Twin Twin Transfusion Syndrome

What is TTTS?

Twin-to-Twin Transfusion Syndrome (TTTS) is a severe, primarily hemodynamic complication affecting approximately 10–15% of monochorionic–diamniotic twin pregnancies. It arises from an imbalance in intertwin blood exchange through placental vascular anastomoses within a shared monochorionic placenta. These placentas contain a complex “third circulation,” composed of arterioarterial (AA), venovenous, and arteriovenous (AV) anastomoses. TTTS develops when this network becomes functionally unbalanced, typically due to a predominance of deep, unidirectional AV anastomoses combined with a relative absence of superficial, bidirectional AA connections. In balanced monochorionic placentation, AA anastomoses act as low-resistance pressure-equalizing conduits that buffer transient intertwin differences in blood pressure and volume.

Their paucity in TTTS allows unopposed, chronic shunting of blood from the donor to the recipient twin through AV capillary beds. The resulting disorder is not simply a volume-transfer disease but a sustained hemodynamic and endocrine derangement affecting both fetuses. TTTS is diagnosed antenatally by sonographic evidence of the twin oligohydramnios–polyhydramnios sequence (TOPS), defined by a deepest vertical pocket ≤2 cm in the donor sac and ≥8 cm in the recipient sac. Growth discordance frequently coexists but is not required for diagnosis. Disease severity is classically staged using the Quintero system, ranging from isolated amniotic fluid discordance (Stage I) to absent donor bladder (Stage II), critically abnormal Dopplers (Stage III), hydrops (Stage IV), and fetal demise (Stage V). Beyond volume imbalance, TTTS is characterized by intertwin transfer of vasoactive mediators, leading to a hostile endocrine milieu that amplifies cardiovascular and renal maladaptation and drives progressive myocardial and vascular remodeling.

Fetal Hemodynamic Effect

Recipient twin

The recipient twin is exposed to a dual hemodynamic insult: chronic hypervolemia and sustained pressure overload. Increased circulating volume leads to myocardial stretch and activation of atrial and brain natriuretic peptides, resulting in profound polyuria and polyhydramnios. In parallel, the recipient develops severe systemic hypertension driven by paradoxical activation of the renin–angiotensin–aldosterone system (RAAS). Although renal renin production in the recipient is appropriately downregulated, high circulating levels of renin, angiotensin II, and endothelin-1 persist due to placental transfer from the hypovolemic donor. This endocrine configuration closely resembles a “two kidneys–one clip” model of hypertension, in which the recipient behaves as a normal kidney exposed to excessive vasoconstrictive hormones. The result is malignant fetal hypertension, with systolic pressures that may reach twice the normal range for gestational age. Angiotensin II exerts direct trophic effects on cardiomyocytes and fibroblasts, promoting myocardial hypertrophy and fibrosis that is disproportionate to volume loading alone.

Echocardiographically, recipient twins demonstrate a characteristic progression in cardiac dysfunction. Diastolic impairment typically precedes systolic failure and is reflected by reduced ventricular compliance, fusion of early and late filling waves, and a markedly elevated myocardial performance index. As pressure loading intensifies, atrioventricular valve regurgitation—most commonly tricuspid—becomes prevalent. In a subset of recipients, diminished forward flow across the pulmonary valve leads to acquired right ventricular outflow tract obstruction (RVOTO), manifesting as functional pulmonary stenosis or, in severe cases, pulmonary atresia.

Donor Twin

The donor twin experiences the converse physiology: chronic hypovolemia and hypoperfusion. Reduced renal blood flow triggers robust activation of the RAAS and antidiuretic hormone secretion in an attempt to preserve blood pressure. The resulting oliguria produces oligohydramnios, often with a non-visualized bladder and the classic “stuck twin” appearance. While systolic cardiac function in the donor is often preserved at diagnosis, the cardiovascular system is subjected to persistently high placental resistance and elevated afterload. Chronic neurohormonal activation promotes arterial smooth-muscle hypertrophy, collagen deposition, and reduced vascular distensibility—a process increasingly recognized as fetal vascular programming. Reduced preload and diminished antegrade flow through the left ventricular outflow tract impair normal development of the aortic arch, substantially increasing the risk of coarctation or arch hypoplasia. These donor-specific effects are suggested antenatally by abnormal umbilical artery Doppler patterns, including absent or reversed end-diastolic flow, and by persistent fetal growth restriction.

Postnatal Cardiovascular Phenotypes

The transition to postnatal life reveals persistent cardiovascular phenotypes that mirror each twin’s intrauterine hemodynamic exposure.

