(Circulation. 1999;99:1678-1684.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Coronary Flow Reserve in Young Men With Familial Combined Hyperlipidemia
From the Departments of Medicine (O.-P.P., P.N., I.N., T.R., J.V.) and Clinical Physiology (O.T.R.) and the Turku PET Centre (J.K.), Turku University, Turku, Finland; National Public Health Institute, Helsinki, Finland (K.P., C.E.); Department of Medicine (M.-R.T.), Helsinki University, Helsinki, Finland; and Research Institute for Brain and Blood Vessels-Akita (H.I.), Akita, Japan.
Correspondence to Professor Juhani Knuuti, Turku PET Centre, c/o Turku University Central Hospital, PO Box 52 FIN-20521 Turku, Finland. E-mail jknuuti{at}utu.fi
Background—Familial combined hyperlipidemia (FCHL) is a common hereditary disorder of lipoprotein metabolism estimated to cause 10% to 20% of premature coronary heart disease. We investigated whether functional abnormalities exist in coronary reactivity in asymptomatic patients with FCHL.
Methods and Results—We studied 21 male FCHL patients (age, 34.8±5.4 years) and a matched group of 21 healthy control subjects. Myocardial blood flow (MBF) was measured at baseline and during dipyridamole-induced hyperemia with PET and 15O-labeled water. The baseline MBF was similar in patients and control subjects (0.79±0.19 versus 0.88±0.20 mL · g-1 · min-1, P=NS). An increase in MBF was seen in both groups after dipyridamole infusion, but MBF at maximal vasodilation was lower in FCHL patients (3.54±1.59 versus 4.54±1.17 mL · g-1 · min-1, P=0.025). The difference in coronary flow reserve (CFR) was not statistically significant (4.7±2.2 versus 5.3±1.6, P=NS, patients versus control subjects). Considerable variability in CFR values was detected within the FCHL group. Patients with phenotype IIB (n=8) had lower flow during hyperemia (2.5±1.2 versus 4.2±1.5 mL · g-1 · min-1, P<0.05) and lower CFR (3.4±2.1 versus 5.4±2.0, P<0.05) compared with phenotype IIA (n=13).
Conclusions—Abnormalities in coronary flow regulation exist in young asymptomatic FCHL patients expressing phenotype IIB (characterized by abnormalities in both serum cholesterol and triglyceride concentrations). This is in line with previous observations suggesting that the metabolic abnormalities related to the pathophysiology of FCHL are associated with the phenotype IIB.
Key Words: lipids • blood flow • myocardium • hyperlipidemia, familial combined • tomography
This article has been cited by other articles:
 |
|
 |
|
  M. Juonala, J. S.A. Viikari, T. Ronnemaa, J. Marniemi, A. Jula, B.-M. Loo, and O. T. Raitakari Associations of Dyslipidemias From Childhood to Adulthood With Carotid Intima-Media Thickness, Elasticity, and Brachial Flow-Mediated Dilatation in Adulthood: The Cardiovascular Risk in Young Finns Study Arterioscler. Thromb. Vasc. Biol., May 1, 2008; 28(5): 1012 - 1017. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. O. Kiviniemi, A. Snapir, M. Saraste, J. O. Toikka, O. T. Raitakari, M. Ahotupa, J. J. Hartiala, M. Scheinin, and J. W. Koskenvuo Determinants of coronary flow velocity reserve in healthy young men Am J Physiol Heart Circ Physiol, August 1, 2006; 291(2): H564 - H569. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. C. Brunken, J. K. Perloff, J. Czernin, R. Campisi, S. Purcell, P. D. Miner, J. S. Child, and H. R. Schelbert Myocardial perfusion reserve in adults with cyanotic congenital heart disease Am J Physiol Heart Circ Physiol, November 1, 2005; 289(5): H1798 - H1806. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Wieneke, C. von Birgelen, M. Haude, H. Eggebrecht, S. Mohlenkamp, A. Schmermund, D. Bose, C. Altmann, T. Bartel, and R. Erbel Determinants of coronary blood flow in humans: quantification by intracoronary Doppler and ultrasound J Appl Physiol, March 1, 2005; 98(3): 1076 - 1082. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. A. Kaufmann and P. G. Camici Myocardial Blood Flow Measurement by PET: Technical Aspects and Clinical Applications J. Nucl. Med., January 1, 2005; 46(1): 75 - 88. [Full Text] [PDF]
