ANTIBIOTIC‐INDUCED CARDIAC ARRHYTHMIA IN ELDERLY PATIENTS

American men than in the general population. This racial disparity has been attributed to the higher prevalence and worse severity of hypertension in this cohort. A contributing factor may be the higher prevalence of cardiac amyloidosis from TTR misfolding. In the Beta-blocker Evaluation of Survival Trial, 10% of African-American participants aged 60 and older were found to be carriers of the mutant TTR allele v122I. This mutation, which results in misfolded TTR proteins that are precursors to the amyloid deposits, has an age-dependent penetrance and rarely manifests before the age of 60. Accordingly, it has been found to contribute to cardiac function decline and high mortality after the age of 65. Recently, pharmacological therapies have been developed that stabilize the TTR protein, preventing it from forming intermediate forms that have a strong tendency to misfold and subsequently deposit in the myocardium. Such therapies are preventive in nature and ideally would be initiated before irreversible cardiovascular structural and functional changes. African-American men are also at high risk of developing prostate cancer, a disease that strikes at the age when misfolded TTR would begin to accumulate in the myocardium, but prostate biopsies are not routinely evaluated for the presence of amyloid because this requires specialized staining. As such, no studies have investigated the concomitant deposition of amyloid in the myocardium and prostate. Using standard amyloid staining techniques, it was possible to identify the presence of amyloidosis in an individual with a congestive heart failure phenotype and echocardiographic evidence of severe diastolic dysfunction. Furthermore, with genetic testing, it was possible to identify the presence of the V122I allele. Further investigation is warranted to determine whether staining of prostate specimens in target populations could identify individual at risk of developing heart failure secondary to cardiac ATTR.