The original article, titled “The importance of classifying central hypopneas: a call to action,” argued that hypopneas—shallow or reduced breathing events during sleep—should not all be lumped together. Hypopneas can arise through obstructive mechanisms, in which the upper airway narrows or collapses despite ongoing respiratory effort, or through central mechanisms, in which the brain’s drive to breathe transiently wanes. The distinction matters in principle because the two phenomena reflect fundamentally different physiology: one is a mechanical problem of airway patency, the other a problem of neural control of ventilation. Standard polysomnography, however, scores both events under a single apnea-hypopnea index, or AHI, and most clinical practice proceeds as though the difference were inconsequential.

Dr. Kumari’s letter, “Central hypopnea classification: bridging the gap between event identification and clinical utility,” pressed on precisely the point where the call to action was most vulnerable. She noted that the original manuscript proposed no quantitative threshold to guide clinical decision-making and offered no evidence that classifying hypopneas changes disease categorization, treatment response, or patient-centered outcomes. In other words, even if central hypopneas can be identified, no one knows how many of them constitute a meaningful disease burden, and no one has demonstrated that knowing the proportion of central events improves any measurable outcome. These are not pedantic objections; they are the standard demands of evidence-based medicine, and the reply concedes them almost entirely.

Ahn and Malhotra’s response is notable for its candor. They write that research in this area is lacking, that the field has simply not focused on classifying hypopneas, and that very little data exists to understand how hypopnea classification may impact disease categorization and treatment outcomes. The motivation behind the original paper, they explain, was exactly that—to highlight a need to better understand and classify these events. Rather than presenting a finished clinical framework, the authors describe their manuscript as a deliberate act of awareness-raising, intended to provoke research, reflection, and discussion rather than to prescribe thresholds or algorithms.

What gives the argument its urgency is the arrival of mechanistically specific treatments for sleep-disordered breathing. For most of the modern history of the field, the therapeutic arsenal was relatively blunt: continuous positive airway pressure, oral appliances, weight loss, and positional therapy, all aimed primarily at keeping the upper airway open. That era is ending. Pharmacotherapy for obstructive sleep apnea has entered clinical practice, and neurostimulation—whether hypoglossal nerve stimulation for airway control or emerging approaches targeting respiratory drive—offers interventions that act on specific physiological pathways. A drug or a stimulator designed to stabilize airway mechanics may do little for a patient whose events are predominantly central, and vice versa. If treatments are becoming mechanism-specific, the authors argue, then proper classification of hypopneas may be critical to guide interventions while optimizing health outcomes for patients with various conditions.

The reply also makes a broader and arguably more provocative point: sleep medicine cannot even agree on thresholds for the disease it knows best. The authors observe that the field struggles to identify an exact threshold for treating obstructive sleep apnea using the well-established AHI. Treatment decisions are usually based on a combination of AHI, hypoxemia, clinical symptoms, and comorbidities rather than on the index alone. The conventional severity categories—mild, moderate, and severe, corresponding to cutoffs of fewer than 5, 5 to 15, 15 to 30, and more than 30 events per hour—are explicitly described as arbitrary or consensus-based rather than biological. There is no physiological discontinuity at 15 events per hour that justifies calling one patient’s disease moderate and another’s severe; the boundaries exist because committees drew them.

The limitations of the AHI run deeper than arbitrary cutoffs. As the authors note, AHI is a poor predictor of OSA complications in general, and a clinically important improvement in AHI is challenging to define. A patient whose event count drops from 30 to 15 per hour has halved their index, but whether that change translates into reduced cardiovascular risk, improved cognition, better daytime function, or longer life is far from clear. This weakness has driven interest in alternative metrics, including the sleep apnea–specific hypoxic burden, or SASHB, a measure that quantifies the cumulative oxygen desaturation a patient experiences rather than simply counting discrete events. The authors report that SASHB may do a better job at predicting mortality and cardiovascular disease than AHI, though they immediately temper that promise: minimal data are available to establish SASHB as a validated surrogate measure. The lesson they draw is that the optimum metrics for studies in sleep-disordered breathing likely vary with the outcome of interest, and that treatment decisions are often guided, in part, by patient preferences.

This framing reframes Kumari’s critique in an instructive way. Her demand for validated thresholds and outcome data is exactly right by the standards of clinical science, but applying that standard uniquely to central hypopnea classification would hold the new question to a bar the rest of the field has never cleared. The AHI itself, the foundation of sleep medicine for decades, rests on consensus cutoffs with weak predictive power for the complications it is supposed to forecast. If the field waits for perfect validation before distinguishing central from obstructive hypopneas, it may repeat the pattern of the AHI: adopting a metric on convention, using it for decades, and only later discovering its predictive limitations. The authors’ implicit argument is that the time to start generating outcome data on hypopnea classification is now, before mechanistically specific treatments make the question unavoidable.

The scientific process, as the reply acknowledges, will take time. Building the evidence base requires studies that score hypopneas by mechanism, track patients with different central-versus-obstructive event proportions, and measure whether classification changes disease categorization, treatment selection, or patient-centered outcomes such as symptoms, quality of life, and cardiovascular risk. It requires agreement on how to identify central hypopneas reliably in the first place, since scoring rules for hypopneas have historically been contentious even before mechanism is considered. And it requires the kind of broad multidisciplinary consensus that the original call to action assembled, with authors spanning multiple institutions and subspecialties. Ahn and Malhotra report that there was broad agreement among the authors of their manuscript that investigation into hypopnea classification and how it changes management is important to pursue, and they credit Dr. Kumari with helping raise awareness of these proposed next steps.

What emerges from the exchange is a rare public acknowledgment of how much foundational work remains in a mature field. Sleep medicine can detect breathing events with exquisite precision, stage sleep across multiple physiological channels, and generate indices to many decimal places—yet the meaning of those numbers, and the boundaries of the disease they describe, rest on conventions that were never biologically derived. The central hypopnea debate is a microcosm of that larger condition. As pharmacological and neurostimulation therapies multiply, the pressure to match patients to mechanisms will only intensify, and the field will need thresholds, surrogate markers, and outcome data that currently do not exist. The reply’s authors do not pretend otherwise. Their contribution is to insist, in print and with unusual candor, that the gap between identifying an event and knowing what to do about it is the most important problem sleep medicine is not yet studying—and that filling it will take the kind of patient, unglamorous research that begins with a call to action and ends, years later, with evidence.

Subject of Research: Classification of central hypopneas in sleep-disordered breathing and its clinical utility

Article Title: Reply to “Central hypopnea classification: bridging the gap between event identification and clinical utility”

Article References: Reply to “Central hypopnea classification: bridging the gap between event identification and clinical utility”. (n.d.). https://doi.org/10.1007/s44470-026-00211-7

Image Credits: AI Generated

DOI: 10.1007/s44470-026-00211-7

Keywords: central hypopnea, sleep apnea, apnea-hypopnea index, polysomnography, sleep-disordered breathing, hypoxic burden, neurostimulation, pharmacotherapy, obstructive sleep apnea, clinical thresholds, outcomes research, sleep medicine