Cardiac manifestations in polymyositis.

Twenty-one patients with polymyositis were prospectively examined with echocardiography, phonocardiography and electrocardiography. Cardiac performance, estimated with echocardiography, was enhanced as shown by a significant (P less than 0.01) increase in ejection phase indexes of left ventricular function compared with values in a matched control group. Known causes of the high output state, such as anemia or thyrotoxicosis, were not clinically evident. There was no evidence of left ventricular enlargement, left ventricular wall hypertrophy, or left atrial enlargement in the echocardiogram or chest X-ray film. The echocardiogram showed systolic mitral valve prolapse in 11 of 17 patients (65 percent) with an adequately imaged mitral valve; midsystolic clicks were present in 7 of these. One patient, who did not have prolapse, had echocardiographic evidence of a small pericardial effusion. Electrocardiographic abnormalities were present in 11 of 21 patients (52 percent) and included evidence of atrioventricular conduction disturbances, atrial and ventricular arrhythmias and left atrial abnormality. The pathophysiology of mitral valve prolapse and increased systolic left ventricular function in polymyositis remains uncertain; however, the spectrum of cardiac abnormalities, detected noninvasively in 16 of 21 of our patients (76 percent) may represent a high frequency rate of cardiac involvement in this disease.

Mid-systolic click and mitral valve prolapse following mitral commissurotomy.

Five patients with rheumatic mitral stenosis were observed to have mid-systolic clicks with murmurs of mitral regurgitation at various intervals after mitral commissurotomy. In two patients echocardiography showed an unusually rapid posterior deflection of the mitral valve coinciding exactly with a systolic nonejection click. It is speculated that the shortened, fused chordae tendineae, compromised by mitral commissurotomy, rigidly hold the valve leaflets fixed at the onset of systole. During systole, ventricular conformational changes, in the face of marginal coaptation of thickened and fibrotic mitral leaflets, allow the mitral valve to be forced abruptly towards the left atrium with great velocity. This is manifested by a loud systolic click and, in some patients, a near vertical posterior systolic deflection of the mitral valve on the echocardiogram. The systolic click may occur without echocardiographic or angiographic evidence of mitral valve prolapse. Unusually loud mid-systolic clicks can be heard in patients with rheumatic heart disease after mitral commissurotomy and may be accompanied by a distinctive echocardiographic appearance of the mitral valve.

Distance correction for precordial electrocardiographic voltage in estimating left ventricular mass: an echocardiographic study.

This study was undertaken to assess both the relation between echocardiographic measurement of left ventricular (LV) mass and commonly used electrocardiographic criteria for LV hypertrophy and the effect of the distance from the center of LV mass to the anterior chest wall on precordial voltage. Echocardiograms and standard 12-lead electrocardiograms were obtained on 100 persons, ages 3 to 79. The correlation coefficients of echocardiographically determined LV mass with ECG precordial voltage (SV1 + RV5 or V6), the Estes point score system, and a VL4 wave voltage were .686, .721, and .531, respectively. Extrapolating from the dipole nature of the heart, the precrodial voltage was multiplied by the square of the chest wall to mid-LV distance to correct for the loss of energy across the distance from LV to recording electrode. Utilizing this correction, a much improved precordial voltage estimation of LV mass (r = .846) was obtained. We conclude that the distance of the center of LV mass from the chest wall influences the amplitude of recorded precordial voltage and that correction for this influence improved the correlation of precordial voltage with LV mass.

Paradoxical motion of the interventricular septum in a patient with normal right heart hemodynamics.

A 32-year-old man with paradoxical motion of the interventricular septum at the level of the chordae tendineae and with normal right heart hemodynamics is presented. It appears that, in absence of severe left ventricular dysfunction or intraventricular conduction defect, paradoxical septal motion is not entirely specific for right ventricular volume overload and may represent a rare normal variant.