British societies guideline on the management of emergencies in implantable left ventricular assist device recipients in transplant centres.

An implantable left ventricular assist device (LVAD) is indicated as a bridge to transplantation or recovery in the United Kingdom (UK). The mechanism of action of the LVAD results in a unique state of haemodynamic stability with diminished arterial pulsatility. The clinical assessment of an LVAD recipient can be challenging because non-invasive blood pressure, pulse and oxygen saturation measurements may be hard to obtain. As a result of this unusual situation and complex interplay between the device and the native circulation, resuscitation of LVAD recipients requires bespoke guidelines. Through collaboration with key UK stakeholders, we assessed the current evidence base and developed guidelines for the recognition of clinical deterioration, inadequate circulation and time-critical interventions. Such guidelines, intended for use in transplant centres, are designed to be deployed by those providing immediate care of LVAD patients under conditions of precipitous clinical deterioration. In summary, the Joint British Societies and Transplant Centres LVAD Working Group present the UK guideline on management of emergencies in implantable LVAD recipients for use in advanced heart failure centres. These recommendations have been made with a UK resuscitation focus but are widely applicable to professionals regularly managing patients with implantable LVADs.

Extending the reach of expert amyloidosis care: A feasibility study exploring the staged implementation of a UK amyloidosis network.

There has been an exponential increase in the diagnosis of transthyretin amyloid cardiomyopathy (ATTR-CA). In response, the Midlands Amyloidosis Service was launched with the aim of providing patients with a timely diagnosis, remote expertise from the National Amyloidosis Centre and access to emerging transthyretin (TTR)-directed therapies. This was a descriptive study of a pilot hub-and-spoke model of delivering specialist amyloidosis care. Patients with suspected amyloidosis were referred from the wider Midlands region, and seen in a consultant-led multidisciplinary clinic. The diagnosis of ATTR-CA was established according to either the validated non-biopsy criteria or histological confirmation of ATTR deposits with imaging evidence of amyloid. Study endpoints were the volume of service provision and the time to diagnosis from the receipt of referral. Patients (n=173, age 75±2 years; male 72 %) were referred between 2019 and 2021. Eighty patients (46 %) were found to have cardiac amyloidosis, of whom 68 (85 %) had ATTR-CA. The median time from referral to diagnosis was 43 days. By removing the need for patients to travel to London, an average of 187 patient-miles was saved. Fifteen (9 %) patients with wild-type ATTR-CA received tafamidis under the Early Access to Medicine scheme; 10 (6 %) were enrolled into phase 3 clinical trials of RNA interference or antisense oligonucleotide therapies. Our results suggest that implementing a UK amyloidosis network appears feasible and would enhance equity of access to specialised amyloidosis healthcare for the increasing numbers of older patients found to have ATTR-CA.

Predictors and clinical implications of residual mitral regurgitation following left ventricular assist device therapy.

BACKGROUND: Correction of mitral regurgitation (MR) at the time of left ventricular assist device (LVAD) implantation remains controversial. There is conflicting evidence regarding the clinical impact of residual MR, and studies have not examined whether MR aetiology or right heart function impacts the likelihood of residual MR. METHODS: This is a retrospective single-centre study of 155 consecutive patients with LVAD implantation from January 2011 to March 2020. Exclusion criteria were no MR pre-LVAD (n=8), inaccessible echocardiography (n=9), duplicate records (n=10) and concomitant mitral valve repair (n=1). Statistical analysis was performed using STATA V.16 and SPSS V.24. RESULTS: Carpentier IIIb MR aetiology was associated with more severe MR pre-LVAD (severe 18/27 (67%) vs non-severe 32/91 (35%), p=0.004) and a higher likelihood of residual MR (8/11 (72%) vs 30/74 (41%), p=0.045). Of 95 patients with significant MR pre-LVAD, 15 (16%) had persistent significant MR, which was associated with higher mortality (p=0.006), post-LVAD right ventricle (RV) dilatation (10/15 (67%) vs 28/80 (35%), p=0.022) and RV dysfunction (14/15 (93%) vs 35/80 (44%), p<0.001). Aside from ischaemic aetiology, other pre-LVAD parameters that were associated with significant residual MR included left ventricular end-systolic diameter (LVESD) (6.9 cm (5.7-7.2) vs 5.9 cm (5.5-6.5), p=0.043), left atrial volume index (LAVi) (78 mL/m2 (56-88) vs 57 mL/m2 (47-77), p=0.021), posterior leaflet displacement (2.5 cm (2.3-2.9) vs 2.3 cm (1.9-2.7), p=0.042) and basal right ventricular end-diastolic diameter (RVEDD) (5.1±0.8 cm vs 4.5±0.8 cm, p=0.010). CONCLUSION: LVAD therapy improves MR and tricuspid regurgitation severity in the majority, but 14% have persistent significant residual MR, associated with right ventricular dysfunction and higher long-term mortality. This may be predicted pre-LVAD by greater LVESD, RVEDD and LAVi and by ischaemic aetiology.

