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- W2010332852 abstract "Amyloid cardiomyopathy is caused by protein deposition in the myocardial interstitium, which leads to increased thickness of the ventricular walls and, eventually, congestive heart failure (1,2). The heart failure is often associated with normal or mildly reduced ventricular ejection fraction (3) and, as such, may be refractory to standard therapies aimed at improving systolic function. Although amyloid heart disease is commonly referred to as a “restrictive cardiomyopathy,” which implies rapid early ventricular filling followed by abrupt restriction to further expansion (4), this characterization is controversial. Historical investigation of diastolic function in cardiac amyloidosis. For many years it had been suspected that the heart failure of amyloid cardiomyopathy was related to the thickened, noncompliant ventricular walls found at postmortem examination. Because amyloid cardiomyopathy exhibited many of the clinical features of pericardial constriction (5,6), clinicians surmised that amyloid-associated heart failure was caused by restriction to filling on a myocardial (not pericardial) basis. Hemodynamic confirmation of this hypothesis was provided in 1950 by Fisher et al. (7), who performed right heart catheterization on a patient with amyloidosis, noting that volume infusion failed to increase cardiac output but did increase venous pressure, which suggested “mechanical limitations of diastolic filling. . . .” Other early reports (8-10) confirmed the hemodynamic similarities between amyloid cardiomyopathy and constrictive pericarditis. Both conditions were found to have “dip and plateau” or “square root” diastolic ventricular pressure patterns that, in combination with the rapid early diastolic" @default.
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- W2010332852 title "Diastolic dysfunction in amyloid heart disease: Restrictive cardiomyopathy or not?" @default.
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- W2010332852 doi "https://doi.org/10.1016/0735-1097(89)90548-2" @default.
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