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J Coromilas

Publications and source records attributed to J Coromilas.

43 records · Page 3Linked to original sources
PubMed1983

Left ventricular function and rapid release of creatine kinase MB in acute myocardial infarction. Evidence for spontaneous reperfusion.

Intracoronary thrombolysis during acute myocardial infarction in human beings is associated with rapid release of creatine kinase and improvement of the cardiac ejection fraction. To examine the phenomenon of spontaneous coronary-artery recanalization, we studied the release of creatine kinase MB and sequential radionuclide ventriculograms in 52 patients with transmural myocardial infarction. Patients were divided into two groups according to whether the release of creatine kinase MB (time from base-line to peak serum level) was rapid (n = 24) or slow (n = 28). Patients with slow release had no significant change in global or regional ejection fraction from the time of admission to discharge. However, global ejection fraction in patients with rapid release improved from 0.38 +/- 0.09 (mean +/- S.D.) to 0.48 +/- 0.08 (P less than 0.001). The regional ejection fraction of Q-wave regions also improved, from 0.33 +/- 0.11 to 0.43 +/- 0.13 (P less than 0.001). A negative correlation (r = -0.52, P less than 0.001) existed between time to peak enzyme level and degree of improvement in ejection fraction. With increasing left ventricular damage, patients with rapid release had greater increments in creatine kinase MB than comparable patients with slow release (P = 0.03), suggesting enzyme washout. These data are consistent with the idea that spontaneous reperfusion, leading to altered enzyme release and improvement in ventricular function, is not uncommon after acute myocardial infarction.

Adult↗
PubMed1982

Mechanisms of quinidine-induced depression of maximum upstroke velocity in ovine cardiac Purkinje fibers.

A major advance in understanding how quinidine depresses maximum upstroke velocity (Vmax) is the Hondeghem-Katzung mathematical model which incorporates voltage-independent rate constants for binding to and unbinding from resting, open, and inactive Na channels, and a voltage shift of -40 mV for the Hodgkin-Huxley h-kinetics of quinidine-associated Na channels. Using a double microelectrode voltage clamp technique to control transmembrane voltage and apply conditioning pulses, we found that quinidine blockade increased as transmembrane voltage became more positive in the range -60 to +40 mV, and that the rate of quinidine dissociation increased as transmembrane voltage became more negative in the range -60 to -140 mV. The relationship of Vmax to transmembrane voltage obtained at drive cycles from 500 msec to 20 seconds conformed to the model modified to include voltage-dependent rate constants without the postulated -40-mV shift for quinidine-associated channels. Thus binding of quinidine to inactive Na channels and unbinding from resting channels are both voltage-dependent and can explain frequency and voltage dependent actions of quinidine on Vmax without any voltage shift for quinidine-associated channels.

Action Potentials↗
PubMed1980

Digitalis and myocardial infarction in man.

The use of digitalis after acute myocardial infarction is controversial. The effect of digoxin on computer-quantitated thallium-201 perfusion scintigrams (Tl-201), left ventricular (LV) ejection fraction (EF), and percentage of abnormally contracting LV regions (% ACR) was determined in 23 patients. A correlation was established between creatine kinase MB isoenzyme release and initial radionuclide-gated blood pool wall motion estimates of EF (r = -0.73) and % ACR (r = 0.71). After radionuclide assessments, 14 patients received digoxin 18 +/- 23 hours (mean +/- SD) after the rise in CK-MB from baseline, while the remaining nine patients served as controls. In the control group, the mean EF was 0.33 +/- 0.12 on the first study and 0.30 +/- 0.08 on the second study (p = NS). In the digoxin group, the EF after digoxin administration (mean 0.33 +/- 0.11) was significantly different from the initial EF (mean 0.29 +/- 0.09, p less than 0.03); however, digoxin had no apparent effect on infarct size as assessed by sequential % ACR and Tl-201 perfusion data. These data indicate that digoxin resulted in a minimal but significant improvement in EF that did not occur at the expense of LV perfusion or regional wall motion.

Adult↗
PubMedDate not supplied

Localized spatial discrimination of epicardial conduction paths after linear transformation of variant information.

We present a method for the localized statistical discrimination of class populations based on the Karhunen-Loève and Fukunaga-Koontz transforms. These transforms provide features that model the variance of a sample distribution. The spatial series of a 196 channel epicardial electrogram recording from an arrythmogenic postinfarct canine were analyzed. For each type of rhythm studied, Karhunen-Loève and Fukunaga-Koontz expansions were computed from five training sets of spatial data, corresponding to five locations across the surface of the heart. Nonparametric statistical tests were then used for discriminant analysis to compare properties representative of the distribution from each proposed class. In a comparison of properties from sinus rhythm to those of two ventricular tachycardias, several spatial regions exhibited statistically significantly different propagation characteristics. These areas were observed by visual inspection of electrogram activation maps to be characterized by conductive gradients, which differed in magnitude and direction from one rhythm to another. The regions in which the propagation characteristics are of greatest difference in each tachycardia were centered upon sites of conduction block, manifested by reentrant circuit rhythms. Therefore, the importance of the technique for the localization of specific electrophysiologic events is demonstrated. This study extends previous work of our group on biosignal pattern recognition to encompass localized spatial data.

Analysis of Variance↗