CARDIOVASCULAR JOURNAL OF AFRICA • Vol 24, No 3, April 2013
AFRICA
75
in neonates.
13,15
This could possibly provide an explanation for the
mild to moderate AR observed in our patients.
Left ventricular hypocontractility was observed in a significant
number of our patients. Acute decompensation can be explained
on the basis of normal neonatal cardiac physiology. The neonatal
heart has, by way of its structure, function and unique changes
in loading conditions, limited cardiac reserves and therefore also
less compensatory ability. After birth, volume load on the left
heart increases sharply, from less than 35% of the total output
to 50% of combined ventricular output. Afterload also increases
due to marked increase in the systemic vascular resistance. If
an additional insult such as the acute pressure load of arterial
hypertension is added to an ‘untrained’, adapting left ventricle,
acute left ventricular failure becomes a realistic scenario.
The dilated coronary arteries in two-thirds of our patients
are intriguing. Adult studies have shown coronary arteries
to proportionately increase in diameter in association with
left ventricular hypertrophy.
16,17
Furthermore, coronary arteries
rapidly dilate in response to increased myocardial demand.
18
Taken as a constellation of findings, one can therefore deduce
that the combination of all these echocardiographic findings
would indicate acute cardiac overload of recent onset.
Cardiac failure was treated using milrinone, which in our
clinical judgment gave a beneficial response in all our patients
and improved cardiac function. Milrinone is a treatment of
choice under these circumstances since the phosphodiesterase
inhibitors decrease systemic and pulmonary vascular resistances
and increase cardiac contractility.
19
It should be noted that the reference ranges for plasma renin
activity show marked variation and vary from laboratory to
laboratory. Although transient elevation of PRA or/and plasma
aldosterone levels, with subsequent normalisation after control
of hypertension, was observed in all patients, underlying renal
causes could only be demonstrated in two patients during
admission. Whether this renin–angiotensin–aldosterone system
activation was part of a reactive stress response or a causative
event remains unclear.
18,20,21
Nevertheless, outcome in general
was good, with gradual disappearance of hypertension and the
normalisation of PRA and aldosterone levels in all patients.
Limitations
The study was limited by the small number of patients and
its retrospective nature. In order to reduce observer bias and
variability, all echocardiograms were independently re-examined
by a single cardiologist. As a consequence of the small sample
of patients, the true incidence of hypertension cannot be
determined. Only patients with circulatory failure were included,
therefore patients with milder forms of disease may not have
been detected. Diastolic functional assessments were not carried
out at admission and are therefore not available. Further studies
are required to elucidate the underlying pathophysiology.
Conclusion
Findings of this study are based on a limited number of
patients. However, early neonatal circulatory collapse due to
arterial hypertension is a rare but potentially life-threatening
condition. The echocardiographic presence of mild aortic
regurgitation combined with left ventricular hypocontractility in
an otherwise structurally normal heart should alert the physician
to the possibility of underlying hypertension. Clinicians and
echocardiographers should be aware that at presentation,
hypotension, especially in the presence of a dysfunctional left
ventricle, does not exclude a hypertensive crisis and failure to
consider the diagnosis may lead to death. Long-term cardiac
outcome in survivors appears good.
Grant sponsors: Rotary Tienen Foundation and Eddy Merckx Research
Foundation. RH was supported by a grant of the Research Foundation
Flanders (FWO, Klinische Doctoraatsbeurs), Belgium.
References
1.
Ingelfinger JR. Hypertension in the first year of life. In: Inglefinger
JR (ed).
Pediatric hypertension
. Philadelphia: WB Saunders, 1982:
229–240.
2.
Friedman AL, Hustead VA. Hypertension in babies following discharge
from a neonatal intensive care unit.
Pediatr Nephrol
1987;
1
: 30–34.
3.
Flyn JT. Neonatal hypertension: diagnosis and management.
Pediatr
Nephrol
2000;
14
: 332–341.
4.
Watkinson M. Hypertension in the newborn baby.
Arch Dis Child Fetal
Neonatal Ed
2000;
86
: F78–-81.
5.
Saland JM, Mahony L, Baum M. Perinatal renal ischemia resulting in
hypertensive cardiomyopathy.
Pediatrics
2001;
107
: 185–186.
6.
Wilson DI, Appleton RE, Coulthard MG,
et al
. Fetal and infantile
hypertension caused by unilateral renal arterial disease.
Arch Dis Child
1990;
65
(8): 881–884.
7.
Hegde S, Wright C, Shenoy M,
et al
. Renovascular hypertension
commencing during fetal life.
Arch Dis Child Fetal Neonatal Ed
2007;
92
: F301–304.
8.
Seliem WA, Falk MC, Shadbolt B,
et al
. Antenatal and postnatal risk
factors for neonatal hypertension and infant follow-up.
Pediatr Nephrol
2007;
22
: 2081–2087.
9.
Hawkins KC, Watson AR, Rutter N. Neonatal hypertension and cardiac
failure.
Eur J Pediatr
1995;
154
(2): 148–149.
10. Kim ES, Caiati JM, Tu J,
et al
. Congenital abdominal aortic aneurysm
causing renovascular hypertension, cardiomyopathy, and death in a
19-day-old neonate. J
Pediatr Surg
2001;
36
(9): 1445–1449.
11. Güzeltas A, Ero
ğ
lu AG. Reference values for echocardiographic meas-
urements of healthy newborns.
Cardiol Young
2012;
22
: 152–157.
12. First T, Skovránek J, Marek J. Normal values of 2-dimensional echo-
cardiographic parameters in children.
Cesk Pediatr
1992;
47
: 260–264.
13. Peterson AL, Frommelt PC, Mussatto K. Presentation and echocardio-
graphic markers of neonatal hypertensive cardiomyopathy.
Pediatrics
2006;
118
: e782–785.
14. Gewillig M, Brown SC, De Catte L,
et al.
Premature closure of the
arterial duct: clinical presentations and outcome.
Eur Heart J
2009;
30
: 1530–1536.
15. Okubo M, Ino T, Takahasi K,
et al.
Age dependency of stiffness of the
abdominal aorta and the mechanical properties of the aorta in Kawasaki
disease in children.
Pediatr Cardiol
2001;
22
: 198–203.
16. O’Keefe JH, Owen RM, Bove AA. Influence of left ventricular mass
on coronary artery cross-sectional area.
Am J Cardiol
1987;
59
:
1395–1397.
17. Vassalli G, Kaufmann P, Villari B,
et al
. Reduced epicardial coronary
vasodilator capacity in patients with left ventricular hypertrophy.
Circulation
1995;
91
: 2916–2923.
18. Duncker DJ, Bache RJ. Regulation of coronary blood flow during exer-
cise.
Physiol Rev
2008;
88
: 1009–1086.
19. Hoffman TM, Wernovsky G, Atz AM, et al. Efficacy and safety
of milrinone in preventing low cardiac output syndrome in infants
and children after corrective surgery for congenital heart disease.
Circulation
2003;
107
: 996–1002.
20. Fiselier T, Monnens L, Moerman E,
et al.
Influence of the stress of
venepuncture on basal levels of plasma renin activity in infants and
children.
Int J Pediatr Nephrol
1983;
4
(3): 181–185.
21. Martinerie L, Pussard E, Foix-L’Hélias L,
et al
. Physiological partial
aldosterone resistance in human newborns.
Pediatr Res
2009;
66
(3):
323–328.
