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Introduction: Nonsteroidal anti-inflammatory drugs (NSAIDs) are associated with adverse cardiovascular outcomes and reportedly overused in American-style football (ASF). However, assessment of ASF NSAID use in the context of cardiovascular risk has not been performed. We sought to characterize NSAID use patterns and the association with cardiovascular risk in a diverse cohort of high school and collegiate ASF athletes., Methods: A total of 226 ASF athletes, 60 endurance athletes, and 63 nonathletic controls were studied pre- and postseason with echocardiography, vascular applanation tonometry, and clinical data assessment. Qualitative NSAID use throughout the season was recorded at postseason., Results: ASF athletes gained weight (Δ0.86 ± 3.9 kg, P < 0.001), increased systolic blood pressure (SBP, Δ3.1 ± 12 mm Hg, P < 0.001) and pulse wave velocity (Δ0.2 ± 0.6 m·s, P < 0.001), and decreased E' (Δ-1.4 ± 2.8 cm·s, P < 0.001) across one athletic season. Seventy-seven percent (n = 173) of ASF athletes reported that sport-specific NSAID use began in middle school. ASF NSAID use was more frequent with "weekly" (n = 42.19%) and "daily" (n = 32.14%) use compared with endurance athletes (P < 0.001) and controls (P = 0.02). ASF NSAID use increased in parallel with postseason SBP and weights. "Daily" ASF NSAID users demonstrated the highest postseason SBP (137 ± 13 vs 128 ± 13 mm Hg, P = 0.002) and weight (109.0 ± 18.6 vs 95.8 ± 20.5 kg, P = 0.002) compared with "never/rare" users. Adjusting for player position, SBP, pulse wave velocity, and E', increased weight (odds ratio = 1.04, 95% confidence interval = 1.0-1.08, P = 0.037) was associated with more frequent NSAID use., Conclusions: Habitual NSAID use commonly begins during adolescence, before full physical maturation, and is associated with cardiovascular risk, particularly increased weight, in ASF athletes. NSAID use frequency should be considered when risk stratifying high-risk ASF athletes.

Background: Low diastolic blood pressure (DBP) is associated with increased risk of cardiovascular events. In patients with coronary artery disease (CAD), limitations in coronary blood flow and immune activity are implicated mechanisms, but evidence is lacking. We investigated the association between DBP, biomarkers of myocardial injury, inflammation, immune activation and incident events in patients with CAD., Methods: We studied 2448 adults (mean age 65 ± 12 years, 68% male, median follow-up 4.5 years) with CAD. DBP was categorized into 10 mm Hg increments. Biomarkers of myocardial injury (high sensitivity cardiac troponin-I [hs-cTnI]) and immune activity/inflammation (soluble urokinase plasminogen activator receptor [suPAR]) were dichotomized at their median values. DBP 70-79 mm Hg was used as the referent group, and individuals were followed prospectively for adverse outcomes., Results: After adjusting for demographic and clinical covariates, individuals with DBP < 60 mm Hg had increased odds of elevated levels of hs-cTnI (OR = 1.68; 95% CI = 1.07, 2.65) and suPAR (OR = 1.71; 95% CI = 1.10, 2.65) compared to the referent group. Additionally, DBP < 60 mm Hg was associated with increased adjusted risk of cardiovascular death or MI (HR = 2.04; 95% CI = 1.32, 3.16) and all-cause mortality (HR = 2.41; 95% CI = 1.69, 3.45)., Conclusion: In patients with CAD, DBP < 60 mm Hg is associated with subclinical myocardial injury, immune/inflammatory dysregulation and incident events. Aggressive BP control may be harmful in these patients, and further investigation is warranted to determine appropriate BP targets in patients with CAD., (Copyright © 2018 Elsevier B.V. All rights reserved.)

