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ORIGINAL ARTICLE

Impact of Coronary Disease After Aortic Valve Replacement

Jürg Grünenfelder, MD, Iram Kilb, MD, Andre Plass, MD, Silvano Cominelli, MD1, Daniela Zeller, MD1, Michele Genoni, MD

Clinic for Cardiovascular Surgery, University Hospital Zürich
1 Heart Center, City Hospital Triemli Zürich, Switzerland

Jürg Grünenfelder, MD, Tel: +41 1 2553298, Fax: +41 1 2554446, Email: jurg.grunenfelder{at}usz.ch, Clinic for Cardiovascular Surgery, University Hospital Zürich, Rämistrasse 100, CH-8091 Zürich, Switzerland.

ABSTRACT

Left ventricular dimensions tend to reduce after aortic valve replacement in patients with aortic stenosis. Whether concomitant coronary artery disease has an influence on postoperative ventricular dimensions has not been evaluated. Between 1998 and 2002, 112 patients underwent aortic valve replacement for aortic stenosis; 68 had isolated aortic valve replacement, and 44 had combined coronary artery bypass grafting. Left ventricular dimensions were assessed by echocardiography preoperatively and at 3 and 12 months postoperatively. Transvalvular mean gradient, left ventricular end-diastolic diameter, and left ventricular mass index decreased significantly postoperatively, while left ventricular ejection fraction improved. Preoperative left ventricular dimensions in patients with isolated aortic stenosis were worse than in those with aortic stenosis and coronary artery disease. After aortic valve replacement with coronary artery bypass, left ventricular mass index regression was less than that after valve replacement alone, and there was no improvement in ejection fraction. This suggests that coronary artery disease has a negative impact on postoperative myocardial recovery.

Key Words: Aortic Valve Replacement • Aortic Valve Stenosis • Coronary Artery Bypass • Coronary Artery Disease

INTRODUCTION

In aortic stenosis (AS), there is left ventricular (LV) outflow obstruction that results in increased LV systolic pressure. In response to chronic pressure overload, there is an increase in LV mass, which ultimately progresses to LV dysfunction and heart failure. Survival in such patients is very poor without surgery.1 However, if aortic valve replacement (AVR) is carried out in those with significant AS, there is substantial clinical and hemodynamic improvement, and long-term survival improves dramatically.2,3 LV mass is reduced to near normal within 18 months postoperatively.47 When restudied 5 years postoperatively, LV mass may even have returned to normal.8 Because it was unclear whether the presence of coronary artery disease (CAD) in patients undergoing AVR would influence the degree of myocardial regression, we compared LV dimensions in patients having isolated AVR and those having AVR combined with coronary artery bypass grafting (CABG).

PATIENTS AND METHODS

Between 1998 and 2002, 112 patients who underwent AVR with a St. Jude Medical mechanical valve (St. Jude Medical, Inc., St. Paul, MN) were studied; 68 had isolated AVR and 44 had combined AVR and CABG. The indication for surgery was significant AS (onset of symptoms, depressed LV function, mean gradient>50 mm Hg) in all patients. Other associated valve procedures and previous operations were exclusion criteria. Demographic data of the 2 groups are given in Table 1Go.


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Table 1. Preoperative demographic data of 112 patients undergoing aortic valve replacement
 
At operation, the heart was exposed through a median sternotomy. After heparinization, the ascending aorta and right atrium were cannulated, and cardiopulmonary bypass was initiated. The patient was cooled to 28°C. The aorta was crossclamped, and blood cardioplegia was infused antegradely and retrogradely. In patients undergoing CABG, distal anastomoses were performed. The aortic valve was exposed through an oblique/transverse aortotomy. The native aortic valve was excised, and the annulus thoroughly decalcified. Prosthesis size was chosen after sizing the annulus with appropriate valve sizers. Valve implantation was typically in a supraannular position, using a non-everting suture technique with 2/0 Ti-Cron suture (Ethicon, Norderstedt, Germany). Rewarming was started, the aortotomy was closed, and the aorta was declamped. Proximal anastomoses were undertaken when necessary. The patient was weaned from cardiopulmonary bypass, and the cannulas were removed. Protamine was administered, and the operation was terminated in a standardized way.

