The aim of this study was to investigate the expression of cardiac strain and damage in 18 male marathoners with average age of 52.8 ± 5.0 years running at a 308 km ultra-marathon. Blood samples were collected at pre-race, 100 km, 200 km and 308 km check points for the analysis of cardiac muscle injury markers, creatine kinase (CK), creatine kinase-myocardial band (CK-MB), cardiac troponin I (cTnI) and cardiac muscle strain marker, N-terminal pro-brain natriuretic peptide (NT-proBNP). The CK levels increased 1127.2 ± 507.9 IU/L, 5133.8 ± 2492.7 IU/L and 4958.4 ± 2087.9 IU/L at 100 km, 200 km and 308 km, respectively, compared to the pre-race levels. The CK-MB levels increased 20.2 ± 11.2 ng/mL, 73.3 ± 35.6 ng/mL and 68.6 ± 42.6 ng/mL at 100, 200 and 308 km, respectively, compared to the pre-race levels. The CK-MB/CK ratio showed that the CK-MB mass index was within the normal range (<2.5%) at 100 km, 200 km and 308 km. The cTnI levels showed no significant difference in all check points. The NT-proBNP levels increased 146.55 ± 92.7 pg/mL, 167.95 ± 111.9 pg/mL and 241.23 ± 121.2 pg/mL at 100, 200 and 308 km, respectively, compared to the pre-race levels. The normal CK-MB mass index (<5.0 ng/mL) and the absence of an increase in the cTnI levels during the 308 km ultra-marathon suggested that no myocardial injury despite an elevation in CK-MB. The increase in NT-proBNP levels probably resulted from continuous hemodynamic cardiac stress and represents a transient physiological myocardial protective response.
The aim of the present study was to determine the changes in cardiac makers and endothelin-1 (ET-1) in marathoners with exercise induced hypertension compared to normotensive controls before and after running a marathon. Among a total of 70 volunteers, 10 marathoners with systolic blood pressure (SBP) greater than 210 mmHg during a treadmill exercise stress test were selected as an exercise-induced hypertension group (EIH) and 10 marathoners with normal SBP were selected as a control group (CON). Blood was collected from all volunteers 2 h before and immediately after a marathon: creatinine kinase (CK), CK-MB, cardiac tropoin-I (cTnI), N-terminal pro-brain natriuretic peptide (NT-proBNP), and endothelin-1(ET-1). Cardiac markers, CK, CK-MB, and CK-MB/CK ratio significantly increased in both EIH and CON; significance was not observed between the groups. Significant increases were not observed in high sensitive-C reactive protein (hs-CRP) after the race nor between the groups. Significant increases in cTnI and NT-proBNP were observed after the race in both groups. In addition, EIH showed greater increase than CON after the race. In conclusion, increased vascular tone in EIH during a marathon increased blood pressure and myocardial burden which in turn increased myocardial cell membrane permeability to further increase myocardial tension to the point of cTnI release.
We have developed a knowledge based approach for arterial stiffness estimation. The proposed new approach reliably estimates arterial stiffness based on the analysis of age and heart rate normalized reflected wave arrival time. The proposed new approach reduces cost, space, technical expertise, specialized equipment, complexity, and increases the usability compared to recently researched noninvasive arterial stiffness estimators. The proposed method consists of two main stages: pulse feature extraction and linear regression analysis. The new approach extracts the pulse features and establishes a linear prediction equation. On evaluating proposed methodology with pulse wave velocity (PWV) based arterial stiffness estimators, the proposed methodology offered the error rate of 8.36% for men and 9.52% for women, respectively. With such low error rates and increased benefits, the proposed approach could be usefully applied as low cost and effective solution for ubiquitous and home healthcare environments.
Background and Objectives Determining the presence of viable myocardium has prognostic and therapeutic implications in the treatment of acute myocardial infarction AMI . The aim of this study was to assess the ability of dobutamine echocardiography DE to detect viable myocardium and predict the late improvement of regional left ventricular dysfunction after AMI. Methods Twenty-five patients male 24, mean age 57 9.6 with AMI underwent DE dobutamine 0, 5, 10 and 20 gm/kg/min in 4.8 2.2 days after infarction. Revascularization of infarct related artery was performed in 20 patients percutaneous coronary angioplasty 18, coronary artery bypass graft surgery 2 . A follow-up 2D-echocardiography was performed at 7.1 2.3 months after AMI. Results 1 Improvement of regional wall motion abnormality RWMA was observed in 12 patients during DE [DE group]. Thirteen patients showed no improvement of RWMA [DE group]. 2 In follow-up 2D-echocardiography, 10 patients showed improvement of RWMA among DE group positive predictive value 83.3 . Two patients showed improvement of RWMA among DE group negative predictive value 84.6 . Sensitivity and specificity of DE in predictiong late recovery of RWMA were 83.3 and 84.6 each. DE performed in the early stage of AMI seems to be useful in prediction of late recovery of regional left ventricular dysfunction.
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