Atrial Natriuretic Peptide and Hemodynamic Response to Pericardiectomv for Chronic Conktrictive Pericarditis -
operative test. Invasive hemodynamic varameters and ANP were measured hefore during and after the test. In agreement with the fact that the patient had few symptoms of cardiac failure before the operation, cardiac output was normal and did not improve significantly after operation However, as shown in Figure 1, the stroke volume did not increase during exercise before pericardiectomy, so the change in cardiac output wasalmost due to the increasein heart rate. As shown in Figure 2, beforepericardiectomy, the mean right atria1 pressure was elevated at rest and increasedfrom 8 to 20 mm Hg at maximal exercise, the mean pulmonary arterial pressure increased from 15 to 34 mm Hg and the mean pulmonary capillary wedgepressure increasedfrom IO to 24 mm Hgdur-
Jens Svanegaard, MD, Per Thayssen, PhD, and Henrik K. Arendrup, MD trial compliance, intraluminal A pressure, transmural pressure and atria1 stretch have been suggested as major stimuli for the production of atria1 natriuretic peptide (ANP). These assumptions are mainly based on observations showing good correlations between pressures and ANP levels in heart failure due to heart diseases of various etiology.’ Increasing pressure in the left and/or right atrium is followed by an increased stretch of the atria1 wall in most heart diseases, except in cardiac tamponade and constrictive pericarditis. In an experiment with dogs, the rise of ANP during rapid volume expansion was decreased in the presence of cardiac tamponade, even if the right atria1 pressure and the left end-diastolic pressure increased during the induced tamponade.2 This indicates that pressure is not the only determinant, as has been presumed previously. To investigate this relation, we studied the relation between ANP and some important hemodynamic parameters in a patient during exercise before and after pericardiectomy. A 37-year-old man was admitted to the hospital becauseof symptoms of pleuritis, the origin of which was never revealed. The patient had no complaints of dyspnea. However, in the preceding 2 to 3 weeks, he had modest lower extremity edema together with a slightly elevated serum alanine aminotransferase, serum lactate dehydrogenaseand serum bilirubin. Oneyear before hospital admission, an ultrasound examination of the liver, because of transitory abdominal pain, had shown unexplained enlargement of the hepatic veins. Chest x-ray, echocardiography and left ventriculography From the Departments of Cardiology, Clinical Physiology, and Cardiac Surgery, Odense University Hospital, Kloevervaenget 26 C 2, Odense, Denmark, DK-5000. Manuscript received November 28, 1989; revised manuscript received and accepted February 20. 1990.
showedmanifest pericardial calcification in the whole circumference of the heart. All segmentsof the heart were contracting normally. Ejection fraction was 66%. Three weeks before and 3 months after pericardiectomy, echocardiography at rest and a graded bicycle exercise test were achieved. The exercise test was performed by increasing workload by 30 watts every 3 minutes during right-sided cardiac catheterization, until the preoperative maximal work load of 150 watts was reached. The patient had no medical therapy at the preoperative test or at the post-
Heart
rate
.’
\
j. ‘. ‘.b
Cardiac
output
L/min 20
5-
0
rest FIGURE exerctse
1. Cardiac and before
150 output,
stroke
votume
(dotfed line) and after THE AMERICAN
watt
and heart rate pertcardiectmy
JOURNAL
15 min at rest, during (c~nfhmus
OF CARDIOLOGY
and after line).
JULY 1, 1990
117
ing exercise. The concentration of ANP, measured in the subclavian vein, increased from 217 pg/ml at rest (normal 82 f 38.4 [mean f I standard deviation], n = 51) to 510 pg/ml at 150 watts. After pericardiectomy, the hemodynamic parameters and ANP normalized at rest. During exercise, the right atria1 pressure was decreasing, while the arterial pulmonary pressure and pulmonary capillary wedge pressure increased slightly. The course of the arterial blood pressure at rest and during exercise was unchanged before and after operation. Echocardiographically, the diameter of the left atrium decreased from 51 to 48 mm. A high correlation between the change in pressures and ANP was observed before the operation. After the operation, both ANP and the hemodynamic parameters were lowered and RIGHT ATRIAL
10-
ANP pg/m, - 600
40-
500
35.
