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. 2023 Jun 20;9(6):e17373. doi: 10.1016/j.heliyon.2023.e17373

A rare case of diagnosed absent aortic valve and severely hypoplastic pulmonary valve with double outlet right ventricle: A case report

VV Suvorov a,∗, EP Fedotova b, VV Zaitsev a, EV Dolgova c, LL Popova c, AE Glazunova d, MU Novak c, RA Nasyrov b
PMCID: PMC10333606  PMID: 37441373

Abstract

Agenesis of the aortic and pulmonary valves is a very rare congenital malformation of the semilunar valves. The literature describes no more than thirty cases of such anomaly in combination with congenital heart disease. Most descriptions include aplasia of either the aortic or pulmonic valve. The combination of such defect in both valves has been described in a much smaller number of scientific papers.

In this article, we present a clinical case of the treatment of a patient with agenesis of aortic valve and severely hypoplastic pulmonary valve. As a result circulatory arrest occurred immediately after birth, which required the implementation of cardiopulmonary resuscitation. The child was resuscitated and transferred to the intensive care unit for further examination and treatment.

Keywords: Aortic valve, Pulmonary valve, Absent aortic valve, Aplasia of semilunar valve leaflets, Case report

1. Introduction

Aplasia of one of the semilunar valves is a rare anomaly and occurs in no more than 0.4% of live births with congenital heart disease (CHD) [1,2]. The combination of agenesis of the aortic (AV) and pulmonary valve (PV) is extremely rare [3]. The absence of the semilunar valve is characterized by its agenesis, the presence of rudiments, or severe dysplasia of the aortic and/or pulmonary valve cusps.

The development of this anomaly is accompanied by severe hemodynamic disturbances, often not after the birth of a child, but in utero. This fact is confirmed by some publications that witness to antenatal death of the fetus with a registered case of the absence of semilunar valves [[3], [4], [5], [6]]. The most likely cause of intrauterine fetal death is associated with the development of severe volume overload of both ventricles against the background of severe aortic and pulmonary regurgitation, which leads to the development of severe heart failure and fetal hydrops.

1.1. Pathological anatomy

From the point of view of the development of the semilunar valves, the concepts of absence and agenesis/aplasia cannot be identified. This is mainly due to the fact that the rudiments for the development of these structures are always present, therefore, one of the most appropriate formulation of this anomaly of development is hypoplasia of the semilunar valves. On the other hand, neither the development of the structure, nor the development of the signs of severe impaired differentiation of the anatomical structure, called “agenesis/aplasia” can be justified.

Developmental disorders of the semilunar valves are most likely to be often associated with anomalies of the conotruncus, which lead to the development of, for example, tetralogy of Fallot, a double outlet of great vessels from the right ventricle and other CHD of this group [5]. At the same time, cases of the absence of one or both semilunar valves without concomitant pathology of the conotruncus have been described [4]. There is also a version that developmental disorders of the embryogenesis of the endocardial pads during the formation of the ventriculo-arterial junction may be the cause of agenesis of the semilunar valves [3,7].

To determine the strategy of clinical treatment, it is more important to take into account not the features of the anatomy, but the pathological physiology of the disease in such anomalies that lead to hemodynamic disorders. Thus, the tactics of treatment directly depends on the understanding of the hemodynamic features that occur in acute severe insufficiency of the aortic and pulmonary valve.

1.2. Pathophysiology of acute severe aortic and pulmonary valve insufficiency

Acute severe AV insufficiency leads not only to a significantly increased afterload, but also to the rapid development of excessive volumetric load to the left ventricular (LV), which leads to a sharp increase of the LV diastolic pressure [8]. In this situation, the pressure in the LV exceeds the pressure in the left atrium during diastole. As a result, the ventriculo-atrial gradient greatly increases and causes premature closure of the mitral valve before the start of the next ventricular systole. In the future, a progressive increase of the ventriculo-atrial gradient leads to the fact that the mitral valve begins to open at late diastole, which leads to the appearance of not only the systolic, but also the diastolic mitral regurgitation.

