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Asian Cardiovasc Thorac Ann 2004;12:41-46
© 2004 Asia Publishing EXchange Ltd

ORIGINAL CONTRIBUTION

Clinical Implication of Atrial and Brain Natriuretic Peptide in Coronary Artery Bypass Grafting

Min-Ho Song, MD, Yoshie Kobayashi, RN, Hiroyasu Michi, BS

Department of Cardiovascular Surgery, Shizuoka Saiseikai General Hospital, Shizuoka, Japan

For reprint information contact: Min-Ho Song, MD Tel: 81 54 285 6171 Fax: 81 54 285 5179 Email: songmhmd{at}yahoo.co.jp Department of Cardiovascular Surgery, Shizuoka Saiseikai General Hospital, 1-1-1 Oshika, Shizuoka-shi, Shizuoka 422-8527, Japan.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Atrial natriuretic peptide and brain natriuretic peptide are known to be indices for heart failure. Atrial natriuretic peptide and brain natriuretic peptide changes in off-pump and on-pump coronary artery bypass grafting is hypothesized to be correlated to clinical implications of coronary artery bypass grafting. 20 consecutive off-pump and 20 consecutive on-pump coronary artery bypass grafting patients were studied. Perioperative atrial natriuretic peptide and brain natriuretic peptide values were measured and statistically analyzed in terms of 14 factors related to myocardial damage and recovery. Postoperative atrial natriuretic peptide plateaued on the third postoperative day and it decreased gradually down to the preoperative level by one month in the off-pump group. Postoperative brain natriuretic peptide plateaued, showed very slow decrease and it never reached down to the preoperative level. The peak brain natriuretic peptide level was correlated with aortic cross-clamp time, postoperative pleural effusion, and postoperative atrial fibrillation ( p < 0.01). The atrial natriuretic peptide change reflected surgical prevention of ventricular remodeling. Brain natriuretic peptide > 450 µg·mL-1 had strong predictive power for atrial fibrillation and pleural effusion and is a useful marker for management of coronary surgery patients.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Since the rekindling of off-pump coronary artery bypass grafting (OPCAB), many cardiac surgeons have been trying to identify the specific superiority of OPCAB over conventional cardioplegic coronary artery bypass grafting (CABG). There has been supporting evidence that indirect factors related to operative myocardial damage have improved such as operation time, time needed for respirator, intensive care unit stay, transfusion rate, hospital stay, and amount of medical cost.1 Favorable impact of revascularization by OPCAB on myocardial function is, however, not yet distinctively delineated except in a few reports.2

Several recent studies have demonstrated that cardiac natriuretic hormones are reliable indices of left ventricular (LV) dysfunction. Brain natriuretic peptide (BNP) is released predominantly by the cardiac ventricles and blood concentrations are inversely correlated with the ventricular ejection fraction.3 Atrial natriuretic peptide (ANP) presents a high degree of structural homology with BNP and is primarily synthesized in and secreted from the atrium. The plasma half-life of ANP is shorter, and ANP has less pressure-lowering effects than BNP.4 It has been shown that natriuretic peptides reduce myocardial pre and after load, improve left ventricular function, dilate coronary arteries and ameliorate exercise-induced myocardial ischemia. Although protective effects of ANP and BNP against acute myocardial remodeling have been demonstrated,5 their observed increases in response to CABG occur by means not yet known.6 It is not yet decided whether myocardial stabilizer and simple ischemia is superior to cardioplegic myocardial protection.7 BNP can be a sensitive indicator of postischemic dysfunction even in minor perioperative myocardial ischemia.8

The aim of this study was to investigate ANP and BNP changes in on-pump and off-pump CABG perioperatively, to correlate them with clinical factors of myocardial function, and to identify predictive roles of them on the recovery of the LV function and postoperative management.


