Transient Bradycardia Induced by Carotid Sinus Pressure Increases Outflow Obstruction in Hypertrophic Obstructive Cardiomyopathy but Not in Valvular Aortic Stenosis: Aortic StenosisThe maximum instantaneous pressure gradient in the 21 patients was 41 ±25 mm Hg and the mean pressure gradient was 32±21 mm Hg. Heart rate decreased with CSP in all 21 patients; the Doppler velocity pattern and calculated pressure gradient and murmur intensity did not change in 18 (Fig 2, 4, B). The pressure gradient increased in only three patients (Fig 2) canadian health mall. The murmur intensity increased only in one of these three patients. The maximal instantaneous pressure gradient for the entire group increased to 44±28 mm Hg during CSP (p>0.05).
Mitral Valve Motion and LV Size
Figure 6 illustrates four additional observations noted in the HOCM patients during CSP: (1) the slope of the mitral SAM became steeper, indicating more rapid eversion of the mitral leaflet into the outflow tract; (2) the QRS-SAM onset interval became abbreviated by approximately 10 ms, indicating earlier onset of this movement; (3) the duration of the SAM increased and septal-mitral apposition became more complete; and (4) LV end-diastolic and end-systolic dimensions and mean velocity of posterior ventricular wall systolic motion remained unchanged. This was observed in all 25 HOCM patients in whom the subendocardium was adequately visualized.
Discussion
The present Doppler echocardiographic study clearly demonstrates that (1) the LV outflow tract pressure gradient and the systolic ejection period increase in most HOCM patients (92% in this study) whose heart rate is slowed by CSP, indicating increased outflow tract obstruction; (2) the increase in obstruction is unique to HOCM and is almost never seen in valvular AS; and (3) the increase in obstruction is also seen when the heart rate is slowed down by manipulation of the atrial pacing rate without CSP (Fig 5), thus confirming the previous hemodynamic observation of van der Wall and identifying the longer diastolic pause itself (and not CSP-induced peripheral vasodilation) as the most important factor in the increase in obstruction.

Figure 6. Comparison of mitral valve motion before CSP (left) and during CSP (right). The SAM (black arrow) became steeper, as shown by the slope of the dotted lines and more prominent after cardiac slowing, the mitral leaflet reaching the septum and contacting it. Thus, the outflow tract was narrower, and this state persisted for a longer period of time. In addition, the SAM began earlier after slowing. The brachial pulse also became more typical of obstruction and rose earlier after slowing. The three arrowheads show the endocardial surface of the posterior wall. Systolic motion was not influenced appreciably. End-diastolic LV dimension clearly did not change in this (or any other) patient. BRA=brachial artery pulse; MAC'-mitral annul us calcification; PW=posterior wall; SEP=septum.Figure 6. Comparison of mitral valve motion before CSP (left) and during CSP (right). The SAM (black arrow) became steeper, as shown by the slope of the dotted lines and more prominent after cardiac slowing, the mitral leaflet reaching the septum and contacting it. Thus, the outflow tract was narrower, and this state persisted for a longer period of time. In addition, the SAM began earlier after slowing. The brachial pulse also became more typical of obstruction and rose earlier after slowing. The three arrowheads show the endocardial surface of the posterior wall. Systolic motion was not influenced appreciably. End-diastolic LV dimension clearly did not change in this (or any other) patient. BRA=brachial artery pulse; MAC’-mitral annul us calcification; PW=posterior wall; SEP=septum.