Left atrial appendage thrombus is not uncommon in patients with acute atrial fibrillation and a recent embolic event: A transesophageal echocardiographics tudy

AbstractObjectives. The objective of this study was to determine the frequency of left atrial thrombus in patients with acute atrial fibrillation.Background. It is commonly assumed but unproved that left atrial thrombus in patients with atrial fibrillation begins to form after the onset of atrial fibrillation and that it requires ≥3 days to form. Thus, patients with acute atrial fibrillation (i.e., <3 days) frequently undergo cardioversion without anticoagulation prophylaxis.Methods. Three hundred seventeen patients (250 men, 67 women; mean [±SD] age 64 ± 12 years) with acute (n = 143) or chronic (n = 174) atrial fibrillation were studied by two-dimensional transesophageal echocardiography.Results. Left atrial appendage thrombus was present in 20 patients (14%) with acute and 47 patients (27%, p < 0.01) with chronic atrial fibrillation. In patients with a recent embolic event, the frequency of left atrial appendage thrombus did not differ between those with acute (5 [21%] of 24) and those with chronic (12 [23%] of 52, p = NS) atrial fibrillation. Patients with acute versus chronic atrial fibrillation, respectively, did not differ (p = NS) in mean age (64 ± 13 vs. 65 ± 11 years), frequency of concentric left ventricular hypertrophy (32% vs. 26%), hypertension (32% vs. 41%), coronary artery disease (35% vs. 39%), congestive heart failure (43% vs. 48%), mitral stenosis (4% vs. 7%) or mitral valve replacement (1.4% vs. 6%). The minimally detectable difference in proportions between patients with acute and chronic atrial fibrillation based on a power of 0.80 and base proportion of 0.20 was 14%.Conclusions. Left atrial thrombus does occur in patients with acute atrial fibrillation <3 days in duration. The frequency of left atrial thrombus in patients with recent emboli is comparable between those with acute and chronic atrial fibrillation. These data suggest that patients with acute atrial fibrillation for <3 days require anticoagulation prophylaxis or evaluation by transesophageal echocardiography before cardioversion and should not be assumed to be free of left atrial thrombus

Prolongation of isovolumetric relaxation time as assessed by Doppler echocardiography predicts doxorubicin-induced systolic dysfunction in humans

AbstractA reasonably sensitive and specific noninvasive test for doxorubicin cardiotoxicity is needed. In addition, few data exist on the short- and long-term effects of doxorubicin on diastolic filling. To determine if pulsed Doppler indexes of diastolic filling could predict doxorubicin-induced systolic dysfunction, 26 patients (mean age 48 ± 12 years) were prospectively studied before receiving chemotherapy (control) and 3 weeks after obtaining cumulative doses of doxorubicin.In nine patients developing doxorubicin-induced systolic dysfunction (that is, a decrease in ejection fraction by ≥ 10 ejection fraction units to <55% the isovolumetric relaxation time was prolonged (from 66 ± 18 to 84 ± 24 ms, p < 0.05) after a cumulative doxorubicin dose of 100 to 120 mg/m2. This prolongation preceded a significant decrease in ejection fraction. Other Doppler indexes of filling were impaired after doxorubicin therapy but occurred simultaneously with the decrease in ejection fraction.A >37% increase in isovolumetric relaxation time was 78% (7 of 9) sensitive and 88% (15 of 17) specific for predicting the ultimate development of doxorubicin-induced systolic dysfunction. In 15 patients studied 1 h after the first treatment, doxorubicin enhanced Doppler indexes of filling and shortened isovolumetric relaxation time. In 22 patients, indexes of filling remained impaired and isovolumetric relaxation time was prolonged 3 months after the last doxorubicin dose.In conclusion, doxorubicin-induced systolic dysfunction is reliably predicted by prolongation of Doppler-derived isovolumetric relaxation time. Early after administration, doxorubicin enhances filling and isovolumetric relaxation time. The adverse effects of doxorubicin on both variables persist at least 3 months after cessation of treatment

