03075nas a2200421 4500008004100000022001400041245018900055210006900244260001300313300001200326490000700338520176300345653000902108653002202117653002502139653002702164653003602191653001102227653001502238653001102253653000902264653001302273653003102286653002002317653001702337653003202354653002202386653001802408100002202426700002402448700002302472700002802495700002602523700002402549700002102573700002302594856003602617 2008 eng d a1540-816700aNovel measures of heart rate variability predict cardiovascular mortality in older adults independent of traditional cardiovascular risk factors: the Cardiovascular Health Study (CHS).0 aNovel measures of heart rate variability predict cardiovascular  c2008 Nov a1169-740 v193 a

UNLABELLED: Novel HRV Predicts CV Mortality in the Elderly.

BACKGROUND: It is unknown whether abnormal heart rate turbulence (HRT) and abnormal fractal properties of heart rate variability identify older adults at increased risk of cardiovascular death (CVdth).

METHODS: Data from 1,172 community-dwelling adults, ages 72 +/- 5 (65-93) years, who participated in the Cardiovascular Health Study (CHS), a study of risk factors for CV disease in people >or=65 years. HRT and the short-term fractal scaling exponent (DFA1) derived from 24-hour Holter recordings. HRT categorized as: normal (turbulence slope [TS] and turbulence onset [TO] normal) or abnormal (TS and/or TO abnormal). DFA1 categorized as low (1). Cox regression analyses stratified by Framingham Risk Score (FRS) strata (low = <10, mid = 10-20, and high >20) and adjusted for prevalent clinical cardiovascular disease (CVD), diabetes, and quartiles of ventricular premature beat counts (VPCs).

RESULTS: CVdths (N = 172) occurred over a median follow-up of 12.3 years. Within each FRS stratum, low DFA1 + abnormal HRT predicted risk of CVdth (RR = 7.7 for low FRS; 3.6, mid FRS; 2.8, high FRS). Among high FRS stratum participants, low DFA1 alone also predicted CVdth (RR = 2.0). VPCs in the highest quartile predicted CVdth, but only in the high FRS group. Clinical CV disease predicted CVdth at each FRS stratum (RR = 2.9, low; 2.6, mid; and 1.9, high). Diabetes predicted CVdth in the highest FRS group only (RR = 2.2).

CONCLUSIONS: The combination of low DFA1 + abnormal HRT is a strong risk factor for CVdth among older adults even after adjustment for conventional CVD risk measures and the presence of CVD.

10aAged10aAged, 80 and over10aArrhythmias, Cardiac10aDeath, Sudden, Cardiac10aElectrocardiography, Ambulatory10aFemale10aHeart Rate10aHumans10aMale10aMaryland10aReproducibility of Results10aRisk Assessment10aRisk Factors10aSensitivity and Specificity10aSurvival Analysis10aSurvival Rate1 aStein, Phyllis, K1 aBarzilay, Joshua, I1 aChaves, Paulo, H M1 aMistretta, Stephanie, Q1 aDomitrovich, Peter, P1 aGottdiener, John, S1 aRich, Michael, W1 aKleiger, Robert, E uhttps://chs-nhlbi.org/node/104202581nas a2200229 4500008004100000022001400041245011900055210006900174260001600243520184500259100002102104700002602125700002302151700001902174700002002193700002202213700001702235700002102252700001802273700002402291856003602315 2023 eng d a1879-148400aNon-esterified fatty acids and risk of peripheral artery disease in older adults: The cardiovascular health study.0 aNonesterified fatty acids and risk of peripheral artery disease  c2023 Jan 293 a

BACKGROUND AND AIMS: Non-esterified fatty acids have been implicated in the pathogenesis of diabetes and cardiovascular disease. No longitudinal study has assessed their effects on peripheral artery disease (PAD). We determined the relationships between NEFAs and incident clinical PAD and abnormal ankle-brachial index (ABI) in a population-based cohort of older persons.

METHODS: We evaluated 4575 community living participants aged >65 years who underwent measurement of circulating NEFAs in fasting specimens and ABI in 1992-1993. Participants were assessed annually for clinical PAD until 2015 and underwent repeat ABI in 1998-1999. We used Cox proportional hazards regression to model the associations between NEFAs and risk of clinical PAD and logistic regression to model the associations of NEFAs with incident abnormal ABI.

RESULTS: Mean age was 74.8 years, 59% were female, and 17% were Black. NEFAs were associated with higher risk of clinical PAD in unadjusted and adjusted models. The adjusted hazard ratios for incident clinical PAD were 1.51 (95%CI = 1.06-2.13, p = 0.02) across extreme tertiles, and 1.14 (95%CI = 0.99-1.31, p = 0.08) per standard deviation higher NEFA. The corresponding odds ratios for abnormal ABI were 0.95 (95%CI = 0.69-1.32, p = 0.76) across extreme tertiles, and 1.03 (95%CI = 0.89-1.20, p = 0.68) per standard deviation higher NEFA. Relationships appeared similar irrespective of sex, race, or pre-existing cardiovascular disease, but were stronger later than earlier in follow-up.

CONCLUSIONS: Higher serum levels of NEFAs are significantly associated with increased likelihood of clinical PAD over long-term follow-up but not with 6-year decline in ABI. NEFAs may offer a potential target for intervention against clinical PAD.

1 aAhiawodzi, Peter1 aSolaru, Khendi, White1 aChaves, Paulo, H M1 aIx, Joachim, H1 aKizer, Jorge, R1 aTracy, Russell, P1 aNewman, Anne1 aSiscovick, David1 aDjoussé, Luc1 aMukamal, Kenneth, J uhttps://chs-nhlbi.org/node/9284