589 CLINICAL VALIDATION OF A NEW 3D STRAIN METHOLOGY FOR THE ASSESSMENT OF LEFT VENTRICULAR DEFORMATION IMAGING IN HYPERTENSIVE PATIENTS

Background: Atrial fibrillation (AF) is the most frequently encountered cardiac arrhythmia globally and substantially increases the risk for thromboembolic disease. Albeit, 20% of all cases of AF remain undiagnosed. On the other hand, hypertension amplifies the risk for both AF occurrences through hemodynamic and non-hemodynamic mechanisms and cerebrovascular ischemia. Under this prism, prompt diagnosis of undetected AF in hypertensive patients is of pivotal importance. Method: We conducted a review of the literature for studies with biomarkers that could be used in AF diagnosis as well as in predicting the transition of paroxysmal AF to sustained AF, especially in hypertensive patients. Results: Potential biomarkers for AF can be broadly categorized into electrophysiological, morphological and molecular markers that reflect the underlying mechanisms of adverse atrial remodeling. We focused on P-wave duration and dispersion as electrophysiological markers, and left atrial (LA) and LA appendage size, atrial fibrosis, left ventricular hypertrophy and aortic stiffness as structural biomarkers, respectively. The heterogeneous group of molecular biomarkers of AF encompasses products of the neurohormonal cascade, including NT-pro BNP, BNP, MR-pro ANP, polymorphisms of the ACE and convertases such as corin and furin. In addition, soluble biomarkers of inflammation (i.e. CRP, IL-6) and fibrosis (i.e. TGF-1 and matrix metalloproteinases) were assessed for predicting AF. Conclusion: The reviewed individual biomarkers might be a valuable addition to current diagnostic tools but the ideal candidate is expected to combine multiple indices of atrial remodeling in order to effectively detect both AF and adverse characteristics of high risk patients with hypertension.

Download Full-text

Left Ventricular Filling Profiles in Young White-Coat Hypertensive Patients Without Hypertrophy

Hypertension ◽

10.1161/01.hyp.30.3.746 ◽

1997 ◽

Vol 30 (3) ◽

pp. 746-752 ◽

Cited By ~ 8

Author(s):

Nen-Chung Chang ◽

Zhi-Yang Lai ◽

Paul Chan ◽

Tze-Che Wang

Keyword(s):

Left Ventricular ◽

Left Ventricular Filling ◽

White Coat ◽

Hypertensive Patients ◽

Ventricular Filling

Download Full-text

Common Carotid Artery Stiffness and Patterns of Left Ventricular Hypertrophy in Hypertensive Patients

Hypertension ◽

10.1161/01.hyp.25.4.651 ◽

1995 ◽

Vol 25 (4) ◽

pp. 651-659 ◽

Cited By ~ 99

Author(s):

Pierre Boutouyrie ◽

Stéphane Laurent ◽

Xavier Girerd ◽

Athanase Benetos ◽

Patrick Lacolley ◽

...

Keyword(s):

Carotid Artery ◽

Left Ventricular Hypertrophy ◽

Common Carotid Artery ◽

Ventricular Hypertrophy ◽

Left Ventricular ◽

Hypertensive Patients ◽

Artery Stiffness

Download Full-text

Effects of irbesartan on phenotypic alterations in monocytes and the inflammatory status of hypertensive patients with left ventricular hypertrophy

BMC Cardiovascular Disorders ◽

10.1186/s12872-021-02004-7 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Jingsi Zhang ◽

Lina Yang ◽

Yanchun Ding

Keyword(s):

Ventricular Hypertrophy ◽

Target Organ Damage ◽

Organ Damage ◽

Left Ventricular ◽

Target Organ ◽

Dependent Manner ◽

Concentration Dependent Manner ◽

Hypertensive Patients ◽

Inflammatory Status ◽

Tnf Α

Abstract Background Circulating monocytes and tissue macrophages play complex roles in the pathogenesis of hypertension and the resulting target organ damage. In this study, we observed alterations in the monocyte phenotype and inflammatory state of hypertensive patients with left ventricular hypertrophy (LVH) and studied the effects of irbesartan in these patients. This study might reveal a novel mechanism by which irbesartan alleviates LVH, and it could provide new targets for the prevention and treatment of hypertensive target organ damage. Methods CD163 and CD206 expression on monocytes and IL-10 and TNF-α levels in the serum of hypertensive patients with or without LVH and of healthy volunteers were detected. Furthermore, we treated monocytes from the LVH group with different concentrations of irbesartan, and then, CD163, CD206, IL-10 and TNF-α expression was detected. Results We found, for the first time, that the expression of CD163, CD206 and IL-10 in the LVH group was lower than that in the non-LVH group and healthy control group, but the TNF-α level in the LVH group was significantly higher. Irbesartan upregulated the expression of CD163 and CD206 in hypertensive patients with LVH in a concentration-dependent manner. Irbesartan also increased the expression of IL-10 and inhibited the expression of TNF-α in monocyte culture supernatants in a concentration-dependent manner. Conclusions Our data suggest that inflammation was activated in hypertensive patients with LVH and that the monocyte phenotype was mainly proinflammatory. The expression of proinflammatory factors increased while the expression of anti-inflammatory factors decreased. Irbesartan could alter the monocyte phenotype and inflammatory status in hypertensive patients with LVH. This previously unknown mechanism may explain how irbesartan alleviates LVH. Trail registration The study protocols were approved by the Ethical Committee of the Second Affiliated Hospital of Dalian Medical University. Each patient signed the informed consent form.

Download Full-text