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Background: In clinical practice, the right heart filling status is assessed using the respirophasic variation of the inferior vena cava (IVC) assessed by transthoracic echocardiography (TTE) showing moderate correlations with the catheter‐based reference standard. Purpose: To develop and validate a similar approach using MRI. Study Type: Prospective. Population: 37 male elite cyclists (mean age 26 ± 4 years). Field Strength/Sequence: Real‐time balanced steady‐state free‐precession cine sequence at 1.5 Tesla. Assessment: Respirophasic variation included assessment of expiratory size of the upper hepatic part of the IVC and degree of inspiratory collapse expressed as collapsibility index (CI). The IVC was studied either in long‐axis direction (TTE) or using two transverse slices, separated by 30 mm (MRI) during operator‐guided deep breathing. For MRI, in addition to the TTE‐like diameter, IVC area and major and minor axis diameters were also assessed, together with the corresponding CIs. Statistical Tests: Repeated measures ANOVA test with Bonferroni correction. Intraclass correlation coefficient (ICC) and Bland–Altman analysis for intrareader and inter‐reader agreement. A P value <0.05 was considered statistically significant. Results: No significant differences in expiratory IVC diameter were found between TTE and MRI, i.e., 25 ± 4 mm vs. 25 ± 3 mm (P = 0.242), but MRI showed a higher CI, i.e., 76% ± 14% vs. 66% ± 14% (P < 0.05). As the IVC presented a noncircular shape, i.e., major and minor expiratory diameter of 28 ± 4 mm and 21 ± 4 mm, respectively, the CI varied according to the orientation, i.e., 63% ± 27% vs. 75% ± 16%, respectively. Alternatively, expiratory IVC area was 4.3 ± 1.1 cm2 and showed a significantly higher CI, i.e., 86% ± 14% than diameter‐based CI (P < 0.05). All participants showed a CI >50% with MRI versus 35/37 (94%) with TTE. ICC values ranged 0.546–0.841 for MRI and 0.545–0.704 for TTE. Conclusion: Assessment of the respirophasic IVC variation is feasible with MRI. Adding this biomarker may be of particular use in evaluating heart failure patients. Level of Evidence: 1 Technical Efficacy Stage: 2 [ABSTRACT FROM AUTHOR]

Background: Atrial fibrillation (AF) is the most common performance limiting arrhythmia in racehorses. High dose exercise and airway disease promote AF in humans. Few studies have investigated epidemiological factors associated with AF in horses. Objectives: Explore variables relating to performance, exercise volume and postrace endoscopic findings in horses with AF. Animals: A total of 164 horses with poor race performance and postrace AF were compared to 321 horses with poor performance without AF (PP) and 314 horses performing to expectation (TE). Methods: Horse‐level and race‐level variables for horses racing in Australia and Hong Kong from 2009 to 2021 were compared using univariable and multivariable logistic regression. Postrace endoscopic exercise‐induced pulmonary hemorrhage (EIPH) and tracheal mucus accumulation (TMA) grades for AF and PP horses were compared using chi‐squared analysis. Results: Variables that were significant in the multivariable model of AF compared to TE were distance (lengths) behind the winner, (odds ratio [OR]; 95% confidence interval [95% CI], 1.41 [1.32‐1.51], P <.0001), cumulative prize money per start before the event (OR [95% CI] 1.02 [1.01‐1.03], P =.01) and age (OR [95% CI] 0.72 [0.55‐0.92], P =.01). More AF horses had EIPH grade ≥3 (23/109; 21.1%) than PP horses (7/213; 3.3%; OR [95%CI] 7.9 [3.3‐20.2], P <.0001). Conclusions and Clinical Importance: Acute race performance was substantially impaired by AF but career earnings before the event were not inferior. Exercise volume did not promote AF. Higher grades of EIPH found in AF horses suggests a mechanistic relationship between these conditions. [ABSTRACT FROM AUTHOR]

