in subclinical diabetic cardiomyopathy? Validation against T1 mapping and collagen biomarkers C. Jellis1, J. Wright2, J Sacre1, D. Kennedy3, L Jeffriess1, C. Jenkins1, J Fenwick3, J. Martin1, T. Marwick1,4 1. The University of Queensland, Brisbane, Australia; 2. Heart’s 1st, Greenslopes Private Hospital, Brisbane, Australia; 3. Queensland X-ray Brisbane, Australia; 4. Cleveland Clinic, Cleveland, OH.

Background: Subclinical diabetic cardiomyopathy (DCM) may occur in asymptomatic pts with type 2 diabetes (T2DM). The aetiology is multifactorial, but myocardial fibrosis is a possible contributor. We assessed the anti-fibrotic effect of spironolactone on myocardial structure and function with TDI echo, T1 mapping and pro-collagen biomarkers. Methods: DCM (diastolic dysfunction without occult coronary disease) was sought in 225 asymptomatic pts with T2DM. Biochemical, anthropometric and 2D echo data were measured. Myocardial function was evaluated with deformation imaging. cIB was derived from the posterior wall, anteroseptum and pericardium. T1 mapping was performed with a modified Look-Locker technique using saturation recovery imaging. Amino-terminal propeptides of pro-collagens type I (PINP) and III, carboxy-terminal propeptide of pro-collagen type I and transforming growth factor beta-1 were assayed from blood or urine to assess myocardial collagen turnover. Results: DCM was identified in 81 pts (36%), of whom 49 (25 men, age 60 ± 10y) were randomised to spironolactone 25 mg/day or placebo for six months. Groups were well matched at baseline. Spironolactone was associated with improved diastolic filling and tissue reflectivity on cIB but not alterations in systolic parameters, T1 values or any biomarker levels (Table). ΔcIB was independently associated with spironolactone therapy (Beta = −0.30, p = 0.04) but not Δblood pressure or TDI functional parameters. Conclusion: Spironolactone modulates myocardial structure and function in DCM. Disparity between cIB, T1 and biomarker results suggests that myocardial dysfunction featured in early DCM cannot be directly attributed to underlying myocardial fibrosis.Tabled 1Change with interventionSpironolactone (n = 24)Placebo (n = 25)pE/A ratio−0.1 ± 0.30.2 ± 0.2<0.001cIB (dB)−5.1 ± 6.8−1.3 ± 5.20.030Post-contrast T1 (ms)−12.4 ± 89.0−33.8 ± 134.20.543PINP (μg/L)−18.2 ± 15.8−17.8 ± 15.90.919 Open table in a new tab

Background: Paradoxical shunting via a patent foramen ovale (PFO) has a recognised association with embolic events in younger patients. The use of agitated saline contrast imaging (ASCi) for detecting atrial shunting is well documented, however optimal technique is not well described. This study describes a single-centre experience of ASCi in 1162 patients. Method: A retrospective review was undertaken of 1162 consecutive transthoracic (TTx) ASCi studies, of which 195 also underwent transoesophageal (TEE) echo. ASCi shunt results were compared with colour flow imaging (CFI) and the role of provocative manoeuvres (PM) assessed. Results: 403 TTx studies (35%) had paradoxical shunting seen during ASCi. Of these, 48% were positive with PM only. There was strong agreement between TTx ASCi and reported TEE findings (99% sensitivity, 85% specificity), with six false positive and two false negative results. In hindsight, the latter were likely due to suboptimal right atrial opacification, and the former due to transpulmonary shunting. TTx CFI was found to be insensitive (47%) for the detection of a PFO compared with TTx ASCi. Conclusions: TTx ASCi is minimally invasive and highly accurate for the detection of PFO, provided PM are used. TTx CFI was found to be inaccurate for PFO screening. It is recommended that TTx ASCi should be considered the initial diagnostic tool for the detection of PFO in clinical practice. Guidelines to ensure adequate agitated saline contrast delivery have been proposed including performance of provocative manoeuvres.

