Christine Jellis

Exercise limitation associated with asymptomatic left ventricular impairment: Analogy with Stage B heart failure

BACKGROUNDnStage B heart failure (SBHF) describes asymptomatic ventricular disease that may presage the development of heart failure (HF) symptoms. This entity has been largely defined by structural changes; the roles of sensitive indicators of nonischemic left ventricular (LV) dysfunction, such as LV strain, are undefined.nnnOBJECTIVESnThis study sought to define the association of exercise capacity with left ventricular hypertrophy (LVH) and systolic/diastolic dysfunction in asymptomatic patients with HF risk factors.nnnMETHODSnWe used echocardiography to study 510 asymptomatic patients (age 58 ± 12 years) with type 2 diabetes mellitus, hypertension, or obesity. The results of cardiopulmonary exercise testing in patients with structural evidence of SBHF were compared with those in patients with subclinical dysfunction, defined by reduced LV strain (>-18%) or increased LV filling pressure (E/e >13).nnnRESULTSnCompared with healthy subjects, groups with LV abnormalities differed in terms of oxygen uptake (peak VO2): 25.5 ± 8.2 versus 21.0 ± 8.2 for strain >-18% (pxa0< 0.001); 26.4 ± 8.0 versus 19.0 ± 7.2 for E/e >13 (pxa0< 0.0001); and 26.0 ± 7.7 versus 15.9 ± 6.9 ml/kg/min for LVH (pxa0< 0.0001). SBHF, defined asxa0≥1 imaging variable present, was associated with lower peak VO2 (betaxa0=xa0-0.20; pxa0< 0.0001) and metabolic equivalents (betaxa0=xa0-0.21; pxa0< 0.0001), independent of higher body mass index and insulin resistance, older age, male sex, and treatment with beta-blockers.nnnCONCLUSIONSnLVH, elevated LV filling pressure, and abnormal myocardial deformation were independently associated with impaired exercise capacity. Including functional markers may improve identification of SBHF in nonischemic heart disease.

Clinical Implications of Echocardiographic Phenotypes of Patients With Diabetes Mellitus

BACKGROUNDnType 2 diabetes mellitus (T2DM) may alter cardiac structure and function, but obesity, hypertension (HTN), or aging can induce similar abnormalities.nnnOBJECTIVESnThis study sought to link cardiac phenotypes in T2DM patients with clinical profiles and outcomes using cluster analysis.nnnMETHODSnBaseline echocardiography and a composite endpoint (cardiovascular mortality and hospitalization) were evaluated in 842 T2DM patients from 2 prospective cohorts. A cluster analysis was performed on echocardiographic variables, and the association between clusters and clinical profiles and outcomes was assessed.nnnRESULTSnThree clusters were identified. Cluster 1 patients had the lowest left ventricular (LV) mass index and ratio between early mitral inflow velocity and mitral annular early diastolic velocity (E/e) ratio, had the highest left ventricular ejection fraction (LVEF), and were predominantly male with the lowest rate of obesity or HTN. Cluster 2 patients had thexa0highest strain and highest E/e ratio, were the oldest, were predominantly female, and had the lowest rate of isolated T2DM (without HTN or obesity). Cluster 3 patients had the highest LV mass index and volumes and the lowest LVEF andxa0strain, were predominantly male, and shared similar age and rate of obesity and HTN as cluster 1 patients. Afterxa0follow-up of 67xa0months (interquartile range: 40 to 87), the composite endpoint occurred in 56 of 521 patients (10.8%). Clusters 2 (hazard ratio: 2.37; 95% confidence interval: 1.15 to 4.88) and 3 (hazard ratio: 2.19; 95% confidence interval: 1.00 to 4.82) had a similar outcome, which was worse than clusterxa01.nnnCONCLUSIONSnCluster analysis of echocardiographic variables identified 3 different echocardiographic phenotypes of T2DM patients that were associated with distinct clinical profiles and highlighted the prognostic value of LVxa0remodeling and subclinical dysfunction.

Focal fibrosis and diffuse fibrosis are predictors of reversed left ventricular remodeling in patients with non-ischemic cardiomyopathy

BACKGROUNDnPrognostic value of myocardial fibrosis in patients with non-ischemic idiopathic dilated cardiomyopathy (DCM) is not well-defined. We sought to assess the association of focal and diffuse myocardial fibrosis with left ventricular reversed remodeling (LVRR).nnnMETHODSnPatients with DCM who underwent cardiac MRI with baseline and subsequent follow-up echocardiography were included in the study. Post-contrast T1 times were corrected for renal function, body size, gadolinium dose and time after Gadolinium injection. Patients were followed over a median time of 29months to evaluate changes of left ventricular end-systolic volume (LVESV). A Linear Mixed Model was used to assess the relationship between the LVESV during follow-up, corrected post-T1 value delayed hyperenhancement (DHE), and modified Seattle Heart Failure Score (SHFS).nnnRESULTSnA total of 103 patients (mean age 51±15years, 61% male) were evaluated. The mean LVEF was 33±11%, LVESVi 62±39ml/m(2), and T1 time 416±98. DHE was identified in 45 patients (44%). Patients with focal DHE (n=45) had higher LVESVi at baseline and during follow-up (p=0.024). Post T1 value >450 was an independent predictor of LVRR at the follow-up (Δ=24.6ml/m(2) SE 14.6ml/2, p=0.0480) in patients despite the presence of DHE, even after adjusting for their SHFS.nnnCONCLUSIONnWhile DCM patients with focal DHE demonstrated greater adverse LV remodeling than those without focal fibrosis, diffuse fibrosis independently predicts LVRR in DCM patients in patients despite the presence of focal fibrosis.

