暂无摘要。

BACKGROUND: Many pathological conditions of both cardiovascular and non-cardiac origin in the course of their development cause damage to contractile cardiac muscle cells-cardiac myocytes (CMCs). One of the most sensitive and specific criteria for detecting CMCs are cardiac troponins (CTs), which are regulatory protein molecules that are released into the blood serum from CMCs upon their death or damage. New (high-sensitive) methods for detecting CTs allow the detection of minor CMCs damages at the earliest stages of cardiovascular diseases and can therefore change the understanding of disease development mechanisms and open up new diagnostic possibilities. One of the most common and dangerous early diseases of the cardiovascular system is arterial hypertension. The purpose of this paper is to summarize the pathophysiological mechanisms underlying CMCs damage and CTs release into the bloodstream in the case of arterial hypertension and to state the clinical significance of increased CTs levels in patients with arterial hypertension.
METHODS: This is a descriptive review, which was prepared using the following databases: Embase, Pubmed/Medline and Web of Science. The following key words were used in the literature search: \"myocardial injury\" and \"arterial hypertension\" in combination with the terms \"cardiac troponins\" and \"mechanisms of increase\".
CONCLUSIONS: According to a literature analysis, CMCs damage and CTs release in the case of arterial hypertension occur according to the following pathophysiological mechanisms: myocardial hypertrophy, CMCs apoptosis, damage to the CMC cell membrane and increase in its permeability for CTs molecules, as well as changes in the glomerular filtration rate. Most often, increased CTs serum levels in case of arterial hypertension indicate an unfavorable prognosis. Data on the CTs predictive significance in case of arterial hypertension open the prospects for the use of these biomarkers in the choice of patient management plans.

BACKGROUND: Myocarditis refers to a variety of myocardial inflammatory lesions. A variety of factors such as infection and physical and chemical factors can cause myocarditis. Depending on the severity of myocardial damage, myocarditis patients can manifest heart failure, cardiogenic shock, and even sudden death. Here we present a case of viral myocarditis that mimicked acute coronary syndrome.
METHODS: A middle-aged male patient presented with chest pain and elevated troponin I after a flu-like infection. This patient had a history of hypertension and a habit of alcohol and tobacco use. Electrocardiography showed typical changes in acute myocardial infarction, with the T-wave increasing. Coronary angiogram revealed no stenosis. Cardiac magnetic resonance imaging revealed edema of the middle and apical septal and apical anterior walls on T2-weighted images and the T1 mapping. Late gadolinium enhancement of the middle and apical septal and apical anterior walls could be found. Rubella virus immunoglobulin G and immunoglobulin M antibodies were abnormally elevated. The patient was given antiviral and antibiotic treatments, and serum biomarkers and electrocardiograph returned to normal after 5 d of treatment. After one-year follow-up, the patient showed no symptoms, and cardiac magnetic resonance showed that myocardial thickness was significantly thinner than before, and fibrosis was less than before.
CONCLUSIONS: This case illustrates the utility of cardiac magnetic resonance for diagnosis of infarction-like myocarditis when the angiogram is normal.