Cardiopulmonary complications of connective tissue diseases (CTDs), particularly pulmonary arterial hypertension (PAH) and interstitial lung disease (ILD), are major determinants of morbidity and mortality. Multidisciplinary meetings may improve diagnostic accuracy and optimise treatment. We review the literature regarding multidisciplinary meetings in CTD‐ILD and PAH and describe our tertiary centre experience of the role of the multidisciplinary meeting in managing CTD‐PAH. [ABSTRACT FROM AUTHOR]

Background: Administrative coding of out‐of‐hospital cardiac arrest (OHCA) is heterogeneous, with the prevalence of noninformative diagnoses uncertain. Aim: To characterize the prevalence and type of non‐informative diagnoses in a young cardiac arrest population. Methods: Hospital discharge diagnoses provided to a statewide OHCA registry were characterised as either 'informative' or 'noninformative.' Informative diagnoses stated an OHCA had occurred or defined OHCA as occurring due to coronary artery disease, cardiomyopathy, channelopathy, definite noncardiac cause, or no known cause. Noninformative diagnoses were blank, stated presenting cardiac rhythm only, provided irrelevant information or presented a complication of the OHCA as the main diagnosis. Characteristics of patients receiving informative versus noninformative diagnoses were compared. Results: Of 1479 patients with OHCA aged 1 to 50 years, 290 patients were admitted to 15 hospitals. Ninety diagnoses (31.0%) were noninformative (arrest rhythm = 50, blank = 21, complication = 10 and irrelevant = 9). Two hundred diagnoses (69.0%) were informative (cardiac arrest = 84, coronary artery disease = 54, noncardiac diagnosis = 48, cardiomyopathy = 8, arrhythmia disorder = 4 and unascertained = 2). Only 10 diagnoses (3.5%) included both OHCA and an underlying cause. Patients receiving a noninformative diagnosis were more likely to have survived OHCA or been referred for forensic assessment (P = 0.011) and had longer median length of stay (9 vs 5 days, P = 0.0019). Conclusion: Almost one third of diagnoses for young patients discharged after an OHCA included neither OHCA nor any underlying cause. Underestimating the burden of OHCA impacts ongoing patient and at‐risk family care, data sampling strategies, international statistics and research funding. [ABSTRACT FROM AUTHOR]

Background: Sudden cardiac death (SCD) during physical exercise is devastating. Aims: To evaluate causes and circumstances of exercise‐related SCD in the young in Australia. Methods: We reviewed the National Coronial Information System database for deaths in Australia relating to cardiovascular disease in cases aged 10–35 years between 2000 and 2016. Cases who had undertaken physical exercise at the time of the event were included. We collected demographics, circumstances of death, type of physical exercise, bystander cardiopulmonary resuscitation (CPR) and automated external defibrillator (AED) use prior to ambulance arrival. Results: Over a 17‐year period, 1925 SCD cases were identified, of which 110 (6%) cases (median age 27 years (interquartile range 21–32 years); 92% male) were related to sports/physical exercise. Thirteen (12%) cases occurred in active athletes. Most common causes were coronary artery disease (CAD; 37%) and sudden arrhythmic death syndrome (SADS; 20%). Among Aboriginal and Torres Strait Islanders (n = 10), all deaths were related to CAD. Australian Rules Football (24%), running/jogging (14%) and soccer (14%) were the most frequent physical exercise activities. Prior symptoms were present in 39% (chest pain 37%, pre‐syncope/syncope 26%). Most (87%) were witnessed, with bystander CPR in 70%. AED use prior to ambulance arrival was 8%. Conclusions: The present study demonstrates the high occurrence of CAD and SADS in SCD in the young related to physical exercise. Aboriginal and Torres Strait Islanders were disproportionately affected by CAD. Although events were commonly witnessed, AED was seldom used prior to ambulance arrival and highlights an important opportunity to improve outcomes in the post‐arrest chain of survival. [ABSTRACT FROM AUTHOR]

