Between May and September 2006, transthoracic stress-pacing echocardiography was performed on 15 patients (9 men and 6 women, median age: 71.1±11.0 years) with atypical angina and a permanent pacemaker. All the patients gave us their written informed consent for this study's protocol. Patients with recent myocardial infarction (<2 months), clinical signs of unstable angina, congestive heart failure, significant valvular heart disease, a prior coronary angiographic history or poor echocardiographic images were excluded.

PASE was performed by a single trained cardiologist, who was blinded to the clinical data, and with using commercially available Sequoir C-512 Ultrasound equipment (Acuson Inc., Mountain View, CA, USA) with a 3.5 MHz transducer. The images were obtained with the patient in the left lateral decubitus position and they were acquired before the stress test and every 2 minutes throughout the stress test using the standard parasternal and apical views. Continuous pacing was started at 100 beats per minute (bpm) and the heart beat was increased every 2 min (maximum-150 bpm) until a test endpoint was reached. Test endpoints were achieved by reaching the maximal ventricular pacing (heart rate 150 bpm), severe angina, systolic blood pressure decreases greater than 40 mmHg, regional wall motion abnormality or significant cardiac arrhythmias. The echocardiograms were recorded in a quad-screen format. Two experienced cardiologists, who were unaware of the clinical data, scored the echocardiograms using a standard 16-segment model as suggested by the American Society of Echocardiography.6) Regional wall motion and systolic wall thickening were scored on a 5-point scale. A segment with normal motion was scored as 1, a mild hypokinetic segment as 2, a severe hypokinetic segment as 3, an akinetic segment as 4 and a dyskinetic segment as 5. Ischemia was defined as new or worsened wall motion abnormalities during stress, as indicated by an increase of the wall motion score ≥1 grade in at least one segment. Ischemia was not present when the akinetic segments were at rest became the seg-ments became dyskinetic during stress. The myocardial septal and apical functions were evaluated on the basis of systolic thickening because the wall motion could be influenced by ventricular pacing.

Coronary angiograms were performed via the femoral approach on the 8 patients with positive test results. The angiograms were analyzed independent of the echocardiographic results by two experienced cardiologists. Coronary lesions were assessed with multiple orthogonal views and they were visually evaluated for the morphologic features that were similar to those reported by the American College of Cardilology/American Heart Association (ACC/AHA). Significant coronary stenosis was defined as a 70% or more narrowing of the luminal diameter in one or more major coronary arteries. Coronary artery disease was defined as the presence of at least one coronary vessel with significant stenosis.

The study population consisted of 15 patients (9 men, mean age: 71.1±11.0 years). The clinical and laboratory data is summarized in Table 1. All patients had hypertension and two patients had diabetes mellitus. The pacemaker had been implanted for a mean period of 61±52 months. The electrocardiogram (ECG) data and pacemaker characteristics are presented in Table 2.

The echocardiographic images were interpretable in all the patients. No significant side effects were observed. The left ventricular systolic function was preserved in all the patients [mean left ventricular ejection fraction (LVEF): 63.5%±8.0%]. No tests were stopped due to chest pain or severe hypotension, and 8 of 15 patients showed wall motion abnormalities during pacemaker pacing. Fig. 1 shows a positive example of PASE. All the 8 patients had coronary angiography performed, but only 5 (62.5%) patients showed significant coronary artery disease as documented by coronary angiography. The other 3 patients showed correct correlation between their coronary angiography and the PASE in the coronary territories. Fig. 2 shows an example of a positive coronary angiogram with significant right coronary artery stenosis, which correlated with the PASE results (Figs. 1 and 2). One patient underwent a coronary artery bypass graft due to disease in 3 vessels and there was little indication for performing percutaneous coronary intervention in that patient.

We showed that the prognosis obtained with the PASE test matched with an invasive coronary angiogram performed in the patients with atypical angina and a permanent pacemaker. The major pathophysiologic limitation is that pacing stress only increases in heart rate, leading to a lower rate-pressure product than is produced during exercise stress testing. Despite the small number of patients, our single-center experience implies that noninvasive PASE is a simple, rapid, safe and diagnostically efficient tool to test for coronary artery disease following chest discomfort in patients with a permanent pacemaker. Larger studies are necessary to validate our findings.