Preprocedural valvuloarterial impedance as a predictor of left ventricular ejection fraction improvement after transcatheter aortic valve replacement in patients with reduced left ventricular ejection fraction.

BACKGROUND: Predictors of left ventricular ejection fraction (LVEF) improvement after transcatheter aortic valve replacement (TAVR) in patients with a preoperative reduced LVEF are limited. OBJECTIVES: This study aimed to investigate the relationship between preprocedural valuvuloarterial impedance (ZVa), which represents the global LV afterload, and LVEF improvement after TAVR. METHODS: This was a single-center, retrospective study, which included patients with symptomatic aortic valve stenosis (AS) with a reduced baseline LVEF (< 50%) underwent TAVR. Based on the difference in the LVEF before and 1 month after the procedure, they were divided into two groups: improved group (≥ 10% improvement) and non-improved group (< 10% improvement or worsening). Preprocedural ZVa and clinical outcomes were then compared. ZVa was calculated using preprocedural transthoracic echocardiography data. RESULTS: Among 473 cases of TAVR performed from May 2012 to July 2017 at Queen's Medical Center (Honolulu, HI, USA), 99 patients (improved group, n = 42; mean age 82.0 ± 8.6 years vs. non-improved group, n = 57, mean age 81.4 ± 9.5 years) were included. The improved group had a higher baseline ZVa {4.83 (4.15-6.89) mmHg/ml/m2 vs. 4.04 (3.56-4.63) mmHg/ml/m2, respectively, p = 0.0009} and prevalence of ZVa > 5 mmHg/ml/m2 (45.2% vs. 17.5%, respectively, p = 0.0028). Multivariable analysis of predictors of LVEF improvement ≥ 10% at 1 month identified ZVa > 5 mmHg/ml/m2 [odds ratio (OR): 3.31, 95% confidence interval (CI): 1.05-11.8] as a predictor. The improved group had a lower readmission rate due to heart failure than the non-improved group (log-rank test, p = 0.043). CONCLUSION: In conclusion, Zva is a simple, noninvasive marker that shows promise as a predictor of LVEF improvement after TAVR in reduced LVEF patients.

Two-step approach of percutaneous closure of a paravalvular leak and atrial septal defect after mitral valve reoperation.

Severe paravalvular leakage following mitral valve replacement, a rare but potentially serious complication, may result in heart failure and significant hemolysis. Reoperation is considered standard of care. However, in selected patients, re-do sternotomy carries excessively high surgical risk. Percutaneous closure of paravalvular leaks has become a viable option for these patients. We present a case of a highly symptomatic 42-year-old male who underwent successful percutaneous closure of two paravalvular leaks and a post-operative atrial septal defect after re-do mitral valve replacement surgery. As access to the left atrium was expected to be difficult following percutaneous atrial septal defect closure, a two-step approach of paravalvular leak closure followed by atrial septal defect closure was chosen. Difficulties of atrial septal defect closure following closure of a paravalvular leak next to the inter-atrial septum will be discussed.

Ventricular structure and function in aged dogs with renal hypertension: a model of experimental diastolic heart failure.

BACKGROUND: Heart failure (HF) with normal ejection fraction (diastolic HF [DHF]) usually occurs in elderly patients with hypertension. The presence and significance of altered systolic and diastolic ventricular function in DHF is increasingly controversial. Our objective was to develop a clinically relevant large-animal model to better understand the pathophysiology of DHF. METHODS AND RESULTS: Ventricular structure and function were characterized in young control (YC group; n=6), old control (OC group; n=7), and old dogs made hypertensive by renal wrapping (experimental DHF [ExDHF] group; n=8). The ExDHF group was associated with normal left ventricular (LV) volume, increased LV mass, and myocardial fibrosis. LV relaxation was impaired in ExDHF (tau=53+/-6 ms) compared with OC (tau=35+/-3 ms; P<0.05) and YC (tau=33+/-6 ms; P<0.05) dogs. The percent diastole at which relaxation is complete was increased in ExDHF (116+/-30%) compared with OC (69+/-8%; P<0.05) and YC (35+/-5%; P<0.05) dogs. The coefficient of LV diastolic stiffness was similar in OC, YC, and ExDHF dogs. Diastolic pressures increased dramatically in response to increases in blood pressure. End-systolic LV stiffness was enhanced in ExDHF dogs and after load enhancement of myocardial performance was maintained. Arterial stiffness was increased in ExDHF dogs. CONCLUSIONS: Aged dogs with chronic hypertension exhibit LV hypertrophy and fibrosis with impaired LV relaxation but no increase in the coefficient of LV diastolic stiffness. LV systolic and arterial stiffness are increased, which may exacerbate load-dependent impairment of relaxation and contribute to increased filling pressures with hypertensive episodes. This model mimics many of the structural and functional characteristics described in the limited studies of human DHF and provides insight into the pathogenesis of DHF.