Aims: The contribution of adverse ventricular interdependence remains undervalued in heart failure or pulmonary vascular disease, and not much is known about its dynamic nature during exercise and respiration. In this study, we evaluated ventricular interaction during exercise in patients with heart failure with preserved ejection fraction (HFpEF) and patients with chronic thromboembolic pulmonary hypertension (CTEPH) as compared with healthy controls. Methods and results: Forty‐six subjects (10 controls, 19 CTEPH patients, and 17 HFpEF patients) underwent cardiac magnetic resonance imaging during exercise. Ventricular interaction was determined through analysis of the septal curvature (SC) of a mid‐ventricular short‐axis slice at end‐diastole, end‐systole, and early‐diastole, both in expiration and inspiration. Exercise amplified ventricular interaction in CTEPH patients and to a lesser extent in HFpEF patients (P < 0.05 for decrease in SC with exercise). Adverse interaction was most profound in early‐diastole and most pronounced in CTEPH patients (P < 0.05 interaction group * exercise) because of a disproportionate increase RV afterload (P < 0.05 to both controls and HFpEF) and diastolic pericardial restraint (P < 0.001 for interaction group * exercise) during exercise. Inspiration enhanced diastolic interdependence in CTEPH and HFpEF patients (P < 0.05 vs. expiration). Both at rest and during exercise, SC strongly correlated with RV volumes and pulmonary artery pressures (all P < 0.05). Conclusions: Exercise amplifies adverse right–left ventricular interactions in CTEPH, while a more moderate effect is observed in isolated post‐capillary HFpEF. Given the strong link with RV function and pulmonary hemodynamic, assessing ventricular interaction with exCMR might be valuable from a diagnostic or therapeutic perspective. [ABSTRACT FROM AUTHOR]

Objective: To determine whether young rural Australians have higher rates or different underlying causes of out‐of‐hospital cardiac arrest (OHCA). Design: A case–control design identified patients experiencing an OHCA, then compared annual OHCA rates and underlying causes in rural versus metropolitan Victoria. OHCA causes were defined as either cardiac or non‐cardiac, with specific aetiologies including coronary disease, cardiomyopathy, unascertained cause of arrest, drug toxicity, respiratory event, neurological event and other cardiac and non‐cardiac. For OHCAs with confirmed cardiac aetiology, cardiovascular risk profiles were compared. Setting: A state‐wide prospective OHCA registry (combining ambulance, hospital and forensic data) in the state of Victoria, Australia (population 6.5 million). Participants: Victorians aged 1–50 years old experienced an OHCA between April 2019 and April 2020. Main outcome measures: Rates and underlying causes of OHCA in young rural and metropolitan Victorians. Results: Rates of young OHCA were higher in rural areas (OHCA 22.5 per 100 000 rural residents vs. 13.4 per 100 000 metropolitan residents, standardised incidence ratio 168 (95% CI 101–235); confirmed cardiac cause of arrest 12.1 per 100 000 rural residents versus 7.5 per 100 000 metropolitan residents, standardised incidence ratio 161 (95% CI 71–251). The underlying causation of the OHCA and cardiovascular risk factor burden did not differ between rural and metropolitan areas. Conclusion: Higher rates of OHCA occur in young rural patients, with standardised incidence ratio of 168 compared to young metropolitan residents. Rural status did not influence causes of cardiac arrest or known cardiovascular risk factor burden in young patients experiencing OHCA. [ABSTRACT FROM AUTHOR]

