Transcatheter aortic valve implantation (TAVI) has become an established treatment for patients with severe aortic stenosis (AS) in an ever-growing patient population. It is not uncommon for patients who are undergoing TAVI to have technically difficult anatomy, simultaneous severe left ventricular (LV) impairment and/or extensive coronary artery disease. In this case series we present examples where the use of mechanical circulatory support (MCS) facilitated a safe aortic and coronary intervention in extremely complex patients who would have otherwise carried prohibitive procedural risk.

We were presented with a 60-year-old SARS-CoV-2- (Covid-19) positive gentle-man who was transferred to our intensive care unit from a district general hospital. The patient was intubated and required mechanical ventilation prior to transfer for type 1 respiratory failure secondary to pneumonitis. His past medical history included hypertension and hypercholes-terolaemia. Admission blood tests dem-onstrated markedly elevated troponin I of 593 ng/L and C-reactive protein of 360 mg/L. D-dimer levels were elevated at 32 ng/L. Bedside echocardiogram showed a dilated right ventricle (base 45 mm, mid 42 mm) with severely impaired right ventricular

Left ventricular pseudoaneurysm is a type of rare and lethal mechanical complication derived from rupture of the ventricular free wall but enclosed by the adherent pericardium or scar tissue. We present a rare case of a massive pseudoaneurysm with a large thrombotic burden. Echocardiography had a pivot role on early diagnosis of the pseudoaneurysm allowing for appropriate downstream diagnostic testing. Cardiac magnetic resonance confirmed a large pseudoaneurysm. Furthermore, late gadolinium enhancement imaging demonstrated large thrombotic burden within the pseudoaneurysm. Due to eminent risk of rupture and danger of an embolic event our patient underwent a successful ventricular aneurysectomy. The defect was closed with a 5cm patch of bovine pericardium. An echocardiogram day 6 post-op showed an intact patch repair with no residual pseudoaneurysm.

BackgroundTrastuzumab improves dramatically the prognosis of HER2‐positive breast cancer patients, but it may lead to cardiotoxicity with left ventricular (LV) systolic dysfunction. Its effects on right ventricular (RV) function have not however been elucidated. We sought to assess LV and RV deformation mechanics during treatment with trastuzumab in breast cancer patients.Methods and resultsWe studied 101 consecutive women (mean age 54.3 ± 11.4 years) receiving trastuzumab for 12 months; 62 of them (61.4%) had previously received anthracyclines and 26 (25.7%) were receiving taxanes concurrently with trastuzumab. Comprehensive two‐dimensional echocardiography with speckle tracking imaging of LV and RV global longitudinal strain (GLS) and RV free wall longitudinal strain (FWLS) analyses were performed at baseline and every 3 months up to treatment completion. Cardiotoxicity was defined as a decrease of baseline LV ejection fraction > 10 percentage units to a value < 50%. At 3 months, only LV GLS was significantly reduced (−19.5 ± 2.7 to −18.7 ± 2.8, P = 0.0410), while at 6 months, LV GLS, RV GLS and RV FWLS had significantly declined reaching their lowest values (−17.9 ± 6.1, P = 0.002, −19.6 ± 5.2, P = 0.003 and −19.7 ± 5.6, P = 0.004, respectively). Ten women (9.9%) developed cardiotoxicity. A RV GLS percent change of −14.8% predicted cardiotoxicity with 66.7% sensitivity and 70.8% specificity (area under the curve 0.68, 95% confidence interval 0.54–0.81), classifying correctly 90% of women with cardiotoxicity. This cut‐off is quite similar to the 15% change of LV GLS previously suggested as predictive of cardiotoxicity.ConclusionsDeformation mechanics of both the left and right ventricle follow similar temporal pattern and degree of impairment during trastuzumab therapy, confirming the global and uniform effect of trastuzumab on myocardial function.

Patients with chronic kidney disease (CKD) carry a high cardiovascular risk. An abundance of evidence has emerged in recent years establishing minor reductions in estimated glomerular filtration rate as an independent risk factor for cardiovascular mortality. Additionally, cardiac changes, such as left ventricular hypertrophy and impaired left ventricular systolic function, have been associated with an unfavorable prognosis. Despite the significant prevalence of underlying cardiac abnormalities, symptoms may not manifest in many patients with CKD. A range of available and emerging echocardiographic modalities may assist with diagnosing heart disease in CKD. Furthermore, some of these emerging techniques can give an important insight into the pathophysiology of subclinical dysfunction in CKD. This review discusses how current and emerging echocardiographic modalities such as speckle tracking echocardiography and 3D echocardiography might help cardiologists in providing important information to help with diagnosis and risk stratification of cardiac-related morbidity and mortality in patients with renal disease, as well applicability of these tools to current clinical practice.