   PATIENTS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
From April 2002 to December 2002, 20 on-pump CABG patients (Group On) and 20 off-pump CABG patients (Group Off) were enrolled in this study. Selection of on-pump or off-pump was randomized. Emergent cases and concomitant valve procedures were excluded from this study. The demographic data of both groups is summarized in Table 1Go.


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  		Table 1. Demographic data
 
ANP and BNP were measured at 6 time points; the day before surgery, the 1st, 3rd, 7th and 14th postoperative day, and one month after the surgery. Blood sampling was done from the antecubital vein after the patient had rested supine for 20 minutes. All blood samples were placed in chilled plastic tubes containing 1 mg·mL-1 ethylene-diamine-tetra-acetic acid (EDTA) and 1000 kallikrein inhibitory units per mL aprotinine and immediately placed on ice. Thereafter, the blood was centrifuged at 4°C, and the plasma was stored at -70°C until assay. Plasma concentrations of ANP and BNP were measured by radioimmunoassay using commercially available kit (Shionogi Pharmaceuticals, Ltd., Japan) at our hospital.

All CABGs were done by a single surgeon (MHS). The techniques of off-pump and on-pump CABG were standard. Both on-pump and off-pump CABG were performed through midline sternotomy. Mammary arteries were skeletonized and harvested by Harmonic scalpel (Ethicon, Sommerville, NJ). On-pump CABG was carried out in a standard way of cardiopulmonary bypass with antegrade and retrograde cardioplegia (cold blood) with mild systemic hypothermia. Off-pump CABG was undertaken with the use of Octopus (Octopus 2; Octopus tissue stabilization system; Medtronic Inc, Mineapollis, MN, USA) and intracoronary shunts (Baxter Anasta Flo Intravascular Shunt, Irvine, CA, USA). The anastomosis was done by 8-0 Prolene (Ethicon, Sommerville, NJ, USA) in a usual manner. All patients received at least both left and right internal mammary arteries.

Clinicopathological data are expressed as the mean ± standard deviation. Statistical comparisons were performed by chi-squared analysis, Student t test, or one-way analysis of variance with multiple comparisons, when appropriate. Significance was designated at the probability value of p < 0.01. Linear regression analysis was used to assess the relation between natriuretic peptide levels and hemodynamic variables.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Perioperative BNP changes in group On and group Off are shown in Figure 1Go and Figure 2Go, respectively. In group On, BNP increase was maximal on the 3rd postoperative day and it tended to decrease gradually down to the preoperative level. This trend was the same in group Off. There was no statistical significant difference between two groups at each point.



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  		Figure 1. BNP change of group On

 


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  		Figure 2. BNP change of group Off

 
Perioperative ANP changes in group On and group Off are shown in Figure 3Go and Figure 4Go, respectively. The peak ANP was observed on the 3rd postoperative day in both groups. Group On patients tended to remain increased even after one month postoperatively. ANP on the 3rd postoperative day was significantly higher in group Off than in group On. One month after operation, group Off patients’ ANP returned to the preoperative level.



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  		Figure 3. ANP change of group On

 


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  		Figure 4. ANP change of group Off

 
Tables 2GoGoGo to 5Go show correlations of BNP and ANP with the clinical factors shown in Table 1Go. The statistically correlated factors were aortic crossclamp time, postoperative pleural effusion on the chest X-ray, and postoperative atrial fibrillation. Univariate and multivariate analysis identified peak BNP of more than 450 µg·mL-1 to be the most powerful predictor of postoperative pleural effusion and atrial fibrillation. Improvement of ejection fraction was not correlated with either peak BNP or peak ANP.


