Hemodynamic responses to ergometer exercise in children and young adults with left ventricular pressure or volume overload

This study determines (1) the hemodynamic responses to exercise in groups of young patients with either left ventricular (LV) pressure or volume overload, (2) whether these responses differed from healthy subjects when the variables of sex, age, race and body surface area were controlled (analysis of covariance), and (3) whether any of the exercise variables could predict noninvasively the severity of the gradient in aortic valve stenosis (AS). We tested 137 patients, including 70 with AS, 25 with aortic isthmic coarctation, 20 with aortic regurgitation and 22 with mitral regurgitation, and compared them with a control population of 405 healthy children. The children underwent a continuous, graded, maximal test with 3-minute stages. The variables evaluated were peak heart rate, systolic blood pressure, maximal work load (kgm/min), peak working capacity index (kg-m/min/ kg body weight) and ischemia on electrocardiography.In patients with pressure overload, the maximal exercise values for work load, heart rate and peak working capacity index were significantly different (p < 0.05) from control values. The patients with volume overload had higher blood pressure values than either control subjects or patients with pressure overload. Similarly, the values for heart rate in patients with volume overload were lower than values for control subjects and patients with pressure overload. No exercise variable was predictive of severity of AS. These data confirm some previous investigators' findings with respect to LV volume and pressure overload, but do not support the concept that exercise test results are sensitive and specific for the prediction of severity in AS.     

Comparison of left ventricular geometry and left atrial size and function in patients with aortic stenosis versus those with pure aortic regurgitation

Chronic aortic valve disease can result in distinct adaptive left ventricular (LV) geometric patterns, which has different effects on LV function and left atrial (LA) performance. In this study we assessed the effect of LV geometry on LA size and function, and we verified the relation between LA size and LV mass in patients with distinct LV overload subsets. We analyzed 183 patients with aortic valve disease who underwent a complete echocardiographic evaluation. Based on the type of valvular dysfunction, patients were classified into 2 groups: 141 patients with aortic stenosis (group AS) and 42 patients with pure aortic regurgitation (group AR). Each of these 2 groups were then divided into those with a concentric LV pattern and those with an eccentric pattern. Both LA size and LA ejection force were significantly greater in group AS than group AR, particularly in patients with a concentric LV pattern. The degree of LA enlargement depended on LV mass in the patients with a concentric LV pattern (group AS r = 0.61, p <0.00001; group AR r = 0.38, p = 0.04). In contrast, no relation was found between LA size and LV mass in the patients with an eccentric pattern, independently of the type of valve dysfunction. Our results indicate that the influence of LV geometry on LA size and function in patients with aortic valve disease is relevant. A concentric LV pattern is associated with greater LA size and higher ejection than an eccentric pattern, suggesting that chronic LV pressure overload more than volume overload has a greater effect on stimulating increases in LA performance. The degree of LA enlargement depends on LV mass in patients with a concentric LV pattern, whereas it was unpredictable in those with an eccentric LV pattern.     

Assessment of left ventricular relaxation in patients with valvular regurgitation

Impaired left ventricular (LV) relaxation has been demonstrated in patients with coronary heart disease and in patients with hypertrophic or congestive cardiomyopathy but not yet in those with aortic or mitral regurgitation. Indeed, in patients with valvular regurgitation the lack of isovolumic relaxation and variations in the filling rate invalidate most relaxation indexes. The aim of this study was to assess ventricular relaxation in patients with valvular insufficiency. The hemodynamic and angiographic data were analyzed during the phase of decreasing left ventricular elastance (that is, when pressure is decreasing while volume is increasing) in 57 patients (27 with valvular regurgitation, 17 normal subjects, and 13 patients with coronary heart disease). Starting from a fixed level of wall stress (40 kdyne/cm²), we determined the incremental LV elastance (ratio $\text{solΔAP}\text{ΔV}$) and the changes in velocity of lengthening produced by a constant increase in LV volume (+ 20 ml/m²). In aortic and mitral regurgitation, both the incremental elastance (?0.52 versus —0.95 mm Hg/ml per m² in normal subjects: p <0.001) and the changes in velocity of lengthening (+ 0.76 versus +1.17 circ/s; p <0.05) were abnormal. These indexes were also impaired in patients with coronary heart disease. Further, significant correlations were found in the whole group between incremental elastance and ejection fraction (r = 0.63), mean velocity of fiber shortening (r = 0.62), and end-systolic volume (r = 0.53), suggesting a relation between impaired incremental elastance and alterations in inotropic state or afterload, or both. This hypothesis was confirmed by the fact that patients who had a peak systolic wall stress of less than 400 kdyne/cm² and a normal index of inotropic state also had normal incremental elastance: in contrast, all but 1 patient with the same afterload but abnormal contractility had abnormal incremental elastance. It is concluded that abnormalities in early diastolic filling are common in patients with valvular regurgitation and are likely to be related to impaired LV relaxation.     