Aims: Identifying early right ventricular (RV) dysfunction and impaired vasodilator reserve is challenging in heart failure with preserved ejection fraction (HFpEF). We hypothesized that cardiac magnetic resonance (CMR)‐based exercise imaging and serial cyclic guanosine monophosphate (cGMP) measurements can identify dynamic RV‐arterial uncoupling and responsiveness to pulmonary vasodilators at early stages of the HFpEF syndrome. Methods and results: Patients with HFpEF (n = 16), impaired left ventricular relaxation due to concentric remodelling (LVCR, n = 7), and healthy controls (n = 8) underwent CMR at rest and during supine bicycle exercise with simultaneous measurements of central haemodynamics and circulating cGMP levels, before and after oral administration of 50 mg sildenafil. At rest, mean pulmonary artery pressures (mPAP) were higher in HFpEF, compared with LVCR and controls (27 ± 2, 18 ± 1, and 11 ± 1, respectively; P = 0.01), whereas biventricular volumes, heart rate, and stroke volume were similar. During exercise, LVCR and HFpEF had a greater increase in the ratio of mPAP over cardiac output than controls (5.50 ± 0.77 and 6.34 ± 0.86 vs. 2.24 ± 0.55 in controls, P = 0.005). The ratio of peak exercise to rest RV end‐systolic pressure‐volume, a surrogate of RV contractility, was significantly reduced in LVCR and HFpEF (2.32 ± 0.17 and 1.56 ± 0.08 vs. 3.49 ± 0.35 in controls, P < 0.001) and correlated with peak exercise VO2 (R2 = 0.648, P < 0.001). cGMP levels increased with exercise across the HFpEF spectrum (P < 0.05 vs. baseline), except when postcapillary pulmonary hypertension was present at rest (P = 0.73 vs. baseline). A single sildenafil administration failed to increase circulating cGMP levels and did not improve RV performance. Conclusion: Exercise CMR identifies impaired RV‐arterial coupling at an early stage of HFpEF. Circulating cGMP levels phenocopy the haemodynamic spectrum in HFpEF but fail to increase after phosphodiesterase type 5 inhibition, endorsing the need for alternative interventions to increase cGMP signalling in HFpEF. [ABSTRACT FROM AUTHOR]

Cancer therapy related cardiac dysfunction (CTRCD) is an area of increasing focus, particularly during the survivorship period, for paediatric, adolescent and adult cancer survivors. With the advent of immunotherapy and targeted therapy, there is a new set of mechanisms from which paediatric and young adult patients with cancer may suffer cardiovascular injury. Furthermore, cardiovascular disease is the leading cause of morbidity and mortality in the survivorship period. The recently established Australian Cardio‐Oncology Registry is the largest and only population‐based cardiotoxicity database of paediatric and adolescent and young adult oncology patients in the world, and the first paediatric registry that will document cardiotoxicity caused by chemotherapy and novel targeted therapies using a prospective approach. The database is designed for comprehensive data collection and evaluation of the Australian practice in terms of diagnosis and management of CTRCD. Using the Australian Cardio‐Oncology Registry critical clinical information will be collected regarding predisposing factors for the development of CTRCD, the rate of subclinical left ventricular dysfunction and transition to overt heart failure, further research into protectant molecules against cardiac dysfunction and aid in the discovery of which genetic variants predispose to CTRCD. A health economic arm of the study will assess the cost/benefit of both the registry and cardio‐oncology clinical implementation. Finally, an imaging arm will establish if exercise cardiac magnetic resonance imaging and VO2 max testing is a more sensitive predictor of cardiac reserve in paediatric and adolescent and young adult oncology patients exposed to cardiac toxic therapies. [ABSTRACT FROM AUTHOR]

