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Right arrow Myocardial infarction

J Thorac Cardiovasc Surg 2004;128:38-43
© 2004 The American Association for Thoracic Surgery

Surgery for acquired cardiovascular disease

Neurohormonal response to left ventricular reconstruction surgery in ischemic cardiomyopathy

Soren Schenk, MDa, Patrick M. McCarthy, MDa,b,c,d,*, Randall C. Starling, MD, MPHc,d,e, Katherine J. Hoercher, RNb,c,d, Melanie D. Hail, BSNc, Yoshio Ootaki, MD, PhDa, Gary S. Francis, MDc,d,e, Kazuyoshi Doi, MDa, James B. Young, MDc,d,e, Kiyotaka Fukamachi, MD, PhDa

a Department of Biomedical Engineering, Lerner Research Institute, The Cleveland Clinic Foundation, Cleveland, Ohio, USA
b Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic Foundation, Cleveland, Ohio, USA
c George M. and Linda H. Kaufman Center for Heart Failure, The Cleveland Clinic Foundation, Cleveland, Ohio, USA
d Transplant Center, The Cleveland Clinic Foundation, Cleveland, Ohio, USA
e Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio, USA

* Address for reprints: Patrick M. McCarthy, MD, Department of Thoracic and Cardiovascular Surgery/F25, The Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195, USA
mccartp{at}ccf.org


   Abstract
Top
 Abstract
Materials and methods
 Results
 Discussion
 Conclusions
 References
 
OBJECTIVES: Activation of the neuroendocrine axis in congestive heart failure is of prognostic significance, and neurohumoral blocking therapy prolongs survival. The hypothesis that surgical reduction of left ventricular size and function decreases neuroendocrine activation is less established. We evaluated the neurohormonal response to left ventricular reconstruction surgery in ischemic cardiomyopathy.

METHODS: Norepinephrine, plasma renin activity, and angiotensin II were measured in 10 patients before and 12 months after left ventricular reconstruction. In an additional 5 patients, brain natriuretric peptide was measured before and 3 months postoperatively. Three-dimensional cardiovascular imaging was used to assess ejection fraction and left ventricular end-diastolic volume index.

RESULTS: Concurrent with improvements of New York Heart Association functional class (2.9 ± 0.5 preoperatively vs 2.0 ± 0.4 postoperatively, P < .001), ejection fraction (23.9% ± 6.6% vs 36.2% ± 6.2%, P < .01), and left ventricular end-diastolic volume index (140.8 ± 33.8 mL/m2 vs 90.6 ± 18.3 mL/m2, P < .01), considerable reductions were observed for median plasma profiles of norepinephrine (562.0 pg/mL vs 319.0 pg/mL, P < .05), plasma renin activity (5.75 µg/L/h vs 3.45 µg/L/h, P < .05), angiotensin II (41.0 ng/mL vs 23.0 ng/mL, P = .051), and brain natriuretric peptide (771.0 pg/mL vs 266.0 pg/mL, P < .05). The more plasma renin activity or angiotensin II decreased after left ventricular reconstruction, the higher was the increase in ejection fraction (R = –.745, P < .05 [plasma renin activity]; R = –.808, P < .05 [angiotensin II]).

CONCLUSIONS: Surgical improvements of ejection fraction and left ventricular end-diastolic volume index by left ventricular reconstruction were accompanied by improvement of both the neuroendocrine activity and the functional status in patients with congestive heart failure. Whether this favorable neurohormonal response is predictive of an improved survival requires further evaluation.

Myocardial infarction is a common cause of congestive heart failure (CHF).1 Following injury, ventricular remodeling ensues, resulting in infarct expansion, left ventricular (LV) enlargement, and occasionally aneurysm formation.2 Concomitant activation of neurohumoral systems occurs and is of prognostic importance.3 Increased plasma norepinephrine (NE) and plasma renin activity (PRA) are historically associated with poor survival.4 Plasma angiotensin II (A-II) is elevated in patients with CHF.5 Plasma brain natriuretric peptide (BNP) is increased in patients with CHF and also predicts long-term survival after myocardial infarction.6-8 Neuroendocrine activation can be altered by neurohumoral blocking therapy (beta-blockers and angiotensin-converting enzyme [ACE] inhibitors), reducing mortality in CHF.9,10

LV reconstruction (LVR) surgery effectively treats CHF due to ischemic cardiomyopathy by removing nonviable, scarred tissue and restoring more normal ventricular geometry.11 We hypothesized that surgical intervention would initiate beneficial LV remodeling. If prognosis is improved, there should also be reduced neurohumoral activation. We analyzed the level of neuroendocrine activation before and up to 1 year after LVR surgery and we present the results here.


