Heart Failure in Newborns and Older Children
Etiology, Different Characteristics and Causes of Heart Failure According to Age of Onset
The classic definitions of Heart Failure (HF) issued by the WHO (an energetic syndrome with inability of the heart to provide adequately for tissue metabolic needs and disposal of metabolites) as well as the Task Force’s (abnormal heart function due to pump failure that does not allow the supply of normal tissue metabolic requirements, or that this can only be accomplished with high filling pressures)  might now be considered incomplete as neither definition includes the causes that tend to perpetuate the HF. With current knowledge it is best to define it as a syndrome characterized by complex alterations due to the interaction of hemodynamic and neurohormonal factors [2,3,4,5]. Six neurohormonal factors have now been detected in cases of congestive heart failure, and three of them (the sympathic nervous system, the renin-aldosterone-angiotensin system, and arginine-vasopressin) induce arteriolar vasoconstriction and sodium retention, whereas the other three (prostaglandins [PG] E1 and E2, the dopaminergic system, and the atrial natriuretic peptide [ANP]) act like counter regulators by limiting the effect of the first three in the initial stages of the disease .
In asymptomatic patients or during the initial stages of ventricular dysfunction, vasodilators and ANP seem to be the main neurohormonal factors maintaining circulatory balance. The cardiac natriuretic peptides (CNP) are a structurally related family playing a key role in sodium homeostasis and body fluid volumes. It includes, besides the ANP, the cerebral natriuretic peptide (CNP) and natriuretic peptide type C (NPC). All rise during ventricular dysfunction causing diuresis and natriuresis, arteriolar vasodilation and inhibition of the renin-angiotensin system, thus benefiting the patient .
In the opposite direction goes the action of norepinephrin, angiotensin II and arginine-vasopressin, all producing vasoconstriction .
In more severe forms of HF and in chronic HF, vasoconstrictors and sodium retainers increase their activities as the disease progresses [2-5].
Bases of Actual Treatment in Heart Failure
During the last 20 years many studies have focused on the untoward effects that sympathomimetic neurohormones produce in HF. Paradoxically, beta-blockers are now used with good results in cases of chronic HF. The rationale for their use is to abolish the vasoconstrictor and Na-retaining effects of such neurohormones .
Other studies have documented the benefit of angiotensin converting enzyme inhibitors (ACEI) such as enalapril, with additive effects to those of spironolactone in order to regulate the deleterious effect from the renin-angiotensin-aldosterone system.[7,8,9,10].
Both angiotensin II as norepinephrine, can induce, in high concentrations, myocardial cell death by apoptosis. Their replacement in the near future might be accomplished by stem cell therapy [5,6,7,8,9].
Other drugs such as carvelidol, a non selective antagonist of alfa 1 and beta receptors with vasodilating effect, are being used more frequently with promising results even in pediatric patients  as are new drugs such as Levosimendan, a calcium sensitizer with positive inotropic and peripheral vasodilating actions now being used in acute HF and in cardiogenic shock in adults, children and neonates, with good results when used for a short period [11,12].
Likewise, other studies have evaluated the effects of nesiritide, a synthetic CNP; and an inhibitor of vasopeptidase, an enzyme that degrades the natriuretic peptides .
Nowadays, several studies address the issue of inflammatory causes, other than the cardiomyopathies and myocarditis, that might cause, induce, aggravate or prolong HF. This line of work might produce new treatment options.
Yet another set of therapeutic trials deal with the likelihood of modifying ventricular geometry or altering heart rate through ablation, surgery or pace-makers, in order to improve failing ventricular function.
This newer insight on the pathophysiology of HF led to a better understanding of mechanisms that either cause, induce, trigger, worsen or prolong HF, but also to newer and better drugs, some of which were formerly contraindicated or not used at all in this setting [1-31].
These new drugs however, have not totally replaced digoxin or other already known inotropic agents such as dopamine and dobutamine (beta agonists). Modern agents that are both inotropic and systemic and pulmonary vasodilators like amrinone and milrinone are still very much used in acute HF or in the immediate post-op period after heart surgery. The classic diuretics and vasodilators remain useful, moreso when associated to the newer drugs, with promising results [1,7,8,15,19-22,32,34].
These new treatments, widely proven in adults, are being used successfully in pediatric patients [35-38].
