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Cardiac metabolic effects of heparin differentiate between patients with normal and stenotic coronary arteries
A Thomassen1, T T Nielsen, J P Bagger
1Department of Cardiology, Skejby Sygehus, Aarhus N, Denmark.
Insights
Heparin affects cardiac metabolism by increasing free fatty acid uptake, but its metabolic effects are diminished in patients with ischemic heart disease, likely due to altered substrate regulation.
Area of Science:
- Cardiology
- Biochemistry
- Metabolic Research
Background:
- Heparin is commonly used in cardiovascular procedures.
- Its effects on cardiac metabolism, particularly in ischemic conditions, require further elucidation.
- Understanding substrate utilization is crucial for managing heart disease.
Purpose of the Study:
- To investigate the impact of heparin on cardiac metabolism in patients with and without coronary arterial disease.
- To compare the metabolic responses to heparin between healthy individuals and those with stable angina.
Main Methods:
- Intravenous administration of heparin (12,500 units) in 16 patients (8 with coronary arterial disease, 8 controls).
- Cardiac catheterization of the coronary sinus at rest and during rapid atrial pacing.
- Measurement of myocardial substrate uptake and release (free fatty acids, glucose, lactate, glutamate, alanine, citrate) and oxygen consumption.
Main Results:
- Heparin increased arterial free fatty acid levels and myocardial uptake, but only in non-ischemic conditions.
- In normal coronary arteries, heparin reduced myocardial uptake of glucose and lactate, and alanine release.
- These metabolic effects of heparin were diminished in patients with ischemic heart disease.
- Myocardial oxygen consumption remained unchanged; angina and ST-segment depression were not influenced by heparin.
Conclusions:
- Heparin's metabolic effects on the heart are less pronounced in patients with ischemic heart disease compared to controls.
- Altered substrate preference regulation in ischemic hearts may explain the diminished metabolic response to heparin.
- Further research into substrate metabolism in ischemic heart disease is warranted.
Abstract:
We studied the effects of heparin, given as 12,500 units intravenously, on cardiac metabolism during catheterization of the coronary sinus at rest and during repeated rapid atrial pacing in 8 patients with stable angina pectoris, positive stress tests and coronary arterial disease and in 8 patients with normal coronary arteries without objective signs of ischemic heart disease. Heparin did not influence angina, ST-segment depression or myocardial lactate production induced by pacing in the group with diseased coronary arteries. In both groups, heparin increased the arterial levels (70%) and the myocardial uptake (40-50%) of free fatty acids, the latter only during non-ischemic conditions. Myocardial net uptakes of glucose, lactate and glutamate and the release of alanine were reduced by heparin in the subjects with normal coronary arteries but not in those with ischemic heart disease. Myocardial oxygen consumption was unchanged. In the patients with normal coronary arteries, the levels of free fatty acid in the arteries were positively related to myocardial uptake of fatty acids and the release of citrate but inversely related to cardiac uptake of lactate and glucose. These relations were lacking in the patients with diseased coronary arteries. The metabolic effects of heparin on the heart, therefore, were diminished in patients with ischemic heart disease when compared to controls. This is probably due to an altered regulation of substrate preference in ischemic hearts.