PubMed · 8005937
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A K Pande, V M Kohli, A K Omar, R R Kasliwal, N Trehan. 1993. Left ventricular pseudoaneurysm.. https://pubmed.ncbi.nlm.nih.gov/8005937/
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The development of a clinically correlated human pericardial fluid bank and database is described. A unique feature of this registry is the availability of a large number of pericardial fluid samples for testing with respect to multiple factors and for correlation with angiographic findings and clinical syndromes expressed by the patients. The collection of data at the present time comprises frozen pericardial fluid samples obtained from patients who have undergone cardiac surgery; and historical, clinical, and laboratory data obtained from the patient records. Nearly 400 samples have been stored and analyzed thus far, with sample entry continuing. This registry is designed to evaluate the local factors that play a role in mediating or reflecting myocardial or coronary responses. Pathophysiologic processes of particular interest include restenosis, plaque ruptures, and angiogenesis. Study of the pericardial fluid bank should lead to enhanced understanding of molecular mechanisms, as well as to the explanation for the reasons underlying interpatient variability in these processes. It is further anticipated that this information might provide a foundation for the diagnostic use of pericardial fluid to individualize therapies targeting angiogenesis or plaque physiology.
BACKGROUND: Early identification of patients in whom left ventricular dilatation is likely to occur may have important therapeutic implications. Thus the purpose of this study was to evaluate the relation between Killip class on admission and subsequent left ventricular dilatation after acute myocardial infarction. METHODS AND RESULTS: We serially evaluated 129 consecutive patients by two-dimensional and Doppler echocardiography on days 1, 2, 3, and 7, at 3 and 6 weeks, and at 3, 6, and 12 months after infarction. Killip class on admission >1 was found in 29 of 129 (22.5%) patients, and they had significantly higher end-systolic and end-diastolic volume indexes and wall motion score index from day 1 onward compared with patients with Killip class 1, whereas ejection fraction was lower during the follow-up period in these patients. Patients with Killip class >1 showed the progressive increase of end-diastolic (68.2 +/- 2.99 to 88.0 +/- 7.55 ml/m2, p = 0.001) and end-systolic volume indexes (43.9 +/- 2.67 to 56.3 +/- 6. 18 ml/m2, p = 0.004) during the follow-up period, whereas ejection fraction and wall motion score index remained unchanged. In patients with Killip class 1, end-systolic volume index did not change (30.8 +/- 1.06 to 33.8 +/- 2.15 ml/m2, p = 0.064), ejection fraction increased (49.3% +/- 0.99% to 51.8% +/- 1.17%, p = 0.027), and wall motion score index decreased (1.50 +/- 0.03 to 1.35 +/- 0.04, p < 0. 001). End-systolic volume index was the major independent correlate of Killip class, followed by history of diabetes and peak creatine kinase level. No association was found between Doppler indexes of diastolic filling and Killip class on admission. CONCLUSIONS: Killip class >1 on admission is associated with both acute and long-term left ventricular dilatation. On the other hand, Killip class 1 is associated with favorable left ventricular functional indices, and it appears that left ventricular function in these patients may improve over time. Initial end-systolic volume index but not ejection fraction is the major correlate of Killip class.
Little information is available concerning the effects of nitrates and potassium channel openers on local poststenotic blood flow in coronary artery disease (CAD). Combined quantitative digital angiography (QCA) and intracoronary Doppler (IVADO) velocity measurements were used to determine changes in absolute poststenotic blood flow after intracoronary injection of 0.2 mg nitroglycerin and 0.5 mg nicorandil. Quantitative blood flow (QBF) was calculated from average peak-flow velocity (APV) and angiographic cross-sectional area (CSA): QBF (ml/min) = CSA x APV x 0.5. In group I (n = 9), 0.5 mg nicorandil i.c. was identified as optimal to achieve maximal vasodilatation. In patients with CAD (group II, n = 12), i.c. injection of 0.5 mg nicorandil induced a significant increase in poststenotic CSA (+38%) and QBF (+50%). In contrast, 0.2 mg nitroglycerin (group III, n = 12) increases poststenotic CSA (+38%) without a significant change in QBF (+23%). Additional application of nicorandil in these patients induced further significant increases in CSA (+55%) and QBF (+48%) compared with baseline. There were no significant changes in stenosis area. Poststenotic blood flow can be increased by nicorandil after application of nitroglycerin. This effect is most likely mediated by the potassium channel-opening effect of nicorandil. Combined use of QCA and IVADO is a unique approach to measure local poststenotic QBF in patients with CAD.