Relationship between thiazolidinedione use and cardiovascular outcomes and all-cause mortality among patients with diabetes: a time-updated propensity analysis.

PURPOSE: To investigate the association of the thiazolidinediones (TZDs), rosiglitazone, and pioglitazone, together and individually on the risk of cardiovascular outcomes and all-cause mortality, using time-updated propensity score adjusted analysis. METHODS: We conducted a retrospective cohort study in a large vertically integrated health system in southeast Michigan. Cohort inclusion criteria included adult patients with diabetes treated with oral medications and followed longitudinally within the health system between 1 January 2000 and 1 December 2006. The primary outcome was fatal and non-fatal acute myocardial infarction (AMI). Secondary outcomes included hospitalizations for congestive heart failure (CHF), fatal, and non-fatal cerebrovascular accidents (CVA) and transient ischemic attacks (TIA), combined coronary heart disease (CHD) events, and all-cause mortality. RESULTS: 19,171 patients were included in this study. Use of TZDs (adjusted hazard ratio (aHR) with propensity adjustment (PA), 0.92; 95% confidence interval (CI) 0.73-1.17), rosiglitazone (aHR with PA, 1.06; 95%CI 0.66-1.70), and pioglitazone (aHR with PA, 0.91; 95%CI 0.69-1.21) was not associated with a higher risk of AMI. However, pioglitazone use was associated with a reduction in all-cause mortality (aHR with PA, 0.60; 95%CI 0.42-0.96). Compared with rosiglitazone, pioglitazone use was associated with a lower risk of all outcomes assessed, particularly CHF (p = 0.013) and combined CHD events (p = 0.048). CONCLUSIONS: Our findings suggest that pioglitazone may have a more favorable risk profile when compared to rosiglitazone, arguing against a singular effect for TZDs on cardiovascular outcomes.

Prognostic predictors and outcomes in patients with abnormal myocardial perfusion imaging and angiographically insignificant coronary artery disease.

BACKGROUND: Abnormal stress myocardial perfusion imaging studies (SMPI) with angiographically insignificant coronary artery disease (ICAD) have often been labeled "false positive" scans. We evaluated the prognostic predictors and outcomes in an unselected patient population having abnormal SMPI and ICAD (study group) over a 24 month period of follow-up. METHODS: Retrospective study of consecutive patients who had SMPI and subsequent coronary angiography showing ICAD within 6 months of index scan with matched control group with normal scans. Major Adverse Cardiac Events (MACE) were defined as the first occurrence of death or myocardial infarction (MI). Patients were followed up to 24 months from the time of their SMPI to identify the development of MACE. RESULTS: One hundred and twenty five patients formed the study group and one hundred and thirty six patients formed the control group. Over a two-year follow up, approximately 13% of the study group had MACE as compared to 4.2% in the control group (P = .022). Abnormal SMPI, EF < 40% and chronic kidney disease (GFR < 60 ml/min) were independent predictors of MACE in the study group. In multivariate analysis for MACE prediction, chronic kidney disease remained the sole independent predictor regardless of size or severity of perfusion abnormalities (P = <.001). CONCLUSION: Patients with abnormal SMPI and ICAD have a 13% event rate of MACE over a two-year follow up. CKD seems a very important marker of a higher risk subgroup amongst such patients.

Electrocardiographic features and prevalence of bilateral bundle-branch delay.

BACKGROUND: Definitive diagnosis of bilateral bundle-branch delay/block may be made when catheter-induced right bundle-branch block (RBBB) develops in patients with baseline left bundle-branch (LBB) block. We hypothesized that a RBBB pattern with absent S waves in leads I and aVL will identify bilateral bundle-branch delay/block. METHODS AND RESULTS: Fifty patients developing transient RBBB pattern in lead V1 during right heart catheterization were studied. Patients were grouped according to whether the baseline ECG demonstrated a normal QRS, left fascicular blocks, or LBB block pattern. The RBBB morphologies in each group were compared. The prevalence of bilateral bundle-branch delay/block pattern was examined in our hospital ECG database. All patients with baseline normal QRS complexes (n=30) or left fascicular blocks (4 anterior, 5 posterior) developed a typical RBBB pattern. Among the 11 patients with a baseline LBB block pattern, 7 developed an atypical RBBB pattern with absent S waves in leads I and aVL and the remaining 4 demonstrated a typical RBBB. The absence of S waves in leads I and aVL during RBBB was 100% specific and 64% sensitive for the presence of pre-existing LBB block. Among the consecutive 2253 hospitalized patients with RBBB, 34 (1.5%) had the bilateral bundle-branch delay/block pattern. CONCLUSIONS: An ECG pattern of RBBB in lead V1 with absent S wave in leads I and aVL indicates concomitant LBB delay. Pure RBBB and bifascicular blocks are associated with S waves in leads I and aVL.

Natural history of the Sprint Fidelis lead: survival analysis from a large single-center study.

PURPOSE: The purposes of our study were to: (1) determine lead failure rate in a large single-center cohort of Sprint Fidelis 6949 (Fidelis) leads, (2) define the risk of lead failure over time, (3) assess the impact of the Lead Integrity Alert (LIA) on lead failure presentation, and (4) identify independent predictors of Fidelis lead failure. METHODS: All patients who underwent implantation of a Fidelis lead between September 2004 and July 2007 were included. Demographic, clinical, and device characteristics at the time of implant and prior to failure were collected and analyzed. RESULTS: A total of 971 Fidelis leads (706 men, 265 women,mean age 68.4±12.8 years) were implanted. Over a mean follow-up of 46.3 months, there were 69 lead failures(7.1%). The 5-year lead survival rate was 90.3%. The risk of lead failure demonstrated a double-peaked pattern at 34 and 61 months. In multivariate analysis, there were no independent predictors of lead failure. Inappropriate shocks(IS) were the first sign of lead failure in 29 patients (42%).The incidence (32.6% vs. 65.2%, p=0.01) and number ofIS (2.8±7.2 vs. 11.3±18.7, p=0.01) were significantly lower in patients with LIA. CONCLUSIONS: This study presents a single-center experience on the natural history of the Fidelis lead. In our experience, lead survival declines at a lower rate when compared to prior reports. The risk of lead failure demonstrated a double peaked pattern at approximately 3 and 5 years. No identified variable was predictive of lead failure. LIA was effective in reducing the incidence and number of IS.