Cardiovascular Risk Assessment in the Older Athlete.

CONTEXT: Limited data are available to guide cardiovascular screening in adult or masters athletes (≥35 years old). This review provides recommendations and the rationale for the cardiovascular risk assessment of older athletes. EVIDENCE ACQUISITION: Review of available clinical guidelines, original investigations, and additional searches across PubMed for articles relevant to cardiovascular screening, risk assessment, and prevention in adult athletes (1990-2020). STUDY DESIGN: Clinical review. LEVEL OF EVIDENCE: Level 3. RESULTS: Atherosclerotic coronary artery disease (CAD) is the leading cause of exercise-induced acute coronary syndromes, myocardial infarction, and sudden cardiac death in older athletes. Approximately 50% of adult patients who experience acute coronary syndromes and sudden cardiac arrest do not have prodromal symptoms of myocardial ischemia. The risk of atherosclerotic cardiovascular disease (ASCVD) can be estimated by using existing risk calculators. ASCVD 10-year risk is stratified into 3 categories: low-risk (≤10%), intermediate-risk (between 10% and 20%), and high-risk (≥20%). Coronary artery calcium (CAC) scoring with noncontrast computed tomography provides a noninvasive measure of subclinical CAD. Evidence supports a significant association between elevated CAC and the risk of future cardiovascular events, independent of traditional risk factors or symptoms. Statin therapy is recommended for primary prevention if 10-year ASCVD risk is ≥10% (intermediate- or high-risk patients) or if the Agatston score is >100 or >75th percentile for age and sex. Routine stress testing in asymptomatic, low-risk patients is not recommended. CONCLUSION: We propose a comprehensive risk assessment for older athletes that combines conventional and novel risk factors for ASCVD, a 12-lead resting electrocardiogram, and a CAC score. Available risk calculators provide a 10-year estimate of ASCVD risk allowing for risk stratification and targeted management strategies. CAC scoring can refine risk estimates to improve the selection of patients for initiation or avoidance of pharmacological therapy.

Predictive value of the Seattle Heart Failure Model in patients undergoing left ventricular assist device placement.

BACKGROUND: Left ventricular assist devices (LVADs) are increasingly used in advanced heart failure patients. Despite proven efficacy, optimal timing of LVAD implantation is not well defined. METHODS: Patients receiving an LVAD were prospectively recorded. Laboratory and clinical data were extracted and used to calculate the predicted survival with medical therapy using the Seattle Heart Failure Model (SHFM). This was compared with observed survival, hospital length of stay and timeliness of discharge. RESULTS: We identified 104 patients. Survival with an LVAD vs SHFM predicted survival was 69% vs 11% at 1 year, corresponding to a hazard ratio of 0.17 (p < 0.0001). SHFM-estimated 1-year survival with medical therapy increased from 4% in 1997 to 2004 to 25% in 2007-2008 (p < 0.0001). Subgroup analysis of higher vs lower risk LVAD patients showed observed 1-year survival of 83% vs 57% (p = 0.04). The lower risk group had a shorter length of stay (46 vs 75 days, p = 0.03), along with higher rates of discharge prior to transplant (88% vs 61%, p = 0.01) and discharge within 60 days of LVAD placement (77% vs 52%, p = 0.03). CONCLUSIONS: The SHFM allows prediction of important features of a patient's hospital course post-operatively, including length of stay and 1-year survival. Given evidence of improved survival and shorter hospital stay in lower risk patients, earlier LVAD placement based on a prediction model like the SHFM should be considered in advanced heart failure patients. The SHFM may have utility as a virtual control arm for single-arm LVAD trials.

In patients with heart failure elevated soluble TNF-receptor 1 is associated with higher risk of depression.

BACKGROUND: Pro-inflammatory cytokines may contribute to the development and progression of heart failure (HF) and are also implicated in depressive disorders. In this cross-sectional study, we investigated whether systemic inflammation, as assessed by circulating levels of inflammatory cytokines, was associated with comorbid depression in patients with heart failure. METHODS AND RESULTS: Baseline clinical variables, depression status, and inflammatory marker levels were measured in 129 ambulatory HF patients. We hypothesized that pro-inflammatory cytokines, specifically tumor necrosis factor (TNF)-alpha, interleukin (IL)-1, and IL-6, would be elevated in HF patients with comorbid depression. In unadjusted analyses, levels of soluble TNF-alpha receptor1 (sTNFr1) were significantly higher among depressed (1.6 ng/mL), compared with nondepressed (1.1 ng/mL), HF patients (P = .01). After multivariate adjustment, compared with patients in the lowest quartile of sTNFr1 levels, those in the highest quartile had an adjusted near 5-fold higher risk of depression (OR 4.6, 95% CI 1.2-17.3; P for trend .008). The subgroup of patients on antidepressants but not currently depressed had a trend toward higher levels of sTNFr1, suggesting that antidepressants may not lower cytokine levels even when adequately treating depressive symptoms. IL-1beta and IL-6 levels were not significantly different among depressed versus nondepressed HF patients. CONCLUSIONS: In this cross-sectional analysis, HF patients with comorbid depression, compared with nondepressed HF patients, had higher levels of sTNFr1 and trend toward higher levels of sTNFr1 even when adequately treated for depression.