Acute exercise-induced changes in cardiac function relates to right ventricular remodeling following 12-wk hypoxic exercise training.

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.

Exercise-Induced Cardiac Fatigue after a 45-Minute Bout of High-Intensity Running Exercise Is Not Altered under Hypoxia.

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.

Hypertrophic cardiomyopathy and exercise restrictions: time to let the shackles off?

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.

Scaling to produce size-independent indices of echocardiographic derived aortic root dimensions in elite Rugby Football League players.

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.

Electrocardiogram reference intervals for clinically normal wild-born chimpanzees (Pan troglodytes).

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.

Inadvertent left ventricular pacing through a patent foramen ovale: identification, management and implications for postpacemaker implantation checks.

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.

Peripheral vascular structure and function in hypertrophic cardiomyopathy.

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.

Myopericarditis in giant cell arteritis: case report of diagnostic dilemma and review of literature.

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.

Lesson of the month (2). Angina without 'strangling and anxiety of the breast'.

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'.

QT peak prolongation is not associated with left ventricular hypertrophy in teenage professional football players.

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.