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Review
. 2022 May;15(5):e011664.
doi: 10.1161/CIRCINTERVENTIONS.121.011664. Epub 2022 Apr 29.

Neonatal Myocardial Infarction: A Proposed Algorithm for Coronary Arterial Thrombus Management

Affiliations
Review

Neonatal Myocardial Infarction: A Proposed Algorithm for Coronary Arterial Thrombus Management

Hannah El-Sabrout et al. Circ Cardiovasc Interv. 2022 May.

Abstract

Background: Neonatal myocardial infarction is rare and is associated with a high mortality of 40% to 50%. We report our experience with neonatal myocardial infarction, including presentation, management, outcomes, and our current patient management algorithm.

Methods: We reviewed all infants admitted with a diagnosis of coronary artery thrombosis, coronary ischemia, or myocardial infarction between January 2015 and May 2021.

Results: We identified 21 patients (median age, 1 [interquartile range (IQR), 0.25-9.00] day; weight, 3.2 [IQR, 2.9-3.7] kg). Presentation included respiratory distress (16), shock (3), and murmur (2). Regional wall motion abnormalities by echocardiogram were a key criterion for diagnosis and were present in all 21 with varying degrees of depressed left ventricular function (severe [8], moderate [6], mild [2], and low normal [5]). Ejection fraction ranged from 20% to 54% (median, 43% [IQR, 34%-51%]). Mitral regurgitation was present in 19 (90%), left atrial dilation in 15 (71%), and pulmonary hypertension in 18 (86%). ECG was abnormal in 19 (90%). Median troponin I was 0.18 (IQR, 0.12-0.56) ng/mL. Median BNP (B-type natriuretic peptide) was 2100 (IQR, 924-2325) pg/mL. Seventeen had documented coronary thrombosis by cardiac catheterization. Seventeen (81%) were treated with intracoronary tPA (tissue-type plasminogen activator) followed by systemic heparin, AT (antithrombin), and intravenous nitroglycerin, and 4 (19%) were treated with systemic heparin, AT, and intravenous nitroglycerin alone. Nineteen of 21 recovered. One died (also had infradiaphragmatic total anomalous pulmonary venous return). One patient required a ventricular assist device and later underwent heart transplant; this patient was diagnosed late at 5 weeks of age and did not respond to tPA. Nineteen of 21 (90%) regained normal left ventricular function (ejection fraction, 60%-74%; mean, 65% [IQR, 61%-67%]) at latest follow-up (median, 6.8 [IQR, 3.58-14.72] months). Two of 21 (10%) had residual trivial mitral regurgitation. After analysis of these results, we present our current algorithm, which developed and matured over time, to manage neonatal myocardial infarction.

Conclusions: We experienced a lower mortality rate for infants with neonatal infarction than that reported in the literature. We propose a post hoc algorithm that may lead to improvement in patient outcomes following coronary artery thrombus.

Keywords: dilatation; infant; stroke volume; troponin I; umbilical cord.

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Figures

Figure 1.
Figure 1.. Neonatal myocardial infarction management algorithm.
Cath Lab indicates catheterization laboratory; Echo, echocardiography; IV, intravenous; LA, left atrium; LMWH, low-molecular-weight heparin; LV, left ventricle; max, maximum; MR, magnetic resonance; MRI, magnetic resonance imaging; PTT, partial thromboplastin time; and tPA, tissue-type plasminogen activator.
Figure 2.
Figure 2.. ECG with Q waves in inferior leads and an inferior-lateral infarct pattern.
Right axis deviation, right bundle branch block, and poor R-wave progression are also noted.
Figure 3.
Figure 3.. Magnetic resonance images.
A and B demonstrate myocardial thinning and delayed myocardial enhancement. C depicts subendocardial enhancement. Yellow arrows point to areas of myocardial thinning and delayed enhancement.
Figure 4.
Figure 4.. Anatomic specimen and original angiogram in comparison.
Images demonstrate the explanted heart (A) oriented in a way that matches the angiographic images (B) in left anterior oblique/cranial view and (C) in straight lateral. A, Explanted heart with left ventricular assist device in place at the apex. The infarcted area matches the area of coronary perfusion paucity in the distribution of the obtuse marginal, ramus, and distal circumflex (yellow circles.) Note the nonocclusive thrombus in the left main coronary artery (top arrows).
Figure 5.
Figure 5.. Histopathologic correlation to gross specimen.
A, Large transmural infarction (white), posterior-lateral wall of left ventricle. B, Infarcted area with complete loss of cardiac muscle. C, Trichrome stain highlights the fibrous tissue (blue) and few residual cardiac muscles (red). D, Noninfarcted area. E, Hypertrophic cardiac muscle with interspersed fibrous tissue. F, Trichrome stain highlights the interspersed fibrous tissue, adjacent to the infarcted area. Middle, Explanted heart.

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