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Objective: QT peak prolongation is associated with left ventricular hypertrophy (LVH) in patients with hypertension. This study tests the hypothesis that QT peak prolongation correlates with LV mass index in apparently healthy young football players.Methods: QT peak and other ECG criteria for LVH were assessed in 117 male professional footballers (mean age 16.4 years +/- SD 0.76). Their left ventricular mass index (LVMI) was assessed by transthoracic echocardiography. Heart rate-corrected QT peak (QTpc) interval was measured in lead I using Bazett's formula. Spearman (2-tailed) test and UNIANOVA was used to assess if there were correlations between QT peak and the various echocardiographic and ECG indices of LVH.Results: Echocardiographic LVH, defined as LVMI > or = 134 g/m(2), was seen in 79 (70.5%) subjects. ECG-defined LVH was present in 54 (50 %) players by Sokolow-Lyon criteria, in 19 (16 %) players by Romhilt Score, in 5 (4 %) players by Cornell voltage criteria, and in 7 (6 %) players by Cornell product >2436 mm ms. There was no correlation between QT peak (QTpc) and LVMI on echocardiography (Spearman r = 0.058, 2-tailed P = 0.54). In addition, there was no relation between LVH and QTpc of lead I using any of the following ECG criteria: Sokolow-Lyon (P = 0.6), Romhilt (P = 0.3), Cornell voltage (P = 0.8), or Cornell product (P = 0.6).Conclusion: QT peak interval, which is associated with pathological LVH in hypertensive patients and is a measure of risk of cardiac death, does not correlate with LVH characterized by myocyte hypertrophy in young apparently healthy professional footballers. [ABSTRACT FROM AUTHOR]

Objective: To assess physiological cardiac adaptation in adolescent professional soccer players.Subjects and Design: Over a 32 month period 172 teenage soccer players were screened by echocardiography and ECG at a tertiary referral cardiothoracic centre. They were from six professional soccer teams in the north west of England, competing in the English Football League. One was excluded because of an atrial septal defect. The median age of the 171 players assessed was 16.7 years (5th to 95th centile range: 14-19) and median body surface area 1.68 m(2) (1.39-2.06 m(2)).Main Outcome Measures: Standard echocardiographic measurements were compared with predicted mean, lower, and upper limits in a cohort of normal controls after matching for age and surface area. Univariate regression analysis was used to assess the correlation between echocardiographic variables and the age and surface area of the soccer player cohort. ECG findings were also assessed.Results: All mean echocardiographic variables were greater than predicted for age and surface area matched controls (p < 0.001). All variables except left ventricular septal and posterior wall thickness showed a modest linear correlation with surface area (r = 0.2 to 0.4, p < 0.001); however, left ventricular mass was the only variable that was significantly correlated with age (r = 0.2, p < 0.01). Only six players (3.5%) had structural anomalies, none of which required further evaluation. All had normal left ventricular systolic function. Sinus bradycardia was found in 65 (39%). The Solokow-Lyon voltage criteria for left ventricular hypertrophy were present in 85 (50%) and the Romhilt-Estes points score (five or more) in 29 (17%). Repolarisation changes were present in 19 (11%), mainly in the inferior leads.Conclusions: Chamber dimensions, left ventricular wall thickness and mass, and aortic root size were all greater than predicted for controls after matching for age and surface area. Sinus bradycardia and the ECG criteria for left ventricular hypertrophy were common but there was poor correlation with echocardiographic left ventricular hypertrophy. The type of hypertrophy found reflected the combined endurance and strength based training undertaken. [ABSTRACT FROM AUTHOR]

