scholarly journals Relationship between myocardial edema and left ventricular wall thickness in acute myocardial ischemia: A Magnetic Resonance Imaging study

2014 ◽  
Vol 1 (2) ◽  
pp. 23
Author(s):  
Yoko Mikami ◽  
Andreas Kumar ◽  
Hassan Abdel-Aty ◽  
Matthias G. Friedrich

Purpose: We sought to assess the relationship between left ventricular regional end-diastolic myocardial wall thickness (EDWT) and myocardial edema defined using T2-weighted Cardiovascular Magnetic Resonance (CMR) after acute myocardial ischemia and reperfusion. Methods: T2-weighted and cine CMR images for 7 dogs at baseline, during coronary occlusion (mean 33 ± 4 minutes) and after reperfusion were studied. The EDWT was measured in segments with high signal intensity (SI) on T2-weighted images, adjacent segments and remote segments according to a 16-segment model. Results: The EDWT after reperfusion in segments with high SI on T2-weighted images was significantly increased compared to baseline (6.28 ± 1.06 mm and 5.51 ± 1.40 mm, p < 0.05), whereas EDWT after the reperfusion in adjacent and remote segments did not show significant difference compared to baseline (adjacent: 6.48 ± 1.55 mm and 6.38 ± 1.26 mm, p = N.S., remote: 6.41 ± 1.11mm and 6.42 ± 1.27mm, p = N.S.). The % increase in EDWT after reperfusion from baseline in segments with high SI on T2-weighted images was higher than those in adjacent and remote segments (19 ± 30%, 1.3 ± 15% and 1.5 ± 16%, respectively, p < 0.05). Conclusions: After a brief period of ischemia and reperfusion, edema as defined by high SI on T2-weighted CMR is related to an increase in EDWT. This increase however is too small to be clinically relevant to be used for the detection of acute myocardial injury. Edema imaging is more sensitive and is an essential part of the reliable assessment of acute ischemic myocardial injury.

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
T Keteepe-Arachi ◽  
A Malhotra ◽  
J Basu ◽  
G Parry-Williams ◽  
B Ensam ◽  
...  

Abstract Background Structural cardiac adaptations due to hypertension (HTN) present a diagnostic challenge when differentiating from hypertrophic cardiomyopathy (HCM), using traditional imaging techniques such as echocardiography (echo). Cardiac magnetic resonance imaging (CMR) offers reproducible anatomical, functional quantification and myocardial tissue characterisation which discriminates between hypertension and HCM. Purpose To identify hypertensive individuals with undiagnosed HCM using CMR imaging. Methods 100 consecutive hypertensive patients underwent CMR at a tertiary centre dedicated blood pressure clinic (55% male, mean age 51 years). In keeping with ESC guidelines, end diastolic wall thickness (EDWT) ≥15mm identified individuals within the “grey zone” between hypertension and with a potential HCM diagnosis. 19 individuals were referred on to the dedicated inherited cardiac conditions clinic for further evaluation. Four patients expressed a definitive LV phenotype and were diagnosed with HCM. CMR parameters were compared in three groups: Hypertensive (HTN), “grey zone” Hypertensive (GZH) and HCM. Results CMR demonstrated end diastolic wall thickness (EDWT) >11 mm in 50% of hypertensives. 73% of the referred patients were Afro-Caribbean (AC) and all 4 HCM patients were AC. All referrals demonstrated EDWTs ≥14mm, 9 (47%) demonstrated late gadolinium enhancement of which 3 (16%) had HCM. Three had asymmetrical septal hypertrophy – 2 were in the HCM cohort and one underwent endomyocardial biopsy confirming HTN. Left ventricular mass index (LVMI) was significantly higher in GZH compared to HTN (p<0.0001) and in HCM compared to HTN (p=0.0004). EDWT was significantly greater in GZH compared to HTN (p<0.0001) and in HCM compared to HTN (p=0.0002). There was no significant difference in these parameters between GZH and HCM. Table 1. P-values for CMR data in hypertensive (HTN), gray zone hypertensive (GZH) and hypertrophic cardiomyopathy (HCM) cohorts CMR Parameter HCM vs. HTN GZH vs. HTN GZH vs. HCM EDVI NS p=0.025 NS EDWT p=0.0002 p<0.0001 NS LVMI p=0.0004 p<0.0001 NS Conclusion This study reports a 4% prevalence of HCM among hypertensive patients - 20 x greater than in the general population - which would be left undiagnosed using echo alone. Screening hypertensive individuals with CMR is not routine but we advocate its use in these individuals especially in Afro Caribbeans and in those in the “grey zone”, to identify undiagnosed HCM, which has significant implications for lifestyle modification and family screening. Acknowledgement/Funding Cardiac Risk in the Young


