Physiology-Guided Heart Rate Modulation in Cardiogenic Shock With Myocardial Bridging: Reversing the Inotrope Paradox

Myocardial bridging is a dynamic coronary anomaly in which systolic compression may extend into early diastole, particularly under conditions of increased heart rate and contractility. In patients with cardiogenic shock, this creates a potential physiological conflict, as catecholaminergic support may worsen coronary flow impairment rather than improve haemodynamics. A 66-year-old man presented with inferolateral ST-segment elevation myocardial infarction due to thrombotic occlusion of the proximal left circumflex artery, successfully treated with primary percutaneous coronary intervention. Coronary angiography also showed a long myocardial bridge involving the mid left anterior descending artery. After revascularization, the patient devoped cardiogenic shock requiring norepinephrine and dobutamine, but remained haemodinamically unstable, with persistent tachycardia, low cardiac index, reduced stroke volume index, and progressive respiratory failure. Given the presence of myocardial bridging, a tachicardia-mediated limitation of dyastolic coronary perfusion was hypothesized. Low-dose landiolol, an ultra-short-acting and highly β1-selective blocker, was introduced under continuous haemodynamic monitoring. Heart rate decreased from 127 to 83 bpm and was accompained by a marked improvement in stroke volume index, cardiac index, and lactate levels, while vasopressor requirements remained stable. This case illustrates an "inotrope paradox" in which adrenergic stimulation may aggravate haemodynamic compromise in the presence of myocardial bridging by increasing heart rate and contractility, thereby intensifying systolic compression and shortening diastolic perfusion time. In this setting, physiology-guided heart rate reduction may restore coronary flow dynamics and improve systemic output. In selected patients with cardiogenic shock and myocardial bridging, ultra-short-acting β1-blockade may represent a targeted strategy to reverse tachycardia-mediated haemodynamic deterioration and support a diastole-centered approach to resuscitation.