The HF syndrome can be classified into five types :
- Acute (if compensating mechanisms have no time to act) or chronic (compensation occurs with or without previous acute events).
- High cardiac output HF (tachycardia, systemic hypertension, warm skin, wide pulses such as it occurs in anemia, hyperthyroidism, etc) or low cardiac output (tachycardia, cold extremities, weak pulses, pallor and oliguria as it usually happens in myocarditis, cardiomyopathies, coronary anomalies, post-op, etc).
- Right-sided HF (systemic venous congestion, and enlarged liver) or left-sided HF dyspnea and fatigue) although it is always global in fetus and neonates.
- Forward or backward (retrograde) HF, related to the previous and following types.
- Systolic (Poor ventricular ejection with decreased contractility, non-thickened ventricular walls, and increased telediastolic left ventricular pressure. Common pediatric causes include Kawasaki disease, cardiomyopathies, aortic stenosis, and aortic coarctation with critical myocardial failure. Diastolic (altered ventricular filling with clear-cut ventricular hypertrophy in spite of good telediastolic pressure, contractility and ejection fraction. It relates to mitral stenosis, pericardial effusions, increase in pressure after the Glenn procedure.
So, the HF syndrome acknowledges multiple etiologies (especially so in pediatric patients) with high morbidity and mortality in spite of adequate treatment. In adults, survival after initial diagnosis is 3-5 years. In newborns with HF, without structural heart disease, one out of three, and one in two cases of HF in the presence of congenital heart lesions, will die before age one month if treatment is not adequate [2, 40-45].
HF in neonates: Differences with older children and adults
The cardiovascular system will behave different, both in health and in disease, according to the age of the patient. The fetal-neonatal heart shows marked disadvantages compared to adults; these must be known in order to understand its behavior, both normal and abnormal [2, 26, 40-44].
This higher liability of the newborn heart results from several factors which diminish its performance, such as [2, 40-46]:
1. The neonatal cardiac output
During fetal life the combined biventricular output is nearly 450 ml/Kg/min of which 300 ml (66%) belongs to the right ventricle, although both ventricular chambers handle equal pressures as they both eject towards the Aorta (the right ventricle into the descending portion via the ductus arteriosus, whereas the left ventricle flows into the transverse and ascending aorta). Thus fetal life maintains two ventricles working “in parallel” or “in association”. This fact provides some relief to the ventricles, unlike the “series” arrangement, typical of extra uterine life [2, 40-46]. See Figure 1.
Figure 1. Combined ventricular output in the fetal heart: the right ventricle (VD) handles 66% of the total blood flow and ejects it towards the of the pulmonary artery truncus (TAP); only 7% goes into the right and left Pulmonary Artery branches (RdAP; RiAP), because the lungs cannot handle more volume during fetal life. The remaining 59% goes to the descending Aorta through the ductus arteriosus (DA). The 34% of left ventricular flow is distributed as follows: 3% to the coronary arteries (AC) and 21% to the neck vessels (TBC, CI, SI). The remaining 10% that reaches the aortic isthmus (Istmo Ao) meets the flow from the ductus arteriosus in the descending aorta (Ao desc). The actual size of the chambers and blood vessels are the reflection of the flow volumes they really handle. Thus TAP (66%), the DA (59%), and the Ao desc (69%) will show similar sizes because they handle similar flows. The VD has higher development than the VI (see text)
After birth the left ventricle will increase its flow from 150 to 450 ml/Kg/min because the “parallel” display must be changed to the “series” type. Thus, each ventricle must handle its own volume. This physiological rearrangement stresses the LV to its limit, making it very hard for it to compensate when facing structural anomalies resulting in additional pressure-volume loads. In fact, anatomically normal neonatal hearts have a hard time adjusting to simple factors such as cold stress, hypoglycemia, hypocalcemia, infections, and water overloads, due to lack of adequate compensatory mechanisms which develop as the infant grows. This limited reserve of the newborn heart over the older child’s or even the fetus, determines the difficulties faced by the newborn right after birth [2, 41-46].
After the first postnatal week, the cardiac output decreases from 450 to 300 ml/Kg/min by the 3rd postnatal week (33% less than at birth) reaching 150 ml/Kg/min by age six weeks and 70-80 ml/Kg/min after the 6th postnatal month (adult cardiac output is 70 ml/Kg/min) [2, 40-46]. See Figure 2.
