Final answer:
A myocardial infarction impairs the heart muscle, leading to a diminished pumping capacity and potential heart failure. Left-sided damage increases back pressure in the lungs, affecting the right heart and leading to right-sided heart failure. New research targets cellular-level processes to improve heart muscle contractions in heart failure treatment.
Step-by-step explanation:
How Myocardial Infarction Leads to Heart Failure
A myocardial infarction (MI), or heart attack, occurs when blood flow is obstructed to a part of the heart, leading to the damage or death of the heart muscle tissue. This event can lead to a cascade of detrimental effects, including heart failure. During an MI, the blockage of a coronary artery, often due to a blood clot or the rupture of atherosclerotic plaque, restricts the flow of oxygen and nutrients to the myocardium (heart muscle). As a result, affected myocardial cells perish. The resulting scar tissue can weaken the heart muscle, diminish its pumping ability, and contribute to arrhythmias, potentially escalating to heart failure.
When the left side of the heart is damaged, it may lead to left-sided heart failure, characterized by a rise in pressure entering the left heart chambers and a decrease in aortal pressure. Over time, this can result in the inadequate circulation of blood throughout the body. Subsequently, the damaged left heart can cause back pressure in the pulmonary circulation, which might increase the workload on the right heart, setting the stage for right-sided heart failure. The right side of the heart might fail to pump blood effectively through the lungs due to increased pressures in the vena cavae and decreased pressures in the pulmonary arteries. Consequently, fluid can accumulate in the extremities and organs, causing swelling and organ congestion, symptoms indicative of right-sided heart failure.
Appropriately, heart failure is also determined by the functioning of the cardiac muscle cells. At the molecular level, heart failure can be caused by improper functioning of the endoplasmic reticulum in cardiac cells, leading to insufficient calcium ions for proper muscle contractions. New research, such as that conducted by the University of Texas Southwestern Medical Center, has revealed potential therapeutic targets to increase the contractile force of cardiac muscle in heart failure patients by influencing the calcium-ion pump and muscle contraction process.