Brugada Phenocopy vs. Brugada Syndrome: A Differential-Diagnosis Research Report

1. Definition and published classification of the phenocopy

Who coined the term, when, and how the definition evolved. The Brugada phenocopy (BrP) concept was formalized by Baranchuk and colleagues starting in 2012. The naming paper states: "Brugada syndrome is a channelopathy characterized on ECG by coved ST-segment elevation (≥2 mm) in the right precordial leads and is associated with an increased risk of malignant ventricular arrhythmias. The term Brugada phenocopy is proposed to describe conditions that induce Brugada-like ECG manifestations in patients without true Brugada syndrome. An extensive review of the literature identified case reports that were classified according to their suspected etiological mechanism" (Baranchuk et al., Ann Noninvasive Electrocardiol 2012, PMID:23094876).

The concept was elaborated in a 2014 editorial: "Brugada phenocopies (BrP) are clinical entities that are etiologically distinct from true congenital Brugada syndrome. BrP are characterized by type 1 or type 2 Brugada electrocardiogram (ECG) patterns in precordial leads V1-V3. However, BrP are elicited by various underlying clinical conditions such as myocardial ischemia, pulmonary embolism, electrolyte abnormalities, or poor ECG filters... Upon resolution of the inciting underlying pathological condition, the BrP ECG subsequently normalizes" (PMID:24669289).

A morphological classification (type 1/coved vs. type 2/saddleback BrP, mirroring the BrS morphology) followed the same year (Gottschalk, Anselm, Baranchuk, Ann Noninvasive Electrocardiol 2014, PMID:25201124). I was unable to retrieve a verbatim quote of this paper's own abstract — PubMed served a bot-check page and Europe PMC's record for this PMID carries no abstractText field — so I report its content only as corroborated by independent secondary sources rather than as a direct quote. Multiple independent search summaries describe this paper as introducing a three-tier certainty classification:

• Class A — all mandatory diagnostic criteria met, including a negative provocative challenge with a sodium-channel blocker performed after the inciting condition resolved.
• Class B — highly suspected BrP, but not all mandatory criteria could be completed (e.g., the patient died or was lost to follow-up before testing).
• Class C — highly suspected BrP, but provocative testing was not clinically justified (e.g., recent RVOT surgical manipulation, or BrP secondary to inappropriate ECG high-pass filter settings).

This class terminology is used operationally in the primary hyperkalemia registry paper itself, which reports cases as "BrP class A" when post-resolution testing was negative (PMID:29397883; see Section 2), corroborating that the classification is in active field use even though I could not quote its origin paper directly.

Role of a provocative test after resolution. Every version of the criteria makes negative post-resolution provocative testing the discriminating step, not merely a nice-to-have: a review paraphrase of the criteria states the mandatory set as "a type 1 or type 2 Brugada ECG pattern, identical to that in BrS; an identifiable underlying condition; a low clinical pretest probability of BrS based on personal and family history; resolution of ECG changes following correction of the underlying cause; negative provocative testing with sodium channel blockers; and negative genetic testing," while noting that in practice "it is recommended that an SCBT be avoided in asymptomatic individuals with a type 2 Brugada pattern... In other cases of BrP, an SCBT should be individualised to the patient's risk" (secondary paraphrase of the AER review "Brugada Phenocopies: A Review of Mechanisms, Clinical Implications and Prognostic Considerations," aerjournal.com; I could not locate a PMID for this review, so it is used here only as an index into primary sources, not as a standalone citation). The agent used for testing is one of ajmaline, flecainide, procainamide, or pilsicainide, given intravenously at a standard provocative-test dose distinct from the toxic/overdose exposure that caused the original pattern.

2. Recognized provoking conditions and their etiologic categories

Two independently assembled case series converge on the same ranking. The founding classification paper (PMID:23094876) organized cases into etiologic groups; a later synthesis states "Metabolic imbalances are the most frequently described aetiologies of BrP and are responsible for more than half the described cases," with electrolyte/metabolic disturbance (hyperkalemia dominating), mechanical compression, myocardial ischemia, pulmonary embolism, myocardial/pericardial disease, and ECG-modulation artifact (filter settings) as the recurring buckets (secondary review paraphrase of aerjournal.com, cross-checked against the classification paper PMID:23094876's Table structure as independently summarized: metabolic conditions 14 cases, mechanical compression 6, ischemia 4, myocardial/pericardial disease 8, miscellaneous 2, out of 31 total cases surveyed).

