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1.
Artif Organs ; 44(11): 1150-1161, 2020 Nov.
Article in English | MEDLINE | ID: mdl-32416628

ABSTRACT

Gastrointestinal bleeding (GIB) is a common adverse event after continuous-flow left ventricular assist device (CF-LVAD) implantation. We sought to evaluate patterns of GIB development and related outcomes in CF-LVAD recipients. An electronic search was performed to identify all articles related to GIB in the setting of CF-LVAD implantation. A total of 34 studies involving 1087 patients were pooled for analysis. Mean patient age was 60 years (95% CI 57-64) and 24% (95% CI 21-28%) were female. The mean time from CF-LVAD implantation to the first GIB was 54 days (95% CI 24-84) with 40% (95% CI 34-45%) of patients having multiple episodes of GIB. Anemia was present in 75% (95% CI 41-93%) and the most common etiology of bleeding was arteriovenous malformations (36% [95% CI 24-50%]). The mean duration of follow-up was 14.6 months (95% CI 6.9-22.3) during which the all-cause mortality rate was 21% (95% CI 12-36%) and the mortality rate from GIB was 4% (95% CI 2-9%). Thromboembolic events occurred in 32% (95% CI 22-44%) of patients with an ischemic stroke rate of 16% (95% CI 3-51%) and a pump thrombosis rate of 8% (95%CI 3-22%). Heart transplantation was performed in 31% (95% CI 18-47%) of patients, after which 0% (95% CI 0-10%) experienced recurrent GIB. GIB is a major source of morbidity among CF-LVAD recipients. While death due to GIB is rare, cessation of anticoagulation during treatment increases the risk of subsequent thrombotic events. Heart transplant in these patients appears to reliably resolve the risk of future GIB.


Subject(s)
Gastrointestinal Hemorrhage/etiology , Heart-Assist Devices/adverse effects , Humans , Intensive Care Units , Length of Stay , Survival Analysis
2.
J Card Surg ; 35(5): 1062-1071, 2020 May.
Article in English | MEDLINE | ID: mdl-32237166

ABSTRACT

BACKGROUND AND AIM OF THE STUDY: Ventricular septal defect (VSD) following myocardial infarction (MI) is a relatively infrequent complication with high mortality. We sought to investigate the effect of concomitant coronary artery bypass graft (CABG) on outcomes following post-MI VSD repair. METHODS: Electronic search was performed to identify all relevant studies published from 2000 to 2018. Sixty-seven studies were selected for the analysis comprising 2174 patients with post-MI VSD. Demographic information, perioperative variables, and outcomes including survival data were extracted and pooled for systematic review and meta-analysis. RESULTS: Single-vessel disease was most common (47%, 95% confidence interval [CI], 42-52), left anterior descending coronary artery was the most commonly involved vessel (55%, 95% CI, 46-63), and anterior wall was the most commonly affected territory (57%, 95% CI, 51-63). Concomitant CABG was performed in 52% (95% CI, 46-57) of patients. Of these, infarcted territory was re-vascularized in 54% (95% CI, 23-82). A residual/recurrent shunt was present in 29% (95% CI, 24-34) of patients. Of these, surgical repair was performed in 35% (95% CI, 28-41) and transcatheter repair in 11% (95% CI, 6-21). Thirty-day mortality was 30% (95% CI, 26-35) in patients who had preoperative coronary angiogram, and 58% (95% CI, 43-71) in those who did not (P < .01). No significant survival difference observed between those who had concomitant CABG vs those without CABG. CONCLUSIONS: Concomitant CABG did not have a significant effect on survival following VSD repair. Revascularization should be weighed against the risks associated with prolonged cardiopulmonary bypass.


