ASDs, VSDs, PDA, and AVSDs are part of the everyday landscape of pediatric cardiology. These lesions are well understood, have apparently straightforward pathophysiology, and are managed using well-established treatments. Nevertheless, this familiarity does not always translate into consistent care. Patients with similar defects may undergo markedly different follow-up depending on the institution, the clinician responsible, or simply the inertia inherited from previous visits.
The American College of Cardiology concise clinical guidance document, Outpatient Management of Isolated Left-to-Right Shunt Lesions in Pediatric Patients, seeks to bring order to this area. Its aim is not to redefine anatomy or introduce new closure techniques, but to provide a common framework for the outpatient follow-up of isolated left-to-right shunt lesions.
This distinction is important. The document is not intended to replace clinical judgment or resolve every controversy surrounding the timing of intervention. Its main contribution is more pragmatic: identifying which patients require specialist surveillance, how frequently they should be reviewed, and when it is reasonable to extend follow-up intervals or discharge them from cardiology care. The result is guidance focused less on the appeal of innovation and more on the discipline of everyday practice. In medicine, effective standardization may ultimately contribute more than an isolated breakthrough.
One of the document’s most relevant messages is that the presence of an anatomical communication does not necessarily indicate clinically active heart disease. A small muscular VSD, an ASD without hemodynamic consequences, or a silent PDA should not automatically commit a patient to indefinite specialist follow-up.
The guidance supports reducing or discontinuing follow-up for selected trivial lesions when their natural history, impact on the cardiac chambers, and clinical examination indicate a benign course. This does not mean trivializing the diagnosis, but rather matching the intensity of care to the patient’s actual risk.
This recommendation has two important implications. First, it avoids repetitive testing, low-yield consultations, and unnecessary medicalization of the child. Second, it frees resources so that greater attention can be directed toward patients with volume overload, progressive chamber dilation, pulmonary hypertension, valvular regurgitation, or symptoms.
Discharge from cardiology, however, should not be presented as a discontinuation of care, but as an organized transfer to primary care pediatrics. To ensure safety, both the family and the pediatrician should understand which findings warrant reassessment: the appearance of a new or different murmur, exercise intolerance, recurrent infections, impaired growth, or any unexpected clinical change.
The algorithms are structured around each individual lesion, but they follow the same principle: follow-up frequency should not depend exclusively on defect diameter. Its physiological consequences are more important.
In VSD and PDA, hemodynamic impact is primarily reflected by volume overload of the left-sided chambers. Changes in LV size, shunt magnitude, estimated pulmonary pressures, associated aortic regurgitation in selected VSDs, and the child’s growth trajectory are more informative than any isolated measurement.
In ASD, attention shifts to the RV. Right-sided chamber dilation, septal motion, pulmonary blood flow, and the presence of symptoms or arrhythmias are more relevant than anatomical size alone. The defect should be interpreted according to the imprint it leaves on the heart.
AVSD requires a different surveillance strategy. In complete AVSD, initial follow-up is not intended to determine whether surgery will be required, but to identify the safest time for repair before pulmonary overcirculation, common atrioventricular valve regurgitation, or pulmonary vascular disease worsens the patient’s condition. In partial AVSD, valvular regurgitation and chamber dilation may progress more gradually, but they are no less important.
The guidance appropriately places these indicators at the center of clinical decision-making. Qp:Qs can help quantify the shunt, but it should not be interpreted in isolation. Two patients with similar values may exhibit different ventricular responses. Follow-up must therefore assess the interaction between anatomy, flow, pressure, and myocardial adaptation.
The indication for closure does not arise from the defect itself, but from the point at which the heart can no longer compensate for it. The biological cost may become apparent as chamber dilation, heart failure, growth failure, pulmonary hypertension, secondary valvular regurgitation, or reduced exercise tolerance.
The guidance reinforces a principle already embedded in modern practice: the absence of symptoms does not necessarily mean the absence of hemodynamic impact. Children adjust their level of activity to their functional capacity and rarely report limitations spontaneously. Waiting for overt heart failure or a clear decline in growth percentiles may mean that the heart has already been exposed to prolonged overload.
Conversely, mild chamber dilation does not invariably mandate immediate intervention. The decision must consider age, longitudinal trends, the likelihood of spontaneous closure, procedural risk, and the consistency of the findings. A single measurement, particularly from a technically challenging echocardiographic study, should not by itself become a surgical mandate. In this setting, the guidance functions as a safety framework rather than an autopilot system. Its purpose is to identify when the patient’s course is no longer reassuring and should be discussed at a specialized center.
Another strength of the document is its reminder that success does not end in the catheterization laboratory or when the patient is weaned from cardiopulmonary bypass. After closure, follow-up should confirm the absence of a significant residual shunt and assess ventricular function, pulmonary pressures, valvular regurgitation, and, when applicable, device position and integrity.
Reverse remodeling begins early, but its pace varies between patients and lesions. A reduction in ventricular volumes is a favorable sign, although not all parameters normalize simultaneously. Persistent dilation should not automatically be attributed to a residual defect: age at closure, duration of the preoperative overload, and subsequent loading conditions all influence recovery.
Evidence from myocardial strain and ventricular mechanics suggests that functional abnormalities may exist even when EF remains preserved. Nevertheless, these measurements still vary across scanners, software platforms, and laboratories, and there are no widely validated thresholds that would justify using them as isolated triggers for intervention.
