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Objective: The TIMI Risk Score for secondary prevention (TRS2°P), a simple scoring system based on presence/absence of nine clinical factors, was developed to stratify the risk of secondary events in patients with a history of myocardial infarction (MI), but its performance has not been evaluated in patients with peripheral artery disease (PAD). Since MI and PAD are caused by similar biology and underlying atherosclerotic disease it is possible that TRS2°P is also informative in PAD patients. Methods: TRS2°P was calculated with a point value of 1 assigned for heart failure, hypertension, age ≥75 years, diabetes, stroke, coronary artery bypass graft, PAD, kidney dysfunction, and current smoking (since all patients had PAD, the lowest possible score was 1). We evaluated prediction statistics of TRS2°P for major adverse cardiovascular disease (MACE) (a composite of cardiovascular death, myocardial infarction, or ischemic stroke) in 386,458 patients with PAD in five international cohorts from New Zealand, South Korea, Sweden, and the US participating in the Chronic Kidney Disease Prognosis Consortium. Results: Overall, there were 134,827 cases of MACE outcomes reported across five cohorts over a mean follow-up of 5 years, and overall MACE rate ranged from 1.5 to 8.6 (per 100 person-years). The TRS2°P showed modest calibration (Brier score ranged from 0.061 to 0.160) and discrimination (c-statistics ranged from 0.59 to 0.69) across cohorts (Brier score was 0.098 and c-statistic was 0.67 in the TRS2°P derived dataset). Although there was some heterogeneity across cohorts, the predictors in the TRS2°P were generally associated with MACE in patients with PAD, with the strongest association for a history of heart failure (meta-analyzed adjusted hazard ratio [HR] 2.1), followed by age ≥75 years (HR 1.8), stroke (HR 1.7), kidney dysfunction (HR 1.4), and current smoking (HR 1.2). Hypertension and coronary artery bypass graft surgery did not reach statistical significance. Conclusion: TRS2°P was reasonably predictive of MACE outcomes when applied in patients with PAD and thus can be a reasonable tool for risk assessment in two common leading atherosclerotic diseases, MI and PAD. [ABSTRACT FROM AUTHOR]

Background: High-sensitivity cardiac troponin T (hs-cTnT) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) at the time of myocardial infarction (MI) are strong prognostic predictors. However, whether their pre-morbid (before MI occurrence) levels at middle age are associated with prognosis after incident MI is unknown. Methods: In 1,192 participants from the Atherosclerosis Risk in Communities (ARIC) study with incident MI after baseline (1990-92), we evaluated premorbid levels of hs-cTnT (<3 [reference], 3-5, 6-8, 9-13, and ≥14 ng/L) and NT-proBNP (<35.2 [reference], 35.2-68.4, 68.5-121.2, 121.3-223.9, and ≥224.0 pg/mL; divided at the same percentiles) measured, on average, 8.0 [IQR 3.7-13.5] years prior to incident MI, and evaluated their associations with composite and individual outcomes of all-cause mortality, cardiovascular mortality, recurrent MI, heart failure, and stroke through 2016. Cox regression models were used to adjust for potential confounders at the time of incident MI. Results: During a median follow-up of 2.7 years after MI, 911 participants developed the composite outcome. Both hs-cTnT and NT-proBNP were independently associated with composite outcome after incident MI (e.g., HR 1.60 [95%CI 1.27-2.02] for hs-cTnT ≥14 vs. <3 ng/L and 1.76 [1.41-2.21] for NT-proBNP ≥224.0 vs.<35.2 pg/mL). Both cardiac markers were associated with all-cause and cardiovascular mortality, and heart failure after incident MI, and NT-proBNP generally demonstrated a dose-response relationship with heart failure after incident MI. The associations were consistent even after accounting for MI severity score. The addition of hs-cTnT and NT-proBNP to conventional risk factors significantly improved risk prediction of heart failure after incident MI (C-statistic differences of 0.009 [95% CI 0.001-0.018] for heart failure, from 0.706 with conventional risk factors). Conclusions: Premorbid levels of hs-cTnT and NT-proBNP assessed, on average, almost a decade prior to incident MI were associated with adverse outcomes after incident MI. These results may highlight a prognostic value of pre-MI cardiac condition. [ABSTRACT FROM AUTHOR]

Background: The association between low systolic blood pressure (SBP) and vascular disease is unclear, especially in nonclinical populations., Methods and Results: We studied 1 235 246 individuals who participated in routine medical examinations between 1992 and 1995. The hazard ratios (HRs) were adjusted for potential confounders. During 22.7 million person-years of follow-up, 34 816 individuals died of atherosclerotic vascular diseases. An increase in SBP was directly related to an increase in vascular mortality at SBP above ≈100 mmHg. The group with the lowest SBP (<90 mm Hg) had a higher HR for mortality from atherosclerotic vascular disease (HR, 1.53; 95% confidence interval, 1.15-2.03) in comparison with those with an SBP of 90 to 99 mm Hg. The HR associated with the lowest SBP was 2.54 (95% confidence interval, 1.51-4.29) for ischemic heart disease and 1.21 (95% confidence interval, 0.79-1.85) for stroke. Regarding stroke subtype, mortality from hemorrhagic stroke (HR per 10 mm Hg increase, 0.53; 95% confidence interval, 0.29-0.96), rather than mortality from ischemic stroke (HR per 10 mm Hg increase, 1.00; 95% confidence interval, 0.51-1.97), was inversely associated with SBP when SBP fell to <100 mm Hg. Even when excluding the first 5 years of follow-up, the HRs associated with the lowest SBP did not decrease. The inverse association between SBP and vascular mortality in the range <100 mm Hg tended to be apparent in people aged 60 to 95 years in comparison with individuals aged 30 to 59 years., Conclusions: J-curve associations exist between SBP and vascular mortality, which reach a nadir at ≈100 mm Hg. SBP of <90 mm Hg may portend death from vascular disease, particularly from ischemic heart disease., (© 2016 American Heart Association, Inc.)