Circulation ◽  
1995 ◽  
Vol 92 (12) ◽  
pp. 3549-3559 ◽  
Author(s):  
Tamás Simor ◽  
Wen-Jang Chu ◽  
Lynne Johnson ◽  
Andras Safranko ◽  
Mark Doyle ◽  
...  

Author(s):  
Fabian Strodka ◽  
Jana Logoteta ◽  
Roman Schuwerk ◽  
Mona Salehi Ravesh ◽  
Dominik Daniel Gabbert ◽  
...  

AbstractVentricular dysfunction is a well-known complication in single ventricle patients in Fontan circulation. As studies exclusively examining patients with a single left ventricle (SLV) are sparse, we assessed left ventricular (LV) function in SLV patients by using 2D-cardiovascular magnetic resonance (CMR) feature tracking (2D-CMR-FT) and 2D-speckle tracking echocardiography (2D-STE). 54 SLV patients (11.4, 3.1–38.1 years) and 35 age-matched controls (12.3, 6.3–25.8 years) were included. LV global longitudinal, circumferential and radial strain (GLS, GCS, GRS) and strain rate (GLSR, GCSR, GRSR) were measured using 2D-CMR-FT. LV volumes, ejection fraction (LVEF) and mass were determined from short axis images. 2D-STE was applied in patients to measure peak systolic GLS and GLSR. In a subgroup analysis, we compared double inlet left ventricle (DILV) with tricuspid atresia (TA) patients. The population consisted of 19 DILV patients, 24 TA patients and 11 patients with diverse diagnoses. 52 patients were in NYHA class I and 2 patients were in class II. Most SLV patients had a normal systolic function but median LVEF in patients was lower compared to controls (55.6% vs. 61.2%, p = 0.0001). 2D-CMR-FT demonstrated reduced GLS, GCS and GCSR values in patients compared to controls. LVEF correlated with GS values in patients (p < 0.05). There was no significant difference between GLS values from 2D-CMR-FT and 2D-STE in the patient group. LVEF, LV volumes, GS and GSR (from 2D-CMR-FT) were not significantly different between DILV and TA patients. Although most SLV patients had a preserved EF derived by CMR, our results suggest that, LV deformation and function may behave differently in SLV patients compared to healthy subjects.


Author(s):  
Shinya Ito ◽  
Akihiro Isotani ◽  
Kyohei Yamaji ◽  
Kenji Ando

Abstract Background  Löffler endocarditis is a condition characterized by cardiac infiltration of eosinophils. Cardiac magnetic resonance imaging (MRI) is a modality for the diagnosis of myocardial damage. Case summary  This is the case of a 77-year-old man with acute decompensated heart failure who was admitted. Transthoracic echocardiography showed preserved left ventricular (LV) systolic function along with LV thrombi attached to the septo-apical wall and the posterior wall, consistent with Löffler endocarditis. Cardiac MRI revealed obliteration of the LV apex and partial filling of the LV cavity, as well as near circumferential subendocardial late gadolinium enhancement (LGE) in the mid- and apical segments. T2-weighted images showed a near circumferential high-intensity area of the LV subendocardial muscle in the mid- and apical segments. High-dose corticosteroids and intravenous heparin were initiated, followed by maintenance warfarin therapy. At 18 months, follow-up cardiac MRI revealed the disappearance of the LV thrombi, and a reduction of LGE, as well as high-intensity areas in the T2-weighted images. Discussion  The high-intensity area of T2-weighted images indicate the presence of subendocardial oedema. Eosinophil-mediated heart damage evolves through three stages: (i) acute necrotic, (ii) thrombotic, and (iii) fibrotic stages. Since the deposition of toxic eosinophil granule proteins and eosinophil infiltration injured the endocardium, the first-line treatment for Löffler endocarditis is corticosteroid therapy. In this case, LGE in the subendocardium and the high-intensity area in the T2-weighted images were reduced at 18 months. High-intensity areas of T2-weighted images in the acute phase might indicate the possibility of therapeutic response to corticosteroid therapy.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Jose A Barrabes ◽  
Javier Inserte ◽  
Maribel Mirabet ◽  
Adoracion Quiroga ◽  
Victor Hernando ◽  
...  

