Valvular heart disease: aortic regurgitation

Aortic regurgitation (AR) is characterized by diastolic reflux of blood from the aorta into the left ventricle (LV). Acute AR typically causes severe pulmonary edema and hypotension and is a surgical emergency. Chronic severe AR causes combined LV volume and pressure overload. It is accompanied by systolic hypertension and wide pulse pressure, which account for peripheral physical findings, such as bounding pulses. The afterload excess caused by systolic hypertension leads to progressive LV dilation and systolic dysfunction. The most important diagnostic test for AR is echocardiography. It provides the ability to determine the cause of AR and to assess the severity of AR and its effect on LV size, function, and hemodynamics. Many patients with chronic severe AR may remain clinically compensated for years with normal LV function and no symptoms. These patients do not require surgery but can be followed carefully for the onset of symptoms or LV dilation/dysfunction. Surgery should be considered before the LV ejection fraction falls below 55% or the LV end-systolic [corrected] dimension reaches 55 mm. Symptomatic patients should undergo surgery unless there are excessive comorbidities or other contraindications. The primary role of medical therapy with vasodilators is to delay the need for surgery in asymptomatic patients with normal LV function or to treat patients in whom surgery is not an option. The goal of vasodilator therapy is to achieve a significant decrease in systolic arterial pressure. Future therapies may focus on molecular mechanisms to prevent adverse LV remodeling and fibrosis.     

Value of partial ejection fraction, volume increment, and regional wall motion in identifying patients with clinically significant coronary artery disease

Recent studies suggest that the partial ejection fraction (EF) in early systole is a more sensitive index of left ventricular (LV) dysfunction than the holosystolic EF. We examined LV volume, partial EF, and volume increment at each of 12 time points in systole to determine which parameter best distinguishes normal subjects from patients with coronary artery disease (CAD). Contrast ventriculograms, obtained either in the right anterior oblique projection (60 frames/sec) or in the biplane projection (30 frames/sec), of 58 normal subjects and 68 patients with CAD were studied. The endocardial contour in each frame of a sinus beat was traced to derive a volume curve. At each twelfth of systole, LV volume was extrapolated from the curve and the partial EF was calculated. The increment in volume between successive time points was also calculated. Both partial EF and LV volume in patients with CAD became progressively more abnormal with time; peak abnormality occurred at end-systole. In a subgroup of patients with CAD who had normal holosystolic EF, both partial EF and volume were normal throughout systole. The increment in volume with each twelfth of systole in patients with CAD deviated less than 1 SD from normal throughout systole. Thus, maximum abnormality in partial EF and volume occurs at end-systole. Of the parameters of global LV function tested, holosystolic EF best distinguishes patients with CAD from normal subjects. However, regional wall motion measured in the area of interest is more sensitive to localized abnormality, the severity of which may be overestimated or underestimated by the EF due to hyperkinesis or hypokinesis in other regions of the left ventricle.     

二维超声心动图对术前法乐四联症左心室重量与心功能的评价

目的：研究法乐四联症左心发育与心功能的关系。方法：用二维超声心动图评价９０例法乐四联症的左心室容积、左心室重量与心功能的关系（各测值均与年龄相匹配的４０名正常人对照）。结果：法乐四联症病人的左心室容积、左心室前壁、后壁厚度及左心室心肌重量各测值明显小于正常对照组（Ｐ＜０．０１）；而心室间隔厚度、左心室舒张末容积／左心室心肌容积比值、左心室射血分数各测值在两组间比较均无显著差异（Ｐ＞０．０５）；法乐四联症组的左心室舒张末容积与左心室心肌容积测值呈高度相关（ｒ＝０．８６）。结论：法乐四联症病人大多有左心室发育障碍，但左心室收缩功能仍可保持正常。     

Influence of age on the relationship between left atrial performance and left ventricular systolic and diastolic function in systemic arterial hypertension

