Changes in left ventricular diastolic function 6 months after nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy

BACKGROUND: Nonsurgical septal reduction therapy (NSRT) decreases left ventricular outflow tract (LVOT) gradient and improves symptoms in patients with hypertrophic obstructive cardiomyopathy (HOCM). NSRT effects on LV/left ventricular diastolic function are currently unknown. METHODS AND RESULTS: HOCM patients (n=29) had Doppler echocardiography at baseline and 6 months after NSRT to evaluate changes in LV volume, pre-A-wave pressure, early diastolic mitral annulus velocity (Ea) by tissue Doppler, and tau. At 6 months, a significant reduction in LVOT gradient (from 53.6+/-15 to 6+/-5 mm Hg; P<0.001) was accompanied by improvement in exercise duration (from 284+/-147 to 408+/-178 seconds; P=0.04) and New York Health Association class (from III to I; P<0.001). Pre-A pressure (18+/-6 to 14+/-5 mm Hg; P<0.01) and tau (62+/-8 to 51+/-8 ms; P<0.01) decreased, whereas Ea (5.8+/-1.8 to 8+/-1.8 cml/s; P<0.01) and LV end-diastolic volume (117+/-16 to 130+/-22 mL; P<0.01) increased. CONCLUSIONS: NSRT improves LV relaxation and compliance, which contributes to the symptomatic relief seen at 6 months.     

Differentiation method-dependent expression of leptin in adipocyte cell lines

OBJECTIVES: This study was undertaken to evaluate the ability of myocardial contrast echocardiography (MCE) to guide the targeted delivery of ethanol during nonsurgical septal reduction therapy (NSRT) and to assess the relation between the MCE risk area and infarct size determined by enzymatic and radionuclide methods. BACKGROUND: NSRT with intracoronary ethanol is a new promising treatment for patients with hypertrophic obstructive cardiomyopathy (HOCM). Proper localization and quantification of the septal infarct before ethanol injection are highly desirable. MCE can provide accurate delineation of the vascular territory of the coronary arteries. METHODS: Twenty-nine patients with HOCM and maximal medical therapy underwent NSRT. The left ventricular outflow tract (LVOT) gradient by Doppler echocardiography at baseline was 53 +/- 16 mm Hg (mean +/- SD). Before NSRT, MCE was performed in all patients with intracoronary sonicated albumin (Albunex). Diluted sonicated albumin (Albunex) was selectively injected into the septal perforator arteries during simultaneous transthoracic imaging. Immediately after MCE, ethanol was injected into the same vessel. Plasma total creatine kinase (CK), total CK-MB fraction and CK-MB fraction subforms were measured at baseline and serially for 36 h. RESULTS: LVOT gradient decreased to 12 +/- 6 mm Hg (p < 0.001) after NSRT. Accurate mapping of the vascular beds of the septal perforators was successfully attained in all patients by MCE. Furthermore, the MCE risk area correlated well with peak CK (r = 0.79, p < 0.001). Six weeks after NSRT, 23 patients underwent myocardial perfusion studies performed with single-photon emission computed tomography (SPECT). Mean SPECT septal perfusion defect size involved 9.5 +/- 6% of the left ventricle and correlated well with MCE area (r = 0.7), with no statistically significant difference between the risk area estimated by MCE and that by SPECT. CONCLUSIONS: Estimation of the size of the septal vascular territory with MCE is accurate, safe and feasible in essentially all patients during NSRT. MCE can delineate the perfusion bed of the septal perforators and can predict the infarct size that follows ethanol injection.     

The effect of the ingestion of ethanol on obstruction of the left ventricular outflow tract in hypertrophic cardiomyopathy

BACKGROUND: Ethanol causes vasodilation, which might have an adverse effect, due to increased obstruction of the left ventricular outflow tract, in patients with hypertrophic obstructive cardiomyopathy. We assessed the hemodynamic effects of the ingestion of ethanol, in an amount commonly consumed socially, in patients with hypertrophic cardiomyopathy. METHODS: We performed echocardiography in 36 patients before and several times after the ingestion of either 50 ml of 40 percent ethanol or an isocaloric placebo with the aroma of rum. Each patient received both ethanol and placebo, on different days. The patients, but not the physicians, were blinded to the content of the drink. We measured the sizes of the left atrium and left ventricle, the left-ventricular-wall thickness, blood pressure, heart rate, the degree of systolic anterior motion of the mitral valve, and the pressure gradient across the left ventricular outflow tract. RESULTS: The ingestion of ethanol regulated in a significant drop in the mean (+/- SD) systolic blood pressure (from 130.5 +/- 18.6 to 122.5 +/- 20.3 mm Hg, P<0.001), a significant increase in systolic anterior motion of the mitral valve (from a grade of 2.1 to a grade of 2.5, P<0.001), and a 63 percent increase in the mean gradient across the left ventricular outflow tract (from 38.1 +/- 26.5 to 62.2 +/- 42.4 mm Hg, P<0.001). These changes, which were not associated with symptoms, did not occur after the ingestion of placebo. CONCLUSION: The ingestion of a small amount of ethanol caused an increase in the gradient across the left ventricular outflow tract in patients with hypertrophic obstructive cardiomyopathy, which could have and adverse clinical effect.     

