19 research outputs found

    How I do it: Minimally invasive Cox-Maze IV procedure

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    Clinical vignette Our patient is a 66-year-old female with a 2-year history of atrial fibrillation (AF) and mitral valve prolapse who presented with dyspnea on exertion. She was found to be in AF upon her admission electrocardiogram. A transthoracic echocardiogram was performed demonstrating moderate-to-severe mitral regurgitation (MR) with a left atrial (LA) diameter of 5.1 cm and normal left ventricular (LV) function. After completion of her workup, it was decided that the patient would best be treated by a minimally invasive Cox-Maze IV (CMIV) and concomitant mitral valve procedure given her significant MR and symptoms. This article and accompanying video will discuss how the minimally invasive CMIV procedure is performed. Surgical technique

    Comparison of the stand-alone Cox-Maze IV procedure to the concomitant Cox-Maze IV and mitral valve procedure for atrial fibrillation

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    BACKGROUND: The majority of patients undergoing surgical ablation for atrial fibrillation (AF) worldwide receive a concomitant mitral valve (MV) procedure. This study compared outcomes of the Cox-Maze IV (CMIV) in patients with lone AF to those with AF and MV disease. METHODS: A retrospective review of 335 patients receiving either a stand-alone CMIV for AF (n=151) or a CMIV with a MV procedure (n=184) was performed from January 2002 through December of 2012. Data were obtained at 3, 6, 12, 24, and 48 months and patients were evaluated for recurrence of AF. Twenty-four preoperative and perioperative variables were evaluated to identify predictors of AF recurrence at one year. RESULTS: The two groups differed in that stand-alone CMIV patients were younger, had AF of longer duration and had more failed catheter ablations, while patients with AF and MV disease had larger left atria and worse New York Heart Association class (P≀0.001). Operative mortality was higher in the concomitant MV group (1% vs. 5%, P=0.015). Freedom from AF and antiarrhythmic drugs at 12 and 24 months were similar between the two groups (73% and 76% at 12 months; 77% vs. 78% at 24 months). Predictors of recurrence included failure to use a box-lesion to isolate the pulmonary veins and posterior left atria, early recurrence of atrial tachyarrhythmias (ATAs) and the presence of a preoperative pacemaker (P=0.001). CONCLUSIONS: The efficacy of the CMIV procedure was similar in patients with and without co-existent MV pathology. Patients receiving a concomitant CMIV and MV procedure represented an older and sicker patient population and had higher mortality rates than those receiving a stand-alone CMIV procedure

    Diazoxide maintains human myocyte volume homeostasis during stress

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    BACKGROUND: Exposure to hypothermic hyperkalemic cardioplegia, hyposmotic stress, or metabolic inhibition results in significant animal myocyte swelling (6% to10%) and subsequent reduced contractility (10% to 20%). Both are eliminated by the adenosine triphosphate-sensitive potassium channel opener diazoxide (DZX). The relationship between swelling and reduced contractility suggests that the structural change may represent one mechanism of postoperative myocardial stunning. This study evaluated human myocyte volume during stress to investigate if similar phenomena exist in human myocytes. METHODS AND RESULTS: Human atrial myocytes isolated from tissue obtained during cardiac surgery were perfused with Tyrode's physiological solution (20 minutes, 37°C), test solution (20 minutes), and Tyrode's (37°C, 20 minutes). Test solutions (n=6 to 12 myocytes each) included Tyrode's (37°C or 9°C), Tyrode's+DZX (9°C), hyperkalemic cardioplegia (9°C)±DZX, cardioplegia+DZX+HMR 1098 (sarcolemmal adenosine triphosphate-sensitive potassium channel inhibitor, 9°C), cardioplegia+DZX+5-hydroxydeconoate (mitochondrial adenosine triphosphate-sensitive potassium channel inhibitor, 9°C), mild hyposmotic solution±DZX, metabolic inhibition±DZX, and metabolic inhibition+DZX+5-hydroxydeconoate. Myocyte volume was recorded every 5 minutes. Exposure to hypothermic hyperkalemic cardioplegia, hyposmotic stress, or metabolic inhibition resulted in significant human myocyte swelling (8%, 7%, and 6%, respectively; all P<0.05 vs control). In all groups, the swelling was eliminated or lessened by DZX. The addition of channel inhibitors did not significantly alter results. CONCLUSIONS: DZX maintains human myocyte volume homeostasis during stress via an unknown mechanism. DZX may prove to be clinically useful following the elucidation of its specific mechanism of action. (J Am Heart Assoc. 2012;1:jah3-e000778 doi: 10.1161/JAHA.112.000778.

