THE ORIGIN AND DIAGNOSIS OF INFILTRATIVE HEART DISEASE IN A MODERN INTERPRETATION

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THE ORIGIN AND DIAGNOSIS OF INFILTRATIVE HEART DISEASE IN A

MODERN INTERPRETATION

¹Toshboyeva Shaxlo Yusup qizi

²Mardonova Ruxsora Sodikjonovna

³Baxriddinov Numonjon Fazliddin o‘g‘li

¹'²'³Samarkand State Medical University, Cardiology Department,

Clinical Residency, 1st Stage Residents.

https://doi.org/10.5281/zenodo.14984460

Introduction: I

mmunoglobulin light chains (AL amyloidosis, a consequence of

monoclonal gammopathy), 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), and

transthyretin (two variants of transthyretin - ATTR amyloidosis:

Research methods and materials:

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. ATTRv amyloidosis, here

ATTRv amyloidosis is associated with a non-hereditary type of transthyretin amyloidosis). The

prognosis of cardiac amyloidosis is very unfavorable. Below we briefly review the main

provisions of the European document. 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].

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 14 mm or more, in combination with the following features: heart

failure or aortic stenosis at age ≥63 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

longitudinal strain with preserved cardiac apex, low-voltage QRS complexes and pseudo Q waves

on ECG, atrioventricular conduction disturbances, and family history.

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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:

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. No radiopharmaceutical uptake

by the myocardium during scintigraphy, monoclonal protein studies are negative - the probability

of ATTR and AL amyloidosis is very low.

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

: 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. 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.

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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Pathogenetic therapy of amyloidosis includes chemotherapeutic drugs in AL amyloidosis,

as well as several drugs that slow and stabilize transthyretin synthesis in ARRT amyloidosis:

patisiran, inotersen, tafamidis, etc. In the ATTR-ACT study, tafamidis was associated with lower

cardiomyopathy in patients [3].

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