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"The failing heart is not just an enlarged version of a normal heart." I know Dr. Louis Katz said it, but I never found out where. At any rate, he posthumously alerted me to recognize that patients with heart failure do not demonstrate the lower range of normal physiology, but rather their own special ranges. I recognize this in the exquisite load sensitivity of the failing heart or in noting how much atrioventricular synchrony contributes to the failing heart. I try to teach this all the time-I'll know it's time to retire when I overhear the medical students joking about me having them graph the relationship between cardiac output and vascular resistance. Nevertheless, it's a concept I use every day.-Marc A. Silver Similar to all disease states, the primary approach to and ultimate treatment of heart failure is prevention. For the entire human population, this means bringing systemic blood pressure into the currently recommended range, controlling the risk factors for atherosclerosis, aggressively managing ischemic syndromes, reversing valvular and congenital lesions before cardiac damage occurs, and so forth. Hopefully, over time, we'll be able to counter and reverse many of the predisposing genetic factors as well.-Carl V. Leier Ask patients to describe exactly how they take their medications. Heart failure patients are frequent victims of polypharmacy, and despite the best intentions of the health care providers and patients, inadvertent medication errors are common. For example, one of my patients mixed up his digoxin and isosorbide dinitrate; as a result, he was taking digoxin three times a day (and wondering why he was nauseated)! Ask routinely about the use of over-the-counter medications, especially cold preparations, "diet pills," and nonsteroidal anti-inflammatory drugs (NSAIDs). These widely available agents are frequently used by heart failure patients, who fail to recognize the potential for drug-drug and drug-disease interactions.-Michael W. RichThere are several things I routinely do for each patient who comes to see me. On the first visit, I examine current medications and simplify the regimen. I eliminate calcium channel blockers, NSAIDs, and albuterol (unless there is a pressing need to continue these). We routinely check digoxin levels and adjust the medication to keep the plasma level between 0.7 and 1.0 ng/mL. This is based on data from our laboratory showing that most of the benefit of this drug is at low dose (J Am Coll Cardiol. 1997;29:1206) and a post hoc analysis of the DIG study, which showed a relationship of plasma level and mortality with more toxicity at higher doses (Am Heart J. 1997;134:3). I optimize angiotensin-converting enzyme (ACE) inhibitor doses (in an attempt to use the doses shown to be efficacious in the clinical trials) and use a longer-acting, preferably once-a-day ACE inhibitor to simplify the patient's regimen. I often give this dose prior to bedtime so that any hypotension will be at night while the patient is sleeping. I also give nitrates to my heart failure pat...

Funding Acknowledgements Type of funding sources: None. Introduction High-sensitivity C-reactive protein (hs-CRP), a marker of inflammation, is associated with atherosclerosis, and recent studies indicate that therapies targeting inflammation are associated with reductions in cardiovascular (CV) risk. However, factors predictive of elevated hs-CRP in the general population have not been elucidated. Purpose To determine independent predictors of hs-CRP levels in an ambulatory adult population in the US. Methods This study included 5412 adults from the NHANES 2015-2016 cohort and 5856 adults from the NHANES 2017-2018 cohort. The sample was scientifically selected to ensure representativeness of the larger US population. Multivariable logistic regression analysis was used to identify independent predictors of elevated hs-CRP (≥3 mg/L) utilizing the NHANES 2015-2016 cycle (derivation set). The model was verified utilizing the independent NHANES 2017-2018 cycle (validation set). Candidate variables comprised demographic, behavioral, and clinical factors, including standard CV risk factors. Models based on diet and nutrition were developed separately on a subsample of subjects who answered dietary questions. Model discrimination was assessed using area under the receiver-operator characteristic curve (c-statistic). Results Significant independent predictors of high hs-CRP included: increased age (OR 1.09; 95% CI 1.03-1.14 per decade; P=0.024), increased BMI (OR 1.12; 95% CI 1.10-1.14; P<0.001), elevated white blood cell count (OR 1.21; 95% CI 1.15-1.28 per 1000 white blood cells/uL; P=0.002), Black vs White race (OR 1.31; 95% CI 1.10-1.56; P=0.037), female sex (OR 1.57; 95% CI 1.36-1.80; P=0.003), and self-reported poor vs excellent health (OR 1.73; 95% CI 1.04-2.22; P=0.012). The model had excellent discrimination with a c-statistic of 0.77 in the 2015-2016 derivation cycle and 0.76 in the 2017-2018 validation cycle. None of the standard CV risk factors contributed to the model. The only significant nutritional predictor of lower hs-CRP was fiber intake (OR 0.99; 95% CI 0.98-0.99; P=0.035) and the only significant dietary predictor was fruit intake (OR 0.67; 95% CI 0.4-0.934; P=0.045). The dietary and nutrition models had poor discrimination with c-statistics of 0.60 in the 2015-2016 cohort and 0.61 in the 2017-2018 cohort for both models. In a sensitivity analysis, adding dietary factors to the main model did not improve discrimination. Conclusion Older age, female sex, Black race, increased BMI, higher white blood cell count, and self-reported poor health were independent predictors of elevated hs-CRP levels. Higher fruit and fiber consumption were associated with lower hs-CRP levels in univariate but not multivariable models. Additional studies are needed to determine if behavioral modifications (weight loss, increased fiber and fruit intake) can lower hs-CRP and whether this translates to reduced risk for cardiovascular disease.