BACKGROUND: Changes in left ventricular (LV) systolic and diastolic properties may generate variations in left atrial (LA) size and function in many pathophysiological models of LV overload. Besides these states, increasing age may independently influence and magnify LA changes. OBJECTIVE: To investigate the relation of LA size and function to increasing age in hypertensive patients, and to evaluate whether this relationship is influenced by LV function. METHODS: Three hundred thirty-six patients were evaluated using Doppler echocardiography. Maximal LA volume and ejection force were used as indexes of LA size and performance, respectively. RESULTS: Age was positively associated with LA ejection force (r=0.34, P<0.001) and maximal volume (r=0.25, P<0.001). The effect of age was independent of LV mass and LV concentric geometry, which independently influenced LA parameters. The relationship between age and LA ejection force was maintained in patients with and without LV systolic dysfunction, and in those with normal diastolic function, whereas it was lost in those with LV diastolic dysfunction. The relationship between age and LA size was not influenced by either LV systolic or diastolic function. LA ejection force was associated with LV mass and LV concentric geometry in all groups of patients 56 years or older, while no association was found between these variables in patients younger than 56 years. LV mass was systematically linked to maximal LA volume in all classes of age, together with LV end-diastolic volume in all groups of patients 56 years of age or older, and LV concentric geometry in patients 68 years of age or older. CONCLUSIONS: There is a positive relationship between age and LA size and performance in hypertensive patients, which is independent of LV mass and geometry. The effect of age on LA performance is insignificant when diastolic dysfunction occurs.     

A new classification of left ventricular geometry in patients with cardiac disease based on M-mode echocardiography.

M-mode echocardiograms of 202 cardiac patients were studied with respect to the pattern of left ventricular (LV) geometry. Patients with normal LV mass and volume were separated from those who had LV hypertrophy or enlargement on the basis of LV mass and volume indexed to body surface area. The relative wall thickness that is currently used to classify LV hypertrophy/enlargement was found to be inadequate for differentiating between concentric and eccentric types of LV hypertrophy. A new M-mode echocardiographic classification is therefore proposed that accurately separates the different types of LV enlargement; it also allows identification of patients who have chronically dilated left ventricles at the expense of thin walls and thus have normal LV mass.     

Diagnostic implications of figure-of-eight and clockwise QRS loop rotation on the horizontal vectorcardiogram in chronic aortic valve disease

In chronic aortic valve disease the left ventricular (LV) volumes, mass and ejection fraction (EF), as well as selected Frank ECG measurements of patients with a normal counterclockwise rotation (Type A) of the horizontal QRS vector loop are compared with those of patients showing an abnormal figure-of-eight or clockwise configuration (Type B) to investigate whether the different QRS patterns reflect ventriculographic alterations or depends on a conduction delay. In aortic stenosis (AS,n = 21) and combined AS and aortic insufficiency (AS + AI,n = 23) the Type B vectorcardiograms (VCGs) correlate with significantly increased LV end-diastolic volumes (p. .01, .01, respectively) and depressed EF (p .07, .009, respectively). In pure AI (n = 39) LV volumes, mass and EF do not differ between the Type A and Type B patterns. As compared to Type B VCGs of AS (n = 6), the LV end-diastolic volume index is clearly higher in Type A VCGs of pure AI (n = 21)(p .028). The only ECG change which is significant at the p .01 level in each group is the increase of the R peak time in lead X in the Type B VCGs. This can be related to greater volume and mass only in AS and AS+ AI, but is not substantiated by equivalent ventriculographic alterations in pure AI. The findings indicate that Type B VCGs are very likely caused by a left ventricular conduction delay since they cannot be strictly correlated with increases in LV volume and mass alone.     

