Table III.

Detrimental effects of periprocedural patient stress (stress as a foe)

Hyperthrombotic state: Hyper-enhanced blood clot formation is associated with the development of thrombosis (DVT/PE) as well as STEMI, and may also be associated with other thromboembolic complications (e.g., ischemic stroke, acute limb ischemia) In some conditions can precipitate disseminated intravascular clotting (DIC)

Immune overactivation/inflammation: Promotes plaque rupture and can contribute to oxygen supply demand mismatch in type 2 myocardial infarction and myocardial injury after noncardiac surgery (MINS) Can progress to cytokine storm in some severe cases

Autonomic hyperactivity: May induce lethal arrhythmia Causes hemodynamic instability: Hypertensive crisis Vasovagal hypotension and bradycardia Responsible for neurogenic stunning that causes or exacerbates heart failure Impairs microcirculation, probably both directly and indirectly

High anxiety: May worsen the compliance of the patient: Weakens the informed consent process Impairs periprocedural cooperation of the patient Negatively affects the rehabilitation course

Various and unclear mechanisms: Causes stress ulcer Induces renal failure, plays a role in contrast induced nephropathy (CIN)

Overly prolonged/chronic stress: Leads to atherosclerosis, at least through the induction of metabolic syndrome Is most likely responsible for impaired wound healing after procedures