Ethnicity and Left Ventricular Hypertrophy: Tools and Uncertainties
- PDF / 613,289 Bytes
- 4 Pages / 595.276 x 790.866 pts Page_size
- 55 Downloads / 242 Views
COMMENTARY
Ethnicity and Left Ventricular Hypertrophy: Tools and Uncertainties Daniel Piskorz1 Received: 6 July 2018 / Accepted: 16 July 2018 © Springer Nature Switzerland AG 2018
Although the hemodynamic load generated by hypertension and the loss of the viscoelastic properties of the great central arteries are the main stimuli for the development of left ventricular hypertrophy, several other variables are strongly involved in hypertensive mediated cardiac damage. Left ventricular afterload is determined largely by the elastic properties of the great arteries (arterial stiffness), arteriolar diameter, and the return of wave reflection, and it is composed by a steady and a pulsatile component. The increase in the latter causes a mismatch between the left ventricle and the vascular tree coupling which is supposed to be the main mechanism that promotes the development of left ventricular hypertrophy [1, 2]. Beyond these mechanical variables, biological stimuli also can be translated into signals that generate both synthesis and degradation of cellular and extracellular proteins, and the disbalance between these stimuli is what generates the increase in the left ventricular mass index and remodeling. The genetic burden is another variable to be considered, since more than one hundred gene mutations have been detected that could be liable to myocardial damage, among them, the genes that encode the converting angiotensin enzyme, the angiotensin type 2 receptor, or the alpha 1 adrenergic receptors are the best well-known [3–5]. Both myocytes and non-myocytic cells are biomechanical sensors of neurohumoral and pressor stimuli. The growth signals are generated by the release of growth factors and cytokines such as endothelin 1, which is a peptide that stimulates a G protein coupled to the receptor, angiotensin II, cardiotrophin 1, which is a cytokine related to interleukin 6, and insulin growth factor type 1, which is a growth factor that activates tyrosine kinases receptors, among others. This means that there are many signaling pathways that activate cellular responses which could increase cell size, re-express
* Daniel Piskorz [email protected] 1
Sanatorio Británico Cardiology Institute, Paraguay 40, 2000 Rosario, Argentina
embryonic genes, or accumulate and assemble contractile proteins [6]. The diagnosis of left ventricular hypertrophy is supported either on expert’s consensus criteria based on the distribution of the left ventricular mass index in healthy or hypertensive populations, or on the basis of clinical evolution and cardiovascular events in hypertensive patients. The left ventricular mass index shows a normal distribution in the population, so that the individuals in the right part of the Gaussian curve are those who have left ventricular hypertrophy. This is the most commonly used way to consider the cut off points, even though it does not necessarily have a close relationship to cardiovascular risk. The variability of the left ventricular mass index distribution in different populations
Data Loading...