Influence of left ventricular mass on coronary artery cross-sectional area

Observations from cardiac catheterization suggest that coronary artery cross-sectional area (CSA) is increased in patients with left ventricular (LV) hypertrophy and is proportional to LV mass. This hypothesis was tested using computer-based quantitative analysis of LV mass and CSA from angiographic images of the left ventricle and proximal coronary arteries from 19 men and 21 women, aged 23 to 78 years (mean 56). Twenty-seven patients had valvular heart disease, 16 of whom had multivalvular involvement; diagnoses included aortic stenosis in 19, aortic regurgitation in 13 and mitral regurgitation in 12. Thirteen patients had normal valvular and ventricular function. All patients had normal coronary arteries. Significant differences between normal patients and those with valvular disease were noted in LV mass (88 +/- 7 vs 165 +/- 12 g/m2, p less than 0.001) and coronary CSA (26 +/- 2 vs 46 +/- 3 mm2, p less than 0.001). Furthermore, a linear relation between LV mass and coronary CSA was noted (r = 0.788, p less than 0.001). Thus, proximal coronary artery CSA is significantly larger in valvular heart disease patients with LV hypertrophy than in those with normal ventricles, and proximal coronary artery area increases in proportion to LV mass in hypertrophied ventricles.     

Role of inadequate adaptive left ventricular hypertrophy in the genesis of mitral regurgitation in patients with severe aortic stenosis: implications for its prevention

BACKGROUND AND AIM OF THE STUDY: Mitral regurgitation (MR) is frequent in patients with severe calcific aortic stenosis (AS). This complicates not only the clinical course of AS, but also its surgical management. The aim of the present study was to investigate the mechanism of genesis of MR in patients with severe AS. METHODS: The echocardiographic database was searched for subjects with severe AS defined as a calculated (continuity equation) aortic valve area < 0.7 cm2. Patients with previous valve surgery were excluded; thus, the study group comprised 123 patients. RESULTS: Among 123 patients (mean age 75 +/- 10 years) with severe AS, 54 (44%) had no MR, 37 (30%) had mild MR, 20 (16%) had moderate MR, and 12 (10%) had severe MR. Hence, moderate or severe MR was present in approximately 25% of patients. Patients with moderate or severe MR had a larger left ventricular (LV) end-diastolic diameter (5.1 +/- 1.0 versus 4.8 +/- 0.8 cm; p = 0.08), larger LV end-systolic diameter (3.8 +/- 1.2 versus 3.1 +/- 0.8 cm; p = 0.001), lower LV ejection fraction (40 +/- 16 versus 58 +/- 18%; p = 0.0001), higher degree of aortic regurgitation (p = 0.002), larger left atrial diameter (4.7 +/- 0.9 versus 4.1 +/- 0.6 cm; p = 0.001), lower LV free wall thickness (1.1 +/- 0.2 versus 1.3 +/- 0.4 cm; p = 0.05), and lower combined wall thickness (2.4 +/- 0.3 versus 2.7 +/- 0.5 cm; p = 0.02) and relative wall thickness (0.5 +/- 0.1 versus 0.6 +/- 0.1 cm; p = 0.02). Both groups had similar degrees of AS and mitral annular calcification. CONCLUSION: MR in severe AS is associated with a larger LV size and lesser wall thickness, and this may result from failure of adequate adaptive LV hypertrophy necessitated by the pressure overload imposed by AS. This might have important clinical implications in terms of timing of aortic valve replacement before the left ventricle begins to dilate, and also in the choice of pharmacologic therapy that may modulate the adaptive response of the left ventricle.     

