Transient Ventricular Wall Thickening in Acute Myocarditis. A Serial Echocardiographic and Histopathologic Study.

Abstract

n the acute phase of myocarditis, 1-3 ventricular wall thickening is sometimes observed 4-18 and is believed to be caused by interstitial edema. However, no reports have characterized the wall thickening in a large number of cases and, furthermore, its cause is not yet fully understood. This prompted us to investigate whether ventricular wall thickening in the acute phase of myocarditis is attributable to interstitial edema, by focusing on the echocardiographic changes in left ventricular wall thickness and dimensions, as well as the histologic findings in myocardial biopsy specimens. Methods The study group comprised 25 patients selected out of 55 patients hospitalized and diagnosed with acute myocarditis during the 11-year period from 1987 to 1997 at Fujita Health University or Nagoya Dai-ni Red Cross Hospital. The selected patients were chosen because they were able to undergo echocardiography and endomyocardial biopsy during both the acute and convalescent phases of myocarditis. Lymphocytic myocarditis was present in 17 patients, and eosinophilic myocarditis 19 in 8 patients (Table 1). Lymphocytic myocarditis was characterized by the onset of flu-like symptoms, cardiac failure associated

Left Ventricular Diastolic Dysfunction Induced by Cyclophosphamide in Blood Stem Cell Transplantation.

“…Furthermore, repetitive follow-up UCG examination may have revealed that the transient increase in IVSd was due to tissue edema, but not hypertrophy, as observed in acute myocarditis. [30][31][32][33] In spite of these limitations, the present study, which provides valuable information concerning early cardiac complications induced by cyclophosphamide, may contribute in the near future to an increase in the success rate for BSCT.…”

Fulminant myocarditis treated with high doses of steroids

“…The highest severity of edema is observed in the first three days of myocarditis and it undergoes gradual regression during the next eight days. Myocardial biopsies obtained after 30 days from the beginning of myocarditis do not show any characteristics of interstitial edema [3,4].…”

“…Hiramitsu et al, who on the basis of a careful histological analysis of biopsies demonstrated that myocardial cells do not undergo edema, also confirm this. The authors did not observe any changes of the longitudinal and transverse dimensions of the myocytes and emphasized that the edema is located only in the parenchymal cells [3]. The highest severity of edema is observed in the first three days of myocarditis and it undergoes gradual regression during the next eight days.…”

“…For about 20 years we have observed in the literature reports indicating LV myocardial thickening in the acute phase of myocarditis [1][2][3]. It can be located both in the IVS and in the LV free wall.…”

Cardiogenic Shock due to Left Ventricular Outflow Obstruction and Complete Atrioventricular Block in a Patient with Hypertrophic Cardiomyopathy with Acute Myocarditis

“…In patients with acute myocarditis, myocardial injury leads to transient interstitial edema, which induces thickening of the ventricular wall (1,2), occasionally also causing asymmetrical septal hypertrophy (ASH) and narrowing of the cavity of the left ventricle (LV), producing hypertrophic obstructive cardiomyopathy (HOCM) (3). Patients with acute myocarditis may also present with complete atrioventricular (AV) block.…”