Type:
Poster Presentation
Keywords:
Cardiac, MR, CT, Echocardiography, Diagnostic procedure, Hyperplasia / Hypertrophy, Education and training, Image verification
Authors:
E. Pershina, O. Larina, E. A. Mershina, V. Sinitsyn; Moscow/RU
Results
Focuses of LGE were determined in 13 of 21 patients (61,9%).
- 9 patients had small punctuate,
patchy mid-wall hyper-enhancement – typical patterns of LGE corresponded to the most hypertrophied part of the myocardium and at the junction of the septum to the anterior and posterior walls of LV (Fig.2)
4 of 13 patients with LGE focuses (30%) had atypical pattern of contrast-enhancement.
- 2 patients had subendocardial type of enhancement mimicked ischemical disorders.
No significant coronary stenoses were found in both cases.
- 1st patient was diagnosed with mid-ventricular HCM (myocardial mass - 235 g,
thickness of anterobasal septum - 21 mm and mid-vetricular septum - 23 mm) - Fig. 4. This patient had transmural ischemic pattern with thinning of the apex wall,
apical aneurism of LV and small apical thrombus without enhancement in the most hypertrophied middle segments of myocardium (Fig. 5, Fig. 6).
“Freeze” ECG-feature of apical aneurism (Fig. 3) and mid-ventricular systolic gradient measured 20mmHg by Echo was found.
- 2nd patient was diagnosed with apical HCM (myocardial mass - 215g,
thickness of anterobasal septum - 20 mm and mid-ventricular septum - 26 mm).
This patient had circular subendocardial (10-15% of myocardial thickness) hyperenhancement in the most hypertrophied apical segments.
Corresponded perfusion deficit was found by CT (Fig. 7.
Fig. 8).
The ischemical pattern of hyperenhancement in these cases may be explained by dysplasia of small arteries,
reduced arteriolar density,
small vessel intramural coronary artery disease (SICAD).
The apical chamber is a subject to greater and sustained systolic stress due to the high mid-ventricular gradient [4].
The apical aneurysm («burned-out apex») observed in this patient could appear due to microvascular dysfunction and mid-ventricular obstruction.
- 3rd patient with ASH had curved septal contour and no outflow tract obstruction (myocardial mass - 301g,
the anteromiddle septum measured 17 mm and mid-vetricular septum mesuard 24 mm). A patchy mid-wall hyperenhancement in the non-most-hypertrophied left ventricular arterial segments was observed and absence of hyperenhancement in the most hypertrophied mid-ventricular segments was noted (Fig. 9,
Fig. 10)
Late enhancement of the non-hypertrophied segments in HCM should not be considered exceptional,
since the myopathic process (i.e.
disarray,
fibrosis or necrosis) affects the entire left ventricle irrespectively of the wall thickness [6].
- 4th pateint with ASH had curved septal contour and no outflow tract obstruction (myocardial mass - 199g,
basal mid-vetricular segment mesuared 16 mm,
middle - 18 mm,
apical -14 mm).
This patient had subepicardial hyperenchancement in apical and posterobasal segments.
The ejection fraction was about 42%.
Despite of myocardium mass increase eventually it was considered as inflammatory disorder and patient was diagnosed with myocarditis (Fig. 11).
This example of atypical hyperenhancement should be consider in the framework of HCM pathogenesis too.