The document summarizes the pathophysiology of heart and cardiovascular disease. It describes how LDL and triglycerides damage endothelial cells, leading platelets and monocytes to adhere and abnormal proliferation of smooth muscles. This causes inflammation and narrowing of blood vessels from atherosclerotic plaque formation. Over time, plaque rupture can decrease blood flow and increase vascular resistance, raising afterload and preload on the heart. As a compensatory mechanism, the heart undergoes hypertrophy but eventually fails in oxygen compensation, leading to tissue ischemia, injury, and infarction which decreases cardiac output and causes systemic hypoxia and multiorgan failure and death.
The document summarizes the pathophysiology of heart and cardiovascular disease. It describes how LDL and triglycerides damage endothelial cells, leading platelets and monocytes to adhere and abnormal proliferation of smooth muscles. This causes inflammation and narrowing of blood vessels from atherosclerotic plaque formation. Over time, plaque rupture can decrease blood flow and increase vascular resistance, raising afterload and preload on the heart. As a compensatory mechanism, the heart undergoes hypertrophy but eventually fails in oxygen compensation, leading to tissue ischemia, injury, and infarction which decreases cardiac output and causes systemic hypoxia and multiorgan failure and death.
The document summarizes the pathophysiology of heart and cardiovascular disease. It describes how LDL and triglycerides damage endothelial cells, leading platelets and monocytes to adhere and abnormal proliferation of smooth muscles. This causes inflammation and narrowing of blood vessels from atherosclerotic plaque formation. Over time, plaque rupture can decrease blood flow and increase vascular resistance, raising afterload and preload on the heart. As a compensatory mechanism, the heart undergoes hypertrophy but eventually fails in oxygen compensation, leading to tissue ischemia, injury, and infarction which decreases cardiac output and causes systemic hypoxia and multiorgan failure and death.
The document summarizes the pathophysiology of heart and cardiovascular disease. It describes how LDL and triglycerides damage endothelial cells, leading platelets and monocytes to adhere and abnormal proliferation of smooth muscles. This causes inflammation and narrowing of blood vessels from atherosclerotic plaque formation. Over time, plaque rupture can decrease blood flow and increase vascular resistance, raising afterload and preload on the heart. As a compensatory mechanism, the heart undergoes hypertrophy but eventually fails in oxygen compensation, leading to tissue ischemia, injury, and infarction which decreases cardiac output and causes systemic hypoxia and multiorgan failure and death.