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Altered coronary flow reserve in the hypertrophied heart: implications for therapy
E O McFalls1, D J Duncker, L M Sassen
1Experimental Cardiology, Thoraxcenter, Erasmus University Rotterdam, The Netherlands.
Insights
Abnormal coronary flow reserve in left ventricular hypertrophy may be reversed by chronic therapy. Acute drug administration can alter measurements, requiring careful interpretation in hypertrophy models.
Area of Science:
- Cardiovascular Physiology
- Cardiac Hypertrophy Research
- Pharmacology
Background:
- Left ventricular hypertrophy (LVH) is linked to reduced coronary flow reserve (CFR).
- LVH increases risks for subendocardial ischemia and sudden cardiac death.
- Restoring impaired CFR in LVH may offer therapeutic benefits.
Purpose of the Study:
- To review mechanisms causing abnormal vasodilator capacity in hypertrophied hearts.
- To explore how chronic therapies might reverse CFR abnormalities.
- To report the acute effects of various drugs on CFR measurements.
Main Methods:
- Review of existing literature on LVH and CFR.
- Analysis of data from anesthetized swine models.
- Investigation of pharmacological agent effects on CFR.
Main Results:
- Chronic therapy may reverse abnormal vasodilator capacity in LVH.
- Acute administration of drugs significantly alters CFR measurements.
- Swine models provide insights into drug effects on CFR.
Conclusions:
- Understanding mechanisms of impaired CFR in LVH is crucial.
- Chronic treatments hold potential for improving CFR in hypertrophic hearts.
- Acute drug effects necessitate cautious interpretation of CFR data in LVH models.
Abstract:
Coronary flow reserve has been shown to be abnormally low in several models of left ventricular hypertrophy induced by long-standing pressure overload. Because the presence of hypertrophy is a risk factor for the development of subendocardial ischaemia and sudden death, efforts to restore alterations in flow reserve may prove beneficial. In the following review, we discuss potential mechanisms which might contribute to this abnormal vasodilator capacity in the hypertrophied heart, with particular emphasis on how chronic therapy may potentially reverse such abnormalities. In addition, we report how the acute administration of various classes of pharmacological agents can alter measurements of coronary flow reserve, as observed in our anaesthetised swine model. Such factors must be considered before interpreting any changes in coronary flow reserve in models of hypertrophy following chronic administration of drugs.