Myocardial perfusion in patients with typical chest pain and normal angiogram


  • Department of Cardiology (S. Graf, A. Khorsand, M. Gwechenberger, H. Sochor, G. Maurer, M. Zehetgruber), Department of Nuclear Medicine (M. Schütz, K. Kletter, R. Dudczak), Medical University of Vienna, Vienna; Department of Nuclear Medicine, Private Medical University of Salzburg, Salzburg (C. Pirich); Department of Nuclear Medicine, Rudolfinerhaus, Vienna (G. Porenta), Austria.

Senta Graf, MD, Department of Cardiology, Medical University of Vienna, Waehringer Guertel 18–20, A−1090 Vienna, Austria. Tel.: +43 140400–4618; fax: +43 1408 1148; e-mail:


Background  Approximately 10–30% of patients with typical chest pain present normal epicardial coronaries. In a proportion of these patients, angina is attributed to microvascular dysfunction. Previous studies investigating whether angina is the result of abnormal resting or stress perfusion are controversial but limited by varying inclusion criteria. Therefore, we investigated whether microvascular dysfunction in these patients is associated with perfusion abnormalities at rest or at stress.

Patients and methods  In 58 patients (39 female, 19 male, mean age 58 ± 10 years) with angina and normal angiogram as well as 10 control patients with atypical chest pain and normal coronaries (six female, four male, mean age 53 ± 11 years) myocardial blood flow (MBF) was measured at rest and under dipyridamole using 13N–ammonia PET. Resting MBF and coronary flow reserve (CFR) as the ratio of hyperaemic to resting MBF were corrected for rate – pressure – product (RPP): normalized resting MBF (MBFn) = MBF × 10 000/RPP and CFRn = CFR × RPP/10 000.

Results  Sixteen/58 patients had a normal CFRn (= 2·5; group I; CFRn: 3·1 ± 0·88); the same as the controls (CFRn: 3·3 ± 0·74). Forty-two/58 patients presented a reduced CFRn (group II; CFRn: 1·78 ± 0·57). Group II had both a higher MBFn (group II: 1·30 ± 0·33 vs. Group I: 1·03 ± 0·26; P < 0·05 and vs. controls: 1·07 ± 0·19; P < 0·01) and a lower hyperaemic MBF (group II: 2·25 ± 0·76 mL g−1 min−1 vs. Group I: 3·07 ± 0·78 mL g−1 min−1; P < 0·001 and vs. controls: 3·41 ± 0·94 mL g−1 min−1; P < 0·0001).

Conclusion  Impaired CFRn in patients with typical angina and normal angiogram is owing to both an increased resting and reduced hyperaemic MBF. Therefore, PET represents a prerequisite for further studies to optimize treatment in individuals with anginal pain and normal coronary angiogram.