Faculty Bibliography

Heart failure continues to be a leading cause of morbidity and mortality throughout the United States. The pathophysiology of heart failure involves activation of complex neurohormonal pathways, many of which mediate not only hypertrophy and fibrosis within ventricular myocardium and interstitium, but also activation of platelets and alteration of vascular endothelium. Platelet activation and vascular endothelial dysfunction may contribute to the observed increased risk of thromboembolic events in patients with chronic heart failure. However, current data from clinical trials do not support routine use of chronic antiplatelet or oral anticoagulation therapy for ambulatory heart failure patients without other indications (atrial fibrillation and/or coronary artery disease) as the risk of bleeding seems to outweigh the potential benefit related to reduction in thromboembolic events. In this review, we consider the potential clinical utility of targeting specific pathophysiological mechanisms of platelet and vascular endothelial activation to guide clinical decision making in heart failure patients.

Cardiogenic shock is a life-threatening condition that occurs in response to reduced cardiac output in the presence of adequate intravascular volume and results in tissue hypoxia. Cardiogenic shock has several underlying aetiologies, with the most common being acute myocardial infarction (AMI). Refractory cardiogenic shock presents as persistent tissue hypoperfusion despite administration of adequate doses of two vasoactive medications and treatment of the underlying aetiology. Investigators of the SHOCK trial reported a long-term mortality benefit of emergency revascularization for shock complicating AMI. Since the publication of the SHOCK trial and subsequent guideline recommendations, the increase in community-based use of percutaneous coronary intervention for this condition has resulted in a significant decline in mortality. Despite these successes in the past 15 years, mortality still remains exceptionally high, particularly in patients with refractory cardiogenic shock. In this Review, we discuss the aetiology and pathophysiology of cardiogenic shock and summarize the data on the available therapeutics and their limitations. Although new mechanical circulatory support devices have been shown to improve haemodynamic variables in patients with shock complicating AMI, they did not improve clinical outcomes and are associated with high costs and complications.

Patients with continuous flow left ventricular assist devices (CF-LVADs) are at increased risk of bleeding. We reviewed our institutional experience with bleeding in the urinary tract following CF-LVAD implantation andquantified the impact on hospital resource utilization in comparison to bleeding in the gastrointestinal tract, the most commonly reportedmucosal site of bleeding following LVAD implantation. Records were retrospectively reviewed for patients undergoing CF-LVAD implantation at our institution between October 2011 and April 2015. Major adverse events of gross hematuria and gastrointestinal bleeding were identified, and patient demographics and hospital course were reviewed.

We present a case of rapidly ascending left ventricular assist device driveline and tunnel infection in a patient with a long length of driveline buried beyond the distal velour coating. Device salvage with radical debridement, exit site relocation, and local tissue advancement is described. The findings in this case suggest that the interface between nonvelour covered driveline and subcutaneous tissue can become the nidus of a virulent ascending infection because of poor tissue ingrowth.