Clinical and hemodynamic follow-up of left ventricular to aortic conduits in patients with aortic stenosis

To assess the long-term results of left ventricular outflow tract reconstruction utilizing an apical left ventricular to aortic valved (porcine) conduit the clinical and hemodynamic data were reviewed from 24 patients who had placement of an apico-aortic conduit. Eighteen of the patients are asymptomatic and taking no cardiac medications. Three patients were reoperated on, one patient 1.5 years after his original operation for subacute bacterial endocarditis and two patients 3 to 4 years after their original operation for severe conduit valve insufficiency. None of the patients is taking anticoagulants and no thromboembolic events have occurred. Postoperative catheterization has been performed 1 to 1.5 years (mean 1.2) after repair in 15 of 21 patients. The rest left ventricular outflow tract gradient has decreased from 102.5 +/- 20 mm Hg preoperatively to 14.8 +/- 9.9 mm Hg postoperatively (probability [p] less than 0.001). Some degree of conduit obstruction was demonstrated by catheter passage in 11 of the 15 patients. In these 11 patients, the obstruction occurred at three distant sites: at the egress of the left ventricle in 9, at the porcine valve in 5 and at the aortic to conduit junction in 1. Isometric exercise in five and supine bicycle exercise in six patients increased the left ventricular outflow tract gradient by 2.5 +/- 1.1 and 20.8 +/- 11.8 mm Hg, respectively, despite an increase in cardiac index of 1 +/- 0.3 and 3.7 +/- 0.4 liters/min per m2, respectively. The data suggest that a left ventricular to aortic conduit is an effective form of therapy for severe left ventricular outflow tract obstruction.     

Hypertrophic obstructive cardiomyopathy in pediatric patients: results of surgical treatment

Between April 1975 and May 1995, 25 pediatric patients on one hospital service underwent extended left ventricular septal myectomy because of hypertrophic obstructive cardiomyopathy. Ages ranged from 2 months to 20 years (mean, 11.2 years). Seventeen patients had moderate to severe mitral valve insufficiency. Medical therapy had failed in all patients and one patient had undergone dual-chamber pacemaker implantation without improvement. Left ventricular outflow tract gradients ranged from 50 to 154 mm Hg (mean, 99.9 +/- 25.2). Concomitant cardiac procedures included mitral valve repair (n = 2), automatic implantable cardioverter defibrillator implantation (n = 1), and closure of atrial septal defect (n = 1). Intraoperative premyectomy left ventricular outflow tract gradients ranged from 20 to 117 mm Hg (mean, 60.4 + 26.2) and postmyectomy gradients ranged from 0 to 20 mm Hg (mean, 6.6 +/- 5.9). Postmyectomy mitral insufficiency was reduced to a regurgitant fraction of 0% to 12%, and no patient required mitral valve replacement. One patient required a pacemaker because of complete heart block; on subsequent follow-up, normal sinus rhythm had returned. There was no early mortality and no instance of aortic or mitral valve injury or ventricular septal defect. Follow-up ranged from 10 months to 20 years (mean, 6.4 years). There were no late deaths. Left ventricular outflow tract gradients by echocardiography were a mean of 14.2 mm Hg with a median of 5.0 mm Hg. All patients had normal sinus rhythm. Reoperation because of recurrent left ventricular outflow tract obstruction was necessary in two patients at 3.2 years and 12.4 years after initial myectomy, respectively. All patients but one have New York Heart Association class I or II function. We conclude that extended septal myectomy is a safe and effective means of relieving cardiac symptoms and left ventricular outflow tract obstruction in pediatric patients with severe hypertrophic obstructive cardiomyopathy unresponsive to medical management, and late survivorship compares favorably with the natural history of the disease.     

Quantitative assessment of the operative results after extended myectomy and surgical reconstruction of the subvalvular mitral apparatus in hypertrophic obstructive cardiomyopathy using dynamic three-dimensional transesophageal echocardiography

OBJECTIVES: The aim of this study was to examine the value of dynamic three-dimensional (3D) transesophageal echocardiography (TEE) for the postoperative evaluation after extended myectomy and surgical reconstruction of the subvalvular mitral valve apparatus in patients with hypertrophic obstructive cardiomyopathy (HOCM). BACKGROUND: Two-dimensional imaging techniques such as echocardiography, computed tomography and magnetic resonance imaging have not been able to precisely quantify the effects of surgical therapy on the morphology of the left ventricular outflow tract (LVOT). METHODS: Multiplane TEE with 3D reconstruction was performed in 11 patients before and after the operation and in 16 normal control subjects for comparison. The preoperative maximal systolic pressure gradient in the LVOT was 69 +/- 59 mm Hg. The following variables were measured within the dynamic 3D data set: depth, width, length and cross-sectional area (CSA) gain caused by the myectomy trough, minimal CSA of the LVOT at each time point and its cyclic changes and maximal mitral leaflet deviation during systole. RESULTS: Functional class improved from 3.0 +/- 0.2 before the operation to 1.5 +/- 0.6 after it. The maximal systolic pressure gradient in the outflow tract decreased to 26 +/- 21 mm Hg postoperatively (p < 0.001). Minimal CSA of the outflow tract increased from 1.1 +/- 1.2 to 3.8 +/- 1.9 cm2 postoperatively (p < 0.001), similar to the value of the control group (4.2 +/- 1.5 cm2, p = NS). The area gain due to the myectomy trough was 1.3 +/- 1.0 cm2, corresponding to 48 +/- 12% of the total operative area difference. Maximal systolic depth of the myectomy was 7 +/- 2 mm, maximal width was 20 +/- 8 mm and length was 28 +/- 7 mm. Maximal deviation of the mitral leaflets fell from 15 +/- 7 to 6 +/- 7 mm postoperatively (p < 0.01). In five patients mass measurements of the intracavitary portion of the papillary muscle (PM) revealed an increase from 7.3 +/- 1.0 to 12.1 +/- 2.5 g due to surgical mobilization of PMs (p < 0.01). CONCLUSIONS: 3D TEE quantifies the differences in outflow tract morphology before and after surgery for HOCM. This technique may have an impact on the planning of operative interventions and allow for the evaluation of its results.     