Safety of expedited anticoagulation in patients undergoing transesophageal echocardiographic-guided cardioversion.

BACKGROUND: In patients undergoing transesophageal echocardiography-guided cardioversion, we evaluated the use and safety of an expedited in-hospital anticoagulation regimen that incorporates shorter-than-standard durations of precardioversion intravenous unfractionated heparin and postcardioversion bridging therapy with a low-molecular-weight heparin. METHODS: Adult patients who underwent successful transesophageal echocardiography-guided cardioversion for atrial fibrillation or atrial flutter between May 2000 and August 2003 were classified into 2 groups by duration of intravenous unfractionated heparin therapy (<24 h or > or =24 h) before transesophageal echocardiography and cardioversion. Safety end points evaluated included all-cause death, stroke or other thromboembolic events, and major bleeding complications within 1 month after successful cardioversion. RESULTS: The study population of 386 patients included 199 (52%) who received expedited intravenous unfractionated heparin (<24 h; minimum duration, <4 h) and 193 patients (50%) who were discharged on low-molecular-weight heparin therapy. The adverse event rates at 1-month follow-up were not significantly different between the 2 unfractionated heparin patient groups, and the rate of stroke among patients dismissed on low-molecular-weight heparin was less than 1%. No adverse events occurred among patients who received intravenous unfractionated heparin for less than 12 hours and who were dismissed on low-molecular-weight heparin bridging therapy. CONCLUSIONS: The use of an expedited heparin anticoagulation regimen in patients with atrial fibrillation or atrial flutter undergoing transesophageal echocardiography-guided cardioversion appears to be safe. Cardioversion can be performed as early as a few hours after initiation of intravenous unfractionated heparin, and bridging therapy with a low-molecular-weight heparin can be used after cardioversion until the international normalized ratio is therapeutic.

Failing atrial myocardium: energetic deficits accompany structural remodeling and electrical instability.

The failing ventricular myocardium is characterized by reduction of high-energy phosphates and reduced activity of the phosphotransfer enzymes creatine kinase (CK) and adenylate kinase (AK), which are responsible for transfer of high-energy phosphoryls from sites of production to sites of utilization, thereby compromising excitation-contraction coupling. In humans with chronic atrial fibrillation (AF) unassociated with congestive heart failure (CHF), impairment of atrial myofibrillar energetics linked to oxidative modification of myofibrillar CK has been observed. However, the bioenergetic status of the failing atrial myocardium and its potential contribution to atrial electrical instability in CHF have not been determined. Dogs with (n = 6) and without (n = 6) rapid pacing-induced CHF underwent echocardiography (conscious) and electrophysiological (under anesthesia) studies. CHF dogs had more pronounced mitral regurgitation, higher atrial pressure, larger atrial area, and increased atrial fibrosis. An enhanced propensity to sustain AF was observed in CHF, despite significant increases in atrial effective refractory period and wavelength. Profound deficits in atrial bioenergetics were present with reduced activities of the phosphotransfer enzymes CK and AK, depletion of high-energy phosphates (ATP and creatine phosphate), and reduction of cellular energetic potential (ATP-to-ADP and creatine phosphate-to-Cr ratios). AF duration correlated with left atrial area (r = 0.73, P = 0.01) and inversely with atrial ATP concentration (r = -0.75, P = 0.005), CK activity (r = -0.57, P = 0.054), and AK activity (r = -0.64, P = 0.02). Atrial levels of malondialdehyde, a marker of oxidative stress, were significantly increased in CHF. Myocardial bioenergetic deficits are a conserved feature of dysfunctional atrial and ventricular myocardium in CHF and may constitute a component of the substrate for AF in CHF.