A Critical Evaluation of Patient Pathways and Missed Opportunities in Treatment for Heart Failure.

BACKGROUND: Heart failure (HF) is a global problem responsible for significant morbidity and mortality. METHODS: This review describes the patient pathways and missed opportunities related to treatment for patients with HF. RESULTS: The contemporary management strategies in HF, including medical therapies, device therapy, transplant, and palliative care. Despite the strong evidence base for therapies that improve prognosis and symptoms, there remains a large number of patients that are not optimally managed. The treatment of patients with HF is highly influenced by those who are caring for them and varies widely across geographical regions. HF patients can be broadly classified into two key groups: those who have known HF, and those who are incidentally found to have reduced left ventricular systolic dysfunction or other cardiac abnormality when an echocardiogram is performed. While all patients are under the care of a general practitioner or family doctor, in other instances, non-cardiologist physicians, cardiologists, and specialist HF nurses-each will have varying levels of expertise in managing HF-are part of the broader team involved in the specialist management of patients with HF. CONCLUSIONS: There are many potential missed opportunities in HF treatment, which include general opportunities, medications, etiology-specific therapy, device therapy, therapies when initial treatments fail, and palliative care.

Outcomes of temporary mechanical circulatory support in cardiogenic shock due to end-stage heart failure.

Background: There are few reports of mechanical circulatory support (MCS) in patients with cardiogenic shock (CS) due to end-stage heart failure (ESHF). We evaluated our institutional MCS strategy and compared the outcomes of INTERMACS 1 and 2 patients with CS due to ESHF. Methods: Retrospective analysis of prospectively collected data (November 2014 to July 2019) from a single centre. ESHF was defined by a diagnosis of HF prior to presentation with CS. Other causes of CS (eg: acute myocardial infarction) were excluded. We compared the clinical course, complications and 90-day survival of patients with CS due to ESHF in INTERMACS profile 1 and 2. Results: We included 60 consecutive patients with CS due to ESHF Differences in baseline characteristics were consistent with the INTERMACS profiles. The duration of MCS was similar between INTERMACS 1 and 2 patients (14 (10-33) vs 15 (7-23) days, p = 0.439). There was no significant difference in the number of patients with complications that required intervention. Compared to INTERMACS 2, INTERMACS 1 patients had more organ dysfunction on support and significant lower 90-day survival (66% vs 34%, p = 0.016). Conclusion: Our temporary MCS strategy, including earlier intervention in patients with CS due to ESHF at INTERMACS 2 was associated with less organ dysfunction and better 90-day survival compared to INTERMACS 1 patients.

Cardiac transplantation in transthyretin amyloid cardiomyopathy: Outcomes from three decades of tertiary center experience.

