subclinical’ focal fibrosis, with a substantial proportion of these scars consistent with probable historical myocarditis events. Further work will now explore the life-course determinants of this scar burden in the older age human heart.

Apical Sparing of Longitudinal Strain as a Specific Pattern of Myocardial Fibrosis in Patients with Severe Left Ventricular Hypertrophy: A Comparison between Deformation Imaging and Histological Findings.

Objectives: This study aimed to investigate the correlation between apical sparing of longitudinal strain (LS), as measured by speckle-tracking echocardiography (STE), and the histological presence of myocardial fibrosis (MF), in patients with hypertrophic obstructive cardiomyopathy (HOCM). Methods: Twenty-seven HOCM patients who underwent elective Morrow procedures +/- aortic valve replacement (AVR) were included. All patients had standard echocardiography, with STE pre- and post-operatively. Intraoperative probes of the interventricular septum were sent for histological analysis. Correlation of different regional LS patterns with the histological findings of MF and with clinical outcome were analyzed. In addition, a logistic regression and ROC analysis were performed. Results: All patients underwent the Morrow procedure for HOCM, with 33.3% also undergoing AVR. A total of 74.1% showed evidence of MF in the histological analysis. Patients with MF had significantly lower GLS than patients without MF (-12.7 ± 2.7% vs. -23.0 ± 5.7%, p < 0.001). The LS in patients with MF was significantly lower at the basal regions of the LV segments and increased significantly towards the apex as compared to the patients without MF (mean basal-strain %: -10.6 ± 2.6 vs. -17.3 ± 4.6, p < 0.001; mean apical strain %: -21.8 ± 4.8 vs. -16.7 ± 5.6, p = 0.032). In the logistic regression, only the GLS remained as an independent predictor of MF with an Odds ratio of 1.07 (95%-CI: 1.05-1.09, p < 0.001). Conclusions: Our study highlights the significant correlation between GLS and MF in HOCM patients. These findings contribute to the growing understanding of MF in HOCM and may inform future approaches to patient management and risk stratification.

The natural history of CVB3 myocarditis in C57BL/6J mice: an extended in-depth characterization

Background and aimsViral infections are the leading cause of myocarditis. Besides acute cardiac complications, late-stage sequelae such as myocardial fibrosis may develop, importantly impacting the prognosis. Coxsackievirus B3 (CVB)-induced myocarditis in mice is the most commonly used translational model to study viral myocarditis and has provided the majority of our current understanding of the disease pathophysiology. Nevertheless, the late stages of disease, encompassing fibrogenesis and arrhythmogenesis, have been underappreciated in viral myocarditis research to date. The present study investigated the natural history of CVB-induced myocarditis in C57BL/6J mice, expanding the focus beyond the acute phase of disease. In addition, we studied the impact of sex and inoculation dose on the disease course. Methods and resultsC57BL/6J mice (12 weeks old; n=154) received a single intraperitoneal injection with CVB to induce viral myocarditis, or vehicle (PBS) as control. Male mice (n=92) were injected with 5 × 105 (regular dose) (RD) or 5 × 106 (high dose) (HD) plaque-forming units of CVB, whereas female mice received the RD only. Animals were sacrificed 1, 2, 4, 8, and 11 weeks after CVB or PBS injection. Virally inoculated mice developed viral disease with a temporary decline in general condition and weight loss, which was less pronounced in female animals (P<.001). In male CVB mice, premature mortality occurred between days 8 and 23 after inoculation (RD: 21%, HD: 20%), whereas all female animals survived. Over the course of disease, cardiac inflammation progressively subsided, with faster resolution in female mice. There were no substantial group differences in the composition of the inflammatory cell infiltrates: predominance of cytotoxic T cells at day 7 and 14, and a switch from arginase1-reactive macrophages to iNOS-reactive macrophages from day 7 to 14 were the main findings. There was concomitant development and maturation of different patterns of myocardial fibrosis, with enhanced fibrogenesis in male mice. Virus was almost completely cleared from the heart by day 14. Serum biomarkers of cardiac damage and cardiac expression of remodeling genes were temporarily elevated during the acute phase of disease. Cardiac CTGF gene upregulation was less prolonged in female CVB animals. In vivo electrophysiology studies at weeks 8 and 11 demonstrated that under baseline conditions (i.e. in the absence of proarrhythmogenic drugs), ventricular arrhythmias could only be induced in CVB animals. The cumulative arrhythmia burden throughout the entire stimulation protocol was not significantly different between CVB and control groups. ConclusionCVB inoculation in C57BL/6J mice represents a model of acute self-limiting viral myocarditis, with progression to different patterns of myocardial fibrosis. Sex, but not inoculation dose, seems to modulate the course of disease.

