Narrowing of the Left Ventricular Cavity Associated With Transient Ventricular Wall Thickening Reduces Stroke Volume in Patients With Acute Myocarditis

It has been reported that some patients with acute myocarditis have transient ventricular thickening associated with narrowing of the left ventricular cavity caused by interstitial edema. The present study investigated this phenomenon in 20 patients with acute myocarditis. Based on the sum of the interventricular septal wall thickness and left ventricular posterior wall thickness (IVST + PWT), measured by M-mode echocardiography, patients were divided into group A (IVST + PWT >/=25 mm, n=12) and group B (IVST + PWT <25 mm, n=8). The IVST + PWT was 31.8 +/-3.5 mm in group A and 21.9+/-2.7 mm in group B (p<0.0001). The left ventricular end-diastolic dimension (LVDd) was 42.3+/-6.0 mm in group A and 49.4+/-6.7 mm in group B (p<0.05). The stroke volume (SV) was 41.1+/-20.5 ml and 73.0+/-32.3 ml in groups A and B, respectively (p<0.05). The left ventricular ejection fraction (LVEF) was similar in group A (47.9+/-13.0%) and group B (56.9+/-9.0%). The SV correlated inversely with IVST + PWT (r=-0.62, p<0.01), and directly with both the LVDd (r=0.95, p<0.0001) and LVEF (r=0.64, p<0.01). The LVDd correlated inversely with IVST + PWT (r=-0.62, p<0.01). In conclusion, the reduction in SV that occurs during the acute phase of myocarditis is not only the result of systolic dysfunction, but also of the concentric left ventricular wall thickening associated with myocardial interstitial edema, which results in narrowing of the left ventricular cavity at end diastole.