Biventricular Function is Impaired in Right Ventricular Septal Pacing-A Prospective Study Using Myocardial Strain Imaging.

BACKGROUND: Left ventricular (LV) dysfunction is known to occur after right ventricular (RV) pacing; the effect on RV function is less well studied. The aim of this study was to assess the impact of RV mid-septal pacing upon RV function using the novel parameters of speckle-tracking derived RV global longitudinal strain (RV GLS) and RV free wall strain (RV FWS), as well as the conventional parameters RV fractional area change (FAC), tricuspid annular plane systolic excursion (TAPSE), and tricuspid annular systolic velocity (RV S'). METHODS: Thirty-two (32) consecutive patients with normal baseline LV and RV function requiring permanent pacemaker insertion (for high-grade AV block or sinus node dysfunction) were prospectively recruited. Echocardiography was performed prior to implantation, at 1 day, 1 month and 1 year after implantation, with 29 patients completing follow-up. RESULTS: After 1 year, three patients (10%) with otherwise normal RV parameters developed abnormal RV strain patterns. Compared to 1 day after implantation, at 1 year significant reductions were observed in mean RV GLS (-24.8 to -21.8%) RV S' (15.1 to 12.2 cm/s), TAPSE (24.2 to 21.9 mm), RV GLS (-24.8 to -21.8%), left ventricular ejection fraction (LVEF) (66.0 to 57.9%), LV GLS (-19.9 to 17.0), all p<0.01. There was a non-significant reduction for RV FWS (-29.0 to -26.7%, p=0.06) and there was no change in RV FAC (49.1 to 46.9%, p=0.24). CONCLUSION: We report abnormalities of RV strain developing 1 year after pacemaker insertion. Measurement of myocardial strain is emerging as an additional method to detect patients at risk of RV dysfunction in those who have undergone pacemaker implantation.

Invasive versus conservative management in patients aged ≥85 years presenting with non-ST-elevation myocardial infarction.

BACKGROUND: Guidelines recommend early coronary angiography (CA) in patients with non-ST-elevation myocardial infarction (NSTEMI) irrespective of age. However, elderly patients are less likely to be treated according to these guidelines due to their perceived high risk and medical comorbidities. Whether an invasive strategy is associated with improved survival in patients aged ≥85 years remains uncertain due to their exclusion from randomised trials. AIMS: Patients were stratified based on whether they underwent invasive management with CA with a view to revascularisation versus conservative management. The primary outcome was long-term mortality. METHODS: Consecutive patients aged ≥85 years presenting to a tertiary centre with NSTEMI between 2008 and 2018 were included in this retrospective cohort study. RESULTS: Of 7591 patients with NSTEMI, 1052 patients aged ≥85 years were included. Ninety-nine (9.4%) patients underwent CA. Those undergoing CA were more likely to be younger, male, live independently, without mobility or cognitive issues (all P < 0.01). Overall, 495 (47%) patients died during a mean follow up of 1.3 ± 1 year. On Cox regression, after adjusting for age, pre-morbid functional status, cognition and cardiovascular risk factors, invasive management was the strongest predictor for survival (hazard ratio 0.47; 95% confidence interval 0.26-0.85; P = 0.01). Invasive management was associated with a trend to increased risk of in-hospital bleeding (6.1% vs 2.6%; P = 0.054) with no significant difference in stroke (2.0% vs 3.8%; P = 0.37). CONCLUSION: In patients aged ≥85 years who presented with NSTEMI, invasive management was associated with improved survival without significant differences in bleeding or stroke. A randomised controlled study assessing the efficacy and safety of invasive management in very elderly patients with NSTEMI is warranted.

Role of Cardiac Computed Tomography in Planning Transcatheter Mitral Valve Replacement (TMVR).