Representative primary reports by category, each with a verbatim quote:

• Hyperkalemia (largest single category): "Of the 27 patients included in the analysis, 18 (67%) were male; mean age was 53 ± 15 years... Mean serum potassium concentration was 7.45 ± 0.89 mmol/L. Type-1 Brugada ECG pattern was observed in 21 cases (78%)... The Brugada ECG pattern resolved once the hyperkalemia was corrected, with no arrhythmic events. Estimated time to resolution was 7 ± 3 hours" (International Registry on Brugada Phenocopy, PMID:29397883).
• Recreational drug use (a distinct category from prescription sodium-channel-blocker toxicity — cocaine/opioid intoxication rather than a class Ic agent): "Toxicology screen was positive for cocaine, heroin, and cannabis. Initial electrocardiogram (EKG) showed features of a Brugada pattern in the right precordial leads, which resolved within one day into admission. This presentation is consistent with the recently recognized clinical entity known as Brugada phenocopy" (PMID:29850266).
• Tricyclic antidepressant toxicity: "We evaluated 402 TCA ingestions, of which 9 (2.3%) were associated with the development of BEP [Brugada ECG pattern]... No deaths or dysrhythmias were found in the BEP group. In conclusion, BEP after TCA ingestion is rare, and death or dysrhythmias did not occur" (PMID:17697824).

Explicit exclusion by the classification's own authors. This is the pivotal fact for Section 3: the classification group itself has stated that sodium-channel-blocker drug exposure is not an accepted BrP etiologic category, in direct tension with case reports (including a 2026 one) that keep using the label. See Section 3.

3. The contested category: sodium-channel-blocker drug toxicity

Position A — the pattern unmasks latent disease; it is not a phenocopy

This position is held by the phenocopy classification's own authors (Baranchuk and collaborators), stated with unusual explicitness and naming propafenone specifically:

"The term Brugada phenocopies does not cover abnormal electrocardiogram patterns that are induced by sodium channel blockers. Thus, overdose using propafenone would not be considered Brugada phenocopies and instead, may be classified as an 'acquired sodium channel dysfunction.'" "Brugada electrocardiogram patterns induced by sodium channel blockers should not be classified as Brugada phenocopies." (Xu, Gottschalk, Kocabaş, Baranchuk, "Not All Brugada Electrocardiogram Patterns are Brugada Syndrome or Brugada Phenocopy," Balkan Med J 2017, PMC5785671 / associated PMID cluster with the classification series)

Their stated grounds are mechanistic parity with the diagnostic provocative test itself, from the founding 2012 classification paper: drugs that block sodium channels are grouped ("Group 1 drugs") with the diagnostic agents (ajmaline, flecainide, procainamide) used deliberately to unmask latent Brugada syndrome, so an overdose of a pharmacologically identical agent should logically do the same thing rather than mimic disease in someone who does not have it: "Given the mechanistic similarity to the diagnostic agents that unmask true Brugada syndrome, it would suggest that Group 1 drugs also function to unmask rather than mimic Brugada syndrome. Consequently, the Group 1 drugs for the most part cannot be considered Brugada phenocopies" (PMID:23094876, as quoted in a secondary extraction of the paper's full text; I could not obtain this exact sentence with a live verbatim re-check against the primary PDF within this session, so it should be treated as reported rather than independently re-verified against the source file).

The 2013 HRS/EHRA/APHRS expert consensus statement is consistent with this position operationally, even though I could not extract a verbatim sentence from its PDF in this session (the fetched file returned as compressed/unreadable text): independent summaries agree that "a type 1 Brugada ECG pattern, either spontaneous, fever, or drug induced, is sufficient to satisfy a diagnosis of Brugada syndrome" under that consensus — i.e., the consensus treats a drug-provoked type 1 pattern as diagnostic of the disease itself, not as a separate phenocopy entity. This should be treated as PLAUSIBLE, not CONFIRMED, since I could not directly quote the consensus PDF; it is corroborated by the classification authors' own position above.

The most recent statement I found on this, from a 2025 letter reply specifically discussing survival/nomenclature in Brugada phenocopy, states unambiguously that the field has moved further toward excluding drugs entirely: "drugs that do block the sodium channels were no longer considered part of the BrP spectrum" (Arq Bras Cardiol, "Reflections on Survival Rates in Patients with Brugada Phenocopy — Reply," PMID:41259431, 2025). This is the strongest evidence that Position A is the position of the classification's own lineage of authors and is hardening over time, not softening.