Analysis of genetic variant associated with heart failure mortality implicates thymic stromal lymphopoietin as mediator of strain-induced myocardial fibroblast-mast cell crosstalk and fibrosis.

Heart failure (HF) is a leading cause of death and disability globally. Heritable factors and the extent and pattern of myocardial fibrosis are important determinants of outcomes in patients with HF. In a genome-wide association study of mortality in HF, we recently identified a genetic polymorphism on chromosome 5q22 associated with HF mortality. Here, we sought to study the mechanisms by which this variant may influence myocardial disease processes. We find that the risk allele is located in an enhancer motif upstream of the TSLP gene (encoding thymic stromal lymphopoietin), conferring increased binding of the transcription factor nescient helix-loop helix 1 (NHLH1) and increased TSLP expression in human heart. Further, we find that increased strain of primary human myocardial fibroblasts results in increased TSLP expression and that the TSLP receptor is expressed in myocardial mast cells in human single nuclei RNA sequence data. Finally, we show that TSLP overexpression induces increased transforming growth factor β expression in myocardial mast cells and tissue fibrosis. Collectively, our findings based on follow-up of a human genetic finding implicate a novel pathway in myocardial tissue homeostasis and remodeling.

Abstract P2042: Linking Extracellular Matrix Stiffness With Cardiomyocyte Structure And Function

The composition and organization of the extracellular matrix (ECM) provides cues to myocardial cells that direct normal function and responses to stress. However, little is known about how exactly a change in environmental tension leads to alterations in cardiomyocyte cell size and contractile force. Collagen I comprises the majority of cardiac ECM where it is crosslinked and matured by the lysyl oxidase (LOX) family of enzymes that includes LOX and LOX-like (LOXL) proteins. LOX and LOXLs are frequently upregulated in the heart after injury, and their inhibition has been shown to alleviate increases in tissue stiffness. Cardiac injury models result in activation and recruitment of many cells that secrete growth factors and modify the ECM, which makes it difficult to address specifically how cardiomyocytes are responding to changes in matrix tension alone. Therefore, we utilized LOX or LOXL overexpression as a tool to stiffen the ECM in the absence of pathophysiologic injury and paracrine factors. Transgenic overexpression of LOX increases myocardial stiffness and results in mild cardiac dysfunction by 9 months of age. While younger adult mice do not display a phenotype at baseline, they have an exaggerated response to pressure overload hypertrophy. In a different set of experiments, adeno-associated viruses (AAV9) for LOXL1, -2, or -3 were administered to mouse pups via cardiac injection at perinatal day 7. By 12 weeks of age, LOXL1 overexpression leads to cardiac hypertrophy with preserved ejection fraction, while increased LOXL2 or LOXL3 results in decreased cardiac function (each with differential patterns of myocardial fibrosis). Ongoing studies are assessing how these functional changes are associated with alterations in tissue stiffness and cardiomyocyte behavior. Determining how cardiomyocytes respond to alterations in the physical properties of the ECM will improve our understanding of the etiology of progressive cardiomyopathies and fibrosis.