Propranolol in mitral stenosis during sinus rhythm

Patients with early symptomatic mitral stenosis usually suffer from pulmonary congestion on the basis of left atrial and pulmonary venous hypertension. They are often in sinus rhythm, and cardiac output is usually well maintained. Symptoms occur most often when heart rate, cardiac output, or both are increased. In this study, intravenous propranolol administered to patients with pure mitral stenosis in sinus rhythm resulted in significant reductions in mitral diastolic gradient (-7.1 mm. Hg +/- 1.6 SED), mean pulmonary wedge pressure (--6.9 mm. Hg +/- 1.2) and mean pulmonary artery pressures (--9.0 mm. Hg +/- 1.2). This was due to simultaneous reduction of heart rate (--13.0 beats/minute +/- 2.6 and cardiac output (--0.5 L./minute +/- 0.2). A small associated reduction of left ventricular systolic pressure (--5.1 mm. Hg +/- 2.6) was not accompanied by adverse clinical effects. A potential role for propranolol in medical management of pure mitral stenosis in the presence of sinus rhythm is suggested.     

Impact of size mismatch and left ventricular function on performance of the St. Jude disc valve after aortic valve replacement

BACKGROUND: The hemodynamic function of the St. Jude valve may change relative to changes in left ventricular function after aortic valve replacement for aortic stenosis. From theoretical reasons one may hypothesize that prosthetic valve hemodynamic function is related to left ventricular failure and mismatch between valve size and patient/ventricular chamber size. METHODS: Forty patients aged 24 to 82 years who survived aortic valve replacement for aortic stenosis with a standard St. Jude disc valve (mean size, 23.5 mm; range, 19 to 29 mm) were followed up prospectively with Doppler echocardiography and radionuclide left ventriculography preoperatively and 9 days, 3 months, and 18 months after the operation with assessment of intravascular hemolysis at 18 months. Follow-up to a maximum of 7.4 years (mean, 6.3 years) was 100% complete. RESULTS: Left ventricular muscle mass index decreased from 198 +/- 62 g.m-2 preoperatively to 153 +/- 53 g.m-2 at 18 months (p < 0.001), paralleled by a significant increase in left ventricular ejection fraction, peak ejection rate, and peak filling rate; only 18% of the patients had normal left ventricular muscle mass index and only 32% normal ventricular function (normal left ventricular ejection fraction, peak ejection rate, peak filling rate, early filling fraction, and late filling fraction during atrial contraction) at 18 months. Prosthetic valve peak Doppler gradient dropped from 20 +/- 6 mm Hg at 9 days to 17 +/- 5 mm Hg at 18 months (p < 0.05). Reduction of left ventricular muscle mass index was unrelated to peak gradient and size of the valve. Peak gradient at 18 months rose with valve orifice diameter of 17 mm or less (by 6 mm Hg), orifice diameter/body surface area of 9 mm.m-2 or less (by 5 mm Hg), left ventricular enddiastolic dimension (by 23 mm Hg per 10 mm increase), and impaired ventricular function (by 3 mm Hg). All but 2 patients (5%) had intravascular hemolysis; none had anemia. Two patients with moderate paravalvular leak had the highest serum lactic dehydrogenase levels; 4 patients with trivial leak had higher serum lactic dehydrogenase levels than those without leak. Serum lactic dehydrogenase levels rose with moderate paravalvular leak, impaired ventricular function, and valve orifice diameter. Six patients with trivial or moderate paravalvular leak had a cumulative 7-year freedom from bleeding and thromboembolism of 44% +/- 22% compared with 87% +/- 5% for those without leak (p < 0.05). CONCLUSIONS: The peak gradient of the St. Jude aortic valve dropped marginally over the first 18 postoperative months in association with incomplete left ventricular hypertrophy regression and marginal improvement of ventricular function. Mismatch between valve size and ventricular cavity size or patient size and impaired function of a dilated ventricle significantly compromised the performance of the St. Jude valve. Probably explained by platelet destruction or activation, paravalvular leak was related to bleeding and thromboembolic complications.     

