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J Thorac Cardiovasc Surg 1998;116:590-598
© 1998 Mosby, Inc.
SURGERY FOR ADULT CARDIOVASCULAR DISEASE |
Rome, Italy
From the Cardiac Surgery Department, Tor Vergata University of Rome, Italy.
Received for publication Dec 22, 1997. Revisions requested Jan 29, 1998; revisions received May 26, 1998. Accepted for publication May 28, 1998. Address for reprints: Ruggero De Paulis, MD, Cattedra di Cardiochirurgia, Università di Roma, Tor Vergata, European Hospital, via Portuense 700, 00149 Rome, Italy.
| Abstract |
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| Introduction |
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In a recently published study
3 in which we compared 2 groups of patients with aortic stenosis receiving bileaflet mechanical valves of different sizes, we did not find a significant difference in the regression of left ventricular hypertrophy 3 years after the operation. In the present study we wanted to test the hypothesis that the better hemodynamic performances of stentless valves were also reflected by a greater reduction in left ventricular mass when compared with conventional prosthetic valves. Therefore we analyzed the regression of hypertrophy in 3 groups of patients who received a stentless, a stented, or a mechanical valve.
| Patients and methods |
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Ten patients (group II) received a Hancock stented valve (Hancock Extracorporeal Inc, Anaheim, Calif), size 21 mm (8 cases) or size 23 mm (2 cases). Ten patients (group III) received a CarboMedics bileaflet mechanical valve (Sulzer Carbomedics Inc, Austin, Tex), size 21 mm (8 cases) or size 23 mm (2 cases). A fourth group of 10 healthy subjects, without heart disease on routine diagnostic echocardiography and without a history of systemic hypertension, served as a control group.All patients were evaluated before the operation and after a mean time of 13 ± 6 months for group I, 15 ± 4 months for group II, and 12 ± 7 months for group III. For patients of groups I and III, an echocardiographic study was also available after a mean of 2 years' follow-up. The time frame of the study was 15 months. Medical ethics committee approval and informed patient consent for participation in the study were obtained in all cases.Patient characteristics are shown in Table I. Because our policy is to implant biologic valves after the age of 70 years, patients receiving bioprostheses were slightly older than both the patients receiving mechanical valves and the control subjects. Although the difference was not significant, the group receiving stented bioprostheses contained a higher proportion of women than did the other groups. All patients had pure aortic stenosis; however 2 patients in each group had minimal evidence of aortic regurgitation. None of the patients had postoperative prosthetic valve insufficiency. Two patients in the groups receiving biologic valves and 1 patient in the group receiving mechanical valves had associated coronary artery disease. The diameter of the implanted prosthesis was significantly larger for patients receiving stentless valves than for the other patient groups. Diastolic pressure was an average of blood pressure as measured before the operation 3 times a day over a period of more than 4 consecutive days. Three patients in each group were receiving a daily dose of angiotensin-converting enzyme inhibitors (10 to 20 mg).
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Then the following parameters were calculated: (1) the ratio between interventricular septum and posterior wall thickness; (2) the ratio between left ventricular wall thickness (interventricular septum plus posterior wall thickness) and left ventricular chamber radius; (3) the left ventricular mass, which was calculated from the M-mode measurements by means of the formula modified by Devereux and Reicher
4; (4) maximum and mean gradient, which were calculated by means of the modified Bernoulli equation. All values were indexed for the body surface area.All parameters were measured and calculated independently by 2 expert echocardiographers. The echocardiograms were reviewed by a third investigator if the first 2 investigators were not in agreement.
Statistical analysis.
Two-factor repeated-measures analysis of variance with repeated measures on 1 factor was used to compare echocardiographic parameters in the 4 groups of patients. When significant differences were detected, pairwise comparisons were made by the Scheffé F test. Comparisons of the remaining continuous or discrete variables among groups were performed by means of an unpaired Student t test or a
2 test, respectively (SPSS for Windows Software, SPSS, Inc, Chicago, Ill). Data are expressed as mean ± 1 standard deviation unless otherwise indicated.
| Results |
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Preoperatively, left ventricular diameters and function were comparable among study groups and not significantly different from the control group. At follow-up, all values changed slightly, remaining within the normal range (Table II).
