Troponin elevation in supraventricular tachycardia: A narrative review

Table 1 Assay-specific 99^th percentile cut-offs, delta thresholds, and universal definition of myocardial infarction classification criteria for high-sensitivity cardiac troponin

Category	Details
Universal definition of myocardial infarction categories	Acute myocardial injury: Hs-cTn ≥ 99th percentile + significant rise/fall. Chronic myocardial injury: Persistent elevation without dynamic change. Type 1 MI: Acute injury + ischemia evidence due to coronary thrombosis/plaque rupture. Type 2 MI: Acute injury + imbalance in supply-demand (e.g., tachyarrhythmia, hypotension) with supportive clinical/electrocardiogram/echo evidence
99th percentile cut-offs (assay-specific examples)1	Roche hs-cTnT (gen 5): 14 ng/L (general); some United States reports: 14 ng/L women, 22 ng/L men. Abbott hs-cTnI: 17 ng/L (women), 35 ng/L (men). Siemens hs-cTnI: Approximately 18 ng/L (women), approximately 27 ng/L (men)
Delta thresholds (European Society of Cardiology 0/1 hour and 0/2 hours algorithms; assay-specific)1	Roche hs-cTnT 0/1 hour: Rule-out: < 5 ng/L or < 12 ng/L with Δ < 3 ng/L; rule-in: ≥ 52 ng/L or Δ ≥ 5 ng/L. Roche hs-cTnT 0/2 hours: Rule-out: Δ ≤ 3 ng/L below 99th percentile; rule-in: Δ ≥ 10 ng/L. Abbott hs-cTnI 0/1 hour (examples): Rule-out: Baseline < 4 ng/L + Δ < 2 ng/L; rule-in: ≥ approximately 64 ng/L or Δ ≥ approximately 6 ng/L. Abbott hs-cTnI 0/2 hours: Rule-out Δ < 2 ng/L; rule-in Δ ≥ 15 ng/L

¹Values are derived from the 2023 European Society of Cardiology Guidelines for the management of acute coronary syndromes and corresponding assay manufacturer data. Thresholds are assay-specific and may vary by platform; institutions should apply values validated for their own laboratory.

Thresholds and algorithms are assay-specific; institutions should apply values validated for their laboratory platform. European Society of Cardiology 2023 guidelines endorse 0/1 hour and 0/2 hours strategies as class I recommendations. hs-cTn: High-sensitivity cardiac troponin; MI: Myocardial infarction.

Table 2 Summary of published studies evaluating the prognostic significance of troponin elevation in patients presenting with supraventricular tachycardia

