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David Gaze

Publications and source records attributed to David Gaze.

At least 19 recordsLinked to original sources

Altered left ventricular diastolic filling following a marathon is a reproducible phenomenon.

The present study examined the reproducibility of alterations in left ventricular function and cardiac biomarkers in a cohort of athletes following two marathons, one year apart. Eight participants in the 2004 and 2005 London Marathons were tested pre- and post-race via echocardiography and humoral analysis. Reductions in diastolic filling, unrelated to loading or heart rate, following both marathons were reproducible within individuals, which may be a function of exercise duration. In contrast, exercise-induced cardiac troponin release was inconsistent.

Adult↗

Impact of repeated prolonged exercise bouts on cardiac function and biomarkers.

PURPOSE: The present study examined the impact of repeated bouts of prolonged (< 60 min) exercise on left ventricular function and cardiac biomarkers. METHODS: Ten athletes completed a 15.3-mile hill run on three consecutive days and were assessed before, immediately after, 1 h after, and 20 h after each bout. Six of the athletes completed a fourth bout. Left ventricular (LV) function was examined echocardiographically using two-dimensional M-mode, Doppler, and flow propagation velocity (Vp). Venous blood samples were analyzed for cardiac biomarkers including cardiac troponin T (cTnT). RESULTS: Ejection fraction (EF) significantly decreased (P = 0.027) after the third exercise bout compared with baseline (mean +/- SD: 56.3 +/- 4.4 vs 51.3 +/- 5.9%), accompanied by a nonsignificant decrease in systolic blood pressure/end systolic volume (SBP/ESV) ratio. A sustained depression in systolic function 20 h after bout 3 also persisted in the subset who completed a fourth bout, yet this did not reach clinical levels. Significant (P < 0.01) reductions in early to late diastolic filling (E:A) ratio pre-to post-bout 1 (mean +/- SD: 1.9 +/- 0.5 vs 1.4 +/- 0.3) and pre- to post-bout 3(2.0 +/- 0.5 vs 1.3 +/- 0.4) normalized after each 20-h recovery period. A similar pattern of change was observed in Vp. Cardiac troponin T was elevated in four individuals 1 h after bout 1 (range: 0.013-0.125 microg.L(-1)) but was undetectable thereafter except in one athlete. CONCLUSION: Repeated bouts of prolonged exercise induce short-term reductions in diastolic filling and a cumulative decrease in systolic function, yet these alterations seem to have minimal clinical or functional impact. Elevated cTnT after the initial bout, but not thereafter, may represent an adaptive response to prolonged exercise.

Adult↗

Value of primary care electrocardiography for the prediction of left ventricular systolic dysfunction in patients with suspected heart failure.

To compare electrocardiogram (ECG) with measurement of N-terminal pro-B-type natriuretic peptides (NTproBNP) as the General Practitioner's (GP) initial test for suspected heart failure patients from the community. We prospectively studied 137 suspected heart failure patients who underwent ECG and NTproBNP estimation; were referred from primary care to a specialist unit for echocardiography. We demonstrated that sensitivity of ECG interpreted by GP was significantly lower than both by ECG interpreted by Hospital Physician (HP) and NTproBNP estimation for the detection of left ventricular systolic dysfunction (LVSD). Therefore, measurement of NTproBNP is a better investigation in primary care than ECG for the detection of significant LVSD.

Aged↗

Novel application of flow propagation velocity and ischaemia-modified albumin in analysis of postexercise cardiac function in man.