Radionuclide evaluation of aortic regurgitation: assessment of ventricular function by Fourier phase analysis

Forty patients with chronic isolated aortic regurgitation werestudied by phase analysis of equilibrium radionuclide ventriculographyto see whether this technique could detect changes in left ventricular(LV) function before the onset of symptoms. This technique wascompared to the radionuclide ejection fraction and echocardiography.The severity of LV volume overload was assessed using the radionuclideregurgitant index.Patients with clinically severe aortic regurgitationhad severe volume overload (high regurgitant index), increasedechocardiographic left ventricular dimensions and significantlyincreased phase spread (loss synchrony of wall motion) comparedto mild and moderate groups. All but one had well maintainedglobal left ventricular function assessed by the ejection fraction.All seven patients with definite symptoms had a marked increasein phase spread and severe volume overload.     

Combined first-pass and equilibrium radionuclide ventriculography and comparison with left ventricular/right ventricular stroke count ratio in mitral and aortic regurgitation

Effective and total left ventricular (LV) stroke volume were assessed in 31 patients with verified aortic or mitral regurgitation, or both, and in 22 patients with normal valvular function using combined first-pass and equilibrium radionuclide ventriculography. The difference between these 2 volumes as a fraction of LV stroke volume was taken as the radionuclide regurgitant fraction. The results were compared with the LV/right ventricular (RV) stroke count ratio and with the angiographic regurgitant fraction according to the method of Sandler and Dodge. Radionuclide regurgitant fraction derived from 2 determinations with a time interval of 1 week showed good reproducibility (n = 15, r = 0.96, SEE = 9.1). Sensitivity was 100% for radionuclide regurgitant fraction and 87% for LV/RV stroke count ratio at equal specificity (100%). Radionuclide regurgitant fraction was more sensitive, especially in severely ill patients, in whom additional RV volume overload led to false-low or false-negative ratios. Angiographic and radionuclide regurgitant fraction showed linear correlation (r = 0.79, p less than 0.001). In contrast, because 5 patients had RV volume overload, only a weak correlation could be noticed between angiography and LV/RV stroke count ratio (r = 0.47, p less than 0.05). Excluding these patients, correlation substantially improved (r = 0.74, p less than 0.001). The combination of first-pass and equilibrium radionuclide ventriculography is a sensitive, specific and well reproducible method for the evaluation of mitral and aortic regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Percutaneous balloon pulmonary valvuloplasty

Percutaneous balloon pulmonary valvuloplasty (BPV) was performed in 18 consecutive patients with valvular pulmonary stenosis (PS) with no associated cardiac defects. The patients were 11 months to 19 years of age. The balloon was positioned across the pulmonary valve and inflated to pressures of 80, 100, and 120 pounds/square inch (psi). Each inflation lasted approximately 10 seconds. Peak systolic pulmonary valve gradient (ΔP) and cardiac output were measured before and 15 minutes after BPV. There was no change in cardiac output, but all patients had an improved ΔP. The prevalvuloplasty ΔP was 81 ± 31 mm Hg, decreasing to 23 ± 11 mm Hg after BPV (p < 0.01). The right ventricular peak systolic pressure decreased from 106 ± 31 to 50 ± 12 mm Hg (p < 0.01). No pulmonary regurgitation was noted after BPV. The balloons were 12 or 15 mm in diameter, chosen according to the diameter of the pulmonary valve anulus. Pressures of 100 to 120 psi were required to achieve full inflation of the balloons. BPV also was performed in a patient with tetralogy of Fallot. Subsequent total repair provided an opportunity to observe the mechanism of the dilatation. Evidence of a small tear alongside the anterior valve raphe was noted. BPV induced a significant decrease in ΔP and may offer an alternative method for treating PS.     