Objective: Platelets activated during experimental acute myocardial infarction (AMI) contribute to myocardial injury. We aimed to investigate whether platelets from patients with AMI increase myocardial damage after transient ischemia in isolated rat hearts and the modification of this effect by the P2Y 12 receptor antagonist cangrelor and the GPIIb/IIIa receptor blocker abciximab. Methods: Platelets were obtained from 9 AMI patients (7 thrombolyzed, all on aspirin) within 24 h after symptom onset. Incubation with 100 μM cangrelor or 50 μg/ml abciximab resulted, respectively, in 78 ± 4 and 90 ± 2% inhibition of aggregation (optical aggregometry). Isolated rat hearts (four simultaneous experiments per patient) were subjected to 40 min of global ischemia and 60 min of reperfusion. Hearts received no additional intervention (Control) or were infused during the 5 min prior to ischemia with platelets (22.5x10 6 /min), either untreated or treated with cangrelor or abciximab. Results: P-selectin expression (flow cytometry) in isolated platelets before infusion was 31 ± 3% (P = NS between groups). Platelets augmented myocardial injury, as demonstrated by worse left ventricular developed pressure (LVDevP), higher left ventricular enddiastolic pressure (LVEDP) and coronary resistance, and greater LDH release and infarct size (TTC staining), and both cangrelor and abciximab greatly attenuated these effects (Table ). Conclusions: Activated platelets from patients with AMI increase myocardial injury after ischemia and reperfusion, and cangrelor and abciximab attenuate this effect. The results support the notion that very early antiplatelet treatment may increase myocardial salvage by direct effects on the microcirculation in these patients.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Pedro V Staziaki ◽  
Hoshang Farhad ◽  
Otávio Coelho-Filho ◽  
Ravi V Shah ◽  
Richard N Mitchell ◽  
...  

Introduction: Anthracyclines are a standard chemotherapeutic agent. However, the anthracyclines are associated with a late reduction in left ventricular ejection fraction (LVEF) and heart failure. Pathologically, anthracycline-induced cardiotoxicity (AIC) is characterized by the development of cardiac edema and fibrosis and cardiac magnetic resonance (CMR) is the gold-standard imaging technique for edema and fibrosis. Hypothesis: We hypothesized that a) cardiac edema and fibrosis would be detected by CMR after anthracyclines and b) edema and fibrosis would provide prognostic information. Methods: We performed a longitudinal CMR and histological study of 45 wild-type mice randomized to doxorubicin (DOX, n=30, 5 mg/kg/week for 5 weeks) or placebo (n=15). Measurements were performed at baseline, 5, 10, and 20 weeks after DOX or placebo. Measures of interest were LVEF, myocardial edema and fibrosis. Edema was assessed by T2 mapping, fibrosis by calculating the extracellular volume (ECV) from pre- and post-contrast T1 measurements. Results: In DOX-treated mice vs. placebo, myocardial edema at 5 weeks was increased (T2 values of 32±4 vs. 21±3 ms, P<0.05, Fig. A), while LVEF was unchanged. At 10 weeks, there was a reduction in LVEF (54±6 vs. 63±5% μL, P<0.05) and an increase in myocardial fibrosis (ECV of 0.34±0.03 vs. 0.27±0.03, P<0.05, Fig. B). There was a correlation between T2 measures and cardiac water weight (r=0.79, P=0.007, Fig. C) and between the ECV and histological myocardial fibrosis (r=0.90, P<0.001; Fig. D). Both the early increase in edema and the sub-acute increase in fibrosis predicted the late DOX-induced mortality (P<0.001, Fig. E and F). Conclusions: Our data suggest that, in mice, CMR can detect the early increase in edema and sub-acute increase in fibrosis after anthracyclines, that an increase in edema precedes a reduction in LVEF, that the increase in edema and fibrosis are linked and both are predictive of late animal mortality.


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