The present study employed novel echocardiographic tools and cardiac markers to obtain a greater understanding of the aetiology and time course of altered cardiac function and cardiac damage following prolonged exercise and, in particular, the possible role of transient ischaemia within these phenomena. Fourteen runners in the 2004 London Marathon were assessed pre-, immediately post-, 1 h post- and 24 h postcompletion of the race. Left ventricular function was examined echocardiographically using 2-D, M-mode, tissue Doppler imaging and flow propagation velocity (Vp). Venous blood samples were analysed for N-terminal pro-B-type natriuretic peptide (proBNP), cardiac troponin T (cTnT) and ischaemia-modified albumin (IMA). Left ventricular (LV) diastolic filling was altered on completion of the race, as indicated by significant decreases in mean early to late diastolic myocardial wave (E':A') ratio and Vp (from 1.82 +/- 0.9 to 1.32 +/- 0.32, and from 67.5 +/- 9.3 to 60.2 +/- 8.2 cm s(-1), respectively, P < 0.05), accompanied by an increase in proBNP (from 21.6 +/- 11 to 47.08 +/- 19.5 pg l(-1), P < 0.05). The observed reduction in LV diastolic filling following completion of a marathon, unrelated to changes in heart rate or loading parameters, indicates an intrinsically mediated change in diastolic filling. Exercise-induced elevations in cTnT in nine individuals (range, 0.023-0.37 microg l(-1)) were indicative of minor cardiac damage. A significant reduction in IMA was observed after the marathon (from 63.68 +/- 9.83 to 44.94 +/- 16.13 Um l(-1), P < 0.05), unrelated to the alterations in cardiac function, proBNP or cTnT. The absence of an elevation in IMA suggests that exercise-induced myocardial ischaemia did not occur and therefore could not explain the changes in cardiac function or biomarkers. Future studies in this area should investigate alternative diagnostic tools for the detection of transient ischaemia, and other potential mechanisms, in order to extend the understanding of this phenomenon.

Adult↗

Risk stratification of chest pain patients by point-of-care cardiac troponin T and myoglobin measured in the emergency department.

A prospective multicenter study including 1410 chest pain patients with suspected acute coronary syndromes was carried out to examine the predictive value of biological cardiac markers for adverse events measured by a point-of-care system. Admission cardiac troponin T (cTnT) and myoglobin were measured in parallel on a point-of-care system in the emergency department and -- together with CK-MB mass -- on lab analyzers. In a one-year follow-up, cardiac and non-cardiac death, acute myocardial infarction, unstable angina pectoris and need for revascularization were registered. Median time between onset of symptoms and admission was 285 min; 172 patients (12.2%) had no event during follow-up. If the cTnT, measured either by the point-of-care system or a conventional lab analyzer, was >0.05 microg/L, then the chance of a cardiac event during the follow-up period was doubled (18% vs. 9%). Serial cTnT measurement did not add any further value to the predictive power of the admission cTnT. Myoglobin and CK-MB mass identified increasing risk with increasing concentration quartiles; cardiac event rates were 2.8- to 4.4-fold higher between the quartiles with the lowest and those with the highest analyte concentration, respectively. There was no difference in non-cardiac death rates between any concentration quartiles. In conclusion, the prediction of clinical events by cardiac troponin T and myoglobin measured with a point-of-care analyzer in the emergency department was as good as that of the same cardiac markers and CK-MB mass measured on lab analyzers.

Aged↗

Mitral annular myocardial velocity assessment of segmental left ventricular diastolic function after prolonged exercise in humans.

We assessed segmental and global left ventricular (LV) diastolic function via tissue-Doppler imaging (TDI) as well as Doppler flow variables before and after a marathon race to extend our knowledge of exercise-induced changes in cardiac function. Twenty-nine subjects (age 18-62 year) volunteered to participate and were assessed pre- and post-race. Measurements of longitudinal plane TDI myocardial diastolic velocities at five sites on the mitral annulus included peak early myocardial tissue velocity (E'), peak late (or atrial) myocardial tissue velocity (A') and the ratio E'/A'. Standard pulsed-wave Doppler transmitral and pulmonary vein flow indices were also recorded along with measurements of body mass, heart rate, blood pressures and cardiac troponin T (cTnT), a biomarker of myocyte damage. Pre- to post-race changes in LV diastolic function were analysed by repeated measures ANOVA. Delta scores for LV diastolic function were correlated with each other and alterations in indices of LV loading. Diastolic longitudinal segmental and mean TDI data were altered post-race such that the mean E'/A' ratio was significantly depressed (1.51 +/- 0.34 to 1.16 +/- 0.35, P < 0.05). Changes in segmental and global TDI data were not related to an elevated post-race HR, a decreased post-race pre-load or an elevated cTnT. The pulsed wave Doppler ratio of peak early transmitral flow velocity (E)/peak late (or atrial) flow velocity (A) was also significantly reduced post-race (1.75 +/- 0.46 to 1.05 +/- 0.30, P < 0.05); however, it was significantly correlated with post-race changes in heart rate. The lack of change in E/E' from pre- to post-race (3.4 +/- 0.8 and 3.3 +/- 0.7, respectively) suggests that the depression in diastolic function is likely to be due to altered relaxation of the left ventricle; however, the exact aetiology of this change remains to be determined.