Severe isolated aortic stenosis with normal left ventricular systolic function and low transvalvular gradients: pathophysiologic and prognostic insights

BACKGROUND AND AIM OF THE STUDY: A significant proportion of patients with severe valvular aortic stenosis (AS) and preserved left ventricular (LV) systolic function have low transvalvular gradients. The study aim was to determine the mechanisms and outcome of patients with this hemodynamic profile of AS. METHODS: Among 1,679 patients who underwent transthoracic echocardiography for the evaluation of AS at the authors' institution, 215 (105 females, 110 males; mean age: 77 +/- 10 years) had isolated AS (mean aortic valve area index 0.39 +/- 0.1 cm2/m2), normal sinus rhythm and normal LV ejection fraction. The mean follow up was 23 +/- 12 months, and the end-points were mortality, aortic valve replacement (AVR), or mortality or AVR. RESULTS: Forty-seven patients had a transvalvular mean gradient (MG) <30 mmHg (MG(low)) and 168 had MG > or = 30 mmHg (MG(high)). Compared to MG(high), the MG(low) group had a higher prevalence of hypertension, lower LV end-diastolic volume index (47 +/- 9 versus 56 +/- 12 ml/m2, p <0.0001), lower LV stroke vol-ume index (37 +/- 12 versus 41 +/- 11 ml/beat, p <0.0002), a lesser severity of stenosis (aortic valve area index 0.37 +/- 0.09 versus 0.46 +/- 0.09 cm2/m2, p <0.0001) and a higher systemic vascular resistance (2163 +/- 754 versus 1879 +/- 528 dyne cm s(-5). The LV end-diastolic volume index, systemic vascular resistance and energy loss index were predictors of MG <30 mmHg (OR = 0.30, 95% CI, 0.12, 0.62; OR = 3.05, 95% CI, 1.71, 6.26; and OR = 6.76, 95% CI, 3.44,15.38, respectively). MG <30 mmHg (MGhigh) was associated with almost 50% lower referral to surgery and a two-fold increase in preoperative mortality. CONCLUSION: In severe AS with a normal LV ejection fraction, MG <30 mmHg is related to a lesser severity of stenosis, a smaller LV volume, a lower flow rate and a higher systemic vascular resistance. Compared to the MG(high) group, these patients were less frequently referred to surgery and had a higher mortality.     

Progression of isolated aortic stenosis: Analysis of 29 patients having more than 1 cardiac catheterization

Factors related to progression of nonrheumatic aortic stenosis (AS) were analyzed in 29 adult patients who underwent serial hemodynamic studies over a mean of 71 months. AS was congenital in 8 patients and degenerative in 21. The patients were divided into 2 groups on the basis of the change in aortic valve area between the 2 studies. Twelve patients had a ≥ 25% reduction in aortic valve area (Group I) and 17 patients had < 25% decrease in aortic valve area (Group II). There were no significant differences between the 2 groups in age, interval between studies, cardiac output, left ventricular end-diastolic pressure, left ventricular peak systolic pressure and origin of AS (congenital or degenerative). Group I patients had significantly larger initial aortic valve areas than did Group II patients (1.3 ± 0.9 cm² versus 0.8 ± 0.4 cm², p = 0.02). Also, the initial peak transaortic pressure gradients were lower in Group I than in Group II (27 ±19 versus 58 ± 38 mm Hg, p = 0.01). Group I patients had a significantly greater increase in pressure gradient and a greater reduction in cardiac output than did Group II patients (24 ± 21 mm Hg in Group I versus?0.1 ± 24.5 mm Hg in Group II, p = 0.01, and ?1.0 ± 1.3 liters/min in Group I versus 0.10 ± 1.4 liters/min in Group II, p = 0.03). Thus, AS progressed in 41 % of a selected group of patients who underwent repeated cardiac catheterization. The progression was not predictable. Although 10 patients (34%) had moderate aortic regurgitation (AR) in the second study, it was not related to the origin or rate of progression of AS. Mild AS tends to progress more than severe AS. Congenital AS appears to progress at the same rate as degenerative AS.     