As a result of the progression of such changes, the diastolic dimension of the LV rapidly increases. This, on the one hand, leads to the progression of mitral valve insufficiency, and on the other hand, increases the stress on the ventricular wall. Against the background of coronary blood flow disorders existing by this time, myocardial perfusion significantly and rapidly deteriorates, which leads to the development of ischemia, decrease in myocardial contractility, and the occurrence of the hemodynamically significant arrhythmias.

In acute severe pulmonary valve insufficiency, the right ventricle (RV) is the first to be affected by the increase in volumetric load, provided that the pulmonary artery pressure is normal, which is compensated by a change in compliance [9]. But in the situations with increased afterload, the hemodynamic negative consequences for the RV are greatly exacerbated. This is the main difference of acute severe aortic regurgitation, when the physiological response of the LV depends mainly on the severity and speed of its development, since changes in LV compliance do not occur quickly. Therefore, the combination of volume and pressure overload can lead to a rapid deterioration of the RV function.

In acute severe PV insufficiency without the increase of the pulmonary artery pressure, there is only a moderate elevation of the RV end-diastolic pressure and the right atrial pressure, despite the fact that the volume of regurgitation is large. If the pulmonary artery pressure is elevated, the RV end-diastolic pressure will be significantly increased. The systolic pressure in the RV will rise to the level of the systolic pressure in the pulmonary artery. In addition, compensatory hypertrophy of the RV does not occur in this condition.

Therefore, the combination of pressure and volume overload will lead to a rapid increase of the load to the ventricular wall and to the decrease of the RV systolic function. The development of the RV dysfunction and insufficiency against the background of such hemodynamic changes is the cause of decrease of the effective stroke volume and the preload to the LV.

2. Case report

2.1. Clinical and instrumental examination

A newborn boy was born at the clinic of St. Petersburg State Pediatric Medical University at a gestational age of 39 weeks. Birth weight was 2970 g, body length was 49 cm. Congenital heart disease was detected prenatally during the 2nd trimester of pregnancy as: D-transposition of the great arteries. Double outlet of great arteries from the right ventricle. Ventricular septal defect. Pulmonary valve dysplasia. Pericardial effusion.

During the first minutes after birth the child's condition began to worsen. Apgar score was 3/3/4b. The clinical picture included the following: the child's condition was extremely severe, the cry was weak, there was muscle hypotension, the skin was pale pink, there was pronounced acrocyanosis. The heart rate was 58 beats per minute. On auscultation of the heart there was a pronounced systolic-diastolic murmur. Breathing was spontaneous of the Gasping type. There was dyspnea, the respiratory rate was 90 per minute. On auscultation of the lungs the breathing was sharply weakened on both sides, with moist rales. Tracheal intubation was performed on the background of parallel cardiopulmonary resuscitation. Vasoprostan infusion was started through the catheter in the umbilical vein at a dose of 0.05 μg/kg/min. Transesophageal pacing was started, as VVI mode with a frequency of 110 beats per minute with a maximum stimulation amplitude. Pacing response was poor, the rhythm was unstable. After 35 minutes, there was a restoration of cardiac sinus rhythm with the heart rate of 110 beats per minute and improved blood pressure (55/45 mm Hg).

A transthoracic echocardiographic (ECHO) examination was performed (Fig. 1, Fig. 2, Fig. 3): Situs solitus. The heart was located correctly. Atrioventricular connections were concordant. There was no mitral-semilunar contact (Fig. 1A and B; 3B). There was a double outlet of great vessels from the right ventricle with transposition. The left ventricle was enlarged (Fig. 3 B). The right and left atria were not dilated (Fig. 3A). The ventricular septal defect (VSD) was visualized in the inflow part of the septum as a non-restrictive one (20 mm in diameter) (Fig. 3B). The mitral and tricuspid valves were normal (Fig. 3A). In the aortic valve the leaflets were not defined, an antegrade flow and severe insufficiency were visualized (Fig. 1A and B). In the pulmonary valve there were dysplastic leaflets, severe hypoplasia, an antegrade flow and severe insufficiency were visualized. The pulmonary artery trunk and branches were dilated (Fig. 2A and B). The patent ductus arteriosus (PDA) with bidirectional blood shunt (6 mm in diameter) was observed in the patent (Fig. 2A and B). The open foramen ovale (6 mm in diameter) with left to right shunting of blood without signs of restriction was identified. The aortic arch was filled ante- and retrograde, with pronounced diastolic reversal of blood flow (Fig. 2A and B). In the abdominal aorta the blood flow was of the main type with pronounced diastolic reverse. Fluid was determined in the right pleural cavity and in the abdominal cavity.