Evaluation of diastolic dysfunction in children with hypertrophic cardiomyopathy and its relationship with development of myocardial fibrosis

BackgroundPatients with hypertrophic cardiomyopathy may develop symptoms of shortness of breathing due to diastolic dysfunction which is not related to the severity of left ventricular outflow tract obstruction. As these patients usually develop a non-ischemic pattern of myocardial fibrosis, this may represent a mechanism for increased myocardial stiffness leading to impaired diastolic filling. The study aimed to determine the prevalence of myocardial fibrosis assessed by magnetic resonance imaging in children with hypertrophic cardiomyopathy and to evaluate its relationship with echocardiographic parameters including left ventricle diastolic dysfunction and to find echocardiographic indices which correlates with myocardial fibrosis as detected by cardiac magnetic resonance. A cross-sectional study was done for data of 50 children with hypertrophic cardiomyopathy from July 2018 to July 2021, patients were divided into (group 1) having myocardial fibrosis and (group 2) with no myocardial fibrosis, and results of echocardiographic parameters were compared between the two groups.ResultsResults showed strong relationship between presence of myocardial fibrosis and each of the following: Interventricular septum thickness, lower lateral and septal early diastolic tissue velocities (E′), E/E′ ratio, presence of left ventricular out flow tract obstruction and the grade of diastolic dysfunction.ConclusionsThe trans-mitral lateral and septal E/E′ (early mitral inflow to early diastolic mitral annular velocity ratio) allows early detection of left ventricular diastolic dysfunction in children with hypertrophic cardiomyopathy. The prevalence of diastolic dysfunction is higher in obstructive hypertrophic cardiomyopathy. The diastolic dysfunction severity is higher in patients with myocardial fibrosis.

ASSOCIATION OF PATTERN OF MYOCARDIAL FIBROSIS WITH ADVANCED AND EARLY HEART FAILURE

Background: The cardiomyopathies are defined as “hetrogenous group of diseases of the myocardium associated with mechanical or electrical dysfunction that usually (but not invariably) exhibit inappropriate ventricular hypertrophy or dilatation and are due to variety of causes that frequently are genetic. They usually present clinically with heart failure.&#x0D; Methods: The cross sectional hospital based study was conducted in the Department of Radiodiagnosis in patients with heart failure with LVEF (Left Ventricular Ejection Fraction) of &lt;45% without RWM(Regional Wall Motion) abnormality on echocardiography evaluated in department of cardiology at IGMC, Shimla over a period of one year.&#x0D; Results: The myocardial fibrosis was seen in the 10 (47.62%) patients of advanced heart failure and 6(35.29%) patients of early heart failure with insignificant P value of 0.52 and odd ratio of 1.64.The subendocardial myocardial fibrosis in coronary territory was seen in the 3(14.29%) patients of advanced heart failure and 2(11.76%) patients of early heart failure with insignificant P value of 1.00 and odd ratio of 1.24.&#x0D; Conclusion: The association of pattern of myocardial fibrosis with advanced and early heart failure was found statistically Insignificants&#x0D; Keywords: MRI, Myocardial, Heart failure.

Segmental longitudinal strain as the most accurate predictor of the patchy pattern late gadolinium enhancement in hypertrophic cardiomyopathy