PURPOSE OF REVIEW: Transcatheter mitral valve replacement (TMVR) is an evolving and rapidly expanding field within structural interventions, offering renewed treatment options for patients with high-risk mitral valve disease. We aim to highlight and illustrate the importance of cardiac CT in the planning of TMVR. RECENT FINDINGS: As TMVR has evolved, so has the specific nuances of cardiac CT planning, we now understand the importance of accurate annular sizing and valve simulation to predict complications such as neo-LVOT obstruction and paravalvular leak (PVL). More so than any other modality, cardiac CT remains instrumental in accurately planning TVMR from feasibility, device sizing, access, and fluoroscopic angles. Cardiac CT remains the key modality in TMVR evaluation, often the first step in determining patient eligibility through comprehensive procedural planning as well as informing potential outcomes and prognosis. In this review, we discuss the critical role of cardiac computed tomography (CT) and the specific considerations involved in TMVR.

Impaired Cardiac Reserve on Dobutamine Stress Echocardiography Predicts the Development of Hepatorenal Syndrome.

OBJECTIVES: Cardiac dysfunction has been implicated in the genesis of hepatorenal syndrome (HRS). It is unclear whether a low cardiac output (CO) or attenuated contractile response to hemodynamic stress can predict its occurrence. We studied cardiovascular hemodynamics in cirrhosis and assessed whether a diminished cardiac reserve with stress testing predicted the development of HRS on follow-up. METHODS: Consecutive patients undergoing liver transplant workup with dobutamine stress echocardiography (DSE) were included. CO was measured at baseline and during low-dose dobutamine infusion at 10 µg/kg/min. HRS was diagnosed using guideline-based criteria. RESULTS: A total of 560 patients underwent DSE, of whom 488 were included after preliminary assessment. There were 64 (13.1%) patients with established HRS. The HRS cohort had a higher baseline CO (8.0 ± 2 vs 6.9 ± 2 L/min; P < 0.001) and demonstrated a blunted response to low-dose dobutamine (ΔCO 29 ± 22% vs 44 ± 32%, P < 0.001) driven primarily by inotropic incompetence. Optimal cutpoint for ΔCO in patients with HRS was determined to be <25% and was used to define a low cardiac reserve. Among the 424 patients without HRS initially, 94 (22.1%) developed HRS over a mean follow-up of 1.5 years. Higher proportion with a low cardiac reserve developed HRS (52 [55.0%] vs 56 [16.9%]; hazard ratio 4.5; 95% confidence interval 3.0-6.7; P < 0.001). In a Cox multivariable model, low cardiac reserve remained the strongest predictor for the development of HRS (hazard ratio 3.9; 95% confidence interval 2.2-7.0; P < 0.001). DISCUSSION: Patients with HRS demonstrated a higher resting CO and an attenuated cardiac reserve on stress testing. On longitudinal follow-up, low cardiac reserve was an independent predictor for the development of HRS. Assessment of cardiac reserve with DSE may provide a novel noninvasive risk marker for developing HRS in patients with advanced liver disease.HRS is a life-threatening complication of liver disease. We studied whether an inability to increase cardiac contraction in response to stress can assist in the prediction of HRS. We demonstrate that patients with liver disease who exhibit cardiac dysfunction during stress testing had a 4-fold increased risk of developing HRS. This may improve our ability for early diagnosis and treatment of patients at a higher risk of developing HRS.

Mapping the Minnesota Living with Heart Failure Questionnaire (MLHFQ) onto the Assessment of Quality of Life 8D (AQoL-8D) utility scores.