Recipient Twin

Former recipients typically present with a hypertensive cardiomyopathy phenotype characterized by biventricular hypertrophy, cardiomegaly, and an elevated risk of early congestive heart failure. In infants not treated prenatally with fetoscopic laser surgery, three postnatal trajectories have been described: no immediate impairment, isolated systemic hypertension, and severe cardiac failure within the first 24 hours of life. Even after successful laser therapy, recipients remain vulnerable—particularly if delivery occurs within two months of the procedure—reflecting delayed endocrine and myocardial recovery. Right-sided pathology predominates. RVOTO may persist postnatally as pulmonary stenosis or functional pulmonary atresia. While many obstructions resolve after circulatory separation, approximately 5–8% of recipients develop permanent pulmonary valve stenosis requiring catheter-based or surgical intervention.

Chronic intrauterine hypertension and vascular “intoxication” also increase susceptibility to persistent pulmonary hypertension of the newborn, complicating cardiopulmonary transition. Blood pressure trajectories are characteristic: markedly elevated systolic pressures in the first hours of life may be followed by abrupt hypotension if left ventricular systolic dysfunction ensues. Diastolic dysfunction almost invariably precedes systolic failure and is readily detected by Doppler and MPI abnormalities. The persistence of neonatal instability after laser therapy is attributed to hormonal lag—continued exposure to RAAS mediators and endothelin-1, combined with ongoing natriuretic peptide secretion from hypertrophied myocardium. This hormonal lag exists in all TTTS recipients, but it is clinically relevant mainly when delivery occurs close to the time of laser surgery. With sufficient interval between laser and birth, it usually resolves and becomes clinically silent. The hormonal lag refers to the persistence of vasoactive and neurohormonal disturbances in the recipient twin after the intertwin circulation has been interrupted by fetoscopic selective laser coagulation (FSLC). These include: elevated circulating angiotensin II and renin transferred prenatally from the donor; persistently high endothelin-1; ongoing secretion of atrial and brain natriuretic peptides from a hypertrophied, pressure-loaded myocardium. Importantly, laser immediately stops (or at least limits) further transfer, but it does not instantly normalize the recipient’s endocrine or myocardial state. When delivery occurs close to fetoscopic laser photocoagulation therapy (approximately within 6–8 weeks), hormonal lag is clinically significant and often dominates the postnatal presentation. The recipient myocardium typically remains hypertrophied and stiff, systemic vascular resistance stays elevated, and the effects of RAAS activation and endothelin exposure persist despite placental separation. Natriuretic peptides may also remain elevated due to residual chamber dilation. Clinically, this translates into a high risk of neonatal systemic hypertension, early diastolic dysfunction that may progress to systolic failure, and acute heart failure within the first 12–24 hours of life, with an increased likelihood of persistent RVOT obstruction and PPHN. This group characteristically follows a trajectory of early severe hypertension followed by myocardial decompensation and subsequent hypotension with low cardiac output. In contrast, when delivery occurs remote from laser therapy (approximately 8–10 weeks or more), hormonal lag is largely resolved: circulating vasoactive mediators normalize, vascular tone gradually resets, myocardial hypertrophy regresses in utero, and diastolic function improves before birth. As a result, most infants are hemodynamically stable at delivery, with a markedly lower incidence of neonatal hypertension or heart failure; although fixed structural lesions such as pulmonary stenosis may persist, endocrine-driven cardiovascular instability is uncommon, explaining why the majority of later-delivered, laser-treated recipients show no significant postnatal cardiovascular phenotype.

Donor Twin

In contrast, the donor twin’s postnatal phenotype is dominated by vascular rather than myocardial pathology. Cardiac contractility and ejection fraction are generally preserved, but systemic arteries exhibit increased stiffness and reduced compliance. Structural lesions of the aortic arch are a major concern. Coarctation or arch hypoplasia reflects a flow-dependent growth disturbance caused by chronic low preload and diminished antegrade aortic flow during fetal life. Renal vulnerability is also prominent. A history of intrauterine hypoperfusion predisposes donors to transient acute kidney injury, with oliguria and elevated creatinine that may take up to two weeks to normalize. If delivery follows shortly after laser therapy, abrupt interruption of chronic shunting can result in transient volume overload or hydrops, requiring close hemodynamic surveillance. Donor twins also remain at risk for ischemic or hemorrhagic cerebral injury, mandating systematic neuroimaging and long-term follow-up.

