2024 CSANZ Position Statement on Indications, Assessment and Monitoring of Structural and Valvular Heart Disease With Transthoracic Echocardiography in Adults.

Transthoracic echocardiography (TTE) is the most widely available and utilised imaging modality for the screening, diagnosis, and serial monitoring of all abnormalities related to cardiac structure or function. The primary objectives of this document are to provide (1) a guiding framework for treating clinicians of the acceptable indications for the initial and serial TTE assessments of the commonly encountered cardiovascular conditions in adults, and (2) the minimum required standard for TTE examinations and reporting for imaging service providers. The main areas covered within this Position Statement pertain to the TTE assessment of the left and right ventricles, valvular heart diseases, pericardial diseases, aortic diseases, infective endocarditis, cardiac masses, pulmonary hypertension, and cardiovascular diseases associated with cancer treatments or cardio-oncology. Facilitating the optimal use and performance of high quality TTEs will prevent the over or under-utilisation of this resource and unnecessary downstream testing due to suboptimal or incomplete studies.

Right ventricular functional recovery assessment with stress echocardiography and cardiopulmonary exercise testing after pulmonary embolism: a pilot prospective multicentre study.

BACKGROUND: Data on right ventricular (RV) exercise adaptation following acute intermediate and high-risk pulmonary embolism (PE) remain limited. This study aimed to evaluate the symptom burden, RV functional recovery during exercise and cardiopulmonary exercise parameters in survivors of intermediate and high-risk acute PE. METHODS: We prospectively recruited patients following acute intermediate and high-risk PE at four sites in Australia and UK. Study assessments included stress echocardiography, cardiopulmonary exercise testing (CPET) and ventilation-perfusion (VQ) scan at 3 months follow-up. RESULTS: Thirty patients were recruited and 24 (median age: 55 years, IQR: 22) completed follow-up. Reduced peak oxygen consumption (VO2) and workload was seen in 75.0% (n=18), with a persistent high symptom burden (mean PEmb-QoL Questionnaire 48.4±21.5 and emPHasis-10 score 22.4±8.8) reported at follow-up. All had improvement in RV-focused resting echocardiographic parameters. RV systolic dysfunction and RV to pulmonary artery (PA) uncoupling assessed by stress echocardiography was seen in 29.2% (n=7) patients and associated with increased ventilatory inefficiency (V̇E/V̇CO2 slope 47.6 vs 32.4, p=0.03), peak exercise oxygen desaturation (93.2% vs 98.4%, p=0.01) and reduced peak oxygen pulse (p=0.036) compared with controls. Five out of seven patients with RV-PA uncoupling demonstrated persistent bilateral perfusion defects on VQ scintigraphy consistent with chronic thromboembolic pulmonary vascular disease. CONCLUSION: In our cohort, impaired RV adaptation on exercise was seen in almost one-third of patients. Combined stress echocardiography and CPET may enable more accurate phenotyping of patients with persistent symptoms following acute PE to allow timely detection of long-term complications.

Right heart strain assessment on CTPA following acute pulmonary embolism: Interobserver variability between expert radiologists and physicians.

BACKGROUND: Accuracy of right heart strain (RHS) measured on computed tomography pulmonary angiogram (CTPA) scans by non-radiologists is unknown. We assessed inter-observer variability of four RHS features and determined the accuracy of measurements by respiratory physicians. METHOD: 1560 consecutive patients with acute PE were identified, and those who had a CTPA and an echocardiogram within 24-h included. CTPAs were independently scored prospectively by two radiologists, two thoracic physicians and a specialist registrar. Inter-observer variability was assessed, and diagnostic accuracy compared to echocardiography. RESULTS: 182 patients (median age 62.8 years, IQR 49.8-71.5) with acute PE (7.7% high-risk, 40.7% intermediate high-risk, 31.3% intermediate low-risk and 20.3% low-risk) were included. Right ventricle to left ventricle diameter ratio (RV:LV) measurement had low inter-observer variability among the radiologists and non-radiologists with interclass correlation coefficient (ICC) of 0.95 (95%CI 0.92-0.97) and 0.96 (95%CI 0.94-0.97) respectively. RV:LV ratio had high diagnostic accuracy compared to RV dilatation on echocardiography (AUC 0.89, 95%CI 0.84-0.94 for radiologists and AUC 0.84, 95%CI 0.77-0.90 for non-radiologists). Main pulmonary artery to ascending aorta diameter ratio (MPA:Ao) measurement also had excellent agreement amongst the radiologists and non-radiologists (ICC 0.93 (95%CI 0.88-0.96) and 0.92 (95%CI 0.81-0.96) respectively). Significant variability was seen in the assessment of subjective features of RHS (leftward bowing of interventricular septum and contrast reflux into inferior vena cava) amongst the non-radiologists. CONCLUSION: RV:LV and MPA:Ao diameter ratios on CTPA measured by non-radiologists have low inter-observer variability and good agreement with radiologists, and can be reliably used where an expert report is unavailable.