PURPOSE: The Minnesota Living with Heart Failure Questionnaire (MLHFQ) is a widely used condition-specific measure of quality of life (QoL) in patients with heart failure. To use information from the MLHFQ in an economic evaluation, the MLHFQ must be mapped onto a preference-based measure of QoL. This study aims to develop a mapping algorithm between the MLHFQ and the Assessment of Quality of Life (AQoL) 8D utility instrument in patients with dilated cardiomyopathy (DCM). METHODS: MLHFQ and AQoL-8D data were collected on 61 Australian adults with idiopathic DCM or other non-hypertrophic cardiomyopathies. Three statistical methods were used as follows: ordinary least squares (OLS) regression, the robust MM estimator, and the generalised linear models (GLM). Each included a range of explanatory variables. Model performance was assessed using key goodness-of-fit measures, the mean absolute error (MAE), and the root-mean-square error (RMSE). RESULTS: The MLHFQ summary score and AQoL-8D utility scores were strongly correlated (r = - 0.83, p < 0.0001) and the two subscales of the MLHFQ were correlated with the eight dimensions of the AQoL-8D. Utility scores were predicted with acceptable precision based on responses to the MLHFQ physical, emotional, social, and other subscales. OLS and GLM performed similarly with MAE and RMSE ranging 0.086-0.106 and 0.114-0.130, respectively. CONCLUSION: The mapping algorithm developed in this study allows the derivation of AQoL-8D utilities from MLHFQ scores for use in cost-effectiveness analyses and most importantly, enables the economic evaluation of alternative heart failure therapy options when only the MLHFQ has been collected.

Renin-angiotensin system inhibition and risk of infection and mortality in COVID-19: a systematic review and meta-analysis.

BACKGROUND: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of COVID-19, enters human cells by binding of its viral protein to the aminopeptidase angiotensin-converting enzyme 2 (ACE2). This has led to speculation whether treatment with renin-angiotensin system (RAS) inhibitors was associated with an increased likelihood of a positive test for COVID-19 and risk of mortality. AIMS: We performed a systematic review and meta-analysis to investigate whether RAS inhibitors increased the likelihood of a positive test or death/severe illness in patients with COVID-19. METHODS: A systematic search of MEDLINE, PubMed and EMBASE was conducted for studies stratified by the use of angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor blockers (ARB). Pooled analysis was performed using a random-effects model. RESULTS: Seven trials of 73 122 patients were included. Overall, 16 624 (22.7%) patients had a positive COVID-19 test and 7892 (10.8%) were on a RAS inhibitor. RAS inhibitors were not associated with higher likelihood of a positive COVID-19 test result (odds ratio (OR) 0.97 (95% CI 0.97-1.05, P = 0.48) with low heterogeneity. This was comparable when stratifying by use of each medication class. The use of RAS inhibitors was also not associated with mortality or severe illness (OR 0.89, 95% CI 0.73-1.07, P = 0.21) with moderate heterogeneity. CONCLUSION: Use of ACEI or ARB was not associated with a heightened susceptibility for a positive diagnosis of COVID-19. Furthermore, they were not associated with increased illness severity or mortality due to COVID-19. Randomised controlled trials are needed to address definitively the potential benefits or harms of RAS inhibitors in patients with COVID-19.

Erdheim-Chester Disease: a Rare but Important Cause of Recurrent Pericarditis.

PURPOSE OF REVIEW: Erdheim-Chester disease (ECD) is a very rare neoplasm of the non-Langerhans cell histiocytes. Pericardial involvement is uncommon, and we aim to review the current knowledge on the epidemiology, clinical manifestations, and management of recurrent pericarditis due to ECD. We also aim to raise awareness of the importance of considering ECD as a differential diagnosis for recurrent pericarditis in the appropriate clinical settings. RECENT FINDINGS: The prevalence of pericardial involvement in ECD is estimated to be 40% and is getting more recognized recently. Up to 68% of patients carry the BRAFV600E mutation, and targeted treatment with vemurafenib, an inhibitor of BRAF kinase, showed an excellent response in those who carry this mutation. Pericardial disease appears to be the most common cardiac presentation (in 80% of cases). Although pericardial involvement is frequently asymptomatic, patients with ECD can present with typical pericarditis chest pain and signs of right heart failure if constriction is present. The diagnosis of ECD requires a biopsy of the pericardium or another affected organ. If BRAFV600E mutation is absent, limited data exist, and many medications have been tried, like interferon alfa, anakinra, and infliximab.

