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. 2022 Jun 12;S0002-9149(22)00531-8.
doi: 10.1016/j.amjcard.2022.05.003.
Online ahead of print.
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Am J Cardiol.
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Abstract
Heart failure with preserved ejection fraction is a heterogeneous clinical syndrome that includes distinct subtypes with different pathophysiologies, genetics, and treatment. Distinguishing heart failure with preserved ejection fraction caused by transthyretin cardiac amyloidosis (ATTR-CA) is critical given its specific treatment. We analyzed a single-center retrospective cohort to determine the association of body mass index (BMI) with a composite of either ATTR-CA or the valine-to-isoleucine substitution (Val122Ile) variant genotype (ATTR-CA+Val122Ile). These BMI differences were prospectively evaluated in the multicenter Screening for Cardiac Amyloidosis using nuclear imaging for Minority Populations (SCAN-MP) study of Black and Hispanic patients with heart failure. The association of BMI with ATTR-CA+Val122Ile was compared by Wilcoxon rank sum analysis and combined with age, gender, and maximum left ventricle wall thickness in multivariable logistic regression. In the retrospective analysis (n = 469), ATTR-CA+Val122Ile was identified in n = 198 (40%), who had a lower median BMI (25.8 kg/m2, interquartile range [IQR] 23.4 to 28.9) than other patients (27.1 kg/m2, IQR 23.9 to 32.0) (p <0.001). In multivariable logistic regression, BMI <30 kg/m2 (odds ratio 2.6, 95% confidence interval 1.5 to 4.5) remained independently associated with ATTR-CA+Val122Ile with a greater association in Black and Hispanic patients (odds ratio 5.8, 95% confidence interval 1.7 to 19.6). In SCAN-MP (n = 201), 17 (8%) had either ATTR-CA (n = 10) or were Val122Ile carriers (n = 7) with negative pyrophosphate scans. BMI was lower (25.4 kg/m2 [IQR 24.3 to 28.2]) in ATTR-CA+Val122Ile patients than in non-amyloid patients (32.7 kg/m2 [28.3 to 38.6]) (p <0.001), a finding that persisted in multivariable analysis (p = 0.002). In conclusion, lower BMI is associated with ATTR-CA+Val122Ile in heart failure with increased left ventricle wall thickness, particularly in Black and Hispanic patients, and may aid in the identification of those benefiting from ATTR-CA evaluation.
Copyright © 2022 Elsevier Inc. All rights reserved.
Conflict of interest statement
Disclosures Dr. Poterucha owns stock in Abbott Laboratories and Baxter International, with research support provided to his institution from the Amyloidosis Foundation, Eidos Therapeutics, Pfizer, Edwards Lifesciences, and the Glorney-Raisbeck Fellowship Award from the New York Academy of Medicine. Dr. Maurer has had consulting income from Pfizer, Eidos, Prothena, Intellia, Akcea, Jansen, and Alnylam and his institution received clinical trial funding from Pfizer, Prothena, Eidos, and Alnylam. Dr. Ruberg acknowledges research support from Pfizer, Akcea Therapeutics, and Alnylam Therapeutics. Dr. Einstein reports speaker’s fee from Ionetix, consulting fees from W. L. Gore & Associates and authorship fees from Wolters Kluwer Healthcare – UpToDate; the institution has grants/grants pending from Attralus, Canon Medical Systems, Eidos Therapeutics, GE Healthcare (Little Chalfont, United Kingdom), Pfizer (New York, New York), Roche Medical Systems, W. L. Gore & Associates, and XyloCor Therapeutics. The remaining authors have no conflicts of interest to declare.
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