Angiology: Open Access

Angiology: Open Access
Open Access

ISSN: 2329-9495

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Commentary - (2023)Volume 11, Issue 1

Pathogenesis of Pericarditis and its Diagnosis

Kentro Hayashida*
 
*Correspondence: Kentro Hayashida, Department of Cardiology, Keio University School of Medicine, Tokyo, Japan, Email:

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Description

Pericarditis is swelling and irritation of the thin, saclike tissue surrounding the heart (pericardium). Pericarditis is a polyetiological infectious or non-infectious (aseptic) inflammatory disease, the most common visceral leaf that occurs as a complication of various diseases. Pericardium is a fibrous sac consisting of two fibrous leaves (visceral and parietal) surrounding the heart, containing normally up to 20-25 ml of physiologically essential fluid. On large vessels near the heart, the leaves of the pericardium pass directly to one another. In the left-sided defect of the pericardium it is possible to bulge the pulmonary trunk and left atrium, in rare cases the left atrium is infringed, which leads to sudden death.

Functions of pericardium

• Pericardium does not allow the heart to expand dramatically with FN and hypervolemia.

• In the systole of the ventricles there is a negative intra pericardial pressure it contributes to the filling of the atria.

• Pericardium reduces friction between the heart and neighboring organs, prevents the displacement of the heart and the inflection of large vessels.

• Serves as a barrier to infection from the pleural cavities and lungs.

However, the complete absence of pericardium (congenital malformation) is not clinically manifested.

Pathogenesis

Acute pericarditis begins with limited catarrhal and then fibrous inflammation, a small amount of effacing is subjected to reverse absorption, and fibrin strands are deposited on the visceral and parietal leaves of pericardium dry pericarditis. Then there is total inflammation, exudate accumulates in large quantities effusion.

Inflammatory fluid is first located in the lower diaphragmatic and posterior pericardium cavity, and then spreads to the entire cavity. The volume of liquid can reach 1-2 litters. As the inflammatory process subsides, the exudate is absorbed, and in the pericardium sheets the granular tissue grows, which is then replaced by connective tissue fibers, if connective tissue adhesives are formed between pericardium leaves. If the scar tissue absorbs the entire pericardium cavity, it tightens the visceral and parietal leaves, which leads to a pronounced compression of the heart. This outcome of sweaty pericarditis was called a constrictor, or squeezing. In some cases, calcium is deposited in the scar-changed pericardium and the pericardium is calcified, which turns into a rigid, dense and sedentary bag (shell) surrounding the heart (shell heart).

Diagnostics

Laboratory: Possible leucocytosis, shift ingestion of blood formula to the left, increase of SEE, CRB, hyperglobulinemia.

ECG: The concordant (one-directional) rise of the RS-T segment in many ECG withdrawals

ECHOKG: Thickening of pericardium leaves is revealed Pericarditis mostly causes acute chest pain. The chest pain occurs when the irritated layers of the pericardium rub against each other. Pericarditis is usually mild and gets into control without any treatment. Non-drug treatment is the restriction of physical activity until symptoms subside and PSA normalize. Patients who do not have the effect of treatment ASC/NSPVP, have a large effusion in pericardium and are suspected for specific ethology pericarditis, need hospitalization for further examination and treatment, colchicine is recommended in low doses, respectively, weight to improve the effectiveness of therapy and prevent relapses, colchicine can double the risk of relapse.

Author Info

Kentro Hayashida*
 
Department of Cardiology, Keio University School of Medicine, Tokyo, Japan
 

Citation: Hayashida K (2023) Pathogenesis of Pericarditis and its Diagnosis. Angiol Open Access. 11:318 .

Received: 04-Jan-2023, Manuscript No. AOA-23-21965; Editor assigned: 06-Jan-2023, Pre QC No. AOA-23-21965 (PQ); Reviewed: 20-Jan-2023, QC No. AOA-23-21965; Revised: 27-Jan-2023, Manuscript No. AOA-23-21965 (R); Published: 03-Feb-2023 , DOI: 10.35248/2329-9495.23.11.318

Copyright: © 2023 Hayashida K. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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