Christopher Troyanos

Cardiac arrest during long-distance running races

BACKGROUND Approximately 2 million people participate in long-distance running races in the United States annually. Reports of race-related cardiac arrests have generated concern about the safety of this activity. METHODS We assessed the incidence and outcomes of cardiac arrest associated with marathon and half-marathon races in the United States from January 1, 2000, to May 31, 2010. We determined the clinical characteristics of the arrests by interviewing survivors and the next of kin of nonsurvivors, reviewing medical records, and analyzing postmortem data. RESULTS Of 10.9 million runners, 59 (mean [±SD] age, 42-13 years; 51 men) had cardiac arrest (incidence rate, 0.54 per 100,000 participants; 95% confidence interval [CI], 0.41 to 0.70). Cardiovascular disease accounted for the majority of cardiac arrests. The incidence rate was significantly higher during marathons (1.01 per 100,000; 95% CI, 0.72 to 1.38) than during half-marathons (0.27; 95% CI, 0.17 to 0.43) and among men (0.90 per 100,000; 95% CI, 0.67 to 1.18) than among women (0.16; 95% CI, 0.07 to 0.31). Male marathon runners, the highest-risk group, had an increased incidence of cardiac arrest during the latter half of the study decade (2000-2004, 0.71 per 100,000 [95% CI, 0.31 to 1.40]; 2005-2010, 2.03 per 100,000 [95% CI, 1.33 to 2.98]; P=0.01). Of the 59 cases of cardiac arrest, 42 (71%) were fatal (incidence, 0.39 per 100,000; 95% CI, 0.28 to 0.52). Among the 31 cases with complete clinical data, initiation of bystander-administered cardiopulmonary resuscitation and an underlying diagnosis other than hypertrophic cardiomyopathy were the strongest predictors of survival. CONCLUSIONS Marathons and half-marathons are associated with a low overall risk of cardiac arrest and sudden death. Cardiac arrest, most commonly attributable to hypertrophic cardiomyopathy or atherosclerotic coronary disease, occurs primarily among male marathon participants; the incidence rate in this group increased during the past decade.

Be Prepared — The Boston Marathon and Mass-Casualty Events

The fact that there was not more loss of life in the Boston Marathon bombings is attributable in large part to the medical communitys prior efforts to build and sustain emergency-preparedness programs and to practice its response in exercises and drills.

Effect of Statins on Creatine Kinase Levels Before and After a Marathon Run

We measured the serum levels of myoglobin, total creatine kinase (CK), and the CK myocardial (CK-MB), muscle (CK-MM), and brain (CK-BB) isoenzymes in 37 subjects treated with statins and 43 nonstatin-treated controls running the 2011 Boston Marathon. Venous blood samples were obtained the day before (PRE) and within 1 hour (FINISH) and 24 hours after (POST) the race. The hematocrit and hemoglobin values were used to adjust for changes in the plasma volume. The CK distribution was normalized using log transformation before analysis. The exercise-related increase in CK 24 hours after exercise, adjusted for changes in plasma volume, was greater in the statin users (PRE to POST 133 ± 15 to 1,104 ± 150 U/L) than in the controls (PRE to POST 125 ± 12 to 813 ± 137 U/L; p = 0.03 for comparison). The increase in CK-MB 24 hours after exercise was also greater in the statin users (PRE to POST 1.1 ± 3.9 to 8.9 ± 7.0 U/L) than in the controls (PRE to POST 0.0 ± 0.0 to 4.2 ± 5.0 U/L; p <0.05 for comparison). However, the increases in muscle myoglobin did not differ at any point between the 2 groups. Increases in CK at both FINISH and POST race measurements were directly related to age in the statin users (r(2) = 0.13 and r(2) = 0.14, respectively; p <0.05) but not in the controls (r(2) = 0.02 and r(2) = 0.00, respectively; p >0.42), suggesting that susceptibility to exercise-induced muscle injury with statins increases with age. In conclusion, our results show that statins increase exercise-related muscle injury.