BackgroundThe prognostic value of myocardial fibrosis in patients with hypertrophic cardiomyopathy (HCM) has been well-established. Although cardiac magnetic resonance (CMR) is the method of choice in its revealing as the presence of late gadolinium enhancement (LGE), this technique still has limited availability in daily clinical practice. Two-dimensional speckle tracking echocardiography (2D STE) seems to be helpful in verification which HCM patient has the highest probability of LGE presence and hence needs to be qualified to CMR. While the majority of HCM patients have a patchy pattern of myocardial fibrosis, the aim of this study was to evaluate whether segmental rather than global longitudinal strain is more accurate in the identification of the presence of LGE. MethodsForty-six HCM patients had transthoracic echocardiography and CMR imaging performed. Each patient had global longitudinal strain and rotation parameters calculated, as well as segmental analyses for wall thickness, longitudinal strain, and LGE presence based on 736 segments of the left ventricle (LV). The presence of LGE in CMR was confirmed on a per-segment basis, which was similar to LV segments in the echocardiographic examination. All patients were divided into two groups according to the CMR result: LGE (+) and LGE (−). ResultsReceiver-operating characteristic analyses identified peak global longitudinal strain and peak twisting velocity with the cut-off values −14.4% and 116°/s respectively as the accurate predictors of LGE presence in CMR, whereas segmental longitudinal strain of −12.5% cut-off value had the highest area under the curve value (87.4%, confidence interval 84.5–90.3%), with 93.7% sensitivity, 86.5% negative predictive value, and 55% specificity. ConclusionsSegmental longitudinal strain with the cut-off value of −12.5% has the highest discriminatory power for LGE presence and seems to be more adequate than global speckle tracking parameters in identification of HCM patients with strong indications for CMR for more accurate risk stratification.

Heart failure with improved ejection fraction in advanced heart failure clinic

Abstract Objectives The aims of the study were: (1) to determine the pattern of myocardial fibrosis assessed by delayed gadolinium enhancement cardiac MRI (DGE-CMRI) in patients with heart failure improved ejection fraction (HF-iEF) in an advanced heat failure clinic; and (2) to examine the dosage of beta-blocker and angiotensin converting enzyme inhibitor/ angiotensin receptor blockage/angiotensin neprilysin inhibitor (ACE-I/ARB/ARNI) in those patients. Methods HF-iEF was defined as patients with LVEF &amp;gt;40% with previously documented LVEF &amp;lt;35% at baseline. Results Among 312 consecutive patients with HF-rEF who were referred for an advanced HF clinic, 18% (56 patients) had HF-iEF within 12 months after referral. Of these, 84% (47 patients) had non-ischemic cardiomyopathy (CM); complete data on MRI for analysis were available for 25 of these patients (62%). Myocardial scar was found in 52% of patients with nonischemic CM (13 of 25). All patients with nonischemic CM had the myocardial scar of less than 10% of the total LV volume. Mid-wall DGE of the interventricular septum was the most common scar pattern. Among patients with HF-iEF, 36% (20 patients) were referred for heart transplant. Two patients with peripartum related and nonischemic etiologies were listed for heart transplant, and delisted 12 months after. No patient died during 1-year follow up. At 12 months, the mean LVEF change was +27±12%. Improvement of the LVEF to ≥50% occurred in 31 patients (55%). The percentage use of ACE-I/ARB/ARNI and beta-blocker was significantly increased, at 1-year-follow-up. Fourteen percent and 48% of patients achieved target dose of ACE-I/ARB/ARNI and beta-blocker, respectively. There was no significant association between myocardial scar pattern or extent and dosage of medical titration. Conclusions HF-iEF was present in 18% of patients with HF-rEF after 1-year follow-up in advanced heart failure clinic. Mid-wall DGE of the interventricular septum was the most common scar pattern in nonischemic HF-iEF. None of patients with nonischemic HF-iEF had myocardial scar &amp;gt;10% of the total LV volume. Improvement of LVEF to ≥50% occurred in approximately half of the study patients, and led to delisting patients from heart transplant waiting list. The majority of patients had recovery of the LVEF when the target dose of beta-blocker or ACE-I/ARB/ARNI had not been achieved during medical up-titration. Funding Acknowledgement Type of funding source: None

Cardiac magnetic resonance imaging in Chagas’ disease: a parallel with electrophysiologic studies

