The value of NT-proBNP in early risk stratification of acute coronary syndromes.

INTRODUCTION: The N-terminal portion of brain natriuretic peptide (NT-proBNP) has been identified as an indicator of prognosis in different cardiovascular diseases. Its role in risk stratification in patients with acute coronary syndromes (ACS) is still under evaluation. OBJECTIVE: We aimed to evaluate the prognostic value of NT-proBNP measured in the first 48 hours after admission due to an acute coronary syndrome. METHODS: Our study included 142 patients (aged 62.7 +/- 12.0 years, 70.4% males) admitted to a cardiology unit with an ACS. All laboratory evaluations were performed in the first 48 hours after admission. The mean follow-up was 200 days. Death from any cause or hospitalization because of a major acute cardiovascular event (whichever occurred first) was defined as the end-point. RESULTS: Cardiovascular risk factors were found in a significant proportion of our sample (hypertension in 56.3%, diabetes mellitus in 38.0%, current or previous smoking in 51.4%, dyslipidemia in 67.6%). Fifty-eight patients had left ventricular systolic dysfunction (LVSD). Serum levels of NT-proBNP were 2174 +/- 4801 pg/ml. Variables associated with event-free survival in univariate analysis were: NT-proBNP (HR 1.007, 95% CI 1.003-1.011, for each 100 pg/ml increment), serum glucose (hazard ratio [HR] 1.007, 95% CI 1.001-1.012, for each 1 mg/dl increment) and maximum cardiac troponin I (cTnI) level (HR 1.005, 95% CI 1.001-1.009, for each 1 ng/ml increment). The white blood count (WBC) was marginally associated with a poor prognosis (HR 1.152, 95% CI 0.994-1.335, for each 1000/mm3 increment). After adjustment for the above variables, age, sex, left ventricular systolic dysfunction, diabetes, coronary anatomy and coronary revascularization using a forward likelihood ratio Cox regression model, NT-proBNP remained the only variable with significant prognostic value (HR 1.007, 95% CI 1.003-1.011, for each 100 pg/ml increment). CONCLUSIONS: These data suggest that NT-proBNP is a strong clinical predictor of prognosis in acute coronary syndromes. Its early measurement should be included in the risk stratification strategy in this setting.

Left ventricular function in adults with muscular dystrophies: genotype-phenotype correlations.

BACKGROUND: Left ventricular dysfunction (LVD) is a clinical manifestation of muscular dystrophy (MD) in adults and an important prognostic factor. However, there is a lack of recommendations concerning cardiac followup of these patients. The aim of this work was to evaluate the prevalence of systolic LVD in adults with MD. METHODS: The patients, referred from a Neuromuscular Diseases Unit, underwent clinical evaluation, ECG and transthoracic echocardiogram. Serum troponin I and NT-proBNP were also evaluated. Systolic LVD was defined by an ejection fraction of <0.45 and/or shortening fraction of <0.25. RESULTS: During a one-year period, we evaluated 24 consecutive patients, 16 men, age 33 +/- 12 years (age at myopathy diagnosis 23 +/- 12 years). They had the following MD: dystrophinopathies--four patients (Duchenne: 1, Becker: 3); Steinert myotonic dystrophy--nine patients; limb-girdle myopathies--six patients; facioscapulohumeral (FSH) myopathies--four patients; and one dysferlinopathy (Miyoshi myopathy). The MD diagnosis, based on clinical and histological criteria, was genetically confirmed in 18 cases (75%). Five patients (20.8%) had thoracic pain, four (16.6%) dyspnea and one a history of syncope. ECG abnormalities were present in 14 cases (58.3%). Stolic LVD or left ventricular remodeling were present in six patients (25%): three with dystrophinopathies, one with limb-girdle myopathy, one with FSH dystrophy and one with myotonic dystrophy. Three patients (12.5%) were diagnosed with heart failure according to the European Society of Cardiology criteria. Three of the five patients with left ventricular dysfunction had elevation of NT-proBNP. One patient with Becker dystrophy had slight elevation of troponin I. In patients with systolic LVD or LV remodeling, the mutations identified were: deletion in intron 1 to exon 49 (one Duchenne MD patient) and deletions in exons 45 to 51 (two Becker MD patients) in the dystrophin gene; deletion of D4Z4 repeats in the DFS locus (4q35) (one patient with FSH MD); and 1300-1500 CTG triplet repeats in the DMPK gene (one patient with myotonic dystrophy). CONCLUSIONS: These results, although preliminary, show that a high percentage of patients with genetically determined skeletal myopathies exhibit cardiac myocyte functional impairment, with severe LVD and heart failure, justifying periodic cardiovascular evaluation. In the future, phenotype-genotype correlations could help to determine the best cardiac surveillance in MD patients.