Myocardial Adaptations to Recreational Marathon Training Among Middle-Aged Men

Background—Myocardial adaptations to exercise have been well documented among competitive athletes. To what degree cardiac remodeling occurs among recreational exercisers is unknown. We sought to evaluate the effect of recreational marathon training on myocardial structure and function comprehensively. Methods and Results—Male runners (n=45; age, 48±7 years; 64% with ≥1 cardiovascular risk factor) participated in a structured marathon-training program. Echocardiography, cardiopulmonary exercise testing, and laboratory evaluation were performed pre and post training to quantify changes in myocardial structure and function, cardiorespiratory fitness, and traditional cardiac risk parameters. Completion of an 18-week running program (25±9 miles/wk) led to increased cardiorespiratory fitness (peak oxygen consumption, 44.6±5.2 versus 46.3±5.4 mL/kg per minute; P<0.001). In this setting, there was a significant structural cardiac remodeling characterized by dilation of the left ventricle (end-diastolic volume, 156±26 versus 172±28 mL, P<0.001), right ventricle (end-diastolic area=27.0±4.8 versus 28.6±4.3 cm2; P=0.02), and left atrium (end-diastolic volume, 65±19 versus 72±19; P=0.02). Functional adaptations included increases in both early (E′=12.4±2.5 versus 13.2±2.0 cm/s; P=0.007) and late (A′=11.5±1.9 versus 12.2±2.1 cm/s; P=0.02) left ventricular diastolic velocities. Myocardial remodeling was accompanied by beneficial changes in cardiovascular risk factors, including body mass index (27.0±2.7 versus 26.7±2.6 kg/m2; P<0.001), total cholesterol (199±33 versus 192±29 mg/dL; P=0.01), low-density lipoprotein (120±29 versus 114±26 mg/dL; P=0.01), and triglycerides (100±52 versus 85±36 mg/dL; P=0.02). Conclusions—Among middle-aged men, recreational marathon training is associated with biventricular dilation, enhanced left ventricular diastolic function, and favorable changes in nonmyocardial determinants of cardiovascular risk. Recreational marathon training may, therefore, serve as an effective strategy for decreasing incident cardiovascular disease.

Influence of chronic exercise on carotid atherosclerosis in marathon runners

Objectives The effect of habitual, high-intensity exercise training on the progression of atherosclerosis is unclear. We assessed indices of vascular health (central systolic blood pressure (SBP) and arterial stiffness as well as carotid intima-medial thickness (cIMT)) in addition to cardiovascular risk factors of trained runners versus their untrained spouses or partners to evaluate the impact of exercise on the development of carotid atherosclerosis. Setting field study at Boston Marathon. Participants 42 qualifiers (mean age±SD: 46±13 years, 21 women) for the 2012 Boston Marathon and their sedentary domestic controls (46±12 years, n=21 women). Outcomes We measured medical and running history, vital signs, anthropometrics, blood lipids, C reactive protein (CRP), 10 years Framingham risk, central arterial stiffness and SBP and cIMT. Results Multiple cardiovascular risk factors, including CRP, non-high-density lipoprotein cholesterol, triglycerides, heart rate, body weight and body mass index (all p<0.05), were reduced in the runners. The left and right cIMT, as well as central SBP, were not different between the two groups (all p>0.31) and were associated with age (all r≥0.41; p<0.01) and Framingham risk score (all r≥0.44; p<0.01) independent of exercise group (all p>0.08 for interactions). The amplification of the central pressure waveform (augmentation pressure at heart rate 75 bpm) was also not different between the two groups (p=0.07) but was related to age (p<0.01) and group (p=0.02) in a multiple linear regression model. Conclusions Habitual endurance exercise improves the cardiovascular risk profile, but does not reduce the magnitude of carotid atherosclerosis associated with age and cardiovascular risk factors.

Effect of air travel on exercise-induced coagulatory and fibrinolytic activation in marathon runners.

Objective:Air travel and exercise change hemostatic parameters. This study investigated the effect of air travel on exercise-induced coagulation and fibrinolysis in endurance athletes. Design:A prospective longitudinal study. Setting:The 114th Boston Marathon (April 19, 2010). Participants:Forty-one adults were divided into travel (T: 23 participants, living >4-hour plane flight from Boston) and nontravel (C: 18 participants, living <2-hour car trip from Boston) groups. Independent Variables:Age, anthropometrics, vital signs, training mileage, and finishing time were collected. Main Outcome Measures:Subjects provided venous blood samples the day before (PRE), immediately after (FINISH), and the day following the marathon after returning home (POST). Blood was analyzed for thrombin–antithrombin complex (TAT), tissue plasminogen activator (t-PA), hematocrit (Hct), and the presence of Factor V Leiden R506Q mutation. Results:Thrombin–antithrombin complex increased more in T subjects in PRE to FINISH samples (5.0 ± 4.0 to 12.9 ± 15.6 μg/L) than in C subjects (4.0 ± 1.2 to 6.1 ± 1.2 μg/L; P = 0.02 for comparison). The t-PA increased in both the T (5.4 ± 2.3 to 25.1 ± 12.2 ng/mL) and C (5.6 ± 2.0 to 27.7 ± 11.3 ng/mL) groups in PRE to FINISH samples, and this response did not differ between groups (P = 0.23 for comparison). Both groups exhibited similar t-PA and TAT values at POST that were not different than PRE (all P > 0.35). Age was related to the FINISH TAT values in T (r2 = 0.19; P = 0.04) but not in C (r2 = 0.03; P = 0.53) subjects. Conclusions:Results suggest that the combination of air travel and marathon running induces an acute hypercoaguable state; this hemostatic imbalance is exaggerated with increasing age.