Impact and Predictors of Noncircular Left Ventricular Outflow Tract Shapes on Estimating Aortic Stenosis Severity by Means of Continuity Equations

Determining aortic stenosis (AS) severity is clinically important. Calculating aortic valve (AV) area by means of the continuity equation assumes a circular left ventricular outflow tract (LVOT). The full impact of this assumption in calculating AV area is unknown. Predictors of noncircular LVOT shape in patients with AS are undefined. In 109 adult patients with AS who underwent multiplanar transesophageal echocardiography, we calculated AV area by means of the standard continuity method and by a modified method involving planimetric LVOT area. We found 54 circular, 37 horizontal-oval, 8 vertical-oval, and 10 irregular LVOTs. Area derived by direct planimetry correlated better with the modified than the standard continuity method (r=0.89 vs r=0.85; both P=0.0001). Valve areas of patients with mild, moderate, or severe AS by planimetry were more often mischaracterized with use of the standard than modified method (29 vs 18; P \u3c0.0001). Horizontal-oval AV area derived by planimetry (1.28 ± 0.55 cm2) was underestimated by the standard method (1.05 ± 0.47 cm2; P=0.001), but not by the modified method. Congenital AV morphology and low cardiac index were the only multivariate predictors of horizontal-oval shape. Low cardiac index was the only predictor of noncircular shape. More than half our patients with AS had noncircular LVOTs. Using the modified method reduces mischaracterizations of AS severity. Congenital AV morphology and low cardiac index predict horizontal-oval or noncircular shape. These data suggest the value of direct LVOT measurement to calculate AS severity in patients who have congenital AV or a low cardiac index

The Overestimation of Concentric Hypertrophy In Patients With HFpEF as Determined By 2D-Echocardiography

Background: Heart failure with preserved ejection fraction continues to pose multiple challenges in terms of accurate diagnosis, treatment, and associated morbidity. Accurate left ventricular (LV) mass calculation yields essential prognostic information relating to structural heart disease. Two-dimensional (2D) echocardiography-based calculations are solely limited to LV geometric assumptions of symmetry, whereas three-dimensional (3D) echocardiography could overcome these limitations. This study aims to compare the performance of 2D and 3D LV mass calculations. Methods: A prospective review of echocardiography findings at the University of Louisville, Kentucky, was conducted and assessed. Normal ejection fraction (EF) was defined as \u3e=52% in males and \u3e=54% in females. The following calculations were performed: relative wall thickness (RWT) = 2x posterior wall thickness/LV internal diastolic dimension (LVIDd) and 2D LV mass = 0.8{1.04([LVIDd + IVSd +PWd]3 - LVIDd3)} + 0.6. Concentric hypertrophy was RWT \u3e 0.42 and LV mass \u3e95 kg/m2 in females or \u3e 115 kg/m2 in males. The same cut-offs were used for 2D and 3D echocardiography. Results: Echocardiographic findings for a total number of 154 patients in the study were investigated. There was a weak positive correlation between 2D and 3D LV mass indices (R= 0.534, r2= 0.286, p= 0.001). Seventy patients had 3D EF \u3e=45% with clinical heart failure (HFpEF). Among HFpEF patients, LV hypertrophy (LVH) was present in 74% of patients by 2D echocardiography and 30% by 3D echocardiography (McNemar test p= 0.001). Using 3D echocardiography as the reference, 68% of normal patients were misdiagnosed with LV hypertrophy by 2D echocardiography. Two-thirds of the patients with concentric remodeling by 3D echocardiography were misclassified as having concentric hypertrophy by 2D echocardiography (p=0.001). Conclusion: Adapting necropsy-proven LV mass index cutoffs, 2D over-diagnosed LV hypertrophy through overestimation of the mass, compared to 3D echocardiography. In turn, the majority of HFpEF patients showed no structural hypertrophy of the LV on 3D imaging. This suggests that the majority of patients with HFpEF may qualify for pharmacological prevention to prevent further progression to LV remodeling or LVH

