Marie-France Poulin

Impact of Physical Inactivity on Mortality in Patients With Heart Failure.

The impact of physical inactivity on heart failure (HF) mortality is unclear. We analyzed data from the HF Adherence and Retention Trial (HART) which enrolled 902 patients with New York Heart Association class II/III HF, with preserved or reduced ejection fraction, who were followed for 36 months. On the basis of mean self-reported weekly exercise duration, patients were classified into inactive (0 min/week) and active (≥1 min/week) groups and then propensity score matched according to 34 baseline covariates in 1:2 ratio. Sedentary activity was determined according to self-reported daily television screen time (<2, 2 to 4, >4 h/day). The primary outcome was all-cause death. Secondary outcomes were cardiac death and HF hospitalization. There were 196 inactive patients, of whom 171 were propensity matched to 342 active patients. Physical inactivity was associated with greater risk of all-cause death (hazard ratio [HR] 2.01, confidence interval [CI] 1.47 to 3.00; p <0.001) and cardiac death (HR 2.01, CI 1.28 to 3.17; p = 0.002) but no significant difference in HF hospitalization (p = 0.548). Modest exercise (1 to 89 min/week) was associated with a significant reduction in the rate of death (p = 0.003) and cardiac death (p = 0.050). Independent of exercise duration and baseline covariates, television screen time (>4 vs <2 h/day) was associated with all-cause death (HR 1.65, CI 1.10 to 2.48; p = 0.016; incremental chi-square = 6.05; p = 0.049). In conclusion, in patients with symptomatic chronic HF, physical inactivity is associated with higher all-cause and cardiac mortality. Failure to exercise and television screen time are additive in their effects on mortality. Even modest exercise was associated with survival benefit.

Clinical or Symptomatic Leaflet Thrombosis Following Transcatheter Aortic Valve Replacement: Insights from the U.S. FDA MAUDE Database

ABSTRACT Background: Data on clinical or symptomatic leaflet thrombosis after transcatheter aortic valve replacement (TAVR) are limited. Whether clinical leaflet thrombosis has significance beyond peri-TAVR stroke or transient ischemic attacks (TIA) is yet to be elucidated. Methods: Between January 2012 and October 2015, we searched the MAUDE database for all entries with the identifier code, “NPT,” designated by the U.S. FDA to identify TAVR-related adverse events (AEs). Selected entries were searched further for the terms “leaflet,” “central aortic regurgitation,” and “aortic stenosis” to capture all events related to leaflet thrombosis causing structural valve dysfunction (SVD). Presentation of leaflet thrombosis (aortic stenosis or regurgitation or mixed valve lesion), mode of diagnosis (echocardiography, computed tomography, surgical explantation, or autopsy), and timing of presentation after TAVR were recorded. For all AEs of SVD due to leaflet thrombosis, the following outcomes were recorded: stroke or TIA, cardiogenic shock, and death from any cause. Results: A total of 5691 TAVR-related AEs were reported in the MAUDE database. SVD due to leaflet thrombosis was reported in 30 cases. Most cases (n = 18/30, 60.0%, 95% CI 0.41–0.77) occurred in the first year following TAVR. SVD manifested as either aortic stenosis (n = 16/30, 53.3%, 95% CI 0.34–0.72), or regurgitation (n = 7/30, 23.3%, 95% CI 0.10–0.42), or both (n = 4/30, 13.3%, 95% CI 0.04–0.31). Interventions to address leaflet thrombosis included either escalation of antiplatelet or anticoagulant therapy (n = 9/30, 30.0%, 95% CI 0.15–0.49), valve-in-valve TAVR (n = 5/30, 16.7%, 95% CI 0.06–0.35), or surgery (n = 14/30, 46.7%, 95% CI 0.28–0.66), or their combination. Outcome following leaflet thrombosis included stroke/TIA (n = 3/30, 10.0%, 95% CI 0.02–0.27), cardiogenic shock (n = 2/30, 6.7%, 95% CI 0.01–0.22), and death (n = 9/30, 30.0%, 95% CI 0.15–0.49). Conclusion: Clinically manifest leaflet thrombosis was associated with serious manifestations that included stroke, cardiogenic shock, and death.

Clinical Benefits of Stem Cells for Chronic Symptomatic Systolic Heart Failure A Systematic Review of the Existing Data and Ongoing Trials.

The benefits of stem cell therapy for patients with chronic symptomatic systolic heart failure due to ischemic and nonischemic cardiomyopathy (ICM and NICM, respectively) are unclear. We performed a systematic review of major published and ongoing trials of stem cell therapy for systolic heart failure and compared measured clinical outcomes for both types of cardiomyopathy. The majority of the 29 published studies demonstrated clinical benefits of autologous bone marrow-derived mesenchymal stem cells (BM-MSCs). Left ventricular ejection fraction (LVEF) was improved in the majority of trials after therapy. Cell delivery combined with coronary artery bypass grafting was associated with the greatest improvement in LVEF. Left ventricular end-systolic volume (or diameter), New York Heart Association functional classification, quality of life, and exercise capacity were also improved in most studies after cell therapy. Most ICM trials demonstrated a significant improvement in perfusion defects, infarct size, and myocardial viability. Several larger clinical trials that are in progress employ alternative delivery modes, cell types, and longer follow-up periods. Stem cells are a promising therapeutic modality for patients with heart failure due to ICM or NICM. More data are required from larger blinded trials to determine which combination of cell type and delivery mode will yield the most benefit with avoidance of harm in these patient populations.