Subject(s)
Cardiac Catheterization/methods , Cardiac Surgical Procedures/methods , Coronary Artery Bypass , Heart Septal Defects, Ventricular/surgery , Cardiopulmonary Bypass/adverse effects , Female , Heart Septal Defects, Ventricular/etiology , Heart Septal Defects, Ventricular/mortality , Humans , Male , Myocardial Infarction/complications , Survival Rate , Treatment Outcome
3.
Interact Cardiovasc Thorac Surg ; 25(1): 41-46, 2017 07 01.
Article in English | MEDLINE | ID: mdl-28387838

ABSTRACT

OBJECTIVES: There are various strategies in the use of temporary mechanical circulatory support following orthotopic heart transplant (OHT). We sought to examine the outcomes following different temporary mechanical circulatory support strategies for acute graft failure. METHODS: Patients who received an OHT between 2001 and 2015 at a single institution were retrospectively reviewed. Patients were divided into 2 groups based on the need for temporary mechanical circulatory support (TMCS). RESULTS: A total of 9.9% (19 of 192) of patients required TMCS following OHT. There were no significant differences in the preoperative demographics between groups. Six patients (32%) required a biventricular assist device, 9 patients (47%) required a right ventricular assist device and 4 patients (21%) required a veno-arterial extracorporeal membrane oxygenator. Perioperative morbidity was comparable between all groups. Our entire TMCS cohort had 94.7% 30-day and 61.1% 1-year survival. When compared with the OHT patients with no TMCS (97.1% at 30 days and 92.8% at 1 year), survival was inferior in TMCS patients ( P = 0.01 at 30 days, P < 0.001 at 1 year, P < 0.001 overall). CONCLUSIONS: Acute graft failure requiring TMCS has inferior overall survival. Larger, multi-institutional studies are needed to further elucidate these differences and identify the best TMCS mode.


Subject(s)
Heart Transplantation , Heart-Assist Devices , Oxygenators, Membrane , Postoperative Care/methods , Primary Graft Dysfunction/prevention & control , Female , Humans , Male , Middle Aged , Morbidity/trends , Primary Graft Dysfunction/epidemiology , Retrospective Studies , Survival Rate/trends , Treatment Outcome , United States/epidemiology
4.
Am J Physiol Heart Circ Physiol ; 300(5): H1841-52, 2011 May.
Article in English | MEDLINE | ID: mdl-21335464

ABSTRACT

Mammalian enabled (Mena) of the Drosophila enabled/vasodilator-stimulated phosphoprotein gene family is a cytoskeletal protein implicated in actin regulation and cell motility. Cardiac Mena expression is enriched in intercalated discs (ICD), the critical intercellular communication nexus between adjacent muscle cells. We previously identified Mena gene expression to be a key predictor of human and murine heart failure (HF). To determine the in vivo function of Mena in the heart, we assessed Mena protein expression in multiple HF models and characterized the effects of genetic Mena deletion on cardiac structure and function. Immunoblot analysis revealed significant upregulation of Mena protein expression in left ventricle tissue from patients with end-stage HF, calsequestrin-overexpressing mice, and isoproterenol-infused mice. Characterization of the baseline cardiac function of adult Mena knockout mice (Mena(-/-)) via echocardiography demonstrated persistent cardiac dysfunction, including a significant reduction in percent fractional shortening compared with wild-type littermates. Electrocardiogram PR and QRS intervals were significantly prolonged in Mena(-/-) mice, manifested by slowed conduction on optical mapping studies. Ultrastructural analysis of Mena(-/-) hearts revealed disrupted organization and widening of ICD structures, mislocalization of the gap junction protein connexin 43 (Cx43) to the lateral borders of cardiomyoycytes, and increased Cx43 expression. Furthermore, the expression of vinculin (an adherens junction protein) was significantly reduced in Mena(-/-) mice. We report for the first time that genetic ablation of Mena results in cardiac dysfunction, highlighted by diminished contractile performance, disrupted ICD structure, and slowed electrical conduction.


Subject(s)
Cytoskeletal Proteins/physiology , Heart Failure/physiopathology , Heart/physiopathology , Microfilament Proteins/physiology , Animals , Connexin 43/metabolism , Cytoskeletal Proteins/deficiency , Cytoskeletal Proteins/genetics , Disease Models, Animal , Gap Junctions/metabolism , Gap Junctions/ultrastructure , Heart Failure/metabolism , Humans , Mice , Mice, Inbred C57BL , Mice, Knockout , Myocardial Contraction/physiology , Myocardium/metabolism , Myocardium/ultrastructure , Phosphorylation
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