State of the Art Review of Surgical Techniques for Microaxial Flow Pump Implantation.

Recently, temporary mechanical circulatory support (tMCS) has been increasingly used for cardiogenic shock therapy. Originally designed as a bail-out option for patients who could not be weaned from cardiopulmonary bypass, the indications for tMCS have been expended and now enable us to support a wide range of patients with various cardiac pathologies. Modern tMCS devices include microaxial flow pumps (mAFP) which are small, versatile systems that can provide both acute cardiac support and cardiac protection for high-risk interventions. In this paper, we review different surgical implantation techniques with modern mAFP as well as specific aspects of preoperative indications and patient evaluation.

Physical preconditioning on biventricular temporary mechanical circulatory support while awaiting heart transplantation.

Temporary mechanical circulatory support (tMCS) is increasingly used in patients with cardiogenic shock as a bridge to further treatment. We present the case of a 52-year-old female patient with biventricular heart failure who was bridged to heart transplantation employing biventricular tMCS through a non-femoral access. The 'groin-free' tMCS concept facilitates pre-habilitation while awaiting heart transplantation.

Determinants of seeding and spreading of α-synuclein pathology in the brain.

In Parkinson's disease (PD), fibrillar forms of α-synuclein are hypothesized to propagate through synaptically coupled networks, causing Lewy pathology (LP) and neurodegeneration. To more rigorously characterize the determinants of spreading, preformed α-synuclein fibrils were injected into the mouse pedunculopontine nucleus (PPN), a brain region that manifests LP in PD patients and the distribution of developing α-synuclein pathology compared to that ascertained by anterograde and retrograde connectomic mapping. Within the PPN, α-synuclein pathology was cell-specific, being robust in PD-vulnerable cholinergic neurons but not in neighboring noncholinergic neurons. While nearly all neurons projecting to PPN cholinergics manifested α-synuclein pathology, the kinetics, magnitude, and persistence of the propagated pathology were unrelated to the strength of those connections. Thus, neuronal phenotype governs the somatodendritic uptake of pathological α-synuclein, and while the afferent connectome restricts the subsequent spreading of pathology, its magnitude and persistence is not a strict function of the strength of coupling.