Background— Metabolic and vascular disturbances contribute to diabetic cardiomyopathy, but the role of interstitial fibrosis in early disease is unproven. We sought to assess the relationship between imaging markers of diffuse fibrosis and myocardial dysfunction and to link this to possible causes of early diabetic cardiomyopathy. Methods and Results— Hemodynamic and metabolic data were measured in 67 subjects with type 2 diabetes mellitus (age 60±10 years) with no cardiac symptoms. Myocardial function was evaluated with standard echocardiography and myocardial deformation; ischemia was excluded by exercise echocardiography. Calibrated integrated backscatter was calculated from parasternal long-axis views. T1 mapping was performed after contrast with a modified Look-Locker technique using saturation recovery images. Amino-terminal propeptides of procollagens type I and III, as well as the carboxy-terminal propeptide of procollagen type I, were assayed to determine collagen turnover. Subjects with abnormal early diastolic tissue velocity (E m ) had shorter postcontrast T1 values ( P =0.042) and higher calibrated integrated backscatter ( P =0.007). They were heavier ( P =0.003) and had worse exercise capacity ( P <0.001), lower insulin sensitivity ( P =0.003), and blunted systolic tissue velocity ( P =0.05). Postcontrast T1 was associated with diastolic dysfunction (E m r =0.28, P =0.020; E/E m r =−0.24, P =0.049), impaired exercise capacity ( r =0.30, P =0.016), central adiposity ( r =−0.26, P =0.046), blood pressure (systolic r =−0.30, P =0.012; diastolic r =−0.49, P <0.001), and insulin sensitivity ( r =0.30, P =0.037). The association of T1 with E/E m (β=−0.31, P =0.017) was independent of blood pressure and metabolic disturbance. Amino-terminal propeptide of procollagens type III was linked to diastolic dysfunction (E m r =−0.32, P =0.008) and calibrated integrated backscatter ( r =0.30, P =0.015) but not T1 values. Conclusions— The association between myocardial diastolic dysfunction, postcontrast T1 values, and metabolic disturbance supports that diffuse myocardial fibrosis is an underlying contributor to early diabetic cardiomyopathy.

Background: A 12-lead electrocardiography (ECG) is a well established pre-operative test. Conventional workflow strategies result in significant delays in cardiology reporting time. Previous data supports negligible impact of wireless local area networks (WLAN) on other medical equipment. This study aims to test the hypothesis that secure, low-cost WLAN data transmission in combination with automated ECG prioritisation will significantly decrease the confirmation time of ECGs for pre-operative theatre screening. Methods: Standard 12 lead ECGs (Mortara ELI-250) were digitally acquired in a single-centre preoperative ward and wirelessly transmitted to a central digital storage and reporting server (Mortara EScribe) using a readily available 802.11g wireless network card. ECGs were automatically assigned a high priority for cardiology review by the digital system. We retrospectively reviewed pre-operative ECGs performed on the 14 days prior to, and 14 days post installation of the WLAN, using mean time to confirmation and total ECGs performed as markers of efficiency. Results: No significant difference (p = NS) was observed in the number of ECGs performed (261 ECGs prior to, 288 after installation). There was a significant decrease in mean time to confirmation, from 42 hours 52 minutes to 4 hours 42 minutes (p ≤ 0.001) following WLAN implementation. Conclusion: WLAN transfer ensures almost real-time transfer of the ECG. Automatic prioritisation of the digital ECG ensures timely review by a cardiologist and drastically reduces confirmation time. In conjunction with automated prioritisation, WLAN is a safe, inexpensive and effective method for improved ECG delivery workflow in pre-operative theatre screening.

Introduction: Treadmill stress echocardiography (TSE) is well validated, however accuracy is dependent on adequate endocardial border definition. Incremental benefit of Definity® (perflutren in lipid microsphere) is well described, particularly in technically challenging studies. Definity usage in TSE remains low, partly due to presumed negative impact on clinical workflow. This project sought to test the hypothesis that routine clinical use of Definity in TSE is feasible and does not impact negatively on workflow.

