Publications

BACKGROUND: Early readmission after PCI is an important contributor to healthcare expenditures and a target for performance measurement. The extent to which 30-day readmissions after PCI are preventable is unknown yet essential to minimizing their occurrence.

METHODS AND RESULTS: PCI patients readmitted to hospital at which PCI was performed within 30 days of discharge at the Massachusetts General Hospital and Brigham and Women's Hospital were identified, and their medical records were independently reviewed by 2 physicians. Each reviewer used an ordinal scale (0, not; 1, possibly; 2, probably; and 3, definitely preventable) to rate clinical preventability, and a total sum score ≥2 was considered preventable. Characteristics of preventable and unpreventable readmissions were compared, and predictors of clinical preventability were assessed by using multivariate logistic regression. Of 9288 PCIs performed, 9081 (97.8%) patients survived to initial hospital discharge and 1007 (11.1%) were readmitted to the index hospital within 30 days. After excluding repeat readmissions, 893 readmissions were reviewed. Fair agreement between physician reviewers was observed (weighted κ statistic 0.44 [95% CI 0.39 to 0.49]). After aggregation of scores, 380 (42.6%) readmissions were deemed preventable and 513 (57.4%) were deemed not preventable. Common causes of preventable readmissions included staged PCI without new symptoms (14.7%), vascular/bleeding complications of PCI (10.0%), and congestive heart failure (9.7%).

CONCLUSIONS: Nearly half of 30-day readmissions after PCI may have been prevented by changes in clinical decision-making. Focusing on these readmissions may reduce readmission rates.

AIMS: To determine the incidence and predictors of atrial fibrillation (AF) and its impact on survival in patients with other forms of supraventricular arrhythmias (SVAs) including atrial flutter (AFL), atrial tachycardia (AT), atrioventricular reentrant (AVRT), and AV nodal reentrant tachycardia (AVNRT). We hypothesized that SVA may increase risk of AF and concomitant AF may influence long-term survival.

METHODS AND RESULTS: All patients who underwent catheter ablation for SVA from 2000 to 2010 were included in this study. The patients were identified retrospectively and the vital status determined prospectively. Observed survival in the study cohort was compared with survival rates in the age- and sex-matched general population. The study group included 1573 patients (mean age 50.5 ± 18 years, 47% female) with AVNRT (38.5%), AFL (29.6%), AVRT (22.6%) and AT (9.3%). The patients were followed for a mean of 35 months (median 23 months). Atrial fibrillation was documented in 424 patients (27%) with a higher incidence in males (35 vs. 18%). Atrial fibrillation was present in 19.6% of patients before the ablation and developed in 9.07% after ablation. Atrial fibrillation commonly occurred in patients with AFL (57.5%), AT (27.4%), AVRT (13.5%), and AVNRT (9.7%). Older age, prolonged PR interval, dilated left atrium, low left ventricular ejection fraction and presence of AFL were independent predictors for concomitant AF. Long-term survival was worse in the presence of AF.

CONCLUSION: The incidence of AF is high in patients with other forms of SVA. The most common association is between AFL and AF. Long-term survival is decreased in those who have concomitant AF, although AF did not emerge as an independent predictor of mortality when adjusted for other covariates.

OBJECTIVE: To derive and internally validate a clinical prediction rule for virologic response based on CD4 cell count increase after initiation of HAART in a resource-limited setting.

DESIGN AND METHODS: A retrospective cohort study at two HIV care clinics in Gaborone, Botswana. The participants were previously treatment-naive HIV-1-infected individuals initiating HAART. The main outcome measure was a plasma HIV-1 RNA level (viral load) < or = 400 copies/ml (i.e. undetectable) 6 months after initiating HAART.

RESULTS: The ability of CD4 cell count increase to predict an undetectable viral load was significantly better in those with baseline CD4 cell counts < or = 100 cells/microl [area under the ROC curve (AUC), 0.78; 95% confidence interval (CI), 0.67-0.89; versus AUC, 0.60; 95% CI, 0.48-0.71; P = 0.018]. The sensitivity, specificity, and positive and negative predictive values of a CD4 cell count increase of > or = 50 cells/microl for an undetectable viral load in those with baseline CD4 cell counts < or = 100 cells/microl were 93.1, 61.3, 92.5 and 63.3%, respectively. Alternatively, these values were 47.8, 87.1, 95.0 and 24.5%, respectively, if a increase in CD4 cell count of > or = 150 cells/microl was used.

CONCLUSIONS: CD4 cell count increase after initiating HAART has only moderate discriminative ability in identifying patients with an undetectable viral load, and the predictive ability is higher [corrected] in patients with lower baseline CD4 cell counts. Although HIV treatment programs in resource-constrained settings could consider the use of CD4 cell count increases to triage viral load testing, more accurate approaches to monitoring virologic failure are urgently needed.