Echocardiographic studies were performed using standard ultrasound machines. Transthoracic Doppler echocardiography was carried out preoperatively, at discharge, 3 and 12 months postoperatively. Examinations included M-mode, 2-dimensional, continuous wave, and pulsed Doppler, with color Doppler analyses. Left parasternal, apical, right parasternal, and subcostal views were employed to interrogate for paravalvular leak and regurgitation. Peak and mean pressure gradients were calculated using the modified Bernoulli equation.9 LV mass was calculated by the modified American Society of Echocardiography cube method:


Formula

where LVIDD is left ventricular end-diastolic internal dimension, IVST is end-diastolic thickness of the interventricular septum, and PWT is posterior LV wall thickness.10 Normal values of echocardiographic LV dimensions according to the literature are listed in Table 2Go.10


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Table 2. Normal left ventricular echocardiographic data
 
Data analysis was performed with SPSS II software (SPSS Inc., Chicago, IL, USA). Values are reported as mean ±standard deviation. Comparison of nominal variables was made by chi-squared test, and continuous variables were analyzed by the Mann Whitney U test. Values of p less than 0.05 were considered significant.

RESULTS

There was no early mortality, and no patient died within 12 months after AVR. Patients who had combined AVR and CABG were significantly older than those undergoing isolated AVR (p =0.009). There were significantly more males in the group having a combined procedure (p =0.005; Table 1Go). Preoperative echocardiographic data are given in Table 3Go. Transvalvular peak gradient, mean gradient, LV end-diastolic diameter, and LV mass index were significantly higher in patients undergoing isolated AVR. At 3 and 12 months, there was a significant difference in LV ejection fraction (LVEF). Patients who had combined AVR and CABG had a lower LVEF at follow-up compared to the group with isolated AVR (Table 3Go). Preoperative LV mass index was significantly higher in patients undergoing isolated AVR; it was within the normal range in those who had AVR combined with CABG. After 3 and 12 months, LV mass index had decreased in both groups, but the values were still not within the normal range after 12 months (Table 2Go). However, changes within the groups demonstrated significant improvement in LVEF, LV mass regression, and LV end-diastolic diameter during the 12-month follow-up (Table 4Go).


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Table 3. Echocardiographic data of 68 patients undergoing isolated AVR and 44 undergoing AVR and CABG
 

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Table 4. Echocardiographic changes during follow-up
 
DISCUSSION

There is a long latent period in AS, during which there is gradually increasing obstruction and pressure load on the myocardium, while the patient remains asymptomatic.11 The cardinal manifestations of AS, which commence most commonly in the 6th decade of life, are angina pectoris, syncope, and heart failure.5 In patients in whom the obstruction remains unrelieved, once these symptoms become manifested, the prognosis is poor.1 Angina occurs in approximately two-thirds of patients with critical AS, about half of whom have associated significant CAD.1 In our population, 61% had isolated AVR and 39% needed concomitant CABG.

According to the literature, operative mortality for AVR with or without CABG varies between 1% and 5%.1214 It was believed in the past that only the most important coronaries should be bypassed to minimize aortic crossclamp time.15 With modern myocardial protection, cardiopulmonary bypass technology, and anesthesia, this concern is obsolete. There was no operative mortality in our study group. One reason might be that mean LVEF was only slightly reduced in our patients. In those with severe AS, survival after AVR improves significantly, even in patients who have a normal preoperative LVEF.2,3 All of our patients were still alive after 12 months.

