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An 81-year-old woman with severe symptomatic aortic stenosis underwent aortic valve replacement. The postoperative course was complicated by new subvalvular left ventricular outflow tract obstruction created by systolic anterior motion of the anterior mitral leaflet. The condition was recognized by echocardiography and was successfully treated medically.
A patient with localized upper septal hypertrophy and medically uncontrolled severe outflow obstruction is described. His outflow obstruction was controlled by the implantation of a dual-chamber (DDD) permanent pacemaker.
To determine their internal consistency, M-mode and Doppler echocardiography were used to estimate the gradient across the left ventricular outflow tract during 74 evaluations of 50 infants, children, and young adults with congenital valvular (n = 43), subvalvular (n = 6), and supravalvular (n = 1) aortic stenosis. By M-mode the gradient was estimated from the wall-stress formula (left ventricular pressure = 225 x wall thickness/end-systolic diameter) minus systolic blood pressure determined by sphygmomanometry. Doppler (pulsed or continuous wave) methods utilized the Bernoulli formula (gradient = 4 x V2). There was good agreement between the M-mode and Doppler estimates of outflow gradient in most patients (r = 0.69, standard error of the estimate = 26.9). In 46 of 74 comparisons (62%) the two estimates differed by less than 20 mm Hg, and the estimates placed the patient in the same clinical class (mild, moderate, or severe). In 22 patients undergoing cardiac catheterization, there was only a fair correlation between the M-mode (r = 0.50) and Doppler (r = 0.58) gradients and those obtained at catheterization. Each noninvasive technique yielded major overestimates or underestimates of the gradient in several instances. The M-mode and Doppler techniques for estimating the severity of congenital aortic stenosis are complementary. Their combined use minimizes but does not totally eliminate errors of overestimation or underestimation of outflow gradient.
To determine predictors of exercise benefit in patients with hypertrophic cardiomyopathy after operative relief of left ventricular (LV) outflow tract obstruction, 30 patients underwent catheterization and exercise testing before and 6 months after operation, and hemodynamic measurements were obtained. The increase in maximal oxygen consumption (VO2max) during treadmill exercise testing was chosen as an index of exercise benefit. Univariate analysis showed a significant positive correlation of operative change in VO2max with preoperative LV end-diastolic and pulmonary arterial wedge pressures, operative change in exercise duration, and operative reductions in LV end-diastolic and pulmonary arterial wedge pressures and resting LV outflow tract gradient, and a significant negative correlation with preoperative VO2max and percent predicted VO2max. Multivariate analysis by stepwise linear regression of only significant univariate variables selected only preoperative percent predicted VO2max, and operative reduction in LV end-diastolic pressure and resting LV outflow tract gradient as significant predictors of postoperative change in VO2max. Stepwise regression analysis, applied only to preoperative exercise and catheterization hemodynamic variables, selected only preoperative percent predicted VO2max and preoperative LV end-diastolic pressure as predictors of improvement in exercise capacity. Thus, patients with obstructive hypertrophic cardiomyopathy, after failing medical therapy, are most likely to demonstrate improvement in exercise capacity if preoperative exercise testing demonstrates limited exercise capacity and if surgery achieves reduction in elevated resting LV outflow tract gradients and LV filling pressures.
Obstruction to pulmonary blood flow as a result of neoplasia in the right ventricular outflow tract is described in two dogs. Whereas one dog had exertional syncope and a systolic ejection murmur, the other had signs of congestive failure and hypoxia. In both animals the mass was detected in the right ventricle with two-dimensional echocardiography and confirmed angiographically. Although rare, primary right ventricular neoplasia represents a potentially treatable form of cardiac disease and should be considered as a cause of acquired outflow tract obstruction.
Reconstructive surgery of the mitral valve has been an alternative to mitral valve replacement in patients with mitral regurgitation. Previously, we reported on postoperative left ventricular outflow tract obstruction associated with systolic anterior motion of the anterior mitral leaflet. The current study was designed to evaluate the incidence of this complication and the long-term results of mitral valve reconstructive surgery. Sixty-five patients, aged 19 to 78 years, had mitral valve reconstructive surgery. Two patients died perioperatively, and three died late after surgery. The 60 surviving patients were studied by M mode, two-dimensional, and Doppler echocardiography 1 to 55 months postoperatively (mean 21). Fifty patients had no evidence of postoperative mitral regurgitation, two patients had moderate mitral regurgitation, three patients had mild mitral regurgitation, and five patients had trace mitral regurgitation. No significant mitral stenosis was detected in any patient postoperatively. After surgery, the diameter of the left ventricular outflow tract was significantly smaller than that before surgery. The echocardiograms of six patients showed abnormal systolic anterior motion of the anterior mitral leaflet that was not observed preoperatively. Doppler echocardiography demonstrated pressure gradients across the left ventricular outflow tract between 10 and 64 mm Hg. Inhalation of amyl nitrite increased these gradients. An additional patient who had systolic anterior motion but no gradient developed a 36 mm Hg gradient after inhalation of amyl nitrite. The remaining patients had no gradient induced by amyl nitrite. Abnormal systolic anterior motion of the anterior mitral leaflet may be surgically induced by changes in left ventricular geometry and the size of the left ventricular outflow tract during systole.(ABSTRACT TRUNCATED AT 250 WORDS)
This report presents a case of an unusually large unruptured sinus of Valsalva aneurysm complicated by right ventricular outflow tract obstruction, right coronary artery occlusion and incomplete right bundle branch block. Two-dimensional and Doppler echocardiography were instrumental in preoperative diagnosis and postoperative follow-up.