For the time being, strain should therefore be regarded as a complementary tool. It may enrich the assessment of remodeling, but it cannot replace clinical evaluation, conventional echocardiography, or multidisciplinary discussion.
The main strength of the guidance—its concision—is also its principal limitation. Algorithms simplify decision-making, but inevitably omit clinical nuance. Many recommended follow-up intervals are based on expert consensus and observational evidence rather than trials designed to compare surveillance strategies. This pediatric guidance should also not be conflated with recommendations for adults with congenital heart disease. Pulmonary vascular resistance thresholds and closure strategies in adults with pulmonary hypertension address a different clinical setting and cannot simply be transferred to a child with an isolated shunt lesion.
The document also excludes PDA in premature infants, whose pathophysiology, associated comorbidities, and therapeutic evidence represent a distinct clinical problem. This is not an accidental omission, but rather an acknowledgment that including this population would have exceeded the intended scope of outpatient guidance for isolated lesions.
Overall, the publication provides a useful and prudent framework. It does not change the rules of the game; it helps ensure that we all play by the same ones.
COMMENTARY:
From a surgeon’s perspective, the most interesting question is not how often a VSD or ASD should be reviewed. The question is whether that frequency allows us to recognize, in time, the point at which continued observation ceases to be harmless.
Pediatric cardiac surgery has advanced to the point that closure of many simple defects can now be performed with low procedural risk. This safety may push us toward two opposing extremes. The first is intervening before sufficient hemodynamic impact has developed, exposing the child to a procedure that may never have been necessary. The second is prolonging follow-up because the patient “is doing well,” while the heart remains exposed to silent volume overload for years.
The guidance attempts to find a balance between these extremes. Its proposal is sound: do not operate on anatomy alone, but on its consequences. The difficulty is that these consequences do not always emerge in a binary fashion. Ventricular remodeling is a continuous process, and the boundary between adaptation and injury remains a line that we cannot yet define precisely.
We can measure diameters, volumes, and Z-scores, estimate Qp:Qs, and assess pulmonary pressures. Nevertheless, we still do not know exactly when apparently compensated dilation begins to consume myocardial reserve. Nor do we know whether certain subclinical strain abnormalities translate into meaningful long-term consequences or fully normalize after closure.
It would therefore be premature to turn myocardial deformation or biomarkers into new surgical “triggers.” However, it would also be a mistake to dismiss them as merely academic findings. Their true value may lie in identifying trajectories. A patient with preserved EF but progressive chamber dilation and reproducible deterioration in strain should probably not be interpreted in the same way as another patient whose parameters remain stable.
In Spain, the main value of this guidance may not lie in changing surgical indications, but in reducing variability in follow-up. We have highly specialized referral centers, high-quality echocardiography, and multidisciplinary discussion involving cardiology, surgery, interventional cardiology, and imaging. However, access to these resources is not identical across regions or levels of care.
The algorithms may provide a common language between institutions. They may also help avoid two frequent practices: maintaining indefinite specialist follow-up for trivial lesions and allowing excessively long intervals between reviews in patients with progressive hemodynamic consequences.
The recommendation to discharge selected insignificant defects is particularly relevant in a health care system with overloaded outpatient clinics. However, this will only be safe if communication with primary care is clear and families receive understandable instructions. Discharge does not mean abandoning follow-up; it means recognizing that surveillance can safely continue outside the Pediatric Cardiology Unit.
At the opposite end of the spectrum, patients with progressive chamber dilation, valvular regurgitation, suspected pulmonary hypertension, or discordance between clinical and echocardiographic findings should be referred early to specialized centers. The usefulness of an algorithm ends where uncertainty begins. In such cases, image review, CMR, cardiac catheterization, or discussion within a congenital Heart Team may prevent both premature intervention and unnecessary delay.
Not every center needs access to advanced strain imaging or artificial intelligence applied to cardiovascular imaging. What is essential is the ability to recognize when conventional data do not adequately explain the patient’s clinical course and when specialist assessment is required.
The future will probably not replace traditional criteria, but refine them. Advanced imaging, strain, biomarkers, and automated analysis of serial echocardiographic studies may help us distinguish more accurately between a heart that remains successfully adapted and one that is beginning to lose reserve.
Nevertheless, no technology will fully resolve the question of optimal timing. Decision-making will continue to require integration of anatomy, physiology, longitudinal progression, technical risk, and the individual clinical context. A guidance document can identify the safest route for most patients, but it cannot anticipate every bend in the road.
The principal virtue of this document is that it reminds us that follow-up is itself a clinical intervention. Excessive surveillance may lead to medicalization. Insufficient surveillance may delay a necessary decision. Successful treatment is not simply a matter of closing a shunt, but of doing so when the expected benefit clearly outweighs both procedural risk and the biological cost of continued observation.
Perhaps this is the question that should remain with us after reading the guidance: not only how large the defect is or how much blood flows through it, but how long that heart can continue to adapt before adaptation ceases to be protective and begins to become harmful.
REFERENCE:
Sachdeva R, Parthiban A, Birnbaum B, Hancock HS, Jayaram NM, Plummer ST, et al. Outpatient Management of Isolated Left-to-Right Shunt Lesions in Pediatric Patients: 2026 ACC Concise Clinical Guidance: A Report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. 2026 Jun 9;87(22):3185-3206. doi: 10.1016/j.jacc.2025.11.020. Epub 2026 Mar 26. PMID: 41885674.