Adolescent↗

Cardiac troponins in intensive care.

The cardiac troponins are integral components of the myofibrillary apparatus and they regulate muscle contraction. The measurement of cardiac troponins has replaced other biomarkers for the specific detection of myocardial necrosis and for the diagnosis of myocardial infarction. The tissue specificity plus sensitivity of the measurement technology has meant that cardiac damage can be detected in circumstances other than conventional acute coronary syndromes. The ability to specifically detect cardiac damage as part of multiple organ failure in intensive care patients has been shown to provide prognostic information, but it is unclear whether this is a dependent or an independent marker of outcome.

Biomarkers↗

Impact of marathon running on cardiac structure and function in recreational runners.

The present study examined the relationship between LV (left ventricular) function, markers of cardiac-specific damage and markers of oxidative stress in recreational runners following a marathon. Runners (n=52; 43 male and nine female; age, 35+/-10 years; height, 1.74+/-0.08 m; body mass, 75.9+/-8.9 kg) were assessed pre- and immediately post-marathon. LV function was assessed using standard M-mode two-dimensional Doppler echocardiography and TDI (tissue-Doppler imaging) echocardiography. Serum was analysed for cTnT (cardiac troponin-T), TEAC (Trolox equivalent antioxidant capacity; a measure of total antioxidant capacity), MDA (malondealdehyde) and 4-HNE (4-hydroxynonenal). A strong relationship was observed between standard and TDI echocardiography for all functional measures. Diastolic function was altered post-marathon characterized by a reduction in E (peak early diastolic filling: 0.79+/-0.11 compared with 0.64+/-0.16 cm/s; P<0.001), an increase in A (peak late diastolic filling: 0.48+/-0.11 compared with 0.60+/-0.12 cm/s; P<0.001) and a resultant decrease in E/A (ratio of E to A; 1.71+/-0.48 compared with 1.10+/-0.31; P<0.001). Ejection fraction remained unchanged post-marathon. Thirty-two runners presented with cTnT values above the lower limit of detection for the assay (0.01 microg/l), and 20 runners presented post-marathon with cTnT values above the acute myocardial infarction cut-off value (0.05 microg/l). No significant correlations were observed between cTnT and any functional measurements. MDA (2.90+/-1.58 compared with 3.59+/-1.47 micromol/l) and TEAC (1.80+/-0.12 compared with 1.89+/-0.21 mmol/l) were significantly increased post-marathon, but were unrelated to changes in function or cTnT. In conclusion, the present study demonstrated a reduction in diastolic function and widespread evidence of minimal cardiac damage following a marathon in recreational runners. The mechanism(s) underpinning the altered function and appearance of cTnT appear unrelated to reactive oxygen species.

Adolescent↗

Ischemia-modified albumin concentrations in patients with peripheral vascular disease and exercise-induced skeletal muscle ischemia.

