Elsevier

The American Journal of Cardiology

Volume 136, 1 December 2020, Pages 140-148
The American Journal of Cardiology

Predictors and Mechanisms of Atrial Fibrillation in Patients With Hypertrophic Cardiomyopathy

https://doi.org/10.1016/j.amjcard.2020.09.006Get rights and content

Atrial fibrillation (AF) in hypertrophic cardiomyopathy (HC) is associated with significant symptomatic deterioration, heart failure, and thromboembolic disease. There is a need for better mechanistic insight and improved identification of at risk patients. We used cardiovascular magnetic resonance (CMR) to assess predictors of AF in HC, in particular the role of myocardial fibrosis. Consecutive patients with HC referred for CMR 2003 to 2013 were prospectively enrolled. CMR parameters including left ventricular volumes, presence and percentage of late gadolinium enhancement in the left ventricle (%LGE) and left atrial volume index (LAVi) were measured. Overall, 377 patients were recruited (age 62 ± 14 years, 73% men). Sixty-two patients (16%) developed new-onset AF during a median follow up of 4.5 (interquartile range 2.9 to 6.0) years. Multivariable analysis revealed %LGE (hazard ratio [HR] 1.3 per 10% (confidence interval: 1.0 to 1.5; p = 0.02), LAVi (HR 1.4 per 10 mL/m2[1.2 to 1.5; p < 0.001]), age at HC diagnosis, nonsustained ventricular tachycardia and diabetes to be independent predictors of AF. We constructed a simple risk prediction score for future AF based on the multivariable model with a Harrell's C-statistic of 0.73. In conclusion, the extent of ventricular fibrosis and LA volume independently predicted AF in patients with HC. This finding suggests a mechanistic relation between fibrosis and future AF in HC. CMR with quantification of fibrosis has incremental value over LV and LA measurements in risk stratification for AF. A risk prediction score may be used to identify patients at high risk of future AF who may benefit from more intensive rhythm monitoring and a lower threshold for oral anticoagulation.

Section snippets

Methods

From December 2003 to April 2013, consecutive patients referred with a diagnosis of known or suspected HC underwent a CMR scan including myocardial perfusion and late gadolinium enhancement at the Royal Brompton Hospital in London UK. All patients met the American College of Cardiology Foundation/American Heart Association (ACCF/AHA) diagnostic criteria for HC.11 Exclusion criteria were previous or current AF, metabolic diseases resulting in HC phenocopies such as Anderson-Fabry disease,

Results

A total of 377 patients (mean age 62 ± 14, 73% male) were recruited. Exclusions were prior or current AF (n = 18, 5%), inadequate baseline data (n = 5, 1%) and patients lost to follow up (n = 6, 2%), giving a final population of 348 patients (Figure 1, Table 1).

The median follow-up period was 4.5 years (2.9, 6.0) with a total of 1532 patient-years of follow-up. During follow-up, 62 patients (16%) developed new AF. The incidence of AF was 4.0 (CI: 3.2 to 5.2) per 100 person-years. There were 22

Discussion

Patients with HC who develop AF are known to be at increased risk for heart failure and thromboembolic events, including stroke. We demonstrated that the extent of myocardial fibrosis and LA volume determined by CMR were strong independent predictors of AF. Our results suggest that myocardial replacement fibrosis may have a mechanistic role in development of AF. We formulated a risk prediction that may be used to identify high risk patients. Compared with those with minimal or no LGE and LAVi

Authors Contribution

Conceptualization and methodology: SKP, DJP, ROH. Investigation: CER, ACL, FM, GSK, FRA, EDP. Formal analysis: SN, RO, JG. Writing – original draft: ACL, CER. Writing – Review and Editing – RC, PGm VV, SE, MF

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    Funding: The work was supported by CORDA and the Rosetrees Foundation Trust, United Kingdom. Dr. Raphael supported by a British Heart Foundation Clinical Research Training Fellowship, United Kingdom.

    Disclosures: Dr. Pennell has received a grant from Siemens; is the Director of and shareholder with CVIS; and has received personal fees from Bayer. Dr. Prasad has received personal fees from Bayer-Schering. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

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