Long-term effect of angiotensin-converting enzyme inhibitor in volume overloaded heart during growth: a controlled pilot study

OBJECTIVES: This study examined whether long-term therapy with an angiotensin-converting enzyme (ACE) inhibitor reduces excessive increases in left ventricular (LV) mass as well as volume in growing children with aortic regurgitation or mitral regurgitation. BACKGROUND: The ACE inhibitor reduces volume overload and LV hypertrophy in adults with aortic or mitral regurgitation. METHODS: This study included 24 patients whose ages ranged from 0.3 to 16 years at entry to the study. On echocardiography, we measured LV size, systolic function and mass. After obtaining baseline data, patients were allocated into two groups. Twelve patients were given an ACE inhibitor (ACE inhibitor group), and 12 patients were not (control group). Echo parameters were again assessed after an average 3.4 years of follow-up. RESULTS: Left ventricular parameters at baseline in the two groups were similar. The Z value of LV end-diastolic dimensions decreased from +0.82 +/- 0.55 to +0.57 +/- 0.58 in the ACE inhibitor group, whereas it increased from +0.73 +/- 0.85 to +1.14 +/- 1.04 in the control group (mean change -0.25 +/- 0.33 for the ACE inhibitor group vs. +0.42 +/- 0.48 for the control group, p = 0.0007). The mass normalized to growth also reduced from 221 +/- 93% to 149 +/- 44% of normal in the ACE inhibitor group and increased from 167 +/- 46% to 204 +/-59% of normal in the control group (mean change -72 +/- 89% of normal for the ACE inhibitor group vs. +37 +/- 35% of normal for the control group, p = 0.0007). CONCLUSIONS: Long-term treatment with ACE inhibitors is effective in reducing not only LV volume overload but also LV hypertrophy in the hearts of growing children with LV volume overload.     

Concentric left ventricular hypertrophy in patients with aortic regurgitation

Chronic aortic regurgitation (AR) is a disease incorporating volume overload of the left ventricle (LV) which is characterized by hyperactive left ventricular dilatation (LVD). However, we have encountered several patients who had concentric LV hypertrophy (LVH) instead of LVD. We therefore studied 50 consecutive patients with isolated AR but without aortic stenosis and found seven patients with concentric LVH having LV wall thickness (determined by summing ventricular septal and posterior wall thicknesses) exceeding 30 mm and LV diastolic diameters of less than 60 mm. These seven patients with AR and LVH were older (55 +/- 27 vs 42 +/- 11 years) and tended to have milder degree of AR, compared with the remaining 43 patients having AR and LVD. However, patients with AR and LVH did not differ from AR and LVD as to the cardiothoracic ratio, SV1 + RV5, T-waves, ejection fraction, operative findings of valvular morphology and underlying etiologies. In contrast, patients with AR and LVH presented higher systolic (196 +/- 41 vs 149 +/- 26 mmHg, p less than 0.01) and diastolic pressures (74 +/- 14 vs 51 +/- 13 mmHg, p less than 0.01) and higher systemic vascular resistance (1,854 +/- 399 vs 1,388 +/- 352 dyne.sec.cm-5, p less than 0.05) during catheterization than did those with AR and LVD. However, blood pressure at the time of admission was not different in the two groups. These observations indicate that concentric LVH is not rare among patients with AR, and that an association of pressure overload with volume overload of the LV, particularly during exercise or stress, may lead to concentric LVH, even in patients with chronic AR.     

Impact of valvular regurgitation on left ventricular geometry and function in hypertensive patients with left ventricular hypertrophy: the LIFE study

Mild-to-moderate aortic and mitral regurgitation are frequently detected by echocardiogram in asymptomatic hypertensive patients. Our goal was to assess the prevalence and impact of mild-to-moderate mitral and/or aortic regurgitation on left ventricular (LV) structure and function in patients with hypertension and LV hypertrophy (LVH). Hypertensive patients with ECG LVH enrolled in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiography substudy were evaluated. Among 939 patients with needed LV measurements and Doppler data, 242 had mild (1+) valvular regurgitation, and 51 patients had moderate (2+ or 3+) regurgitation of one or both valves. In analyses adjusting for gender, patients with mild mitral and/or aortic regurgitation had larger LV internal dimensions (5.25 vs 5.33 cm, P<0.05), higher LV mass indexed for body surface area (122 vs 125 g/m(2), P<0.05) or height(2.7) (55.4 vs 57.3, P<0.05), and larger left atrial diameter. Patients with moderate regurgitation of one or both valves had larger LV chambers (5.25 vs 5.9 cm, P<0.001), greater mean LV mass (232 vs 248 g, P<0.001) and LV mass indexed for body surface area or height(2.7), and higher Doppler stroke volume. Patients with moderate valvular regurgitation also had a higher prevalence of LVH due to an increased prevalence of eccentric LVH. There were no differences among groups defined by the presence and severity of valvular regurgitation in cardiac output, total peripheral resistance, or pulse pressure/stroke volume, indicating that the observed inter-group differences in LV geometry were not due to differences in the haemodynamic severity of hypertension. Hypertensive patients with mild-to-moderate mitral or aortic valvular insufficiency have additional LV structural and functional changes that may affect prognosis.     

