HeartMate 3: new challenges in ventricular tachycardia ablation.

AIM: To describe clinical characteristics, procedural details, specific challenges, and outcomes in patients with HeartMate3™ (HM3), a left ventricular assist device system with a magnetically levitated pump, undergoing ventricular tachycardia ablation (VTA). METHODS AND RESULTS: Data were collected from patients with an HM3 system who underwent VTA in seven tertiary centres. Data included baseline patient characteristics, procedural data, mortality, and arrhythmia-free survival. The study cohort included 19 patients with cardiomyopathy presenting with ventricular tachycardia (VT) (53% with VT storm). Ventricular tachycardias were induced in 89% of patients and a total of 41 VTs were observed. Severe electromagnetic interference was present on the surface electrocardiogram. Hence, VT localization required analysis of intra-cardiac signals or the use of filter in the 40-20 Hz range. The large house pump HM3 design obscured the cannula inflow and therefore multi imaging modalities were necessary to avoid catheter entrapment in the cannula. A total of 32 VTs were mapped and were successfully ablated (31% to the anterior wall, 38% to the septum and only 9% to the inflow cannula region). Non-inducibility of any VT was reached in 11 patients (58%). Over a follow-up of 429 (interquartile range 101-692) days, 5 (26%) patients underwent a redo VT ablation due to recurrent VTA and 2 (11%) patients died. CONCLUSIONS: Ventricular tachycardia ablation in patients with HM3 is feasible and safe when done in the appropriate setup. Long-term arrhythmia-free survival is acceptable but not well predicted by non-inducibility at the end of the procedure.

Assessment of left ventricular function: comparison of cardiac multidetector-row computed tomography with two-dimension standard echocardiography for assessment of left ventricular function.

OBJECTIVE: To compare global Left Ventricular (LV) systolic function assessment by 16-detector row Computed Tomography (MDCT) with Two-Dimensional Standard Echocardiography (2DSE) in a routine cardiology practice setting and to ascertain the degree of correlation between LV volumes and measurements obtained by 2DSE with those measured by MDCT. METHODS: In 52 patients with suspected coronary artery disease, a contrast enhanced MDCT study was performed using retrospective gating without dose modulation for better endocardial delineation. Eight phases of the cardiac cycle were analyzed to identify the end-diastolic and end-systolic phases. 2DSE was performed on the same day. Left ventricular systolic and diastolic volumes and ejection fraction were calculated in 4-chamber, 2-chamber and biplane (average of the two) views. Endocardial tracing was used to measure ventricular volumes by area length method for CT and Simpson's method for echocardiography. RESULTS: On MDCT, mean LV ejection fraction (LVEF) in 4-chamber, 2-chamber and biplane views were 58.4 +/- 12, 59.3 +/- 12 and 59.7 +/- 12% respectively. On 2DSE, mean LVEF in 4-chamber, 2-chamber and biplane views were 58 +/- 14, 57 +/- 16 and 58 +/- 13% respectively. LVEF correlated best using the biplane views (r = 0.59 and P < 0.01) compared to 2-chamber (r = 0.57 and P < 0.01) and 4-chamber views (r = 0.32 and P = 0.02). Biplane measurement by these two techniques correlated well for LV volumes in both diastole (r = 0.69 and P < 0.01) and systole (r = 0.73 and P < 0.01), although MDCT consistently gave higher values. CONCLUSIONS: MDCT can be a useful tool to measure LVEF while patients are undergoing CT coronary angiography.

Oxidized-LDL through LOX-1 increases the expression of angiotensin converting enzyme in human coronary artery endothelial cells.

BACKGROUND AND OBJECTIVES: Our previous studies have shown that oxidized low-density lipoprotein (ox-LDL) and angiotensin II (Ang II) influence each other's action in endothelial cells. This study was designed to examine the regulation by ox-LDL of the expression of angiotensin converting enzyme (ACE) gene in human coronary artery endothelial cells (HCAECs). In addition, we studied the effect of the HMG CoA reductase inhibitor simvastatin on this interaction. METHODS AND RESULTS: Cultured HCAECs were incubated with ox-LDL (10-80 microg/ml) for 1-24 h. Ox-LDL increased the expression of ACE in a concentration- and time-dependent fashion. The upregulation of ACE expression in response to ox-LDL was mediated by its endothelial receptor LOX-1, since pretreatment of HCAECs with a blocking antibody to LOX-1 prevented the expression of ACE (P<0.01). Native-LDL had no significant effect on ACE expression. In this process, ox-LDL-induced activation of mitogen-activated protein kinase (MAPK p42/44) played an important role, since pretreatment of HCAECs with the MAPK p42/44 inhibitor (PD98059, 10 microM) inhibited MAPK activation and subsequently attenuated the expression of ACE (P<0.01 vs. ox-LDL alone). In other experiments, we pretreated HCAECs with simvastatin (10 microM) and then exposed the cells to ox-LDL. Simvastatin markedly attenuated ox-LDL-induced MAPK activation, and concurrently reduced ACE expression (P<0.01 vs. ox-LDL alone). CONCLUSIONS: Our observations provide direct evidence that ox-LDL via LOX-1 activation induces ACE gene expression in HCAECs, and MAPK activation plays a signal transduction role in this process. Simvastatin, which inhibits MAPK activation, also blocks ox-LDL-mediated upregulation of ACE.