[Amyl nitrite test in the evaluation of left ventricular function: application to ischemic heart disease and Duchenne's progressive muscular dystrophy].

The effect of amyl nitrite (AN) inhalation on the left ventricular function was evaluated by mechanocardiography and echocardiography. The patient's group consisted of 110 cases with ischemic heart disease (IHD) and 25 cases of dystrophia musculorum progressiva (DMP) of Duchenne type. The former was a representative of impairment of blood supply and myocardial involvement, and the latter was of predominant myocardial disease. The control was age-matched 32 normals for IHD group and 17 cases for DMP group. Left ventricular function was mainly evaluated by systolic time intervals (STI) and the echocardiographic correlates. Fifty-five cases of IHD group were tested by coronary angiography and left ventriculography and these data were compared with the noninvasive measures. The results were as follows: I. IHD group: The ratio of ejection time (ET) to pre-ejection period (PEP), ET/PEP, did not change so much as in controls after AN inhalation, and this percent change was much smaller in cases with lesions of the left anterior descending artery (LAD) than in cases with lesions of the right coronary artery (RCA). On the other hand, mean posterior wall velocity (mPWV) and posterior wall excursion (PWE) changed greater in patients with LAD lesion than in those with RCA lesion. In cases with LAD stenosis, percent change in ET/PEP was smaller in cases with asynergy than in cases without it, disclosing more significant impairment of the left ventricle in the former. II. DMP group: In severe cases, ET/PEP was small even at rest, and percent change by AN inhalation was smaller than control in mild cases and smallest in severe cases. This seems to be useful in evaluating the severity of the diseased process. The mPWV and PWE showed impairment of left ventricular motion even at rest, but it was clearly showed in severe cases after AN inhalation. These results indicate that impairment of left ventricular function induces the poor response to AN inhalation and this, in turn, results in the lack of hyperactivity of the heart produced by this drug.