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Left ventricular mass index at 2 years in groups I (stentless valves) and III (mechanical valves) did not change significantly (137 ± 33 g/m2 and 136 ± 35 g/m2; P = NS vs values at 1 year of follow-up, respectively).
| Discussion |
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Very recently, many studies have shown a greater regression in left ventricular mass after aortic valve replacement with stentless valves than with classic valve substitutes.
8,9 Christakis and associates
10 did not find that the type of prosthesis could influence the extent of mass regression in the early postoperative period.
10 However, the same group reported an optimized mass regression with stentless valves after 1 year of follow-up.
11 Jin and colleagues,
12 who evaluated the regression of left ventricular hypertrophy in a large number of patients after aortic valve replacement with different types of valve substitutes, showed that the patient with a stentless or homograft valve had a greater reduction in the left ventricular mass than the patient who received a stented biologic or mechanical valve. After a follow-up period of more than 3 years, they reported a left ventricular mass index of 145 g/m2 for all patients with aortic stenosis and 144 g/m2 for patients with a stentless valve. Similarly, Gonzalez-Juanatey and associates,
13 who observed the changes in left ventricular mass in a group of patients with different sizes of biologic or mechanical valves, demonstrated a more complete regression in left ventricular hypertrophy in patients with larger valves. The left ventricular mass index was 137 g/m2 for patients receiving 19 mm aortic prostheses and 124 g/m2 for those receiving 25 mm aortic prostheses, with a rate of reduction of about 10% and 28%, respectively. However, although both studies demonstrated a greater reduction in left ventricular mass index in patients with lower transprosthetic gradients (homograft valve in 1 case and larger biologic or mechanical valve in the second case), the postoperative values in left ventricular mass and the rate of reduction from preoperative levels were similar to ours and still different from control values. Sim and associates,
14 who also demonstrated, after a follow-up period of 3 years, a less-pronounced reduction in left ventricular mass in patients with 19 mm stented or mechanical valves compared with similar valves of larger diameters, reported a postoperative mass index of 120 g/m2 (with a preoperative value of only 129 g/m2) that was not different from the postoperative mass index of patients with larger valves (ie, 125 g/m2 for patients receiving 25 mm aortic prostheses). Finally, Lund and coworkers
15 recently analyzed the impact of size mismatch in a group of patients operated on for aortic stenosis with different sizes of St Jude Medical valves. After a mean period of 18 months their left ventricular mass index was 153 ± 53 g/m2 with a posterior wall thickness of 12 ± 2 mm. Noteworthy, they found that small valve orifice diameter and valve prosthesis size mismatch (along with left ventricular end-diastolic dimension and impaired left ventricular function) were independent determinants of Doppler gradients. Most interestingly, they did not find a correlation between the 18-month gradient and the left ventricular mass index or the rate of reduction in the left ventricular mass index from the preoperative level. These results led them to the conclusion that the incomplete hypertrophy regression could not be ascribed to the relatively obstructive mechanical prostheses.
There are several reasons why regression of left ventricular hypertrophy is incomplete after aortic valve replacement for aortic stenosis. First, the left ventricular myocardial collagen fibrosis especially in the interventricular septum might take a much longer time to return to normal or the myocardial structural abnormality might never regress in patients with truly pathologic hypertrophy.
16 Second, other host-related factors should be taken into consideration. Age is known to be an independent factor of left ventricular hypertrophy.
17 Lindroos and associates,
18 who evaluated the amount of left ventricular hypertrophy in an old patient population, found that the increase of left ventricular mass is due partly to age-related disease but also partly to an independent effect of age. The left ventricular mass was often found to exceed 70% of the standard limits in the oldest patient cohort (85 years old). Although our patients receiving mechanical valves or control valves were slightly younger than patients receiving biologic valves, the differences seem too small to justify an age-dependent difference in left ventricular mass index. Gender should also be considered, because left ventricular mass, when indexed either for body surface area or height, has been found to be greater in men than women.
19 However, female patients show a greater increase in left ventricular mass with advanced age, apparently because of the higher incidence of obesity in elderly women. Therefore it is unlikely that the high proportion of women in the group receiving stented biologic valves could have influenced the differences in left ventricular mass regression among our patient groups. Hypertension that is often present in an elderly patient population might significantly influence the rate of regression of left ventricular hypertrophy. In our study we excluded patients with evidence of hypertension, but we cannot rule out that patients with a blunted nocturnal fall in blood pressure might have an increased left ventricular mass. However, Verdecchia and coworkers
20 demonstrated that, at least in hypertensive men, daytime hypertension was a sufficient determinant of left ventricular wall thickening independent of the presence or absence of a nocturnal fall in blood pressure. Finally, the classic index of left ventricular mass for body surface area might be inappropriate. Lauer and associates
21 recently suggested a new method of indexing, independent of obesity, that might reduce the variability associated with body size and gender.