Aims: Transthyretin cardiac amyloidosis (ATTR-CM) is a progressive and fatal cardiomyopathy. Treatment options in patients with advanced ATTR-CM are limited to cardiac transplantation (CT). Despite case series demonstrating comparable outcomes with CT between patients with ATTR-CM and non-amyloid cardiomyopathies, ATTR-CM is considered to be a contraindication to CT in some centers, partly due to a perceived risk of amyloid recurrence in the allograft. We report long-term outcomes of CT in ATTR-CM at two tertiary centers. Materials and methods and Results: We retrospectively evaluated ATTR-CM patients across two tertiary centers who underwent transplantation between 1990 and 2020. Pre-transplantation characteristics were determined and outcomes were compared with a cohort of non-transplanted ATTR-CM patients. Fourteen (12 male, 2 female) patients with ATTR-CM underwent CT including 11 with wild-type ATTR-CM and 3 with variant ATTR-CM (ATTRv). Median age at CT was 62 years and median follow up post-CT was 66 months. One, three, and five-year survival was 100, 92, and 90%, respectively and the longest surviving patient was Censored > 19 years post CT. No patients had recurrence of amyloid in the cardiac allograft. Four patients died, including one with ATTRv-CM from complications of leptomeningeal amyloidosis. Survival among the cohort of patients who underwent CT was significantly prolonged compared to UK patients with ATTR-CM generally (p < 0.001) including those diagnosed under age 65 years (p = 0.008) or with early stage cardiomyopathy (p < 0.001). Conclusion: CT is well-tolerated, restores functional capacity and improves prognosis in ATTR-CM. The risk of amyloid recurrence in the cardiac allograft appears to be low.

Pathophysiology of severe primary graft dysfunction in orthotopic heart transplantation.

BACKGROUND: A series of insults on the donor heart result in pathophysiological changes that manifest as primary graft dysfunction (PGD) post-orthotopic heart transplantation. The objectives of this study were: (i) describe the pathophysiology of severe PGD using an established cardiovascular model; and (ii) the evolution of the pathophysiology during recovery from severe PGD. METHODS: Hemodynamic data from 20 consecutive patients with severe PGD (need for mechanical circulatory support, MCS) at baseline (T0), 6 h (T6) and "recovery" (explant of support), and 20 consecutive patients without severe PGD were used to model the pathophysiology using the cardiovascular model described by Burkhoff and Dickstein. RESULTS: There was a progressive (from T0 to T6) up- and leftward shift in the diastolic pressure-volume relationship, especially of the right ventricle (RV), resulting in reduced capacitance. RV end-systolic elastance (Ees) was significantly elevated in severe PGD but preload-recruitable stroke work (PRSW) was significantly lower compared to patients without severe PGD. "Recovery" (after liberation from MCS) was associated with improvement in RV Ees, chamber capacitance and PRSW, although they remained significantly lower than patients without severe PGD. CONCLUSION: Severe PGD of the dominant right heart failure phenotype is characterized by reduced chamber capacitance, increased "stiffness" and impaired contractility. Complete normalization was not required for successful weaning of MCS.

Cardiac Power Output Index and Severe Primary Graft Dysfunction After Heart Transplantation.

OBJECTIVES: To evaluate the value of cardiac power output index (CPOi) in predicting severe primary graft dysfunction (PGD) after heart transplantation (defined as mechanical circulatory support [MCS] and/or mortality <30 days after transplant). DESIGN: Observational cohort study. SETTING: A heart transplant center in the United Kingdom. PARTICIPANTS: Consecutive patients who underwent heart transplantation from January 2014 to December 2019 (n = 160). Twenty patients were excluded, as MCS was instituted immediately after transplant. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Hemodynamic data on return to the intensive care unit (time 0, T0) and at 6 hours (T6) were collected to calculate CPOi at both points in 140 consecutive patients-22 patients developed severe PGD. The CPOi at T0 correlated with donor-recipient predicted heart mass and inversely with inotrope score. Patients who developed severe PGD had significantly lower CPOi at T0 and T6. The areas under the receiver operating characteristic curve for CPOi at T0 and T6 for the development of severe PGD were 0.90 and 0.92, respectively. Adjusting for vasoactive-inotrope score did not improve discrimination. The probability of severe PGD if CPOi at T0 <0.34 W/m2 and T6 <0.33 W/m2 was 79%, but was only 2% if both CPOi at T0 and T6 were >0.34 W/m2 and >0.33 W/m2, respectively. After adjusting for baseline differences, CPOi at T6 (odds ratio 0.78; 95% CI 0.67-0.91, p = .001) was significantly associated with severe PGD. CONCLUSION: Low CPOi at T0 is associated with severe PGD. Serial assessment of CPOi increases the diagnostic probability of severe PGD.