Figure 2. The changes in cardiac output right after birth. Immediately after delivery, the cardiac output of the newborn is 450 ml/Kg/min as in utero. By the 3rd week it is 300 ml/Kg/min and 150 ml/Kg/min at 6 weeks. At age six months, it reaches the adult value of 70 ml/Kg/min (see text).
This so called physiologic hemodilution of the normal newborn, may, in part, explain the decreased effect of inotropic drugs administered to neonates as opposed to older children or adults . See Figure 2.
This progressive decrease of the neonatal cardiac output, mainly achieved through large urine outputs, partially explains the greater lability of the neonatal heart right after birth. As such, the only compensatory mechanism of the newborn heart in the early days of life remains the heart rate, although limited, as it is already normally elevated [2, 40-46].
2. The number of contractile units
The newborn heart has lees contractile units per mm2 than older children and adults. Thus, contraction is less efficient [2, 40, 41,46]. Inside the neonatal myocite, the contractile elements are limited to about 30% (70% in adults). One advantage, however, of the neonatal heart is its ability to produce hyperplasia through circulating growth factors .
3. Preload, afterload, and Frank-Starling’s law
Preload is the end-diastolic maximum length of the ventricular muscle fiber, and it depends on: a) the ventricular compliance (the ventricle distending ability), and b) the venous return.
Ventricular compliance is rarely affected in neonates with the exceptions of fibroelastosis, restrictive cardiomyopathies or severe myocardial ischemia.
The venous return, on the other hand, is normally high in newborns due to the high cardiac output. Thus, the Frank-Starling’ law is fully acknowledged, stretching the fiber to its maximal limit, leaving little or no margin for tolerating additional overloads due to either excess volume or congenital heart disease. This law also known as recoil law implies that the more the fiber is stretched the contraction will be stronger, up to a point after which overstretching ensues, and the elastic recoil breaks down.
The Afterload can be defined as the maximum tension reached by the ventricular wall at the beginning of the systolic interval. It is directly related to ventricular radius and intraventricular pressure, but inversely related to wall thickness, according to the following equation:
Pressure x r2
2 wall thickness
Intraventricular pressure is not nearly important in newborns as the other two variables which condition the poor performance of the neonatal left ventricle. The larger radius is due to the higher neonatal preload. The wall thickness lacks the necessary time to compensate, as it would in older children. This fact explains the fast, frequent, and severe compromise that can be expected in cases, for instance, of aortic coarctation, or moderate aortic stenosis, unlike the light clinical picture that both disease will have in older patients [2, 40-42, 46].
4. Sympathic innervations and catecholamines
Both α 1 and β 2 receptors modify actively heart rate, contractility and peripheral vascular tone whereas α 2 inhibit these processes. Sympathic nerve endings are poorly developed in newborns. Nature replaces this disadvantage by providing the neonate with a serum concentration of catecholamines nearly 30 times higher that the one found in adults. However, as they are rapidly released after birth, their stores are soon depleted, so if needed they will not be available [2, 45, 47-49].
It is clear that newborns and young infants with HF and low output have higher sympathic tone and high concentration of circulating catecholamines, as well as a smaller number and density of beta receptors than infants without HF. Besides, their physiologic hemodilution may limit the action of exogenously administered catecholamines [45,46,47,48,49].
In summary, compensatory mechanisms are late and limited in newborns, although age will correct this problem. Both adrenergic and dopaminergic receptors will require time in order to improve their functioning [2,40,49].
5. Myocardial metabolism, calcium and fetal hemoglobin
The neonatal heart muscle can only use glucose-6-phosphate as its only fuel. As newborn glycogen stores are very limited, hypoglycemia can result in HF. In due course, new pathways (mainly fatty acids) will develop as alternative fuel sources, thus minimizing the effect of low blood sugar. Calcium disorders, however, frequently coexist with hypoglycemia. Hypocalcemia results from poor calcium sources plus inadequate calcium-phosphorus exchanges. Because of the poor sarcoplasmic reticulum set-up in newborns, calcium uptake is limited. Fetal Hb remains the major Hb in newborns. Its low levels of 2,3 diphosphoglycerate shifts the oxyhemoglobin dissociation curve to the left; thus it is easily saturated at relatively low oxygen tensions, but it will not easily release the oxygen load at the tissue level, requiring more blood flow. The neonatal heart cannot adequately meet this demand. At a later age, fetal Hb will disappear, so this problem will no longer bear any significance [2, 41].