A cost-effectiveness model of genetic testing and periodical clinical screening for the evaluation of families with dilated cardiomyopathy.

PURPOSE: To assess the relative cost-effectiveness of cascade genetic testing in asymptomatic relatives of patients with dilated cardiomyopathy (DCM) compared with periodical clinical surveillance. METHODS: A decision-analytic model, combining a decision tree and a Markov model, was used to determine the lifetime costs and quality-adjusted life years (QALYs) for the two strategies. Deterministic and probabilistic sensitivity analyses were undertaken to assess the robustness of findings and to explore decision uncertainty. RESULTS: The incremental cost per additional QALY of cascade genetic testing prior to periodical clinical surveillance of first-degree relatives compared with periodical clinical surveillance alone was estimated at approximately AUD $6100. At established thresholds of cost-effectiveness, there is a 90% probability that cascade genetic testing is cost-effective. Extensive sensitivity analyses, including the addition of second-degree relatives, did not alter the conclusions drawn from the main analysis. CONCLUSION: Using cascade genetic testing to guide clinical surveillance of asymptomatic relatives of patients with DCM is very likely to be cost-effective. As the DCM pathogenic variant detection rate rises and new evidence for personalized treatment of at-risk individuals becomes available, the cost-effectiveness of cascade testing will further increase.

Evaluation of Modified Look-Locker Inversion Recovery and Arrhythmia-Insensitive Rapid Cardiac T1 Mapping Pulse Sequences in Cardiomyopathy Patients.

OBJECTIVE: The aim of this study was to compare the performance of arrhythmia-insensitive rapid (AIR) and modified Look-Locker inversion recovery (MOLLI) T1 mapping in patients with cardiomyopathies. METHODS: In 58 patients referred for clinical cardiac magnetic resonance imaging at 1.5 T, we compared MOLLI and AIR native and postcontrast T1 measurements. Two readers independently analyzed myocardial and blood T1 values. Agreement between techniques, interreader agreement per technique, and intrascan agreement per technique were evaluated. RESULTS: The MOLLI and AIR T1 values were strongly correlated (r = 0.98); however, statistically significantly different T1 values were derived (bias 80 milliseconds, pooled data, P < 0.01). Both techniques demonstrated high repeatability (MOLLI, r = 1.00 and coefficient of repeatability [CR] = 72 milliseconds; AIR, r = 0.99 and CR = 184.2 milliseconds) and produced high interreader agreement (MOLLI, r = 1.00 and CR = 51.7 milliseconds; AIR, r = 0.99 and CR = 183.5 milliseconds). CONCLUSIONS: Arrhythmia-insensitive rapid and MOLLI sequences produced significantly different T1 values in a diverse patient cohort.

Left ventricular hypertrophy in experimental chronic kidney disease is associated with reduced expression of cardiac Kruppel-like factor 15.

BACKGROUND: Left ventricular hypertrophy (LVH) increases the risk of death in chronic kidney disease (CKD). The transcription factor Kruppel-like factor 15 (KLF15) is expressed in the heart and regulates cardiac remodelling through inhibition of hypertrophy and fibrosis. It is unknown if KLF15 expression is changed in CKD induced LVH, or whether expression is modulated by blood pressure reduction using angiotensin converting enzyme (ACE) inhibition. METHODS: CKD was induced in Sprague-Dawley rats by subtotal nephrectomy (STNx), and rats received vehicle (n = 10) or ACE inhibition (ramipril, 1 mg/kg/day, n = 10) for 4 weeks. Control, sham-operated rats (n = 9) received vehicle. Cardiac structure and function and expression of KLF15 were assessed. RESULTS: STNx caused impaired kidney function (P < 0.001), hypertension (P < 0.01), LVH (P < 0.001) and fibrosis (P < 0.05). LVH was associated with increased gene expression of hypertrophic markers, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP, P < 0.01) and connective tissue growth factor (CTGF) (P < 0.05). Cardiac KLF15 mRNA and protein expression were reduced (P < 0.05) in STNx and levels of the transcription regulator, GATA binding protein 4 were increased (P < 0.05). Ramipril reduced blood pressure (P < 0.001), LVH (P < 0.001) and fibrosis (P < 0.05), and increased cardiac KLF15 gene (P < 0.05) and protein levels (P < 0.01). This was associated with reduced ANP, BNP and CTGF mRNA (all P < 0.05). CONCLUSION: This is the first evidence that loss of cardiac KLF15 in CKD induced LVH is associated with unchecked trophic and fibrotic signalling, and that ACE inhibition ameliorates loss of cardiac KLF15.

