AN ECHOCARDIOGRAPHIC STUDY OF THE FLUID-MECHANICS OF OBSTRUCTION IN HYPERTROPHIC CARDIOMYOPATHY

Objectives. The goal of this study was to investigate the hydrodynamic cause of mitral-septal contact and obstruction in patients with hyper trophic cardiomyopathy. Background. Mitral-septal apposition has been shown to be the cause of obstruction in patients with hypertrophic car diomyopathy. With obstruction, characteristic continuous wave Doppler tracings show an increasing acceleration of flow. (Tracing is concave to the left.) Methods. We studied 24 consecutive patients who had a Do ppler echocardiographic pressure gradient greater-than-or-equal-to 36 mm Hg. We pursued two lines of inquiry. 1) Before the onset of obstruc tion, we systematically measured the angle between the direction of le ft ventricular Doppler color flow and the protruding mitral leaflet in early systole. 2) After the onset of obstruction, we qualitatively an alyzed the concave contour of the continuous wave Doppler tracings in our patients and developed a hydrodynamic theory of the obstruction ph ase to explain the characteristic tracings. We present a mathematic mo del to support this concept. Results. We measured 129 angles. Just bef ore mitral-septal contact, the protruding mitral leaflet projects at a mean 40-degrees and 45-degrees relative to flow in the apical long-ax is and apical five-chamber views, respectively. At mitral-septal conta ct, the obstructing leaflet projects at a mean 52-degrees and 58-degre es relative to flow in the same respective views. Even very early in s ystole, at leaflet coaptation, 11 of 23 patients had angles >15-degree s relative to flow. After mitral-septal apposition, obstruction across a cowl-shaped orifice begins. During this stage, the obstructing leaf let projects at a mean 55-degrees and 63-degrees relative to flow. In 22 patients, the continuous wave Doppler tracing of the left ventricul ar outflow jet showed an increasing acceleration of flow. Conclusions. Just before mitral-septal contact, the protruding leaflets project at high angles relative to flow. At these high angles, flow drag, the pu shing force of flow, is the dominant hydrodynamic force on the protrud ing leaflet and appears to be the immediate cause of obstruction. The high angle between flow direction and the protruding leaflet precludes significant Venturi effects. Even earlier in systole, at leaflet coap tation, flow drag is dominant in half of the patients, with angles rel ative to flow >15-degrees. After obstruction is triggered, it appears from our data and model that the leaflet is forced against the septum by the pressure difference across the orifice. The increasing accelera tion of Doppler flow is explained by a time-dependent amplifying feedb ack loop in which the rising pressure difference across the orifice le ads to a smaller orifice and a higher pressure difference.