BackgroundChronic 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.ObjectiveTo 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.MethodsThirty-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 ± 6% in VHD patients, while in LVAD patients the mean apical myocardial fibrosis rate was 38 ± 9%. In VHD patients, fibrosis was also present in the lateral wall (9 ± 4%) and in the septum (9 ± 6%).ConclusionOur 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.

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. Twentythree 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±6% in VHD patients, while in LVAD patients the mean apical myocardial fibrosis rate was 38±9%. In VHD patients, fibrosis was also present in the lateral wall (9±4%) and in the septum (9±6%). 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.

Purpose. Amiodarone is a source of excess iodine that may induce thyroid dysfunction. The aim of the present analysis was to evaluate the magnitude and time course of 24-hr urinary iodine excretion and its potential relationship with thyroid disorders in patients on antiarrhythmic prophylaxis with amiodarone. Methods. 24-hr urinary iodine excretion and thyroid function were evaluated in 67 patients on chronic amiodarone therapy. All patients were clinically and biochemically euthyroid before starting treatment and were followed up by 6-month measurements of 24-hr urinary iodine excretion and plasma TSH levels. Results. Since amiodarone initiation, 20 patients developed thyroid dysfunction (14 hypothyroidism, 3 subclinical hypothyroidism, 3 hyperthyroidism). No differences were observed in terms of treatment length or urinary iodine levels between patients remaining euthyroid and those developing thyroid dysfunction: urinary iodine in the euthyroid group was 8094 µg/24h (IQR 4082-10766) vs 10851 µg/24h (IQR 8529-12804) in the thyroid dysfunction group at 6 months (p = 0.176) and 8651 µg/24h (IQR 6924-11574) vs 8551 µg/24h([IQR 4916-13580) (p = 0.886) at one year from amiodarone initiation. The occurrence of thyroid dysfunction was equally distributed among patients taking amiodarone for more than one year versus those under treatment for less than one year. Upon amiodarone withdrawal, normal range of urinary iodine was achieved after a mean time of 15.2 ± 7.7 months. Conclusion. These results suggest no correlation between 24-hr urinary iodine excretion and thyroid dysfunction in patients on amiodarone therapy. Thyroid disorders following amiodarone administration likely depend on the individual predisposition to iodine load.