This study sought to determine the cardiovascular physiologic correlates of sleep-disordered breathing (SDB) in American-style football (ASF) participants using echocardiography, vascular applanation tonometry, and peripheral arterial tonometry. Forty collegiate ASF participants were analyzed at pre- and postseason time points with echocardiography and vascular applanation tonometry. WatchPAT (inclusive of peripheral arterial tonometry) used to assess for SDB was then performed at the postseason time point. Twenty-two of 40 (55%) ASF participants demonstrated SDB with an apnea-hypopnea index (pAHI) ≥5. ASF participants with SDB were larger (109 ± 20 vs 92 ± 14 kg, p = 0.004) and more likely linemen position players (83% vs 50%, p = 0.03). Compared with those without SDB, ASF participants with SDB demonstrated relative impairments in left ventricular diastolic and vascular function as reflected by lower lateral e' (14 ± 3 vs 17 ± 3 cm/s, p = 0.007) and septal e' (11 ± 2 vs 13 ± 2 cm/s, p = 0.009) tissue velocities and higher pulse wave velocity (5.4 ± 0.9 vs 4.8 ± 0.5 m/s, p = 0.02). In the total cohort, there were significant positive correlations between pAHI and pulse wave velocity (r = 0.42, p = 0.008) and inverse correlations between pAHI and the averaged e' tissue velocities (r = -0.42, p = 0.01). In conclusion, SDB is highly prevalent in youthful collegiate ASF participants and associated with relative impairments in cardiac and vascular function. Targeted efforts to identify youthful populations with SDB, including ASF participants, and implement SDB treatment algorithms, represent important future clinical directives., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Although hypertension is common in American-style football (ASF) players, the presence of concomitant vascular dysfunction has not been previously characterized. We sought to examine the impact of ASF participation on arterial stiffness and to compare metrics of arterial function between collegiate ASF participants and nonathletic collegiate controls. Newly matriculated collegiate athletes were studied longitudinally during a single season of ASF participation and were then compared with healthy undergraduate controls. Arterial stiffness was characterized using applanation tonometry (SphygmoCor). ASF participants (n = 32, 18.4 ± 0.5 years) were evenly comprised of Caucasians (n = 14, 44%) and African-Americans (n = 18, 56%). A single season of ASF participation led to an increase in central aortic pulse pressure (27 ± 4 vs 34 ± 8 mm Hg, p <0.001). Relative to controls (n = 47), pulse wave velocity was increased in ASF participants (5.6 ± 0.7 vs 6.2 ± 0.9 m/s, p = 0.002). After adjusting for height, weight, body mass index, systolic blood pressure, and diastolic blood pressure, ASF participation was independently predictive of increased pulse wave velocity (β = 0.33, p = 0.04). In conclusion, ASF participation leads to changes in central hemodynamics and increased arterial stiffness., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Background: Hypertension, a strong determinant of cardiovascular disease risk, has been documented among elite, professional American-style football (ASF) players. The risk of increased blood pressure (BP) and early adulthood hypertension among the substantially larger population of collegiate ASF athletes is not known., Methods and Results: We conducted a prospective, longitudinal study to examine BP, the incidence of hypertension, and left ventricular remodeling among collegiate ASF athletes. Resting BP and left ventricular structure were assessed before and after a single season of competitive ASF participation in 6 consecutive groups of first-year university athletes (n=113). ASF participation was associated with significant increases in systolic BP (116±8 versus 125±13 mm Hg; P<0.001) and diastolic BP (64±8 mm Hg versus 66±10 mm Hg; P<0.001). At the postseason assessment, the majority of athletes met criteria for Joint National Commission (seventh report) prehypertension (53 of 113, 47%) or stage 1 hypertension (16 of 113, 14%). Among measured characteristics, lineman field position, intraseason weight gain, and family history of hypertension were the strongest independent predictors of postseason BP. Among linemen, there was a significant increase in the prevalence of concentric left ventricular hypertrophy (2 of 64 [3%] versus 20 of 64 [31%]; P<0.001) and change in left ventricular mass correlated with intraseason change in systolic BP (R=0.46, P<0.001)., Conclusions: Collegiate ASF athletes may be at risk for clinically relevant increases in BP and the development of hypertension. Enhanced surveillance and carefully selected interventions may represent important opportunities to improve later-life cardiovascular health outcomes in this population.

