Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 2001;104:e151-e152

This Article
Right arrow Extract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Auer, J.
Right arrow Articles by Berman, D. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Auer, J.
Right arrow Articles by Berman, D. S.
Right arrowPubmed/NCBI databases
Medline Plus Health Information
*Nuclear Scans
Related Collections
Right arrow Cardiovascular Pharmacology
Right arrow Cardiovascular imaging agents/Techniques
Right arrow Pathophysiology
Right arrow Risk Factors
Right arrow Nuclear cardiology and PET
Right arrow Chronic ischemic heart disease
Right arrow Genetics of cardiovascular disease
Right arrow Endothelium/vascular type/nitric oxide
Right arrow Mechanism of atherosclerosis/growth factors

(Circulation. 2001;104:e151.)
© 2001 American Heart Association, Inc.


Correspondence

Anti-Ischemic Therapy and Myocardial Ischemia Shown by Single Photon Emission Computed Tomography Imaging

Johann Auer, MD; Robert Berent, MD; Bernd Eber, MD

Department of Cardiology and Intensive Care, General Hospital Wels, Wels, Austria

To the Editor:

O‘Rourke and colleagues1 describe a case of resolution of stress-induced myocardial ischemia during aggressive medical therapy demonstrated by single photon emission computed tomography (SPECT) imaging. They conclude that a 1-year period of aggressive medical treatment led to this favorable result in a patient, who initially had typical angina pectoris and a 80% mid-left anterior descending coronary artery stenosis. We do not agree with their interpretation, and we think that the effect demonstrated on SPECT imaging can be shown within hours after the administration of effective antianginal therapy with ß-blockers,2 calcium antagonists, or nitrates.3

Sensitivity for the detection of stress-induced myocardial ischemia by SPECT imaging depends on several factors, including the administration of anti-ischemic medications, non-flow-limiting coronary stenoses, overlap circulation, "balanced" hypoperfusion or hypoperfusion in segments with attenuation, and collateral circulation.4

Antianginal therapy can abolish the effects of pharmacological stress with consecutive "false-negative" SPECT imaging results. Therefore, serial testing using pharmacological stress with dipyridamole or adenosine is not appropriate to assess the adequacy of medical therapy.5

References

1. O‘Rourke RA, Chaudhuri T, Shaw L, et al. Resolution of stress-induced myocardial ischemia during aggressive medical therapy as demonstrated by single photon emission computed tomography imaging. Circulation. 2001; 103: 2315.

2. Thadani U, Davidson C, Singleton W, et al. Comparison of the immediate effects of five beta-adrenoreceptor-blocking drugs with different ancillary properties in angina pectoris. N Engl J Med. 1979; 300: 750–755.[Abstract]

3. Kaski JC, Plaza LR, Meran DO, et al. Improved coronary supply: prevailing mechanism of action of nitrates in chronic stable angina. Am Heart J. 1985; 110: 238–245.[Medline] [Order article via Infotrieve]

4. Kwok JM, Christian TF, Miller TD, et al. Identification of severe coronary artery disease in patients with a single abnormal coronary territory on exercise thallium-201 imaging: the importance of clinical and exercise variables. J Am Coll Cardiol. 2000; 35: 335–344.[Abstract/Free Full Text]

5. San Roman JA, Vilacosta I, Castillo JA, et al. Selection of the optimal stress test for the diagnosis of coronary artery disease. Heart. 1998; 80: 370–376.[Abstract/Free Full Text]


 

Robert A. O’Rourke, MD; Tuhin Chaudhuri, MD

Division of Cardiology, University of Texas Health Science Center, San Antonio, Texas

Leslee Shaw, PhD

Department of Radiology, University of Texas Health Science Center, San Antonio, Texas

Daniel S. Berman, MD

Department of Health Policy and Management, Emory University, Atlanta, Georgia
University of California at Los Angeles School of Medicine, Los Angeles, California

Response

We appreciate the comments by Auer and associates on our article.1 Although perfusion defects on single photon emission computed tomography (SPECT) imaging can improve within hours of effective anginal therapy, this observation does not diminish the usefulness of sequential vasodilator stress myocardial perfusion SPECT in documenting effective medical therapy. Several prior publications have established this fact. Sharir et al2 performed dipyridamole SPECT in 21 patients with coronary artery disease before and after the administration of calcium antagonists, nitrates, or ß-blockers. A 24% to 33% reduction in perfusion defect size occurred with anti-ischemic medications. Mostaza et al3 examined the effects of cholesterol reduction using dipyridamole thallium-201 SPECT. After 16 weeks of therapy, the summed stress score was lower with pravastatin than with placebo (7.2 versus 5.9, P=0.012). Quantitative analysis showed a smaller defect with pravastatin (29.2% versus 33.8%, P=0.021).

