The impact of carnosine on myosin for a possible intervention or prevention of systolic heart failure

Abstract

Heart failure is a common but serious condition that affects approximately 5.7 million adults in the United States and costs the economy $30.7 billion each year. More specifically, systolic heart failure, otherwise known as heart failure with reduced ejection fraction (HFrEF), is the most common form of heart failure that occurs when the muscle of the left ventricle loses its ability to contract, preventing enough oxygen and blood from circulating throughout the body. Although a myriad of treatment options have emerged in recent years for the treatment of heart failure and left ventricular systolic heart dysfunction, there is yet to be an established and definite treatment for this condition. Thus, it is paramount to develop a more effective therapeutic treatment by specifically targeting the carnosine protein. Through an analysis on the ATP activity of myosin with and without carnosine, it was discovered that myosin activity increases in the presence of carnosine. This is a significant discovery as carnosine allows for contractions of the heart to increase. As heart contractions increase from an increase in myosin, increasing actin activity through a directly proportional relationship, it allows for an increased amount of blood to be pumped from the heart. Thus, the hypothesis was supported as the carnosine protein can be seen to enhance muscle contractions of the heart and allow for the treatment or possible prevention of systolic heart failure, which can be caused by any condition that impairs the heart muscle’s ability to pump blood.

Keywords

• carnosine
• myosin
• myosin ATPase activity
• systolic heart failure
• contractile function Introduction Heart failure is a serious condition that affects approximately 5.7 million adults in the United States and costs the economy $30.7 billion each year (Division for Heart Disease and Stroke Prevention
• 2016). It occurs when the heart is not pumping enough blood to meet all of the body’s needs
• leading to a loss in vital functions
• and can affect both left and right sides of the heart (Nic
• 2012). The reasons for this reduced pumping of blood lie in cardiac enlargement
• or the enlargement of the heart
• and when heart muscles become too stiff to properly contract (McMullen and Jennings
• 2007). More specifically
• systolic heart failure is the most common form of heart failure and occurs when the muscle of the left ventricle of the heart loses its ability to contract
• preventing enough oxygen and blood from circulating throughout the body (“Heart Failure Signs and Symptoms
• which helps to classify the certain type of heart failure. Those possessing heart failure with reduced ejection fraction have 40% and below of the blood in the left ventricle of the heart pumped out to the rest of the body
• which is below the normal ejection fraction of more than 55% (Pai et. al
• 2017). Although a myriad of treatment options have emerged in recent years for the treatment of heart failure
• such as the use of Beta blockers or Angiotensin-converting enzyme (ACE) inhibitors
• there is yet to be an established and definite treatment for this condition (McConaghy & Smith
• 2004). This is due to the fact that even though current treatment options are effective to some extent in serving as a base-line treatment
• it is rather recommended by Becher
• Blankenberg
• and Westermann from the World Journal of Cardiology that future treatments focus on “augmentation of heart rate in order to increase cardiac output
• 2015). With this
• a promising approach to the development of an effective intervention of heart failure lies in a dipeptide that has been reasoned to increase cardiac contractility (Black et. al
• contractile function