English to Russian Medical Medical: Cardiology сердечная недостаточность

For patients with ATTR-CM and EF #40%, GDMT may be poorly tolerated. The vasodilating effects of ARNi, ACEi, and ARB may exacerbate hypotension, especially with amyloid-associated autonomic dysfunction. Beta blockers may worsen HF symptoms as patients with ATTR-CM rely on heart rate response to maintain cardiac output. The benefit of ICDs in ATTR-CM has not been studied in randomized trials, and a case-control study showed unclear benefit (5). CRT has not been studied in ATTR-CM with HFrEF. Disease-modifying therapies include *TTR silencers* (disrupt hepatic synthesis via mRNA inhibition/degradation: inotersen and patisiran), TTR stabilizers (prevent misfolding/deposition: diflunisal and tafamidis), and TTR disruptors (target tissue clearance: doxycycline, tauroursodeoxycholic acid [TUDCA], and epigallocatechin-3-gallate [EGCG] in green tea). Light chain cardiac amyloidosis is managed by hematology-oncology specialists and beyond the scope of cardiologists, but diagnosis is often made by cardiologists when cardiac amyloid becomes manifest (Figure 13). AL amyloidosis is treatable, and patients with AL amyloidosis with cardiac involvement should promptly be referred to hematology-oncology for timely treatment. Inotersen and patisiran are associated with slower progression of
amyloidosis-related polyneuropathy in ATTRv-CM (6,7). There are ongoing trials of the impact of inotersen and patisiran and newer generation mRNA inhibitors-degraders on cardiovascular morbidity or mortality. There is limited benefit of diflunisal (8), doxycycline plus TUDCA (9,10), and EGCG (11), on surrogate endpoints such as LV mass, but the impact of these agents on cardiovascular morbidity and mortality has not been assessed. Evaluation and management of autonomic dysfunction, volume status, and arrhythmia are important.