Association between vascular dysfunction and reduced myocardial flow reserve in patients with hypertension: A LIFE substudy
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Association between vascular dysfunction and reduced myocardial flow reserve in patients with hypertension : A LIFE substudy. / Olsen, M. H.; Wachtell, K.; Meyer, C.; Hove, J. D.; Palmieri, V.; Dige-Petersen, H.; Rokkedal, J.; Hesse, B.; Ibsen, H.
I: Journal of Human Hypertension, Bind 18, Nr. 6, 06.2004, s. 445-452.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Association between vascular dysfunction and reduced myocardial flow reserve in patients with hypertension
T2 - A LIFE substudy
AU - Olsen, M. H.
AU - Wachtell, K.
AU - Meyer, C.
AU - Hove, J. D.
AU - Palmieri, V.
AU - Dige-Petersen, H.
AU - Rokkedal, J.
AU - Hesse, B.
AU - Ibsen, H.
N1 - Funding Information: We thank Paulette A Lyle for assistance with preparation of the manuscript. This work was supported in part by Grants from Merck & Co., Inc., Copenhagen, Denmark, and The Danish Medical Association Research Fund, Copenhagen, Denmark, as part of the LIFE ICARUS substudy.
PY - 2004/6
Y1 - 2004/6
N2 - Impaired myocardial flow reserve (MFR) has been demonstrated in hypertension, and has been associated with peripheral vascular changes. We investigated whether MFR was impaired and associated with structural and/or functional vascular changes in hypertensive patients without evidence of coronary artery disease (CAD). We measured left ventricular (LV) mass index by echocardiography and MFR by positron emission tomography in 33 unmedicated, hypertensive patients with electrocardiographic LV hypertrophy without CAD, and 15 age- and gender-matched normotensive subjects. We also measured 24-h ambulatory blood pressure, minimal forearm vascular resistance (MFVR) by plethysmography, media:lumen ratio in isolated, subcutaneous resistance arteries by myography, intima-media cross-sectional area of the common carotid artery, and flow-mediated (FMD) and nitroglycerin-induced dilatation (NID) of the brachial artery by ultrasound. Compared to the controls, the patients had impaired MFR (2.4 (95% CI 1.95-2.8) vs 3.4 (2.7-4.2), P<0.01) due to increased resting myocardial blood flow (MBF) (0.82 (0.73-0.91) vs 0.65 (0.56-0.75) ml/g min), and decreased dipyridamole-stimulated MBF (1.80 (1.55-2.1) vs 2.3 (1.80-2.8) ml/gmin, both P<0.05). The difference in resting MBF disappeared (80 (74-87) vs 86 (74-97) μl/kg mmHg, NS) when normalized for blood pressure and heart rate. MFR correlated negatively to median 24-h systolic blood pressure (r = -0.50, P < 0.01) as well as to LV mass index (r = -0.45, P < 0.05) and MFVR in men (r = -0.47, P < 0.05), and positively to FMD (r = 0.44, P < 0.05) and NID (r = 0.40, P < 0.05). Hypertensive patients with electrocardiographic LV hypertrophy without CAD had impaired MFR associated with cardiovascular hypertrophy and vasodilatory dysfunction. This suggests that MFR is impaired by LV hypertrophy and structural/functional vascular damage in the coronary and noncoronary circulation.
AB - Impaired myocardial flow reserve (MFR) has been demonstrated in hypertension, and has been associated with peripheral vascular changes. We investigated whether MFR was impaired and associated with structural and/or functional vascular changes in hypertensive patients without evidence of coronary artery disease (CAD). We measured left ventricular (LV) mass index by echocardiography and MFR by positron emission tomography in 33 unmedicated, hypertensive patients with electrocardiographic LV hypertrophy without CAD, and 15 age- and gender-matched normotensive subjects. We also measured 24-h ambulatory blood pressure, minimal forearm vascular resistance (MFVR) by plethysmography, media:lumen ratio in isolated, subcutaneous resistance arteries by myography, intima-media cross-sectional area of the common carotid artery, and flow-mediated (FMD) and nitroglycerin-induced dilatation (NID) of the brachial artery by ultrasound. Compared to the controls, the patients had impaired MFR (2.4 (95% CI 1.95-2.8) vs 3.4 (2.7-4.2), P<0.01) due to increased resting myocardial blood flow (MBF) (0.82 (0.73-0.91) vs 0.65 (0.56-0.75) ml/g min), and decreased dipyridamole-stimulated MBF (1.80 (1.55-2.1) vs 2.3 (1.80-2.8) ml/gmin, both P<0.05). The difference in resting MBF disappeared (80 (74-87) vs 86 (74-97) μl/kg mmHg, NS) when normalized for blood pressure and heart rate. MFR correlated negatively to median 24-h systolic blood pressure (r = -0.50, P < 0.01) as well as to LV mass index (r = -0.45, P < 0.05) and MFVR in men (r = -0.47, P < 0.05), and positively to FMD (r = 0.44, P < 0.05) and NID (r = 0.40, P < 0.05). Hypertensive patients with electrocardiographic LV hypertrophy without CAD had impaired MFR associated with cardiovascular hypertrophy and vasodilatory dysfunction. This suggests that MFR is impaired by LV hypertrophy and structural/functional vascular damage in the coronary and noncoronary circulation.
KW - Carotid arteries
KW - Endothelium
KW - Hypertrophy
UR - http://www.scopus.com/inward/record.url?scp=2942711717&partnerID=8YFLogxK
U2 - 10.1038/sj.jhh.1001716
DO - 10.1038/sj.jhh.1001716
M3 - Journal article
C2 - 15014539
AN - SCOPUS:2942711717
VL - 18
SP - 445
EP - 452
JO - Journal of Human Hypertension
JF - Journal of Human Hypertension
SN - 0950-9240
IS - 6
ER -
ID: 308766337