Fig. 1.

Fig. 1

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ECHO. (A) Parasternal long-axis view. Systole phase of the LV. Displacement of the great arteries to the right with transposition. Turbulent flow to the aorta and pulmonary artery are visualized. Aortic and pulmonary valves are not visualized. No mitral-semilunar contact (marked with an asterisk). (B) Parasternal long-axis view. Diastole phase of the LV. Severe pulmonary regurgitation (marked with an arrow on the right part of the picture). Abbreviations: RV, the right ventricle; LA, the left atrium; PA, the pulmonary artery; Ao, the ascending aorta.

Fig. 2.

Fig. 2

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ECHO. (A) Parasternal shot-axis view. Systole phase of the ventricles. Antegrade flow to the aorta and pulmonary artery are visualized. Left to right shunt through the PDA. (B) Parasternal shot-axis view. Diastole phase of the ventricles. Retrograde flow at the aortic arch level is visualized. Right to left shunt through the PDA. Abbreviations: RV, the right ventricle; PA, the pulmonary artery; LPA, the left pulmonary artery; Ao, the ascending aorta; PDA, the patent ductus arteriosus; DesAo, the descending aorta.

Fig. 3.

Fig. 3

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ECHO. (A) Subcostal view. The right and left atrium are normal. The atrioventricular valves are normal. (B) Parasternal long-axis view. Enlargement of the left ventricle. No mitral-semilunar contact (marked with an asterisk). Huge ventricular septum defect. Abbreviations: RV, the right ventricle; LV, the left ventricle; LA, the left atrium; RA, the right atrium; PA, the pulmonary artery; IVS, the interventricular septum; VSD, the ventricular septum defect.

The newborn was diagnosed with: CHD. Double outlet of great arteries from the right ventricle with transposition of the great arteries. Agenesis of aortic valve. Severely hypoplastic pulmonary valve. Severe insufficiency of the AV. Severe insufficiency of the PV. The PDA.

Based on the data of ECHO, the severe critical condition of the child, the futility of intensive therapy, the indications for performing emergency surgical correction were determined. For 30 minutes the child's condition remained extremely severe and unstable. Against the background of intensive therapy with high doses of inotropic and vasoactive drugs, circulatory arrest occurred again with severe violations of the pumping function of the heart and electromechanical dissociation by ECG on the monitor. The resuscitation was unsuccessful.

2.2. Postmortem examination

Pathological anatomical examination of the heart and great vessels confirmed the data of instrumental examination (Fig. 4, Fig. 5). The aorta and pulmonary artery was arisen from the right ventricle. The aorta was located to the right of the pulmonary artery and anteriorly, and it was dilated (the width at the orifice was 28 mm), cusps of the semilunar valve were not developed (Fig. 4, Fig. 5A). The pulmonary artery was located to the left of the aorta and posteriorly, closer to the VSD than the aorta. Three leaflets of the pulmonary valve were severely hypoplastic and deformed (Fig. 4, Fig. 5B).

Fig. 4.

Fig. 4

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Macroscopic specimen of the heart. The displacement of the great vessels to the right, aplasia of the semilunar aortic valve (marked with blue arrows), and pronounced hypoplasia of the cusps of the pulmonary valve were determined. Abbreviations: RV, the right ventricle; LV, the left ventricle; PA, the pulmonary artery; Ao, the ascending aorta; PV, the pulmonary valve; VSD, the ventricular septum defect. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

Fig. 5.

Fig. 5

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Macroscopic specimen of the heart. (A) The aorta was arisen from the right ventricle, aplasia of the aortic semilunar valve (marked with blue arrows), VSD were determined. (B) The pulmonary artery was located closer to the ventricular septal defect. Severe hypoplasia of the pulmonic valve leaflets was noted (marked with blue arrows). Abbreviations: RV, the right ventricle; LV, the left ventricle; PA, the pulmonary artery; Ao, the ascending aorta; VSD, the ventricular septum defect. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

The left atrium on the posterior surface was a slit-like one. All pulmonary veins drain into the left atrium. The mitral valve was correctly formed. The left ventricle was enlarged with a thickness of the posterior wall of 30 mm, spongy, with a flabby consistency protruding above the surface on the cut. The interventricular septum in the region of the apex of the heart was pronouncedly hypertrophied (30 mm), passed into a thin translucent cone-shaped membrane 10 mm long. At the base of the heart under the mitral valve, an ellipsoid-shaped hole (a septal defect) with a size of 24 × 25 mm was determined.