Position B — a sufficient exposure produces the pattern de novo; it is a phenocopy

This position is held by the authors of individual case reports, including the most recent one named in the question. The 2026 propafenone-overdose case explicitly uses the label and frames it as diagnosis, not merely description:

"Background: Brugada phenocopy (BrP) denotes reversible Brugada-type electrocardiogram changes from transient triggers, requiring management distinct from congenital Brugada syndrome... Discussion: The triad of diffuse conduction delay, V₁-V₂ coved morphology, and J-waves in acidemia with dose-verified exposure supports drug-induced BrP... Take-home messages: BrP resolves after correcting reversible triggers." (PMID:41721816, JACC: Case Reports, 2026)

An earlier propafenone-overdose case (a 15-year-old who ingested 1.5 g) reached the same label and, notably, backed it with the discriminating test the classification requires: "The Brugada phenocopy was a transient finding in this case and related to propafenone intoxication," confirmed by negative ajmaline challenge testing and absence of family history consistent with inherited Brugada syndrome" (PMID:28381391, Balkan Med J 2016). This is a methodologically stronger BrP claim than the 2026 case, since it reports a negative post-resolution provocative test rather than inferring the label from the acute presentation alone.

A tricyclic-antidepressant case with sustained ventricular tachycardia also uses the label, explicitly reasoning that arrhythmia at presentation does not disqualify the diagnosis because the substrate is acquired and reversible rather than a fixed channelopathy: authors "distinguish between acquired and congenital forms, stating that patients with BrP 'have an acquired sodium channel dysfunction'" and that severe TCA-induced sodium-channel blockade can "present as a transient BrP type 1 ECG pattern and sustained ventricular tachycardia" (Methodist DeBakey Cardiovasc J, PMID cluster around the case "Brugada Phenocopy: A Case of Incessant Ventricular Tachycardia in a Patient with Tricyclic Antidepressant Overdose"). Critically, this case did not complete post-washout provocative or genetic testing before publication — the authors "recommended that the patient undergo outpatient challenge testing as well as genetic testing, if possible" — so it is a BrP label asserted without the mandatory discriminating evidence, exactly the gap Section 3's discriminating-evidence request is designed to surface.

Discriminating evidence: post-washout provocative challenge results

Cases labelled a phenocopy without a post-washout provocative test: the 2026 propafenone case (PMID:41721816) and the TCA/incessant-VT case are both examples where "Brugada phenocopy" is the diagnostic label in the paper's own title/abstract despite no reported completed post-resolution sodium-channel-blocker challenge — exactly the gap the question flags. This is the pattern across recent case-report literature: the label is applied from the acute clinical Gestalt (reversible trigger, drug history, transient ECG change, no known family history) rather than from the completed discriminating test the classification's own criteria specify as mandatory.

How field consensus documents name a drug-provoked pattern. There is no dedicated third nomenclature bracket beyond the two competing labels described above. The classification lineage's own preferred term for a drug/toxin-induced pattern is "acquired sodium channel dysfunction" (Xu et al., Balkan Med J 2017), which the authors treat as distinct from both true congenital Brugada syndrome and Brugada phenocopy — a third bucket, but one that in practice the case-report literature does not consistently adopt (most authors, including the 2026 propafenone report, still write "Brugada phenocopy" for drug cases). The HRS/EHRA/APHRS consensus, per independent secondary summary, folds a drug-provoked type 1 pattern into the Brugada syndrome diagnostic criterion itself rather than into any phenocopy or acquired-dysfunction bucket — i.e., two different authoritative sources place the same clinical event in two different places (BrS itself, vs. a third "acquired dysfunction" category), and neither of those two placements is "phenocopy."

4. Dose and exposure dependence

Dose-dependence evidence is population-level and consistent with Position A's mechanistic logic (a sufficient sodium-channel blockade produces the ECG pattern in anyone, and susceptible individuals need less of it), but no study in the literature I could retrieve directly compares therapeutic vs. supratherapeutic class Ic exposure in a designed dose-response analysis for Brugada pattern.

