Search

The article discusses a study focusing on the left ventricular hypertrophy (LV) and its potential role in coronary heart disease. Topics discussed include the link of ischemic heart diseases with LV hypertrophy, the assessment of the burden of atherosclerosis using coronary artery calcifications (CACs), and the use of calcium-channel blockers for treatment.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) rapidly spread across the world, killing more than 4 million individuals globally, with 240 million individuals being confirmed by laboratory tests. Among different therapeutic strategies to prevent SARS-CoV-2 infection, vaccines are the most promising approach for curbing the pandemic. They elicit an immune neutralizing response and thus offer protection against coronavirus disease 2019 (COVID-19). However, some questions regarding the safety of COVID-19 vaccines have been raised and based on sparse reports of severe systemic reactions after vaccination. Among these, evidences on the potential effect of vaccination on the acute rise in blood pressure have been recently accrued. Approved vaccines in Europe increase the endogenous synthesis of SARS-CoV-2 Spike proteins from a variety of cells. Once synthetized in the cells reached by the vaccine, the Spike proteins first assemble in the cytoplasm and then migrate to the cell surface to protrude with a native-like conformation. Spike proteins are recognized by the immune system which rapidly develops an immune response. Furthermore, the Spike proteins assembled in the cells which are eventually destroyed by the immune response circulate in the blood as free-floating forms. Free-floating Spike proteins may interact with angiotensin-converting enzyme 2 (ACE2) receptors leading to internalization, degradation, and dysregulation of the catalytic activities of these receptors. The consequent loss of ACE2 receptor activity leads to a rapid drop in the generation of angiotensin1,7 resulting from inactivation of angiotensin II. The imbalance between angiotensin II (overactivity) and of angiotensin1,7 (deficiency) might play a role in the genesis of acute elevation in blood pressure.