Influence of statins on distinct circulating microRNAs during prolonged aerobic exercise.

Statins exacerbate exercise-induced skeletal muscle injury. Muscle-specific microRNAs (myomiRs) increase in plasma after prolonged exercise, but the patterns of myomiRs release after statin-associated muscle injury have not been examined. We examined the relationships between statin exposure, in vitro and in vivo muscle contraction, and expression of candidate circulating myomiRs. We measured plasma levels of myomiRs, circulating microRNA-1 (c-miR-1), c-miR-133a, c-miR-206, and c-miR-499-5p from 28 statin-using and 28 nonstatin-using runners before (PRE), immediately after (FINISH), and 24 h after they ran a 42-km footrace (the 2011 Boston marathon) (POST-24). To examine these cellular-regulation myomiRs, we used contracting mouse C2C12 myotubes in culture with and without statin exposure to compare intracellular and extracellular expression of these molecules. In marathoners, c-miR-1, c-miR-133a, and c-miR-206 increased at FINISH, returned to baseline at POST-24, and were unaffected by statin use. In contrast, c-miR-499-5p was unchanged at FINISH but increased at POST-24 among statin users compared with PRE and runners who did not take statins. In cultured C2C12 myotubes, extracellular c-miR-1, c-miR-133a, and c-miR-206 were significantly increased by muscle contraction regardless of statin use. In contrast, extracellular miR-499-5p was unaffected by either isolated statin exposure or isolated carbachol exposure but it was increased when muscle contraction was combined with statin exposure. In summary, we found that statin-potentiated muscle injury during exercise is accompanied by augmented extracellular release of miR-499-5p. Thus c-miR-499-5p may serve as a biomarker of statin-potentiated muscle damage.

Effect of WBGT Index Measurement Location on Heat Stress Category Classification.

UNLABELLED The location of the wet bulb globe temperature (WBGT) index measurement may affect heat stress flag category classification. PURPOSE This study aimed to compare WBGT measurements at three locations along the Boston Marathon race course and compare WBGT estimates for meteorological stations and 72-h advanced WBGT forecasts. METHODS WBGT was measured hourly from 1000 to 1400 h at approximately 7 km, approximately 18 km, and approximately 30 km on the Boston Marathon race course. Simultaneous WBGT estimates were made for two meteorological stations southeast of the course via a commercial online system, which also provided 72-h advanced forecasts. RESULTS The measurement difference (mean ± SD) among course locations was 0.2°C ± 1.8°C WBGT (ANOVA, P > 0.05). The difference between course and stations was 1.9°C ± 2.4°C WBGT (t-test, P < 0.05). Station values underestimated (n = 98) or overestimated (n = 13) course values by >3°C WBGT (>0.5 flag category) in 111 of 245 paired comparisons (45%). Higher black globe and lower wet bulb temperatures explained over- and underestimates, respectively. Significant underestimates of WBGT resulted in misclassification of green (labeled white) and black (labeled red) course flag categories (χ2, P < 0.05). Forecast data significantly underestimated red (labeled amber) and black (labeled red) course flag categories. CONCLUSIONS Differences in WBGT index along 23 km of the Boston Marathon race route can be small enough to warrant single measurements. However, significant misclassification of flag categories occurred using WBGT estimates for meteorological stations; thus, local measurements are preferred. If the relation between station WBGT forecasts and the race sites can be established, the forecast WBGT values could be corrected to give advanced warning of approximate flag conditions. Similar work is proposed for other venues to improve heat stress monitoring.

Statins Attenuate the Increase in P-Selectin Produced by Prolonged Exercise

Strenuous endurance exercise increases inflammatory markers and acutely increases cardiovascular risk; however, statins may mitigate this response. We measured serum levels of p-selectin in 37 runners treated with statins and in 43 nonstatin treated controls running the 2011 Boston Marathon. Venous blood samples were obtained the day before (PRE) as well as within 1 hour after (FINISH) and 24 hours after (POST) the race. The increase in p-selectin immediately after exercise was lower in statin users (PRE to FINISH: 20.5 ± 19.4 ng/mL) than controls (PRE to FINISH: 30.9 ± 27.1 ng/mL; P < 0.001). The increase in p-selectin 24 hours after exercise was also lower in statin users (PRE to POST: 21.5 ± 26.6 ng/mL) than controls (PRE to POST: 29.3 ± 31.9 ng/mL; P < 0.001). Furthermore, LDL-C was positively correlated with p-selectin at FINISH and POST (P < 0.01 and P < 0.05, resp.), irrespective of drug treatment, suggesting that lower levels of LDL-C are associated with a reduced inflammatory response to exercise. We conclude that statins blunt the exercise-induced increase in p-selectin following a marathon and that the inflammatory response to a marathon varies directly with LDL-C levels.