Omecamtiv mecarbil in chronic heart failure with reduced ejection fraction, GALACTIC‐HF: baseline characteristics and comparison with contemporary clinical trials

Aims: The safety and efficacy of the novel selective cardiac myosin activator, omecamtiv mecarbil, in patients with heart failure with reduced ejection fraction (HFrEF) is tested in the Global Approach to Lowering Adverse Cardiac outcomes Through Improving Contractility in Heart Failure (GALACTIC‐HF) trial. Here we describe the baseline characteristics of participants in GALACTIC‐HF and how these compare with other contemporary trials. Methods and Results: Adults with established HFrEF, New York Heart Association functional class (NYHA) ≥ II, EF ≤35%, elevated natriuretic peptides and either current hospitalization for HF or history of hospitalization/ emergency department visit for HF within a year were randomized to either placebo or omecamtiv mecarbil (pharmacokinetic‐guided dosing: 25, 37.5 or 50 mg bid). 8256 patients [male (79%), non‐white (22%), mean age 65 years] were enrolled with a mean EF 27%, ischemic etiology in 54%, NYHA II 53% and III/IV 47%, and median NT‐proBNP 1971 pg/mL. HF therapies at baseline were among the most effectively employed in contemporary HF trials. GALACTIC‐HF randomized patients representative of recent HF registries and trials with substantial numbers of patients also having characteristics understudied in previous trials including more from North America (n = 1386), enrolled as inpatients (n = 2084), systolic blood pressure &lt; 100 mmHg (n = 1127), estimated glomerular filtration rate &lt; 30 mL/min/1.73 m2 (n = 528), and treated with sacubitril‐valsartan at baseline (n = 1594). Conclusions: GALACTIC‐HF enrolled a well‐treated, high‐risk population from both inpatient and outpatient settings, which will provide a definitive evaluation of the efficacy and safety of this novel therapy, as well as informing its potential future implementation

Systolic and diastolic function in chronic spinal cord injury.

Individuals with spinal cord injury develop cardiovascular disease more than age-matched, non-injured cohorts. However, progression of systolic and diastolic dysfunction into cardiovascular disease after spinal cord injury is not well described. We sought to investigate the relationship between systolic and diastolic function in chronic spinal cord injury to describe how biological sex, level, severity, and duration of injury correlate with structural changes in the left ventricle. Individuals with chronic spinal cord injury participated in this study (n = 70). Registered diagnostic cardiac sonographers used cardiac ultrasound to measure dimensions, mass, and systolic and diastolic function of the left ventricle. We found no significant relationship to severity or duration of injury with left ventricle measurements, systolic function outcome, or diastolic function outcome. Moreover, nearly all outcomes measured were within the American Society of Echocardiography-defined healthy range. Similar to non-injured individuals, when indexed by body surface area (BSA) left ventricle mass [-14 (5) g/m2, p < .01], end diastolic volume [-6 (3) mL/m2, p < .05], and end systolic volume [-4 (1) mL/m2, p < .01] were significantly decreased in women compared with men. Likewise, diastolic function outcomes significantly worsened with age: E-wave velocity [-5 (2), p < .01], E/A ratio [-0.23 (0.08), p < .01], and e' velocity [lateral: -1.5 (0.3) cm/s, p < .001; septal: -0.9 (0.2), p < .001] decreased with age while A-wave velocity [5 (1) cm/s, p < .001] and isovolumic relaxation time [6 (3) ms, p < .05] increased with age. Women demonstrated significantly decreased cardiac size and volumes compared with men, but there was no biological relationship to dysfunction. Moreover, individuals were within the range of ASE-defined healthy values with no evidence of systolic or diastolic function and no meaningful relationship to level, severity, or duration of injury. Decreases to left ventricular dimensions and mass seen in spinal cord injury may result from adaptation rather than maladaptive myocardial remodeling, and increased incidence of cardiovascular disease may be related to modifiable risk factors