The mechanisms by which CHF predisposes patients to thrombo-inflammation are diverse and involve a complex interplay between hemodynamic and cardiac factors, such as increased wall tension, mechanical stress, volume overload, activation of the renin–angiotensin–aldosterone system (RAAS), and mitochondrial oxidative stress, with eventual organ cross-talk and activation of the innate immune system, especially the NLRP3 inflammasome [42,44,45,46,47,48]. Here, NLRP3 is linked to congestive heart failure.