Advanced Anderson-Fabry disease presenting with left ventricular apical aneurysm and ventricular tachycardia

A 54-year-old female with Anderson-Fabry disease (AFD)-R342Q missense mutation on exon 7 in alpha-galactosidase A (GLA) gene - presented with sustained ventricular tachycardia. Imaging confirmed the presence of a new left ventricular apical aneurysm (LVAA) and a significantly reduced intra-cavitary gradient compared to two years prior. AFDcv is an X-linked lysosomal storage disorder caused by GLA enzyme deficiency. The phenotypic expression of AFD in the heart is not well described. Cardiac involvement can include left ventricular hypertrophy (LVH), which is typically symmetric, but can also mimic hypertrophic cardiomyopathy (HCM). Left ventricular apical aneurysm is a rare finding in HCM. We suggest a shared mechanism of LVAA formation in AFD and HCM, independent of the underlying cardiomyopathy. Mechanisms of LVAA formation in HCM include genetic predisposition and long-standing left ventricular wall stress from elevated intra-cavitary systolic pressures due to mid-cavitary obstruction. Both mechanisms are supported in this patient (a brother with AFD also developed a small LVAA). Screening for AFD should be considered in cases of unexplained LVH, particularly in patients with the aneurysmal variant of HCM.

Coronary Computed Tomographic Angiography in the Evaluation of Liver Transplant Candidates

The feasibility, safety, and value of coronary computed tomographic angiography (CCTA) in evaluating orthotopic liver transplant (OLT) candidates are unknown. We studied a cohort of consecutive OLT candidates with intermediate-to-high risk of coronary artery disease (CAD). Intermediate risk candidates received CCTA, and those at high risk or with abnormal noninvasive testing underwent invasive coronary angiography (ICA). One hundred consecutive patients were evaluated. Fifty patients underwent a CCTA, 71.4% were β-blocked, the image quality was “good” or “excellent” in 71.4% of cases, and there was no event of significant contrast-induced nephropathy. Twenty (20%) patients were found to have severe CAD (≥70% stenosis) by CCTA and/or ICA. Independent predictors of severe CAD were age (odds ratio [OR] = 5.4 per 10-year increment, 95% confidence interval [CI] = 1.7-17.0; P = .004), dyslipidemia (OR = 12.3, 95% CI = 2.6-57.6; P = .001), and chest pain (OR = 6.0, 95% CI = 1.2-29.1; P = .03). Implementing CCTA in the evaluation of intermediate/high CAD risk OLT candidates is challenging but feasible and seems safe.

Hyperthyroid Atrial Fibrillation: Does It Matter for Stroke Risk?

patients found hyperthyroidism not to be independently predictive of stroke by multivariate analysis [13] . The prothrombotic state in hyperthyroidism has a biological basis. Many derangements in the coagulation system such as increased factors VIII and X activity, shorter activated partial thromboplastin time, higher fibrinogen levels and increased synthesis of acute phase reactants have been described [14] . Moreover, D-dimer level, a marker for fibrinolysis, has been found to be significantly higher in hyperthyroidism and to correlate with disease severity. D-dimer level was also identified as a predictor of thromboembolic events in AF [15] . In the present report, the authors studied 62 patients with hyperthyroid AF, comparing them to two control groups: non-thyroid AF (n = 107) and hyperthyroidism without AF (n = 100); all prospectively followed for a mean of 34 months. The authors found that the annual incidence of ischemic stroke was highest among hyperthyroid AF patients at 7.6% versus 3.6 and 0.7% in the non-thyroid AF and hyperthyroidism without AF groups, respectively [1] . Although the study groups were matched for stroke risk according to the CHA 2 DS 2 -VASc score, the Cox proportional hazards analysis indicated that hyperthyroid AF patients were at significantly higher stroke risk than non-thyroid AF patients with a hazard ratio of 3.2 (95% CI 1.01–5.59, p = 0.04), indicating that hyperthyroid AF is predictive of stroke risk above and beyond the CHA 2 DS 2 -VASc score. The study by Chen et al. [1] has many strengths, including consecutive patient selection and prospective followIn a recent issue of Cardiology , Chen et al. [1] reported on hypercoagulable state and stroke risk in hyperthyroid atrial fibrillation (AF). The existing evidence is not completely settled as to whether hyperthyroid AF is associated with a hypercoagulable state and constitutes an excess stroke risk, since the existing studies are small and observational in nature. This is reflected in discordant published guidelines [2, 3] and an inadequate adjudication of stroke risk in hyperthyroid AF as assessed by the CHADS 2 and CHA 2 DS 2 -VASc scores [4, 5] . Thus, the present study is quite relevant as the authors prospectively compared stroke risk in a cohort of patients with hyperthyroid AF to two control groups: non-thyroid AF and hyperthyroid patients without AF. In this editorial comment, we examine the internal and external validity of this study and weigh-in on the controversy of stroke risk and recommendation for anticoagulation in hyperthyroid AF. It is well established that patients with hyperthyroidism are at significant risk for AF. However, stroke risk among hyperthyroid AF patients remains controversial. Many reports indicate that hyperthyroidism alone is associated with an increased stroke risk, with a reported incidence ranging from 2.4 to 26.7% [6–11] . Furthermore, strokes have even been observed with sinus rhythm and in young adults with hyperthyroidism and no other risk factors [6, 9, 12] . A study by Sheu et al. [12] suggested that thyrotoxic patients (without AF), as compared to euthyroid individuals, are at increased risk for ischemic stroke with a hazard ratio of 1.44. On the other hand, the Swedish Atrial Fibrillation cohort study of 182,678 AF Received: November 26, 2013 Accepted: November 27, 2013 Published online: February 12, 2014