Vasculogenic properties of adventitial Sca-1+CD45+ progenitor cells in mice: a potential source of vasa vasorum in atherosclerosis.

The cellular origins of vasa vasorum are ill-defined and may involve circulating or local progenitor cells. We previously discovered that murine aortic adventitia contains Sca-1+CD45+ progenitors that produce macrophages. Here we investigated whether they are also vasculogenic. In aortas of C57BL/6 mice, Sca-1+CD45+ cells were localised to adventitia and lacked surface expression of endothelial markers (<1% for CD31, CD144, TIE-2). In contrast, they did show expression of CD31, CD144, TIE-2 and VEGFR2 in atherosclerotic ApoE-/- aortas. Although Sca-1+CD45+ cells from C57BL/6 aorta did not express CD31, they formed CD31+ colonies in endothelial differentiation media and produced interconnecting vascular-like cords in Matrigel that contained both endothelial cells and a small population of macrophages, which were located at branch points. Transfer of aortic Sca-1+CD45+ cells generated endothelial cells and neovessels de novo in a hindlimb model of ischaemia and resulted in a 50% increase in perfusion compared to cell-free control. Similarly, their injection into the carotid adventitia of ApoE-/- mice produced donor-derived adventitial and peri-adventitial microvessels after atherogenic diet, suggestive of newly formed vasa vasorum. These findings show that beyond its content of macrophage progenitors, adventitial Sca-1+CD45+ cells are also vasculogenic and may be a source of vasa vasorum during atherogenesis.

Mechanical circulatory support in the heart failure population.

PURPOSE OF REVIEW: Use of durable left ventricular assist devices (LVADs) has increased considerably in recent years because of the insufficient supply of donor hearts for cardiac transplantation and improvement in outcomes from refinements in technology. This review examines clinical utility of these devices and summarizes the most recent evidence supporting the use of LVAD therapy. RECENT FINDINGS: There continues to be significant advancements made in LVAD technology, which has resulted in improvements in the rates of adverse events and overall patient quality of life. Specifically, less invasive and improved surgical techniques have resulted in fewer incidence of pump thrombosis and stringent blood pressure management have been shown to significantly decrease stroke rates. SUMMARY: The continued advances in LVAD therapy have resulted in significant improvement in overall survival; however, complication rates remain relatively high. Future work will focus on improvements in adverse outcomes and ultimately the possibility that LVADs will be a viable alternative to transplantation in patients with end-stage heart failure.

Coronary Vasospasm Following Heart Transplantation: Rapid Progression to Aggressive Cardiac Allograft Vasculopathy.

Coronary artery vasospasm (CVS) has been described in orthotopic heart transplant patients but is rare in the post-transplanted, denervated heart. Severe CVS has been associated with accelerated cardiac allograft vasculopathy (CAV) and allograft rejection. Allograft vasculopathy is the leading cause of decreased long-term survival in orthotopic heart transplant. The prognostic significance and relationship of the presence and severity of CVS with CAV are not well understood. We present a case of severe symptomatic CVS with rapid development of severe CAV. Our case emphasizes the need for close angiographic surveillance and intracoronary imaging for early detection of CAV in the presence of vasospasm.

Mechanical Circulatory Support for Decompensated Heart Failure.

