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Reduced coronary vasodilator function in infarcted and normal myocardium after myocardial infarction
N G Uren1, T Crake, D C Lefroy
1Division of Cardiology, Hammersmith Hospital, London, United Kingdom.
Insights
Following myocardial infarction, coronary vasodilator dysfunction occurs in both infarcted and normal artery regions. This impaired blood flow response may worsen myocardial ischemia and necrosis.
Area of Science:
- Cardiology
- Vascular Biology
- Nuclear Cardiology
Background:
- Coronary artery disease can impair the heart's ability to increase blood flow.
- This impairment may persist even in areas supplied by normal-appearing arteries.
- Such dysfunction after myocardial infarction could worsen heart muscle damage.
Purpose of the Study:
- To investigate coronary vasodilator function after acute myocardial infarction.
- To assess blood flow in both infarcted and remote myocardial regions.
Main Methods:
- Studied 13 patients with single-vessel coronary artery disease post-myocardial infarction.
- Used positron-emission tomography (PET) with oxygen-15-labeled water to measure myocardial blood flow.
- Assessed blood flow under basal conditions and after dipyridamole administration at 1 week and 6 months post-infarction.
Main Results:
- One week post-infarction, vasodilator response was significantly lower in the infarct-related region compared to the remote region.
- Six months post-infarction, vasodilator response improved in the infarcted region but remained impaired in the remote region compared to controls.
- Remote myocardium showed persistently lower vasodilator response than in control patients.
Conclusions:
- Acute myocardial infarction causes significant vasodilator dysfunction in both infarcted and non-infarcted myocardial regions.
- This widespread vasomotor abnormality impacts myocardial ischemia and necrosis extent.
- Impaired vasodilation in remote regions suggests a systemic effect post-myocardial infarction.
Background:
The ability of the coronary vascular bed to dilate and thus increase blood flow to the myocardium may be impaired in coronary artery disease, even in regions of myocardium supplied by an angiographically normal coronary artery. If this kind of vasomotor dysfunction was present or accentuated after acute myocardial infarction, it might influence the extent of ischemia and necrosis in areas not directly injured by the infarction.
Methods:
We studied 13 patients (mean [+/- SD] age, 62 +/- 11 years) with single-vessel coronary artery disease after they had received thrombolytic therapy for myocardial infarction. Using positron-emission tomography (PET) with oxygen-15-labeled water, we measured regional myocardial blood flow under basal conditions and after the intravenous administration of dipyridamole (0.5 mg per kg of body weight over a period of four minutes) 8 +/- 3 days after infarction in all 13 patients (1-week study) and 6 +/- 2 months after infarction in 9 of the 13 (6-month study). On both occasions we measured blood flow both in the infarcted region and in a region of myocardium that was remote from the infarcted region and supplied by a normal artery.
Results:
At the one-week PET study, the coronary vasodilator response (the ratio of the myocardial blood flow after the administration of dipyridamole to basal blood flow) was 1.12 +/- 0.50 in the infarct-related artery and 1.53 +/- 0.36 in the remote region (P = 0.015). At the six-month study, the coronary vasodilator response was 1.42 +/- 0.37 in the infarcted region and 2.19 +/- 0.69 in the remote region (P = 0.004 for the comparison with the infarcted region; P = 0.011 for the comparison with the remote region at the one-week study). The value in remote myocardium remained lower than that in similar regions in 10 control patients, who had single-vessel coronary artery disease but no evidence of myocardial infarction (3.17 +/- 0.72; P = 0.009).
Conclusions:
After acute myocardial infarction, there is a severe vasodilator abnormality involving not only resistance vessels in infarcted myocardium, but also those in myocardium perfused by normal coronary vessels. This dysfunction may affect the extent of myocardial ischemia and necrosis after coronary occlusion.