An echocardiographic analysis of the long-term effects of carvedilol on left ventricular remodeling, systolic performance, and ventricular filling patterns in dilated cardiomyopathy

BACKGROUND: The long-term clinical benefit of beta blockade is well recognized, but data quantifying long-term effects of beta blockade on remodeling of the left ventricle (LV) is limited. METHODS: This consecutive series evaluates the long-term response of the LV to the addition of carvedilol to conventional therapy for dilated cardiomyopathy. There were 33 patients who had a LV ejection fraction <45%, LV enlargement and symptomatic heart failure. Quantitative Doppler echocardiography was performed at baseline 6, 12, 24, and 36 months after initiation of carvedilol to evaluate LV ejection fraction, LV volume, wall stress, mass, regional function, and diastolic performance. RESULTS: Compared to baseline there was a significant and sustained reduction in end-systolic volume and end-systolic wall stress with a corresponding improvement in LV ejection fraction. The LV mass did not decline but relative wall thickness increased toward normal. An analysis of regional wall motion responses showed an improvement in all areas, particularly the apical, septal, and lateral walls that was significantly more frequent in patients with a nonischemic etiology. Filling patterns of the LV remained abnormal throughout the study but changed with therapy suggesting a decline in filling pressures. These changes were sustained for 3 years. CONCLUSION: (1) The addition of carvedilol to conventional therapy for a dilated cardiomyopathy significantly improves LV ejection fraction and reduces LV end-systolic volume and wall stress for at least 3 years, (2) the response to 6 months of treatment predicts the long-term response, (3) the typical response is partial improvement of the LV, complete return to normal size, and function is uncommon, and (4) abnormalities of LV filling persist in virtually all patients throughout the course of treatment.     

Cardiac remodelling and myocardial recovery: lost in translation?

The insight that decreases in left ventricular (LV) volume and mass occur secondary to the recovery of the myocardium at the cellular and molecular level has engendered a wider appreciation of the importance of LV remodelling as a mechanism for worsening heart failure. Despite these recent insights into the recognition of the importance of LV reverse remodelling in heart failure, many clinicians do not consider simple measurements of LV structure (i.e. LV volume) in their routine clinical decision‐making process, preferring instead to rely on measurements of LV function [e.g. ejection fraction (EF)] when making decisions about medical and surgical treatment options. Although there are probably multiple reasons of why the use of LV volumes has not gained wider acceptance in day‐to‐day clinical management of heart failure patients, the most likely reason is that clinicians remain extremely comfortable using the LVEF to assess their heart failure patients. Importantly, LV volumes predict outcome more reliably than does the EF. Moreover, knowledge regarding LV volumes is extremely useful in optimizing patient selection for surgical and device therapies. Based on the foregoing arguments, we suggest that it is time to begin developing individualized clinical strategies based upon a consideration of the important role that LV remodelling plays in the pathogenesis of heart failure, and that we begin to incorporate measurements of LV volume and mass into the clinical decision‐making process.     

Gender differences in left ventricular function in patients with isolated aortic stenosis

BACKGROUND AND AIM OF THE STUDY: Hypertrophic response of the left ventricle to systolic overload in aortic stenosis appears to be gender-dependent. METHODS: To examine gender-related differences in left ventricular (LV) function in patients with isolated severe aortic stenosis, 145 patients (65 women, 80 men; mean age 66 +/- 8 years; range: 50 to 89 years) with aortic valve area <0.8 cm2 who underwent cardiac catheterization were studied. No patient had associated myocardial, coronary or other valve disease; patients with diabetes mellitus and systemic hypertension were excluded. RESULTS: No significant differences were seen in aortic valve area between men and women. Neither were there any significant gender-related differences in LV end-systolic and end-diastolic volumes, LV end-diastolic pressure, LV mass indexed by body surface area, LV mass:volume ratio, LV mass:height ratio, elastic stiffness constant, ejection fraction, pulmonary wedge pressure, pulmonary arteriolar resistance and preload. Women showed significantly higher mean transaortic gradient, LV peak systolic pressure and peak systolic stress, end-systolic stress:end-systolic volume ratio, heart rate and cardiac index. In the subgroup of patients with LV pressure >199 mmHg, the mass:volume ratio was increased in men compared with women; of note, the mass:volume ratio in women was not increased in this subgroup compared with the general population. LV pump function in this subgroup was normal and did not differ between men and women. CONCLUSION: Although no clear-cut difference in hemodynamic parameters was seen, there was a trend towards a less compensatory increase in LV mass in females.     