Assessment of cardiac structure and function in kidney failure: understanding echocardiography and magnetic resonance imaging for the nephrologist.

Cardiovascular disease is the leading cause of death in patients with kidney failure or on chronic dialysis. Patients on chronic dialysis have a 10- to 50-fold increased risk of sudden cardiac death compared to patients with normal kidney function. Adverse changes in cardiac structure and function may not manifest with clinical symptoms in patients with kidney failure and, therefore, pose a challenge in identifying cardiac dysfunction early. Fortunately, there are multi-modality cardiac imaging techniques available, including echocardiography and cardiac magnetic resonance imaging, that can help our understanding of the pathophysiology of cardiac dysfunction in kidney failure. This review describes the benefits and limitations of these two commonly available cardiac imaging modalities to assess cardiac structure and function, thereby aiding nephrologists in choosing the most appropriate investigative tool based on individual clinical circumstances. For the purposes of this review, cardiac imaging for detection of coronary artery disease has been omitted.

Echocardiographic assessment of raised pulmonary vascular resistance: application to diagnosis and follow-up of pulmonary hypertension.

OBJECTIVE: To optimise an echocardiographic estimation of pulmonary vascular resistance (PVR(e)) for diagnosis and follow-up of pulmonary hypertension (PHT). DESIGN: Cross-sectional study. SETTING: Tertiary referral centre. PATIENTS: Patients undergoing right heart catheterisation and echocardiography for assessment of suspected PHT. METHODS: PVR(e) ([tricuspid regurgitation velocity ×10/(right ventricular outflow tract velocity-time integral+0.16) and invasive PVR(i) ((mean pulmonary artery systolic pressure-wedge pressure)/cardiac output) were compared in 72 patients. Other echo data included right ventricular systolic pressure (RVSP), estimated right atrial pressure, and E/e' ratio. Difference between PVR(e) and PVR(i) at various levels of PVR was sought using Bland-Altman analysis. Corrected PVR(c) ((RVSP-E/e')/RVOT(VTI)) (RVOT, RV outflow time; VTI, velocity time integral) was developed in the training group and tested in a separate validation group of 42 patients with established PHT. RESULTS: PVR(e)>2.0 had high sensitivity (93%) and specificity (91%) for recognition of PVR(i)>2.0, and PVR(c) provided similar sensitivities and specificities. PVR(e) and PVR(i) correlated well (r=0.77, p<0.01), but PVR(e) underestimated marked elevation of PVR(i)-a trend avoided by PVR(c). PVR(c) and PVR(e) were tested against PVR(i) in a separate validation group (n=42). The mean difference between PVR(e) and PVR(i) exceeded that between PVR(c) and PVR(i) (2.8±2.7 vs 0.8±3.0 Wood units; p<0.001). A drop in PVR(i) by at least one SD occurred in 10 patients over 6 months; this was detected in one patient by PVR(e) and eight patients by PVR(c) (p=0.002). CONCLUSION: PVR(e) distinguishes normal from abnormal PVR(i) but underestimates high PVR(i). PVR(c) identifies the severity of PHT and may be used to assess treatment response.