Transient Constrictive Pericarditis: Current Diagnostic and Therapeutic Strategies

Transient constrictive pericarditis is increasingly recognized as a distinct sub-type of constrictive pericarditis. The underlying pathophysiology typically relates to impaired pericardial distensibility, associated with acute or sub-acute inflammation, rather than the fibrosis or calcification often seen in chronic pericardial constriction. Accordingly, patients may present clinically with concomitant features of pericarditis and constrictive physiology. Non-invasive multimodality imaging is advocated for diagnosis of transient constrictive pericarditis. Echocardiography remains the mainstay for initial evaluation of the dynamic features of constriction. However, cardiac magnetic resonance imaging can provide complimentary functional information, with the addition of dedicated sequences to assess for active pericardial edema and inflammation. Although transient pericardial constriction can spontaneously resolve, institution of anti-inflammatory therapy may hasten resolution or even prevent progression to chronic pericardial constriction. Non-steroidal anti-inflammatory agents remain the initial treatment of choice, with subsequent consideration of colchicine, steroids, and other immune-modulating agents in more refractory cases.

3D Imaging of Device Leads: “Taking the Lead With 3D”∗

Pacemaker lead–associated tricuspid regurgitation (TR) has been anecdotally described for many years, but investigation has been limited to a small number of observational studies [(1)][1]. Overall, it seems that worsening of TR is common after transvenous lead placement [(2)][2]. Perhaps the lack

Correlation between right ventricular T1 mapping and right ventricular dysfunction in non-ischemic cardiomyopathy

Right ventricular (RV) fibrosis is increasingly recognized as the underlying pathological substrate in a variety of clinical conditions. We sought to employ cardiac magnetic resonance (CMR) techniques of strain imaging and longitudinal relaxation time (T1) mapping to better examine the relationship between RV function and structure. Our aim was to initially evaluate the feasibility of these techniques to evaluate the right ventricle. We then sought to explore the relationship between RV function and underlying fibrosis, along with examining the evolution of RV remodeling according to the amount of baseline fibrosis. Echocardiography was performed in 102 subjects with non-ischemic cardiomyopathy. Right ventricular parameters were assessed including: fractional area change (FAC) and longitudinal strain. The same cohort underwent CMR. Post-contrast T1 mapping was performed as a marker of fibrosis with a Look-Locker technique using inversion recovery imaging. Mid-ventricular post-contrast T1 values of the RV free wall, RV septum and lateral LV were calculated using prototype analysis software. Biventricular volumetric data including ejection fraction was measured by CMR using a cine short axis stack. CMR strain analysis was also performed to assess 2D RV longitudinal and radial strain. Simultaneous biochemical and anthropometric data were recorded. Subjects were followed over a median time of 29 months (IQR 20–37 months) with echocardiography to evaluate temporal change in RV FAC according to baseline post-contrast T1 values. Longitudinal data analysis was performed to adjust for patient loss during follow-up. Subjects (62% men, 51u2009±u200915 years) had mild to moderately impaired global RV systolic function (RVEFu2009=u200939u2009±u200915%; RVEDVu2009=u2009187u2009±u200969xa0ml; RVESVu2009=u2009119u2009±u200968xa0ml) and moderate left ventricular dysfunction at baseline (LVEF 30u2009±u200917%). Good correlation was observed between mean LV and RV post-contrast T1 values (ru2009=u20090.652, pu2009<u20090.001), with similar post-contrast T1 values maintained in both the RV free wall and septum (ru2009=u20090.761, pu2009<u20090.001). CMR RVEF demonstrated a proportional correlation with echocardiographic measures of RV longitudinal function and CMR RV strain (longitudinal ru2009=u2009−0.449, pu2009=u20090.001; radial ru2009=u2009−0.549, pu2009<u20090.001). RVEF was related to RV post-contrast T1 values, particularly in those with RV dysfunction (free wall T1 ru2009=u20090.259 pu2009=u20090.027; septal T1 ru2009=u20090.421 pu2009<u20090.001). RV strain was also related to RV post-contrast T1 values (ru2009=u2009−0.417, pu2009=u20090.002). Linear regression analysis demonstrated strain and post-contrast T1 values to be independently associated with RVEF. Subjects with severe RV dysfunction (CMR RVEF <25%) demonstrated lower RV CMR strain (longitudinal pu2009=u20090.018; radial pu2009<u20090.001), RV T1 values (free wall pu2009=u20090.013; septum <0.001) and RV longitudinal echocardiography parameters despite no difference in afterload. During follow-up, those with RV free wall post-contrast T1 valuesu2009≥u2009350xa0ms demonstrated ongoing improvement in FAC (Δ6%), whilst values <350xa0ms were associated with deterioration in RV function (ΔFACu2009=u2009−5%) (pu2009=u20090.026). CMR provides a comprehensive method by which to evaluate right ventricular function. Post-contrast T1 mapping and CMR strain imaging are technically feasible and provide incremental information regarding global RV function and structure. The proportional relationship between RV function and post-contrast T1 values supports that myocardial fibrosis is a causative factor of RV dysfunction in NICM, irrespective of RV afterload. This same structural milieu also appears integral to the propensity for both positive and negative RV remodeling long-term, suggestive that this is also determined by the degree of underlying RV fibrosis.

