Tree-structured risk stratification of in-hospital mortality after percutaneous coronary intervention for acute myocardial infarction: a report from the New York State percutaneous coronary intervention database.

BACKGROUND: Previous risk scores have shown excellent performance. However, the need for real-time risk score computation makes their implementation in an emergent situation challenging. A more simplified approach can provide practitioners with a practical bedside risk stratification tool. METHODS: We developed an easy-to-use tree-structured risk stratification model for patients undergoing early percutaneous coronary intervention (PCI) for acute myocardial infarction. The model was developed on the New York State PCI database for 1999 to 2000 (consisting of 5385 procedures) and was validated using the subsequent 2001 to 2002 database (consisting of 7414 procedures). RESULTS: Tree-structured modeling identified 3 key presenting features: cardiogenic shock, congestive heart failure, and age. In the validation data set, this risk stratification model identified patient groups with in-hospital mortality ranging from 0.5% to 20.6%, more than a 20-fold increased risk. The performance of this model was similar to the Mayo Clinic Risk Score with a discriminative capacity of 82% (95% confidence interval, 79%-84%) versus 80% (95% confidence interval, 77%-82%), respectively. CONCLUSION: Patients undergoing PCI for acute myocardial infarction can be readily stratified into risk categories using the tree-structured model. This provides practicing cardiologists with an internally validated and easy-to-use scheme for in-hospital mortality risk stratification.

Persistent sex difference in hospital outcome following percutaneous coronary intervention: results from the New York State reporting system.

BACKGROUND: Although sex-related differences in early outcomes have been observed in young women following acute myocardial infarction (AMI) and coronary bypass surgery, evidence for similar differences following percutaneous coronary intervention (PCI) is lacking. METHODS: Using the 1999 to 2002 New York State PCI reporting system, we identified 11,162 men and 2,561 women aged 50 years or younger undergoing a first PCI procedure. In-hospital outcomes were compared by gender after multivariable adjustment for baseline, clinical and procedural characteristics. RESULTS: Young women undergoing an initial PCI procedure were more likely to belong to racial or ethnic minorities and exhibit more comorbidities than young men. However, they had better ejection fraction (52.9% +/- 11.3 vs. 51.9 +/- 11; p = 0.0002) and presented more often with single-vessel disease (75% vs. 67%; p < 0.0001). Despite women receiving glycoprotein IIb/IIIa inhibitors (58.6% vs. 65.1%; p < 0.0001) and stents (92.5% vs. 94.9%; p < 0.0001) less often, procedural success was achieved equally (97% vs. 96%). Young women experienced higher rates of in-hospital mortality (0.70% vs. 0.22%; p < 0.0001), and vascular damage (0.82% vs. 0.24%; p < 0.0001) compared to men. In multivariable analysis, female sex independently predicted in-hospital mortality (OR 4.0, 95% CI: 1.9 to 8.1) after adjustment for urgency of PCI, clinical and procedural characteristics. CONCLUSION: A gender-based difference in early survival exists in young women undergoing a first PCI procedure. Further investigation into the mechanism of this higher risk is warranted.

Effectiveness of glycoprotein IIb/IIIa inhibitor use during primary coronary angioplasty: results of propensity analysis using the New York State Percutaneous Coronary Intervention Reporting System.

Patients undergoing primary angioplasty in clinical practice experience a higher risk for adverse events than those enrolled in clinical trials. Whether glycoprotein (GP) IIb/IIIa inhibitor use during primary angioplasty is both safe and effective in real life is unknown. Therefore, we examined the pattern of GP IIb/IIIa use and its effectiveness in a large population-based cohort of 7,321 patients who underwent primary angioplasty in New York State. Propensity analysis was used to account for the nonrandomized use of GP IIb/IIIa inhibitors. Overall, 78.5% of patients who underwent primary angioplasty received GP IIb/IIIa inhibitors. In-hospital mortality was significantly lower with GP IIb/IIIa use (3% vs 6.2%, p <0.0001) after adjustment for both propensity score (odds ratio 0.57, 95% confidence interval 0.44 to 0.74, p <0.0001) and the combination of propensity score and clinical characteristics (odds ratio 0.63, 95% confidence interval 0.45 to 0.88, p = 0.006). Patients with older age and higher Mayo Clinic Risk Score (MCRS) received GP IIb/IIIa inhibitors less often. However, stratified analysis of patients with low to moderate risk (MCRS <12) versus high risk (>or=12) demonstrated that GP IIb/IIIa use lowered risk of mortality both in low- to moderate-risk (1.39% vs 3.23%, p <0.0001) and high-risk patients (16.15% vs 22.41%, p = 0.03). In conclusion, adjunct GP IIb/IIIa inhibitor use during primary angioplasty is effective and associated with improved in-hospital survival rates.