The patients undergoing concomitant AVR and CABG in our study group were significantly older; as the incidence of CAD is higher in older people, this was not surprising. Studies in patients aged 50 years or older undergoing AVR found 50% had CAD.13,14 We also found significantly more men in the group undergoing combined AVR. It is well known that men are more prone to CAD than women.16 The valve orifice is reduced in AS, resulting in reduced stroke volume, which leads to reduced LVEF.1 LVEF was identical in both patient groups; however, when compared to normal values, both groups had mildly reduced LVEF pre-operatively. Dangas and colleagues17 studied the value of angina pectoris as a predictor of significant CAD in patients ≥ 70 years with AS: angina pectoris had a sensitivity of 78% and a specificity of 82% in predicting obstructive CAD. It can be assumed that angina in patients with CAD and AS occurs earlier, and these patients might have surgery earlier than those undergoing an isolated procedure. This might be the reason why patients having the combined procedure had a lower peak gradient. The same assumption can be made when looking at the mean gradient. Preoperative LVEDD was within the normal range in both groups, but it was significantly higher in the isolated AVR group, presumably because the patients with CAD underwent surgery earlier due to CAD-related symptoms. Increased LV mass index is associated with increased hospital mortality.18 It also influences long-term results due to irreversible myocardial damage.19 Preoperative LV mass index was pathologic in our patients, and it was significantly higher in those with isolated AVR, again probably because those with CAD had earlier AVR.

LVEF was nearly unchanged compared to preoperative values shortly after the operation. This is not surprising as the first echocardiographic examinations were carried out 5 to 8 days postoperatively. After 3 and 12 months, LVEF had increased in the isolated AVR group but remained unchanged in patients who had combined AVR and CABG. We assume that some patients with CAD might have had preoperative myocardial infarction. Peak and mean gradients decreased significantly after AVR for obvious reasons. After 3 and 6 months there were further decreases in transvalvular peak and mean gradients. Hypothetically, a reason for this finding could be that by relieving valve obstruction, the subvalvular component of the outflow tract obstruction appears. With time, this component is reduced as well, and as a result, the gradients decrease.

There was a slight decrease in postoperative LVEDD during follow-up in the group with isolated AVR. However, patients with combined AS and CAD showed no change in postoperative LVEDD. As stated previously, myocardial damage is probably more pronounced in patients with concomitant CAD and therefore, myocardial recovery is reduced in this group. Postoperative interventricular septum thickness was within the normal range in both groups, and there was only a slight decrease during follow-up. De Paulis and colleagues20 also found a reduction of interventricular septum thickness after AVR; however, after 3 years, this variable did not reach normal values. Shortly after AVR, posterior wall thickness was significantly lower in the group with CAD. Although the values were within the normal range in both groups, this particular finding is interesting. One explanation could be that patients with CAD might have immediately profited from revascularization in the posterior wall area. After 3 and 12 months, all values had equalized in both groups. De Paulis and colleagues20 found that only posterior wall thickness reached normal values after AVR, unlike interventricular septum thickness and LV mass index. An interesting result was the change in LV mass index: it was pathologic in both groups before AVR, although significantly less pathologic in patients with a combined procedure. This could be due to more extensive myocardial damage caused by CAD. In the group with isolated AVR, LV mass index declined after 3 and 12 months, whereas it remained stable in the CABG group. Reduction of LV mass index after AVR is well known. Lund and colleagues19 found that a reduction of LV mass index occurred within 18 months postoperatively.19 Others noted that after 5 years, it had returned to normal.8

This study shows that patients with AS combined with CAD have less severe preoperative LV changes than those with isolated AS. However, after AVR, LV dimensions normalize more quickly in the group with isolated AVR. This suggests that CAD has a negative impact on postoperative myocardial recovery.

Presented at the 16th Annual Meeting of the Asian Society for Cardiovascular & Thoracic Surgery, Singapore, March 13–16, 2008.

REFERENCES

  1. Libby P, Bonow RO, Mann DL, Zipes DP, Braunwald’s Heart disease, 8th Edition. Philadelphia: Saunders, 2008.

  2. Horstkotte D, Loogen F. The natural history of aortic valve stenosis [Review]. Eur Heart J 1988;9(Suppl E):57–64.[Abstract]

  3. Schwarz F, Baumann P, Manthey J, Hoffmann M, Schuler G, Mehmel HC, et al. The effect of aortic valve replacement on survival. Circulation 1982;66:1105–10.[Abstract/Free Full Text]