Exercise hemodynamics in small (< or = 21 mm) aortic valve prostheses assessed by Doppler echocardiography

Exercise Doppler echocardiography was used to assess hemodynamics in 25 patients with a < or = 21 mm aortic valve prosthesis (14 with a Medtronic-Hall 21 mm valve, three with a Medtronic-Hall 20 mm valve, three with a Sorin 21 mm valve, one with a Duromedics 21 mm valve, and four with a Carpentier-Edwards 21 mm valve). A symptom-limited upright bicycle exercise test was performed, and Doppler gradients were recorded during exercise. Gradients increased with exercise from 30 +/- 8/16 +/- 4 mm Hg (peak/mean) at rest to 46 +/- 12/24 +/- 7 mm Hg during exercise; both p < 0.001. Mean exercise gradient exceeded 30 mm Hg in five patients, and the highest mean gradient recorded was 37 mm Hg. Within the group of mechanical valves, gradients at exercise were similar for different types of valves. A linear relationship was found between gradients at rest and during exercise (peak r = 0.75, mean r = 0.77; both p < 0.001). Additional findings were midventricular velocities exceeding 1.5 m/sec in late systole in 10 patients (40%) and intraventricular flow (> or = 0.2 m/sec) toward the apex during isovolumic relaxation in 11 patients (44%). The patients with these velocity patterns had significantly smaller left ventricular cavities (end-diastolic diameter 39.8 +/- 4.8 vs 46.5 +/- 4.2 mm, p < 0.01; end-systolic diameter 24.2 +/- 3.0 vs 28.5 +/- 4.5 mm, p = 0.013).(ABSTRACT TRUNCATED AT 250 WORDS)     

Mobilization of the left and right fibrous trigones for relief of severe left ventricular outflow obstruction

BACKGROUND: There is still no agreement about the optimal method of surgical relief of fixed subaortic stenosis, particularly the severe forms. OBJECTIVES: The purpose of this study was to describe a new technique for the relief of subaortic stenosis based on analysis of the functional anatomy of the left ventricular outflow tract and pathophysiologic features of subaortic stenosis. Methods and patients: We propose that one of the basic abnormalities in subaortic stenosis is interference with the hinge mechanism provided by the 2 fibrous trigones with progressive deposition of fibrous tissue in these angles. The technique described in this paper consists of excision of all components of the fibrous "ring," with mobilization of the left and right fibrous trigones. This results in the restoration of the normal dynamic behavior of the left ventricular outflow tract with maximal widening of the outflow tract as the result of backward displacement of the subaortic curtain and anterior leaflet of the mitral valve. This technique has been used in 57 consecutive patients who ranged in age between 5 months and 56 years (mean, 15.5 +/- 10.6 years). Gradients across the left ventricular outflow tract were between 45 and 200 mm Hg (mean, 86.7 mm Hg). Additional lesions were present in 10 patients, and 7 patients had had 8 previous operations on the left ventricular outflow tract. At operation, in addition to resection of subaortic stenosis, 3 patients had aortic valvotomy, 2 patients had homograft replacement of the aortic valve, 7 patients had patch closure of a ventricular septal defect, and 1 patient had open mitral valvotomy. RESULTS: There were 2 early deaths and 1 late sudden death during the follow-up period that ranged from 1 month to 25 years (mean, 15. 2 years). One patient experienced the development of endocarditis on the aortic valve 7 years after operation, which was successfully treated by homograft replacement. Postoperative gradients across the left ventricular outflow tract varied from no gradient to 30 mm Hg (mean, 8 mm Hg). There were no instances of recurrence of a gradient across the left ventricular outflow tract. CONCLUSION: It is concluded that mobilization of the left and right fibrous trigones results in durable relief of subaortic stenosis.     

Stress-induced left ventricular outflow tract obstruction: a potential cause of dyspnea in the elderly

OBJECTIVES: We sought to identify the pattern of disturbed left ventricular physiology associated with symptom development in elderly patients with effort-induced breathlessness. BACKGROUND: Limitation of exercise tolerance by dyspnea is common in the elderly and has been ascribed to diastolic dysfunction when left ventricular cavity size and systolic function appear normal. METHODS: Dobutamine stress echocardiography was used in 30 patients (mean [+/-SD] age 70 +/- 12 years; 21 women, 9 men) with exertional dyspnea and negative exercise test results, and the values were compared with those in 15 control subjects. RESULTS: Before stress, left ventricular end-diastolic and end-systolic dimensions were reduced, fractional shortening was increased, and the basal septum was thickened (2.3 +/- 0.5 vs. 1.4 +/- 0.2 cm, p < 0.001, vs. control subjects) in the patients, but posterior wall thickness did not differ from that in control subjects. Left ventricular outflow tract diameter, measured as systolic mitral leaflet septal distance, was significantly reduced (13 +/- 4.5 vs. 18 +/- 2 mm, p < 0.001). Isovolumetric relaxation time was prolonged, and peak left ventricular minor axis lengthening rate was reduced (8.1 +/- 3.5 vs. 10.4 +/- 2.6 cm/s, p < 0.05), suggesting diastolic dysfunction. Transmitral velocities and the E/A ratio did not differ significantly. At peak stress, heart rate increased from 66 +/- 8 to 115 +/- 20 beats/min in the control subjects, but blood pressure did not change. Transmitral A wave velocity increased, but the E/A ratio did not change. Left ventricular outflow tract velocity increased from 0.8 +/- 0.1 to 2.0 +/- 0.2 m/s, and mitral leaflet septal distance decreased from 18 +/- 2 to 14 +/- 3 mm, p < 0.001. In the patients, heart rate rose from 80 +/- 12 to 132 +/- 26 beats/min and systolic blood pressure from 143 +/- 22 to 170 +/- 14 mm Hg (p < 0.001 for each), but left ventricular dimensions did not change. Peak left ventricular outflow tract velocity increased from 1.5 +/- 0.5 m/s (at rest) to 4.2 +/- 1.2 m/s; mitral leaflet septal distance fell from 13 +/- 4.5 to 2.2 +/- 1.9 mm (p < 0.001); and systolic anterior motion of mitral valve appeared in 24 patients (80%) but in none of the control subjects (p < 0.001). Measurements of diastolic function did not change. All patients developed dyspnea at peak stress, but none developed a new wall motion abnormality or mitral regurgitation. CONCLUSIONS: Although our patients fulfilled the criteria for "diastolic heart failure," diastolic dysfunction was not aggravated by pharmacologic stress. Instead, high velocities appeared in the left ventricular outflow tract and were associated with basal septal hypertrophy and systolic anterior motion of the mitral valve. Their appearance correlated closely with the development of symptoms, suggesting a potential causative link.     

