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J Thorac Cardiovasc Surg 2002;124:206-209
© 2002 The American Association for Thoracic Surgery
Brief Communications |
From the Division of Cardiovascular Surgery, Osaka Minami National Hospital, Osaka, Japan.
Received for publication Dec 18, 2001. Accepted for publication Jan 7, 2002. Address for reprints: Yoshitaka Hayashi, MD, Division of Cardiovascular Surgery, Osaka Minami National Hospital, 2-1 Kido-higashimachi, Kawachinagano City, Osaka 586-8521, Japan (E-mail: yhayashi{at}jun.ncvc.go.jp).
Atrial natriuretic peptide (ANP) has various pharmacologic effects, such as natriuresis, diuresis, vasodilation, inhibition of the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system, and renal protection.
1,2 ANP is stored in secretory granules in the atria, and its secretion is predominantly regulated by stretching of the atria. 3 Plasma levels of ANP increase with the severity of heart failure, 3,4 especially in patients with mitral stenosis (MS), and there has been a significant correlation between plasma ANP concentrations and pulmonary capillary wedge pressure. 5 On the other hand, a few cases of very low plasma ANP level despite chronic congestive heart failure have been reported. 6,7 For these patients, the infusion of synthetic human 
-ANP (h-ANP) is thought to be effective in postoperative management, although it seems difficult to wean the patient from the h-ANP infusion. 6 Here we describe the case of a patient with a very low plasma ANP concentration and giant atria as a result of severe MS and tricuspid regurgitation (TR), and we report the effects of postoperative h-ANP infusion and oral spironolactone administration for the replacement of intravenous h-ANP infusion after cardiac surgery.
Clinical summary
A 64-year-old woman who had undergone closed mitral commissurotomy for MS at the age of 29 years was admitted to our hospital because of severe general malaise, palpitations, orthopnea, hepatocardiomegaly, and dyspnea. These symptoms appeared even at rest, and her New York Heart Association functional class was III. An electrocardiogram demonstrated atrial fibrillation but showed no myocardial ischemic signs. A chest radiograph showed severe pulmonary congestion, pleural effusion, and cardiomegaly (cardiothoracic ratio 90%), indicative of chronic congestive heart failure. On echocardiography, the left atrial dimension measured 87 mm, the left ventricular end-diastolic and end-systolic dimensions measured 43 and 29 mm, respectively, the intraventricular septal thickness measured 7 mm, the left ventricular posterior wall thickness measured 7 mm, the fractional shortening was 33%, and the ejection fraction was 56%. The mitral valve area was 0.66 cm2 according to the pressure half-time method and 0.59 cm2 according to the trace method. Mitral regurgitation was mild. TR was severe, accompanying the enlargement of both the atria. The pulmonary arterial systolic pressure, as calculated by the peak velocity of severe TR (39 mm Hg), was considered to represent severe pulmonary hypertension. Cardiac catheterization and angiography were performed for preoperative evaluation. Neither aortic stenosis nor aortic regurgitation was detected. Left ventricular function, as calculated by left ventriculography, was as follows: left ventricular end-diastolic volume, 207 mL; indexed left ventricular end-diastolic volume, 156 mL/m2; left ventricular end-systolic volume, 78 mL; indexed left ventricular end-systolic volume, 59 mL/m2; and ejection fraction, 62%. Pulmonary capillary wedge pressure was measured at 20 mm Hg, and pulmonary arterial pressure was measured at 50/25 mm Hg (mean 33 mm Hg). Coronary angiography showed no significant coronary artery stenosis. The diagnosis was therefore congestive heart failure as a result of severe MS and TR.
To evaluate the association of neurohormones, the plasma levels of ANP, brain natriuretic peptide (BNP), cyclic guanosine monophosphate, renin activity, and aldosterone were measured by radioimmunoassay. The plasma ANP concentration was very low (7.3 pg/mL), whereas the plasma BNP concentration was high (82.7 pg/mL). The cyclic guanosine monophosphate level was 3.2 pmol/mL. The RAAS was remarkably activated (renin activity 17.4 ng/[mL · h], plasma aldosterone 431 pg/dL). Renal function was within normal limits, with a 0.5 mg/dL creatinine level.
The patient underwent mitral valve replacement and tricuspid annuloplasty 35 days after admission to our institution. Median full sternotomy was done to expose the pericardial cavity. The walls of both the atria were remarkably thinned. Cardiopulmonary bypass (CPB) was established in a routine fashion, and myocardial protection during aortic crossclamping was performed with continuous and intermittent bolus infusions of minimally diluted blood cardioplegia containing 9.8 mmol/L potassium and 4.0 mmol/L magnesium. Mitral valve replacement was performed with a 27-mm bioprosthesis (Carpentier-Edwards; Baxter Healthcare Corporation CardioVascular Group, Irvine, Calif), and tricuspid annuloplasty was performed with a 28-mm annular ring (Cosgrove Edwards Ring; Baxter Healthcare Corporation CardioVascular Group). The operation was finished without any complications, and the process of weaning the patient from CPB with the assistance of inotropic agents was uneventful. After the termination of CPB, however, oliguria developed and did not even respond to the intravenous bolus injection of 100 mg furosemide. Intravenous infusion of h-ANP (HANP; Suntory Inc, Zeria Pharmaceutical, Tokyo, Japan) at a rate of 0.05 µg/(kg · min) was started immediately. After this infusion, systolic aortic pressure decreased to less than 90 mm Hg, and the infusion was therefore reduced to a rate of 0.025 µg/(kg · min). The urinary output increased dramatically without the use of furosemide.
