Post MI Heart Failure

Pathophysiology

In patients with MI, heart failure (HF) usually results from reduced contractile function of one or both ventricles, secondary to loss of viable myocardial tissue. However, mitral valvular regurgitation, due to failure of the papillary muscles, may also play a role, as may arrhythmias.

Reduced contractile function leads to a fall in cardiac output to the systemic circulation (in left-sided HF), pulmonary circulation (in right-sided HF) or both. Venous congestion in these systems contributes to peripheral and pulmonary oedema, resulting in ankle swelling and dyspnoea, respectively.

The physiological response to falling cardiac output includes a number of compensatory mechanisms that initially help to increase cardiac output and maintain perfusion pressure (Figure 1). These include ventricular remodelling, and activation of the sympathetic nervous system and the renin-angiotensinaldosterone system (RAAS). Despite their initial usefulness, these compensatory mechanisms have detrimental effects over time, and ultimately cause a worsening of HF.

A major aim of drug treatment in patients with HF is to mitigate the impact of these compensatory mechanisms.

Figure 1. Compensatory mechanisms in heart failure, and their consequences. 

Adapted from Kumar & Clark.¹
RAAS = renin-angiotensin-aldosterone system; SNS = sympathetic nervous system.