Influence of the angiotensin II antagonist valsartan on left ventricular hypertrophy in patients with essential hypertension

BACKGROUND: Left ventricular hypertrophy (LVH) represents an independent risk factor in patients with essential hypertension. Because reversal of LVH may be associated with an improvement of prognosis, the influence of new antihypertensive compounds, such as angiotensin II AT1 receptor antagonists, on LVH should be determined. METHODS AND RESULTS: In a randomized, double-blind trial, 69 predominantly previously untreated hypertensive patients with echocardiographically proven LVH, ie, left ventricular mass index (LVMI) >134 g/m2 in men and >110 g/m2 in women and/or end-diastolic septal thickness >12 mm, received either the angiotensin II antagonist valsartan or atenolol for 8 months. Echocardiographic data of 58 patients were available. After 8 months of valsartan treatment (n=29), LVMI decreased from 127+/-23 to 106+/-25 g/m2 (ratio [R]=0.83; 95% CI, 0.79 to 0.87; P<0.0001 versus baseline). Under atenolol (n=29), LVMI decreased to a smaller extent, from 127+/-25 to 117+/-27 g/m2 (R=0.92; 95% CI, 0.86 to 0.98; P=0.0082 versus baseline). The mean reduction of LVMI came to 21 g/m2 under valsartan and only to 10 g/m2 under atenolol (R=0.91; 90% CI, 0.85 to 0.97 versus atenolol). Baseline mean blood pressure values were determined to be 163+/-12/101+/-6 mm Hg before treatment with valsartan and 160+/-14/103+/-6 mm Hg before atenolol treatment. After 8 months of treatment, mean blood pressure decreased to 146+/-13/90+/-7 mm Hg with valsartan and to 147+/-18/90+/-7 mm Hg with atenolol. Nine patients in the valsartan group and 8 patients in the atenolol group required additional medication with hydrochlorothiazide. CONCLUSIONS: Antihypertensive treatment with the angiotensin II antagonist valsartan for 8 months produced a significant regression of LVH in predominantly previously untreated patients with essential hypertension. The drug may be safely administered in this subset of hypertensive patients; however, the long-term benefit in terms of risk reduction has still to be evaluated in further trials.     

Afterload reduction therapy with nitroprusside in severe aortic regurgitation: improved cardiac performance and reduced regurgitant volume

To assess the hemodynamic effects of afterload reduction in severe aortic regurgitation, nitroprusside was infused at cardiac catheterization in 12 patients with aortic regurgitation. Cardiac hemodynamics, angiographic variables and regurgitant volumes were quantified during control periods, and nitroprusside was infused to reduce systemic systolic pressure to 110 to 125 mm Hg. The following were reduced by the drug: systolic arterial pressure (from 154 +/- 6.4 to 115 +/- 2.3 mm Hg, P less than 0.001); left ventricular end-diastolic pressure (from 23 +/- 2.2 to 11 +/- 1.0 mm Hg, P less than 0.001); systemic vascular resistance (from 1,782 +/- 133 to 1,148 +/- 94 dynes sec cm-5, P less than 0.001); left ventricular end-diastolic volume (from 242 +/- 25 to 196 +/- 19 ml, P less than 0.001); aortic regurgitant fraction (from 0.53 +/- 0.05 to 0.44 +/- 0.06, P less than 0.01); and aortic regurgitant minute volume (from 5.5 +/- 0.10 to 4.3 +/- 0.09 liters/min, P less than 0.01). Effective cardiac index increased (from 2.49 +/- 0.19 to 3.10 +/- 0.24 liters/min per m2, P less than 0.01), and left ventricular ejection fraction rose (from 0.55 +/- 0.03 to 0.61 +/- 0.03, P less than 0.005). These data indicate that afterload reduction with nitroprusside in severe aortic regurgitation improves cardiac performance, greatly decreases left ventricular preload and reduces aortic regurgitant volume. Thus, nitroprusside therapy has special value in severe aortic regurgitation that is of particular benefit in critical clinical conditions.     