3. Discussion

Agenesis of the aortic and pulmonary valves is a rare congenital anomaly of the heart, manifested by the development of early severe heart failure due to severe aortic and pulmonary valve regurgitation. No more than 30 cases of this pathology have been reported in the literature since Toews et al. reported the first case of this anomaly in 1975 [10]. Severe aortic regurgitation caused by the absence of aortic valve leaflets can affect the circulation of the fetus and the newborn in different ways. Volume overload of the left ventricle leads to severe heart failure and the development of fetal dropsy. One of the reasons for the sudden and rapid deterioration of blood circulation after birth is the syndrome of “coronary steal” due to severe aortic regurgitation [6,8]. Also, a pronounced volume overload of the left ventricle is the cause of the progression of violations of the LV systolic function, mitral regurgitation and pulmonary edema. Stroke volume of the LV also decreases due to the formation of severe mitral regurgitation, which results in a decrease of the left ventricular preload. Against the background of these hemodynamic changes, coronary perfusion and ventricular myocardial contractility deteriorate significantly.

There are few scientific publications devoted to the treatment of newborns with such an anomaly in the development of the semilunar valves, especially those undergoing surgical intervention, and most report the death of infants during the first week of life [2]. Murakami T. et al. reviewed two cases with aortic valve agenesis and analyzed the results of treatment of 24 cases of other authors. Successful palliative surgery has been reported in several publications [[11], [12], [13], [14]]. But it should be noted that in these cases, patients had atresia or severe mitral valve stenosis. With such hemodynamics, the pathological physiology is different and is not accompanied by hemodynamic disorders similar to acute severe insufficiency of AV and PV.

In the presented clinical case, the newborn child had the CHD: Double outlet of great arteries from the right ventricle with transposition of the great arteries. Agenesis of the aortic valve. Severely hypoplastic of the pulmonary valve. Severe insufficiency of the AV. Severe insufficiency of the PV. The PDA. As a result of aortic valve agenesis and severe pulmonic valve dysplasia, the newborn had acute severe insufficiency on both semilunar valves. Hemodynamics with such anatomy of the defect leads to a persistent increase not only of the volume load on both ventricles, but also of the pressure overload. Before the development of severe insufficiency of atrioventricular valves and sufficient systolic ventricular function, cardiac output remains at a sufficient level, albeit borderline. But the presence of a pronounced decrease in coronary perfusion led to a rapid disruption of ventricular myocardial contractility against the background of ischemia, the development of hemodynamically significant bradyarrhythmia, and impaired systemic perfusion. In our case, within a few minutes after birth, the newborn child developed bradycardia with circulatory arrest. As a result of cardiopulmonary resuscitation in the delivery room, the child's condition was stabilized. The child was transferred to the intensive care unit for further examination and treatment. But after 30 minutes, hemodynamically significant arrhythmias with circulatory arrest occurred again. The most likely cause of the development of such conditions was a violation of coronary blood flow, which could be compensated by high doses of inotropic and vasopressor drugs. Such therapy, unfortunately, does not allow to influence the main mechanism of pathogenesis, which, obviously, is primarily associated with acute severe semilunar valve insufficiency. Thus, only the surgical correction is effective and promising method of treatment.

In addition, surgery should be undertaken as a matter of urgency after diagnosis in order to prevent further deterioration of ventricular function against the background of progression of coronary and systemic perfusion disorders.

Given the high risk of fatal complications in the first minutes after birth, and the need to perform the operation as soon as possible after the verification of the diagnosis, a very significant role is given to prenatal diagnosis. In the case of a prenatal diagnosis, delivery should be performed in a hospital with the possibility of providing cardiac surgery [15]. In this case, the cardiac surgical team must be prepared to perform an emergency operation immediately after birth. There are no publications on the preferred method of surgical correction, because this malformation is very rare and most patients die either antenatally or within the first hours after birth.

