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Neonatal acute myocardial infarction (MI) is a rare event, with a high mortality rate. Early recognition and intensive care management can be successful, and it requires a high index of suspicion in cases of unknown cardiogenic shock. The lack of access to cardiac catheterization should not delay management. Furthermore, there is great potential for myocardial regeneration to occur in surviving neonates with MI, emphasizing the importance of early recognition and management. The present report describes a neonate with an anatomically normal heart and coronary arteries who developed clinical, laboratory and electrocardiographic features of MI, and was managed successfully with fluid resuscitation, inotropic drugs and vasodilators.
L’infarctus aigu du myocarde (IM) pendant la période néonatale est un événement rare qui s’associe à un taux de mortalité élevé. Le dépistage précoce et la prise en charge aux soins intensifs peuvent être couronnés de succès, ce qui exige toutefois un fort indice de suspicion dans les cas de choc cardiogène inconnu. Le manque d’accès au cathétérisme cardiaque ne doit pas retarder la prise en charge. De plus, le potentiel de régénération myocardique est élevé chez les nouveau-nés qui survivent à un IM, ce qui fait ressortir l’importance d’un dépistage et d’une prise en charge rapides. Le présent rapport décrit un nouveau-né qui avait un cœur et des artères coronaires à l’anatomie normale, qui a manifesté des caractéristiques cliniques, de laboratoire et électrocardiographiques d’IM et qui a été pris en charge avec succès au moyen de remplacement liquidien, de médicaments inotropes et de vasodilatateurs.
Cases of myocardial infarction (MI) in neonates with or without congenital heart disease are sporadic. Mortality has been estimated at 90% (1), with causes being attributed to enteroviral myocarditis (2), perinatal asphyxia (3), coagulopathy (4) and erythroblastosis (5). Coronary artery thromboembolism is the most commonly described etiology (5). The present report describes a neonate with an anatomically normal heart and coronary arteries who experienced an acute MI on day 1 of life, and was successfully treated with fluid resuscitation, vasodilators and inotropic drugs.
A female infant was born at 34 weeks gestational age (birth weight 2140 g) via spontaneous vaginal delivery following an uncomplicated pregnancy. Amniotic membranes had been ruptured for 21 h and the mother had an elevated peripheral white blood cell count of 29×109/L. She received one dose of penicillin G 1 h before delivery.
The infant was born with a foul odour. Apgar scores were 7 at 1 min and 9 at 5 min. She required several seconds of positive pressure ventilation. She was transferred to the paediatric ward and an umbilical venous catheter (UVC) was inserted. A chest x-ray to assess UVC positioning demonstrated the line tip in the left atrium but was otherwise unremarkable. Within 5 min of the UVC being withdrawn, she developed signs of circulatory collapse with an oxygen saturation of 85% followed by a 30 s apneic period. She required intubation and received fluid boluses (NaCl 0.9%) for poor perfusion and hypotension (30/17 mmHg). The infant was transferred to the paediatric critical care unit.
On arrival, she was afebrile, mottled and dusky, with poor perfusion. She had a heart rate of 194 beats/min and a respiratory rate of 50 breaths/min. Oxygen saturation was 100% on room air. She had normal precordial and respiratory examinations, and her liver was palpated at 2 cm to 3 cm below the right costal margin. Serum cardiac enzymes at 20 h of life were significantly elevated. Total creatine kinase activity was 2413 U/L, troponin I was 16.60 μg/L and serum lactate was 8.4 mmol/L. Coagulation studies at 8 h of life showed a slightly elevated international normalized ratio of 1.8, and partial thromboplastin time of 71 s. The infant’s fibrinogen level was within normal limits at 7.791 μmol/L. All values were normalized by day 3 of life. Complete blood count and full septic workup were unremarkable. A central blood culture was obtained and antibiotics were started empirically. A cranial ultrasound on day 3 of life was unremarkable.
An initial electrocardiogram (ECG) (Figure 1) revealed sinus tachycardia, a northwest axis, ST depression in leads III, V4, V5 and V6, wide QS in leads I and aVL, and QT pro-longation, suggestive of lateral infarction. Echocardiography showed a structurally normal heart and coronary arteries, a moderate sized secundum atrial septal defect (ASD), mild mitral and tricuspid valve regurgitation with an estimated right ventricular pressure greater than two-thirds of the systemic arterial pressure, small patent ductus arteriosus with bidirectional flow, and moderately decreased biventricular function with a fractional shortening (FS) of 0.15. No intra-cardiac or extracardiac thrombus was identified. Dopamine at 7.5 μg/kg/min was started and milrinone was added. She received sodium bicarbonate and nitroprusside for several hours followed by nitric oxide until day 3 of life. The infant remained intubated and ventilated for five days, and by day 3, her dopamine infusion and nitroprusside were discontinued. Daily echocardiograms demonstrated steady improvements in biventricular function, evidenced by increases in FS. Her FS was 0.26 on day 5 when milrinone was discontinued and captopril was started. She was discharged home at four weeks of age on captopril. A repeat ECG at two weeks of age demonstrated pure notched Q waves in leads I and aVL with no ST changes.
