Inglis, Sara

Introduction: Microaxial flow pumps reduce mortality in myocardial infarction (MI) related cardiogenic shock (CS). The Impella 5.5 generates increased flow to provide circulatory support, and optimization relies on mechanistic understanding of pressure-volume (PV) relationships. Aim: Using a porcine model of acute MI in tandem with biventricular (BiV) PV loop conductance catheters, this study aimed to understand the impact of Impella 5.5 on BiV hemodynamics in MI CS. Methods: In 6 Domestic Yorkshire Pigs, an Impella 5.5 (J&J MedTech, NJ) was inserted percutaneously under fluoroscopic guidance via carotid or aortic access. An angioplasty balloon catheter was advanced past the first diagonal and inflated to above nominal pressure with blood flow obstruction for 90 minutes. BiV PV loop conductance catheters (Sigma-M, CD Leycom, Hengelo, The Netherlands) were inserted via femoral venous access. The left ventricle (LV) PV loop catheter is positioned via transeptal puncture using intracardiac echocardiography. BiV PV loops are generated for each level of Impella support from P1 to P7. Results: With increasing Impella 5.5 support, LV PV loops shifted to the left and right ventricular (RV) loops to the right. Without statistical significance, LV end diastolic volume (EDV) decreased by a mean of 12.3 ± 10.7% from baseline and RV EDV increased by 32 ± 40%. Native LV function decreased with increasing Impella 5.5 support, demonstrated by a reduction in stroke volume (SV) (35±13 ml to 27±14 ml; p<0.001), cardiac output (CO) derived from SV&heart rate (2.0±0.5 ml/min to 1.7±0.7 ml/min; p<0.001), and ejection fraction (EF) (37±7% to 29±12%; p<0.001). Less consistent trends were noted in peak positive dP/dt and end-systolic pressure volume relationship. Native RV function increased with higher levels of Impella 5.5 support, noted by increasing SV (27±24 ml to 41±28 ml; p=0.004), CO (1.6±1.2 ml/min to 2.3±1.4 ml/min; p=0.001), and EF (42±16% to 45±9%; p=0.04). Arterial elastance and ventriculo-arterial coupling increased in the LV from baseline to P7 (2.2±1.4 mmHg/ml to 2.8±1.0 mmHg/ml and 1.8±0.5 to 3.2±1.9, respectively; p<0.001) and decreased in the RV (1.3±0.7 mmHg/ml to 0.9±0.7 mmHg/ml (p<0.001) and 2.1±2.2 to 1.3±0.6 (p=0.004)). Conclusions: Impella 5.5 speed modulation highlights significant ventricular interdependence in the setting of acute MI. PV loop derived parameters here visualized parameters that may be utilized to improve optimization of hemodynamic support in CS.

Percutaneous ventricular assist devices (pVAD) decrease mortality in cardiogenic shock (CS) patients, but at a high adverse event rate. Novel pVADs need to improve cardiac power output (CPO) to improve efficacy and reduce profile to reduce adverse events. Venstramedical has developed an impeller with nitinol and polymer which can collapse for low-profile insertion and expand in the body to provide optimal CPO. We have also developed a unique 9 French (9Fr) delivery system. In vitro and in vivo testing have been performed to develop this device. Head-flow (HQ) tests generate 5.0 L/min with a pressure differential of 80 mm Hg and 7.0 L/min against 60 mm Hg. Durability testing demonstrated continuous operation of up to 20 days. In the acute healthy ovine model, we demonstrated full flow (7–9 L against 60–80 mm Hg), transcatheter 9Fr delivery, retrieval of the device, and resting of the native heart during pumping. In a CS animal, we demonstrated survival and resting of the native heart during the acute study with decreased stroke work (SW), decreased stroke volume (SV), while total cardiac output was up to 7 L/min and maintaining adequate pressure with low hemolysis. We also demonstrated multiday functioning of the device in a healthy ovine model with good CO and low hemolysis.

Background: Thoracic aortic aneurysms (TAAs) can be found in 1-2/1000 individuals in the general population and are commonly associated with genetic disorders of connective tissue and bicuspid aortic valve (BAV). Larger size, distal aneurysms, high DBP and presence of BAV are some factors that can accelerate aneurysm growth. Case: A 37-year-old male without a history of recent trauma or stimulant use presented to the emergency room with 2 days of chest tightness. He had acute worsening overnight and awoke with chest pain, discomfort in the suprasternal notch and between the shoulder blades. He had no other medical history, however, was treated with a 10-day course of Ciprofloxacin for epididymitis 3 weeks prior. On presentation, the patient had active pleuritic chest pain, tachycardia and tachypnea with no abnormalities on cardiac auscultation. EKG showed sinus tachycardia, PVCs, and nonspecific ST elevations in leads II, III and aVF with normal troponins and chest X-ray. CT chest angiogram revealed a 60 mm ascending aortic aneurysm ( Fig. 1a ). Doming of the right cusp of the aortic valve in the parasternal view ( Fig. 1b ) raised suspicion for BAV which was confirmed with the classic fish mouth appearance on the TEE ( Fig. 1c ). The patient underwent successful aortic repair with graft placement. First degree relatives were offered screening for BAV. Ciprofloxacin was replaced with Sulfamethoxazole-Trimethoprim for treating his residual epididymal infection. Discussion: TAA rupture is associated with a >90% mortality rate. It is important to be aware of echocardiographic features of BAV as this can predispose to accelerated aneurysm growth. Additionally, fluoroquinolones (FQs) are a commonly prescribed class of antibiotics that may affect the structural integrity of the aorta, associated with aneurysm enlargement and rupture. This case offers an important example to highlight why the FDA recommends against the use of FQs in patients with known TAA or risk factors for it.