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  		Table 2. Relationships between BNP and clinical factors in group On
 

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  		Table 3. Relationships between BNP and clinical factors in group Off
 

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  		Table 4. Relationships between ANP and clinical factors in group On
 

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  		Table 5. Relationships between ANP and clinical factors in group Off
 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
BNP response to CABG or OPCAB became maximal on the 3rd postoperative day and it remained higher than the preoperative level. This transition was the same in both groups. The inference from this study was that BNP did not discriminate the operative invasiveness either on-pump or off-pump, but postoperative peak BNP of more than 450 µg·mL-1 predicted the occurrence of postoperative pleural effusion and atrial fibrillation. Matsusita and colleagues6 discussed that the operative stress included general anesthesia, cardiac herniation, stabilizer compression, regional blood flow blockage and reperfusion injury. Their results were in agreement with ours. They observed that ANP and BNP of the OPCAB group returned to near the preoperative level one month after the surgery, thus supporting the notion that OPCAB is less invasive. In our study the BNP level did not return to the preoperative level in both groups, and this was reflected by the sensitivity of BNP for ventricular function. Since the direct marker for the ventricular insult, creatine kinase MB-isoenzyme (CKMB), was not significantly different among both groups, BNP was thought to be a more precise index for myocardial status. The returned ANP level implies that the prevention of myocardial remodeling was achieved by coronary revascularization.5 ANP levels demonstrate that if the coronary bypass is successful, myocardial remodeling is consecutively prevented. BNP levels, on the other hand, demonstrate that even if the coronary bypass is successful, the operation itself affects the myocardial function.

Postoperative atrial fibrillation is seen in 30% of coronary bypass surgery. Although its etiology remains unclear,ANP was reported to be unable to predict postoperative atrial fibrillation.9 Our study showed that if the peak BNP was more than 450 µg·mL-1, postoperative atrial fibrillation was observed in all patients. BNP has been shown to be an independent predictor for atrial fibrillation and its production is demonstrated in the atrium.10 Stamou and colleagues concluded in 969 off-pump coronary surgery that predictors of atrial fibrillation included age > 75 years old, history of stroke, postoperative pleural effusion, and postoperative pulmonary edema.11 Regarding the recurrence of atrial fibrillation, Mabuchi and coworkers reported that high BNP and relatively low ANP compared with BNP were independent risk factors of atrial fibrillation recurrence in patients with mild congestive heart failure.12 If atrial fibrillation is restored to sinus rhythm by cardioversion, BNP is reported to decrease immediately.13 Also as to atrial fibrillation leading to thromboembolism, BNP is a significant predictor of thromboembolic events.14 In clinical settings, if postoperative BNP is high, the generalized prevention should be undertaken immediately to mitigate unnecessary complications.

BNP was a significant predictor for postoperative pleural effusion in our study. In a large study, Light and colleagues reported that the prevalence of pleural effusions in the patients undergoing only CABG surgery (63%) or CABG surgery plus valve surgery only (62%) was significantly higher than that in the patients undergoing valve surgery only (45%).15 Discussion about the relationship between BNP and postoperative pleural effusion is scarce, but it is possible pleural effusion complicates as myocardial insult and BNP increase, which would originate from the pericardial sac. Also, as pleural effusion was a predictor for atrial fibrillation,11 our result seems to be rational. In clinical settings, if BNP is high, the precaution for pleural effusion should be undertaken and it should be drained by thoracentesis.

In summary, we observed two inferences. First, ANP returned to preoperative level in the off-pump group but not in the on-pump group, which meant that prevention of remodeling was achieved earlier after coronary surgery, especially after OPCAB. Second, BNP showed a very gradual decrease in both groups, which had significant predictive relationship of postoperative atrial fibrillation and pleural effusion, so postoperative measurement of BNP is useful to anticipate such complications.