Pattern of left ventricular diastolic filling associated with right ventricular enlargement

Right ventricular (RV) dilatation associated with pressure overload may alter left ventricular (LV) geometry resulting in abnormal diastolic function as demonstrated by a smaller LV diastolic volume for a given LV diastolic pressure. To determine whether abnormalities in LV geometry due to RV dilatation result in abnormalities in the LV diastolic filling pattern, we obtained pulsed Doppler transmitral recordings from 23 patients with RV dilatation with RV systolic pressure estimated to be less than 40 mm Hg (group 1), 18 patients with RV dilatation and RV systolic pressures greater than or equal to 40 mm Hg (group 2) and 33 normal patients. RV systolic pressures were estimated from continuous wave Doppler peak tricuspid regurgitation velocities using the modified Bernoulli equation. Diastolic filling parameters in group 1 patients were similar to normals. In group 2 patient, increased peak atrial filling velocity (76 +/- 14 vs 57 +/- 12 cm/s, p less than 0.001), decreased peak rapid filling velocity/peak atrial filling velocity (1.1 +/- 0.4 vs 1.5 +/- 0.4, p less than 0.01), increased atrial filling fraction (41 +/- 14 vs 30 +/- 10%, p less than 0.01) and prolongation of the atrial filling period (171 +/- 47 vs 152 +/- 39 ms, p less than 0.05) were noted compared with the normal group. RV end-diastolic size and LV end-systolic shape were significantly correlated with the atrial filling fraction in group 2 patients. In patients with RV dilatation and RV systolic pressures greater than or equal to 40 mm Hg, there is increased reliance on atrial systolic contribution to the LV filling volume.     

Hemodynamic effects of nitroprusside on valvular aortic stenosis.

The effects of acute reduction of left ventricular (LV) loading in valvular aortic stenosis (AS) were examined. Thirty-five consecutive patients with AS (peak-to-peak aortic valve gradient 66 +/- 26 mm Hg, aortic valve area 0.65 +/- 0.22 cm2) were given intravenous sodium nitroprusside (1 to 3 micrograms/kg/min) to reduce systolic aortic pressures by greater than 10 mm Hg (mean aortic pressure 99 +/- 15 to 80 +/- 15 mm Hg; p less than 0.001). Overall, nitroprusside infusion resulted in little change in cardiac index (2.72 +/- 0.61 to 2.67 +/- 0.58 liters/min/m2; p = not significant). Individual patients had a range of responses. Fourteen patients (group 1) had an increase in cardiac index (2.42 +/- 0.59 to 2.74 +/- 0.67 liters/min/m2; p less than 0.001), whereas 21 (group 2) had a decrease or no change (2.93 +/- 0.56 to 2.61 +/- 0.52 liters/min/m2; p less than 0.001). Comparison of these subgroups showed that a cardiac index increase with nitroprusside was significantly predicted by a higher LV end-diastolic pressure (26 +/- 12 vs 15 +/- 6 mm Hg), lower LV ejection fraction (44 +/- 18 vs 62 +/- 12%). smaller aortic valve area (0.52 +/- 0.12 vs 0.74 +/- 0.22 cm2) and lower cardiac index (2.42 +/- 0.59 vs 2.93 +/- 0.56 liters/min/m2) (all values groups 1 and 2, respectively). It is concluded that there is a disparate response to acute vasodilatation in AS. Potentially beneficial effects are seen in a subgroup of patients, especially those with increased filling pressures and impaired LV function.(ABSTRACT TRUNCATED AT 250 WORDS)     