Regression of left ventricular mass one year after aortic valve replacement for pure severe aortic stenosis

The aim of the study was to quantify a 1-year change in left ventricular (LV) mass index (MI) and systolic LV function in 30 patients with pure severe aortic stenosis by means of serial 3-dimensional (3-D) echocardiography. To assess the completeness of LVMI regression after 1 year, we compared the postoperative mass of patients with mass values of 30 normotensive control subjects without a history of cardiac disease. Ejection fraction increased from 64 +/- 14% before surgery to 69 +/- 8% at follow-up (p = 0.067), and functional class improved from 2.9 +/- 0.5 to 1.4 +/- 0.5 (p <0.05), with improvement in each patient. During the same period, LVMI regressed by 23.4% (p <0.001). Postoperative LVMI was related to preoperative LVMI (r = 0.82; p <0.001) and baseline ejection fraction (r = -0.5; p = 0.009). LVMI regressed into the normal range in 64% of patients at follow-up. Patients achieving normal mass values did not differ with respect to patient gender, valve type, or valve size. Patients with reduced preoperative LV function had larger volumes (p <0.01), larger mass values (p <0.01), and a trend toward more mass regression (p = 0.062) than patients with normal preoperative function. Although ejection fraction improved after 1 year in all of these patients (p <0.03), they were less likely to achieve normal mass values at follow-up (p = 0.01). Regression of LVMI in patients with pure aortic stenosis is a positive event that occurs in each patient and that is associated with improvement in functional status. LVMI regressed into the normal range in most patients with normal preoperative function. Preoperative LV function, but not patient gender, valve type, or size, was related to normalization of LVMI at follow-up in this selected study population.     

Functional description of the left ventricle in patients with volume overload, pressure overload, and myocardial disease using cine magnetic resonance imaging

Cine magnetic resonance imaging (MRI) is a three-dimensional imaging technique with sufficient temporal resolution to provide quantitation of left ventricular (LV) dimensions and function. It can be used to describe the three-dimensional geometrical and functional characteristics of various cardiac disease states. Accordingly, the purpose of the study was to noninvasively characterize LV function with cine MRI using LV mass, systolic wall stress, ejection fraction, and fractional wall thickening, and to compare these functional determinants among three major cardiac disease states. Patients were selected from echocardiographic criteria and specific history of disease and divided into the following groups: compensated moderate to severe aortic regurgitation; compensated LV hypertrophy caused by systemic hypertension; and dilated congestive cardiomyopathy. Normal subjects without evidence of heart disease were studied for comparison. Cine MRI was performed at 1.5 Tesla in the short-axis plane. Wall stress was calculated from MRI, along with blood pressure recordings and carotid pulse tracings, according to the Laplacian expression. The end-diastolic volume to LV mass ratio distinguished between concentric and eccentric LV hypertrophy. Peak-systolic wall stress was increased in volume overload lesions and myocardial disease and significantly different (P less than .01) compared with pressure overload lesions and normal subjects. Ejection fraction was significantly decreased (P less than .01) in myocardial disease compared with volume and pressure overload lesions and normal subjects. Among these disease states, LV mass was not different but was significantly higher in all (P less than .01) compared with normal subjects. Fractional wall thickening was increased in pressure overload lesions. Thus, the increase in LV mass in volume overload lesions and primary myocardial disease is not adequate to prevent an increase in wall stress, whereas LV mass increased sufficiently in pressure overload lesions to normalize systolic wall stress. Cine MRI can be used to noninvasively describe the three-dimensional geometry and functional state of the heart in various pathological conditions and might be used to monitor therapeutic effects.     

Effect of electrocardiographic left ventricular hypertrophy on left ventricular systolic function in systemic hypertension (The LIFE Study). Losartan Intervention For Endpoint