Kruppel-Like Factor 15 Is Critical for the Development of Left Ventricular Hypertrophy.

Left ventricular hypertrophy (LVH) is an independent risk factor for adverse cardiovascular events and is often present in patients with hypertension. Treatment to reduce blood pressure and regress LVH is key to improving health outcomes, but currently available drugs have only modest cardioprotective effects. Improved understanding of the molecular mechanisms involved in the development of LVH may lead to new therapeutic targets in the future. There is now compelling evidence that the transcription factor Kruppel-like factor 15 (KLF15) is an important negative regulator of cardiac hypertrophy in both experimental models and in man. Studies have reported that loss or suppression of KLF15 contributes to LVH, through lack of inhibition of pro-hypertrophic transcription factors and stimulation of trophic and fibrotic signaling pathways. This review provides a summary of the experimental and human studies that have investigated the role of KLF15 in the development of cardiac hypertrophy. It also discusses our recent paper that described the contribution of genetic variants in KLF15 to the development of LVH and heart failure in high-risk patients.

Does left ventricular hypertrophy affect cognition and brain structural integrity in type 2 diabetes? Study design and rationale of the Diabetes and Dementia (D2) study.

BACKGROUND: Cognitive impairment is common in type 2 diabetes mellitus, and there is a strong association between type 2 diabetes and Alzheimer's disease. However, we do not know which type 2 diabetes patients will dement or which biomarkers predict cognitive decline. Left ventricular hypertrophy (LVH) is potentially such a marker. LVH is highly prevalent in type 2 diabetes and is a strong, independent predictor of cardiovascular events. To date, no studies have investigated the association between LVH and cognitive decline in type 2 diabetes. The Diabetes and Dementia (D2) study is designed to establish whether patients with type 2 diabetes and LVH have increased rates of brain atrophy and cognitive decline. METHODS: The D2 study is a single centre, observational, longitudinal case control study that will follow 168 adult patients aged >50 years with type 2 diabetes: 50% with LVH (case) and 50% without LVH (control). It will assess change in cardiovascular risk, brain imaging and neuropsychological testing between two time-points, baseline (0 months) and 24 months. The primary outcome is brain volume change at 24 months. The co-primary outcome is the presence of cognitive decline at 24 months. The secondary outcome is change in left ventricular mass associated with brain atrophy and cognitive decline at 24 months. DISCUSSION: The D2 study will test the hypothesis that patients with type 2 diabetes and LVH will exhibit greater brain atrophy than those without LVH. An understanding of whether LVH contributes to cognitive decline, and in which patients, will allow us to identify patients at particular risk. TRIAL REGISTRATION: Australian New Zealand Clinical Trials Registry ( ACTRN12616000546459 ), date registered, 28/04/2016.

Vulnerability to environmental and climatic health provocations among women and men hospitalized with chronic heart disease: insights from the RESILIENCE TRIAL cohort.