Emerging cardiovascular biomarkers, such as speckle tracking echocardiography (STE) and aortic pulse wave velocity (aPWV), have recently demonstrated the presence of subclinical left ventricular dysfunction and arterial stiffening in patients with chronic kidney disease (CKD) and no previous cardiovascular history. However, limited information exists on the prognostic impact of these biomarkers. We aimed to investigate whether STE and aPWV predict major adverse cardiac events (MACE) in this patient population. In this cohort study we prospectively analysed 106 CKD patients with no overt cardiovascular disease (CVD) and normal left ventricular ejection fraction. Cardiac deformation was measured using STE while aPWV was measured using arterial tonometry. The primary end-point was the composite of all-cause mortality, acute coronary syndrome, stable angina requiring revascularization (either using percutaneous coronary intervention or coronary artery bypass surgery), hospitalization for heart failure and stroke. Over a median follow up period of 49 months (interquartile range 11-63 months), 26 patients (24.5%) reached the primary endpoint. In a multivariable Cox hazards model, global longitudinal strain (GLS) (HR 1.12, 95% CI 1.02-1.29, p = 0.041) and aPWV (HR 1.31, 95% CI 1.05-1.41, p = 0.021) were significant, independent predictors of MACE. GLS and aPWV independently predict MACE in CKD patients with normal EF and no clinically overt CVD.

Recent studies hypothesized left ventricular (LV) twist as a potential biomarker for evaluation of sub clinical myocardial disease, however its relationship with aortic stiffness has yet to be investigated. Chronic kidney disease (CKD) has been identified as a risk factor for both myocardial and arterial disease. As such we sought to explore the relationship between aortic stiffness and LV twist in CKD patients without known cardiovascular disease (CVD). In this prospective, observational study we enrolled 106 CKD patients (Stages 1 to 5) with normal LVEF as assessed by conventional echocardiography. Aortic stiffness was measured using aortic pulse wave velocity (aPWV). We defined increased aPWV as ≥10 m/s. LV Twist was measured using two-dimensional speckle tracking echocardiography. Patients with increased aPWV had higher LV twist (p = 0.002) but similar LVEF (p = 0.486). Aortic PWV correlated crudely with age (p < 0.001), the presence of diabetes (p < 0.001), hypertension (p < 0.001), eGFR (p < 0.001), LVMI (p = 0.01), e/e' (p < 0.001) and LV twist (p = 0.003). In multivariable analyses after adjusting for age, gender, cardiovascular risk factors and hypertensive medication, aPWV was independently associated with LV twist (β = 0.163, p = 0.025). Aortic stiffness independently associates with LV Twist in asymptomatic CKD patients. These findings suggest a close interaction between LV twist mechanics and arterial remodeling even before CVD becomes clinically relevant.

AIMSTo identify subclinical left ventricular (LV) myocardial dysfunction using speckle tracking echocardiography (STE) in patients with chronic kidney disease (CKD), preserved LV ejection fraction (LVEF), and no cardiovascular history or symptoms.METHODS AND RESULTSCross-sectional comparisons of conventional and STE parameters were performed between controls and patients with different stages of CKD. CKD patients were followed up for major adverse cardiovascular events (MACEs). We recruited 106 CKD patients and 38 controls. Mean age was 54.4 ± 15.1 and 36.9 ± 11.5 years, respectively (P < 0.001), with 49.1 vs. 52.6% being female (P = 0.705). There were 29 (27.4%) patients with CKD stages 1/2, 38 (35.8%) with stage 3, and 39 (36.8%) with stages 4/5. Global longitudinal strain (GLS) was more impaired when moving from controls to CKD stages 4/5 (-20.67 ± 3.06, -20.39 ± 2.29, -18.33 ± 3.81, -18.01 ± 2.64, controls vs. CKD stages 1/2, vs. CKD stage 3, vs. CKD stages 4/5, respectively, Padjusted = 0.016), whereas LV twist (16.2 ± 4.8, 18.51 ± 4.36, 19.91 ± 5.35, 24.6 ± 5.35, Padjusted < 0.001) and LV twist rate (101.7 ± 30.3, 110.4 ± 30.1, 121 ± 31.4, 154.8 ± 36.7, Padjusted < 0.001) increased. Risk factor-adjusted GLS (standardized beta β = -0.245, P = 0.025), strain rate (SR) [global longitudinal strain rates (GLSRs); β = -0.236, P = 0.019], and early diastolic longitudinal strain rate (GLSRe; β = 0.247, P = 0.019) were significantly associated with estimated glomerular filtration rate (eGFR), whereas LV twist (β = -0.432, P < 0.001), LV twist rate (β = -0.433, P < 0.001), and number of segments with diastolic dysfunction (β = -340, P < 0.001) were inversely and independently associated with eGFR. Impaired GLS (more than -16%) was observed in almost a quarter of CKD patients and associated with a reduced estimated MACE-free survival at 12-month follow-up (88.5 vs 93.7%, Plogrank = 0.038).CONCLUSIONIn CKD patients with no cardiovascular symptoms or history and preserved LVEF, STE can identify subclinical abnormalities of both systolic (decreased GLS and GLSR, increased LV twist, and twist rate) and diastolic (decreased GLSRe and increased number of segments with diastolic dysfunction) LV function.