Purpose: Interstitial fibrosis is believed to be one of several contributors to diabeticcardiomyopathy (DCM), manifesting as myocardial dysfunction in the absenceof ischemic heart disease in subjects with type 2 diabetes (T2DM). Myocardialultrasound reflectivity is proportionate to fibrosis, but use of the pericardiumas a frame of reference (calibrated integrated backscatter, cIB) may be limitedby signal saturation. Recently, diffuse fibrosis has been shown to be inverselyproportionate to T1 time on post-contrast T1 mapping using cardiac magneticresonance imaging. We sought to compare the association of cIB and T1 timewith DCM.Methods: Demographic, anthropometric, hemodynamic and biochemical datawere measured in 107 apparently healthy, asymptomatic subjects with T2DM (65men, 60±9 years). LV dysfunction (LVD) was sought on resting echo (early diastolictissue velocity [Em] < 1SD from mean for age). Ischemia was excludedby exercise echo. Standard 2D and color TDI measures (tissue velocity, strainand strain rate) were acquired in apical long axis views. Calibrated integratedbackscatter (cIB) was calculated from a parasternal long axis view. Tonometricaortic pulse wave velocity (APWV) was used to determine arterial stiffness. T1mapping was performed in those with LVD and matched controls.Results: LVD was identified in 23 subjects (28%) who also demonstrated significantlypoorer diabetic control (HbA1c 8.2±2.0 vs 7.3±1.4 mmol/L) but no relationshipwith cIB. T1 mapping was performed in 26 subjects (17 men, 60±10years) comprising 20 with LVD and 6 controls. Em was independently associatedwith age (β=-0.76 p<0.001), body mass index [BMI] (β=-0.65, p<0.001), strain(β=0.51, p=0.003) and post-contrast T1 time (β=0.36, p=0.04) [model R Square =0.63] but not cIB. Post-contrast T1 time was independently associated with insulinresistance (HOMA-IR β=-0.63, p=0.016) [model R Square = 0.38] but not withcIB, APWV, BMI or low density lipoprotein (LDL). The only independent correlateof cIB was APWV (β=0.59, p=0.009) [model R Square = 0.39] and not HOMA-IR,BMI or LDL.Conclusions: Quantitative tissue characterisation of fibrosis (T1 time) was independentlyassociated with subclinical DCM, in addition to systolic dysfunction(strain), age and BMI. The association of T1 mapping with insulin resistance contrastswith the link between cIB and arterial stiffness, suggesting potential differencesbetween fibrosis in DCM and hypertension.

Introduction: Structural remodelling as left atrial (LA) volume increases is associated with increasing risk of atrial fibrillation and systemic emboli. Traditional ECG indicators of left atrial enlargement have limited sensitivity; but continue to be used in clinical practice due to availability and cost. We have previously shown that time frequency analysis is superior to traditional ECG indicators in predicting LA enlargement by echocardiography. Cardiac magnetic resonance imaging (CMR) is the reference standard for cardiac volumes. This study sought to correlate time–frequency ECG parameters with LA volumes by CMR.

Cardiac magnetic resonance imaging is a new imaging method that has much to offer clinicians caring for patients with ischaemic heart disease. This article describes briefly the basic principles and practical aspects of cardiac magnetic resonance imaging, and summarizes the pathophysiology of ischaemic heart disease. Then it discusses in detail the use of cardiac magnetic resonance imaging for detection of coronary artery disease, and for assessment of acute and stable coronary syndromes.

Introduction: Non-invasive differentiation of “normal” from “pseudo-normal” transmitral flow remains challenging. Velocity Vector Imaging (VVI) is an angle-independent speckle tracking method, allowing analysis of radial, rotational and longitudinal velocity, strain and strain rate. This project sought to test the hypothesis that patients with worsening diastolic dysfunction demonstrate reduced radial strain parameters in early diastole as assessed by VVI.