AIMS: We aimed to recruit a representative cohort of women and men with multi-morbid chronic heart disease as part of a trial testing an innovative, nurse-co-ordinated, multi-faceted intervention to lower rehospitalization and death by addressing areas of vulnerability to external challenges to their health. METHODS AND RESULTS: The prospective, randomized open, blinded end-point RESILIENCE Trial recruited 203 hospital inpatients (mean age 75.7 ± 10.2 years) of whom 51% were women and 94% had combined coronary artery disease, heart failure, and/or atrial fibrillation. Levels of concurrent multi-morbidity were high (mean Charlson Index of Comorbidity Score 6.5 ± 2.7), and 8.9% had at least mild frailty according to the Rockwood Clinical Frailty Scale. Including the index admission, 19-20% of women and men had a pre-existing pattern of seasonally linked hospitalization (seasonality). Detailed phenotyping revealed that 48% of women and 40% of men had ≥3 physiological factors, and 15% of women and 16% of men had ≥3 behavioural factors likely to increase their vulnerability to external provocations to their health. Overall, 61-62% of women and men had ≥4 combined factors indicative of such vulnerability. Additional factors such as reliance on the public health system (63 vs. 49%), lower education (30 vs. 14%), and living alone (48 vs. 29%) were more prevalent in women. CONCLUSION: We successfully recruited women and men with multi-morbid chronic heart disease and bio-behavioural indicators of vulnerability to external provocations to their health. Once completed, the RESILIENCE TRIAL will provide important insights on the impact of addressing such vulnerability (promoting resilience) on subsequent health outcomes. REGISTRATION: ClinicalTrials.org: NCT04614428.

Clinical, functional and prognostic implications of severe atrial dilation in secondary mitral regurgitation.

OBJECTIVE: Atrial dilation is known to be a poor prognostic indicator. However, its clinical, functional and prognostic implications have not been thoroughly explored in secondary mitral regurgitation (SMR). We sought to describe the implications of severe atrial dilation (SAD) in SMR. METHODS: We included all adult patients with severe SMR due to left ventricle dysfunction (with no organic mitral valve disease) who underwent transthoracic echocardiography between January 2012 and March 2021 at our institution. The concomitant presence of severe left atrial (LA) dilation (>48 mL/m2) defined SADMR (SAD in SMR), and these patients were compared with those without SAD. RESULTS: A total of 2011 patients were included (mean age 70% and 41% females), with 71% having SADMR. MR severity and ejection fraction were similar between both groups. Patients with SADMR were older, less females and had more diabetes, but similar rates of atrial fibrillation. Mechanistically, they had lower A wave velocity (0.61 vs 0.72 cm/sec, p<0.001) and more impaired LA reservoir strain (9.7% vs 15.5%, p<0.001). Geometrically, SADMR had shallower leaflets' angulations, lower tenting height, larger annuli and smaller leaflet length/annular diameter ratios (all p<0.001). They underwent fewer MV interventions, although these were associated with better outcomes (log-rank p<0.001). Over the study period, SAD was an independent predictor of mortality (HR 1.26, p=0.04). CONCLUSION: SADMR is associated with specific mechanistic and functional alterations and confers a worse prognosis.

Effect of Myocardial Tissue Characterization Using Native T1 to Predict the Occurrence of Adverse Events in Patients With Chronic Kidney Disease and Severe Aortic Stenosis.

Among patients with chronic kidney disease (CKD), aortic stenosis (AS) is associated with a significantly higher rate of mortality. We aimed to evaluate whether diffuse myocardial fibrosis, determined using native T1 mapping, has prognostic utility in predicting major adverse cardiovascular events (MACEs), including all-cause mortality or heart failure hospitalization, in patients with CKD and severe AS who are evaluated for transcatheter aortic valve implantation. Cardiac magnetic resonance with T1 mapping using the modified Look-Locker inversion recovery technique was performed in 117 consecutive patients with severe AS and CKD (stage ≥3). Patients were followed up to determine the occurrence of MACE. The mean age of the 117 patients in the cohort was 82 ± 8 years. Native T1 was 1,055 ms (25th- to 75th percentiles 1,031 to 1,078 ms), which is higher than previously reported in healthy controls. Patients with higher T1 times were more likely to have higher N-terminal pro-B-type natriuretic peptide levels (4,122 [IQR 1,578 to 7,980] pg/ml vs 1,678 [IQR 493 to 2,851] pg/ml, p = 0.005) and a history of heart failure (33% vs 9%, p = 0.034). After median follow-up of 3.4 years, MACE occurred in 71 patients (61%). The Society of Thoracic Surgeons predicted risk of mortality score (hazard ratio [HR] 1.07, 95% confidence interval [CI] 1.02 to 1.12, p = 0.006), native T1 >1,024 ms (HR 2.10, 95% CI 1.09 to 4.06, p = 0.028), and New York Heart Association class (HR 1.56, 95% 1.09 to 2.34, p = 0.016) were independent predictors of MACE. Longer native T1 was associated with MACE occurrence in patients with CKD and severe AS.