All these considerations indicate that in an elderly population (ie, those most likely to receive a bioprosthesis) with reduced physical activity who often have hypertension and have had aortic stenosis for a great number of years, it might be difficult to observe a complete regression of left ventricular mass and to ascribe it to the type of valve substitute. Conversely, differences in the rate of regression of left ventricular hypertrophy could be easier to detect in a young patient population with a greater increase in cardiac output during daily activity. It is also possible that other parameters rather than the simple assessment of left ventricular mass could be more sensitive markers of the beneficial effects of an optimal reduction of ventricular pressure load. Noteworthy, Jin and colleagues
12 showed that patients with less obstructive valve prostheses (homograft or stentless biologic valves) had a substantially greater increase in the rates of dimensional shortening and wall thickening than patients with stented valve prostheses. They
22 had also previously shown that an early decrease in peak systolic stress was 50% greater after aortic valve replacement with a stentless valve than with a stented one. Additionally or alternatively to these more sensitive parameters, a more appropriate index could better help in distinguishing differences in left ventricular hypertrophy between patients with different valve substitutes.
One year of follow-up appears to be sufficient to assess the regression of left ventricular hypertrophy in patients undergoing aortic valve replacement. Jin and associates
12 found no differences in left ventricular mass or in left ventricular structure and function between 6 months and 3 years of follow-up. We also demonstrated in a group of patients operated on for aortic stenosis with different sizes of mechanical valves that the left ventricular mass index was not different between 1 year and 3 years of follow-up.
3 Similarly, in 2 groups of patients of the present study (group I and group III) in whom a longer follow-up of 2 years was also available, no changes in left ventricular mass index were present. Monrad and coworkers
23 had already clearly demonstrated that the regression of left ventricular hypertrophy is maximal within the first year of follow-up and that more than 8 years are necessary to detect a further reduction of ventricular mass. They considered only patients with different types of stented biologic or mechanical valves; therefore we cannot exclude the possibility that stentless valves or homografts will behave differently. Del Rizzo and colleagues,
11 after a careful follow-up of the Toronto SPV stentless valve, reported a progressive decrease in left ventricular mass index within the first year of follow-up but no differences in left ventricular mass regression between 1 year and 3 years of follow-up.
It is intuitive that an aortic valve prostheses with optimized hemodynamic performance and minimal or no residual postoperative gradient should result in better ventricular structure and function. In this study the simple assessment of left ventricular hypertrophy did not discriminate between patients with different types of valves after an intermediate period of follow-up. However, even when the beneficial effect of stentless valves on left ventricular mass regression becomes clear, it will be necessary to demonstrate that the incomplete regression of left ventricular mass after aortic valve replacement is sufficient to determine differences in clinical status or in overall survival. Large clinical trials comparing survival and cardiac related events within patients with stented and stentless valves are therefore warranted.
Limitations of the study.
The major limitation of this study is the fact that patients were not randomized to receive a different type of valve prosthesis. Although selection criteria were very strict and most of the clinical variables were not different between the population groups, many other factors that could conceivably contribute to differences might not have been included. Selection bias often can be difficult to describe. However, inasmuch as the result of this study was different from what we were expecting, the possibility of selection bias may be attenuated. Our control patients were slightly younger than those in the study groups and might not have been an accurate basis for comparison, especially for patients receiving biologic implants. Nevertheless, control values are easily available in the literature. Finally, the relatively small group of patients considered indicates a low statistical power of the study. On the basis of the data on left ventricular mass regression available in the literature, and to identify a 25% decrease in left ventricular mass, a larger number of patients was necessary. Although, the statistical power of the study calculated from our data appears to be sufficiently high (from 87% to 95% for pairwise comparisons, at an
level of .05) it carries a strong ß error. Obviously, a larger number of patients would have strengthened the results and improved the study. The strict selection of patients and the accuracy of follow-up has prevented us from concluding a larger study in a relatively short period of time. However, we think that the information obtained from this study is sufficient to show the need of a large randomized trial comparing different valve substitutes.
| Acknowledgments |
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| References |
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