|
|
|
|
|
|
T. O. Kiviniemi, M. Saraste, J. W. Koskenvuo, K. E. J. Airaksinen, J. O. Toikka, A. Saraste, J. P. Parkka, and J. J. Hartiala Coronary artery diameter can be assessed reliably with transthoracic echocardiography Am J Physiol Heart Circ Physiol, April 1, 2004; 286(4): H1515 - H1520. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Verseyden, S. Meijssen, H. van Dijk, H. Jansen, and M. C. Cabezas Effects of atorvastatin on fasting and postprandial complement component 3 response in familial combined hyperlipidemia J. Lipid Res., November 1, 2003; 44(11): 2100 - 2108. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Paiva, J. Laakso, H. Laine, R. Laaksonen, J. Knuuti, and O. T. Raitakari Plasma asymmetric dimethylarginine and hyperemic myocardial blood flow in young subjects with borderline hypertension or familial hypercholesterolemia J. Am. Coll. Cardiol., October 2, 2002; 40(7): 1241 - 1247. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Meijssen, H. van Dijk, C. Verseyden, D.W. Erkelens, and M. C. Cabezas Delayed and Exaggerated Postprandial Complement Component 3 Response in Familial Combined Hyperlipidemia Arterioscler. Thromb. Vasc. Biol., May 1, 2002; 22(5): 811 - 816. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. E. Hokanson, S. Cheng, J. K. Snell-Bergeon, B. A. Fijal, M. A. Grow, C. Hung, H. A. Erlich, J. Ehrlich, R. H. Eckel, and M. Rewers A Common Promoter Polymorphism in the Hepatic Lipase Gene (LIPC-480C>T) Is Associated With an Increase in Coronary Calcification in Type 1 Diabetes Diabetes, April 1, 2002; 51(4): 1208 - 1213. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Scognamiglio, A. Avogaro, S. Vigili de Kreutzenberg, C. Negut, M. Palisi, E. Bagolin, and A. Tiengo Effects of Treatment With Sulfonylurea Drugs or Insulin on Ischemia-Induced Myocardial Dysfunction in Type 2 Diabetes Diabetes, March 1, 2002; 51(3): 808 - 812. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Verseyden, S. Meijssen, and M. C. Cabezas Postprandial changes of apoB-100 and apoB-48 in TG rich lipoproteins in familial combined hyperlipidemia J. Lipid Res., February 1, 2002; 43(2): 274 - 280. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. H. Buus, M. Bottcher, F. Hermansen, M. Sander, T. T. Nielsen, and M. J. Mulvany Influence of Nitric Oxide Synthase and Adrenergic Inhibition on Adenosine-Induced Myocardial Hyperemia Circulation, November 6, 2001; 104(19): 2305 - 2310. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Tadamura, H. Iida, K. Matsumoto, M. Mamede, S. Kubo, H. Toyoda, T. Shiozaki, T. Mukai, Y. Magata, and J. Konishi Comparison of myocardial blood flow during dobutamine-atropine infusion with that after dipyridamole administration in normal men J. Am. Coll. Cardiol., January 1, 2001; 37(1): 130 - 136. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. A. Kaufmann, T. Gnecchi-Ruscone, K. P. Schafers, T. F. Luscher, and P. G. Camici Low density lipoprotein cholesterol and coronary microvascular dysfunction in hypercholesterolemia J. Am. Coll. Cardiol., July 1, 2000; 36(1): 103 - 109. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Meijssen, M. C. Cabezas, T. B. Twickler, H. Jansen, and D. W. Erkelens In vivo evidence of defective postprandial and postabsorptive free fatty acid metabolism in familial combined hyperlipidemia J. Lipid Res., July 1, 2000; 41(7): 1096 - 1102. [Abstract] [Full Text]
|
|