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J Geriatr Cardiol. 2015 Jan;12(1):1-10. doi: 10.11909/j.issn.1671-5411.2015.01.001.

Inflammation and oxidative stress caused by nitric oxide synthase uncoupling might lead to left ventricular diastolic and systolic dysfunction in patients with hypertension.

Author information

1
The Heart and Vascular Center of Semmelweis University, Budapest 1122, Gaál József u. 9, Hungary.
2
3rd Department of Internal Medicine, Semmelweis University, School of Medicine, Budapest 1125, Kútvölgyi út 4, Hungary.
3
Institute of Pathophysiology, Semmelweis University, Budapest 1089, Nagyvárad tér 4, Hungary.
4
Department of Neurology, Kútvölgyi Clinical Group, Semmelweis University, Budapest 1125, Kútvölgyi út 4, Hungary.
5
2nd Department of Medicine, Military Hospital, Budapest 1134, Róbert Károly krt. 44, Hungary.
6
St. Istvan and St. Laszlo Hospital, St. Laszlo Hospital Campus, Hematology and Stem Cell Transplantation Department, Hemostasis Laboratory, Budapest 1097, Gyáli út 5-7, Hungary.
7
First Department of Obstetrics and Gynecology, Semmelweis University, Budapest 1085, Baross u. 27, Hungary.
8
MTA-SE, Lendulet" Hereditary Endocrine Tumors Research Group, Budapest 1051, Széchenyi István tér 9, Hungary.

Abstract

OBJECTIVE:

To investigate the role of oxidative stress, inflammation, hypercoagulability and neuroendocrine activation in the transition of hypertensive heart disease to heart failure with preserved ejection fraction (HFPEF).

METHODS:

We performed echocardiography for 112 patients (≥ 60 years old) with normal EF (18 controls and 94 with hypertension), and determined protein carbonylation (PC), and tetrahydrobiopterin (BH4), C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), fibrinogen, plasminogen activator inhibitor type-I (PAI-I), von Willebrand factor, chromogranin A (cGA) and B-type natriuretic peptide (BNP) levels from their blood samples.

RESULTS:

We found that 40% (38/94) of the patients with hypertension (HT) had no diastolic dysfunction (HTDD-), and 60% (56/94) had diastolic dysfunction (HTDD+). Compared to the controls, both patient groups had increased PC and BH4, TNF-α, PAI-I and BNP levels, while the HTDD+ group had elevated cGA and CRP levels. Decreased atrial and longitudinal left ventricular (LV) systolic and diastolic myocardial deformation (strain and strain rate) was demonstrated in both patient groups versus the control. Patients whose LV diastolic function deteriorated during the follow-up had elevated PC and IL-6 level compared to their own baseline values, and to the respective values of patients whose LV diastolic function remained unchanged. Oxidative stress, inflammation, BNP and PAI-I levels inversely correlated with LV systolic, diastolic and atrial function.

CONCLUSIONS:

In patients with HT and normal EF, the most common HFPEF precursor condition, oxidative stress and inflammation may be responsible for LV systolic, diastolic and atrial dysfunction, which are important determinants of the transition of HT to HFPEF.

KEYWORDS:

Heart failure; Hypertension; Inflammation; Oxidative stress

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