Purpose: American-style football (ASF) participation rates in the United States are highest among high school (HS) athletes. This study sought to compare the cardiovascular response to HS versus collegiate ASF participation. Methods: The ASF participants (HS, n = 61; collegiate, n = 87) were studied at preseason and postseason time points with echocardiography and applanation tonometry. Primary outcome variables included: left ventricular (LV) mass index, LV diastolic function (early relaxation velocity [E′]), and arterial stiffness (pulse wave velocity [PWV]). Results: High school (17.1 ± 0.4 yr) and collegiate ASF participants (18 ± 0.4 yr) experienced similar LV hypertrophy (ΔLV mass HS = 10.5 ± 10 vs collegiate = 11.2 ± 13.6 g·m−2, P = 0.97). Among HS participants, increases in LV mass were associated with stable diastolic tissue velocities (ΔE′ = −0.3 ± 2.9 cm·s−1, P = 0.40) and vascular function (ΔPWV = −0.1 ± 0.6 m·s−1, P = 0.13). In contrast, collegiate participants demonstrated a higher burden of concentric LV hypertrophy (21/87, 24% vs 7/61, 11%, P = 0.026) with concomitant reductions in diastolic tissue velocities (ΔE′: −2.0 ± 2.7 cm·s−1, P < 0.001) and increased arterial stiffness (ΔPWV: Δ0.2 ± 0.6 m·s−1, P = 0.003), changes that were influenced by linemen who had the highest post-season weight (124 ± 10 kg) and systolic blood pressure ([SBP], 138.8 ± 11 mm Hg). In multivariable analyses adjusting for age and ethnicity, body mass was an independent predictor of post-season PWV (β estimate = 0.01, P = 0.04) and E′ (β estimate = −0.04, P = 0.05), whereas SBP was an independent predictor of postseason LV mass index (β estimate = 0.18, P = 0.01) and PWV (β estimate = 0.01, P = 0.007). Conclusions: The transition from HS to college represents an important physiologic temporal data point after which differential ASF cardiovascular phenotypes manifest. Future work aimed to clarify underlying mechanisms, and the long-term clinical implications of these findings is warranted. [ABSTRACT FROM AUTHOR]

Key points Left ventricular twist (LVT) results from rotation of the LV apex and base in opposite directions., Although LVT is altered in various cardiac diseases, physiological factors that affect LVT remain incompletely understood., In an experimental model involving healthy humans, isometric handgrip testing (IHGT) was performed to produce a clinically relevant form of LV afterload increase. The impact of IHGT on LV twist mechanics was assessed using speckle-tracking echocardiography., IHGT produced significant increase in systemic blood pressure and acute reduction in LV stroke volume. In this setting, LV apical rotation and LVT significantly decreased., Impairment of LV twist mechanics may in part underlie the LV dysfunction that can occur in the clinical context of acute increase in afterload., Abstract Left ventricular (LV) rotation occurs due to contraction of obliquely oriented myocardial fibres. Left ventricular twist (LVT) results from rotation of the apex and base in opposite directions. Although LVT is altered in various cardiac diseases, physiological factors that affect LVT remain incompletely understood. Isometric handgrip testing (IHGT), a well-established laboratory-based technique to increase LV afterload, was performed for 3 min at 40% maximum force generation in healthy human subjects ( n= 18, mean age 29.7 ± 2.7 years). Speckle-tracking echocardiography was used to measure LV volumes, LV apical and basal rotation, peak systolic LVT and peak early diastolic untwisting rate (UTR) at rest and at peak IHGT. IHGT led to significant increase in systemic blood pressure (systolic, 120.6 ± 9.7 vs. 155.6 ± 14.5 mmHg, P < 0.001; diastolic, 67.5 ± 6.4 vs. 94.1 ± 21.1 mmHg, P < 0.001) and LV end-systolic volume (44.2 ± 7.8 vs. 50.5 ± 10.8 ml, P= 0.005), as well as a significant increase in heart rate (62.8 ± 11.7 vs. 84.7 ± 13.8 beats min−1; P < 0.001). IHGT produced a significant acute reduction in LV stroke volume (63.9 ± 12.0 vs. 49.4 ± 7.8 ml, P < 0.001). In this setting, there was a significant decrease in peak systolic apical rotation (11.9 ± 3.0 vs. 8.6 ± 2.2 deg, P < 0.001) and a resultant 25% decrease in peak systolic LVT (16.6 ± 2.8 vs. 12.5 ± 2.8 deg, P < 0.001). The magnitude of peak early diastolic UTR did not change (−114.5 ± 26.4 vs. −110.6 ± 39.8 deg s−1, P= 0.71). Peak systolic apical rotation and LVT decrease during IHGT in healthy humans. This impairment of LV twist mechanics may in part underlie the LV dysfunction that can occur in the clinical context of acute increase in afterload. [ABSTRACT FROM AUTHOR]