Left atrium volume and function changes during stress in patients with primary mitral regurgitation and preserved left ventricular ejection fraction.

INTRODUCTION: Patients with primary mitral regurgitation (MR) usually remain asymptomatic for a long time due to compensatory mechanisms and an adequate treatment could be delayed. Stress echocardiography and speckle-tracking analysis could help to evaluate impaired left atrium (LA) function before the manifestation of clinically significant myocardial changes in asymptomatic patients with primary MR and preserved left ventricular (LV) ejection fraction (EF). METHODS: This study prospectively enrolled 91 patients with preserved LV EF (≥60%) at rest, of which 60 patients had moderate-to-severe MR and 31 were healthy controls. Rest and stress (bicycle ergometry) echocardiography and speckle-tracking offline analysis were performed. RESULTS: In MR group LA volume indices were higher at rest and during stress, while LA reservoir, conduit, and contractile fractions were decreased (p < .005). LA deformation parameters at rest were similar in both groups. During maximum stress LA conduit, contractile fractions and reservoir strain were lower (p < .05) in patients with MR. Indices of LA volume were related to SPAP at rest and during stress. Higher NT-proBNP concentrations was associated with higher LA volume indices, decreased contractile and reservoir functions during peak stress (p < .05). LA volume indices, LA EF, and filling index at rest could predict exercise-induced pulmonary hypertension (EIPH) (p < .05). CONCLUSIONS: In patients with primary MR and preserved LV EF, LA parameters are related to SPAP and NT-pro-BNP concentration. LA volume indices, LA EF and LA filling index are predictors of EIPH.

Comparative analysis of intracardiac neural structures in the aged rats with essential hypertension.

Persistent arterial hypertension initiates cardiac autonomic imbalance and alters cardiac tissues. Previous studies have shown that neural component contributes to arterial hypertension etiology, maintenance, and progression and leads to brain damage, peripheral neuropathy, and remodeling of intrinsic cardiac neural plexus. Recently, significant structural changes of the intracardiac neural plexus were demonstrated in young prehypertensive and adult hypertensive spontaneously hypertensive rats (SHR), yet structural alterations of intracardiac neural plexus that occur in the aged SHR remain undetermined. Thus, we analyzed the impact of uncontrolled arterial hypertension in old (48-52 weeks) SHR and the age-matched Wistar-Kyoto rats (WKY). Intrinsic cardiac neural plexus was examined using a combination of immunofluorescence confocal microscopy and transmission electron microscopy in cardiac sections and whole-mount preparations. Our findings demonstrate that structural changes of intrinsic cardiac neural plexus caused by arterial hypertension are heterogeneous and may support recent physiological implications about cardiac denervation occurring together with the hyperinnervation of the SHR heart. We conclude that arterial hypertension leads to (i) the decrease of the neuronal body area, the thickness of atrial nerves, the number of myelinated nerve fibers, unmyelinated axon area and cumulative axon area in the nerve, and the density of myocardial nerve fibers, and (ii) the increase in myelinated nerve fiber area and density of neuronal bodies within epicardiac ganglia. Despite neuropathic alterations of myelinated fibers were exposed within intracardiac nerves of both groups, SHR and WKY, we consider that the determined significant changes in structure of intrinsic cardiac neural plexus were predisposed by arterial hypertension.