Reoperation for coarctation of the aorta

Between 1957 and 1980 reoperation for coarctation of the aorta was performed in 21 patients at one institution for an overall incidence rate of 7.9 percent. The incidence rate of reoperation was 38 percent for patients younger than age 3 years and 1.5 percent for patients 3 years or older at initial repair. Before reoperation 14 of the 21 patients were symptomatic, 19 had systolic hypertension of the upper limbs and 20 had a documented coarctation pressure gradient at rest (mean 42.4 mm Hg). Surgical techniques used at reoperation were patch aortoplasty in 12 patients, graft interposition in 4, end to end anastomosis in 3 and end to side left subclavian to descending aorta bypass graft in 2. There was one surgical death. The 20 survivors have been followed up a mean of 4.3 years. There has been significant symptomatic improvement (p < 0.001). Upper limb hypertension has also lessened significantly (p < 0.001) after reoperation;15 patients are no longer hypertensive and 3 have a lesser degree of hypertension. The coarctation pressure gradient at rest has significantly decreased (p < 0.001); 13 patients have no residual gradient and 7 have a mild gradient of 20 mm Hg or less. Graded treadmill exercise testing performed in five patients after reoperation documented upper limb hypertension in four and a marked increase in coarctation gradient with exercise in three.

In conclusion, the incidence of reoperation is significantly increased in patients who are younger than age 3 years at initial coarctation repair. Reoperation is a safe and effective procedure. It has a low mortality rate (4.8 percent), relieves symptoms and decreases hypertension and the coarctation pressure gradient. Patch aortoplasty appears to be the operative procedure of choice. Moderate to severe hemodynamic abnormalities may persist during exercise after reoperation for coarctation of the aorta.     

Factors influencing left ventricular structure and stress-corrected systolic function in men and women with asymptomatic aortic valve stenosis (a SEAS Substudy)

To identify determinants of left ventricular (LV) structure and stress-corrected systolic function in men and women with asymptomatic aortic stenosis (AS), Doppler echocardiography was performed at baseline in 1,046 men and 674 women 28 to 86 years of age (mean 67 +/- 10) recruited in the Simvastatin Ezetimibe in Aortic Stenosis (SEAS) study evaluating placebo-controlled combined simvastatin and ezetimibe treatment in AS. LV hypertrophy was less prevalent in women despite older age, higher systolic blood pressure, and smaller aortic valve area/body surface area (all p values <0.05). In logistic regression analyses, LV hypertrophy was independently associated with male gender, severity of AS, hypertension, higher systolic blood pressure, and lower stress-corrected midwall shortening (scMWS) or stress-corrected fractional shortening (scFS; all p values <0.01). In men aortic regurgitation also was a predictor of LV hypertrophy (p <0.05). Women had greater scFS and scMWS when corrected for LV size or geometry (all p values <0.001). In multivariate analyses, female gender predicted 11% greater scFS and 4% greater scMWS independent of age, body mass index, heart rate, aortic valve area, LV mass, relative wall thickness, aortic regurgitation, hypertension, and end-systolic stress (R(2) = 0.23 and 0.59, respectively, p <0.001). In conclusion, the major determinants of LV hypertrophy in patients with asymptomatic AS are male gender, severity of AS, and concomitant hypertension. Women have higher stress-corrected indexes of systolic function independent of LV geometry or size, wall stress, older age, or more concomitant hypertension.     

End-systolic volume as a predictor of postoperative left ventricular performance in volume overload from valvular regurgitation

Although over-all cardiac performance may remain normal in patients with left ventricular volume overload from valvular regurgitation, impairment of myocardial function may occur and remain undetected by currently accepted methods of assessing ventricular performance. Since end-systolic volume reflects myocardial contractile function yet is independent of preload, we assessed preoperative end-systolic volume as a measure of myocardial function in 41 patients with aortic regurgitation, mitral regurgitation or both. Preoperative end-systolic volume was compared to postoperative left ventricular performance as measured by postoperative echocardiographic per cent dimension change (% ΔD) and New York Heart Association class. Preoperative end-systolic volume correlated well with postoperative left ventricular performance in patients with aortic regurgitation (r = 0.77) or mitral regurgitation (r = 0.73). Much poorer correlations existed for preoperative ejection fraction, enddiastolic volume or left ventricular end-diastolic pressure. Preoperative end-systolic volume also predicted patients at high risk for perioperative cardiac death, with all such cardiac deaths occurring in patients with an end-systolic volume >60 cc/m². Again, both preoperative ejection fraction and end-diastolic volume were less precise predictors of surgical outcome. Patients with aortic regurgitation appeared to tolerate a larger end-systolic volume better than those with mitral regurgitation.End-systolic volume is an easily determinable parameter of left ventricular function which is independent of the abnormal preload that occurs in mitral regurgitation and aortic regurgitation and appears to provide a measure for the onset of myocardial dysfunction in patients with these lesions. Whether this myocardial dysfunction is due to a depressed inotropic state of individual sarcomeres, a stress-shortening imbalance or to other factors is unknown, but its presence has major prognostic importance.     

