Prevalence and prognosis of structural heart disease among athletes with negative T waves and normal transthoracic echocardiography.

INTRODUCTION: The aim of the present study was to evaluate the prevalence and prognosis of structural heart disease (SHD) among competitive athletes with negative T waves without pathological findings at transthoracic echocardiogram. METHODS: From a prospective register of 450 athletes consecutively evaluated during a second-level cardiological examination, we retrospectively identified all subjects with the following inclusion criteria: (1) not previously known cardiovascular disease; (2) negative T waves in leads other than V1-V2; (3) normal transthoracic echocardiogram. Patients underwent cardiac MRI and CT. The primary endpoint was the diagnosis of definite SHD after multimodality imaging evaluation. A follow-up was collected for a combined end-point of sudden death, resuscitated sudden cardiac death and hospitalization for any cardiovascular causes. RESULTS: A total of 55 competitive athletes were finally enrolled (50 males, 90%) with a mean age of 27.5 ± 14.1 years. Among the population enrolled 16 (29.1%) athletes had a final diagnosis of SHD. At multivariate analysis, only deep negative T waves remained statistically significant [OR (95% CI) 7.81 (1.24-49.08), p = 0.0285]. Contemporary identification of deep negative T waves and complex arrhythmias in the same patients appeared to have an incremental diagnostic value. No events were collected at 49.3 ± 12.3 months of follow-up. CONCLUSIONS: In a cohort of athletes with negative T waves at ECG, cardiac MRI (and selected use of cardiac CT) enabled the identification of 16 (29.1%) subjects with SHD despite normal transthoracic echocardiography. Deep negative T waves and complex ventricular arrhythmias were the only clinical characteristic associated with SHD diagnosis.

Myocardial fibrosis in asymptomatic patients undergoing surgery for mitral and aortic valve regurgitation.

BACKGROUND: Chronic heart valve regurgitation induces left ventricular (LV) volume overload, leading to the development of hypertrophy and progressive dilatation of the ventricle to maintain physiological cardiac output. In order to prevent potential irreversible LV structural changes, the identification of the best timing for treatment is pivotal. OBJECTIVE: To assess the presence and extent of fibrosis in myocardial tissue in asymptomatic patients with valvular heart disease (VHD) and preserved LV dimensions and function undergoing cardiac surgery. METHODS: Thirty-nine patients were enrolled. Sixteen patients were affected by aortic or mitral regurgitation: they were all asymptomatic, undergoing valve surgery according to VHD European Society of Cardiology guidelines. Twenty-three patients with end-stage nonischemic dilated cardiomyopathy (DCM) and severe LV dysfunction undergoing cardiac surgery for implantation of a durable left ventricular assist device (LVAD) served as controls. During surgery, VHD patients underwent three myocardial biopsies at the level of the septum, the lateral wall and LV apex, while in LVAD patients the coring of the apex of the LV was used. For both groups, the tissue samples were analyzed on one section corresponding to the apical area. All slides were stained with hematoxylin and eosin and Masson's trichrome staining and further digitalized. The degree of fibrosis was then calculated as a percentage of the total area. RESULTS: Of 39 patients, 23 met the inclusion criteria: 12 had mitral or aortic insufficiency with a preserved ejection fraction and 11 had idiopathic dilated cardiomyopathy. Quantitative analysis of apical sections revealed a myocardial fibrosis amount of 10 ±â€Š6% in VHD patients, while in LVAD patients the mean apical myocardial fibrosis rate was 38 ±â€Š9%. In VHD patients, fibrosis was also present in the lateral wall (9 ±â€Š4%) and in the septum (9 ±â€Š6%). CONCLUSION: Our case series study highlights the presence of tissue remodeling with fibrosis in asymptomatic patients with VHD and preserved LV function. According to our results, myocardial fibrosis is present at an early stage of the disease, well before developing detectable LV dysfunction and symptoms. Since the relationship between the progressive magnitude of myocardial fibrosis and potential prognostic implications are not yet defined, further studies on this topic are warranted.

Vasostatin-1 as a potential novel circulating biomarker in patients with chronic systolic heart failure: A pilot study.

BACKGROUND AND AIMS: Previous studies have shown that circulating chromogranin A (CgA) increases in patients with chronic systolic heart failure (HF). Aim of the present study is to evaluate the potential role of circulating vasostatin-1 (VS-1), a cardioregulatory fragment of CgA, as prognostic marker in patients with chronic HF. MATERIALS AND METHODS: The plasma levels of CgA and VS-1 were determined in 80 patients with chronic systolic HF. Patients were followed-up to evaluate the occurrence of cardiovascular (CV) events. RESULTS: CgA and VS-1 plasma levels were significantly higher in patients with CV events at follow-up. VS-1, but not CgA, was associated to NT-proBNP. No significant association of CgA and VS-1 with left ventricular ejection fraction (LVEF) was observed. CgA, NT-proBNP and age, but not VS-1, were independent predictors of CV events. CONCLUSION: In patients with chronic systolic HF those who experienced CV events had higher levels of VS-1 and CgA. Given its established effect on cardiac cells, the association of VS-1 levels with NT-proBNP levels but not with LVEF, suggests that this fragment might provide complementary information to NT-proBNP and CgA in HF patients.