Chagas' disease (CD), caused by the parasite Trypanosoma cruzi, is the leading cause of cardiac disability from infectious diseases in Central and South America. The disease progresses through an extended, asymptomatic form characterized by latency without clinical manifestations into a symptomatic form with cardiac and gastro-intestinal manifestations. In the terminal phase, chronic Chagas' myocarditis results in extensive myocardial fibrosis, chamber enlargement with aneurysms and ventricular tachycardia (VT). Cardiac magnetic resonance imaging (CMR) has proven useful in characterizing myocardial fibrosis (MF). Sub-epicardial and mid-wall fibrosis are less common patterns of MF in CHD than transmural scar, which resembles myocardial infarction. Commonly involved areas of MF include the left ventricular apex and basal infero-lateral wall, suggesting a role for watershed ischemia in the pathophysiology of MF. Electrophysiology studies have helped refine the relationship between MF and VT in this setting. This article reviews the patterns of MF in CHD and correlate these patterns with electrogram patterns to predict risk of ventricular arrhythmias and sudden death.

Characterization of interstitial diffuse fibrosis patterns using texture analysis of myocardial native T1 mapping.

BackgroundThe pattern of myocardial fibrosis differs significantly between different cardiomyopathies. Fibrosis in hypertrophic cardiomyopathy (HCM) is characteristically as patchy and regional but in dilated cardiomyopathy (DCM) as diffuse and global. We sought to investigate if texture analyses on myocardial native T1 mapping can differentiate between fibrosis patterns in patients with HCM and DCM.MethodsWe prospectively acquired native myocardial T1 mapping images for 321 subjects (55±15 years, 70% male): 65 control, 116 HCM, and 140 DCM patients. To quantify different fibrosis patterns, four sets of texture descriptors were used to extract 152 texture features from native T1 maps. Seven features were sequentially selected to identify HCM- and DCM-specific patterns in 70% of data (training dataset). Pattern reproducibility and generalizability were tested on the rest of data (testing dataset) using support vector machines (SVM) and regression models.ResultsPattern-derived texture features were capable to identify subjects in HCM, DCM, and controls cohorts with 202/237(85.2%) accuracy of all subjects in the training dataset using 10-fold cross-validation on SVM (AUC = 0.93, 0.93, and 0.93 for controls, HCM and DCM, respectively), while pattern-independent global native T1 mapping was poorly capable to identify those subjects with 121/237(51.1%) accuracy (AUC = 0.78, 0.51, and 0.74) (P<0.001 for all). The pattern-derived features were reproducible with excellent intra- and inter-observer reliability and generalizable on the testing dataset with 75/84(89.3%) accuracy.ConclusionTexture analysis of myocardial native T1 mapping can characterize fibrosis patterns in HCM and DCM patients and provides additional information beyond average native T1 values.

Myocardial fibrosis in athletes-Current perspective.

Several previous studies suggested that prolonged and extensive physical activity might lead to increased prevalence of myocardial fibrosis in athletes. The review summarizes these studies focusing on common patterns of myocardial fibrosis observed in athletes, their potential causes and significance. It also presents recent research on parametric imaging shedding new light on diffuse myocardial fibrosis in athletes. Finally, it reviews how these traditional and novel cardiac magnetic resonance (CMR) techniques can be incorporated in the diagnostic work up to differentiate athlete's heart from cardiomyopathies.

Myocardial Fibrosis and Prognosis in Heart Transplant Recipients.

