16 research outputs found

    Chronic Heart Failure and Exercise Intolerance: The Hemodynamic Paradox

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    Heart failure represents a major source of morbidity and mortality in industrialized nations. As the leading hospital discharge diagnosis in the United States in patients over the age of 65, it is also associated with substantial economic costs. While the acute symptoms of volume overload frequently precipitate inpatient admission, it is the symptoms of chronic heart failure, including fatigue, exercise intolerance and exertional dyspnea, that impact quality of life. Over the last two decades, research into the enzymatic, histologic and neurohumoral alterations seen with heart failure have revealed that hemodynamic derangements do not necessarily correlate with symptoms. This “hemodynamic paradox” is explained by alterations in the skeletal musculature that occur in response to hemodynamic derangements. Importantly, gender specific effects appear to modify both disease pathophysiology and response to therapy. The following review will discuss our current understanding of the systemic effects of heart failure before examining how exercise training and cardiac resynchronization therapy may impact disease course

    Catheter ablation of inappropriate sinus tachycardia

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    Catheter ablation for inappropriate sinus tachycardia (IST) is recommended for patients symptomatic for palpitations and refractory to other treatments. The current approach consists in sinus node modification (SNM), achieved by ablation of the cranial part of the sinus node to eliminate faster sinus rates while trying to preserve chronotropic competence. This approach has a limited efficacy, with a very modest long-term clinical success. To overcome this, proper patient selection is crucial and an epicardial approach should always be considered. This brief review will discuss the current role and limitations of catheter ablation in the management of patients with IST

    Difference in thermodynamics between two types of esophageal temperature probes: Insights from an experimental study

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    Luminal esophageal temperature (LET) monitoring is performed with a variety of temperature probes, but little is known on the relationship between the structure of a given probe and its thermodynamic characteristics

    Acute and early outcomes of focal impulse and rotor modulation (FIRM)-guided rotors-only ablation in patients with nonparoxysmal atrial fibrillation

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    Background Focal impulse and rotor modulation (FIRM)-guided ablation targets sites that are thought to sustain atrial fibrillation (AF). Objective The purpose of this study was to evaluate the acute and mid-term outcomes of FIRM-guided only ablation in patients with nonparoxysmal AF. Methods We prospectively enrolled patients with persistent and long-standing persistent (LSP) AF at three centers to undergo FIRM-guided only ablation. We evaluated acute procedural success (defined as AF termination, organization, or ≥10% slowing), safety (incidence of periprocedural complications), and long-term success (single-procedure freedom from atrial tachycardia [AT]/AF off antiarrhythmic drugs [AAD] after a 2-month blanking period). Results Twenty-nine patients with persistent (N = 20) and LSP (N = 9) AF underwent FIRM mapping. Rotors were presents in all patients, with a mean of 4 ± 1.2 per patient (62% were left atrial); 1 focal impulse was identified. All sources were successfully ablated, and overall acute success rate was 41% (0 AF termination, 2 AF slowing, 10 AF organization). There were no major procedure-related adverse events. After a mean 5.7 months of follow-up, single-procedure freedom from AT/AF without AADs was 17%. Conclusion In nonparoxysmal AF patients, targeted ablation of FIRM-identified rotors is not effective in obtaining AF termination, organization, or slowing during the procedure. After mid-term follow-up, the strategy of ablating FIRM-identified rotors alone did not prevent recurrence from AT/AF

    Outcomes of atrioesophageal fistula following catheter ablation of atrial fibrillation treated with surgical repair versus esophageal stenting

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    Atrioesophageal fistula (AEF) is a rare but devastating complication of radiofrequency catheter ablation (RFCA) of atrial fibrillation (AF). Surgical repair and esophageal stents are available treatment options for AEF. We report outcomes of these 2 management strategies

    Novel association of polymorphic genetic variants with predictors of outcome of catheter ablation in atrial fibrillation: new directions from a prospective study (DECAF)

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    Purpose: Non-pulmonary vein (non-PV) triggers and left atrial (LA) scars perpetuate atrial fibrillation (AF) and limit the success rate of catheter ablation. In order to understand the genetic basis of these risk factors, we examined the association of selected single nucleotide polymorphisms (SNPs) with scar and non-PV triggers. Methods: Four hundred AF patients (67 % male, 62 ± 12 years, LA size 45.3 ± 7 mm, 64 % non-paroxysmal) undergoing catheter ablation were prospectively enrolled. DNA extractions for 16 AF-related SNPS from blood samples were performed of which 371 DNA samples were available for genotyping. Multivariate logistic regression analysis was used for assessing predictive role of individual SNP, and logistic kernel-machine approach was applied to test the cumulative effect of multiple SNPs as a group with non-PV triggers and LA scar. False discovery rate (FDR) was computed for all candidate SNPs to address multiple testing. Results: SNPs rs6599230 and rs6843082 were inversely associated (OR 0.68, p = 0.04, and 0.62, p = 0.01, respectively) whereas rs1448817 (OR 1.74, p = 0.04) and rs7193343 (OR 1.66, p = 0.02) predicted higher risk of non-PV triggers. Genotypes for rs6599230 and rs6843082 conferred 51 % reduction in the odds for non-PV triggers (combined OR 0.49, p = 0.019), while rs1448817 and rs7193343 demonstrated a combined OR of 1.93, p = 0.025. FDR was controlled at 16 % to adjust for multiple testing. For LA scar, inverse association was observed with rs1448817 (OR 0.29, p = 0.006), rs17042171 (OR 0.27, p = 0.032), rs3807989 (OR 0.54, p = 0.017), and rs6843082 (OR 0.56, p = 0.009). Two SNPs were associated with increased scar risk: rs17375901 (OR 3.68, p = 0.03) and rs7193343 (OR 1.74, p = 0.037). For global association of SNPs with left atrial scar FDR was controlled at ≤10 % to adjust for multiple testing. Conclusions: This study has a strong clinical significance as it provides important insights into the molecular basis of pertinent therapeutic targets. Our findings demonstrate that the presence of certain genetic polymorphisms increases the risk of scar and non-PV triggers in AF patients. Therefore, PVAI alone will not be enough to eliminate the arrhythmia and the operators may need to identify and isolate the non-PV foci to maximize procedural success in patients carrying these risk variants. Clinical trial registration: clinicaltrials.gov (NCT01751607
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