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 tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Olsen, MH, Wachtell, K, Meyer, C, Hove, JD, Palmieri, V, Dige-Petersen, H, Rokkedal, J, Hesse, B & Ibsen, H 2004, 'Association between vascular dysfunction and reduced myocardial flow reserve in patients with hypertension: A LIFE substudy', Journal of Human Hypertension, bind 18, nr. 6, s. 445-452. https://doi.org/10.1038/sj.jhh.1001716

APA

Olsen, M. H., Wachtell, K., Meyer, C., Hove, J. D., Palmieri, V., Dige-Petersen, H., Rokkedal, J., Hesse, B., & Ibsen, H. (2004). Association between vascular dysfunction and reduced myocardial flow reserve in patients with hypertension: A LIFE substudy. Journal of Human Hypertension, 18(6), 445-452. https://doi.org/10.1038/sj.jhh.1001716

Vancouver

Olsen MH, Wachtell K, Meyer C, Hove JD, Palmieri V, Dige-Petersen H o.a. Association between vascular dysfunction and reduced myocardial flow reserve in patients with hypertension: A LIFE substudy. Journal of Human Hypertension. 2004 jun.;18(6):445-452. https://doi.org/10.1038/sj.jhh.1001716

Author

Olsen, M. H. ; Wachtell, K. ; Meyer, C. ; Hove, J. D. ; Palmieri, V. ; Dige-Petersen, H. ; Rokkedal, J. ; Hesse, B. ; Ibsen, H. / Association between vascular dysfunction and reduced myocardial flow reserve in patients with hypertension : A LIFE substudy. I: Journal of Human Hypertension. 2004 ; Bind 18, Nr. 6. s. 445-452.

Bibtex

@article{66902f54c44a406984b80e99858043b9,
title = "Association between vascular dysfunction and reduced myocardial flow reserve in patients with hypertension: A LIFE substudy",
abstract = "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.",
keywords = "Carotid arteries, Endothelium, Hypertrophy",
author = "Olsen, {M. H.} and K. Wachtell and C. Meyer and Hove, {J. D.} and V. Palmieri and H. Dige-Petersen and J. Rokkedal and B. Hesse and H. Ibsen",
note = "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.",
year = "2004",
month = jun,
doi = "10.1038/sj.jhh.1001716",
language = "English",
volume = "18",
pages = "445--452",
journal = "Journal of Human Hypertension",
issn = "0950-9240",
publisher = "nature publishing group",
number = "6",

}

RIS

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