    The impact of uncorrected mild aortic insufficiency at the time of left ventricular assist device implantation

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    OBJECTIVE: The study objective was to investigate the progression of uncorrected mild aortic insufficiency and its impact on survival and functional status after left ventricular assist device implantation. METHODS: We retrospectively reviewed 694 consecutive patients who underwent implantation of a continuous-flow left ventricular assist device between January 2006 and March 2018. Pre-left ventricular assist device transthoracic echocardiography identified 111 patients with mild aortic insufficiency and 493 patients with trace or no aortic insufficiency. To adjust for differences in preoperative factors, propensity score matching was used, resulting in 101 matched patients in each of the mild aortic insufficiency and no aortic insufficiency groups. RESULTS: Although both groups showed similar survival (P = .58), the mild aortic insufficiency group experienced higher incidence of readmission caused by heart failure (hazard ratio, 2.62; 95% confidence interval, 1.42-4.69; P \u3c .01). By using the mixed effect model, pre-left ventricular assist device mild aortic insufficiency was a significant risk factor for both moderate or greater aortic insufficiency and worsening New York Heart Association functional status (P \u3c .01). CONCLUSIONS: Patients with uncorrected mild aortic insufficiency had a higher risk of progression to moderate or greater aortic insufficiency after left ventricular assist device implantation with worse functional status and higher incidence of readmission caused by heart failure compared with patients without aortic insufficiency. Further investigations into the safety and efficacy of concomitant aortic valve procedures for mild aortic insufficiency at the time of left ventricular assist device implant are warranted to improve patients\u27 quality of life, considering the longer left ventricular assist device use as destination therapy and bridge to transplant with the new US heart allocation system

    Lower survival after coronary artery bypass in patients who had atrial fibrillation missed by widely used definitions

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    OBJECTIVE: To investigate the impact of limiting the definition of post-coronary artery bypass graft (CABG) atrial fibrillation (AF) to AF/flutter requiring treatment-as in the Society of Thoracic Surgeons\u27 (STS) database- on the association with survival. PATIENTS AND METHODS: We assessed in-hospital incidence of post-CABG AF in 7110 consecutive isolated patients with CABG without preoperative AF at 4 hospitals (January 1, 2004 to December 31, 2010). Patients with ≄1 episode of post-CABG AF detected via continuous in-hospital electrocardiogram (ECG)/telemetry monitoring documented by physicians were assigned to the following: Group 1, identified as having post-CABG AF in STS data and Group 2, not identified as having post-CABG AF in STS data. Patients without documented post-CABG AF constituted Group 3. Survival was compared via a Cox model, adjusted for STS risk of mortality and accounting for site differences. RESULTS: Over 7 years\u27 follow-up, 16.0% (295 of 1841) of Group 1, 18.7% (79 of 422) of Group 2, and 7.9% (382 of 4847) of Group 3 died. Group 2 had a significantly greater adjusted risk of death than both Group 1 (hazard ratio [HR]: 1.16; 95% confidence interval [CI], 1.02 to 1.33) and Group 3 (HR: 1.94; 95% CI, 1.69 to 2.22). CONCLUSIONS: The statistically significant 16% higher risk of death for patients with AF post-CABG missed vs captured in STS data suggests treatment and postdischarge management should be investigated for differences. The historical misclassification of missed patients as experiencing no AF in the STS data weakens the ability to observe differences in risk between patients with and without post-CABG AF. Therefore, STS data should not be used for research examining post-CABG AF

    An experimental model of chronic severe mitral regurgitation

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    OBJECTIVE: To develop a minimally invasive, reproducible model of chronic severe mitral regurgitation (MR) that replicates the clinical phenotype of left atrial (LA) and left ventricular dilation and susceptibility to atrial fibrillation. METHODS: Under transesophageal echocardiographic guidance, chordae tendinae were avulsed using endovascular forceps until the ratio of regurgitant jet area to LA area was ≄70%. Animals survived for an average of 8.6 ± 1.6 months (standard deviation) and imaged with monthly transthoracic echocardiography (TTE). Animals underwent baseline and preterminal magnetic resonance imaging. Terminal studies included TTE, transesophageal echocardiography, and rapid atrial pacing to test inducibility of atrial tachyarrhythmias. RESULTS: Eight dogs underwent creation of severe MR and interval monitoring. Two were excluded-one died from acute heart failure, and the other had resolution of MR. Six dogs underwent the full experimental protocol; only one required medical management of clinical heart failure. MR remained severe over time, with a mean terminal regurgitant jet area to LA area of 71 ± 14% (standard deviation) and regurgitant fraction of 52 ± 11%. Mean LA volume increased over 130% (TTE: 163 ± 147%, CONCLUSIONS: Within the 6 dogs that successfully completed the full experimental protocol, this model replicated the clinical phenotype of severe MR, which led to marked structural and electrophysiologic cardiac remodeling. This model allowed for precise measurements at repeated time points and will facilitate future studies to elucidate the mechanisms of atrial and ventricular remodeling secondary to MR and the pathophysiology of valvular atrial fibrillation

    Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

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    IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570
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