Similar results have been shown by Gould4 using dipyridamole positron-emission tomography. Thus, reducing cholesterol levels with statins improves myocardial perfusion during SPECT imaging. This improvement likely relates to the normalization of endothelial function rather than anatomic changes. The action of dipyridamole in the coronary vasculature may be related in part to an increase in perfusion related to endothelial dependent arteriolar vasodilation.5 In another study, Dakik et al6 reported the results of adenosine SPECT in 44 postinfarction patients to compare medical therapy with coronary angioplasty. After 30 days, a 33% reduction in total perfusion defect size and a 23% reduction in reversible perfusion defect size were noted with anti-ischemic therapy. The reduction in total ischemic defect size was similar in both treatment groups. Importantly, event-free survival was 96% for patients who had a significant reduction in perfusion defect size and only 65% for those with no major decrease in SPECT defects.

To assess medical therapy, either exercise or pharmacological vasodilator stress is used with SPECT. We and others7 have demonstrated that exercise SPECT will document a reduction in ischemia with medical therapy. The vasodilator stress is potentially more reproducible because patient effort is not required. Of course, it is essential that the patients be appropriately prepared for the stress SPECT studies. Relative to vasodilator stress, it is important that the patients not be under the influence of caffeine at the time of testing, because caffeine can block the vasodilator effects of adenosine and dipyridamole.

Contrary to the conclusions of Auer and colleagues, extensive evidence suggests that myocardial perfusion SPECT with pharmacological stress is effective in assessing the adequacy of medical therapy.

References

1. O‘Rourke RA, Chaudhuri T, Shaw L, et al. Resolution of stress-induced myocardial ischemia during aggressive medical therapy as demonstrated by single photon emission computed tomography imaging. Circulation. 2001; 103: 2315.

2. Sharir T, Rabinowitz B, Livschitz S, et al. Underestimation of extent and severity of coronary artery disease by dipyridamole stress thallium-201 single-photon emission computed tomographic myocardial perfusion imaging in patients taking antianginal drugs. J Am Coll Cardiol. 1998; 31: 1540–1546.[Abstract/Free Full Text]

3. Mostaza JM, Gomez MV, Gallardo F, et al. Cholesterol reduction improves myocardial perfusion abnormalities in patients with coronary artery disease and average cholesterol levels. J Am Coll Cardiol. 2000; 35: 76–82.[Abstract/Free Full Text]

4. Gould KL, Ornish D, Scherwitz, et al. Changes in myocardial perfusion abnormalities by positron emission tomography after long-term, intense risk factor modification. JAMA. 1995; 274: 894–901.[Abstract/Free Full Text]

5. Kinsella JP, Torielli F, Ziegler JW, et al. Dipyridamole augmentation of response to nitric oxide. Lancet. 1995; 346: 647–648.[Medline] [Order article via Infotrieve]

6. Dakik HA, Farmer J, Kleiman NS. Images in cardiovascular medicine: fistula between left main, left anterior descending, and pulmonary arteries. Circulation. 1998; 97: 2091–2092.[Free Full Text]

7. Mahmarian JJ, Fenimore NL, Marks GF, et al. Transdermal nitroglycerin patch therapy reduces the extent of exercise-induced myocardial ischemia: results of a double-blind, placebo-controlled trial using quantitative thallium-201 tomography. J Am Coll Cardiol. 1994; 24: 25–32.[Abstract]





This Article
Right arrow Extract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Auer, J.
Right arrow Articles by Berman, D. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Auer, J.
Right arrow Articles by Berman, D. S.
Right arrowPubmed/NCBI databases
Medline Plus Health Information
*Nuclear Scans
Related Collections
Right arrow Cardiovascular Pharmacology
Right arrow Cardiovascular imaging agents/Techniques
Right arrow Pathophysiology
Right arrow Risk Factors
Right arrow Nuclear cardiology and PET
Right arrow Chronic ischemic heart disease
Right arrow Genetics of cardiovascular disease
Right arrow Endothelium/vascular type/nitric oxide
Right arrow Mechanism of atherosclerosis/growth factors