Myocardial fibrosis is a well-described histopathologic feature in heart transplant recipients. Whether myocardial fibrosis in heart transplant recipients is independently associated with clinical outcomes is unclear. We sought to determine whether myocardial fibrosis on late gadolinium enhancement cardiovascular magnetic resonance imaging in heart transplant recipients was independently associated with all-cause death or major adverse cardiac outcomes in the long-term. Using a cohort of consecutive heart transplant recipients that had cardiovascular magnetic resonance imaging, we determined the prevalence and the patterns of myocardial fibrosis and analyzed associations between myocardial fibrosis and a composite end point of all-cause death or major adverse cardiac events: retransplantation, nonfatal myocardial infarction, coronary revascularization, and heart failure hospitalization. One hundred and fifty-two heart transplant recipients (age, 54±15 years; 29% women; 5.0±5.4 years after heart transplantation) were included. Myocardial fibrosis was present in 18% (37% infarct pattern, 41% noninfarct pattern, and 22% both). Its prevalence was positively associated with cardiac allograft vasculopathy grade. With a median follow-up of 2.6 years, myocardial fibrosis was independently associated with all-cause death or major adverse cardiac events (hazard ratio, 2.88; 95% CI, 1.59-5.23; P<0.001) after adjustment for cardiac allograft vasculopathy, history of rejection, time since transplantation, left ventricular ejection fraction, and indexed right ventricular end-diastolic volume. Every 1% increase in myocardial fibrosis was independently associated with a 6% higher hazard for all-cause death or major adverse cardiac events (hazard ratio, 1.06; 95% CI, 1.03-1.09; P<0.001). The addition of myocardial fibrosis variables to models with cardiac allograft vasculopathy, history of rejection, time since transplantation, left ventricular ejection fraction, and indexed right ventricular end-diastolic volume resulted in significant improvements in model fit, suggesting incremental prognostic value. In heart transplant recipients, myocardial fibrosis is seen on late gadolinium enhancement cardiovascular magnetic resonance imaging in 18%. Both the presence and the extent of myocardial fibrosis are independently associated with the long-term risk of all-cause death or major adverse cardiac events.

Healing Myocarditis from a Hypertrophied Heart with Multifocal Fibrosis Mimicking Cardiomyopathy

We report the case of an 18 year old man who unexpectedly died of healing myocarditis. His heart was hypertrophied with multifocal fibrosis which can be a common histological feature of primary and secondary cardiomyopathy as well as the healing phase of myocarditis. However, the pattern of myocardial fibrosis, inflammation with myonecrosis, sparing of the right ventricular myocardium, and cardiomyocytes features in the remaining areas of the heart were considered as the key elements in determining a diagnosis of myocarditis. This case illustrates that meticulous histologic examination and the analysis of the histologic findings in the hypertrophied heart with multifocal fibrosis can be helpful to make a correct diagnosis.

Prevalence and prognosis of ischaemic and non-ischaemic myocardial fibrosis in older adults.

Non-ischaemic cardiomyopathies (NICM) can cause heart failure and death. Cardiac magnetic resonance (CMR) detects myocardial scar/fibrosis associated with myocardial infarction (MI) and NICM with late gadolinium enhancement (LGE). The aim of this study was to determine the prevalence and prognosis of ischaemic and non-ischaemic myocardial fibrosis in a community-based sample of older adults. The ICELAND-MI cohort, a substudy of the Age, Gene/Environment Susceptibility Reykjavik (AGES-Reykjavik) study, provided a well-characterized population of 900 subjects after excluding subjects with pre-existing heart failure. Late gadolinium enhancement CMR divided subjects into four groups: MI (n = 211), major (n = 54) non-ischaemic fibrosis (well-established, classic patterns, associated with myocarditis, infiltrative cardiomyopathies, or pathological hypertrophy), minor (n = 238) non-ischaemic fibrosis (remaining localized patterns not meeting major criteria), and a no LGE (n = 397) reference group. The primary outcome was time to death or first heart failure hospitalization. During a median follow-up of 5.8 years, 192 composite events occurred (115 deaths and 77 hospitalizations for incident heart failure). After inverse probability weighting, major non-ischaemic fibrosis [hazard ratio (HR) 3.2, P < 0.001] remained independently associated with the primary endpoint, while MI (HR 1.4, P = 0.10) and minor non-ischaemic LGE (HR 1.2, P = 0.39) did not. Major non-ischaemic fibrosis was associated with a poorer outcome than MI (HR = 2.3, P = 0.001) in the adjusted analysis. Major non-ischaemic patterns of myocardial fibrosis portended worse prognosis than no fibrosis/scar in an older community-based cohort. Traditional risk factors largely accounted for the effect of MI and minor non-ischaemic LGE.