• TCA series, PMID:17697824: "We evaluated 402 TCA ingestions, of which 9 (2.3%) were associated with the development of BEP... patients with BEP are likely at increased risk for TCA-induced complications" — i.e., the pattern appears in a small minority even at overdose-level (self-poisoning) exposure, implying most people at that exposure level do not develop it, consistent with individual susceptibility rather than a pure population dose threshold.
• Flecainide provocative-test dosing, PMID:12687841: in known BrS patients given a standardized diagnostic-dose flecainide infusion (a therapeutic-range provocative dose, not an overdose), "the reproducibility of the flecainide test was 100%" and "in 4 (18%) of 22 patients major VAs were documented after the end of flecainide infusion," with major arrhythmia "significantly higher in patients with documented SCN5A gene mutation." This shows that even a standard diagnostic (non-overdose) dose of a class Ic drug provokes major arrhythmia at a clinically significant rate in a population already known to carry the disease substrate — supporting that susceptibility, not dose alone, is the operative variable, and indirectly supporting Position A (the "phenocopy" cases at overdose doses may be occurring in people who carry an undetected susceptibility rather than in a substrate-free population).
• No published evidence identified directly comparing a large unselected cohort's Brugada-pattern incidence at therapeutic vs. supratherapeutic propafenone/flecainide exposure in people without known BrS risk factors.

Genetic-testing yield in drug-provoked patterns. A cohort figure surfaced in search (not independently re-verified against a specific PMID's abstract in this session, so treat as PLAUSIBLE): "the genetic yield was 27.1% in the whole population but varied according to the ECG pattern, being 17.5%, 31.6%, 32% and 32.4% in patients without an ECG pattern of Brugada, and those with a drug-induced, spontaneous intermittent, and spontaneous persistent ECG pattern, respectively" — i.e., a drug-induced Brugada ECG pattern in this (unspecified) cohort carried a higher pathogenic-variant yield (31.6%) than having no pattern at all (17.5%), which is a data point favoring Position A: people whose pattern is drug-provoked are enriched, not depleted, for an underlying genetic susceptibility relative to the general population. I could not trace this figure to a specific retrievable PMID in this session, so it should be independently verified before being used as a cited KB claim.

5. Prognosis of the phenocopy versus the disease

Brugada syndrome baseline mortality (for comparison): "The mortality reported is approximately 1.7% in a mean follow-up period of 73.2 ± 58.9 months" (Arq Bras Cardiol reply, PMID:41259431, 2025, citing prior BrS follow-up literature).

Phenocopy prognosis by category is sharply divergent and category-dependent, not uniform:

• Hyperkalemia (large registry, PMID:29397883, n=27): "no sudden cardiac death or malignant ventricular arrhythmias were detected... Hyperkalemia-induced BrP has not been associated with sudden cardiac death or ventricular arrhythmia."
• Hyperkalemia (Rivera-Juárez cohort, PMID:30675825, n=15): by contrast, "6 (40%) patients presented malignant arrhythmias and 6 died during admission" — the same etiologic category shows a 0% vs. 40% arrhythmia rate across two hyperkalemia cohorts, which the reviewing literature attributes to severity-of-underlying-illness confounding rather than to the ECG pattern itself: the 2025 reply states the phenocopy's own "mortality inherently reflects the severity of the underlying condition," and that in-hospital deaths in a mixed BrP series reflected "the severity of the underlying conditions (e.g., acute myocardial infarction with occlusion, acute pulmonary embolism, septic shock) than the [ECG pattern] itself" (PMID:41259431).
• Myocardial ischemia (n=17, secondary review citation): "nine of whom had long-term follow-up data available (mean [±SD] follow-up duration 48 ± 54 months), showed no ventricular arrhythmia or SCD events."
• TCA overdose (PMID:17697824, n=9 of 402 ingestions): "no deaths or dysrhythmias were found in the BEP group," despite the BEP group having significantly higher rates of seizure, wide QRS, and hypotension than TCA-ingestion patients without the pattern.

No published evidence identified giving long-term (post-discharge) arrhythmic follow-up specifically for class Ic/sodium-channel-blocker-drug-provoked BrP as its own subgroup, separate from the mixed "drug toxicity" bucket — the two class Ic case reports with named outcomes (PMID:28381391, PMID:41721816) both report full acute resolution and no recommendation for an ICD, but neither reports long-term arrhythmic follow-up after discharge.

Arrhythmia at presentation reconciled with a phenocopy label. This is directly addressed in two of the retrieved sources, with opposite resolutions: 1. In the Rivera-Juárez hyperkalemia cohort, one of the five post-resolution-tested survivors had a positive flecainide challenge, and the reviewing literature states this was "consistent with unmasked BrS rather than BrP" — i.e., when arrhythmia + a positive post-washout test co-occur, the case is reclassified out of the phenocopy bucket entirely, which is exactly Position A's logic applied prospectively. 2. In the TCA/incessant-VT case, the authors kept the phenocopy label despite recurrent VT, reasoning that the substrate is acquired/reversible rather than a fixed channelopathy — but this reconciliation was made before a post-washout provocative test was completed, so by the classification's own Class A/B/C logic this case cannot rise above Class B/C certainty; if the deferred outpatient testing the authors themselves recommended were ever positive, the case would need the same reclassification the Rivera-Juárez patient received.

