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ORIGIN AND MODERN CLINICAL DIAGNOSIS OF INFILTRATIVE HEART
DISEASES
¹Ergashev Davlat
²Xolmatov Mehroj
³Boltayev Husan
⁴Mardonqulov Akmal
⁵Yavg'ashev Asomiddin
¹'²'³'⁴'⁵Samarkand State Medical University, DKTF, Department of Internal Medicine, Cardiology
and Functional Diagnostics, 2nd year clinical residents
https://doi.org/10.5281/zenodo.14885607
Introduction:
To date, nine amyloidogenic proteins have been identified that can
accumulate in the myocardium and cause cardiac amyloidosis. Three of them are common: serum
amyloid A (AA amyloidosis, a consequence of chronic inflammation and infectious diseases),
immunoglobulin light chains (AL amyloidosis, a consequence of monoclonal gammopathy), and
transthyretin (two variants of transthyretin - ATTR amyloidosis: ATTRv amyloidosis, here
ATTRv amyloidosis is associated with a non-hereditary type of transthyretin amyloidosis).
Research methods and materials:
The prognosis of cardiac amyloidosis is very
unfavorable. However, in recent years, certain progress has been made not only in diagnostics, but
also in the development of drug therapy for cardiac amyloidosis, so that experts from the Working
Group on Myocardial and Pericardial Diseases of the European Society of Cardiology have
developed a consensus document on the diagnosis and treatment of cardiac amyloidosis [1].
A similar document was previously published by the American Heart Association [2].
Below we briefly review the main provisions of the European document.
First of all, the authors noted that the prevalence of cardiac amyloidosis may be higher than
currently available data, which is usually associated with imperfect diagnosis of this disease.
In this regard, the following algorithm for diagnosing amyloidosis is proposed, consisting
of two stages: 1. forming an assumption about the presence of cardiac amyloidosis 2. specific
diagnosis of cardiac amyloidosis.
The following factors have been identified as factors that may indicate amyloidosis: left
ventricular wall thickness of 12 mm or more, in combination with the following features: heart
failure or aortic stenosis at age ≥65 years, hypertension, autonomic dysfunction, peripheral
polyneuropathy, proteinuria, bilateral carpal tunnel syndrome, bilateral tendon syndrome, late
gadolinium enhancement on cardiac magnetic resonance imaging (MRI), reduced left ventricular
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longitudinal strain with preserved cardiac apex, low-voltage QRS complexes and pseudo Q waves
on ECG, atrioventricular conduction disturbances, and family history.
In addition, both invasive and noninvasive diagnostic methods can be used to confirm the
diagnosis. Invasive methods include biopsy of the myocardium or other organs, followed by
staining of the biopsy material with Congo red and examination under polarized light, while
noninvasive methods include echocardiography, cardiac MRI, phosphate scintigraphy, and blood
tests for immunoglobulin light chains.
In addition, only ATTR amyloidosis can be diagnosed non-invasively. For this purpose,
scintigraphy, blood tests for monoclonal gammopathies (to exclude AL amyloidosis) and
echocardiography / MRI of the heart are performed. All other forms of amyloidosis are diagnosed
only after confirming the presence of amyloid by biopsy (not necessarily myocardial) and during
imaging studies according to certain criteria.
Results:
No radiopharmaceutical uptake by the myocardium during scintigraphy,
monoclonal protein studies are negative - the probability of ATTR and AL amyloidosis is very
low.
Scintigraphy has revealed myocardial uptake of the radiopharmaceutical, monoclonal
protein studies are negative - if the uptake level is 2/3 (the same as in bones or more), then the
diagnosis of ATTR amyloidosis is considered confirmed. Next, genetic testing should be
performed to determine its form. If the uptake level is 1 (less than in bones), histological
confirmation of amyloid deposition is required.
There is no myocardial uptake of radiopharmaceuticals during scintigraphy, the study of
monoclonal proteins is positive - AL amyloidosis should be excluded using cardiac MRI. If there
are signs of amyloid on MRI, histological examination should be performed.
Scintigraphy revealed myocardial uptake of the radiopharmaceutical, monoclonal protein
studies were positive - differential diagnosis between ATTR and AL amyloidosis should be made
using histological examination.
Conclusion
: Treatment of cardiac amyloidosis involves the use of specific drugs that
should stop or slow the deposition of amyloid in the myocardium and therapy aimed at preventing
cardiovascular complications. When discussing the latter, it should be noted that in general, only
diuretics are used to treat heart failure in amyloidosis, and anticoagulant therapy is prescribed in
atrial fibrillation, regardless of the number of points on the CHA 2 DS 2 VASc scale.
Pathogenetic therapy of amyloidosis includes chemotherapeutic drugs in AL amyloidosis,
as well as several drugs that slow and stabilize transthyretin synthesis in ARRT amyloidosis:
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patisiran, inotersen, tafamidis, etc. In the ATTR-ACT study, tafamidis was associated with lower
cardiomyopathy in patients [3].
Thus, the available diagnostic methods allow for a reliable diagnosis of cardiac
amyloidosis, as well as for determining its specific variant. However, the treatment of cardiac
amyloidosis remains a difficult task, mainly due to the high cost of therapy, especially in relation
to the most common type, transthyretin amyloidosis.
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