Marked adaptation of left ventricular (LV) structure in endurance athletes is well established. However, previous investigations of functional and mechanical adaptation have been contradictory. A lack of clarity in subjects' athletic performance level may have contributed to these disparate findings. This study aimed to describe structural, functional, and mechanical characteristics of the cyclists' LV, based on clearly defined performance levels. Male elite cyclists (EC) (n = 69), sub‐elite cyclists (SEC) (n = 30), and non‐athletes (NA) (n = 46) were comparatively studied using conventional and speckle tracking 2D echocardiography. Dilated eccentric hypertrophy was common in EC (34.7%), but not SEC (3.3%). Chamber concentricity was higher in EC compared to SEC (7.11 ± 1.08 vs 5.85 ± 0.98 g/(mL)2/3, P <.001). Ejection fraction (EF) was lower in EC compared to NA (57 ± 5% vs 59 ± 4%, P <.05), and reduced EF was observed in a greater proportion of EC (11.6%) compared to SEC (6.7%). Global circumferential strain (GCε) was greater in EC (−18.4 ± 2.4%) and SEC (−19.8 ± 2.7%) compared to NA (−17.2 ± 2.6%) (P <.05 and P <.001). Early diastolic filling was lower in EC compared with SEC (0.72 ± 0.14 vs 0.88 ± 0.12 cm/s, P <.001), as were septal E' (12 ± 2 vs 15 ± 2 cm/s, P <.001) and lateral E' (18 ± 4 vs 20 ± 4 cm/s, P <.05). The magnitude of LV structural adaptation was far greater in EC compared with SEC. Increased GCε may represent a compensatory mechanism to maintain stroke volume in the presence of increased chamber volume. Decreased E and E' velocities may be indicative of a considerable functional reserve in EC. [ABSTRACT FROM AUTHOR]

Aims: To quantify acute energy expenditure, supraclavicular skin temperature and cardiovascular responses to four doses of the β3‐adrenoceptor agonist, mirabegron. Materials and methods: A total of 17 individuals (11 men, six women) participated in this ascending‐dose study, receiving single 50‐, 100‐, 150‐ and 200‐mg doses of mirabegron on four separate days with 3 to 14 days wash‐out between each dose. All variables were measured each visit from baseline to 180 minutes post mirabegron treatment. To determine brown adipose tissue (BAT) thermogenic efficacy at each dose, energy expenditure and supraclavicular skin temperature were compared from baseline to 180 minutes post mirabegron treatment. To examine safety, changes in cardiovascular variables at 100, 150 and 200 mg were compared with the standard clinical dose of 50 mg. Results: Energy expenditure significantly increased after the 100‐ (35.6 ± 5.4 kJ/h) and 200‐mg (35.6 ± 13.1 kJ/h) doses (P ≤ 0.05), and trended towards an increase after 150 mg (24.1 ± 13.6 kJ/h). Supraclavicular skin temperature increased after 50‐ (0.22 ± 0.1°C), 100‐ (0.30 ± 0.1°C) and 150‐mg mirabegron doses (0.29 ± 0.1°C; P ≤ 0.05). The change in systolic blood pressure was greater after 150‐ (7.1 ± 1.3 mm Hg) and 200‐mg doses (9.3 ± 1.9 mm Hg) than after the 50‐mg dose (2.2 ± 1.3 mm Hg; P ≤ 0.05). The change in heart rate was greater after 200 mg (9.0 ± 2.2 bpm) compared with 50 mg (2.9 ± 1.4 bpm; P ≤ 0.05). Conclusions: A 100‐mg dose of mirabegron increases energy expenditure and supraclavicular skin temperature in a β3‐adrenoceptor‐specific manner, without the off‐target elevations in blood pressure or heart rate observed at higher doses. [ABSTRACT FROM AUTHOR]