Heart Failure With Preserved Ejection Fraction: Do You Know Your Left Atrial Strain?

Symptomatic heart failure, despite preserved left ventricular (LV) ejection fraction, is a well-recognized phenomenon. This manifestation of diastolic dysfunction is associated with increased morbidity and mortality and can be attributed to a variety of pathogeneses, including diabetes mellitus, hypertension, infiltrative processes, and obesity.1–5 Unlike in systolic heart failure, where LV ejection fraction readily stratifies disease severity, accurate diagnosis and grading of heart failure with preserved ejection fraction (HFpEF) can be a challenging. Without an equivalent, single, noninvasive diagnostic tool in HFpEF, we must instead rely on a myriad of measures to establish diagnosis and severity. This is best illustrated by the current European and American guidelines, which incorporate ≤8 separate imaging indices into their recommended protocols for diagnosis and classification of diastolic dysfunction.6,7 Although, new guidelines from the American Society of Echocardiography and the European Association of Cardiovascular Imaging will attempt to simplify assessment of diastolic dysfunction with the use of 4 key variables, such as mitral annular early diastolic (e′) velocities, average E/e′ ratio, indexed left atrial (LA) volume, and peak tricuspid regurgitant velocity (personal communication, A.L. Klein, MD, unpublished data, 2016).nnSee Article by Freed et al nnLA size, initially measured as area and now revised to indexed volume, has long been felt to be a sentinel marker of diastolic dysfunction. As such, it features prominently in diagnostic algorithms and is measured routinely in all accredited echocardiographic laboratories. Increasing LA size typically reflects worsening diastolic dysfunction and is known to be associated with increased adverse events, including hospitalizations for heart failure and cardiac death.8 It is widely accepted that this increase in LA size is a consequence of chronically increased LV pressures, associated with increased myocardial stiffness and resultant impaired LV myocardial diastolic relaxation. Once dilated, LA volume will reduce but …

An Atlas of Mitral Valve Imaging

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Exercise pulmonary hypertension in primary mitral regurgitation: what does it predict?

Identifying the optimal time for mitral valve surgery in the setting of severe mitral regurgitation (MR) remains an ongoing challenge due to continually improving surgical options and outcomes. Hence, the threshold for surgical intervention has been reduced in successive iterations of the valve disease guidelines of the American and European cardiology communities.1 ,2 Nevertheless, timing of surgical intervention in primary MR remains arbitrary, as patients can remain apparently asymptomatic for prolonged periods and are understandably reluctant to undergo a potentially hazardous procedure without objective evidence of definitive benefit. This is compounded by the diverse variation in outcomes of morbidity, mortality, size of incision and likelihood of repair at different centres. Hence, in the asymptomatic patient, objective evidence of impaired exercise capacity or other pathophysiological surrogates may be valuable in optimising the timing of surgery. Exercise stress echocardiography (ESE) has been widely used for this purpose to assess symptoms and exercise capacity, determine MR severity with exercise, examine LV contractile reserve and establish peak exercise pulmonary pressure.3 These variables have been used to predict the need for surgical intervention based upon the likelihood of adverse outcomes.nnPulmonary hypertension (PHT) is seen in a minority of patients with severe primary MR at rest. It is usually associated with more severe MR and with higher surgical morbidity, although it typically improves and may even normalise after successful mitral valve surgery. The mechanism of PHT relates to high left atrial (LA) pressure from the regurgitant mitral jet, though individual factors related to the pulmonary vasculature may also be important.4 The significance of exercise PHT in primary MR is somewhat more controversial. Prior to the 2014 revision of the American College of Cardiology/American Heart Association guidelines in valve …

ASSESSMENT OF RIGHT VENTRICULAR STRUCTURE AND FUNCTION: NOVEL CMR T1 MAPPING AND STRAIN TECHNIQUES

There is limited knowledge regarding the relationship between right ventricular (RV) structure, fibrosis & systolic function. CMR T1 mapping & strain techniques may provide additional quantitative assessment of RV function & structure.nnCMR was performed in 102 subjects with non-ischemic