Acquired Congenital Heart Disease in TTTS

Cardiac malformations in TTTS are best understood as acquired, flow- and pressure-mediated lesions rather than primary genetic defects. In recipients, sustained hypertension and right ventricular hypertrophy interfere with pulmonary outflow, producing RVOTO that may progress from functional obstruction to fixed valvar disease. In donors, chronic low flow through the aortic isthmus impairs normal arch development in accordance with the flow-growth principle, predisposing to coarctation or hypoplasia. These lesions illustrate the profound capacity of fetal hemodynamics to shape cardiovascular structure.

Long-Term Outcomes

Despite the severity of neonatal illness, long-term cardiovascular outcomes are generally favorable. Elevated blood pressure and residual hypertrophy may be present at two years of age, but studies of older survivors demonstrate near-complete normalization of cardiac structure and systemic pressures by late childhood. This recovery underscores the remarkable plasticity of the developing cardiovascular system once the initiating stressors are removed. Nevertheless, survivors of TTTS carry a substantially increased lifetime risk of congenital heart disease—estimated up to twelve-fold higher than in singletons—necessitating comprehensive postnatal echocardiographic screening and coordinated long-term multidisciplinary care.

Paradoxical activation of the RAAS in the recipient

In a healthy individual, hypervolemia and high blood pressure would naturally suppress RAAS activity; however, in the recipient twin, this feedback loop is bypassed by the continuous influx of hormones from the donor. Consequently, while the recipient's own renal renin production is downregulated, they exhibit paradoxically high systemic levels of renin and angiotensin II. This "intoxication" by vasoactive substances results in a massive increase in afterload through systemic vasoconstriction. The recipient’s heart is thus forced to work against extremely high pressures, leading to fetal hypertension, with systolic blood pressures that can reach twice the normal range for gestational age. The impact of this high-pressure environment on the recipient’s heart is profound and leads to progressive cardiac remodeling. Angiotensin II not only causes hypertension but also acts directly on cardiac myocytes and fibroblasts to stimulate myocardial hypertrophy and fibrosis. This hormonal stimulation often causes ventricular thickening that is out of proportion to what would be expected from volume overload alone. As the myocardium thickens and compliance decreases, diastolic dysfunction typically develops first, characterized by abnormal ventricular filling patterns and increased filling pressures. This eventually progresses to global systolic impairment and high-output cardiac failure. Furthermore, the RAAS-induced hypertension and right ventricular hypertrophy often lead to secondary structural anomalies. The increased right-sided heart pressure and tricuspid valve regurgitation can severely diminish forward flow across the pulmonary valve. This chronic lack of flow can interfere with the development of the pulmonary outflow tract, resulting in acquired right ventricular outflow tract obstruction (RVOTO), which manifests as either functional pulmonary stenosis or pulmonary atresia. The RAAS also acts synergistically with other mediators, such as endothelin-1, which is elevated in the recipient and further contributes to malignant hypertension and the development of fetal hydrops.

Key Points on RAAS activation:

For the recipient, there is increased preload (volume) with an absolute increase in circulating volume compared to that of the donor, with significantly higher cardiac output. The recipient is also subjected to an increased afterload in the form of increased resistance. The renin-angiotensin system (RAAS) is ‘downregulated’ in the recipient's kidneys, but work has shown that the levels are as high as in the donor; it is assumed that this is mainly due to transfer from the donor. All these factors explain the development of significant myocardial ventricular hypertrophy, out of proportion to simple volume overload. A consequence of this progressive cardiomyopathy is an increase in overall heart size, a reduction in myocardial compliance, atrioventricular valvar regurgitation, and abnormal venous Dopplers. RVOT anomalies in the recipient may be in the form of valvar dysplasia, stenosis, regurgitation, or functional atresia; early involvement of the RVOT may be demonstrated by observing that the pulmonary valve annulus is equal in size to or smaller than that of the aortic valve, and this can progress to produce significant valvar pathology. It is not clear whether RVOT anomalies mirror the severity of the TTTS process, or whether the anomalies are simply due to altered hemodynamics or are a consequence of the vasoactive mediators. The prevalence of RVOT anomalies varies in different series but may be seen in some form in up to 20% of MC/DA twins, but only in recipient twins; between 9 and 12.5% had persistent anomalies requiring postnatal treatment, in spite of otherwise successful treatment for the TTTS.

From Free Article - Yoda H. Fetal and Neonatal Circulatory Disorders in Twin to Twin Transfusion Syndrome (The Secondary Publication). J Nippon Med Sch. 2019;86(4):192-200. PMID: 31484880.