P3327The pattern of myocardial fibrosis detected by cardiovascular magnetic resonance imaging provides prognostic information in patients with idiopathic dilated cardiomyopathy

P3327The pattern of myocardial fibrosis detected by cardiovascular magnetic resonance imaging provides prognostic information in patients with idiopathic dilated cardiomyopathy

Comparison of echocardiography with tissue Doppler imaging and magnetic resonance imaging with delayed enhancement in the assessment of children with hypertrophic cardiomyopathy.

IntroductionIn children with hypertrophic cardiomyopathy (HCM) there often occurs a non-ischemic pattern of myocardial fibrosis, which could be the cause of impaired left ventricular (LV) diastolic function assessed by tissue Doppler imaging (TDI). The aim of the study was to determine the prevalence of myocardial fibrosis in children with HCM, and to evaluate its relationship with echocardiographic parameters including LV diastolic dysfunction.Material and methodsSixty-three children with HCM, mean age 12.2 ±4.5 years, underwent magnetic resonance imaging (MRI) and echocardiographic study from January 2010 to April 2014. The results of MRI, echocardiography, and TDI velocities were analyzed and compared between children with and without myocardial fibrosis. Moreover, correlations between the results of echocardiography and MRI were assessed.ResultsOur results showed a significant correlation between magnetic resonance and echocardiographic measurements of septal wall thickness, posterior wall thickness, LV mass and left atrial dimension. Children with myocardial fibrosis (60%) had a significantly thicker interventricular septum (21.3 vs. 1.8 mm; p < 0.0001) and larger left atrial dimension (36.7 vs. 27.8 mm; p = 0.0004) and volume index (42.0 vs. 26.6 ml/m²; p = 0.0011). Tissue Doppler imaging demonstrated significantly decreased lateral E’ (9.02 vs. 13.53 cm/s; p < 0.0001) and septal E′ (7.05 vs. 9.36 cm/s; p = 0.0082) velocities and a significantly increased transmitral lateral (10.34 vs. 6.68; p = 0.0091) and septal (13.1 vs. 9.8; p = 0.046) E/E′ ratio in children with myocardial fibrosis.ConclusionsMyocardial fibrosis in children with hypertrophic cardiomyopathy was associated with markers for disease severity such as larger septum thickness, enlargement of the left atrium as well as impairment of left ventricular diastolic function. Tissue Doppler imaging is a helpful tool to detect the presence of left ventricular diastolic dysfunction in children with hypertrophic cardiomyopathy and myocardial fibrosis.

Acute Reverse Remodelling After Transcatheter Aortic Valve Implantation: A Link Between Myocardial Fibrosis and Left Ventricular Mass Regression

BackgroundDespite the wealth of data showing the positive effects on cardiac reverse remodelling in the long-term, the immediate effects of transcatheter aortic valve implantation (TAVI) on the left ventricle are yet to be comprehensively described using cardiovascular magnetic resonance imaging. Also, the link between myocardial fibrosis and acute left ventricular (LV) mass regression is unknown. MethodsFifty-seven patients with severe aortic stenosis awaiting TAVI underwent paired cardiovascular magnetic resonance scans before and early after the procedure (4 [interquartile range, 3-5] days). LV mass, volume, and function were measured. Late gadolinium enhancement (LGE) imaging was performed to assess for the presence of and pattern of myocardial fibrosis. ResultsAfter the procedure, 53 (95%) patients experienced an immediate (10.1 ± 7.1%) reduction in indexed LV mass (LVMi) from 76 ± 15.5 to 68.4 ± 14.7 g/m2 (P < 0.001). Those with no LGE experienced the greatest LVMi regression (13.9 ± 7.1%) compared with those with a midwall/focal fibrosis pattern LGE (7.4 ± 5.8%) and infarct pattern LGE (7.2 ± 7.0%; P = 0.005). There was no overall change in LV ejection fraction (LVEF; 55.1 ± 12.1% to 55.5 ± 10.9%; P = 0.867), however a significant improvement in LVEF was seen in those with abnormal (< 55%; n = 24; 42%) baseline LVEF (43.2 ± 8.9 to 46.7 ± 10.5%; P = 0.027). Baseline LVMi (P = 0.005) and myocardial fibrosis (P < 0.001) were strong independent predictors of early LVMi regression. ConclusionsLV reverse remodelling occurs immediately after TAVI, with significant LV mass regression in the total population and an improvement in LVEF in those with preexisting LV impairment. Those without myocardial fibrosis at baseline experience greater LV mass regression than those with fibrosis.