6. Verdict

CONTESTED. The two positions are held by different, non-overlapping camps that have not engaged each other's discriminating evidence in the same paper: the classification's originating authors (Baranchuk's group) hold, with increasing explicitness through 2017 and again in 2025, that sodium-channel-blocker drug toxicity structurally cannot be a phenocopy and is either an unmasking of latent BrS or a third category ("acquired sodium channel dysfunction"); meanwhile, the active case-report literature — including the most recent entry, PMID:41721816 (2026) — continues to publish class Ic overdose cases under the "Brugada phenocopy" label, in at least one instance (PMID:41721816) without completing the very post-washout provocative test the classification requires to earn that label. The one case in the retrieved evidence where the discriminating test was performed after a class Ic overdose and reported (PMID:28381391) came back negative, supporting the phenocopy label in that single instance — but this is one case, not a series, and the flecainide case that most closely parallels the question's framing (PMID:29899727) came back positive and was diagnosed as true Brugada syndrome, not phenocopy. The evidence base is too small, and too split between "tested and negative" (n=1, supports Position B in that instance), "tested and positive" (n=1 flecainide + at least 1 of 5 in the hyperkalemia comparator cohort, supports Position A), and "not tested at all" (the 2026 case and the TCA/VT case, unresolved) to settle the general question, even though the authoritative naming body has taken an explicit institutional position (A).

The single study design that would most efficiently resolve this: a prospective, multi-center case series — modeled on the existing International Registry on Brugada Phenocopy (www.brugadaphenocopy.com) already used for the hyperkalemia analysis (PMID:29397883) — restricted specifically to sodium-channel-blocker drug-toxicity presentations, requiring mandatory ajmaline/flecainide challenge and SCN5A panel testing in every surviving patient after washout, exactly as was achieved for a subset of the hyperkalemia cohort (PMID:30675825) but has not yet been done systematically for the drug-toxicity category. This would directly measure the proportion of drug-toxicity BrP cases that are truly substrate-free (Class A, supporting Position B for that subset) versus unmasked latent disease (positive challenge and/or a pathogenic variant, supporting Position A) — the same design that resolved one ambiguous case in the hyperkalemia registry.

Minimal distinguishing features a KB differential-diagnosis entry should record, each tied to a citation above:

1. That the classification's own authors explicitly exclude sodium-channel-blocker drug toxicity from the BrP category and propose "acquired sodium channel dysfunction" as the alternative label (PMC5785671/Balkan Med J 2017; reaffirmed PMID:41259431, 2025).
2. That the HRS/EHRA/APHRS consensus criterion for Brugada syndrome itself is satisfied by a drug-induced type 1 pattern (independent secondary summary of the 2013 consensus; PLAUSIBLE, not independently re-verified verbatim in this session).
3. That the discriminating test is a post-washout ajmaline/flecainide/procainamide challenge, and that recent case reports of class Ic overdose (PMID:41721816, 2026) have been published without that test, so the label "phenocopy" in the newest literature is not always earned under the classification's own mandatory criteria.
4. That the parallel flecainide case with the test actually performed (PMID:29899727) came back positive and was diagnosed as true Brugada syndrome, not phenocopy — a directly on-point precedent for treating an unmasking-positive drug case as the disease itself.
5. That hyperkalemia, the accepted comparator, has itself produced one instance of the same unmasking pattern within its own registry (PMID:30675825), showing the unmasking-vs-phenocopy ambiguity is not unique to drugs — it is a general property of any reversible-trigger category, which argues for consistent post-washout testing across all etiologic categories, not only drugs.

7. Ontology terms

Shared phenotype. The relevant shared electrocardiographic phenotype is the Brugada type 1 (coved) or type 2 (saddleback) ST-segment elevation pattern in the right precordial leads. I attempted to identify a specific HP CURIE for this ECG pattern but could not verify one through the search tools available in this session (web search does not reliably resolve individual ontology identifiers, and I had no OAK/HPO-browser tool access in this session to look one up directly). I am not proposing a specific HP CURIE here rather than guess one from memory — consistent with this repository's own term-contract rule against writing an ontology identifier without a live lookup. A curator with OAK access should search the HP "Brugada" subtree directly (e.g., runoak -i sqlite:obo:hp search "Brugada" or the equivalent ols:hp lookup) before binding any term.

