The value of global longitudinal strain and galectin-3 for predicting cardiovascular events in patients with severe aortic stenosis.

AIMS: Left ventricular global longitudinal strain (GLS) was shown to predict outcomes after valve replacement in patients with aortic stenosis (AS). In the current study, we aimed to test the combined use of GLS and a marker of fibrosis - Galectin-3 - for predicting major cardiovascular adverse events (MACEs) in patients with severe AS. MATERIALS AND METHODS: We conducted a prospective study on 42 patients with severe AS and 42 volunteers. Patient evaluation included biochemistry tests, electrocardiogram, 24-hour Holter monitoring, the 6-minute walk test, and echocardiography. Outcomes of AS patients were defined as the composite of MACEs - sudden cardiac death, non-fatal myocardial infarction, sustained ventricular arrhythmias,atrial arrhythmias, and hospitalization for heart failure. RESULTS: Patients with severe AS had lower GLS, and increased levels of both biomarkers compared to the control group. Both biomarkers correlated to echocardiographic parameters such as left ventricular (LV) mass index, relative wall thickness, GLS, as well as with the 6-minute walk test distance, and glomerular filtration rate (eGFR). GLS and NT-proBNP predicted MACEs reasonably well, while Galectin-3 did not, after adjustments for confounding factors. Kaplan-Meier analysis showed that the probability of freedom from MACEs was significant in patients who exhibited lower GLS [HR 2.73 (95% CI 1.01-7.53), p<0.05] and higher levels of NT-proBNP [HR 5.22 (95% CI 1.85- 14.51), p=0.001]. CONCLUSIONS: Among tested parameters, GLS and NT-proBNP were the most reliable predictors of MACEs in patients with severe AS, while Galectin-3 performed more poorly.

Tuberculous constrictive pericarditis complicated with tuberculous mediastinitis - case report.

Constrictive pericarditis is a rare and severe disease. A 37-year-old patient was admitted in the hospital for dyspnea, precordial pain, right-sided cardiac failure. Chest X-ray showed cardiac enlargement and an opacity suggestive for pleural effusion. Echocardiography revealed an adhesive-effusive-constrictive pericarditis, a very thickened pericardium and bilateral pleural effusion. After a pericardiectomy done to restore cardiac compensation and to identify etiological factors, a tuberculous pericarditis (TBP) was diagnosed. After surgery and starting anti-TB treatment, the patient presented altered clinical status, dyspnea, dry cough, fever and delayed callus formation at sternum level. Thoracic scan revealed mediastinal air collections, pericarditis and pleurisy. Thus, the TBP diagnosis was extended to mediastinal TB and anti-TB therapy was continued. After four months of treatment, another thoracic scan showed disappearance of the mediastinal air-leakage bubbles, multiple new micronodules in both lungs and lymph nodes of up to 15 mm; also increasing pericardial and pleural effusions. This case was interpreted as a TB treatment failure situation. A retreatment regimen was started, resulting in a slow favorable outcome. Pericardial TB is a rare condition, usually with delayed diagnosis and poor treatment benefits. Whenever possible, earlier diagnostic can contribute to better management of these cases.