0
ANP
- 600
0
- 500
0 P
v v
- 400
25 0
D
300
u
20.
iI
-6. 110 vat,
300
:;-
-0 WDI
pglml
0
- 400
0
5o:
PRESSURE
ANP
mmHg
30
o
10
ARTERIAL
versus
6 0
Alterations in the ANP level have, to our knowledge, only been reported in 1 case of chronic constric-
ANP
mmng
16.
manner, the production, use and/or degradation of ANP in the lungs, left atrium, left ventricle and aortic vessels were estimated from the dtfference in the concentration of ANP in the radial artery and the pulmonal artery. Evaluated in this manner, there seems to be a shift from a predominant production of ANP in the left atrium before operation to a larger production in the right atrium after operation (Figure 3). In spite of an increased pressure of the right atrium at rest and during exercise before operation, the right atrium had only a very small production of ANP, while the production of ANP from the right atrium increased although the right atria1 pressure decreased after operation both at rest and during exercise.
PULMONARY
PRESSURE
versus 15 -
the correlation between the changes in concentrations of ANP and right atria1 pressure were not good. However, ANP was still correlating very well to alterations in both the pulmonary capillary wedge pressure and especially changes of thepulmonary arterial pressure, as the alterations in ANP and the pulmonary arterial pressure were nearly parallel. To estimate the production of ANP in the right and the left atrium, respectively, blood samples were taken from the subclavian vein, the pulmonary artery and the radial artery to determine ANP concentrations at rest and at I50 watts. By subtracting the ANP concentration in the superior caval vein from the concentration in the pulmonal artery, an indication of the production, use and/or degradation of ANP in the right atrium and the right ventricle could be achieved. In the same
*
operative test. Invasive hemodynamic varameters and ANP were measured hefore during and after the test. In agreement with the fact that the patient had few symptoms of cardiac failure before the operation, cardiac output was normal and did not improve significantly after operation However, as shown in Figure 1, the stroke volume did not increase during exercise before pericardiectomy, so the change in cardiac output wasalmost due to the increasein heart rate. As shown in Figure 2, beforepericardiectomy, the mean right atria1 pressure was elevated at rest and increasedfrom 8 to 20 mm Hg at maximal exercise, the mean pulmonary arterial pressure increased from 15 to 34 mm Hg and the mean pulmonary capillary wedgepressure increasedfrom IO to 24 mm Hgdur-
Jens Svanegaard, MD, Per Thayssen, PhD, and Henrik K. Arendrup, MD trial compliance, intraluminal A pressure, transmural pressure and atria1 stretch have been suggested as major stimuli for the production of atria1 natriuretic peptide (ANP). These assumptions are mainly based on observations showing good correlations between pressures and ANP levels in heart failure due to heart diseases of various etiology.’ Increasing pressure in the left and/or right atrium is followed by an increased stretch of the atria1 wall in most heart diseases, except in cardiac tamponade and constrictive pericarditis. In an experiment with dogs, the rise of ANP during rapid volume expansion was decreased in the presence of cardiac tamponade, even if the right atria1 pressure and the left end-diastolic pressure increased during the induced tamponade.2 This indicates that pressure is not the only determinant, as has been presumed previously. To investigate this relation, we studied the relation between ANP and some important hemodynamic parameters in a patient during exercise before and after pericardiectomy. A 37-year-old man was admitted to the hospital becauseof symptoms of pleuritis, the origin of which was never revealed. The patient had no complaints of dyspnea. However, in the preceding 2 to 3 weeks, he had modest lower extremity edema together with a slightly elevated serum alanine aminotransferase, serum lactate dehydrogenaseand serum bilirubin. Oneyear before hospital admission, an ultrasound examination of the liver, because of transitory abdominal pain, had shown unexplained enlargement of the hepatic veins. Chest x-ray, echocardiography and left ventriculography From the Departments of Cardiology, Clinical Physiology, and Cardiac Surgery, Odense University Hospital, Kloevervaenget 26 C 2, Odense, Denmark, DK-5000. Manuscript received November 28, 1989; revised manuscript received and accepted February 20. 1990.