BACKGROUND: Ischemia-modified albumin (IMA) is a new marker of myocardial ischemia, there is concern that IMA concentrations may be affected by ischemia occurring in tissues other than the myocardium. METHODS: We assessed 23 consecutive patients (15 males; mean age, 67 years) with typical leg claudication and documented peripheral vascular disease (PVD). All patients underwent both treadmill-exercise stress testing to induce leg ischemia and dobutamine stress echocardiography 1 week apart for the assessment of myocardial ischemia. Blood samples for IMA measurements were obtained at baseline, immediately after peak exercise/stress, and 1 h after exercise/stress. Statistical analysis was performed with the ANOVA repeated-measures test. RESULTS: Compared with baseline, mean (SD) IMA was significantly lower after the induction of skeletal muscle ischemia and returned to baseline values at 1 h: baseline, 74.6 (15.6) kilounits/L; peak stress, 69.5 (14.0) kilounits/L (P <0.0001 vs baseline); 1 h after stress, 75.9 (15.7) kilounits/L (P <0.0001 vs peak stress; P = 0.3 vs baseline). Baseline, peak stress, and 1-h poststress IMA concentrations were inversely correlated with the ankle-brachial index after exercise (r = -0.4; P <0.05). None of the patients showed regional wall motion abnormalities during dobutamine stress echocardiography, and IMA concentrations remained unchanged from baseline. There were no differences in baseline [74.6 (15.6) vs 72.7 (11.5) kilounits/L; P = 0.6], peak stress, or poststress IMA concentrations when exercise testing and dobutamine stress echocardiography values were compared. CONCLUSIONS: The relationship between disease severity (of a noncardiac origin) and baseline IMA values is an important and novel finding. IMA is significantly lower immediately after exercise-induced leg ischemia in patients with PVD and is related to disease severity. IMA concentrations can therefore be affected by the development of skeletal muscle ischemia, and this may have implications regarding the ability of IMA to detect myocardial ischemia in PVD patients.

Aged↗

Effect of radiofrequency catheter ablation on the biochemical marker ischemia modified albumin.

Ischemia-modified albumin (IMA) levels were measured after radiofrequency (RF) catheter ablation to evaluate the effect of direct myocardial necrosis on IMA formation. IMA levels have been shown to increase in patients after RF catheter ablation compared with those who undergo diagnostic electrophysiologic studies. The results of this study suggest that IMA may be a marker of myocardial injury.

Adult↗

Effect of direct-current cardioversion on ischemia-modified albumin levels in patients with atrial fibrillation.

Ischemia-modified albumin (IMA), measured with the albumin cobalt binding test, is a marker of myocardial ischemia. We measured IMA concentrations after elective direct-current cardioversion for atrial fibrillation to determine whether transient myocardial ischemia occurs. Patients with electrocardiographic changes after cardioversion (ST-depression and/or T-wave inversion) had significantly higher IMA levels than those without these changes. Thus, elevated levels of IMA after cardioversion may reflect transient myocardial ischemia.

Aged↗

Ischemia Modified Albumin for the assessment of patients presenting to the emergency department with acute chest pain but normal or non-diagnostic 12-lead electrocardiograms and negative cardiac troponin T.

BACKGROUND: The diagnosis of myocardial ischemia in patients with acute chest pain at rest but non-diagnostic electrocardiograms (ECG) is problematic. Ischemia Modified Albumin (IMA) is a new biochemical marker of ischemia, which may be useful to characterise acute coronary syndrome (ACS) patients. METHODS: We studied 131 patients (mean age 58.5 years; 95 male) presenting to the emergency department with symptoms suggestive of ACS but with normal or non-diagnostic ECGs. Cardiac troponin T (cTnT) and IMA were measured within 3 h of last chest pain episode. Based on hospital diagnostic test results, patients were classified as having ACS or non-ischemic chest pain (NICP), by two independent cardiologists unaware of IMA results. RESULTS: Mean IMA levels (U/ml) were higher in patients with ACS (98.3+/-11) compared to patients with NICP (85.5+/-15); p<0.0001. IMA levels >93.5 U/ml demonstrated a sensitivity and specificity of 75% for the diagnosis of ACS; area under the receiver operator characteristic curve 0.78 (95% CI: 0.70-0.85). If we applied the manufacturer cutoff point of 85 U/ml, the sensitivity of IMA increased to 90.6% with a specificity of 49.3% (negative predictive value=84.6%). In combination with cTnT (6-12 h) (>0.05 ng/ml), the sensitivity increased to 92.2%. After multivariate analysis, IMA levels >85 U/ml (odds ratio=14.6 [95% CI 4.4-48.4]; p<0.0001), age and prior myocardial infarction were independent predictors of ACS. CONCLUSION: IMA may be a useful biomarker for the identification of ACS in patients presenting with typical acute chest pain but normal or non-diagnostic ECGs.

Adult↗

Altered cardiac function and minimal cardiac damage during prolonged exercise.

