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Altered myocardial vasodilatation in patients with hypertriglyceridemia in anatomically normal coronary arteries
I Yokoyama1, T Ohtake, S Momomura
1Second Department of Internal Medicine, University of Tokyo, Japan.
Insights
Myocardial vasodilatation (MVD) is reduced in hypertriglyceridemic patients with normal coronary arteries. Elevated triglycerides are an independent factor contributing to this impaired blood flow, even without coronary artery disease.
Area of Science:
- Cardiology
- Vascular Biology
- Medical Imaging
Background:
- Reduced myocardial vasodilatation (MVD) is observed in hypercholesterolemia.
- The impact of hypertriglyceridemia on MVD in the absence of coronary stenosis is not well understood.
Purpose of the Study:
- To investigate whether MVD is impaired in patients with hypertriglyceridemia and normal coronary arteries.
- To clarify the relationship between MVD and lipid levels in these patients.
Main Methods:
- Positron emission tomography (PET) with [13N]ammonia was used to measure myocardial blood flow (MBF) at baseline and during dipyridamole (DP) stress.
- MVD was calculated by comparing DP-induced hyperemic MBF to baseline MBF.
- Participants included hypertriglyceridemic patients (normocholesterolemic and mixed hyperlipidemic) and age-matched controls, all with angiographically normal coronary arteries.
Main Results:
- Baseline MBF was comparable across all groups.
- DP-induced MBF was significantly lower in mixed hyperlipidemic patients compared to controls.
- MVD was significantly reduced in both hypertriglyceridemic groups compared to controls.
- Plasma triglyceride levels showed a significant inverse relationship with MVD.
- Multivariate analysis identified triglyceride level as an independent predictor of reduced MVD.
Conclusions:
- Myocardial vasodilatation is impaired in hypertriglyceridemic individuals with anatomically normal coronary arteries.
- Hypertriglyceridemia is an independent risk factor for reduced MVD, suggesting a direct impact on coronary microvascular function.
Abstract:
Reduced myocardial vasodilatation (MVD) in hypercholesterolemics without overt coronary stenosis has been reported. However, the status of MVD in hypertriglyceridemics has not yet been clarified. The aim of this study was to investigate whether MVD is impaired in patients with hypertriglyceridemia without overt coronary stenosis. Twenty-three hypertriglyceridemics (10 normocholesterolemic hypertriglyceridemics [HTGs] and 13 mixed combined hyperlipidemics [MCHLs]) and 13 age-matched controls were studied. All patients were proven to have more than one normal coronary artery, as diagnosed by coronary angiography, and those segments that were perfused by anatomically normal coronary arteries were used in the study. Myocardial blood flow (MBF) during dipyridamole (DP) loading and baseline MBF were measured by using positron emission tomography and [13N]ammonia, after which MVD was calculated. Baseline MBF (mL.min(-1).100 g(-1)) was comparable among HTG (76.0+/-26.1), MCHL (77.0+/-26.1), and controls (80.3+/-38.5). However, MBF during DP loading was significantly lower in MCHL (159+/-52.5) than in control subjects (292+/-166, P<.01), while it was comparable in HTG (202+/-104) and controls. MVD was significantly reduced in both HTG (2.70+/-1.09, P<.05) and MCHL (2.07+/-.70, P<.01) compared with controls (3.73+/-1.14). MVD in MCHLs tended to be reduced compared with that in HTGs, but the difference was statistically insignificant (P=.08). There was a significant relationship between MVD and both plasma triglycerides (r=-.47, P<.01) and plasma total cholesterol (r=-.55, P<.01). When controls and HTGs were combined, the relationship between MVD and plasma total triglycerides became more prominent (r=-.55, P<.05), and the significant relationship between cholesterol level and MVD disappeared. Multivariate regression analysis has revealed that the triglyceride level (F=5.2, P<.05) was independently related to MVD (r=.69, P<.01). In conclusion, MVD was reduced in hypertriglyceridemics in anatomically normal coronary arteries. Hypertriglyceridemia is an independent factor for this abnormality.