Coronary artery disease (CAD) is the most common cause of heart failure (HF) in the United States and has a pivotal role in its development and progression.1 Patients with both CAD and HF have substantially higher risks of mortality compared with those with HF from other causes.2 Nevertheless, discerning whether a causal relationship exists and thus revascularization may be of benefit, or if they simply coexist, presents a significant clinical dilemma. This delineation, although complex, holds profound implications for prognosis and management of patients with CAD and HF.

Mitral valve (MV) regurgitation is the most common valvular heart disease in the United States and the second most common in Europe, with a prevalence of about 1.7%, which increases up to 9.3% in those ≥75 years of age.1,2 In the United States, mitral regurgitation (MR) incidence was >2 million adults in 2000 and is expected to double by 2030.3

Amyloid cardiomyopathy is most commonly caused by 1 of 2 precursor proteins: (1) monoclonal immunoglobulin light chain produced in bone-marrow plasma cell disorders; or (2) transthyretin (TTR), also known as prealbumin, a thyroxine and retinol (vitamin A) transport protein produced mainly in the liver. The abbreviations for the associated amyloid cardiomyopathies are termed light-chain cardiac amyloidosis (AL-CA) and transthyretin cardiac amyloidosis (ATTR-CA), respectively. Distinction between these 2 forms of cardiac amyloidosis is critical, because they differ significantly regarding their epidemiology, pathobiology, genetics, outcomes, and treatment (Table 1).