PURPOSE OF REVIEW: Cardiogenic shock from decompensated heart failure is associated with significant morbidity and mortality. Mechanical circulatory support (MCS) improves haemodynamics and reverses organ dysfunction in critically ill patients with cardiogenic shock. This paper summarises the main modalities of mechanical support and their physiological impact, practical considerations, advantages and disadvantages to facilitate a holistic approach in managing a potentially lethal pathology. RECENT FINDINGS: To date, there remains a lack of large randomised controlled trials to support the use of any mechanical support strategy. Consequently, meta-analyses, registry data and expert consensus in the form of society guidelines are relied upon. Currently, randomised trials are in progress to assess the efficacy of a percutaneous assist device (Impella) and extracorporeal membrane oxygenation. Mechanical support options are centred around the use of counter pulsation and percutaneous assist devices and the use of an extracorporeal pump and are hence varied in means of application, degree of haemodynamic benefit and potential complications. Regardless of future innovations, a timely multidisciplinary approach that incorporates both patient and institutional considerations will always be crucial to a successful outcome.

Efficacy and safety of the subcutaneous implantable cardioverter defibrillator: a systematic review.

BACKGROUND: Subcutaneous implantable cardioverter defibrillators (S-ICDs) are considered an alternative to conventional transvenous ICDs (TV-ICDs) in patients not requiring pacing. METHODS: We searched MEDLINE and EMBASE for studies evaluating efficacy and safety outcomes in S-ICD patients. Outcomes were pooled across studies. RESULTS: Sixteen studies were included with 5380 participants (mean age range 33-56 years). Short-term follow-up data were available for 1670 subjects. The most common complication was pocket infection, affecting 2.7%. Other complications included delayed wound healing (0.6%) and wound discomfort (0.8%). 3.8% of S-ICDs were explanted, most commonly for pocket infection. Mortality rates in hospital (0.4%) and during follow-up (3.4% from 12 studies reporting) were low. Incidence of ventricular arrhythmia varied from 0% to 12%. Overall shock efficacy exceeded 96%. Inappropriate shocks affected 4.3% and was most commonly caused by T-wave oversensing. CONCLUSIONS: Although long-term randomised data are lacking, observational data suggest similar shock efficacy and short-term complication rates between the S-ICD and TV-ICD.

Cardiovascular Effects of Unilateral Nephrectomy in Living Kidney Donors.

UNLABELLED: There is a robust inverse graded association between glomerular filtration rate (GFR) and cardiovascular risk, but proof of causality is lacking. Emerging data suggest living kidney donation may be associated with increased cardiovascular mortality although the mechanisms are unclear. We hypothesized that the reduction in GFR in living kidney donors is associated with increased left ventricular mass, impaired left ventricular function, and increased aortic stiffness. This was a multicenter, parallel group, blinded end point study of living kidney donors and healthy controls (n=124), conducted from March 2011 to August 2014. The primary outcome was a change in left ventricular mass assessed by magnetic resonance imaging (baseline to 12 months). At 12 months, the decrease in isotopic GFR in donors was -30±12 mL/min/1.73m(2). In donors compared with controls, there were significant increases in left ventricular mass (+7±10 versus -3±8 g; P<0.001) and mass:volume ratio (+0.06±0.12 versus -0.01±0.09 g/mL; P<0.01), whereas aortic distensibility (-0.29±1.38 versus +0.28±0.79×10(-3) mm Hg(-1); P=0.03) and global circumferential strain decreased (-1.1±3.8 versus +0.4±2.4%; P=0.04). Donors had greater risks of developing detectable highly sensitive troponin T (odds ratio, 16.2 [95% confidence interval, 2.6-100.1]; P<0.01) and microalbuminuria (odds ratio, 3.8 [95% confidence interval, 1.1-12.8]; P=0.04). Serum uric acid, parathyroid hormone, fibroblast growth factor-23, and high-sensitivity C-reactive protein all increased significantly. There were no changes in ambulatory blood pressure. Change in GFR was independently associated with change in left ventricular mass (R(2)=0.28; P=0.01). These findings suggest that reduced GFR should be regarded as an independent causative cardiovascular risk factor. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT01028703.

