Faculty Bibliography

OBJECTIVES: The purpose of this study was to determine whether the dynamic cause for mitral systolic anterior motion (SAM) is a Venturi or a flow drag (pushing) mechanism. BACKGROUND: In obstructive hypertrophic cardiomyopathy (HCM), if SAM were caused by the Venturi mechanism, high flow velocity in the left ventricular outflow tract (LVOT) should be found at the time of SAM onset. However, if the velocity was found to be normal, this would support an alternative mechanism. METHODS: We studied with echocardiography 25 patients with obstructive HCM who had a mean outflow tract gradient of 82 +/- 6 mm Hg. We compared mitral valve M-mode echocardiogram tracings with continuous wave (CW) and pulsed wave (PW) Doppler tracings recorded on the same study. A total of 98 M-mode, 159 CW, and 151 PW Doppler tracings were digitized and analyzed. For each patient we determined the LVOT CW velocity at the time of SAM onset. This was done by first determining the mean time interval from Q-wave to SAM onset from multiple M-mode tracings. Then, CW velocity in the outflow tract was measured at that same time interval following the Qwave. RESULTS: Systolic anterior motion began mean 71 +/- 5 ms after Q-wave onset. Mean CW Doppler velocity in the LVOT at SAM onset was 89 +/- 8 cm/s. In 68% of cases SAM began before onset of CW and PW Doppler LV ejection. CONCLUSIONS: Systolic anterior motion begins at normal LVOT velocity. At SAM onset, though Venturi forces are present in the outflow tract, their magnitude is much smaller than previously assumed; the Venturi mechanism cannot explain SAM. These velocity data, along with shape, orientation and temporal observations in patients, indicate that drag, the pushing force of flow, is the dominant hydrodynamic force that causes SAM.

OBJECTIVES: In this study we attempt to define the clinical and echocardiographic characteristics of patients with left atrial spontaneous echo contrast (LASEC) in sinus rhythm (NSR). BACKGROUND: Left atrial spontaneous echo contrast in atrial fibrillation (AF) is associated with increased risk of thromboembolism. Little is known about its significance in NSR. METHODS: We reviewed reports of 1,288 transesophageal echocardiogram (TEE) studies done with a 5 MHz probe. Patients with swirling LASEC who were in NSR during TEE were analyzed. We compared them with a control group of 45 age matched patients selected to have NSR, left atrium (LA) > 4.0 cm but no SEC. RESULTS: Spontaneous echo contrast in NSR was noted in 24 patients (2%) and formed our study group. All patients with SEC had enlarged LA, mean 5.6 cm +/- 0.6 cm. There was a higher prevalence of cerebrovascular accident (CVA) in patients with SEC when compared with controls with no SEC, 83% versus 56%, p = 0.02. Patients with SEC had larger LA, 5.6 versus 4.9 cm, p < 0.0001 and lower mean peak left atrial appendage emptying velocity (LAAEV), 38 versus 56 cm/s, p = 0.001. Thirteen percent of patients with SEC had LA thrombus as compared with none in the control group, p = 0.02. By multivariate analysis, SEC in NSR was found to be associated with CVA, larger LA size and decreased mean LAAEV. Even after adjusting for LA size, patients with SEC had a higher prevalence of CVA than controls, p = 0.03. CONCLUSIONS: Spontaneous echo contrast in NSR occurs in patients with significantly dilated LA and depressed atrial function. Left atrial thrombus is noted in 13% of such patients despite NSR. Spontaneous echo contrast in NSR is associated with a higher prevalence of CVA. Further, SEC is found to be an independent and more powerful correlate of CVA than reduced LAAEV or atrial size. These data indicate that LASEC in NSR is a prothombotic condition.

Current medical therapy of hypertrophic cardiomyopathy (HCM) is tailored to relieve symptoms of exercise intolerance, angina, or syncope. In recent years, new concepts in the pathophysiology of HCM have evolved. These concepts underlie our medical therapy and are discussed first in this review. Subsequently, the agents available for the medical treatment of HCM are discussed, along with a practical strategy for rapid medical reduction of outflow gradients. The mechanism of benefit of negative inotropes for obstruction is described, and newer agents under investigation are discussed. Finally, antiarrhythmic therapy for troubling atrial and ventricular arrhythmias is considered.

Systolic anterior motion of the mitral valve and mitral-septal contact is the usual cause of dynamic left ventricular outflow obstruction in hypertrophic cardiomyopathy. That true obstruction actually occurs is now established based on cardiac catheterization and echocardiographic evidence. A mid-systolic drop in left ventricular systolic ejection velocity because of obstruction has been demonstrated recently. Echocardiographic data indicate that systolic anterior motion of the mitral valve is initiated by flow drag; the mitral valve is swept toward the septum by the pushing force of flow. After mitral-septal contact, obstruction begets further obstruction as the pressure gradient pushes the mitral valve into the septum. Most symptomatic patients with obstruction can be treated successfully with negatively inotropic drugs. These medications reduce systolic anterior motion and obstruction by decreasing early left ventricular ejection acceleration, decreasing the early systolic pushing force on the protruding mitral leaflet. Patients who do not improve on medication generally benefit from surgery. Newer interventions to relieve obstruction, such as dual-chamber pacing and percutaneous transluminal septal myocardial ablation are under active investigation.

BACKGROUND: Drugs with negative inotropic effect are widely used to decrease obstruction in hypertrophic cardiomyopathy (HCM). However, the mechanism of therapeutic benefit has not been studied. METHODS AND RESULTS: We used M-mode, two-dimensional, and pulsed Doppler echocardiography to study 11 patients with obstructive HCM before and after medical elimination of left ventricular outflow tract obstruction. We measured 148 digitized pulsed Doppler tracings recorded in the left ventricular cavity 2.5 cm apical of the mitral valve. Successful treatment slowed average acceleration of left ventricular ejection by 34% (P=.001). Mean time to peak velocity in the left ventricle was prolonged 31% (P=.001). Mean time to an ejection velocity of 60 cm/s was prolonged 91% (P=.001). Before treatment, left ventricular ejection velocity peaked in the first half of systole; after successful treatment, it peaked in the second half (P=.001). In contrast, after treatment, we found no change in peak left ventricular ejection velocity. We also found no change in the distance between the mitral coaptation point and the septum, as measured in two planes, indicating no treatment-induced alteration of this anatomic relationship. CONCLUSIONS: Medical treatment eliminates mitral-septal contact and obstruction by decreasing left ventricular ejection acceleration. By slowing acceleration, treatment reduces the hydrodynamic force on the protruding mitral leaflet and delays mitral-septal contact. This, in turn, results in a lower final pressure gradient.