Focus on the congenital heart defect in TTTS

RVOT obstruction in the recipient

In Twin-to-Twin Transfusion Syndrome (TTTS), congenital heart disease (CHD) can develop in one of the twins primarily due to physiological stress and altered hemodynamics related to the shared placenta. In TTTS, one fetus (the "donor") transfuses blood to the other (the "receiver") through placental anastomoses. The receiver fetus becomes fluid overloaded and "intoxicated" by hypertensive substances, such as those from the renin-angiotensin system, and also experiences problems with placental resistance. This leads to the receiver fetus becoming hypertensive, larger, and having more amniotic fluid. The increased arterial hypertension and resistance impact both ventricles, leading to cardiac changes. The right ventricle (RV) frequently becomes hypertrophied. This hypertrophy occurs because the RV, to normalize its strain under the increased afterload (due to elevated pulmonary and systemic resistances), thickens significantly. As a consequence of the RV hypertrophy and its reduced filling, an obstruction to pulmonary outflow can develop, leading to pulmonary stenosis. In some rarer cases, this can progress to pulmonary atresia with an intact septum in the receiver fetus. The left ventricle can also experience issues related to hypertension. These cardiac abnormalities in TTTS are considered acquired CHDs that are purely physiological in origin, rather than being related to primary morphogenetic or genetic processes. The distinct physiological conditions and circulatory differences between the two fetuses contribute to the development of these heart conditions.

Reference for Data and Figure: Manning N, Archer N. Cardiac Manifestations of Twin-to-Twin Transfusion Syndrome. Twin Res Hum Genet. 2016 Jun;19(3):246-54. doi: 10.1017/thg.2016.20. Epub 2016 Apr 18. PMID: 27087122.

Coarctation and the donor

The donor twin experiences a unique set of cardiac and vascular challenges distinct from those of the recipient twin. Due to an unbalanced blood flow through placental vascular anastomoses, the donor twin is characteristically hypovolemic, receiving less blood volume than necessary. This reduced blood volume triggers compensatory physiological changes that affect the donor's cardiovascular system. The donor twin's heart typically does not show severe structural cardiac abnormalities during fetal echocardiographic assessment, unlike the recipient twin, which often exhibits signs of volume overload and cardiomegaly. However, the donor twin suffers from increased afterload caused by elevated placental vascular resistance. This increased resistance arises partly because the donor twin’s share of the placenta is often smaller or less functional, leading to a higher vascular resistance that the heart must work against, on top of circulating RAAS byproducts, BNP/ANP and endothelin-1. Consequently, the donor twin’s heart faces a sustained increase in pressure load. The hemodynamic stress on the donor heart is compounded by hypovolemia, which results in decreased renal perfusion and activation of maladaptive neurohormonal mechanisms. These include increased production of vasoactive substances such as angiotensin II and endothelin I, which contribute to systemic vasoconstriction, vascular remodeling, and arterial wall thickening. The outcome is a persistent alteration in arterial structure, with changes such as collagen deposition, smooth muscle hypertrophy, and vascular stiffness, not only affecting fetal circulatory function but also predisposing the donor twin to long-term vascular issues after birth. Congenital heart defects are less common in donor twins than in recipients, but these altered blood flow during fetal life increase the risk of specific left-sided obstruction defects. Coarctation of the aorta or hypoplastic aortic arch are also thought to be related to the chronic reduced blood flow and increased resistance affecting the left heart and systemic circulation. With a combination of high resistances and low preload, there is a net drop in antegrade blood flow through the arch and aortic isthmus, leading to underdevelopment of the aorta. The donor’s cardiovascular system is thus in a state of high afterload with low preload, which can impair cardiac output and promote remodeling and dysfunction over time. The low preload to RA, leads to decrease net shunting via the Foramen Ovale, limiting the LA and LV preload.

In summary, the development of coarctation of the aorta in donor twins affected by Twin-to-Twin Transfusion Syndrome (TTTS) is primarily attributed to the "flow-grow" theory, a fundamental concept in fetal cardiovascular development stating that the growth and structural maturation of cardiac vessels are dependent on the volume of blood flow passing through them. In the specific hemodynamic environment of TTTS, the donor twin suffers from chronic hypovolemia and hypoperfusion due to the continuous shunting of blood volume through placental anastomoses to the recipient co-twin. This chronic state of low blood volume leads to several critical physiological changes that impair the normal growth of the aorta:

