Neurogenic Stunned Myocardium: A Review

Neurogenic stunned myocardium is a form of stress cardiomyopathy. The disorder is sometimes referred to as atypical Takotsubo cardiomyopathy. The pathophysiology of neurogenic stunned myocardium is hypothesized to involve significant overdrive of the sympathetic nervous system after a brain injury. Treatment options for a patient with a brain injury who has progressed to cardiogenic shock remain controversial, with no consistent guidelines. A patient with subarachnoid hemorrhage who progresses to cardiogenic shock with concurrent cerebral vasospasm presents a special treatment challenge. Neurogenic stunned myocardium is reversible; however, it must be recognized immediately to avoid or manage potential complications, such as cardiogenic shock and pulmonary edema. A multifaceted treatment approach is needed for the patient with cardiogenic shock and concurrent vasospasm.

Enteral Lactoferrin Administration Attenuates Myocardial Ischemia-Reperfusion Injury in an Isolated Rat Heart Model

Background While lactoferrin, an iron-binding glycoprotein, has protective effects on intestinal and cerebral ischemia-reperfusion injuries, its cardioprotective effects against stunned myocardium are unknown. This study aimed to test the hypothesis that lactoferrin has cardioprotective effects against stunned myocardium. Methods Rat hearts were perfused using the Langendorff system, and two experiments were performed. In experiment 1, the hearts were divided into the enteral lactoferrin (E-LF) 7.5 m, 15 m, 30 m, and 60 m groups, where lactoferrin (1000 mg/kg) was administered enterally for 7.5, 15, 30, and 60 min, respectively, before perfusion; and a control group, where saline was administered 30 min before perfusion. In experiment 2, hearts were allocated to the perfusate lactoferrin (P-LF) 15 and 100 groups, where 15 mg/L and 100 mg/L lactoferrin were respectively added to the perfusate, and a control group. Each group was perfused for 20 min prior to 15 min of no-flow ischemia with pacing, followed by 20 min of reperfusion. The primary outcome was the maximum left ventricular derivative of pressure development (LV dP/dt max) 15 min after reperfusion. Myocardial phospho-protein kinase B (p-Akt) was assayed by western blotting. Results LV dP/dt max in the E-LF 15 m and 30 m groups was significantly higher than in the control group. In the second experiment, there were no significant differences in LV dP/dt max. Myocardial p-Akt was not significantly activated in any lactoferrin group. Conclusion Cardio-protection was observed with enteral but not parenteral lactoferrin administration, and myocardial p-Akt was not involved in this effect.

Abstract 116: Impella Device Success: Walking Home After Cardiogenic Shock From Ventricular Fibrillation

Ventricular fibrillation is a fatal arrhythmia due to its detrimental impact on cardiac output. Managing patients in V-Fib arrest is often challenging, but newer mechanical support devices such as Impella CP 5.0 (Abiomed, Danvers, MD) are proving to be an excellent adjunct to inotrope and vasopressor therapy. We present a 75-year-old female with a medical history of atrial fibrillation and obstructive sleep apnea that presented to the ER unresponsive. On arrival, the patient was pulseless and initial rhythm on telemetry revealed ventricular fibrillation. The patient demonstrated minimally reactive pupils to light, negative corneal reflex, and lower extremity clonus. ROSC was achieved with electric defibrillation and two rounds of CPR. Chest radiograph revealed mild bilateral pulmonary congestion. Head CT revealed no acute intracranial pathology. The patient was placed on targeted temperature management protocol for the next 48 hours. Emergent left heart catheterization revealed no signs of occlusive coronary disease. TTE revealed left ventricular ejection fraction 5-10%, likely from stunned myocardium. The patient continued to clinically decline and decision was made to place an Impella device for further hemodynamic support. Unlike ECMO, the Impella fully unloaded the LV and allowed diastolic coronary filling. The patient ultimately demonstrated significant improvement and repeat TTE revealed an improved EF of 45-50%. Prior to hospital discharge, an AICD was placed for primary SCD prevention. The patient maintained close outpatient follow-up with her cardiologist and PCP. This case illustrates the importance life-saving mechanical support devices such as Impella in the setting of cardiogenic shock, even from non-ischemic ventricular fibrillation.

Serum neprilysin levels are associated with myocardial stunning after ST-elevation myocardial infarction

Background/Introduction Left ventricular remodeling following ST-elevation myocardial infarction (STEMI) is associated with poor outcome. Neprilysin inhibition leads to improved outcome in patients with altered left ventricular ejection fraction (LVEF). Purpose We aimed to assess the association between serum levels of neprilysin and left ventricular (LV) volumes, function and remodeling in STEMI patients with successful myocardial reperfusion. Methods Sixty-eight patients were admitted for STEMI and had both plasma neprilysin measurement at baseline and 3D transthoracic echocardiogram at baseline and at follow-up (7 months). We compared 3 groups: a group with a low-level of plasma neprilysin (<125 pg/mL, i.e. the lower limit of detection of the assay, 38 patients) and the two other groups were defined as being below or above the median value of the remaining samples (15 patients each). Results Median age was 58.5±12.8 years and 56 (82.4%) were men. Median LVEF was 45.0±8.5%. Baseline characteristics were comparable among groups. At baseline there was a non-significant trend towards lower end-diastolic volume (p=0.07) but significantly lower LVEF in the high neprilysin group (46.4±8.3%, 47.1±8.1% and 39.1±6.9%, p<0.01). At follow-up, the magnitude of LVEF increase was significantly more important in the high neprilysin group compared to the other groups (p=0.022 for relative change in LVEF and 6.6±7.3%, 3.6±9.0% and 11.3±8.4%, p=0.031 for absolute change in LVEF) resulting in similar LVEF levels at follow-up between all groups (53.0±8.9%, 50.6±9.7% and 50.4±9.9%, p=0.55). Conclusion(s) Initial high neprilysin levels may identify patients with stunned myocardium early after STEMI, with a recovery of contractility leading to improved LVEF at follow-up. Funding Acknowledgement Type of funding source: None

Quantitative proteomic and phosphoproteomic profiling of ischemic myocardial stunning in swine

We first used ion current-based proteomics and phosphoproteomics to reliably identify novel alterations in protein expression and phosphorylation contributing to contractile dysfunction, extracellular matrix (ECM) damage, and programmed cell death in stunned myocardium and developed a comprehensive swine heart-specific proteome database, which provides a valuable resource for future research in porcine models of cardiovascular diseases.