Pseudo-infarction pattern in diffuse systemic sclerosis. Evaluation using cardiovascular magnetic resonance.

Diffuse systemic sclerosis (dSSc) is characterized by vascular lesions and fibrosis. Cardiac involvement, although silent, accounts for 36% of deaths. We hypothesized that cardiovascular magnetic resonance (CMR) can clarify the pathophysiology of Q waves in dSSc patients. 105 dSSc, aged 48±2years, with atypical symptoms and normal routine assessment, were evaluated by ECG and CMR using a 1.5 T system. Biventricular function was assessed by steady-state free-precession sequence (SSFP). To identify fibrosis, late gadolinium enhanced areas (LGE) were evaluated 15min after injection of 0.2mmol/kg gadolinium-DTPA and expressed as % of LV mass. Q waves in V1-V5 (Group A), II, III, AVF (Group B) and I, AVL, II, III, AVF, V1-V5 (Group C) were found in 25/105, 8/105 and 5/105 dSSc, respectively. In 25 dSSc with Q in V1-V6, patchy intramyocardial LGE was detected in 24/25 and involved 8±2% of LV mass. LGE involved the intraventricular septum (IVS) in 11/24 and the lateral wall (LAT) in 5/24 dSSc. Only in 1/25 dSSc, an anterior, transmural LGE, due to LAD occlusion, was identified. In 8 dSSc with Q in II, III, AVF, patchy intramyocardial LGE was detected in the inferior wall and involved 5±2% of LV mass. In 5 dSSc with Q in V1-V5, II, III, AVF, patchy intramyocardial LGE was detected in anterior and inferolateral wall and involved 9±2% of LV mass. CMR unveiled that the pattern of myocardial fibrosis in dSSc with Q waves is due to the systemic disease and not to CAD.

Concordant and Discordant Cardiac Magnetic Resonance Imaging Delayed Hyperenhancement Patterns in Patients with Ischemic and Non-Ischemic Cardiomyopathy.

Background and ObjectivesThe diagnosis of ischemic (ICM) and non-ischemic cardiomyopathy (NICM) is conventionally determined by the presence or absence of coronary artery disease (CAD) in the setting of a reduced left systolic function. However the presence of CAD may not always indicate that the actual left ventricular (LV) dysfunction mechanism is ischemia, as other non-ischemic etiologies can be responsible. We investigated patterns of myocardial fibrosis using delayed hyperenhancement (DHE) on cardiac magnetic resonance (CMR) in ICM and NICM.Subjects and MethodsPatients with systolic heart failure who underwent a CMR were prospectively analyzed. The heart failure diagnosis was based on the modified Framingham criteria and LVEF <35%. LV dysfunction was classified as ICM or NICM based on coronary anatomy.ResultsA total of 101 subjects were analyzed; 34 were classified as ICM and 67 as NICM. The DHE pattern was concordant with the conventional diagnosis in 27 (79.4%) of the patients with ICM and 62 (92.5%) of the patients with NCIM. A discordant NICM DHE pattern was present in 8.8% of patients with ICM, and an ICM pattern was detected 6.0% of the patients with NICM. Furthermore, 11.8% of the patients with ICM and 1.5% of those with NICM demonstrated a mixed pattern.ConclusionA subset of patients conventionally diagnosed with ICM or NICM based on coronary anatomy demonstrated a discordant or mixed DHE pattern. CMR-DHE imaging can be helpful to determine the etiology of heart failure in patients with persistent LV systolic dysfunction.