Repeated ventricular exposure to alterations in workload may relate to subsequent cardiac remodeling. We examined whether baseline acute changes in right (RV) and left ventricular (LV) function relate to chronic cardiac adaptation to 12-wk exercise training. Twenty-one healthy individuals performed 12-wk high-intensity endurance running training under hypoxia (fraction of inspired oxygen: 14.5%). Resting transthoracic echocardiography was performed before and after the training program to assess ventricular structure, function, and mechanics (including strain-area/volume loops). In addition, we examined systolic cardiac function during recumbent exercise under hypoxia at baseline (heart rate of 110-120 beats/min, "stress echocardiography"). Fifteen individuals completed training (22.0 ± 2.4 yr, 10 males). Hypoxic exercise training increased RV size, including diameter and area (all P < 0.05). With exception of an increase in RV fractional area change ( P = 0.03), RV function did not change post-training (all P > 0.05). Regarding the RV strain-area loop, lower systolic and diastolic slopes were found post-training ( P < 0.05). No adaptation in LV structure, function, or mechanics was observed (all P > 0.05). To answer our primary aim, we found that a greater increase in RV fractional area change during baseline stress echocardiography ( r = -0.67, P = 0.01) inversely correlated with adaptation in RV basal diameter following 12-wk training. In conclusion, 12-wk high-intensity running hypoxic exercise training induced right-sided structural remodeling, which was, in part, related to baseline increase in RV fractional area change to acute exercise. These data suggest that acute cardiac responses to exercise may relate to subsequent RV remodeling after exercise training in healthy individuals. NEW & NOTEWORTHY During exercise, the right ventricle is exposed to a disproportionally higher wall stress than the left ventricle, which is further exaggerated under hypoxia. In this study, we showed that 12-wk high-intensity running hypoxic exercise training induced right-sided structural remodeling, which was, in part, related to baseline cardiac increase in RV fractional area change to acute exercise. These data suggest that acute RV responses to exercise are related to subsequent right ventricular remodeling in healthy individuals upon hypoxic training.

Background: Acute exercise promotes transient exercise-induced cardiac fatigue, which affects the right ventricle and to a lesser extent the left ventricle. Hypoxic exposure induces an additional increase in right ventricular (RV) afterload. Therefore, exercise in hypoxia may differently affect both ventricles. The aim of this study was to investigate the acute effects of a bout of high-intensity exercise under hypoxia versus normoxia in healthy individuals on right- and left-sided cardiac function and mechanics., Methods: Twenty-one healthy individuals (mean age, 22.2 ± 0.6 years; 14 men) performed 45-min high-intensity running exercise under hypoxia (fraction of inspired oxygen 14.5%) and normoxia (fraction of inspired oxygen 20.9%) in a randomized order. Pre- and post-exercise echocardiography, at rest and during low-to-moderate intensity recumbent exercise ("stress"), was performed to assess RV and left ventricular (LV) cardiac function and mechanics. RV structure, function, and mechanics were assessed using conventional two-dimensional, Doppler, tissue Doppler, speckle-tracking echocardiographic, and novel strain-area loops., Results: Indices of RV systolic function (RV fractional area change, Tricuspid annular plane systolic excursion, RV s', and RV free wall strain) and LV function (LV ejection fraction and LV global longitudinal strain) were significantly reduced after high-intensity running exercise (P < .01). These exercise-induced changes were more pronounced when echocardiography was examined during stress compared with baseline. These responses in RV and LV indices were not altered under hypoxia (P > .05)., Conclusions: There was no impact of hypoxia on the magnitude of exercise-induced cardiac fatigue in the right and left ventricles after a 45-min bout of high-intensity exercise. This finding suggests that any potential increase in loading conditions does not automatically exacerbate exercise-induced cardiac fatigue in this setting., (Copyright © 2020 American Society of Echocardiography. Published by Elsevier Inc. All rights reserved.)

The health benefits of physical activity are well documented. Patients with hypertrophic cardiomyopathy (HCM) are often discouraged from participating in physical activity due to a perceived increase in the risk of sudden cardiac death (SCD). As a result, only 45% of patients with HCM meet the minimum guidelines for physical activity, and many report an intentional reduction in exercise following diagnosis. Despite most SCD being unrelated to HCM, guidelines traditionally focused on the avoidance of potential risk through restriction of exercise, without clear recommendations on how to negate the negative health impact of inactivity. Retrospective reviews have demonstrated that the majority of cardiac arrests in patients with HCM occurred at rest or on mild exertion and that the overall incidence of HCM-related SCD is significantly lower than previously reported. We will discuss current international guidelines and recommendations and consider the outcomes of various studies that have investigated the effects of exercise of different intensities on patients with HCM. In light of the growing evidence suggesting that carefully guided exercise can be both beneficial and safe in patients with HCM, we ask whether it is time to let the shackles off exercise restriction in HCM., Competing Interests: None declared., (Copyright © 2020 Medinews (Cardiology) Limited.)