Phonocardiography and orifice-view aortography for the detection of valvular and subvalvular stenosis is reviewed. Intracardiac phonocardiography may be useful in detecting a left ventricular outflow tract obstruction, and in distinguishing it from other conditions that can produce an apparent pressure gradient during cardiac catheterization. The frequency analysis of heart sounds on noninvasive phonocardiograms may be useful in identifying subclinical aortic stenosis. Orifice-view aortography can show the anatomy of deformed aortic valves and is useful in measuring the orifice area. In patients with heavily calcified valves, plain orifice-view roentgenograms may enable one to assess the valve area. Therefore the use of these techniques in selected patients may help establish a definitive diagnosis.
Thirty-two patients with severe mitral regurgitation underwent Carpentier mitral valvuloplasty. Postoperatively, three of these patients developed clinical and echocardiographic evidence of left ventricular outflow tract obstruction. None of these patients had asymmetric septal hypertrophy or preoperative echocardiographic demonstration of systolic anterior motion of the mitral valve. Outflow obstruction postoperatively was caused by systolic anterior motion of the mitral valve. Because this potential complication of Carpentier mitral valvuloplasty produced significant hemodynamic effects in two patients, echocardiography should be routinely performed after this operation.
A patient with familial hypertrophic cardiomyopathy with exertional near syncope is reported. Intra-right ventricular obstruction was demonstrated by hemodynamic studies during inspiration and the Valsalva maneuver with systemic hypotension. Improvement occurred following the administration of propranolol. It was suggested that syncope might be precipitated by hemodynamic changes such as a high output state and a depressed cardiac volume in relation to intra-right ventricular obstruction in patients with hypertrophic cardiomyopathy.
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A 9-month-old infant with a clinical diagnosis of double outlet from the right ventricle, subaortic ventricular septal defect, and muscular subpulmonary obstruction underwent surgical repair. The defect was corrected and the right ventricular infundibulum enlarged with a patch. Eight hours after the operation there was a sudden collapse which rapidly progressed to cardiac arrest and death. Postmortem examination of the heart confirmed the clinical diagnosis but noted that the subpulmonary obstruction was caused by a "windsock" deformity of the tricuspid valve which was not identified at operation. The variants of malformations of the tricuspid valve causing subpulmonary obstruction are reviewed.
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A new method for correction of right ventricular flow tract obstruction is described. The method combines the advantages of patch-plasty-procedure and external valved conduit by conduit integration into the right ventricular and pulmonary arterial wall. Good results had been achieved in 3 cases (2 cases of Fallot's tetralogy and one case of double outlet right ventricle).
The purpose of this study was to investigate the development of a right ventricular (RV) outflow tract obstruction of sufficient severity to produce a systolic murmur following blunt cardiac trauma. A nonpenetrating impact directly on the anterior surface of the heart was produced in 34 open chest anesthetized dogs. Impact velocity was 12 m/sec in 15 dogs and 18 m/sec in 19 dogs. Seventeen dogs died immediately following impact. Pressures in the pulmonary artery and RV were measured during the control period in all dogs, and intermittently for 90 minutes following impact in ten of the 17 surviving dogs. At 90 minutes following impact a systolic pressure gradient of 9 +/- 2 mm Hg (range, 3 to 22 mm Hg) developed across the RV outflow tract and was associated with a prominent ejection murmur. At autopsy, RV wall thickness measured at the midventricular level was 13.5 +/- 1 mm (mean +/- SEM) which was thicker than in dogs that died immediately following impact, 6 +/- 1 mm (p less than 0.001). Microscopy of the RV myocardium of dogs that survived impact showed interstitial bleeding with prominent accumulations of blood between muscle bundles, whereas dogs that died immediately after impact showed no interstitial bleeding. The obstruction seems to have resulted from the increased RV wall thickness due to interstitial bleeding. In the absence, therefore, of other evidence to explain a new systolic murmur in patients following nonpenetrating cardiac trauma, the possibility of RV outflow obstruction might be considered.
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