What role do pro-inflammatory cytokines such as TNF and IL play in heart failure?

Pro-inflammatory cytokines such as tumor necrosis factor (TNF) and interleukin (IL) play a significant role in the pathophysiology of heart failure, primarily by causing inflammation and exhibiting negative inotropic effects. In heart failure, these cytokines are produced in excess due to the stress placed on the heart, leading to chronic inflammation. This inflammatory response is detrimental and contributes to the progressive deterioration of cardiac function.

The negative inotropic effects refer to the decreased contractility of the heart muscle, which is crucial for effective pumping of blood. Elevated levels of TNF and IL lead to alterations in myocardial function, vascular responsiveness, and can cause apoptosis (cell death) of cardiomyocytes, further compromising heart function. This cycle of inflammation and myocardial damage exacerbates heart failure and worsens symptoms.

In contrast, promoting healing of myocardial tissue, enhancing cardiac metabolism, and reducing myocardial hypertrophy would indicate beneficial effects that aid cardiac function or recovery, which is not the case with the action of these pro-inflammatory cytokines in heart failure.