   ACKNOWLEDGMENTS
 
We appreciate Dr Hajime Nakamura and Dr Takashi Watanabe for their operative assistance at Shizuoka Saiseikai General Hospital. We also thank Ms Liya Jeon for her manuscript preparation.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. Hart JC, Puskas JD, Sabik JF 3rd. Off-pump coronary revascularization: current state of the art. Semin Thorac Cardiovasc Surg 2002;14:70–81.[Medline]

  2. Chello M, Mastroroberto P, Perticone F, Cirillo F, Bevacqua E, Olivito S et al. Plasma levels of atrial and brain natriuretic peptides as indicators of recovery of left ventricular systolic function after coronary artery bypass. Eur J Cardiothorac Surg 2001;20:140–6.[Abstract/Free Full Text]

  3. Clerico A, Iervasi G, Del Chicca MG, Emdin M, Maffei S, Nannipieri M et al. Circulating levels of cardiac natriuretic peptides (ANP and BNP) measured by highly sensitive and specific immunoradiometric assays in normal subjects and in patients with different degrees of heart failure. J Endocrinol Invest 1998;21:170–9.[Medline]

  4. Raine AE, Erne P, Burgisser E, Muller FB, Bolli P, Burkart F et al. Atrial natriuretic peptide and atrial pressures in patients with congestive heart failure. N Engl J Med 1986;315:533–7.[Abstract]

  5. Hayashi M, Tsutamoto T, Wada A, Maeda K, Mabuchi N, Tsutsui T et al. Intravenous atrial natriuretic peptide prevents left ventricular remodeling in patients with first anterior acute myocardial infarction. J Am Coll Cardiol 2001;37:1820–6.[Abstract/Free Full Text]

  6. Matsushita Y, Okamura Y, Iida H, Mochizuki Y, Mori H, Yamada Y et al. Usefulness of OPCAB from the viewpoint of fluctuations in the level of blood natriuretic peptides. Kyobu Geka 2001;54:321–5.[Medline]

  7. Avidan MS, Meehan N, Ponte J, El-Gamel A, Sherwood RA. Changes in brain natriuretic peptide concentrations following open cardiac surgery with cardioplegic cardiac arrest. Clin Chim Acta 2001;303:127–132.[Medline]

  8. Mair P, Mair J, Bleier J, Hormann C, Balogh D, Puschendorf B. Augmented release of brain natriuretic peptide during reperfusion of the human heart after cardioplegic cardiac arrest. Clin Chim Acta 1997;261:57–68.[Medline]

  9. Hakata T, Hedman A, Turpeinen A, Kettunen R, Vuolteenaho O, Hippelainen M. Prediction of atrial fibrillation after coronary artery bypass grafting by measuring atrial peptide levels and preoperative atrial dimensions. Eur J Cardiothorac Surg 2002;22(6):939–43.[Abstract/Free Full Text]

  10. Inoue S, Murakami Y, Sano K, Katoh H, Shimada T. Atrium as a source of brain natriuretic polypeptide in patients with atrial fibrillation. J Card Fail 2000;6:92–6.[Medline]

  11. Stamou SC, Dangas G, Hill PC, Pfister AJ, Dullum MK, Boyce SW et al. Atrial fibrillation after beating heart surgery. Am J Cardiol 2000;86:64–7.[Medline]

  12. Mabuchi N, Tsutamoto T, Maeda K, Kinoshita M. Plasma cardiac natriuretic peptides as biochemical markers of recurrence of atrial fibrillation in patients with mild congestive heart failure. Jpn Circ J 2000;64:765–71.[Medline]

  13. Jourdain P, Bellorini M, Funck F, Fulla Y, Guillard N, Loiret J et al. Short-term effects of sinus rhythm restoration in patients with lone atrial fibrillation: a hormonal study. Eur J Heart Fail 2002;4:263–7.[Medline]

  14. Shimizu H, Murakami Y, Inoue S, Ohta Y, Nakamura K, Katoh H et al. High plasma brain natriuretic polypeptide level as a marker of risk for thrmoboembolism in patients with nonvalvular atrial fibrillation. Stroke 2002;33:1005–10.[Abstract/Free Full Text]

  15. Light RW, Rogers JT, Moyers JP, Lee YC, Rodriguez RM, Alford WC Jr et al. Prevalence and clinical course of pleural effusions at 30 days after coronary artery and cardiac surgery. Am J Respir Crit Care Med 2002;166:1567–71.[Abstract/Free Full Text]




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