Left ventricular (LV) ejection fraction is normal in most patients with uncomplicated hypertension, but the prevalence and correlates of decreased LV systolic chamber and myocardial function, as assessed by midwall mechanics, in hypertensive patients identified as being at high risk by the presence of LV hypertrophy on the electrocardiogram has not been established. Therefore echocardiograms were obtained in 913 patients with stage I to III hypertension and LV hypertrophy determined by electrocardiographic (Cornell voltage duration or Sokolow-Lyon voltage) criteria after 14 days' placebo treatment. The 913 patients' mean age was 66 years, and 42% were women. Fourteen percent had subnormal LV endocardial shortening, 24% had subnormal midwall shortening, and 13% had reduced stress-corrected midwall shortening. Nineteen percent had normal LV geometry, 11% had concentric remodeling, 47% had eccentric hypertrophy, and 23% had concentric hypertrophy. LV systolic performance evaluated by LV endocardial shortening and midwall shortening was impaired in 10% of patients with normal geometry, 20% with concentric remodeling, 27% with eccentric hypertrophy, and 42% with concentric hypertrophy. Relative wall thickness, an important independent correlate of LV chamber function, was related directly to endocardial shortening and negatively to midwall shortening and stress-corrected midwall shortening. LV mass was the strongest independent correlate of impaired endocardial shortening, midwall shortening, or both. In hypertensive patients with electrocardiographic LV hypertrophy, indexes of systolic performance are subnormal in 10% to 42% with different LV geometric patterns. Depressed endocardial shortening is most common in patients with eccentric LV hypertrophy, whereas impaired midwall shortening is most prevalent in patients with concentric remodeling or hypertrophy. Thus, in hypertensive patients with electrocardiographic LV hypertrophy, impaired LV performance occurs most often, and is associated with greater LV mass and relative wall thickness and may contribute to the high rate of cardiovascular events.     

The role of diastolic ventricular interaction in abnormal cardiac baroreflex function in chronic heart failure

Baroreflex abnormalities have been well documented in both patients with chronic heart failure and experimental animal models of heart failure. These abnormalities are associated with increased mortality and probably contribute to neurohumoral activation. While it is likely that several mechanisms contribute to reduced baroreflex sensitivity, it has been difficult to explain why baroreflex control mechanisms during acute volume unloading in patients with severe chronic heart failure should be directionally opposite to those in normal subjects. Volume unloading normally causes a reduction in baroreceptor activity, and hence an increase in sympathetic outflow; however, patients with chronic heart failure develop attenuated increases or paradoxical reductions in forearm vascular resistance, muscle sympathetic nerve activity, and noradrenaline spillover. It has been suggested that this probably represents paradoxical activation of left ventricular (LV) mechanoreceptors, but why LV receptors should behave in such a fashion has not been determined. In the setting of diastolic ventricular interaction, the filling of the left ventricle is constrained by the surrounding pericardium and right ventricle. In these patients, the reduction in right ventricular (RV) volume that normally occurs during acute volume unloading allows for an increase in LV end-diastolic volume (as opposed to the reduction in LV volume that normally occurs). We have demonstrated this to be important in some patients with chronic heart failure, and observed that baroreflex control of forearn vascular resistance was markedly impaired in these patients. We propose that the increase in LV volume that occurred during volume unloading would increase LV mechanoreceptor activity, and could therefore explain the paradoxical reductions in sympathetic outflow. As discussed, this has important therapeutic implications.     

Echocardiographic findings in pheochromocytoma

M-mode and 2-dimensional echocardiography were used to study 26 consecutive, unselected patients with pheochromocytoma over a 3-year period. Only 1 patient had congestive heart failure; more than half had no cardiac symptoms or abnormalities. The most common (80% of patients) echocardiographic pattern was normal left ventricular (LV) mass with normal or even increased systolic performance. When LV mass was increased, LV systolic function was either normal or only borderline depressed in most of the patients. Patients with echocardiographic LV hypertrophy had symmetric thickening of ventricular walls; no case of asymmetric septal hypertrophy was found. There was no correlation between 24-hour urinary norepinephrine excretion and any of the echocardiographic variables studied. In some patients, increased LV wall thicknesses did not correlate with increased LV mass as calculated by the Woythaler echocardiographic method. Left atrial enlargement was not seen in any patient, including those with increased LV mass. The electrocardiogram and echocardiogram may be discordant: Electrocardiographic LV hypertrophy was seen in 6 patients, of whom 5 had normal echocardiographic LV mass. In patients with pheochromocytoma who have no cardiac symptoms or other clinical evidence of cardiac involvement, echocardiographic findings are usually normal.     

