Background Increased intracardiac thrombus formation in light-chain cardiac amyloidosis (AL-CA) has been associated with thrombotic events such as stroke and high rates of mortality and morbidity. Case summary A 51-year-old man was admitted to the emergency department with a sudden change in consciousness. His emergency brain magnetic resonance imaging showed two foci of cerebral infarction on bilateral temporal lobes. His electrocardiogram displayed a normal sinus rhythm with low QRS voltage. Transthoracic echocardiography showed concentric thickened ventricles, dilatation of both atria, a left ventricular ejection fraction of 53% and a grade-three diastolic dysfunction. The bull-eye plot on speckle tracking echocardiography displayed a distinctive apical sparing pattern. Serum free immunoglobulin analysis showed increased lambda free light chains (295.59 milligrams/liter) with a reduced kappa/lambda ratio (0.08). Light-chain amyloidosis was subsequently confirmed by examining histology of the abdominal fat-pad tissue. On transesophageal echocardiography (TEE), an elongated static thrombus and a mobile bouncing oval thrombus were found on the left and right atrial appendages, respectively. Atrial thrombi were managed with a full dose of dabigatran of 150 milligrams twice daily, which achieved a total resolution after 2 months on follow-up TEE. Discussion Complicating intracardiac thrombosis has been considered one of the major contributions of death in cardiac amyloidosis. Transesophageal echocardiography should be established to aid in the detection and management of atrial thrombus in AL-CA.
Background: Several studies have investigated Galectin-3 as a promising biomarker for predicting the short-term and long-term mortality of patients with acute heart failure. This study aimed to examine the usefulness of plasma galectin-3 at the time of admission in predicting long-term mortality in Vietnamese patients with acute heart failure (AHF). Methods: We carried out a cohort study including 117 patients consecutively diagnosed with acute heart failure in a single cardiology department. Plasma galectin-3 and other biomarkers were measured at the time of admission. The patient’s clinical and analytical characteristics were recorded. The main endpoint was one-year all-cause mortality. Results: There were six patients (5%) lost to follow-up and 59 patients (53.2%) reaching primary outcome within one year after hospital admission. The median plasma galectin-3 level (ng/mL) in patients with acute heart failure was 34.6 (26.7 – 44.1). Plasma galectin-3 in the alive group was significantly higher than that in the deceased group at one-year follow-up. In predicting one-year all-cause mortality, galectin-3 had an area under the curve (AUC) of 0.71 (95% confidence interval (CI), 0.62 – 0.81) representing a good prognostic factor while brain natriuretic peptide (BNP) and troponin I were inferior to galectin-3 with an AUC of 0.69 (95% CI, 0.59 – 0.79) and 0.63 (95% CI, 0.53 – 0.74), respectively. The optimal cut-off value for galectin-3 was 40.75 ng/mL with a sensitivity of 50.1% and a specificity of 88.5%. In a multivariate model, patients with galectin-3 levels > 40.75 ng/mL had a hazard ratio (HR) of 2.8 (95% CI, 1.5 – 5; p = 0.001). The best prediction model was the combined model of galectin-3 and BNP, yielding an AUC of 0.78 (95% CI, 0.70 – 0.86; p < 0.001). Conclusions: Our study suggested that galectin-3 levels could predict long-term all-cause mortality in patients with acute heart failure with a good prognostic capacity. Combining galectin-3 and BNP could bring up a better risk-stratification.
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