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Figure 1. Comparison of left ventricular pulsed Doppler tracings, before treatment (left panel) and after successful medical treatment (right panel). The sample volume was 2.5 cm apical of mitral valve coaptation point. Before treatment, ejection acceleration was rapid (arrowhead) and velocity peaked in the first half of systolic. After treatment, ejection acceleration was slowed (arrowhead) and velocity peaked in the second half of a systole. Systolic anterior mitral motion was delayed and a 96 mm Hg gradient was eliminated. Note, that though acceleration slowed, peak velocity remained virtually unchanged. This contrast highlights the importance of acceleration and the timing of ejection in successful medical therapy. The velocity calibration is identical in both panels. The scale is 20 cm/sec between white marks. Reproduced from Sherrid et al (19) by permission from Circulation © 1997 The American Heart Association
The mechanism of benefit of negative inotropes. We have recently studied how negative inotropes improve or eliminate obstruction (19). We studied 11 symptomatic patients with echocardiography before and after elimination of marked obstruction. Successful medical treatment of obstruction slows the acceleration of left ventricular ejection flow, measured at a point 2.5 cm apical of the mitral valve and 1 cm from the septum. Mean acceleration to peak velocity in the left ventricle at this point was decreased 34%, while peak velocity was unchanged. Before treatment, velocity peaked in the first half of the systolic ejection period; after successful treatment, it peaked in the second half. Decreased acceleration is observed easily by visual inspection of pulsed Doppler tracings in the left ventricle 2.5 cm apical of the mitral valve. An example is shown in figure 1. In contrast, the position of the mitral valve coaptation point relative to the interventricular septum, as seen in two echocardiographic planes, was unchanged after treatment.
Since the force of flow drag is directly related to the square of velocity, even small decreases in initial ejection velocity lead to larger decreases in the initial pushing force on the leaflet. We believe the decrease in force on the leaflet delays SAM, the trigger of obstruction, causing the mitral valve to contact the septum later in the systolic ejection period. This leaves less time in systole for the feedback loop to narrow the orifice, reducing the final pressure difference. Thus, delay in SAM leads to delay of the feedback loop, leaving it less time to act and ultimately yielding a lower pressure gradient (19). Figure 2 summarizes this mechanism schematically.
Figure 2. Proposed explanation of pressure gradient development before and after treatment of obstruction. Before treatment - upper tracing: Rapid LV acceleration apical of the mitral valve, shown as a horizontal thick arrow, triggers early systolic anterior motion and early mitral-septal contact. Once mitral-septal contact occurs, a narrowed orifice develops and a pressure difference results. The pressure difference forces the leaflet against the septum which decreases the orifice size and further increases the pressure difference. An amplifying feedback loop is established, shown as a rising spiral. The longer that the leaflet is in contact with the septum the higher the pressure gradient (8). After treatment - lower tracing: Negative inotropes slow early systolic acceleration (shown as a horizontal wavy arrow) and may thereby decrease the force on the mitral leaflet, delaying systolic anterior motion. Mitral-septal contact occurs later, leaving less time in systole for the feedback loop to narrow the orifice. This reduces the final pressure difference. In addition, delaying systolic anterior motion may allow more time for papillary muscle shortening to provide ountertraction. In the figure, for clarity, the "before" arrow is positioned above the "after" arrow, although at the beginning of systole they both actually begin with a pressure gradient of 0 mm Hg. M-S contact = mitral-septal contact; SAM = systolic anterior motion. Reproduced from Sherrid et al (19) by permission from Circulation © 1997 The American Heart Association.
Doppler examinations of left ventricular acceleration help the clinician manage patients who are still obstructed and symptomatic after medical treatment. In these patients it is often difficult to decide whether to increase medications or to recommend intervention. If left ventricular acceleration is not significantly slowed by medical treatment, we increase or add medication. If acceleration in the left ventricle has slowed but there is still significant obstruction, medication alone may not be adequate to eliminate obstruction, due to adverse anatomy. These patients are the ones that will require further measures.
Only a minority of patients encountered requires anything but medication for symptom relief and gradient reduction (1-3). Patients refractory to beta- blockade or verapamil will often respond to disopyramide. Patients should be treated with disopyramide before considering them medically refractory and before proceeding to surgical or septal ablation intervention. In an illustrative case, abolition of a 96 mm Hg gradient followed disopyramide IV while no change occurred following propranolol IV (14); this is consistent with the systematic comparison of the 2 drugs by Pollick (11) and with our own every day experience (19). The emphasis in the recent literature on surgical and pacemaker treatment is an example of referral bias; patients who are referred for tertiary care are often refractory and are reported by these institutions.