   Materials and methods
Top
 Abstract
 Materials and methods
Results
 Discussion
 Conclusions
 References
 
Patients
Plasma levels of NE, PRA, and A-II were measured before (baseline) and 12 months after LVR in 10 patients. Criteria for study enrollment were anticipated LVR surgery judged as previously described,11 the agreement to return for all scheduled follow-up visits, and informed consent in compliance with the Institutional Review Board at The Cleveland Clinic Foundation. Three additional patients were originally recruited but could not return to our institution for a follow-up visit because they moved to a remote location. They were omitted from this study. Plasma BNP was measured in 5 additional patients before and 3 months after surgery. All patients (7 women, 8 men; age 60.7 ± 11.8 years) received optimized medical therapy for heart failure, consisting of ACE inhibitors, beta-blockers, diuretics, spironolactone, and digoxin (Table 1). Blood tests were drawn the same day as either real-time 3-dimensional echocardiography (RT3DE) or magnetic resonance imaging (MRI). We have previously shown that RT3DE and MRI not only accurately reflect the geometry in LV aneurysms but also reproduce LV volumes and ejection fraction (EF) with excellent correlation and agreement.12,13 Pre- and postoperative assessment of LV function by RT3DE and/or MRI was available in 13 patients; 2 patients had only preoperative cardiovascular imaging.


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  		TABLE 1. Medications (n = 15)

 
Surgical technique
Normothermic cardiopulmonary bypass was used in all patients. First, adjunct procedures, for example, coronary artery bypass grafting (CABG) and/or repair of the mitral valve (MVR), were performed under cardioplegic arrest. LV reconstruction was performed on the beating heart.14 The LV aneurysm was opened and adherent thrombi were removed. Any subendocardial scar on the septum and anterior LV wall was resected, and the border zone between infarcted and normal myocardium was identified. Two circular polypropylene purse-string sutures were placed, creating a neck and obliterating the orifice. The ventriculotomy was closed by a horizontal mattress suture. Intraoperative echocardiography was used to assess the appropriate LV cavity size.15 Surgical details are summarized in Table 2.


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  		TABLE 2. Surgical details (n = 15)

 
Quantitative 3-dimensional imaging
An RT3DE system (Volumetrics Medical Imaging, Inc, Durham, NC) or MRI (Siemens Vision, Erlangen, Germany) was used to determine LV end-diastolic (LVEDV) and end-systolic (LVESV) volumes13,16 and to calculate EF, LVEDV index (LVEDVI), and LVESV index (LVESVI).

Neurohormone assays
Venous blood samples were obtained with the patient in the supine position after 30 minutes of rest and immediately transferred to chilled tubes. NE (normal range 80-520 pg/mL), PRA (normal range 0.5-1.8 µg/L/h), and BNP (normal range <100 pg/mL) were measured at our institution; additional probes were sent on dried ice to Quest Diagnostics (San Juan Capistrano, Calif) for measurement of A-II (normal range 10-50 ng/L).

Statistical analysis
Data were expressed as median, mean, and 95% confidence interval. Neurohormones, cardiovascular function, and New York Heart Association (NYHA) functional class were compared by a Wilcoxon signed-rank test. The association between neurohormones and LV function was evaluated by Pearson's correlation test. All analyses were performed with SPSS 11.5 (SPSS Inc, Chicago, Ill).


   Results
Top
 Abstract
 Materials and methods
 Results
Discussion
 Conclusions
 References
 
LVR surgery
The procedure was well tolerated in all 15 patients. Before LVR surgery, 3 patients were in NYHA functional class II, 11 patients in class III, and 1 patient in class IV. NYHA class improved in 13 patients whereas 2 patients had no change (1 patient in class I, 13 patients in class II, and 1 patient in class III [P = .001]; Figure 1). Medical heart failure treatment was similar to preoperative therapy (Table 1); routine laboratory tests did not detect hepatic or renal dysfunction in any patient.