PURPOSE: The purpose of the present study was to examine markers of cardiac function and cardiac damage during a simulated half-ironman triathlon in highly trained athletes. METHODS: Nine highly trained male triathletes volunteered for the study (mean +/- SD; age: 33 +/- 3 yr; height: 1.8 +/- 0.1 m; body mass: 77.7 +/- 3.2 kg). The subjects completed a half-ironman triathlon; 1.9-km swim in an indoor 20-m pool, followed by a laboratory-based 90-km cycle and 21.1-km run. Venous blood samples were drawn and echocardiographic assessment completed before the start of exercise, immediately after each stage, and 24 h postexercise. Serum was analyzed for total creatine kinase activity (CK), creatine kinase isoenzyme MB(mass) (CK-MB(mass)), and cardiac troponin T (cTnT). Left ventricular systolic (stroke volume, and systolic blood pressure/end systolic volume ratio (SBP/ESV)) and diastolic (ratio of early [E] to late [A], ventricular filling E:A) measurements were derived from echocardiographic assessment. RESULTS: The mean completion time of the half-ironman triathlon was 301 +/- 28 min. Left ventricular contractility (SBP/ESV) was significantly reduced after the half-ironman triathlon (P < 0.05). A significant reduction in E:A was observed after the run phase of the half-ironman triathlon (P < 0.05). Significant increases in CK and CK-MB(mass) were observed during and after the half-ironman triathlon (P < 0.05), and cTnT was elevated in four subjects over the course of the half-ironman triathlon. CONCLUSIONS: The physiologic stress imposed by the half-ironman triathlon resulted in a reduced left ventricular contractility and altered diastolic filling, coupled with minimal cardiac damage in a number of highly trained male triathletes. The mechanisms behind such altered cardiac function and cardiac damage after prolonged exercise are yet to be elucidated.

Adult↗

The impact of prolonged exercise in a cold environment upon cardiac function.

PURPOSE: The purpose of the present study was to examine the impact of cold exposure coupled with prolonged exercise upon postexercise left ventricular (LV) function and markers of myocardial damage. METHODS: colon; Eight highly trained male athletes (mean +/- SD; age: 28.2 +/- 8.8 yr; height: 1.78 +/- 0.07 m; body mass: 74.9 +/- 7.6 kg; VO2max: 65.6 +/- 7.0 mL x kg(-1) x min(-1)) performed two 100-mile cycle trials, the first in an ambient temperature of 0 degrees C, the second in an ambient temperature of 19 degrees C. Echocardiographic assessment was completed and blood samples drawn before, immediately postexercise, and 24-h postexercise. Left ventricular systolic (stroke volume [SV], ejection fraction [EF], and systolic blood pressure/end systolic volume ratio [SBP/ESV]) and diastolic (early [E] to late [A] filling ratio [E:A]) parameters were calculated. Serum was analyzed for creatine kinase isoenzyme MB (CK-MBmass) and cardiac troponin T (cTnT). cTnT was analyzed descriptively whereas other variables were assessed using two-way repeated-measures ANOVA. RESULTS: No significant change was observed in systolic function across time or between trials. A significant difference between trials was observed in E:A immediately after exercise (1.4 +/- 0.4 [19 degrees C] vs 1.8 +/- 0.3 [0 degrees C]) (P < 0.05). CK-MBmass was significantly elevated immediately after exercise in both trials (P < 0.05). Positive cTnT concentrations were observed in two subjects immediately after the 19 degrees C trial (0.012 microg x L(-1) and 0.034 microg x L(-1)). CONCLUSIONS: Cycling 100 miles in an ambient temperature of 19 degrees C is associated with an acute change in diastolic filling that is not observed after prolonged exercise at 0 degrees C. Prolonged exercise is associated with minimal cardiac damage in some individuals; it appears that this is a separate phenomenon to the change in diastolic filling.

Adult↗

Postexercise left ventricular function and cTnT in recreational marathon runners.