A Hybrid Model for Advanced Structural Heart Disease Training Programs: The Attending-Fellow-in-Training Model

Structural heart disease (SHD) fellowship programs in the United States are growing, but they are still not accredited by the Accreditation Council for Graduate Medical Education. This results in a lack of standardized curriculum and complicates funding for a dedicated fellowship, as Medicare and

Impact of a novel interventional platform and hospital design on the door-to-balloon time in patients presenting with ST-segment elevation myocardial infarction.

INTRODUCTION Reducing door-to-balloon (DTB) time in ST-segment elevation myocardial infarction improves outcomes. Several hospital factors can delay DTB times and lead to increased morbidity and mortality. The effects of hospital design and an interventional platform (IP) on patient care, particularly on the DTB time, are unknown. METHODS We performed a retrospective analysis of consecutive patients presenting to the emergency department of a medical center from September 2010 to February 2014 who met criteria for a ST-segment elevation myocardial infarction and underwent primary percutaneous coronary intervention. Patients were divided into 2 groups based on whether they presented before or after the opening of the IP in our new hospital on January 6, 2012. Total DTB time and separate systematic intervals were tabulated. RESULTS Fifty-two patients met our inclusion criteria, 21 pre-IP and 31 post-IP. Both groups had overall similar baseline characteristics. The mean DTB time significantly improved by 11.7 minutes after the opening of the IP (P = 0.016), and all cases had a DTB time 90 minutes or less as compared with 90.4% prior. Eighty-nine percent of the overall improvement in DTB happened before the patient reached the catheterization table. Important factors were the new emergency department (ED) design that facilitates rapid patient triage and the direct connection between the ED and cath lab. CONCLUSIONS This study showed that the new hospital design had significant effects on immediate patient care by improving the DTB time at our institution. Further study regarding the long-term impact of hospital designs on patient care is needed.

Pearls for a Successful Early Career in Structural Heart Disease Interventions

Early career (EC) cardiologists are defined as practicing physicians within 10 years of graduation fromcardiology fellowship training. The recent growth of structural heart disease (SHD) interventions has led some interventional cardiologists to dedicate a significant part of their practice to this subspecialty. Some have received formal fellowship training, while others have learned their skills “on the job” throughmentorship and/or dedicated institutional or industry-sponsored courses. In either case, building a successful career in this field can be challenging. This is a very exciting phase when, after years of training, interventionalists finally begin to practice in their field of choice. Nonetheless, the emerging SHD field is very competitive, rapidly evolving, and becoming increasingly regulated. These factors canmake it especially difficult for EC SHD interventionalists to be successful. In this article we discuss tips on how to overcome some of the EC pitfalls in this field.

Training in Structural Heart Disease: Call to Action

Catheter-based therapies for congenital and structural heart diseases (SHDs) have come a long way since the pioneering work of Terry King in 1976 with the first percutaneous atrial septal defect closure, the first mitral balloon valvuloplasty by Kanji Inoue in 1984, and the first percutaneous valve replacements by Philipp Bonhoeffer and Alain Cribier in the early 2000s. More than 100 000 transcatheter aortic valve replacements (TAVRs) have been performed in the United States, and the yearly number of TAVR implants now exceeds that of isolated surgical aortic valve replacements.1 If the ongoing TAVR trials for low-risk patients demonstrate equivalence with surgery, we can expect another surge in demand for TAVR procedures. Similarly, percutaneous mitral valve repair procedures have now climbed to >15 000 in the United States.1 In addition, several percutaneous therapies for tricuspid and mitral valve repair and replacement are currently in the pipeline and will fuel continued growth in percutaneous therapies for SHD in the coming years. Recent Food and Drug Administration approvals of devices to close the left atrial appendage and patent foramen ovale further highlight this point. Furthermore, the number of adults with congenital heart disease (CHD) now exceeds the number of affected children, and many of these patients will require additional catheterization procedures.2 It is paradoxical that this nascent field has been devoid of formalized training paradigms. There is a clear and unmet need for defining the training requirements of physicians intending to perform SHD interventions. We need to ensure that future proceduralists will possess the appropriate cognitive and technical skill sets required to safely and effectively perform these …