In order to study the impact of operation on left ventricular systolic function in hypertrophic cardiomyopathy (HCM), 8 patients underwent simultaneous measurement of left ventricular pressure, and volume during diagnostic study prior to operation, with repeat study approximately 6 months after myotomy-myectomy. Septal myotomy-myectomy reduced the left ventricular outflow gradient form 75 plus or minus 61 to 18 plus or minus 30 mmHg (mean +1 SD, p less than .01). There was no significant change in the heart rate, blood pressure, stroke volume index, or left ventricular end diastolic volume in the post-operative study compared to the pre- operative study. In 4 patients (Group A) the end systolic pressure/volume relationship, an index of contractility, was shifted to the right in the postop study compared to the pre-op study, indicating a decrease in contractility. In the other 4 patients (Group B) there was no alteration in this relationship in the post-op study compared to the preoperative study, indicating no change in contractility. In comparing the two groups, the Group A patients had a higher index of contractility (end systolic pressure divided by end systolic volume = 13.0 plus or minus 9.9) compared to the Group B patients (3.8 plus or minus 1.4 mmHg/ml). Following operation there was a substantial reduction in this relationship in the Group A patients (change from pre-op to post- op 8.6 plus or minus 7.9 compared to -1.2 plus or minus 2.5 mmHg/ml (p less than .05) in the Group B patients. Despite the pre-op ejection fractions being similar in the two groups, there was a substantial fall in the ejection fraction in the Group A patients (17 plus or minus 5) compared to essentially no change in the ejection fraction of the Group B patients (2 plus or minus 1, p less than .05 versus Group A). Thus, myotomy-myectomy appears to reduce contractility in some patients with HCM, especially those with elevated contractility pre-op, and is reflected by a substantial fall in ejection fraction. This may be advantageous by further reducing myocardial oxygen demands, but also potentially deleterious with respect to long-term left ventricular systolic function.