3.1. Surgical options

After median sternotomy, it is necessary to perform cannulation of the ascending aorta, superior and inferior vena cava, and initiate cardiopulmonary bypass. After initiation of cardiopulmonary bypass, it is necessary to clamp the trunk of the pulmonary artery, as well as the left and right branches of the pulmonary artery. It is proposed not to touch the ductus arteriosus, because when choosing the hybrid correction option, the ductus arteriosus must function. After clamping the aorta and pulmonary artery, it is necessary to perform cardioplegia. For this variant it is better to perform retrograde cardioplegia, because of acute severe insufficiency on both semilunar valves. Due to the large ventricular septal defect, there is no need for drainage of the left ventricles during cardioplegia.

The main idea of the safest variant of hemodynamic correction is a model of fetal circulation, but with a normal function of the aortic and pulmonary valves [16,17]. After cardiac arrest, the first step is to perform an intracardiac step. A synthetic patch should be sutured into the aortic position at the level of the annulus of the immature valve: it is necessary to ensure normal coronary perfusion. After completing this stage, it is necessary to restore cardiac activity and continue the operation on a beating heart. The presence of concomitant severe pulmonary insufficiency will lead to significant stealing of coronary blood flow. Therefore, it is necessary to improve the function of the valve: to form a monocusp from the pericardium or synthetic material in the native pulmonary artery. Another more suitable option is the implantation of a valve-containing conduit. The next step is to banding of the pulmonary arteries. Considering that the patient will have ductus-dependent systemic and coronary blood flow, it is necessary to continue the constant infusion of prostaglandins. The PDA stenting is best performed in a planned manner, after stabilization of the clinical condition. But if it is possible to perform the operation in a hybrid operating room, it is possible to perform the PDA stenting at the same time.

An alternative strategy for surgical correction exists, but it is accompanied by a significantly longer duration of aortic cross-clamping and cardiopulmonary bypass. At the same time, hemodynamic efficiency is not accompanied by significant advantages. Such a variant of the surgery can be considered: the implantation of a valve-containing conduit in the aortic position with the reimplantation of the coronary arteries. But there are no prostheses with the required diameter for a newborn, so this operation will require the Konnо procedure. In the pulmonary position, a monocusp should be formed in the native pulmonary artery, or a valve-containing conduit should be implanted. This type of surgical correction will be accompanied by a significantly higher risk of fatal complications.

In case of unsuccessful weaning from cardiopulmonary bypass, it is necessary to continue assisted circulation using extracorporeal membrane oxygenation.

4. Conclusion

The result of the presented clinical case of the rapid development of decompensation of the clinical condition of the newborn with acute insufficiency of both semilunar valves demonstrates the low efficiency of intensive care for such hemodynamic disorders. The peculiarities of pathophysiology and the nature of the clinical course in the first hours after birth emphasize the importance of prenatal diagnosis of critical malformations in children and delivery of pregnant women to multidisciplinary clinics with the possibility of providing cardiac surgery to newborns. In such cases, the cardiac surgical team must be prepared to perform an emergency operation immediately after birth.

Author contribution statement

Suvorov V.V. conceived and designed the experiments; Analyzed and interpreted the data; wrote the paper; Fedotova E.P. сontributed reagents, materials, analysis tools or data, and wrote the paper; Zaitsev V.V. analyzed and interpreted the data; wrote the paper; Dolgova E.V. performed the experiments and wrote the paper; Popova L.L. performed the experiments and wrote the paper; Glazunova A.E. performed the experiments and wrote the paper; Novak M.U. performed the experiments and wrote the paper; Nasyrov R.A. conceived and designed the experiments; wrote the paper; All the authors read and approved the final draft.

Funding statement

The authors received no specific funding for this study.

Data availability statement

Data included in article/supp. material/referenced in article. Some or all data, models, or code generated or used during the study are available from the corresponding author by request.

Additional information

The parents of the child, whose data or images are included in this publication, provided consent for all images and clinical data and other data included in the manuscript to be published.

Declaration of competing interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

Data included in article/supp. material/referenced in article. Some or all data, models, or code generated or used during the study are available from the corresponding author by request.

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