The assessment of aortic root dimensions is important in cardiac pre-participation screening. Scaling of cardiac dimensions removes the impact of body size allowing meaningful inter/intra group comparisons. Developing appropriate scaling approaches, scaling variables and extending the application to major vessels is warranted so underlying pathology can be detected and managed appropriately. The study aims to define relationships between aortic root dimensions and body surface area/height. Two hundred and twenty elite Rugby Football League athletes were recruited. All participants completed anthropometric assessments, a 12-lead ECG and echocardiogram. Aortic root was measured at the aortic annulus, sinus of valsalva, sinotubular junction and the proximal ascending aorta. Linear and allometric scaling were performed on the relationship between aortic measurements and body surface area/height. Absolute aortic root measurements fell within normal population data (mean ± standard deviation (range): aortic annulus: 22 ± 2 (17-28) mm, sinus of valsalva: 28 ± 3 (20-38) mm, sinotubular junction: 22 ± 3 (14-33) mm, proximal ascending aorta: 22 ± 3 (15-31) mm). Linear scaling to height produced size-independent indices at all aortic measurement sites (P < 0.05). Conversely, linear scaling using body surface area did not produce size-independent indices at any site (P > 0.05). Allometric scaling, using both body surface area and height, produced size-independent indices at all sites (P < 0.05). We recommend linearly scaling aortic root dimensions to height in elite Rugby Football League athletes and discourage the use of body surface area as a linear scaling quantity. Allometric scaling is also effective when using both body surface area and height.

Objective: To generate reference intervals for ECG variables in clinically normal chimpanzees (Pan troglodytes)., Animals: 100 clinically normal (51 young [< 10 years old] and 49 adult [≥ 10 years old]) wild-born chimpanzees., Procedures: Electrocardiograms collected between 2009 and 2013 at the Tchimpounga Chimpanzee Rehabilitation Centre were assessed to determine heart rate, PR interval, QRS duration, QT interval, QRS axis, P axis, and T axis. Electrocardiographic characteristics for left ventricular hypertrophy (LVH) and morphology of the ST segment, T wave, and QRS complex were identified. Reference intervals for young and old animals were calculated as mean ± 1.96•SD for normally distributed data and as 5th to 95th percentiles for data not normally distributed. Differences between age groups were assessed by use of unpaired Student t tests. RESULTS Reference intervals were generated for young and adult wild-born chimpanzees. Most animals had sinus rhythm with small or normal P wave morphology; 24 of 51 (47%) young chimpanzees and 30 of 49 (61%) adult chimpanzees had evidence of LVH as determined on the basis of criteria for humans., Conclusions and Clinical Relevance: Cardiac disease has been implicated as the major cause of death in captive chimpanzees. Species-specific ECG reference intervals for chimpanzees may aid in the diagnosis and treatment of animals with, or at risk of developing, heart disease. Chimpanzees with ECG characteristics outside of these intervals should be considered for follow-up assessment and regular cardiac monitoring.

A dual chamber permanent pacemaker was implanted into an asymptomatic man with complete (third degree) heart block because of the risk of asystole. The ventricular lead was thought to have been attached to the right ventricular septum; however, it inadvertently passed through a patent foramen ovale into the left ventricle. Although the postprocedure ECG showed right bundle branch block this was thought to be due to the presumed septal positioning of the pacing lead. Lead misplacement was not detected on posterioanterior chest X-ray but was clearly demonstrated by transthoracic echocardiography, and subsequently on lateral chest X-ray. The lead was successfully removed and repositioned correctly at the next available opportunity without complication or sequelae.