Periprocedural Echocardiographic Guidance of Transcatheter Mitral Valve Edge-to-Edge Repair Using the MitraClip.

Transcatheter edge-to-edge mitral valve repair is a minimally invasive treatment option for selected patients with moderate to severe or severe mitral regurgitation. Although transcatheter edge-to-edge mitral valve repair offers a significant step forward in the management of mitral regurgitation, the rate of procedural-related complications is not trivial. High-quality periprocedural imaging is important for optimal patient selection and procedural success. In this review, we present a step-by-step approach of the recommended echocardiographic views for transcatheter edge-to-edge mitral valve repair.

Role of Computed Tomography Angiography in Setting of Spontaneous Coronary Artery Dissection.

Spontaneous coronary artery dissection (SCAD) is an infrequent cause of acute coronary syndrome, predominantly affecting young women. Catheter-based coronary angiography is the gold standard diagnostic test, especially when coupled with intracoronary imaging. Conservative management in stable patients is the preferred approach given the increased risk of complications associated with percutaneous interventions. Noninvasive coronary computed tomography angiography (CTA) has a potential role in the diagnosis and follow-up of SCAD. CTA also plays a role in screening for extracoronary vascular abnormalities frequently associated with SCAD. The goal of this article is to review the potential role of CTA in evaluating SCAD.

Improvement in left ventricular mechanics following medical treatment of constrictive pericarditis.

OBJECTIVE: Patients with constrictive pericarditis (CP) with active inflammation may show resolution with anti-inflammatory therapy. We aimed to investigate the impact of anti-inflammatory medications on constrictive pathophysiology using echocardiography in patients with CP. METHODS: We identified 35 patients with CP who were treated with anti-inflammatory medications (colchicine, prednisone, non-steroidal anti-inflammatory drugs) after diagnosis of CP (mean age 58±13; 80% male). Clinical resolution of CP (transient CP) was defined as improvement in New York Heart Association class during follow-up. We assessed constrictive pathophysiology using regional myocardial mechanics by the ratio of peak early diastolic tissue velocity (e') at the lateral and septal mitral annulus by tissue Doppler imaging (lateral/septal e') or the ratio of the left ventricular lateral and septal wall longitudinal strain (LSlateral/LSseptal) by two-dimensional speckle-tracking echocardiography. Longitudinal data were analysed using a mixed effects model. RESULTS: During a median follow-up of 323 days, 20 patients had transient CP, whereas 15 patients had persistent CP. Transient CP had higher baseline erythrocyte sedimentation rates (ESR) (p=0.003) compared with persistent CP. There were no significant differences in LSlateral/LSseptal and lateral/septal e'. During follow-up, only transient CP showed improvement in lateral/septal e' (p<0.001) and LSlateral/LSseptal (p=0.003), and recovery of inflammatory markers was similar between the two groups. In the logistic model, higher baseline ESR and greater improvement in lateral/septal e' and LSlateral/LSseptal were associated with clinical resolution of CP using anti-inflammatory therapy. CONCLUSIONS: Improvement of constrictive physiology detected by lateral/septal e' and LSlateral/LSseptal was associated with resolution of clinical symptoms after anti-inflammatory treatment. Serial monitoring of these markers could be used to identify transient CP.