Evaluation of right ventricular systolic pressure during incremental exercise by Doppler echocardiography in adults with atrial septal defect

STUDY OBJECTIVES: Pulmonary hypertension is the most important complication in patients with atrial septal defect (ASD), but its role in limiting exercise has not been examined. This study sought to evaluate exercise performance in adults with ASD and determine the contribution of elevated pulmonary artery pressure in limiting exercise capacity. DESIGN: We used Doppler echocardiography during exercise in 10 adults (aged 34 to 70 years) with isolated ASD (New York Heart Association class I, II) and an equal number of matched control subjects. Incremental exercise was performed on an electrically braked upright cycle ergometer. Expired gases and VE were measured breath-by-breath. Two-dimensional and Doppler echocardiographic images were obtained at rest prior to exercise to determine ASD size, stroke volume (SV), shunt ratio (Qp:Qs), right ventricular outflow tract (RVOT) size, and right ventricular systolic pressure at rest (RVSPr). Doppler echocardiography was repeated at peak exercise to measure right ventricular systolic pressure during exercise (RVSPex). RESULTS: Resting echocardiography revealed that RVOT was larger (21+/-4 vs 35+/-8 mm, mean+/-SD; p=0.0009) and RVSPr tended to be higher (17+/-8 vs 31+/-8 mm Hg; p=0.08) in ASD; however, left ventricular SV was not different (64+/-23 vs 58+/-23 mL; p>0.05), compared with control subjects. Despite normal resting left ventricular function, ASD patients had a significant reduction in maximum oxygen uptake (VO2max) (22.9+/-5.4 vs 17.3+/-4.2 mL/kg/min; p=0.005). RVSPex was higher (19+/-8 vs 51+/-10 mm Hg; p=0.001) and the mean RVSP-VO2 slope (1+/-2 vs 18+/-3 mm Hg/L/min; p=0.003) and intercept (17+/-4 vs 27+/-4 mm Hg; p=0.05) were higher in the ASD group. VO2max correlated inversely with both RVSPr (r=-0.69; p=0.007) and RVSPex (r=-0.67; p=0.01). CONCLUSION: These findings suggest that adults with ASD have reduced exercise performance, which may be associated with an abnormal increase in pulmonary artery pressure during exercise.     

Veterinary ethics in the liberalized market: the Zambian environment

BACKGROUND: This study was performed to assess the functional capacity of the survivors of septal myectomy for the treatment of hypertrophic obstructive cardiomyopathy in long-term follow-up as assessed by dobutamine stress echocardiography. METHODS: Sixty-nine patients with hypertrophic obstructive cardiomyopathy underwent septal myectomy between 1975 and 1996. The mean age was 25.4 +/- 13.6 years (range, 6-58 years), and 10 of the patients were women. The early mortality was 4.3%. Hospital survivors (95.7%) were followed up for a mean of 43.8 +/- 28.7 months (range, 6-114 months). RESULTS: The postoperative mean functional capacity of the group was 1.47 +/- 0.56. No late deaths were reported. Forty-nine patients (74.2%) were evaluated with standard echocardiographic techniques, and 29 (43.9%) patients underwent dobutamine stress echocardiography. There was a significant decrease in the thickness of the interventricular septum after surgery. The mean preoperative and postoperative septal thickness was 1.99 +/- 0.59 cm (range, 1.3-3.8 cm) and 1.55 +/- 0.41 cm (range, 0.96-2.8 cm), respectively (p < 0.004). The mean posterior wall thickness was significantly less than the preoperative value (p = 0.008) and the left ventricular end-diastolic diameter was slightly greater in the postoperative measurements, but the difference was not significant (p = 0.162). Postoperative left ventricular outflow systolic gradients were reduced significantly when compared with preoperative values (preoperative mean, 78.4 +/- 33.6 mm Hg, range, 50-212 mm Hg versus postoperative mean, 17.9 +/- 15.9 mm Hg: range, 0-40 mm Hg; p < 0.0001). CONCLUSION: Septal myectomy for patients with hypertrophic obstructive cardiomyopathy is a safe procedure with excellent clinical and functional results in the long-term follow-up.     

Partial left ventriculectomy with mitral valve preservation in the treatment of patients with dilated cardiomyopathy

