An Overview on the Mechanisms of Myocardial Damage in Hypertension and the Diagnostic Contribution of Cardiospecific Troponins T and I
Aleksey Michailovich Chaulin1, 2, *
Hypertension (HT) is one of the most common cardiovascular (CV) pathologies and a key risk factor for the development of CV disease and its complications. There are two main etiopathogenetic types of HT: primary and secondary. As a result of HT, damage to many organs (heart, blood vessels, retina, etc.) can occur. These organs are considered the main target organs in HT and assessment of their condition plays an important role for optimal management of patients with HT. Increased levels of cardiospecific troponins T and I, localized in the main type of myocardial cells (cardiomyocytes), may indicate myocardial damage. At the same time, the degree of myocardial damage may correlate with the degree of increase in cardiospecific troponins T and I. In recent studies, cardiospecific troponins T and I have established themselves as early and highly specific criteria for myocardial damage not only in myocardial infarction, but also in many other cardiac (e.g., arrhythmias, endocarditis, myocarditis, takotsubo syndrome, or cardiomyopathy) and extra-cardiac (e.g., renal failure, sepsis, or diabetes mellitus) conditions. Many authors suggest using cardiospecific troponins T and I as prognostic markers for the above pathologies. Thus, the determination of cardiospecific troponins T and I can provide additional diagnostic advantages in the management of patients with pathological conditions that damage the myocardium. The purpose of this article is to systematize information about the pathogenetic mechanisms of myocardial damage in HT and to consider the diagnostic contribution of cardiospecific troponins T and I for the management of patients with HT.
* Address correspondence to: Department of Cardiology and Cardiovascular Surgery and Department of Histology and Embryology, Faculty of Medicine, Samara State Medical University, Samara 443099, Russia; Tel: + 7 (927) 770-25-87; E-mail: firstname.lastname@example.org