  4. Rao L, Mohr-Kahaly S, Geil S, Dahm M, Meyer J. Left ventricular remodeling after aortic valve replacement. Z Kardiol 1999;88:283–9.[Medline]

  5. Kennedy JW, Doces J, Stewart DK. Left ventricular function before and following aortic valve replacement. Circulation 1977; 56:944–50.[Abstract/Free Full Text]

  6. Gelsomino S, Frassani R, Morocutti G, Porreca L, Tursi V, Masullo G, et al. Left ventricular mass regression after aortic valve replacement with CryoLife-O’Brien stentless aortic bio-prosthesis. J Heart Valve Dis 2001;10:603–10.[Medline]

  7. Kühl HP, Franke A, Puschmann D, Schöndube FA, Hoffmann R, Hanrath P. Regression of left ventricular mass one year after aortic valve replacement for pure severe aortic stenosis. Am J Cardiol 2002;15:408–13.

  8. Monrad ES, Hess OM, Murakami T, Nonogi H, Corin WJ, Krayenbuehl HP. Time course of regression of left ventricular hypertrophy after aortic valve replacement. Circulation 1988; 77:1345–55.[Abstract/Free Full Text]

  9. Feigenbaum H. Hemodynamic information derived from echocardiography. In: Feigenbaum H, editor. Echocardiography. 5th ed. Philadelphia, PA: Lea & Febiger, 1994:181–215.

  10. Devereux RB, Alonso DR, Lutas EM, Gottlieb GJ, Campo E, Sachs I, et al. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol 1986;57:450–8.[Medline]

  11. Oakley CM. Management of valvular stenosis. Curr Opin Cardiol 1995;10:117–23.[Medline]

  12. Rahimtoola SH. Perspective on valvular heart disease: update 11. In: Knoebel S, editor. An era in cardiovascular medicine. New York; Elsevier, 1991:45–70.

  13. Sethi GK, Miller DC, Souchek J, Oprian C, Henderson WG, Hassan Z, et al. Clinical, hemodynamic and angiographic predictors of operative mortality in patients undergoing single valve replacement. J Thorac Cardiovasc Surg 1987; 93:884–7.[Abstract]

  14. Mullany CJ, Elveback LR, Frye RL, Pluth JR, Edwards WD, Orszulak TA, et al. Coronary artery disease and its management: Influence on survival in patients undergoing aortic valve replacement. J Am Coll Cardiol 1987;10:66–72.[Abstract]

  15. Ståhle E, Bergström R, Nyström SO, Hansson HE. Early results of aortic valve replacement with or without concomitant coronary artery bypass grafting. Scand J Thorac Cardiovasc Surg 1991; 25:29–35.[Medline]

  16. Kannel WB, Cupples A. Epidemiology and risk profile of cardiac failure. Cardiovasc Drugs Ther 1988;2 (Suppl 1):387–95.[Medline]

  17. Dangas G, Khan S, Curry BH, Kini AS, Sharma SK. Angina pectoris in severe aortic stenosis. Cardiology 1999;92:1–3.[Medline]

  18. Fuster RG, Argudo JA, Albarova OG, Sos FH, Lopez SC, Sorli MJ, et al. Left ventricular mass index in aortic valve surgery: a new index for early valve replacement? Eur J Cardiothorac Surg 2003;23:696–702.[Abstract/Free Full Text]

  19. Lund O, Emmertsen K, Dorup I, Jensen FT, Flo C. Regression of left ventricular hypertrophy during 10 years after valve replacement for aortic stenosis is related to the preoperative risk profile. Eur Heart J 2003;24:1437–46.[Abstract/Free Full Text]

  20. De Paulis R, Sommariva L, Colagrande L, De Matteis GM, Fratini S, Tomai F, et al. Regression of left ventricular hypertrophy after aortic valve replacement for aortic stenosis with different valve substitutes. J Thorac Cardiovasc Surg 1998;116:590–8.[Abstract/Free Full Text]

Asian Cardiovasc Thorac Ann 2009; 17:248-252
© 2009 by SAGE Publications
DOI: 10.1177/0218492309104744




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