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Effects of pharmacologic coronary hyperemia on echocardiographic left ventricular function in patients with single
M J Kern1, A C Pearson, A J Labovitz
1Department of Internal Medicine, St. Louis University Hospital, Missouri 63104.
Insights
Pharmacologic coronary vasodilation using papaverine or dipyridamole did not reliably provoke new left ventricular wall motion abnormalities in patients with single vessel coronary artery disease. These tests are insufficient for identifying ischemic regions.
Area of Science:
- Cardiology
- Medical Imaging
- Pharmacology
Background:
- Pharmacologic stress testing is used to assess coronary artery disease.
- Assessing the ability of coronary vasodilation to provoke left ventricular wall motion abnormalities is crucial for diagnosing ischemia.
Purpose of the Study:
- To evaluate if pharmacologic coronary vasodilation can induce new left ventricular wall motion abnormalities in patients with single vessel coronary artery disease.
- To compare the effectiveness of intracoronary papaverine and intravenous dipyridamole in provoking these abnormalities.
Main Methods:
- Two-dimensional echocardiography was used to measure left ventricular wall motion.
- 14 patients with single vessel coronary artery disease received intracoronary papaverine.
- 13 patients with single vessel coronary artery disease received intravenous dipyridamole.
Main Results:
- Intracoronary papaverine induced new left ventricular wall motion abnormalities in 5 of 14 patients before angioplasty.
- Left ventricular wall motion abnormalities persisted in 3 of these 5 patients after angioplasty.
- Intravenous dipyridamole induced new left ventricular regional asynergy in 3 of 13 patients.
Conclusions:
- Selective (papaverine) and global (dipyridamole) augmentation of coronary flow alone do not reliably identify ischemic left ventricular regions.
- These pharmacologic methods may not be sufficient for diagnosing critical single vessel coronary artery disease.
Abstract:
To assess whether pharmacologic coronary vasodilation could provoke new left ventricular wall motion abnormalities in patients with single vessel coronary artery disease, systemic hemodynamics, coronary blood flow velocity and left ventricular wall motion were measured by two-dimensional echocardiography during administration of 10 mg of intracoronary papaverine in 14 patients before and again immediately after left coronary angioplasty (group 1). As a comparison with an intravenous method, left ventricular wall motion was analyzed after 0.56 mg/kg body weight of intravenous dipyridamole in a separate group of 13 patients with single vessel coronary disease (group 2). Heart rate-blood pressure product increased 3% to 6% in papaverine-treated patients and 14 +/- 11% (p = NS) in dipyridamole-treated patients. No angiographic collateral vessels were present in either group. Although intracoronary mean flow velocity measured in the 14 group 1 patients and in 5 normal control subjects during papaverine treatment increased from 125% to 400% of basal flow velocity, papaverine induced new left ventricular wall motion abnormalities in only 5 of the 14 patients before coronary angioplasty. In three of five patients, left ventricular wall motion abnormalities persisted after successful coronary angioplasty. Four of the 14 patients demonstrated augmentation of left ventricular wall motion with papaverine. After intravenous dipyridamole, only 3 of the 13 group 2 patients developed new left ventricular regional asynergy. These data suggest that selective (papaverine) and, most likely, global (dipyridamole) augmentation of coronary flow alone does not reliably identify potential ischemic left ventricular regions affected by critical single vessel coronary artery disease.