Background: Hypertrophic cardiomyopathy (HCM) is characterised by idiopathic cardiac enlargement and represents the most frequent cause of sudden cardiac death in athletes under the age of 35 years. Differentiation between physiological (ie, exercise-related) and pathological (ie, HCM-related) cardiac remodelling is challenging. In line with cardiac remodelling, vascular structure and function are altered following training, but little is known about peripheral vascular adaptations in HCM. We hypothesised that, while HCM patients and athletes would exhibit similar cardiac characteristics, differences would be apparent in their brachial and carotid arteries., Methods: In age-matched groups of HCM patients (n = 18, 39 ± 15 years), highly competitive athletes (n = 18, 38 ± 12 years) and recreational controls (n = 10, 37 ± 14 years), we used high-resolution ultrasound to assess the diameter and wall thickness of the carotid and brachial arteries, with flow-mediated dilator function (FMD) of the brachial arteries also assessed., Results: A significant difference between athletes and HCM was evident in arterial wall thickness (carotid 519 ± 60 vs 586 ± 102 µm, p<0.05; brachial 345 ± 80 vs 456 ± 76 µm, p<0.05) and the brachial artery peak blood flow response following forearm ischaemia, an index of resistance artery remodelling (998 ± 515 vs 725 ± 248 ml/min, p<0.05). Similar differences were noted between athletes and controls, while controls and HCM did not differ. Brachial FMD% was not different between groups., Conclusions: Athletes and HCM subjects, who can be difficult to differentiate on the basis of cardiac measures, exhibit differences in indices of arterial structure. While this may be a disease-related effect, we cannot discount a generic impact of physical activity on arterial structure, as the athlete's arteries were also different to untrained control subjects. Future studies should assess artery function and structure in athletic HCM subjects.

Giant cell arteritis (GCA), also known as granulomatous arteritis is a systemic vasculitis mainly affecting extra cranial branches of carotid arteries. It can rarely affect other vascular beds causing thoracic aorta aneurysm, dissection and rarely cause myocardial infarction through coronary arteritis. It can cause considerable diagnostic dilemma due to varied clinical presentations. The authors report an illustrative case of a 70-year-old woman with GCA who developed symptoms suggestive of acute myocardial infarction with chest pain, localised ST-T changes and echocardiographic left ventricular dysfunction. However, cardiac troponin T biomarkers and coronary angiography were normal. Her symptoms subsided with steroid treatment. Cardiac symptoms at first presentation of GCA are unusual.

Frequently patients with coronary artery disease (CAD) present with chest pain. Anginal equivalents such as dyspnoea and fatigue, or radiation of pain to the neck, jaw and arm, are also well described. Absence of chest pain with chronic left arm and neck pain is more unusual but demonstrates the heterogeneity of presentation. CAD should be considered in those anginal equivalents in the absence of 'strangling and anxiety of the breast'.

We assessed the prevalence and 3-month change in glucose tolerance status in consecutive non-ST-elevation myocardial infarction (NSTEMI; European Society of Cardiology 2007 definition) patients (N=49; mean (S.D.) age 65 (11) years) admitted to a coronary care unit, without known diabetes. These patients underwent an oral glucose tolerance test (OGTT) 36-hour (median, IQR: 18-72) after admission and at 3 months. Undiagnosed abnormal glucose tolerance (AGT: impaired fasting glucose (IFG), impaired glucose tolerance (IGT) or new diabetes) was common (61% at admission and 41% at 3 months, p<0.05) and the majority (approximately 3/4) had IGT. Glucose tolerance status improved in a higher proportion of patients than it worsened (31% vs. 8%, p=0.04). At 3 months, fasting glucose was unchanged but 2-hour OGTT glucose was lower (mean (S.D.): 8.5 (2.7) mmol/L vs. 7.7 (2.7) mmol/L, p=0.004). 'Stress hyperglycaemia' could explain higher admission glucose levels and this raises the question about the optimal timing of OGTT in relation to myocardial infarction. Newly diagnosed diabetes was present in approximately 10% of patients and this was not reliably detected by fasting plasma glucose. In NSTEMI patients OGTT is the only reliable strategy to identify subjects with IGT and diabetes.

