New Drug Guards Heart From Cardiac Rupture Following Myocardial Infarction – ZMR Blog
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New Drug Guards Heart From Cardiac Rupture Following Myocardial Infarction

New Drug Guards Heart From Cardiac Rupture Following Myocardial Infarction

At present, there are several drug types available for heart failure. Of which, a new drug LCZ696 is advised by the US laws as a first-line therapy for chronic heart failure. Compared to conventional drugs, LCZ696 is superior at decreasing hospitalization and cardiac death owing to heart failure. A research team from the Kumamoto University, Japan, has now discovered that LCZ696 can put off heart failure and cardiac rupture subsequent to acute myocardial infarction—one of the reasons for chronic heart failure.

Across the globe, heart disease is the foremost reason of death and the most of those deaths result from acute myocardial infarction and heart failure. Previously, ARBs (Angiotensin II Receptor Blockers) or ACE inhibitors (angiotensin-converting enzyme inhibitors) were utilized in conjunction with other drugs as the primary treatment for acute myocardial infarction and heart failure. ARBs and ACE inhibitors hinder the system accountable for controlling BP, RAAS (Renin—Angiotensin—Aldosterone System), which leads to high BP when it becomes overzealous.

LCZ696 is a drug that blends Sacubitril and Valsartan—one that has an organ-protective effect and other a conventional antihypertensive drug. Sacubitril obstructs neprilysin that crumbles hormones produced primarily from the heart known as B-type natriuretic peptide and atrial natriuretic peptide.

Microvascular obstruction

LCZ696 was recognized as a chronic heart failure therapy as it represses RAAS activity and improves the functioning of the natriuretic peptide system that guards the heart. Nevertheless, it is yet not apparent whether it is helpful in the acute stage of acute myocardial infarction that results in chronic heart failure. The wall between the non-necrotic and necrotic regions of the heart is worn out resulting in bleeding and rupture at the boundary in myocardial infarction. Around 10% of fatality from myocardial infarction is ascribed to cardiac rupture. Thus, the team scrutinized LCZ696’s effect with the use of an artificial myocardial infarction mouse model.

The day after the creation of the myocardial infarction model mice, they were separated into groups that (a) obtained LCZ696, (b) obtained an ACE inhibitor, and (3) did not obtain any therapy (control group). The team discovered that the rate of mortality owing to cardiac rupture taking place within 1 week following myocardial infarction was considerably lesser in the LCZ696 treatment group compared to other 2 groups.

Gene expression in the region of myocardial infarction was examined to look into the means by which LCZ696 could hold back cardiac rupture. The team discovered that the expression of genes concerned with inflammation-related cytokines (IL-6, IL-1) and in tissue degrading MMP-9 was evidently decreased in the LCZ696 treatment group. A rise in the MMP-9 gene function is known to be associated with the reason for cardiac rupture. Thus, this study has given a new approach to prevent the heart from cardiac rupture.

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