6. Hypoxemia and acidosis
These are frequent findings in sick newborns and they can significantly deteriorate myocardial contractility [2,45].
After having reviewed the main factors predisposing to HF in neonates we can now address their triggering mechanisms [2,40,41].
- Volume overload: left-to-right shunts with large pulmonary overflow (mainly in premature babies), arterio-venous fistula, and valvular insufficiencies.
- Pressure overload: left outflow obstructions (aortic stenosis, coarctation) and right outflow obstruction (critical pulmonic stenosis).
- Altered muscle metabolism compromising production, storage or use of energy leading to myocardial dysfunction. (Hypoxemia, acidosis, hypoglycemia, hypocalcemia, electrolyte imbalance and some inflammatory processes leading, at times, to destruction of contractile units and cellular necrosis).
- Abnormal venous return or ventricular filling as in some arrhythmias and in endocardial fibroelastosis.
Etiology of neonatal HF
In the immediate newborn period, and in some younger infants, the etiology of HF is linked to: Non cardiac causes and Cardiac causes.
Non cardiac causes include metabolic alterations such as hypoglycemia, hypocalcemia, hypoxemia, acidosis, or others like as lung diseases, sepsis, anemia, policythemia, or the mere exposure to cold stress. The common pathway that leads to HF in these situations is tissue hypoxia [2,39,40,41,45].
These causes of HF are always amenable to treatment of the primary cause; conversely, they very rarely will respond o digitalis or inotropic agents. Obviously, the lab will provide the needed diagnosis. In cases of hypocalcemia, however, an ECG (at the monitor if the baby has one) will allow identification of a prolonged ST segment. This relates well with ionic hypocalcemia.
It must be borne in mind, that many newborns with mild heart defects causing little hemodynamic compromise, will rapidly deteriorate when facing a metabolic (non cardiac) disturbance. If not properly diagnosed, a confusing clinical picture will develop in which a newborn is thought of having a worsening cardiac problem, when indeed the clinical deterioration is related to metabolic imbalances or sepsis. For instance, a newborn baby with cyanotic heart disease with low pulmonary blood flow becomes severely cyanotic after acute lung illness. Treatment must be directed to the lung problem rather than trying to improve the heart function with medical or surgical procedures, such as Blalock-Taussig shunts performed while the baby is in bad condition [2,41].
The cardiac causes are summarized in three different groups:
- Structural heart disease
Structural heart disease is any defect affecting the heart’s anatomy at early developmental stages (usually before 60 days gestation), such as wide Ventricular Septal Defect (VSD), coarctation syndrome, transposition of the great arteries, type 1 Truncus among many others leading to neonatal HF.
During the newborn period, in term neonates, the highest incidence of HF due to structural defects is originated in left outflow obstruction: aortic coarctation, interrupted aortic arch, critical aortic stenosis, and the syndrome of hypoplastic left heart. Other disorders, listed by frequency, are: transposition of the great arteries, total common A-V canal, critical pulmonary stenosis with intact septum, and type 1 Truncus. Neither VSD nor ductal left-to-right shunts are frequent causes of HF in this period, although they do become important in premies and in older infants. This is due to the fact that prematures have pulmonary arterioles with wide lumen and thin walls, quite opposite to the findings in full-term babies. Thus, preterm babies are at permanent risk of pulmonary plethora, in cases of VSD and PDA, whereas that will not be the case in term infants.
By age 2-6 postnatal months, pulmonary arterioles reduce their wall thickness and become vulnerable to pulmonary overload and pulmonary hypertension .
Neonatal arrhythmias include SV tachycardia and congenital A-V block. In fetal life, however, atrial flutter and atrial fibrillation can occur, leading to severe HF with hidrops fetalis [2, 50].
The endocardiomyopathies can be either dilated (usually of viral origin), or hypertrophic (infant of diabetic mothers and patients with Noonan syndrome). The rest are the so called “unclassified” such as subendocardic fibroelastosis (frequently found in structural diseases with left flow obstruction) .
The incidence of pediatric HF according to age is as follows: 20-30% occurs in the first postnatal week; 40-45% during the first month of life, and 70-80% in the first four months. See Figure 3.