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  		Figure 1. NYHA functional class (mean) before and after surgery (n = 15). Time of postoperative follow-up varied from 3 months (5 patients) to 12 months (10 patients). No difference was observed between groups. NYHA FC, New York Heart Association functional class.

 
LV function
EF increased from 23.9% ± 6.6% to 36.2% ± 6.2% (P = .003) (Table 3). LVEDVI and LVESVI decreased from 140.8 ± 33.8 mL/m2 to 90.6 ± 18.3 mL/m2 (P = .005) and from 107.6 ± 30.9 mL/m2 to 57.6 ± 12.7 mL/m2 (P = .003), respectively. Mitral regurgitation, present preoperatively in 5 patients, was also decreased. There was no difference in EF, LVEDVI, or LVESVI between the 10 patients followed for 12 months and the 5 patients followed for 3 months, confirming our previous observation that improvement of LV function evolved intraoperatively/early postoperatively and was sustained late after LVR.16


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  		TABLE 3. Left ventricular ejection fraction and dimensions, mitral regurgitation (n = 15)*

 
Neurohormones
Plasma levels of NE, PRA, A-II, and BNP significantly improved after LVR (Table 4). Median NE decreased from 562 pg/mL to 319 pg/mL (P < .05). Median PRA and median A-II dropped from 5.7 µg/L/h to 3.4 µg/L/h (P < .05) and from 41 ng/mL to 23 ng/mL (P = .051), respectively. Median BNP decreased from 771 pg/mL to 266 pg/mL (P < .05). Figure 2 depicts the course of NE, PRA, and A-II in each patient.


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  		TABLE 4. Neurohormones

 


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  		Figure 2. NE, A-II, and PRA profiles before and after surgery (n = 10). Considerable improvements of neurohormones were observed during follow-up. Of note, patient 6 experienced only a modest decrease of norepinephrine, corresponding to an improvement of NYHA class IV before surgery to class III at 1 year after surgery.

 
The changes of pre- to postoperative PRA and A-II inversely correlated with the change of EF. The more PRA decreased after surgery, the higher the increase of EF (R = –.745, P < .05). A similar association was found between the decrease of A-II and the increase of EF (R = –.808, P < .05). Furthermore, the decrease of BNP correlated with the decrease of LVEDVI with a trend toward significance (R = .846, P = .071). No association was found between changes of NE and changes of EF, LVEDVI, or LVESVI.


   Discussion
Top
 Abstract
 Materials and methods
 Results
 Discussion
Conclusions
 References
 
Neuroendocrine activation in CHF
Neurohormones participate in many pathologic adaptations and can contribute to the progression of CHF.17 Medical therapy that decreases neuroendocrine activation also reduces the mortality of CHF9,10,18 and may correlate with modest improvements of EF and functional parameters.19-21 However, neurohormonal models may be necessary but are not sufficient to explain all aspects of disease progression in CHF.22 Neurohormones are not deranged without a triggering event; thus the elimination of 1 trigger (eg, surgical reduction of pathologic cardiac wall stress) may result in the reduction of neurohormones. In support of this, lowering cardiac filling pressure alone by diuretics and vasodilators can rapidly suppress the neurohumoral activation in decompensated heart failure with decreased BNP and NE profiles.23

Neurohormonal response to surgical intervention
In this study, we observed improvement in neurohormones that may be attributed to surgical improvement of LV anatomy with increase of EF and decrease of LV volume and mitral regurgitation. Importantly, although LVR was an aspect of additional procedures (eg, CABG or MVR), the impact of each individual surgical therapy on the improvement of neurohormones cannot be determined because all associated aspects of ischemic cardiomyopathy were repaired. We and others24,25 advocate a complete revascularization whenever possible to achieve an optimal result after LVR. Valve repair, if necessary, is also indicated to realize the full benefit of this procedure.26 We expect that the favorable neurohormonal response observed in this study may have been generated by the combined surgical strategy.27

