The role of myocarditis and myocardial fibrosis in dilated cardiomyopathy Analysis of 28 necropsy cases.

Maehashi, N; Yokota, Yoshiyuki; Takarada, Akira; Usuki, Seiichiro; Maeda, Sakan; Yoshida, Hiroshi; Sugiyama, Taketoshi; Fukuzaki, Hisashi

doi:10.1536/ihj.32.1

Cited by 21 publications

(15 citation statements)

References 20 publications

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“…14. In particular, the electrograms from site E (Fig. 14 E) 13.5±15.8% which is similar to that reported previously ( 10,15,18,19,20,23). Patients in group I had minimal fibrosis with a mean fraction of only 4.6±5.6% (Fig.…”

Section: Discussionsupporting

confidence: 87%

“…Although systolic dysfunction in patients with IDC is usually diffuse, the morphologic abnormalities may be heterogeneous (23). Fibrosis is reported to be greater in the left ventricular subendocardium and in the right ventricular segments than in the left ventricular epicardial region where our measurements were obtained (20).…”

Section: Discussionmentioning

confidence: 88%

“…Much less is known about arrhythmia mechanisms in patients with IDC. There is some evidence of disturbed conduction in patients with IDC (2,(5)(6)(7)(8), and there is considerable evidence of abnormal cellular function (9-1 1 ), abnormal passive electrical properties ( 12,13), and abnormal morphologic features that could contribute to abnormal propagation (14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24). However, we are not aware of any previous attempts to systematically examine the spread ofelectrical activity in cardiomyopathic states in humans or in animal models.…”

Section: Introductionmentioning

confidence: 99%

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Myocardial electrical propagation in patients with idiopathic dilated cardiomyopathy.

Anderson¹,

Walker²,

Urie³

et al. 1993

J. Clin. Invest.

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Myocardial propagation may contribute to fatal arrhythmias in patients with idiopathic dilated cardiomyopathy (IDC). We examined this property in 15 patients with IDC undergoing cardiac transplantation and in 14 control subjects. An 8 X 8 array with electrodes 2 mm apart was used to determine the electrical activation sequence over a small region of the left ventricular surface. Tissue from the area beneath the electrode array was examined in the patients with IDC. The patients with IDC could be divided into three groups. Group I (n = 7) had activation patterns and estimates of longitudinal (OL = 0.84±0.09 m/s) and transverse (OT = 0.23±0.05 m/s) conduction velocities that were no different from controls (OL = 0.80±0.08 m/s, OT = 0.23±0.03 m/s). Group II (n = 4) had fractionated electrograms and disturbed transverse conduction with normal longitudinal activation, features characteristic of nonuniform anisotropic properties. Two of the control patients also had this pattern. Group III (n = 4) had fractionated potentials and severely disturbed transverse and longitudinal propagation. The amount of myocardial fibrosis correlated with the severity of abnormal propagation. We conclude that (a) severe contractile dysfunction is not necessarily accompanied by changes in propagation, and (b) nonuniform anisotropic propagation is present in a large proportion of patients with IDC and could underlie ventricular arrhythmias in this disorder. (J.

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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

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Myocardial electrical propagation in patients with idiopathic dilated cardiomyopathy.

Anderson¹,

Walker²,

Urie³

et al. 1993

J. Clin. Invest.

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“…The midwall enhancement seen in DCM subgroup 3 probably reflects the focal segmental fibrosis at autopsy. 17,18 Myocardial fibrosis in DCM can be divided into 3 groups: mild diffuse fibrosis, severe diffuse fibrosis, and segmental fibrosis. Current CMR techniques are unlikely to detect diffuse microscopic fibrosis and hence most patients with DCM will have absent enhancement.…”