Variants of human papillomaviruses 16 and 18 and their natural history in human immunodeficiency virus-positive women.

Highly oncogenic human papillomavirus (HPV) 16 and 18 variants might be expected to be particularly aggressive in HIV-positive women. The association of HPV16 and 18 variant lineages with race, human immunodeficiency virus (HIV) coinfection, CD4+ T-cell count, HIV-RNA level, time-to-clearance of HPV infection and presence of squamous intraepithelial lesions (SIL) among women in the Women's Interagency HIV Study was studied. Subjects were followed semi-annually with Pap smear and cervicovaginal lavage (CVL). HPV DNA was detected in CVLs using MY09/11 L1 PCR assay. Specimens positive for HPV16/18 underwent E6 PCR and sequencing to determine the variant present. Specimens from 195 HPV16- and 162 HPV18-positive women were classified into variant lineages based on sequencing results. African variants of HPV16 and HPV18 were significantly more prevalent among African-Americans than among Caucasians [42 versus 14 % (P=0.001) and 60 versus 13 % (P<0.001), respectively]. However, it was not possible to detect associations between the HPV16 or 18 variant lineages and other factors studied. African variants of HPV16/18 were more common in women of African descent living outside Africa, which could reflect mixing behaviours and/or immunogenetic factors. However, in a large population of HIV-infected women, the variant of HPV16 or 18 was unrelated to persistence of infection or presence of SIL. If non-European variants are more oncogenic, the effect may involve a late stage in cervical tumorigenesis.

Incidence of cervical squamous intraepithelial lesions associated with HIV serostatus, CD4 cell counts, and human papillomavirus test results.

CONTEXT: Recent cervical cancer screening guidelines state that the interval between screenings can be safely extended to 3 years in healthy women 30 years or older who have normal cytology results and have negative test results for oncogenic human papillomavirus (HPV) DNA. OBJECTIVE: To determine the incidence of squamous intraepithelial lesions (SILs) in HIV-seropositive women with normal cytology results, by baseline HPV DNA results. DESIGN, SETTING, AND PATIENTS: Participants were HIV-seropositive (n = 855; mean age, 36 years) and HIV-seronegative (n = 343; mean age, 34 years) US women with normal baseline cervical cytology who were enrolled in the Women's Interagency HIV Study (WIHS), a large, multi-institutional prospective cohort study. Since their recruitment during 1994-1995, WIHS participants have been followed up semi-annually with repeated Pap smears for a median of 7 years. MAIN OUTCOME MEASURE: The cumulative incidence of any SIL and high-grade SIL or cancer (HSIL+) was estimated according to baseline HPV DNA results, stratified by HIV serostatus and CD4 T-cell count. RESULTS: Development of any SIL in women with negative HPV results (both oncogenic and nononcogenic) at 2 years was as follows: in HIV-seropositive women with CD4 counts less than 200/microL, 9% (95% CI, 1%-18%); with CD4 counts between 200/muL and 500/microL, 9% (95% CI, 4%-13%); and with CD4 counts greater than 500/microL, 4% (95% CI, 1%-7%). The CIs for these estimates overlapped with those for HIV-seronegative women with normal baseline cytology who were HPV-negative (3%; 95% CI, 1%-5%), indicating that at 2 years, there were no large absolute differences in the cumulative incidence of any SIL between groups. Furthermore, no HPV-negative participants in any group developed HSIL+ lesions within 3 years. Multivariate Cox models showed that on a relative scale, the incidence of any SIL among HIV-seropositive women with CD4 counts greater than 500/microL (hazard ratio [HR], 1.2; 95% CI, 0.5-3.0), but not those with CD4 counts less than or equal to 500/microL (HR, 2.9; 95% CI, 1.2-7.1), was similar to that in HIV-seronegative women. CONCLUSION: The similar low cumulative incidence of any SIL among HIV-seronegative and HIV-seropositive women with CD4 counts greater than 500/microL and who had normal cervical cytology and HPV-negative test results suggests that similar cervical cancer screening practices may be applicable to both groups, although this strategy warrants evaluation in an appropriate clinical trial.