Background It has long been established that cardiotoxicity occurs as a result of exposure to certain chemotherapeutics, particularly anthracyclines. Historically, clinicians equate cardiotoxicity with a poor prognosis, in a small percentage of patients and deem long-term surveillance as optional. Emerging evidence suggests that anthracycline cardiotoxicity ( ACT) is a life-long risk with an incidence approaching 20%. Aims To elucidate the incidence of anthracycline cardiotoxicity within a current paediatric oncology survivor cohort. Methods Participants were identified through the Haematology-Oncology database at the Royal Children's Hospital, Melbourne. Patients were identified from a retrospective audit of outpatient attendances between January 2008 and December 2015. Patients with a cancer diagnosis exposed to anthracyclines were eligible for the study. Patient demographics and echocardiogram findings were recorded with patients subcategorised according to degree of ACT. More significant ACT defined as fractional shortening ( FS) <24% and less significant if FS 24-28% or a decline in baseline ejection fraction of >10%. Results Two hundred and eighty-six of a total 481 identified patients were eligible for study inclusion. Twenty patients displayed significant ACT with FS <24%. Ten patients had a FS 24-28% and 25 patients with a decline in ejection fraction from baseline of >10%. Overall, 6.6% demonstrated significant cardiac complications, whilst 19.6 % demonstrated some degree of ACT and decline in myocardial function. When stratified for cumulative anthracycline dose, the incidence of severe cardiac dysfunction was 5.1% (<250 mg/m2) and 25% (>250 mg/m2) Conclusion This study demonstrates, in keeping with modern literature, the higher incidence of anthracycline associated cardiac toxicity and a need for better surveillance and follow up. [ABSTRACT FROM AUTHOR]

Long-term intensive exercise training programs lead to numerous progressive cardiac adaptations, which are collectively termed 'athlete's heart.' Noninvasive diagnostic techniques, such as color Doppler echocardiography, have been widely used in the analysis of the athlete's heart. Initial experiences focused mainly on left heart adaptations to training. However, in recent years, substantial structural and functional adaptations of the right heart have been documented. The present review article focuses on recent data defining right heart adaptation to short- and long-term periods of exercise training. Right ventricular (RV) morphology and function may be more profoundly affected by intense exercise and, in some cases, functional recovery may be incomplete. Moreover, there is speculation that such changes may represent a substrate for proarrhythmic RV remodeling in some highly trained athletes, even in the absence of a known familial redisposition. [ABSTRACT FROM AUTHOR]

The article focuses on an analysis of acute coronary syndrome (ACS) cases. It mentions that hospital is a major tertiary receiving hospital for cardiology transfers from the Albury-Wodonga and East Gippsland regions. It also mentions that an increase in ACS cases observed with elderly patients with multiple comorbidities predominantly affected.

Background Latest research shows that the lower resting values of right ventricular ( RV) myocardial % strain may represent a physiologic change rather than subclinical myocardial damage. Therefore, we assessed load-independent changes to the RV as a consequence of high intensity training by measuring the Isovolumic acceleration ( IVA) of the free wall of the RV in conjunction with NT pro- BNP measured by an electrochemiluminescence assay. Methods Seventeen controls (mean age 27 ± 4), 24 soccer footballers (mean age 24 ± 4), and 18 elite rowers (mean age 22 ± 4) were studied. Left ventricular ( LV) and RV % strain were measured using two-dimensional (2D) speckle based automated functional imaging (AFI) software. RV free wall IVA was measured using pulsed-wave tissue Doppler at the lateral tricuspid annulus. Standard 2D echo were used to measured RV parameters including the Tei index (systolic and diastolic function) and the total annular plane systolic excursion ( TAPSE) of the RV annulus. NT pro- BNP was measured by an electrochemiluminescence assay. Results The RV diameter was increased in the footballers and elite rowers compared with controls (P < 0.001). RV wall size was greater in the elite rowers compared with controls and footballers (P = 0.002). The peak IVA of the RV was higher in the rowers, compared with the footballers and to controls (P < 0.001). The mean LV and RV % myocardial strain were lower in the elite athletes and the footballers compared with controls (P < 0.001). There was no difference in RV Tei index, levels of BNP, and TAPSE across all subjects. Conclusions This study showed a significant increase in IVA of the RV of athletes despite reduced myocardial % strain and normal levels in NT-pro BNP. This suggests that the decrease in % strain is not a consequence of myocardial damage, but may represents a part of the physiological response to endurance exercise. Therefore, a reduced IVA in a remodeled RV could herald a pathological response. [ABSTRACT FROM AUTHOR]