At two months of age the patient was doing very well. Her ECG (Figure 2) had corrected and her echocardiogram was remarkable for a small ASD and low normal left ventricular systolic function (FS 0.27). At 20 months of age, her ECG and echocardiogram were normal, with an FS of 0.43 and no wall motion abnormalities. The ASD has spontaneously closed.
There are only a few reported cases of MI in neonates and infants with complete recovery. In contrast to other reports (6–9), our patient improved and survived without the use of thrombolysis. Our case fulfilled sufficient electrocardiographic criteria for acute MI in childhood, as previously described by Towbin et al (6). These include new, wide Q waves (greater than 35 ms) in serial tracings with prolonged corrected QT intervals. Although no certainty exists, there are several risk factors for paradoxical thromboembolism or even air embolism from the UVC.
Neonatal MI has been reported to occur sporadically but with a high mortality rate. The most common congenital anomalies associated with MI are aortic stenosis or atresia, hypoplastic left heart syndrome, pulmonary atresia, total anomalous pulmonary venous return, stenosis of the coronary ostium and anomalous left coronary artery (10).
In neonates with structurally normal hearts, the most common association is with thromboembolism (1,5). Paradoxical embolizations of thrombi from the ductus venosus (11), renal vein (12) and umbilical vein (13) have all been postulated to account for cases of MI. Associations between MI and UVC insertion have also been reported (14,15). A link has been described between MI and disseminated intravascular coagulation (16), and between MI and antithrombin III deficiency (4). Normal coagulation parameters, including thrombocyte count, mitigated against a hypercoagulable state in our patient. Given the sequence of events, it is possible that the umbilical vein was the source of a thromboembolism or air embolus, although cardiac catheterization was not performed to support this assumption.
Although the mortality rate is quite high, survival has been reported following neonatal MI. Bernstein et al (12) reviewed 27 cases of neonatal MI with only two survivors. Boulton et al (1) reviewed 14 cases, two of whom survived, and added two cases of their own, both of whom survived. A thrombus was identified in one of their two survivors. Both infants were managed with inotropes and digoxin. Subsequent to these cases, there have been scant reports of neonates surviving MI. Hruda et al (15) described a neonate who developed MI at 12 days of age complicated by severe mitral valve regurgitation. Hornung et al (2) reported a case of neonatal MI secondary to enteroviral myocarditis on day 6 of life, managed with diuretics, digoxin and angiotensin-converting enzyme inhibitors. Murugan et al (17) discussed a case of a nine-day-old infant with positive enteroviral serology managed with digoxin, dobutamine, captopril and heparin. Peeters et al (4) described a symptomatic neonate at birth found to have a hereditary antithrombin III deficiency. Cardiac function was supported with inotropes, digoxin, captopril and diuretics. Among the reports, inotropes, vasodilators, diuretics and afterload reducing agents are the mainstays of therapy.
In our patient, dopamine was used to improve blood pressure and cardiac output. At the dosing range administered, we expected to achieve improved cardiac contractility and heart rate. Milrinone has a positive effect on myocardial contractility that is complemented by its peripheral vasodilatory properties, thereby increasing cardiac output without an increase in myocardial oxygen demand. Given that the neonate presented with a picture consistent with cardiogenic shock, our objective was to improve cardiac contractility and therefore end organ perfusion. Nitroprusside was used because we believed that there was a component of pulmonary hypertension.
Thrombolysis has been used with varying results in neonatal MI. Tissue plasminogen activator has been tried both unsuccessfully (8) and successfully. Horigome et al (18) described a three-month-old infant with MI following Kawasaki disease. Echocardiography on admission revealed a giant left coronary aneurysm with a massive thrombus in the lumen that resolved by 48 h after tissue plasminogen activator administration. Burtt et al (9) reported a case of streptokinase administration following MI in a seven-month-old male infant, secondary to Kawasaki disease, in which complete echocardiographic resolution of wall motion abnormalities and significant reperfusion of the anterior wall on thallium-201 scintography were demonstrated. Nevertheless, due to potential risk of major intracranial hemorrhage (19) and relatively less progress toward evidence-based risk factor guidelines (20), thrombolysis in neonates still remains a controversial topic.
Extracorporeal membrane oxygenation has been used in a few published cases of survival after neonatal MI (3,7). Our patient recovered cardiac function without the use of extracorporeal membrane oxygenation or thrombolysis. One month after the event, the initial electrocardiographic changes had disappeared, suggesting regeneration of the previously damaged neonatal myocardium.
We have presented a case that is similar to previously published reports of neonatal MI with respect to onset, proposed etiology, management and outcome. The present case attests to the importance of suspecting MI in neonates with acute cardiovascular collapse. Early recognition and cardiac support with inotropes and afterload reduction agents may be instrumental in managing these cases. With our case, we did not reject the use of thrombolytic agents. However, we share the same concerns as other physicians based on limited experience and lack of recommendations for using these agents in neonates with MI and children in general (21). Because of the rarity of this condition, a multicentre study is required to verify the safety and effectiveness of thrombolysis in neonates with MI.