TRANSIENT BRADYCARDIA INDUCED BY CAROTID-SINUS PRESSURE INCREASES OUTFLOW OBSTRUCTION IN HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY BUT NOT INVALVULAR AORTIC-STENOSIS

Background: The murmur of hypertrophic obstructive cardiomyopathy (HOC M) increases in intensity in about 80% of those patients in whom carot id sinus pressure (CSP) slows the heart rate. This does not occur in v alvular aortic stenosis (AS). Study objectives, design, and patients: It was hypothesized that left ventricular (LV) obstruction increases w ith CSP in HOCM and not in AS, Furthermore, it was not clear whether i t was the sudden bradycardia or CSP itself that was responsible for th e effect noted. Therefore, studies were performed using two different interventions: (1) Doppler echocardiography was performed before and d uring CSP in 36 HOCM patients and 21 AS patients; (2) two patients wit h DDD pacemakers and HOCM were examined before and after pacemaker rat e slowing. Finally, atrial pacing was performed in three HOCM patients at catheterization, and atrial pacing was either slowed or stopped (w ithout CSP). Results: LV outflow velocity and pressure gradient increa sed in 28 of 30 HOCM patients (92%) in whom heart rate decreased with CSP. The peak instantaneous pressure gradient increased from 45+/-37 t o 77+/-53 mm Hg (p<0.005), and the velocity contour became more typica l of HOCM. The pressure gradient increased from 30 mm Hg to 64 and 81 mm Hg, respectively, in the two patients with DDD pacemakers after pac emaker rate slowing. Similar results were seen with slewing or cessati on of atrial pacing at catheterization. In contrast, the pressure grad ient increased in only three of 21 AS patients (14%), to 44+/-28 from 41+/-25 mm Hg, and remained unchanged in the other 18. Conclusion: Thi s study shows that LV outflow velocity and pressure gradient increase markedly in most HOCM patients (92%) if CSP succeeds in slowing the he art rate, but not in patients with valvular AS. A similar effect is ob tained by simply decreasing the atrial rate in patients with DDD or at rial pacemakers. This increase in outflow tract obstruction is suffici ent to account for the increase in murmur intensity. Decreased afterlo ad (secondary to greater aortic decompression with the longer diastole ), increased intrinsic force of contraction with the bradycardia (the Woodworth effect), and Starling's law may play independent roles ire t he dynamic increase in obstruction observed during CSP in patients wit h HOCM. Worsening of mitral regurgitation was not clearly shown to con tribute to the increase in murmur, but it cannot readily be ruled out.