OBJECTIVE: This study reports initial results of partial left ventriculectomy performed with preservation of the mitral valve in the treatment of 27 patients with idiopathic dilated cardiomyopathy. METHODS: Patients were in New York Heart Association class III or IV. Partial ventriculectomy was performed as an isolated procedure in four patients and associated with mitral annuloplasty in 23 patients. There were four hospital deaths (14.8%) and the remaining patients were followed for 11.2 +/- 6 months. RESULTS: Decrease of left ventricular diastolic diameter (81.8 +/- 8.7 to 68.5 +/- 7.6 mm, p < 0.001) and improvement of left ventricular wall shortening (12% +/- 3.1% to 18.1% +/- 3.9%, p < 0.001) were demonstrated by echocardiography after the operation. Left ventricular radioisotopic angiography showed reduction of diastolic volume (495 +/- 124 ml to 352 +/- 108 ml, p < 0.001) and increase of ejection fraction (17.7% +/- 4.6% to 23.7% +/- 8.8%, p < 0.001). Right-sided heart catheterization demonstrated improvement of stroke index (24.3 +/- 7.7 ml/m2 to 28.3 +/- 7.6 ml/m2, p < 0.01) and decrease of pulmonary wedge pressure (23.2 +/- 8.8 mm Hg to 17 +/- 7 mm Hg, p < 0.01). Similar results were documented at 6 and 12 months of follow-up. Functional class improved from 3.6 +/- 0.5 to 1.4 +/- 0.6 (p < 0.001). However, seven patients died at midterm follow-up because of heart failure progression or arrhythmia-related events, and survival rate was 59.2% +/- 9.4% from 6 to 24 months of follow-up. CONCLUSIONS: Partial left ventriculectomy performed with preservation of the mitral valve improves left ventricular function and congestive heart failure in patients with dilated cardiomyopathy. Nevertheless, the high incidences of heart failure progression and arrhythmia-related deaths observed after this procedure preclude its wide clinical application.     

Intraventricular obstructions in dobutamine stress echocardiography: determinants of their development and clinical sequelae

Dobutamine stress echocardiography (DSE) leads to strong hypercontraction, tachycardia, and peripheral vasodilatation. In previous studies systolic obstruction of the left ventricular outflow tract (LVOT) was observed as a result of these factors. To evaluate left ventricular function and morphology in patients (pts) with induced systolic LVOT obstruction, we used continuous wave (CW) doppler registrations in combination with quantitative 2-D-echocardiography in 100 pts during routinely performed DSE (5-40 micrograms/kg/min). In addition left ventricular wall thickness was measured. Symptoms were registered using a standardised questionnaire and cardiac arrhythmias were counted over a two minute interval at rest and during the maximal heart rate of each patient. During DSE dynamic flow acceleration with late systolic peak velocity above 2 m/second (s) was considered to represent LVOT obstruction in pts with normal flow profiles in the LVOT before infusion of dobutamine. For invasive studies pts were investigated with femoral catheterisation by the method of Judkins. A greater than 50% stenosis was judged to be significant. RESULTS: Examinations in 73 pts provided data of sufficient quality for echocardiographic and Doppler sonographic evaluations. 39 pts, 26 men, 13 women, mean age 64 +/- 8 years, developed late systolic flow velocities above 2 m/s and therefore formed the obstructive group (grp A). Grp B consisted of 34 pts, 26 men and 8 women, mean age 66 +/- 10 years, who showed normal time velocity integrals during DSE. In 41 pts invasive data provided information concerning the existence and severity of coronary artery disease. There were no significant differences in the increase of heart rate, the product of maximal systolic blood pressure and maximal heart rate or the percentage of pts, who reached their age corrected submaximal heart rate during DSE. Obstructive pts (group A) showed late systolic dynamic acceleration of systolic flow with a mean maximal speed of 315.4 +/- 139.8 cm/s, which peaked 0.12 +/- 0.04 s after the R-wave. From the velocities we calculated a mean pressure gradient of 47.5 +/- 39.7 mm Hg using the modified Bernoulli equation. Group B patients showed lower and earlier maximal speeds with a mean value of 158.2 +/- 37.6 cm/s, 0.09 +/- 0.04 s after the R-wave, corresponding to a pressure gradient of 10.6 +/- 4.9 mm Hg (p < 0.001). Ejection fractions were higher (p < 0.001) before the test in grp A: 68.2 +/- 8% compared to 55.7 +/- 10.4% in B. This difference increased during peak stress: 74.1 +/- 7.7% compared to 59.5 +/- 12.8%. End diastolic (EDVI) and end systolic volume indexes (ESVI) were lower in grp A (p < 0.001). During DSE, the decrease in ESVI was somewhat stronger for pts in grp A. Left ventricular hypertrophy was more often seen with obstruction. Septal thickness was increased in A: 1.45 +/- 0.34 cm compared to 1.13 +/- 0.27 cm in B (p < 0.001). Left ventricular posterior wall measured 1.03 +/- 0.28 cm in A and 0.83 +/- 0.23 cm in B (p < 0.01). 27 pts in grp B and only 9 in grp A had a history of previous myocardial infarction. Showing no difference at rest, wall motion score indexes raised under DSE in both groups and developed significantly higher scores in grp B at peak stress: 1.30 (1.0-1.90) compared to 1.18 (1.0-1.75) in A. We observed typical chest pain more often in grp B. Unspecific symptoms and arrhythmogenic complications were not statistically different, with the exception of ventricular bigeminy which was more often observed in grp B. A decline in the diastolic blood pressure was observed in pts with very severe obstruction (> 3.5 m/s, p < 0.05). Sensitivity of DSE was 84%, specificity 79%. No significant differences between pts with and without obstruction were observed. SUMMARY: Intraventricular obstructions during DSE are often observed in pts with normal systolic function at rest and during peak stress, especially in the case of left ventricular hypertrophy. (ABSTRACT TRU     

Paradoxical hypertension after reversal of heart failure in patients treated with intensive vasodilator therapy

