1. This study was conducted to assess the role of artrial and brain natriuretic peptides during acute myocardial ischaemia associated with dynamic exercise. 2. Study subjects consisted of 35 angiographically proven patients with angina pectoris and 35 angiographically normal control subjects. All subjects underwent 201Tl dynamic exercise testing. The presence and localization of the exercise-induced acute myocardial perfusion defect were assessed by 201Tl single-photon emission computed tomography. The severity score was calculated using the early image for quantitative assessment of the acute myocardial perfusion defect. 3. Plasma levels of atrial natriuretic peptide increased from 21.3 +/- 3.8 to 72.2 +/- 26.7 pg/ml (P < 0.01) in the angina pectoris group, and increased from 19.4 +/- 2.4 to 36.4 +/- 17.4 pg/ml (P < 0.01) in the control group during dynamic exercise. Plasma levels of brain natriuretic peptide increased from 2.8 +/- 0.8 to 6.9 +/- 2.6 pg/ml (P < 0.01) in the angina pectoris group, but did not change significantly in the control group (from 2.7 +/- 0.7 to 2.9 +/- 1.0 pg/ml) during dynamic exercise. At peak exercise, plasma levels of these natriuretic peptides in the angina pectoris group were significantly higher than those in the control group (P < 0.01). 4. At peak exercise, there were correlations between the plasma level of atrial natriuretic peptide and heart rate in both the angina pectoris and control groups (P < 0.01, r = 0.46; P < 0.01, r = 0.51, respectively), but no significant correlations between the plasma level of brain natriuretic peptide and heart rate in either group. The plasma levels of these peptides at peak exercise correlated well with the severity score in the angina pectoris group (atrial natriuretic peptide, r = 0.71, P < 0.01; brain natriuretic peptide, r = 0.69, P < 0.01).

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The mechanism(s) of myocardial ischemia in hypertrophic cardiomyopathy remain unclear. In this report, the authors present a 75-year-old Japanese woman with nonobstructive hypertrophic cardiomyopathy in whom paroxysmal atrial fibrillation caused severe myocardial ischemia and induced sustained ventricular tachycardia. Her coronary angiogram showed normal findings, and no ischemic changes were provoked by either physical exercise testing or dobutamine stress echocardiography under sinus rhythm. In view of these findings, the rapid ventricular response in the absence of atrial contraction may aggravate or induce myocardial ischemia and predispose patients with hypertrophic cardiomyopathy to develop lethal ventricular arrhythmia.

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