Background: Our aim was to study the independent effect of heart rate (HR) on parameters of diastolic function, particularly mitral annular velocities measured by tissue Doppler imaging (TDI), an effect which is not well understood. Methods: Sixteen patients with dual chamber pacemakers attending for routine pacemaker review underwent detailed echocardiographic assessment during atrial pacing with intact atrioventricular conduction at baseline and accelerated HRs. Mitral inflow and annular tissue Doppler velocities and systolic strain parameters were compared. Results: Parameters of systolic function were unaffected by increased HR. When these parameters were compared at baseline (mean 67 bpm) and accelerated HR (mean 80 bpm), the following was observed: a significant decrease in early mitral inflow (E) wave (70.5 ± 5.5 cm/s vs 63.5 ± 4.9 cm/s, P < 0.02) and early mitral annular (E′) velocities (7.0 ± 0.5 cm/s vs 6.3 ± 0.6 cm/s, P < 0.003) and a significant increase in mitral inflow A wave (70.3 ± 4.5 cm/s vs 77.3 ± 4.4 cm/s, P < 0.05) and late mitral annular (A′) velocities (9.3 ± 0.6 cm/s vs 10.8 ± 0.5, P < 0.00004). Conclusion: Changes in HR have previously unrecognized significant effects on tissue Doppler parameters of diastolic function. Further study is required to determine if tissue Doppler derived annular velocities should be corrected for HR. [ABSTRACT FROM AUTHOR]

The cardiac indices assessed included left ventricular mass index, relative wall thickness, left ventricular ejection fraction, mean E/A ratio, mean E/e' ratio, isovolumetric relaxation time, and deceleration time. We found no statistically significant differences between exposed and non-exposed women with regards to left ventricular ejection fraction, isovolumetric relaxation time or deceleration time. In comparison to the non-exposed population they also demonstrated a lower E/A and a higher E/e' ratio with a mean difference of -0.08 (95%CI -0.15, -0.01) and 0.84 (95%CI 0.41, 1.27) respectively. [Extracted from the article]

Background: Quantification of left ventricular torsion may provide new indices of systolic and diastolic function. We sought to characterize the effect of acute manipulation of load on cardiac torsion, plecotropy in human subjects., Methods: Simultaneous Millar LV pressure, micromanometry, and echocardiograms were performed on 18 patients (10 male, mean age 66 years) with normal systolic function. Loading was altered sequentially by the administration of glyceryl trinitrate (GTN) and saline fluid loading. Echocardiographic speckle tracking imaging was used to quantify LV torsion and event timing was recorded relative to mitral valve opening (MVO)., Results: GTN administration decreased preload (LV end diastolic pressure: 15.7 vs 8.4 mmHg, P < 0.001), and afterload (wall stress: 140 vs 84 x10(3)dyn/cm(2), P < 0.02). Administration of fluid increased preload (LVEDP 11.3 vs 18.1 mmHg, P < 0.001) and increased wall stress, but to a lesser extent (102 vs 117 x10(3)dyn/cm(2), P < 0.003). GTN administration augmented peak torsion (8.4 vs 11.0 deg, P < 0.05), increased systolic torsion velocity (46.6 vs 65.3deg/sec, P < 0.01) and resulted in earlier onset of untwisting (-105 vs -127ms, P < 0.05). Fluid loading decreased the proportion of untwisting prior to MVO (39.0 vs 31.0%, P < 0.05), untwisting acceleration (-750 vs -592deg/sec/sec, P < 0.05) and delayed the timing of peak untwisting (-37.0 vs 9.1ms, P < 0.01), but did not affect systolic torsion parameters., Conclusions: Left ventricular torsion parameters are sensitive to acute changes in load and therefore need to be interpreted in the context of current loading conditions.