Chronic aortic regurgitation: the effect of aortic valve replacement on left ventricular volume, mass and function.

Serial echocardiographic left ventricular (LV) studies were performed in 19 patients before (preop) and after (postop) aortic valve replacement (AVR) for chronic aortic regurgitation (AR); the effect of AVR on LV volume, mass and function was determined from the echocardiographic data. In the 12 patients who were considered to have successful surgical results, the average LV end-diastolic dimension fell from a preop value of 6.9 +/- 0.2 cm to 5.5 +/- 0.2 cm (P less than 0.01) at the time of the early postop study (seven to 10 days). Muscle cross-sectional area (CSA) derived from dimension and wall thickness data was used as an index of LV muscle mass (preop CSA = 26 +/- 1.3 cm2); CSA was unchanged at the early postop study, but subsequently fell to near normal within six months after AVR (20 +/- 1 cm2, P less than 0.01). There was a trend toward improvement in systolic performance by the late postop studies (12+ months). In two out of three patients with postop paravalvular AR, LV dimension increased after an initial fall. Four patients without paravalvular AR failed to show a significant reduction in LV dimension in the postop studies. In this group the preop studies showed a tendency toward a large end-diastolic dimension and decreased fractional shortening, but the single preop parameter which differentiated these four from the successfully treated group was an end-diastolic radius-to-wall thickness (R/Th) ratio greater than or equal to 4. Thus, successful AVR for chronic AR results in the normalization of LV volume and a decrease in LV muscle mass to near normal. The R/Th ratio has important prognostic value which appears to be independent of fractional shortening in some patients with chronic AR.     

Left ventricular hypertrophy in hypertension: stimuli, patterns, and consequences.

Left ventricular (LV) size in childhood closely parallels body size, whereas in adulthood LV mass is increasingly affected by effects of obesity, hypertension, the level of cardiac volume load, and the level of LV myocardial contractility. Recently, additional independent associations of diabetes, arterial structure and function and as yet unknown genes with higher LV mass have been defined; angiotensin II and insulin have also been suggested to be additive stimuli to LV hypertrophy. Consideration of the level of LV mass and of the LV wall thickness/chamber radius ratio (relative wall thickness) has identified four different geometric patterns of LV adaptation to hypertension, including concentric LV hypertrophy (increased mass and wall thickness), eccentric hypertrophy (increased mass, normal relative wall thickness), concentric remodeling (increased relative wall thickness with normal mass) and normal LV geometry. Concentric hypertrophy is associated with especially high arterial pressure while eccentric hypertrophy is associated with obesity and elevated volume load. Numerous studies show that increased LV mass predicts cardiovascular events and death independently of all conventional risk factors; initial studies have also identified adverse implications of low LV midwall function and high relative wall thickness. Pioneer studies strongly suggest that reversal of LV hypertrophy is associated with an improved prognosis.     

Relation of left ventricular dilation during acute myocardial infarction to systolic performance, diastolic dysfunction, infarct size and location

The quantification of left ventricular (LV) volumes and assessment of their relation to systolic and diastolic dysfunction, infarct size and anatomic location were performed in 54 patients with a first acute myocardial infarction (AMI). Blood pool radionuclide angiography was used to assess LV end-diastolic, end-systolic, and stroke volume indexes, ejection fraction and peak diastolic filling rate. Infarct size was estimated from plasma MB creatine kinase activity. Substantial LV dilation occurred within the initial 24 hours of AMI. The peak diastolic filling rate was low, even in those patients with a normal ejection fraction. In comparison with inferior AMI (n = 25), patients with anterior AMI (n = 29) had a larger end-diastolic volume index (105 +/- 8 vs 81 +/- 4 ml/m2, p less than 0.01) and end-systolic volume index (64 +/- 7 vs 37 +/- 4 ml/m2, p less than 0.001), but similar stroke volume index (41 +/- 3 vs 43 +/- 2 ml/m2, difference not significant). No significant relation was noted between infarct size estimated by MB creatine kinase and any volumetric index. On repeat study (day 10 after AMI), end-diastolic and end-systolic volume indexes increased further (p less than 0.05 vs day 1) but ejection fraction and peak diastolic filling rate were unchanged. It was concluded that: (1) LV dilation occurs within hours of AMI in both inferior and anterior AMI, but is more marked in the latter; (2) significant LV diastolic dysfunction is the rule, even in patients with preserved LV systolic function; and (3) LV dilation is an early compensatory mechanism that maintains normal stroke volume, even in patients with severely reduced LV function.     