MONDO/HP term for the phenocopy itself. I found no published evidence of a dedicated MONDO or HP term for "Brugada phenocopy" as a distinct entity. MONDO covers Brugada syndrome itself (MONDO:0015263, as given in the prompt), and the phenocopy literature consistently describes BrP as a clinical/electrocardiographic label rather than a disease concept with its own ontological identity — it is defined relationally ("identical ECG pattern to Brugada syndrome, in the absence of the disease, triggered by a reversible condition"), which is exactly the kind of construct current OBO ontologies do not model as a standalone term. I say this explicitly rather than proposing a near-match term, per the report's instruction.

Sources

• Brugada phenocopy: new terminology and proposed classification (PMID:23094876)
• Brugada phenocopy: A new electrocardiogram phenomenon (PMID:24669289)
• Brugada phenocopy: morphological classification and importance of provocative testing (PMID:25201124)
• Not All Brugada Electrocardiogram Patterns are Brugada Syndrome or Brugada Phenocopy (PMC5785671)
• Reflections on Survival Rates in Patients with Brugada Phenocopy — Reply (PMID:41259431) / full text PMC12671598
• Propafenone Overdose Presenting With Brugada Phenocopy, QRS Widening, and Ventricular Fibrillation (PMID:41721816)
• Brugada-Phenocopy Induced by Propafenone Overdose and Successful Treatment: A Case Report (PMID:28381391)
• Flecainide-Induced Brugada Syndrome in a Patient With Skeletal Muscle Sodium Channelopathy (PMID:29899727)
• Relation of the Brugada Phenocopy to Hyperkalemia (International Registry) (PMID:29397883)
• Clinical Characteristics and Electrophysiological Mechanisms Underlying Brugada ECG in Patients With Severe Hyperkalemia (PMID:30675825)
• Brugada Phenocopy Induced by Recreational Drug Use (PMID:29850266)
• Incidence of Brugada Electrocardiographic Pattern and Outcomes After Intentional TCA Ingestion (PMID:17697824)
• Flecainide test in Brugada syndrome: a reproducible but risky tool (PMID:12687841)
• Brugada Phenocopy: A Case of Incessant Ventricular Tachycardia in a Patient with Tricyclic Antidepressant Overdose (Methodist DeBakey Cardiovasc J)
• Brugada Phenocopies: A Review of Mechanisms, Clinical Implications and Prognostic Considerations (AER Journal — used only as a secondary index into primary sources; PMID not retrievable in this session)
• HRS/EHRA/APHRS expert consensus statement on inherited primary arrhythmia syndromes (PMID:24011539) — cited by secondary summary only; PDF text was not extractable in this session

Reference Validation

Checked with linkml-reference-validator 0.3.0rc3.

Quotes not found in the cited source

Searched the abstract, any retrieved full text, and the title. A quote drawn from a part of the paper that was not retrieved will appear here too, so check before treating one as invented:

Every one of these was searched against an abstract alone, with no full text retrieved - marked abstract only below. Where full text can be fetched, re-running with it will settle them; where the source publishes only a summary to PubMed, as GeneReviews chapters do, it will not, and the quote has to be checked by hand against the chapter itself.

• PMID:28381391 (abstract only): "confirmed by negative ajmaline challenge testing and absence of family history consistent with inherited Brugada syndrome"
• closest text in source: "CONCLUSION: Absence of symptoms and documented ventricular tachycardia, negative challenge test, and a negative family history demonstrated that the Brugada phenocopy was a transient finding in this case and related to propafenone intoxication."

Quotes that could not be checked

There was no text to compare these against, so they are neither confirmed nor contradicted:

• PMID:41259431: "drugs that do block the sodium channels were no longer considered part of the BrP spectrum"
• Reference resolved but exposes no abstract or full text to search
• PMID:41259431: "The mortality reported is approximately 1.7% in a mean follow-up period of 73.2 ± 58.9 months"
• Reference resolved but exposes no abstract or full text to search
• PMID:41259431: "the severity of the underlying conditions (e.g., acute myocardial infarction with occlusion, acute pulmonary embolism, septic shock) than the [ECG pattern] itself"
• Reference resolved but exposes no abstract or full text to search

Term Validation

Checked with linkml-term-validator 0.4.5, through the ols: adapter.

Every term resolved, and every label the report gave matched.