A1 Refereed original research article in a scientific journal

Coronary flow reserve in young men with familial combined hyperlipidemia




AuthorsPitkanen OP, Nuutila P, Raitakari OT, Porkka K, Iida H, Nuotio I, Ronnemaa T, Viikari J, Taskinen MR, Ehnholm C, Knuuti J

PublisherLIPPINCOTT WILLIAMS & WILKINS

Publication year1999

Journal: Circulation

Journal name in sourceCIRCULATION

Journal acronymCIRCULATION

Volume99

Issue13

First page 1678

Last page1684

Number of pages7

ISSN0009-7322

DOIhttps://doi.org/10.1161/01.CIR.99.13.1678


Abstract
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 O-15-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) bad lower now during hyperemia (2.5+/-1.2versus 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 phenotypes IIB.



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