What question did this study set out to answer?

To determine whether transient ventricular wall thickening observed in acute myocarditis is caused by interstitial edema or myocyte enlargement.

January 1, 2001Japanese Circulation Journal-english EditionOpen Access

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

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Population

25 patients with histologically diagnosed acute myocarditis (17 idiopathic, 8 eosinophilic)

Comparison

Serial echocardiography and endomyocardial biopsy vs Acute versus convalescent phase

Design

Cohort

Follow-up

convalescent phase (exact duration not stated)

Authors

SHShinya HiramitsuNagoya Heart Center SMShin-ichiro MorimotoFujita Health University SKShigeru KatoFukui Red Cross Hospital

Discussion

Member takes

Implication

Supports edema as driver of reversible wall thickening in acute myocarditis; leaves open prospective validation for imaging-guided management.

Key Points

To determine whether transient ventricular wall thickening observed in acute myocarditis is caused by interstitial edema or myocyte enlargement.
Evaluated 25 patients with histologically confirmed acute myocarditis (17 idiopathic, 8 eosinophilic) during acute and convalescent phases.
Conducted serial echocardiography to measure interventricular septal thickness, left ventricular posterior wall thickness, chamber dimensions, and ejection fraction.
Performed serial endomyocardial biopsies to grade interstitial edema and quantify cardiac myocyte transverse diameter via light microscopy.
Interventricular septum thickness decreased from 14.3 ± 3.7 mm acutely to 9.7 ± 1.7 mm during convalescence (p < 0.001), and left ventricular posterior wall thickness decreased from 13.3 ± 2.4 mm to 10.2 ± 1.7 mm (p < 0.0001).
Interstitial edema was present in 88.0% of patients (22/25) in the acute phase compared with 28.0% (7/25) in the convalescent phase (p < 0.0001).
Transverse cardiac myocyte diameter did not differ significantly between acute (13.6 ± 1.1 µm) and convalescent (13.8 ± 1.8 µm) phases.

Structured PICO

Population

25 patients with histologically diagnosed acute myocarditis (17 idiopathic, 8 eosinophilic)

Intervention

Serial echocardiography and endomyocardial biopsy

Comparator

Acute versus convalescent phase (within-subject comparison)

Outcome

Changes in ventricular wall thickness (interventricular septum and left ventricular posterior wall) and degree of interstitial edemasurrogate

Transient ventricular wall thickening observed in acute myocarditis is primarily caused by interstitial edema rather than myocyte hypertrophy.

Cite This Study

Hiramitsu et al. (2001) studied this question.

synapsesocial.com/papers/6a703ff531a3df8243288345 https://doi.org/10.1253/jcj.65.863

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Implication

Supports edema as driver of reversible wall thickening in acute myocarditis; leaves open prospective validation for imaging-guided management.

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

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

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