Reduced Cardiac Output: The donor twin experiences low preload and decreased venous return from its share of the placenta. Consequently, the donor's heart generates a significantly reduced left ventricular output compared to normal fetal standards.
Aortic Isthmus Flow Patterns: Because of the low circulating volume and high placental resistance, there is a marked drop in antegrade blood flow across the left ventricular outflow tract (LVOT), specifically through the aortic isthmus and the aortic arch. The aortic isthmus acts as a pressure transducer between the left and right ventricles; in the donor, the diminished volume results in inadequate "loading" of this vessel.
Structural Underdevelopment: The persistent lack of sufficient blood flow through the aorta during critical periods of fetal development results in hypoplasia (underdevelopment) of the aortic arch or the formation of a localized narrowing known as a coarctation.
Vasoactive Mediators: The donor's body attempts to compensate for its hypovolemic state by upregulating the renin-angiotensin system (RAAS) and increasing the production of vasoconstrictors like Angiotensin II and Endothelin-1. While these hormones aim to maintain blood pressure, the resulting systemic vasoconstriction and increased vascular resistance may further compromise systemic blood flow and contribute to structural remodeling of the arterial walls. While the donor's heart "pump" function—such as contractility and ejection fraction—often remains normal prenatally, the acquired structural aberration of the aorta is a significant manifestation of the donor's hemodynamic struggle. The incidence of coarctation of the aorta in donor twins has been reported to be as high as 20% in some series, illustrating the severe impact of intrauterine vascular programming. These defects are considered purely physiological and acquired in origin rather than the result of a primary genetic malformation.

TTTS - Hemodynamic evaluation and management by Dr. Anie Lapointe

TTTS_NHRC_FINAL3.pdf

Presentation by Dr Ida Whiteman and Mrs Kristina Huber in the context of Neonatal Cardiology Rounds on TTTS on March 13, 2024

TTTS Final.pdf

Echocardiography of Pulmonary Stenosis in a recipient twin

Parasternal long axis B-Mode. There is a sweep anteriorly. One may appreciate the RV hypertrophy with the significant narrowing of the RVOT and underlying pulmonary stenosis (with small pulmonary valvular annulus)

PLAX with acceleration of flow in at the pulmonary valve (aliasing seen at a velocity filter/Nyquiest of -1.14 m/s)

PDA is seen left to right, potentially contributing to pulmonary blood flow.

PDA measured at 2.2 mm in 2D.

Modified view where one may appreciate that the pulmonary valve is doming and that its opening is narrowed - outlining some 2D evidence of underlying pulmonary stenosis.

Turbulence of flow / alliasing in the RVOT by colour.

2D view clip and 2D still frame with measurement of the pulmonary valvular annulus.

Parasternal short axis with colour and B-mode. The colour showcases aliasing from the turbulence of flow created by the pulmonary stenosis. One may also appreciate some of the PDA flow feeding into the branche pulmonary arteries.

Apical view sweep from posterior to anterior where we can appreciate the RVOT and pulmonary valve. The Pulmonary valve annulus is measured at 0.31 cm.

Colour flow through the RVOT into the branch pulmonary arteries.

Gradient obtained from the Parasternal Long axis view outlining a RV-MPA gradient of 128 mmHg (stenosis of the pulmonary valve). There is a dagger-shaped high-velocity Doppler spectra outlining there is a dynamic component to the obstruction.

Subcostal view with CW-Doppler in the RVOT with a gradient of 133.7 mmHg RV to PA, outlining significant pulmonary stenosis.

Subcostal view with 2D sweep and colour (outlining an inter-atrial shunt that is bidirectional, but significantly right to left due to increase RV end-diastolic pressure).

Case of significant hypertrophy in the context of a recipient twin

Intra-cavitary acceleration from the hypertrophy of the LV.

Systolic anterior motion of the mitral valve on M-Mode secondary to the hypertrophic state.

Intra-cavitary gradient detected by CW Doppler (secondary to hypertrophy and intra-cavitary obstruction)

Important Articles

cm-93-5.pdf

cardiac-manifestations-of-twin-to-twin-transfusion-syndrome.pdf

pr2005724.pdf

NeoHeart2022_GALTIT_-july28_2022.pdf

s41372-019-0524-5.pdf

000053919.pdf

Interesting article discussing a case of recipient TTTS with post-natal biventricular dysfunction and hypertrophy: Sehgal, A., Buckingham, M.R., Hyland, R.M. et al. Diagnostic and therapeutic precision in cardiovascular diseases in the neonatal intensive care. J Perinatol (2025). https://doi.org/10.1038/s41372-025-02317-x

s41372-025-02317-x (1).pdf

References:

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