Caveolin-1 single-nucleotide polymorphism and arterial stiffness in non-dialysis chronic kidney disease.

BACKGROUND: Arteriosclerosis is an independent predictor of increased cardiovascular mortality in chronic kidney disease (CKD). Histologically it is characterized by hypertrophy and fibrosis of the arterial media wall leading to increased arterial stiffness and end-organ damage. Caveolin-1 acts as an intracellular signalling pathway chaperone in human fibrotic and vascular diseases. The purpose of this study was to assess the association between caveolin-1 (CAV1) single-nucleotide polymorphism (SNP) rs4730751 and arterial stiffness as measured by arterial pulse wave velocity (PWV) in an early-stage CKD cohort and in a cohort with more severe CKD. METHODS: Two prospectively maintained patient cohorts with non-dialysis CKD were studied: 144 patients in the Chronic Renal Impairment in Birmingham (CRIB) cohort and 147 patients in the Renal Impairment in Secondary Care (RIISC) cohort, with matched exclusion criteria and DNA sampling availability. At entry to each cohort database, each patient's initial arterial PWV was measured, as well as their anthropomorphic and biochemical data. CAV1 rs4730751 SNP genotyping was performed using Taqman technology. RESULTS: The CAV1 rs4730751 SNP CC genotype was associated with lower arterial PWV in both CRIB early stage CKD patients [8.1 versus 8.6 m/s; coefficient -0.780 (-1.412, -0.149); P = 0.016] and RIISC more advanced stage CKD patients [8.7 versus 9.4 m/s; coefficient -0.695 (-1.288, -0.102); P = 0.022]; these relationships held following adjustment for other important confounders. CONCLUSIONS: This replicated study suggests potential utility of the studied CAV1 SNP as a genetic biomarker in CKD and a role for CAV1 in the development of arteriosclerosis in this setting. Further studies are warranted to further explore the basic science driving these clinical observations.

Endothelial nitric oxide synthase single nucleotide polymorphism and left ventricular function in early chronic kidney disease.

BACKGROUND: Chronic kidney disease (CKD) is associated with accelerated cardiovascular disease and heart failure. Endothelial nitric oxide synthase (eNOS) Glu298Asp single nucleotide polymorphism (SNP) genotype has been associated with a worse phenotype amongst patients with established heart failure and in patients with progression of their renal disease. The association of a cardiac functional difference in non-dialysis CKD patients with no known previous heart failure, and eNOS gene variant is investigated. METHODS: 140 non-dialysis CKD patients, who had cardiac magnetic resonance (CMR) imaging and tissue doppler echocardiography as part of two clinical trials, were genotyped for eNOS Glu298Asp SNP retrospectively. RESULTS: The median estimated glomerular filtration rate (eGFR) was 50 mls/min and left ventricular ejection fraction (LVEF) was 74% with no overt diastolic dysfunction in this cohort. There were significant differences in LVEF across eNOS genotypes with GG genotype being associated with a worse LVEF compared to other genotypes (LVEF: GG 71%, TG 76%, TT 73%, p = 0.006). After multivariate analysis, (adjusting for age, eGFR, baseline mean arterial pressure, contemporary CMR heart rate, total cholesterol, high sensitive C-reactive protein, body mass index and gender) GG genotype was associated with a worse LVEF, and increased LV end-diastolic and systolic index (p = 0.004, 0.049 and 0.009 respectively). CONCLUSIONS: eNOS Glu298Asp rs1799983 polymorphism in CKD patients is associated with relevant sub-clinical cardiac remodelling as detected by CMR. This gene variant may therefore represent an important genetic biomarker, and possibly highlight pathways for intervention, in these patients who are at particular risk of worsening cardiac disease as their renal dysfunction progresses.

Impact of renal function on survival after transcatheter aortic valve implantation (TAVI): an analysis of the UK TAVI registry.

