title: Abdominal obesity and hypertension: a double burden to the heart.
abstract: Abdominal obesity (AO) is strongly associated with increased cardiovascular risk in hypertensives. Visceral adipose tissue has an important part in water retention, the sympathetic nervous system and renin-angiotensin-aldosterone system activation, which may influence central and systemic hemodynamics. The aim of this study was to estimate the relationship between AO and the hemodynamic profile of patients with arterial hypertension (AH). The clinical evaluation of 144 hypertensives included the following: (1) echocardiographic assessment of the left ventricular ejection fraction (LVEF), the global longitudinal systolic strain (GLSS) and diastolic function (E/A-phase ratio of mitral flow early (E) and late (A) and E/e'-ratio of early mitral flow and mitral septal annulus early diastolic velocity (e')); (2) the applanation tonometry including the central pulse pressure (CPP) and augmentation index (AI); and (3) the impedance cardiography, acceleration index (ACI), velocity index (VI), systemic vascular resistance index (SVRI) and total artery compliance (TAC). Obese hypertensives in comparison with non-obese ones were characterized with the following values: (1) lower echocardiographic (GLSS: -17.2±2.5% vs. -19.0±2.8%, P=0.0002) and impedance indices of left ventricular performance (VI: 44.8±12.4 vs. 51.6±14.2 × 1000*Ω* s(-1), P=0.006; ACI: 66.7±27.8 vs. 79.1±31.2 100*Ω* s(-)(2), P=0.003) and (2) worse diastolic function (e': 9.08±2.69 vs. 10.39±2.34 cm*s(-1), P=0.003; E/e': 7.54±1.81 vs. 6.74±1.40, P=0.007; E/A: 1.02±0.34 vs. 1.15±0.33, P=0.008). No relevant differences for gender, age, blood pressure, heart rate, LVEF, SVRI, TAC, CPP and AI were identified. AH and AO have overlapping effects on cardiovascular hemodynamics. At the early asymptomatic stage, this overlap is exhibited in the impaired cardiac function.
authors.affiliation: Department of Cardiology and Internal Diseases, Military Institute of Medicine, Warsaw, Poland.
authors.forename: Paweł
authors.initials: P
authors.lastname: Krzesiński
authors.affiliation: Department of Cardiology and Internal Diseases, Military Institute of Medicine, Warsaw, Poland.
authors.forename: Adam
authors.initials: A
authors.lastname: Stańczyk
authors.affiliation: Department of Cardiology and Internal Diseases, Military Institute of Medicine, Warsaw, Poland.
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Piotrowicz
authors.affiliation: Department of Cardiology and Internal Diseases, Military Institute of Medicine, Warsaw, Poland.
authors.forename: Grzegorz
authors.initials: G
authors.lastname: Gielerak
authors.affiliation: Department of Cardiology and Internal Diseases, Military Institute of Medicine, Warsaw, Poland.
authors.forename: Beata
authors.initials: B
authors.lastname: Uziębło-Zyczkowska
authors.affiliation: Department of Cardiology and Internal Diseases, Military Institute of Medicine, Warsaw, Poland.
authors.forename: Andrzej
authors.initials: A
authors.lastname: Skrobowski
mesh_terms: D000328:Adult; D001794:Blood Pressure / Q000502:physiology; D004452:Echocardiography; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D056128:Obesity, Abdominal / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology*; D012307:Risk Factors; D013318:Stroke Volume; D014655:Vascular Resistance / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*