Table 1 and Figure 2 show the maximum velocities and pressure gradients before and during CSP according to heart rate and echophonocardiographic responses. In the entire group of 30 patients, the mean pressure gradient increased by 33 ±29 mm Hg (median change, 28.6 mm Hg). In the subgroup of 24 patients in whom the murmur clearly increased, the mean pressure gradient increased from 41 ±30 mm Hg to 81±49 mm Hg (p<0.005).
The continuous Doppler signal envelope configuration changed considerably in almost all cases, particularly when the baseline signal velocity had been relatively low (Fig 3, 4); in these cases, the signal pattern that had initially appeared almost normal became characteristic of subvalvular obstruction with the “knee” and concave leftward appearance that give the typical asymmetric contour to the velocity envelope in this disease. A distinct increase in the initial rate of rise of the LV outflow velocity curve was also noted (Fig 3, 4, A), and this was usually seen best with the first beat after the long diastole. http://asthma-inhalers-online.com read more The interval from QRS complex to onset of outflow signals (the pre-ejection period) clearly shortened, as expected from the earlier aortic valve opening previously demonstrated in these patients at catheterization.
The duration of the outflow Doppler signals (systolic ejection time) increased uniformly during application of CSP, from 288±39 ms to 333±45 ms (p<0.005; Fig 4, A). There was no detectable change in the estimated degree of mitral regurgitation by the techniques used in this study, nor was new regurgitation observed.
In the two patients with DDD pacemakers, the pressure gradient increased from 30 to 81 mm f ig and from 30 to 64 mm f ig, respectively, following abrupt reduction of the pacing rate from 70 to 50 beats/min.
In three patients, the pressure gradient across the LV outflow tract increased at catheterization from 65±15 mm Hg to 105±13 mm Hg after slowing or cessation of atrial pacing (Fig 5). This was not preceded by any increase in the steepness of the slope of aortic pressure decline (ie, no peripheral vasodilation), or of the slope of diastolic LV pressure rise during diastasis, during the a wave, or in end-diastole. The only consistent change was a substantial decrease of 12 to 25 mm Hg in end-diastolic aortic pressure during the long diastole.
Table 1—Maximum Instantaneous Velocity and Calculated Pressure Gradient Before and During Application of Carotid Sinus Pressure in Hypertrophic Obstructive Cardiomyopathy
|Response||Velocity, m/s||Pressure Gradient, mm Hg||p Value|
|Heart rate slowed (11=30/36)||3.3±3.0||4.35±3.65||45 ±37||77 ±53||<0.005|
|Increased outflow velocity (n=28/30)||3.4±3.2||4.5±3.6||46 ±38||81 ±52||<0.005|
|Increased murmur (11=24/38)||3.3±2.7||4.5±2.7||41 ±30||81 ±49||<0.005|
Figure 2. Changes in calculated peak gradients in 30 IIOCM patients (left) whose heart rate decreased by more than 5 beats/min during CSP and in 21 AS patients (right). Dotted lines represent two patients in whom the peak velocity did not increase at all. Black circles represent mean values before and during CSP. C=control (before CSP).
Figure 3. A: response of an HOCM patient’s murmur to CSP, which was applied right after the third beat. There was only a slight decrease in heart rate, but this was sufficient to provoke a marked change in the indirect brachial artery pulse tracing (BA), from normal to the bifid pulse of HOCM, ancf an increase in the systolic murmur intensity on the phonocardiogram (PCG). B: the change in the velocity contour recorded from the outflow tract with CSP applied after the second beat. The calculated instantaneous peak pressure gradient (PG) more than tripled in the first beat after the pause and remained elevated in the next three beats. The velocity contour also changed drastically and became typical of HOCM. The duration of the signals also increased, indicating lengthening of the systolic ejection period. Mitral insufficiency was not detected at any time in this patient. Recorded at 50 mm/s paper speed. Vmax=maximal flow velocity’.
Figure 4. Responses in an HOCM patient and an AS patient, recorded at 100 min/s paper speed, are illustrated for comparison. A: in an HOCM patient, CSP (arrow) first produced an increase in the initial flow velocity in the LV outflow tract, then transformed the entire velocity contour to one that was typical of HOCM, and increased peak instantaneous pressure gradient. This is illustrated in the right panel, where baseline (long arrow) and CSP (short arrow) tracings are superimposed. B: in an AS patient, initial velocity was not influenced by CSP; the total velocity contour remained unaffected. VEL=velocity.
Figure 5. Effect of cessation of atrial pacing on the pressure gradient in HOCM. The gradient increased from less than 70 mm Hg to 112 mm Hg in the first beat after cessation of pacing (four vertical arrows point to pacing artifacts). The only evident hemodynamic change that occurred after the last paced beat was a decrease in the end-diastolic aortic pressure resulting from the greater emptying time. The slope of the aortic pressure fall did not change (ie, no vasodilation) and actually tapered off at the end of diastole. LV pressure did not increase: there was no change in pre-a wave pressure (diastasis), a wave pressure, or end-diastolic pressure, suggesting a minimal role, if any, for Starling s law. Ao=aortic pressure; LV=left ventricular pressure; PPG=peak pressure gradient.