Section: Discussionmentioning

confidence: 99%

Differentiation of Heart Failure Related to Dilated Cardiomyopathy and Coronary Artery Disease Using Gadolinium-Enhanced Cardiovascular Magnetic Resonance

et al. 2003

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Background-Heart failure treatment depends partly on the underlying cause of the disease. We evaluated cardiovascular magnetic resonance (CMR) for the problem of differentiating dilated cardiomyopathy (DCM) from left ventricular (LV) dysfunction caused by coronary artery disease (CAD). Methods and Results-Late gadolinium enhancement with CMR was performed in 90 patients with heart failure and LV systolic dysfunction (63 patients with DCM and unobstructed coronary arteries and 27 with significant CAD at angiography). We also studied 15 control subjects with no coronary risk factors and/or unobstructed coronary arteries. None (0%) of the control subjects had myocardial gadolinium enhancement; however, all patients (100%) with LV dysfunction and CAD had enhancement, which was subendocardial or transmural. In patients with DCM, there were 3 findings: no enhancement (59%); myocardial enhancement indistinguishable from the patients with CAD (13%); and patchy or longitudinal striae of midwall enhancement clearly different from the distribution in patients with CAD (28%). Conclusions-Gadolinium CMR is a powerful technique to distinguish DCM from LV dysfunction related to CAD and yields new insights in DCM. These data suggest that using the coronary angiogram as the arbiter for the presence of LV dysfunction caused by CAD could have lead to an incorrect assignment of DCM cause in 13% of patients, possibly because of coronary recanalization after infarction. The midwall myocardial enhancement in patients with DCM is similar to the fibrosis found at autopsy; it has not previously been visualized in vivo and warrants further investigation. CMR may become a useful alternative to routine coronary angiography in the diagnostic workup of DCM.

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“…The effects of a stiff cardiac interstitium on systolic performance in this patient group, however, remain unclear because reported studies have yielded conflicting results [4,5,[7][8][9][10]. In particular, the difficulty of performing accurate quantification of fibrosis and contractile function has been a major limitation of these studies [3,4,6,12,13].…”

Section: Introductionmentioning

confidence: 98%

Quantification of enhancement of left ventricular myocardium in patients with dilated cardiomyopathy using delayed enhanced MR imaging

Sueyoshi

Sakamoto

Hayashida

et al. 2009

Computerized Medical Imaging and Graphics

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The purpose is to evaluate delayed enhancement (DE) of the myocardium in patients with dilated cardiomyopathy (DCM), compared with control subjects. We also evaluated the interrelationships of DE and contractile function.DCM patients (n=42) and 14 control subjects were evaluated by DE MR imaging, acquired using a two-dimensional segmented inversion-recovery prepared gradient-echo sequence (TI=250msec), 15 minutes after intravenous administration of 0.2 mmol/kg gadolinium.For the myocardium of LV, we traced epicardial and endocardial borders, and regions of interest (ROIs) were placed in each slice. For analysis of DE images, the signal-to-noise ratio (SNR) and the contrast-to-noise ratio (CNR) of the LV myocardium were calculated. The averaged SNR (aSNR) and averaged CNR (aCNR) per slice of the LV myocardium were calculated. In the DCM group, we also evaluated the interrelationship of DE and the contractile function of the left ventricle (LV).Mean aSNR was not significantly different between the studied groups; however, mean aCNR was significantly higher in the DCM group (3.5±3.1) than in control subjects 4 (-4.1±2.1).In the DCM group, aCNR was moderately related to LV ejection fraction (LVEF) (r =0.52, P < .0001). Mean aCNR was significantly higher in the DCM group with low LVEF (<25%) (6.0±2.8) than in the DCM group with high LVEF (≥25%) (2.0±2.3).In DE MR imaging, the LV myocardium of DCM usually has high aCNR, which may suggest fibrosis. Quantification of aCNR may contribute to the diagnosis of DCM. The level of aCNR seems to correlate with LVEF. Using this technique, quantification of aCNR is objective and very useful for the diagnosis of DCM and contractile function of LV.

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The role of myocarditis and myocardial fibrosis in dilated cardiomyopathy Analysis of 28 necropsy cases.

Cited by 21 publications

References 20 publications

Myocardial electrical propagation in patients with idiopathic dilated cardiomyopathy.

Myocardial electrical propagation in patients with idiopathic dilated cardiomyopathy.

Differentiation of Heart Failure Related to Dilated Cardiomyopathy and Coronary Artery Disease Using Gadolinium-Enhanced Cardiovascular Magnetic Resonance

Quantification of enhancement of left ventricular myocardium in patients with dilated cardiomyopathy using delayed enhanced MR imaging

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