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To compare left ventricular global and segmental function at rest and during right atrial pacing in patients with unstable angina, non-Q wave myocardial infarction, and stable angina (class III angina), low-dose digital subtraction ventriculography was performed at rest and after abrupt cessation of pacing in 42 patients with unstable angina, 8 patients with non-Q wave myocardial infarction and 15 patients with stable angina during selective coronary arteriography. Left ventricular ejection fraction was significantly lower at rest in patients with unstable angina (P < 0.01) and non-Q wave myocardial infarction (P < 0.05) and during pacing (P < 0.01). These two groups of patients had significantly higher values of left ventricular end-diastolic and end-systolic volumes at rest and during pacing as compared with stable angina group. In comparing various clinical patterns of unstable angina, ejection fraction was significantly (P < 0.05) lower during pacing in patients with crescendo angina than in new-onset angina. However, ejection fraction was significantly (P < 0.01) lower in crescendo angina only at rest as compared with rest angina. The length of zone of severe hypokinesia was greater in unstable angina (P < 0.01) as well as in non-Q wave myocardial infarction (P < 0.05) both at rest and during pacing as compared with stable angina. Contractility of region of hypokinesia during pacing was higher (P < 0.01) in stable angina than in unstable angina and non-Q wave myocardial infarction. In analyzing segmental function in various subgroups of unstable angina, the authors found that the length of total hypokinesia was significantly higher (P < 0.05) during pacing in crescendo angina than in new-onset angina. Contractility of region of hypokinesia was lowest at rest and during pacing in patients with crescendo angina. This study demonstrates that patients with unstable angina as well as non-Q wave myocardial infarction were characterized by more pronounced global and segmental left ventricular dysfunction at rest and during pacing as compared with patients with stable angina, which may explain the poorer prognosis in the former two groups. This study also shows that patients with crescendo angina have more profound left ventricular global and regional dysfunction as compared with patients with new-onset as well as rest angina.

Unstable angina includes a variety of clinical presentations with a different level of risk for an unfavorable outcome. In this study the authors investigated the prognostic significance of crescendo angina and new-onset angina to discuss management strategies, paying attention to the relevance of baseline clinical characteristics, coronary artery lesions, and left ventricular function, as well as their alterations during atrial pacing. Accordingly coronary arteriographic anatomy and changes in left ventricular volumes and ejection fraction before and during atrial pacing were studied by means of digital subtraction ventriculography in 18 patients with crescendo angina and in 18 patients with new-onset angina. Triple-vessel disease was more frequently observed in crescendo angina (56%; P < 0.05) as compared with the patients with new-onset angina (11%). Complex coronary morphology was statistically more likely to be found in crescendo angina. The angiographic evidence of intracoronary thrombi was found in 33% (P < 0.05) patients with crescendo angina and in 4% patients with new-onset angina. Compared with the patients with new-onset angina, patients with crescendo angina had higher end-diastolic and end-systolic volumes and lower ejection fraction at rest. At peak pacing, ejection fraction was significantly (P < 0.05) lower in crescendo angina (0.48 +/- 0.06) than in new-onset angina (0.66 +/- 0.04). In crescendo angina, during pacing, the magnitude of velocity of circumferential fiber shortening was significantly decreased as compared with new-onset angina.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary artery lesions were compared in 71 patients with unstable angina, 15 patients with non-Q wave myocardial infarction (MI), and 40 patients with stable angina. In the unstable angina group, 29 patients had new-onset angina, 31 had crescendo angina, and 11 had rest angina. In a subgroup of patients with unstable angina, three-vessel disease was less frequently (P < 0.05) seen in patients with new-onset angina (10.3%) than in the patients with crescendo angina (51.6%) or rest angina (54.5%). An angina-producing artery could be identified in 59 patients with unstable angina, in 11 with non-Q wave MI, and in 30 with stable angina. Type II eccentric stenosis (asymmetric narrowing with narrow neck and overhanging irregular edges) was present in 31 patients (52.5%; P < 0.01) with unstable angina, in 7 (63.6%; P < 0.01) with non-Q wave MI, and in only 2 (6.7%) with stable angina. Abrupt occlusion of a vessel was observed in 7 patients (11.9%) with unstable angina and in 2 (18.2%) with non-Q wave MI. None of the patients with stable angina had this type of occlusion. In the group of unstable angina and non-Q wave MI, angiographic evidence of intracoronary thrombi was present in 16 (27.1%) and 3 patients (27.3%), respectively, but in stable angina in only 1 patient (3.3%; P < 0.05). Intracoronary thrombi were most frequently found in rest angina (88%; P < 0.001) and crescendo angina (33.3%; P < 0.01) compared with new-onset angina (3.7%).(ABSTRACT TRUNCATED AT 250 WORDS)

To assess the clinical, coronary arteriographic, and hemodynamic differences between the unstable angina patients manifesting ST segment depression and those showing ST segment elevation as well as those demonstrating chest pain only without ST segment deviation during pacing, low-dose digital subtraction ventriculography was performed in 33 patients before and after abrupt cessation of atrial pacing during selective coronary arteriography. Transient ST segment depression during pacing was observed in 17 patients (52%), whereas 6 patients (18%) showed ST segment elevation; however, 10 patients (30%) did not manifest any ST segment deviation in spite of typical chest pain. Hypertension and a history of myocardial infarction were observed in a significantly higher (P < 0.05) proportion of patients with ST segment depression than in those with ST elevation. Patients who manifested ST segment depression during pacing had a higher incidence of triple-vessel disease (65 vs 17%; P < 0.05) as compared with the patients with ST segment elevation. Indirect evidence of intracoronary thrombi (complicated lesion, abrupt occlusion, and intraluminal filling defect) was noticed in a higher frequency (P < 0.05) in the group of patients with ST elevation during pacing. In patients with ST segment depression, no significant changes of global left ventricular (LV) functional parameters were observed. However, the length of the LV severe hypokinetic region was increased significantly (6.2 ±3.1 vs 23.5 ±6.2%; P < 0.05) during pacing in this group of patients. The shortening of the affected segments of the left ventricle was decreased significantly (52.3 ±3.6 vs 38.3 ±4.9%; P < 0.05) in these patients during pacing. In the group of patients with ST segment elevation during pacing, decrease in ejection fraction was associated with significant (P < 0.01) increase in midwall equatorial diastolic stress as compared with the patients with pacing-induced ST segment depression as well as patients without ST segment deviation. In the group of patients without ST segment deviation during pacing there was no considerable aggravation of LV global or regional function. This distinction should be taken into consideration in evaluating patients with unstable angina for diagnostic and therapeutic intervention. [ABSTRACT FROM AUTHOR]