In agreement with the current study, atrial natriuretric peptide (ANP) and BNP profiles were significantly lowered after revascularization in ischemic cardiomyopathy concurrent with an improvement of LV function and NYHA functional class.28 We have previously shown that the insertion of an LV assist device in patients with decompensated CHF was followed by significantly improved NE, PRA, and A-II profiles, concomitant with partial recovery of the native heart.29 Furthermore, preoperatively elevated plasma ANP levels normalized after mitral valve surgery for degenerative valve disease along with an improvement of functional parameters.30

Implications
The favorable neurohormonal response observed in this study may indicate an improved long-term prognosis after LVR surgery. Patients with a considerable percent decrease in NE (and BNP) profiles may experience a profound decline in mortality.31 Further, median NE levels above 393 pg/mL were previously found predictive for an increased mortality.32 In our study, median NE was significantly reduced to 319 pg/mL, a profile similar to that of a matching cohort of control subjects in the SOLVD trial.3 This observation suggests that the mortality of patients with ischemic cardiomyopathy can be significantly reduced by surgery including LVR. In addition, depressed EF (<30%) and increased LVESVI (>70 mL/m2) were associated with an increased mortality of patients with myocardial infarction33 and CHF.34 In this study, baseline EF and LVESVI were even more compromised; thus, the improvement of both parameters by LVR surgery to 36.2% ± 6.2% and 57.6 ± 12.7 mL/m2, respectively, may also prognosticate a better long-term survival. Moreover, PRA and A-II profiles, both markedly reduced by LVR in this study, were elevated in patients with poor LV function and overt CHF.3,35 Accordingly, we found an inverse correlation between changes of PRA and A-II profiles with changes of EF in the current study. Furthermore, the decrease of BNP profiles after LVR in this study may not only be predictive of a reduced mortality6,7,31,36 but may also indicate the suppression of a trigger of neuroendocrine activation. In agreement with the current study, previous reports have shown that BNP is related to LVEDVI36 and the reduction of intracardiac filling pressure decreases BNP profiles.23 Reduction of cardiac wall stress may possibly contribute to the decreased neuroendocrine activation after LVR.

Study limitations
This study analyzed the effect of LVR surgery on neuroendocrine activation in a small number of patients. Importantly, the improvement of LV function in the patients studied is in close agreement with previous reports of larger cohorts of patients from our institution12-16 and elsewhere,11 indicating that the patients enrolled in this study are indeed representative. Continued medical therapy, while unchanged from preoperative therapy, may have contributed to the improvement of neurohormones in addition to the surgical therapy.

Another limitation arises from the different lengths of follow-up in the 5 patients with BNP profiles in comparison with the remaining 10 patients with other neurohormone data. Of note, improvements of LV function and NYHA classification did not differ between groups, suggesting that the trigger of the neurohormonal response was similar and, hence, the course of neurohormone profiles were likely comparable. LV redilation years after surgery may be possible and could lead to reactivation of neurohormones with consecutive decrease of prognosis.


   Conclusions
Top
 Abstract
 Materials and methods
 Results
 Discussion
 Conclusions
References
 
LVR surgery was accompanied by a favorable neurohormonal response. Decreased profiles of selected neurohormones were associated with improved LV function. These results support the hypothesis that direct improvement of cardiovascular function may reduce neuroendocrine activation by removing trigger mechanisms. Because neuroendocrine activation is of prognostic significance in CHF, the favorable neurohormonal response after LVR surgery may be indicative of an improved long-term survival. Further studies are necessary to confirm this prediction.


   Acknowledgments
 
The authors thank Ms Adelaide Jaffe for editorial advice.


   Footnotes
 
Supported by the Department of Thoracic and Cardiovascular Surgery and the George M. and Linda H. Kaufman Center for Heart Failure at The Cleveland Clinic Foundation.


   References
Top
 Abstract
 Materials and methods
 Results
 Discussion
 Conclusions
 References
 

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 J. Thorac. Cardiovasc. Surg.Home page
V. Dor
Left ventricular reconstruction: The aim and the reality after twenty years
J. Thorac. Cardiovasc. Surg., July 1, 2004; 128(1): 17 - 20.
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Patrick M. McCarthy
Randall C. Starling
Yoshio Ootaki
James B. Young
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