Aims: To determine long-term time-related survival and evaluate risk factors for increased mortality in patients following their first permanent pacemaker implantation., Methods and Results: Analysis of patient records from implant to follow-up. Patient-specific time-lines were constructed to date of last review or death. Observed survival was estimated by event-free analysis using the Kaplan-Meier method. Expected survival was derived from age- and gender-matched cohorts. Risk factors for mortality were sought using the multivariate Cox proportional hazards method and risk ratios estimated. Eight hundred and thirty-three patients underwent implantation of their first permanent pacemaker from April 1992 to January 1994, and were locally followed up. Survival data were available for 803 (96.4%) patients (median age, 77.3 years [5th to 95th centile range: 53.5 to 89 5 years]) and follow-up was complete in 94.8%. At implant. dual-chamber systems were implanted in 443 (55.1%). single-chamber ventricular systems in 321 (40.0%), and single-chamber-atrial systems in 39 (4.9%). Observed survival after implantation was significantly worse than expected (P<0.001). Independent predictors of increased mortality were: age at implant (risk ratio [RR] 1.06: 95% confidence interval [CI] 1.01 to 1.12). VVI pacing mode (RR 1.64; 95% CI 1.34 to 1.93), cardiomyopathy (RR 5.86; 95% CI 4.86 to 6.86), male gender (RR 1.27; 95% CI 1.22 to 1 32) and valvular heart disease (RR 2.01: 95% CI 1.98 to 2.04)., Conclusions: At the end of follow-up, mortality was much higher than expected. In this typical pacemaker population. age at implant and VVI pacing mode were independently associated with increased mortality with accompanying heart disease having the greatest individual impact.

Anomalous coronary arteries are rare and single coronary arteries are very rare congenital abnormalities. Significant stenoses within these arteries have been described, but interventional procedures on such anomalies are very infrequently performed. We describe a patient with angina pectoris and a single left coronary artery with multiple lesions treated with percutaneous transluminal coronary angioplasty (PTCA) and intra-coronary stent implantation. Our case shows that when the anatomy is not too abnormal, even multivessel PTCA and stent employment can be performed successfully in single coronary arteries.

Objectives: To determine whether a specialist cardiac nurse would improve delay to thrombolysis in acute myocardial infarction (MI)., Subjects: Patients presenting with chest pain to a district general hospital., Method: Comparison of: a) door-to-needle times of patients with 'definite' MI when the nurse was on and off duty (15 months) and prior to her employment (3 months); b) pain-to-needle times for definite MI; and c) door-to-needle times of patients without definite MI on first electrocardiogram (ECG) but who subsequently qualified for thrombolysis., Results: Of 365 patients included in the study, 289 had definite MI. Before the appointment of a thrombolysis nurse, door-to-needle times were 0% at 30 minutes, 7% at 45 minutes and 34% at 60 minutes. Since the appointment, with the nurse on-duty, they have improved to 58%, 91% and 100% respectively, a saving of 36 minutes in median door-to-needle time (p = 0.0001). There was a median saving of 95 minutes in pain-to-needle times with the thrombolysis nurse on duty compared with off duty (p = 0.0001). Finally, with the nurse on duty there was also a saving of 36 minutes in median door-to-needle time in patients in whom the first ECG was non-diagnostic for MI (p = 0.02)., Conclusions: A thrombolysis nurse produced a dramatic improvement in median door-to-needle and pain-to-needle times in patients presenting with definite MI. This would lead to an additional 41 lives saved at 30 months per 1,000 patients treated. With 24-hour thrombolysis nurse cover, this would potentially lead to 8 additional lives saved at 30 months at a cost of 12,300 Pounds each. There was also a striking improvement in door-to-needle times for patients presenting with a non-diagnostic first ECG who subsequently qualified for thrombolysis.

Thymocyte and Splenocyte cultures from in vivo immunised Xenopus were assayed to test their suppressive capacity. Immunisation with TNP-Polyvinylpyrrolidone induced suppression. Suppression induced by the haptenated antigens, TNP-Red blood cells, TNP-Lipopolysaccharide, and TNP-Ficoll affected the anti-TNP antibody response of splenocytes from TNP-PVP immunised animals. Pretreatment with cyclophosphamide revealed both a sensitive and insensitive suppression capacity in Xenopus laevis.