showedmanifest pericardial calcification in the whole circumference of the heart. All segmentsof the heart were contracting normally. Ejection fraction was 66%. Three weeks before and 3 months after pericardiectomy, echocardiography at rest and a graded bicycle exercise test were achieved. The exercise test was performed by increasing workload by 30 watts every 3 minutes during right-sided cardiac catheterization, until the preoperative maximal work load of 150 watts was reached. The patient had no medical therapy at the preoperative test or at the post-
Heart
rate
.’
\
j. ‘. ‘.b
Cardiac
output
L/min 20
5-
0
rest FIGURE exerctse
1. Cardiac and before
150 output,
stroke
votume
(dotfed line) and after THE AMERICAN
watt
and heart rate pertcardiectmy
JOURNAL
15 min at rest, during (c~nfhmus
OF CARDIOLOGY
and after line).
JULY 1, 1990
117
ing exercise. The concentration of ANP, measured in the subclavian vein, increased from 217 pg/ml at rest (normal 82 f 38.4 [mean f I standard deviation], n = 51) to 510 pg/ml at 150 watts. After pericardiectomy, the hemodynamic parameters and ANP normalized at rest. During exercise, the right atria1 pressure was decreasing, while the arterial pulmonary pressure and pulmonary capillary wedge pressure increased slightly. The course of the arterial blood pressure at rest and during exercise was unchanged before and after operation. Echocardiographically, the diameter of the left atrium decreased from 51 to 48 mm. A high correlation between the change in pressures and ANP was observed before the operation. After the operation, both ANP and the hemodynamic parameters were lowered and RIGHT ATRIAL
10-
ANP pg/m, - 600
40-
500
35.
0
ANP
- 600
0
- 500
0 P
v v
- 400
25 0
D
300
u
20.
iI
-6. 110 vat,
300
:;-
-0 WDI
pglml
0
- 400
0
5o:
PRESSURE
ANP
mmHg
30
o
10
ARTERIAL
versus
6 0
Alterations in the ANP level have, to our knowledge, only been reported in 1 case of chronic constric-
ANP
mmng
16.
manner, the production, use and/or degradation of ANP in the lungs, left atrium, left ventricle and aortic vessels were estimated from the dtfference in the concentration of ANP in the radial artery and the pulmonal artery. Evaluated in this manner, there seems to be a shift from a predominant production of ANP in the left atrium before operation to a larger production in the right atrium after operation (Figure 3). In spite of an increased pressure of the right atrium at rest and during exercise before operation, the right atrium had only a very small production of ANP, while the production of ANP from the right atrium increased although the right atria1 pressure decreased after operation both at rest and during exercise.
PULMONARY
PRESSURE
versus 15 -
the correlation between the changes in concentrations of ANP and right atria1 pressure were not good. However, ANP was still correlating very well to alterations in both the pulmonary capillary wedge pressure and especially changes of thepulmonary arterial pressure, as the alterations in ANP and the pulmonary arterial pressure were nearly parallel. To estimate the production of ANP in the right and the left atrium, respectively, blood samples were taken from the subclavian vein, the pulmonary artery and the radial artery to determine ANP concentrations at rest and at I50 watts. By subtracting the ANP concentration in the superior caval vein from the concentration in the pulmonal artery, an indication of the production, use and/or degradation of ANP in the right atrium and the right ventricle could be achieved. In the same
*