Successful extubation was accomplished 11 hours after the operation. The h-ANP infusion was gradually tapered with the use of furosemide and was discontinued 43 hours after the operation. Soon after cessation of h-ANP infusion, however, the urinary volume decreased and oliguria resumed despite the dose of furosemide. Further h-ANP infusion at 0.025 µg/(kg · min) was restarted 34 hours after the initial discontinuance. At that time, plasma levels of renin activity, angiotensin II, and aldosterone remained high. A 100-mg dose of spironolactone as well as furosemide was administered orally to aid in tapering the h-ANP infusion. Five days after oral spironolactone administration, h-ANP infusion was discontinued successfully. Figure 1 illustrates the entire postoperative course with respect to h-ANP dose and neurohormones. The patient was discharged from our institution 50 days after the operation, at which time the plasma ANP level was 10.2 pg/mL, the plasma BNP level was 148.5 pg/mL, and the plasma aldosterone level was 158 pg/mL.
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The plasma ANP concentration is thought to increase in accordance with the severity of chronic congestive heart failure because the atrial distention stimulates ANP secretion, 3,4 whereas some patients with severe TR and pulmonary hypertension resulting from MS are reported to show a very low plasma ANP concentration or a lack of ANP secretion despite chronic congestive heart failure. 6,7 Nishimura and associates 6 have suggested that sustained MS and TR induce excessive extension of the atria, which might further diminish the granules producing ANP. Maeda and colleagues 7 demonstrated remarkable fibrosis in the histologic specimen of the right atrial myocardium obtained from a patient with MS and a very low plasma ANP concentration, with only a few remaining myocytes and a few ANP-containing cells. However, these two patients had undergone open mitral commissurotomy. Nishimura and coworkers 8 demonstrated in experimental heart failure models that the secretary function of ANP was impaired after resection of atrial appendages. Although the walls of both atria were remarkably thinned in our case, the right atrial appendage had not been removed or ligated. Further clinical and experimental studies are needed to elucidate the mechanism of low plasma ANP concentration in patients with severe MS, TR, and pulmonary hypertension.
ANP has various pharmacologic effects, as mentioned previously, although it remains unclear why its secretion is enhanced during congestive heart failure. In general, heart failure activates the RAAS and enhances the production of vasopressin. 9 Some suggests that the enhanced ANP production in congestive heart failure is an adaptive response to attenuate the RAAS activation and vasopressin-induced vasoconstriction. 10 On the other hand, BNP secretion is considered to increase in accordance with the degree of left ventricular end-diastolic pressure because the ventricular distention stimulates BNP secretion. 11 In patients with MS and severe pulmonary hypertension, BNP production is thought to increase as a result of right ventricular stimulation. In patients with a very low plasma ANP concentration or a lack of ANP secretion, BNP production is enhanced to compensate for the insufficient ANP secretion.
CPB is also thought to activate the RAAS and vasopressin production. 12 Furthermore, venous drainage reduces the atrial stretching, resulting in a decrease in ANP production. 13 Generally, ANP production resumes at the termination of CPB in accordance with the arterial stretching and plays a role in attenuating the RAAS activation. 13 Sezai and associates 13 have demonstrated that the RAAS activation reaches a peak 3 to 6 hours after CPB. In patients with chronic congestive heart failure accompanying insufficient ANP secretion, however, the RAAS is thought to continue to be activated long after the termination of CPB. This may account for the efficacy of continuous h-ANP infusion and the difficulty in the weaning process.
Continuous h-ANP infusion affects plasma BNP concentrations. The inactivation of members of the natriuretic peptide family is mainly associated with the following two factors: natriuretic peptide receptor C and neutral endopeptidase. 14,15 Continuous h-ANP infusion occupies these deleting systems and reduces the clearance of BNP, resulting in an increase in the plasma BNP concentration. After the termination of h-ANP infusion, however, the deleting system is immediately resumed, and the plasma BNP concentration subsequently decreases. These biochemical responses may play a role in the rebound phenomenon seen with the discontinuation of long-term h-ANP infusion.
According to this and previous reports, continuous h-ANP infusion after cardiac surgery in cases of congestive heart failure seems essential, especially for patients with insufficient ANP secretion. 6,7 However, there are no oral substitute drugs to aid in discontinuing h-ANP infusion. In our case, the RAAS was still activated at the first weaning process from intravenous h-ANP infusion, and oral spironolactone administration was effective for the second weaning process. Recently, several studies have demonstrated the various effects of spironolactone on the patient management in cardiovascular care. 16,17 This is the only reported case in which oral spironolactone administration was effective in weaning a patient with insufficient ANP secretion from intravenous h-ANP infusion, and further studies are needed to establish the perioperative management for h-ANP-dependent patients.
In summary, we treated a patient with giant atria and a very low plasma ANP concentration caused by severe MS and TR. After cardiac surgery, oliguria developed, and continuous intravenous h-ANP infusion was effective for its postoperative management. It was difficult to wean the patient from the h-ANP infusion with the administration of furosemide alone. The RAAS was still activated long after the termination of CPB, and oral spironolactone administration was effective in weaning the patient from the intravenous h-ANP infusion.
References
This article has been cited by other articles:
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  B. Geny, A. Charloux, G. Brandenberger, and F. Piquard Despite cardiac denervation, atrial natriuretic peptides possess a cardiac sympathoinhibitory effect after heart transplantation J. Thorac. Cardiovasc. Surg., June 1, 2006; 131(6): 1417 - 1418. [Full Text] [PDF]
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