Incidence is higher if one adds intrauterine HF and the hidrops fetalis leading to fetal death (over 60% of them are of cardiac origin) [50-55].
Older children rarely develop HF unless they already have it since earlier ages. Primary causes of HF in older children are limited to rheumatic fever, cardiomyopathies, and poorly tolerated post-op periods.
Clinical findings in neonatal heart failure
Neonates in HF, whether of cardiac or non cardiac etiology present with a characteristic clinical triad, including: respiratory distress syndrome (RDS), cardiomegaly, and hepatomegaly, all of which can associate with hyperactive precordium and tachycardia [2,3,13,26, 40-45].
Respiratory distress syndrome
It is always found. It is due to pulmonary overflow, or pulmonary hypertension, or both. There is fluid leakage into the extravascular tissues with interstitial edema and increased respiratory effort [2,41,42,44,45].
Two distinct breathing patterns relate to heart disease: tachypnea, with retractions and deep breaths, and tachypnea with shallow breaths. The first is almost always seen in HF; the second form is found in newborns with low pulmonary blood flow without HF. RDS is always present but clearly it is more visible during crying or feeding. After taking barely 20 cc the infant refuses feeding, becomes fussy and cries. Thus, feeding the baby becomes cumbersome and trying. These issues will ultimate hinder weight gain.
Pulmonary congestion facilitates bacterial overgrowth and lung infections. Wheezing is often heard, and the diagnosis between bronchial spasm and heart disease is not straight- forward. Many heart diseases with HF plus pulmonary hypertension can lead to severe lung disease of its own, further complicating management. In these instances, adequate diagnosis and treatment of the lung condition is imperative, as it allows improvement of the heart dysfunction. When air entry occurs bilaterally, and no wheezes or rales are heard on auscultation, primary lung disease can be ruled out most of the times [2,42,44,45].
Hypoxemia of pulmonary origin is often the most important cause of therapeutic failure in the treatment of neonatal HF. In turn, it must be remembered that many primary lung diseases may induce HF of non cardiac origin. In addition, many babies with HF develop several episodes of urinary tract infections manifested solely by a febrile illness. If the suspicion is high and the diagnosis is prompt, adequate treatment will alleviate HF. Similarly iron deficiency, very frequent in many infants, must be looked for and treated promptly.
There is a global enlargement of the neonatal heart during HF. The perceptions of a leftward displacement of the apex, or a hyperactive precordium, are good clinical evidences of this global cardiomegaly. A plain chest x-ray is undoubtedly the best way to ascertain the enlarged heart, usually confirmed if the cardio-thoracic index is over 60% [2,41,42,44,45]. See Figure 4.
Figure 4. Chest x-rays showing the different degrees of cardiomegaly and pulmonary congestion in neonates with heart failure syndrome. From left to right: films of patients with aortic coarctation, with associated pneumonia (white arrow); next to it, the film of a newborn with a double outflow tract of the right ventricle and severe pulmonary hypertension. The third film is typical of the “lying egg” cardiomegaly of type I truncus arteriosus. The last film shows a hypoplastic left heart syndrome, in severe heart failure, with a stent placed at the level of the ductus arteriosus (black arrow) as palliative therapy
Clearly, if the chest film does not show 7 intercostal spaces, its use will be limited, as poor inspiration tends to diminish heart size, whereas excessive espiration may mimic a non existent cardiomegaly. These technical aspects must be looked for. cardiac ultrasound will reveal functioning of the heart, and assess contractility; in many cases it will provide the etiologic diagnosis. See Figure 5.
Figure 5. M-mode ultrasound done on a 22-day old baby with dilated cardiomyopathy of unknown origin. Note the severe dilatation of the diastolic (dd) and systolic diameters (sd) of the left ventricle (VI) with poor contractility. Ejection fraction is barely 18%. There is limited opening of the mitral valve (VM) and the mitral-septal (MS-SIV) distance is very wide. The right atrium is dilated and the Aorta/left atrium ratio = 1.8; the right ventricular outflow tract (TSVD) appears severely dilated due to the associated severe pulmonary hypertension. M-mode ultrasound many times yields important information about myocardial contractility; however, it informs little about etiology
Very few cases of HF do not show cardiomegaly. This is the case of the rapidly fatal cardiomyopathies, supra-ventricular tachycardia in its early stages, and total anomalous pulmonary venous return, in infra diaphragmatic type [2,41,42,44,45]. See Figure 6.