PURPOSE: To assess the impact of prolonged exercise on left ventricular (LV) function and the appearance of cardiac troponin T (cTnT) in older and recreational athletes. METHODS: Heart rate (HR), blood pressures, and cTnT were recorded in 35 subjects (age range 22-57 yr, finishing time 157-341 min) pre- and postrace. Echocardiograms (N = 26) assessed stroke volume (SV), ejection fraction (EF), sBP/LV end-systolic volume (sBP/ESV), diastolic filling (E:A ratio) as well as preload (LV internal dimension at end-diastole [LVIDd]) and afterload (LV wall stress). HR and core temperature were recorded in-event. Prepost changes in LV function were analyzed by repeated measures t-test. Delta scores for LV function and cTnT data were correlated with each other, age, finishing time, alterations in loading, and in-event data. RESULTS: SV was significantly decreased postrace (109 +/- 31 vs 85 +/- 25 mL, P < 0.05) likely due to a significant decrease in LVIDd (5.3 +/- 0.4 vs 4.9 +/- 0.5 cm, P < 0.05; r = 0.80, P < 0.05). LV wall stress was unchanged postrace (90 +/- 25 vs 89 +/- 27 g x cm(-2), P > 0.05). EF (70 +/- 12 vs.70 +/- 10%, P > 0.05) and sBP/ESV (3.7 +/- 2.9 vs 4.0 +/- 2.0, P > 0.05) did not change prepost race and were not related to age or finishing time (P > 0.05). E:A ratio was significantly reduced postrace (1.73 +/- 0.38 vs 1.41 +/- 0.25, P < 0.05) and could not be explained by an increased HR (56 +/- 9 vs 84 +/- 10, P < 0.05; r = 0.08, P > 0.05), a reduced LVIDd (r = 0.11, P > 0.05), age, finishing time, or in-event data. Postrace 26/33 subjects presented cTnT values in the range 0.024-0.080 microg x L(-1) that were not related to changes in LV function, loading, age, finishing time, or in-event data. CONCLUSION: No evidence of load-independent depression in LV systolic function was reported. Changes in cTnT and E:A were not related, and their etiology is uncertain.

Adult↗

Relation of ischemia-modified albumin (IMA) levels following elective angioplasty for stable angina pectoris to duration of balloon-induced myocardial ischemia.

The results in this study confirm and expand previous reports that ischemia-modified albumin (IMA) is an early marker of ischemia in the setting of percutaneous coronary intervention (PCI). We observed that IMA levels are related to the number of inflations, inflation pressure, and duration of inflations. It is therefore likely that IMA reflects the magnitude and duration of ischemia induced during PCI.

Angina Pectoris↗

The cardiospecificity of the third-generation cTnT assay after exercise-induced muscle damage.

PURPOSE: The purpose of the present study was to examine the cardiospecificity of cTnI and the new third-generation cTnT assay, in the presence of exercise-induced muscle damage in highly trained individuals, and to examine the impact of a maximal-ramping treadmill test on cardiac function. METHODS: Eight highly trained male triathletes (mean +/- SD; age: 29 +/- 9 yr; height: 1.79 +/- 0.10 m; body mass: 77 +/- 10 kg; .VO(2max): 67.4 +/- 6.3 mL.kg(-1).min(-1)) completed two bouts of exercise. On the first occasion, subjects completed a maximal-ramping treadmill test. On a separate occasion, the subjects completed 30 min of downhill running (15% gradient) at a speed equivalent to 70% of maximal running velocity attained during the maximal-ramping treadmill test. All subjects were assessed using ECG, echocardiography, and blood analysis. Measurements were taken at rest, immediately after, and 48 h postexercise for each bout of exercise. Echocardiographic analysis was used to determine left ventricular systolic and diastolic function. Blood samples were analyzed for markers of myocyte damage. RESULTS: Echocardiographic results indicated normal left ventricular function before and after both exercise bouts. Total CK and CKMB were significantly elevated 48 h after the downhill run. cTnT and cTnI were not elevated at any stage of the study. CONCLUSIONS: Neither the maximal-ramping treadmill test nor the 30-min downhill run produced cardiac dysfunction or myocardial damage in young, healthy trained subjects. The elevated total CK and CKMB within the downhill study are noncardiac in origin as demonstrated by the lack of cTnT and cTnI. The cTnI and new third-generation cTnT assays may be used to detect cardiac damage in the presence of elevated total CK and CKMB associated with exercise-induced skeletal muscle damage.

Adult↗