Cardiac contractility modulation as a novel therapeutic approach in transthyretin amyloid cardiomyopathy to improve eligibility to stabilizer therapy: a case report

TL;DR

A patient with a rare heart condition improved with a new therapy that boosted heart function and made him eligible for another treatment.

Contribution

This case report demonstrates cardiac contractility modulation (CCM) as a potential bridge therapy for transthyretin amyloid cardiomyopathy.

Findings

CCM improved left ventricular ejection fraction from 44% to 54% in a patient with wild-type transthyretin amyloid cardiomyopathy.

CCM enabled eligibility for Tafamidis therapy in a patient previously ineligible due to reduced ejection fraction.

This is the second worldwide case showing CCM's potential in amyloid cardiomyopathy.

Abstract

Cardiac transthyretin amyloidosis (ATTR-CM) is an infiltrative cardiomyopathy leading to restrictive physiology and, in advanced stages, systolic dysfunction. Conventional heart failure therapy is often poorly tolerated, and Tafamidis access may be restricted in patients with reduced ejection fraction. Cardiac contractility modulation (CCM) enhances contractility and could represent an alternative in this setting.

A 76-year-old man with wild-type transthyretin cardiac amyloidosis (ATTRwt) and mildly reduced left ventricular ejection fraction (LEVF 44%) developed persistent symptoms despite optimized medical therapy and enrolment in a clinical trial. Due to persistent systolic dysfunction (LVEF 43%), he was ineligible for Tafamidis reimbursement. A CCM device was implanted in March 2024, resulting in progressive improvement in LVEF to 54% by February 2025, enabling Tafamidis initiation.

Wild-type transthyretin cardiac amyloidosis is underdiagnosed, and treatment options remain limited, particularly in patients with systolic dysfunction. Cardiac contractility modulation has demonstrated benefit in non-infiltrative cardiomyopathies, but evidence in amyloidosis is scarce. Our case represents the second documented worldwide, showing that CCM may improve ventricular function and clinical status and, importantly, may facilitate access to disease-modifying therapy. This report highlights CCM as a potential bridge strategy in selected patients with ATTR-CM and reduced ejection fraction.

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