Hypertension is a major cause of heart failure, evolving from left ventricular hypertrophy to systolic and diastolic dysfunction. Although effective heart failure therapy has been associated with a lowering or no change in systemic arterial blood pressure in long-term follow-up, this study describes the symptomatic, clinical, and left ventricular functional response of a subgroup of heart failure patients with a prior history of hypertension who demonstrated a paradoxical hypertensive response despite high-dose vasodilator therapy. We prospectively identified 45 patients with a past history of hypertension who had become normotensive with symptomatic heart failure. Of these 45 heart failure patients, 12 became hypertensive while receiving therapy in follow-up, with systolic blood pressure > or = 140 mm Hg (Group A). The remaining 33 patients did not have a hypertensive response to therapy (Group B). In the 12 Group A patients, 60+/-10 years old, with symptomatic heart failure for 6.3+/-4.3 years, vasodilator therapy was intensified in the 2.0+/-0.5 years of follow-up, achieving final doses of enalapril 78+/-19 mg and isosorbide dinitrate 293 +/-106 mg per day. New York Heart Association classification improved from 2.9+/-0.8 to 1.3+/-0.5 (P < or = .0001), with a reduction in heart-failure-related hospitalizations. Left ventricular ejection fraction increased from 17+/-6% to 40+/-10% (P < .0001). Follow-up blood pressure at 1 to 3 months was unchanged. However, both systolic and diastolic blood pressure increased at final follow-up, rising from 116+/-14 to 154+/-13 mm Hg (P = .0001) and from 71+/-9 to 85+/-14 mm Hg (P = .004), respectively. Renal function remained unchanged. Although both groups had similar clinical responses, there were more blacks and women in the hypertensive Group A. Effectively, 12 of 45 (27%) heart failure patients with an antecedent history of hypertension demonstrated a paradoxical hypertensive response to vasodilator therapy. The recurrence of hypertension in a significant portion of patients successfully treated for heart failure has important clinical implications.     

Should atrial septal defects in adults be closed?

BACKGROUND: By assessing current surgical outcome and symptomatic relief, this study attempts to answer whether atrial septal defects in adults should be closed. METHODS: Thirty-nine adult patients aged 35.2 +/- 13.6 years underwent operation for an atrial septal defect between June 1988 and June 1994. Indications for closure were symptoms (33 patients) or a significant left-to-right atrial shunt (6 patients). Data were obtained from hospital records, and the latest status of the patients was determined by a written questionnaire. RESULTS: There were no deaths. Pulmonary embolism in 1 patient was the only complication observed. The QRS duration on the surface electrocardiogram decreased immediately (p < 0.001), and the cardiothoracic ratio on chest radiographs was significantly lower 3 to 6 months after operation (p < 0.001), both findings reflecting improved hemodynamics. No residual shunts were seen on follow-up (mean follow-up, 3.3 +/- 2.2 years). Twenty-seven (81.8%) of the 33 symptomatic patients improved clinically in terms of exercise performance, atrial arrhythmias, or both. Three (50%) of the 6 previously asymptomatic patients reported improved functional capacity post-operatively. CONCLUSIONS: Today, operation for atrial septal defects in adults can be performed with no mortality and low morbidity and results in symptomatic improvement in the majority of patients. Clinical improvement was seen even in patients who considered themselves asymptomatic preoperatively. We advocate closure of atrial septal defects in adult patients with symptoms or significant atrial shunts.     

The management of severe subaortic stenosis, ventricular septal defect, and aortic arch obstruction in the neonate

Neonates with ventricular septal defect and aortic arch obstruction frequently have subaortic stenosis resulting from posterior deviation of the infundibular septum. Because the aortic anulus is often hypoplastic, making direct resection of the infundibular septum through the standard transaortic approach difficult, the optimal method of repair is uncertain. From September 1989 through November 1991, seven patients with ventricular septal defect, coarctation (n = 4), or interrupted aortic arch (n = 3) and severe subaortic stenosis underwent repair with use of a technique that included transatrial resection of the infundibular septum. Their ages ranged from 5 to 63 days (median 15 days) and weights from 1.3 to 5.4 kg (mean 3.1 kg). Only one patient was older than 1 month. The systolic and diastolic ratios of the diameter of the left ventricular outflow tract to that of the descending aorta were 0.53 +/- 0.09 mm (standard deviation) and 0.73 +/- 0.11, respectively. At operation, the posteriorly displaced infundibular septum was partially removed through a right atrial approach by resecting the superior margin of the ventricular septal defect up to the aortic anulus. The resulting enlarged ventricular septal defect was then closed with a patch to widen the subaortic area. In each patient the aortic arch was repaired by direct anastomosis. All patients survived operation; there was one late death from noncardiac causes 3 months after repair. The survivors remain well from 3 to 14 months after repair (mean 8 months). All are in sinus rhythm and none has a residual ventricular septal defect. One patient underwent successful balloon dilation of a residual aortic arch gradient late after repair. No patient has significant residual subaortic stenosis, although one has valvular aortic stenosis. This series suggests that in neonates with ventricular septal defect and severe subaortic stenosis resulting from posterior deviation of the infundibular septum, direct relief can be satisfactorily accomplished from a right atrial approach. This method provides effective widening of the left ventricular outflow tract and is superior to palliative techniques or conduit procedures.