Skip to content

AIC Genotyping Study

Genetic Susceptibility to AF-Induced Cardiomyopathy

Status
Recruiting
Phases
Unknown
Study type
Observational
Source
ClinicalTrials.gov
Registry ID
NCT07574697
Enrollment
299
Registered
2026-05-08
Start date
2026-03-25
Completion date
2027-05-31
Last updated
2026-05-08

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Atrial Fibrillation (AF), Cardiomyopathy, Genetic

Keywords

prospective, case-controlled, genetics

Brief summary

To quantify genetic variants in a focused DCM gene panel among AF-induced cardiomyopathy (AIC) and positive/negative controls

Detailed description

Atrial Fibrillation (AF) is the most common heart rhythm disorder affecting 1 in 3-5 adults over 45. Although most patients tolerate AF, in some people it can weaken the main pump of the heart (left ventricle), causing heart failure. It is not known why some people develop heart failure during AF and others do not. We propose that individual vulnerability is due to specific genetic abnormalities that do not cause problems until they develop AF. These genetic abnormalities have been identified in patients who develop heart failure with the onset of other stressors, such as alcohol or pregnancy. Our study will identify 92 patients with AF-triggered heart failure, defined by having heart failure during AF but resolved after the AF was treated using a procedure called catheter ablation. We will measure how common these genetic variations are seen in patients with AF-triggered heart failure and compare them with 184 patients who have AF but don't develop heart failure (negative comparators) and 23 patients who do develop heart failure but do not recover after AF treatment (positive comparators).We shall only test for a limited number of clearly disease-causing genetic variants to ensure cost- effectiveness and minimise the risk of identifying genes of unclear significance. If we find a genetic association, doctors could: (1) identify patients more likely to develop weakness before the AF becomes persistent, (2) fast-track at-risk patients for catheter ablation treatment, (3) offer family screening where appropriate, and (4) avoid unnecessary testing in low-risk patients. This would directly improve care for people in East London and beyond by personalising AF treatment and preventing avoidable heart failure.

Interventions

None listed

Sponsors

Barts & The London NHS Trust
Lead SponsorOTHER

Study design

Observational model
CASE_CONTROL
Time perspective
PROSPECTIVE

Eligibility

Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
No

Inclusion criteria

INCLUSION: AIC (Cases): * Age ≥18 * Persistent AF before index catheter ablation or cardioversion * LVEF ≤40% during rate-controlled (resting HR \<100bpm, mean HR on 24-hour Holter \<100bpm) AF prior to index catheter ablation or cardioversion * LVEF normalisation (LVEF ≥55%) in SR, post-catheter ablation or cardioversion (≥3 months post-catheter ablation or cardioversion), no AF (\>30 seconds of continuous AF) detected outside blanking period (8 weeks post-catheter ablation), and with no new introduction of any new or increased dose of heart failure guideline-directed medical therapy (GDMT) (renin-angiotensin-aldosterone system inhibitors (RAASi), Sodium Glucose Co-transporter 2 (SLGT2) inhibitors, increased dose of beta-blocker (BB), mineralocorticoid receptor antagonist (MRA)) AF-pEF (Negative controls): * Age ≥18 * Persistent AF before index catheter ablation or cardioversion * LVEF ≥55% during rate-controlled (resting HR \<100bpm) AF. AIC-genotyping study, v1.7, 27.01.26 Page 13 of 28 AF/HF non-responders (Positive controls) * Age ≥18 * Persistent AF before index catheter ablation or cardioversion * LVEF ≤40% during rate-controlled (resting HR \<100bpm) AF before index catheter ablation or cardioversion. * Persistent LVSD (LVEF ≤40%) in SR, post-catheter ablation or cardioversion (≥3 months post-catheter ablation or cardioversion), no AF (\>30 seconds of continuous AF) detected outside blanking period (8 weeks post-catheter ablation) and with no change in heart failure GDMT (RAASi, SGLT2 inhibitors, increased dose of BB, MRA). EXCLUSION: AIC (Cases). * No alternative cause for LVSD (ischemic cardiomyopathy/non-ischaemic cardiomyopathy before AF diagnosis, primary valve disease, inherited cardiomyopathy * Any pregnancy during AF or in the 12 months preceding LVSD onset. * Alcohol intake \>21 units/week * Any history of cardiotoxic chemotherapy AF-pEF (Negative controls) * No known cause for LVSD (ischemic cardiomyopathy/non-ischaemic cardiomyopathy before AF diagnosis, primary valve disease, inherited cardiomyopathy). * Any pregnancy during AF or in the 12 months preceding LVSD onset. * Alcohol intake \>21 units/week. * Any history of cardiotoxic chemotherapy. AF/HF non-responders (Positive controls) * No alternative cause for LVSD (ischemic cardiomyopathy/non-ischaemic cardiomyopathy before AF diagnosis, primary valve disease, inherited cardiomyopathy). * Any pregnancy during AF or in the 12 months preceding LVSD onset. * Alcohol intake \>21 units/week. * Any history of cardiotoxic chemotherapy.

Design outcomes

Primary

MeasureTime frameDescription
DCM gene prevalence relative to negative controlOn day of baseline testing (1 day)Group difference between AIC vs AF-pEF in P/LP prevalence from DCM panel

Secondary

MeasureTime frameDescription
DCM gene prevalence relative to positive controlOn day of baseline testing (1 day)Group difference between AIC vs AF/HF non-responders in P/LP prevalence.

Countries

United Kingdom

Contacts

CONTACTNikhil Ahluwalia, MBBS, PhD
nikhil.ahluwalia@nhs.net+44(0) 20 3465 5398
PRINCIPAL_INVESTIGATORShohreh Honarbakhsh, MBBS, PhD

Queen Mary University of London

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: May 9, 2026