OBJECTIVE: To determine the nature of the association between renal dysfunction and outcomes following transcatheter aortic valve implantation (TAVI) in all cases performed in the UK between 2007 and 2012. METHODS: The UK TAVI registry was established to report outcomes on all TAVI procedures performed within the UK. Data were collected prospectively on 3980 patients from 1 January 2007 until 31 December 2012. RESULTS: In total, 205 patients (5.5%) died during their admission. Moderate to advanced chronic kidney disease (CKD) (estimated glomerular filtration rate (eGFR) <45 mL/min/1.73 m(2)) was significantly associated with increased mortality, even after adjustment for risk factors (OR 1.45, 95% CI 1.03 to 2.05; p=0.04). For every 10 mL/min/1.73 m(2) decrease in eGFR, in-hospital mortality increased by 8.2% (95% CI 1.1% to 14.7%; p=0.03). In total 1119 patients (30.2%) died during the follow-up period (median 543 days). Moderate to advanced CKD (eGFR <45 mL/min/1.73 m(2)) was significantly associated with increased mortality, even after adjustment for risk factors (OR 1.36, 95% CI 1.17 to 1.58; p<0.001). For every 10 mL/min/1.73 m(2) decrease in eGFR, cumulative mortality increased by 4.4% (95% CI 1.2% to 7.5%; p=0.007). Preoperative kidney function and the need for preoperative dialysis treatment discriminated between patients who died and survived. However, predictive power was poor with none of the c-statistics being >0.6. CONCLUSIONS: Pre-procedural renal dysfunction is associated, in a graded fashion independently of dialysis status, with worse outcomes, including mortality in patients undergoing TAVI.

Comparison of magnetic resonance feature tracking for systolic and diastolic strain and strain rate calculation with spatial modulation of magnetization imaging analysis.

PURPOSE: To compare cardiovascular magnetic resonance-feature tracking (CMR-FT) with spatial modulation of magnetization (SPAMM) tagged imaging for the calculation of short and long axis Lagrangian strain measures in systole and diastole. MATERIALS AND METHODS: Healthy controls (n = 35) and patients with dilated cardiomyopathy (n = 10) were identified prospectively and underwent steady-state free precession (SSFP) cine imaging and SPAMM imaging using a gradient-echo sequence. A timed offline analysis of images acquired at identical horizontal long and short axis slice positions was performed using CMR-FT and dynamic tissue-tagging (CIMTag2D). Agreement between strain and strain rate (SR) values calculated using these two different methods was assessed using the Bland-Altman technique. RESULTS: Across all participants, there was good agreement between CMR-FT and CIMTag for calculation of peak systolic global circumferential strain (-22.7 ± 6.2% vs. -22.5 ± 6.9%, bias 0.2 ± 4.0%) and SR (-1.35 ± 0.42 1/s vs. -1.22 ± 0.42 1/s, bias 0.13 ± 0.33 1/s) and early diastolic global circumferential SR (1.21 ± 0.44 1/s vs. 1.07 ± 0.30 1/s, bias -0.14 ± 0.34 1/s) at the subendocardium. There was satisfactory agreement for derivation of peak systolic global longitudinal strain (-18.1 ± 5.0% vs. -16.7 ± 4.8%, bias 1.3 ± 3.8%) and SR (-1.04 ± 0.29 1/s vs. -0.95 ± 0.32 1/s, bias 0.09 ± 0.26 1/s). The weakest agreement was for early diastolic global longitudinal SR (1.10 ± 0.40 1/s vs. 0.67 ± 0.32 1/s, bias -0.42 ± 0.40 1/s), although the correlation remained significant (r = 0.42, P < 0.01). CMR-FT generated these data over four times quicker than CIMTag. CONCLUSION: There is sufficient agreement between systolic and diastolic strain measures calculated using CMR-FT and myocardial tagging for CMR-FT to be considered as a potentially feasible and rapid alternative.