Ref.	Country/setting	Study design	Number (analyzed)	Population and SVT subtype(s)	Troponin assay and cut-off	Sampling timing	Prevalence of elevated troponin (%)	Outcomes and follow-up	Main result (direction)	Effect size	Adjusted covariates	Risk of bias	Key limitations/notes
Aletras et al[5], 2025	Greece, Venizelio General Hospital of Heraklion	Retrospective, single-center observational study	120	Adults ≥ 18 years, PSVT (AVNRT, AVRT, AT); excluded AFL/AF and structural heart disease	Siemens hs-cTnI, > 99th percentile (sex-specific; 53.5 pg/mL men, 38.6 pg/mL women)	ED presentation; repeat at 3 hours in 80%	48.3%	1-year SVT recurrence, rehospitalization, ablation, mortality	Troponin elevation common but not prognostic; independent predictors were chest pain, absence of prior SVT, higher HR, lower SBP	HR cut-off 165 bpm predicted conventional cardiac troponin + (area under the curve = 0.697, sensitivity = 62%, specificity = 73%); CAD found in only 4%	Multivariable logistic regression (HR, SBP, prior SVT, chest pain)	Moderate (retrospective, single-center, limited generalizability)	No routine advanced imaging; incomplete CAD evaluation; predominantly female cohort; retrospective data collection
Camp et al[29], 2025	United States, TriNetX database	Retrospective, propensity-matched cohort	62582 (31k vs 31k)	ED, first-time SVT (International Classification of Diseases, 10th Revision I47.1)	Mixed assays, within 24 hours	ED arrival	21.6%	30-day MACE (MI, heart failure, stroke, death)	Increased 30-day MACE in troponin + group	Risk difference = 11.1%, P < 0.001	Age, sex, comorbidities	Moderate	Confounding by indication, registry data
Laursen et al[16], 2025	Denmark, national registry	Retrospective registry cohort	1203	De novo PSVT, no cardiovascular disease	High-sensitivity troponin T (roche ≥ 14 ng/L)	First 24 hours hospitals	65.8%	30-day and 1-year mortality; composite CV events	Increased 30-day mortality only	HR significant at 30 days; NS at 1 year	Age, comorbidities, laboratories	Low-moderate	No electrocardiogram data, registry limits
Chen et al[30], 2023	Taiwan, 4 hospitals	Retrospective, multicenter	124	Elderly ≥ 65, SVT (exclude AFL/AF)	The cTnI (Beckman ≥ 0.04)	ED, peak	31.5%	5-year MACE and recurrence	No prognostic effect; CAD history predicted	CAD is transformed into MACE HR = 4.30, P = 0.01	Age, smoking, prior SVT	Moderate	Small, Asian elderly pop, conventional assay
Noorvash et al[31], 2018	United States, Texas academic ED	Retrospective chart review	46	Adults with SVT, HEART 1-6	The cTnI > 0.05 ng/mL	ED	Some positive	Admissions, 3-months MACE	Increased admissions, no MACE impact	Admissions 86% vs 21%, P = 0.006	HEART score	High risk	Tiny cohort, resource utilization focus
Ghersin et al[20], 2020	Israel, Rambam Medical Center	Retrospective, single center	165 (131 with cTnI)	Acute PSVT episodes	The cTnI > 0.028 ng/dL	ED admission	43%	23 ± 7 months follow-up, composite death/MI/percutaneous coronary intervention	Adverse outcomes only if CAD present	HR = 3.3, P = 0.05 (CAD subgroup)	HR > 150, CAD	Moderate	Limited sample, few events
Carlberg et al[32], 2011	United States (Virginia ED)	Retrospective chart review	51	Adults with PSVT	The cTnI, Abbott, cut-off 0.02 ng/dL	ED	29%	30-day outcomes	No prognostic effect; 2 non-ST-elevation MI identified	Descriptive	None	Moderate	Small, variable sampling
Wang et al[21], 2022	Taiwan, 5 hospitals (dialysis)	Multicenter retrospective	62	Adult ESKD on dialysis with SVT	The cTnI Beckman ≥ 0.04	ED	82.5%	3-year and 6-week MACE	No prognostic value; CAD predicted MACE	HR CAD 2.73 (1.01–7.41)	Hypertension, LVEF	Moderate	ESKD-specific, high baseline risk
Chow et al[9], 2010	United States (Johns Hopkins)	Retrospective cohort	78	Hospitalized SVT (AVNRT/AVRT/AT)	The cTnI Beckman ≥ 0.06	0.5-8 hours after SVT	37%	≥ 1 year, death/MI/CV rehospitalization	Troponin + predicted adverse outcomes	HR = 3.67 (1.22-11.1), P = 0.02	Peak HR, LVEF	Moderate	Retrospective, limited centers
Bukkapatnam et al[33], 2010	United States (University of California Davis)	Retrospective cohort	104 (80 tested)	Adults with SVT, ED	The cTnI > 0.07 ng/mL	ED	48%	CAD by testing	Troponin elevation not linked to CAD	NS	CAD risk factors	Moderate	Referral bias, CAD not prognosis

The table outlines study design, population, troponin assay, prevalence of elevation, and reported associations with outcomes. AFL/AF: Atrial fibrillation/flutter; AT: Atrial tachycardia; AVNRT: Atrioventricular nodal reentrant tachycardia; AVRT: Atrioventricular reentrant tachycardia; CAD: Coronary artery disease; cTnI: Conventional cardiac troponin I; CV: Cardiovascular; ED: Emergency department; ESKD: End-stage kidney disease; HR: Heart rate; HR: Hazard ratio; LVEF: Left ventricular ejection fraction; MACE: Major adverse cardiac events; MI: Myocardial infarction; NS: Not significant; PSVT: Paroxysmal supraventricular tachycardia; SBP: Systolic blood pressure; SVT: Supraventricular tachycardia.

Table 3 Practical tips and tricks for troponin testing in adult supraventricular tachycardia

Practical tips and tricks
Do not test routinely in young, low-risk patients with typical paroxysmal supraventricular tachycardia and no ischemic symptoms or electrocardiogram changes after conversion
Remember that most troponin elevations reflect demand ischemia or myocardial stretch, not plaque rupture
Short-term risk is modest and confined to selected populations (older age, coronary artery disease, diabetes, significant comorbidities)
Long-term outcomes are inconsistent, and elevations are often prognostically neutral once comorbidities are accounted for
Always prioritize arrhythmia management first – terminate supraventricular tachycardia, relieve symptoms, and then decide whether troponin adds value
Interpret troponin within the universal definition of myocardial infarction framework, using sex-specific 99th percentiles and delta algorithms, and avoid overdiagnosis of ACS
Positive troponin in the absence of ACS features should prompt tailored outpatient evaluation (coronary computed tomography angiography, stress test, echocardiography) rather than reflexive invasive testing
Balance is key: Avoid unnecessary admissions and procedures, but remain vigilant for true ischemic events

ACS: Acute coronary syndrome.