Figure 6. a) Microphotgraph of heart muscle taken at autopsy from a neonate with a fatal enteric.encephalo-myocarditis. The rapid clinical course did not allow cardiomegaly to develop. Note the paucity of muscle cells and the large amount of eosinophils (HE 250x).
b) ECG showing a paroxystic supraventricular tachycardia with a rate of about 280bpm. In the first few hours of the disease, there will be no cardiomegaly in spite of the presence of heart failure.
c, d) The post mortem anatomy of infra diaphragmatic total anomalous pulmonary venous return, which, more often than not, courses with heart failure without cardiomegaly: c) injected contrast material in the collecting conduct (arrow) showing the filling of the 4 pulmonary veins and their anomalous drain at the portal vein. When the ductus venosus closes, the blood present inside the liver remains trapped within the organ; thus no heart dilatation takes place. The liver will show massive enlargement, d) same patient: the heart is not dilated but there is a very large liver. PD: right lung; PI: left lung
This sign is present in almost all cases of neonatal HF. Palpation of the liver along a line joining the umbilical cord with the right shoulder aids in the clinical appraisal of enlarged livers. The normal neonatal liver appears large on palpation and it is found about 2 cm below the right costal edge. Since it lacks the Glisson capsule, the neonatal liver can rapidly enlarge to accommodate large volumes of blood flow. Thus, it becomes an indirect method to evaluate venous pressures, and in limited settings, of the pulmonary pressures as well [2,41,42].
I the enlargement is rather recent, palpation will not generate discomfort and the liver will feel soft; the opposite is true in chronic liver enlargement. Overly aireated lungs, and the common diastasis of the abdominal muscles in Down syndrome, are conditions that imitate hepatomegly because of the downward displacement of the liver. Infants of diabetic mothers who are macrosomic, tend to have large livers as part of their increased visceromegaly [2,41,42].
Other signs of neonatal HF
Tachycardia, systemic hypertension and a hyperactive precordium are clinical signs frequently found in neonates with HF. Tachycardia can be absent in cases of complete A-V blocks, end-stage HF, and in digitalis toxicity. Systemic hypertension is due to the compensatory catecholamine release, leading to peripheral vasoconstriction (“peripheral heart”). It may not be seen in the severe or end-stage forms of HF and in patients treated wit potent vasodilators or beta-blockers [2,41,42,44,45]. The hyperactive precordium (positive Dressler sign) is found in babies with pulmonary hypertension.
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CV of the authors
Felipe J. Somoza
- Autor del libro: Cardiopatías congénitas. Cardiología perinatal. F Somoza (Ed) Editorial Don Bosco ISAG Buenos Aires 2007. ISBN: (13) 978-987-05-0687-4
- Doctor en Medicina y Cirugía. Universidad Nacional de Córdoba
- Especialista en Cardiología Pediátrica
- Especialista en Neonatología
- Especialista en Hemodinamia, Angiografía y Angioplastia
- Presidente del comité de cardiología pediátrica de la Federación Argentina de Cardiología (FAC) 2006-2008
- Ex Presidente de la Sociedad de Cardiología de Córdoba
- Miembro Titular Fundador de la Sociedad Argentina de Cardiología y Cirugía Cardiovascular Infantil
- Miembro Pleno Fundador Sociedad Latinoamericana de Cardiología Intervencionista
- Coordinador de Cardiología Perinatal del Ministerio de Salud de Córdoba Argentina
- Jefe de Cardiología Neonatal de los Hospitales Materno Neonatal y Materno Provincial de Córdoba, Argentina
- Médica de Staff
- Encargada de diagnóstico prenatal
- Hospitales Materno Neonatal y Materno Provincial Córdoba, Argentina
- Profesor Adscripto de Pediatría y Neonatología, Universidad Nacional de Córdoba
- Coordinador Perinatal, Unidad Perinatal Esperanza
- Master en Salud Pública, y Salud Pública Materno Infantil
- Profesor de Bioestadística y Epidemiología, Maestría en Salud Materno Infantil, Universidad Nacional de Córdoba
Publication: November 2007
FORM DEACTIVATED SINCE
November 30th., 2007
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