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Transient Bradycardia Induced by Carotid Sinus Pressure Increases Outflow Obstruction in Hypertrophic Obstructive Cardiomyopathy but Not in Valvular Aortic Stenosis

Herman O. Klein; Gad Keren; Avinoam Bakst; Shlomo Laniado; Roberto Lang; Elieser Kaplinsky; Elio Di Segni
Author and Funding Information

Affiliations: From the Department of Cardiology, Meir General Hospital, Kfar Saba, Israel,  From Ichilov Hospital, Tel Aviv and Sackler School of Medicine, Tel-Aviv University, Israel

Affiliations: From the Department of Cardiology, Meir General Hospital, Kfar Saba, Israel,  From Ichilov Hospital, Tel Aviv and Sackler School of Medicine, Tel-Aviv University, Israel


1998 by the American College of Chest Physicians


Chest. 1998;114(2):469-476. doi:10.1378/chest.114.2.469
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Abstract

Background: The murmur of hypertrophic obstructive cardiomyopathy (HOCM) increases in intensity in about 80% of those patients in whom carotid sinus pressure (CSP) slows the heart rate. This does not occur in valvular aortic stenosis (AS).

Study objectives, design, and patients: It was hypothesized that left ventricular (LV) obstruction increases with CSP in HOCM and not in AS. Furthermore, it was not clear whether it was the sudden bradycardia or CSP itself that was responsible for the effect noted. Therefore, studies were performed using two different interventions: (1) Doppler echocardiography was performed before and during CSP in 36 HOCM patients and 21 AS patients; (2) two patients with DDD pacemakers and HOCM were examined before and after pacemaker rate slowing. Finally, atrial pacing was performed in three HOCM patients at catheterization, and atrial pacing was either slowed or stopped (without CSP).

Results: LV outflow velocity and pressure gradient increased in 28 of 30 HOCM patients (92%) in whom heart rate decreased with CSP. The peak instantaneous pressure gradient increased from 45±37 to 77±53 mm Hg (p<0.005), and the velocity contour became more typical 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 pacemaker rate slowing. Similar results were seen with slowing or cessation of atrial pacing at catheterization. In contrast, the pressure gradient 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: This study shows that LV outflow velocity and pressure gradient increase markedly in most HOCM patients (92%) if CSP succeeds in slowing the heart rate, but not in patients with valvular AS. A similar effect is obtained by simply decreasing the atrial rate in patients with DDD or atrial pacemakers. This increase in outflow tract obstruction is sufficient to account for the increase in murmur intensity. Decreased afterload (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 in the dynamic increase in obstruction observed during CSP in patients with HOCM. Worsening of mitral regurgitation was not clearly shown to contribute to the increase in murmur, but it cannot readily be ruled out.


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