Fixed subaortic stenosis in the young: Medical and surgical course in 83 patients

Eighty-three patients aged 11 months to 25 years were followed up a median of 6.1 years (range 8 days to 24 years) after diagnosis of fixed subaortic stenosis (SAS). Fourteen (17%) had significant noncardiac defects and 47 (57%) had additional cardiac malformations. The left ventricular (LV) outflow gradient increased in 25 of 26 patients catheterized more than once before surgery. Of 15 patients < 12 years old with gradients < 40 mm Hg, 10 ultimately underwent operation after developing severe obstruction; another has progressed to a gradient of 45 mm Hg at 6 years of age. Before surgery (at a median age of 12 years), 55% had aortic regurgitation (AR), which was usually mild. Infective endocarditis occurred in 12% of the group, with a frequency of 14.3 cases per 1,000 patientyears. Seventy-four patients were operated on, with 6 early (8%) and 7 late (9%) deaths. Twelve underwent reoperation to relieve residual obstruction. Surgery reduced gradients in patients with discrete SAS from 83 ± 33 to 29 ± 30 mm Hg, but in 6 patients with tunnel SAS the reduction was less satisfactory. AR was absent or mild in most patients postoperatively. When the gradient was reduced to < 80 mm Hg, infective endocarditis did not occur unless there were other residual lesions. These data suggest that it is reasonable to resect discrete SAS in children < 10 to 12 years old with LV outflow gradients ?- 30 mm Hg.     

Effect of chronic afterload increase on left ventricular myocardial function in patients with congenital left-sided obstructive lesions

The effect of pressure-overloading distance on left ventricular (LV) function in patients with congenital aortic coarctation and aortic stenosis (AS) was investigated. LV long-axis motions were recorded using M-mode and tissue Doppler imaging (TDI) techniques in 46 consecutive patients with severe LV outflow tract obstruction (23 coarctation and 23 AS), and results were compared with those of 23 controls. TDI lateral and septal long-axis systolic velocities, early diastolic velocities, and M-mode systolic amplitudes were lower in patients with coarctation and AS than controls (lateral site long-axis systolic velocity 7.1 +/- 1.7 and 6.4 +/- 1.6 vs 9.7 +/- 1.7 cm/s, septal site long-axis systolic velocity 6.3 +/- 1.3 and 5.4 +/- 1.1 vs 7.7 +/- 1.3 cm/s; lateral site early diastolic velocity 10.5 +/- 2.2 and 8.2 +/- 2.6 vs 13.1 +/- 2.5 cm/s, septal site early diastolic velocity 7.4 +/- 1.9 and 6.0 +/- 1.8 vs 10.8 +/- 1.6 cm/s, lateral site M-mode systolic amplitude 1.4 +/- 0.2 and 1.3 +/- 0.2 vs 1.6 +/- 0.2 cm, septal site M-mode systolic amplitude 1.2 +/- 0.2 and 1.1 +/- 0.2 vs 1.4 +/- 0.2 cm, p <0.01 for all). Compared with patients with coarctation, those with AS had lower TDI velocities, higher early LV filling velocity/long-axis diastolic velocity ratios, and a higher prevalence of long-axis incoordination (p <0.05 for all) despite similar LV mass index, ejection fraction, and systolic wall stress. In conclusion, LV long-axis function is impaired in patients with a chronic increase in afterload. Worse deterioration in LV function and higher prevalence of long-axis incoordination independent of LV outflow resistance is seen in patients with proximally increased LV afterload (AS) compared with distal disease (aortic coarctation).