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.     

Left ventricular remodeling and mechanics after successful repair of aortic coarctation

Forty normotensive patients (mean age 12.3 +/- 6.5 years) followed up after a successful repair of aortic coarctation (mean age at coarctectomy 5.1 +/- 4.8 yrs) were studied by echo-Doppler to (1) evaluate left ventricular (LV) remodeling and endocardial and midwall mechanics, and (2) identify factors that might predispose to persistent abnormalities. Sex- and age-specific cutoff levels for LV mass/height2.7 and relative wall thickness were defined to assess LV geometry. To adjust for age-and growth-related changes in ventricular mechanics, all echocardiographic variables were expressed as a Z-score relative to the normal distribution. In addition, the smallest diameter of the aorta was assessed by magnetic resonance imaging and calculated as percent narrowing compared with the diameter of the aorta at the diaphragmatic level. In the study group, 24 of 40 patients (60%) had normal LV geometry. Among the 16 patients (40%) with abnormal LV geometry, 5 (12.5%) had a pattern of concentric remodeling and 11 (27.5%) an eccentric hypertrophy. LV hypertrophy was marked (LV mass index >51 g/m2.7) in 5 of these patients. No patient had a pattern of concentric hypertrophy. LV contractility was increased (Z-score >95th percentile) in 28 patients (70%) as assessed using the endocardial stress-velocity index. In contrast, LV contractility assessed using midwall stress-velocity index remained elevated (Z-score >95th percentile) in 15 patients (37.5%). The stepwise multiple logistic regression analysis was not able to detect any significant independent predictor of abnormal LV remodeling, including sex, age at surgical repair, length of postoperative follow-up, heart rate, body mass index, systolic and diastolic blood pressure, and smallest diameter of the aorta, as well as indexes of LV geometry (shape, mass, volume, mass/ volume ratio) and function (preload, afterload, pump function, and myocardial contractility). Thus, normotensive patients after surgical repair of aortic coarctation may be in an LV hyperdynamic cardiovascular state (more frequent in those who have undergone late repair) and have multiple patterns of LV geometry.     

Patency of the infarct-related coronary artery and ventricular geometry.

The pathogenesis of acute myocardial infarction (AMI) involves a sudden thrombotic occlusion of a coronary artery. Spontaneous or pharmacologic thrombolysis may lead to myocardial salvage if patency is achieved within a narrow time window. However, patients in whom thrombolysis occurs late seem to demonstrate improved left ventricular (LV) function and prognosis, which may be independent of myocardial salvage. Preservation of normal LV geometry by reducing expansion of the infarcted segment is a likely mechanism for this benefit. Infarct expansion is most pronounced in patients with anterior wall AMI who have a persistently occluded infarct-related vessel. This process of expansion leads to early increases in LV volume and distortions of LV contour (abnormal LV geometry). Patients whose infarct segment is largest, patients who have manifested infarct expansion, and patients with a persistently occluded infarct-related artery are at highest risk for progressive LV dilation. Experimental data support the concept that reperfusion of occluded vessels that occurs too late for myocardial salvage will preserve LV geometry by limiting infarct expansion. Prospective clinical trials should address whether there is a late, "second time window" during which infarct expansion and distortions of LV geometry may be reduced by (1) therapy with thrombolytic agents applied late after infarction, (2) late mechanical reperfusion with percutaneous transluminal coronary angioplasty (PTCA) or related methods, and (3) load-reducing agents to decrease remodeling, such as angiotensin-converting enzyme inhibitors or nitroglycerin.