Vasodilatory capacity and vascular structure in long-standing hypertension: a LIFE substudy

• Published in: American journal of hypertension Vol. 15; no. 5; pp. 398 - 404
• Main Authors: Olsen, Michael H, Wachtell, Kristian, Aalkjaer, Christian, Dige-Petersen, Harriet, Rokkedal, Jens, Ibsen, Hans
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01-05-2002; Oxford University Press; Elsevier Science
• Subjects: Arterial hypertension. Arterial hypotension; Biological and medical sciences; Blood and lymphatic vessels; Cardiology. Vascular system; Clinical manifestations. Epidemiology. Investigative techniques. Etiology; endothelial dysfunction; flow-mediated dilatation; Hypertension; Medical sciences; nitroglycerin; vascular hypertrophy; Hypertension; vascular hypertrophy; flow-mediated dilatation; nitroglycerin; endothelial dysfunction; Human; Systolic pressure; Prognosis; Pathogenesis; Dysfunction; Heart disease; Cardiovascular disease; Vasodilation; Left ventricle; Endothelium; Hypertrophy
• ISSN: 0895-7061; 1879-1905; 1941-7225
• DOI: 10.1016/S0895-7061(01)02338-X

Flow-mediated dilatation (FMD), which is considered a measure of endothelial function, has been found impaired in hypertension. However, it is unclear whether this impairment is explained solely by endothelial dysfunction, or whether it is associated with structural vascular changes and reduced vasodilatory capacity.
In 42 unmedicated patients with hypertension and electrocardiographic left ventricular hypertrophy, we measured the following: 24-h ambulatory blood pressure (BP), minimal forearm vascular resistance (MFVR) by plethysmography, intima-media cross-sectional area of the common carotid arteries (IMA), FMD, and nitroglycerin-induced dilatation (NID) in the brachial artery by ultrasound.
We found that FMD was correlated positively with NID (r = 0.38,
P < .05). However, FMD as well as NID correlated negatively to 24-h systolic BP (r = −0.41,
P = .01 and r = −0.52,
P = .001), IMA/height (r = −0.41,
P < .01 and r = −0.53,
P < .001) and MFVR
men (r = −0.44,
P < .05 and r = −0.42,
P < .05).
Low FMD as well as low NID were related in parallel to high systolic BP and to the severity of vascular changes in different vascular beds, suggesting that elevated BP load in hypertension induces parallel abnormalities in conduit artery structure and overall vasodilatory capacity. Therefore, the decrease in FMD observed in severe hypertension may be caused by endothelial dysfunction as well as by structural vascular changes, suggesting difficulties in interpreting FMD solely as a measure of endothelial dysfunction in hypertensive patients with left ventricular hypertrophy.