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Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From a study of 34 cases, the authors have tried to define the characteristic features of this very specialised type of coronary artery disease. From the clinical standpoint, if the common combination of uncontrolled angina and a past history of myocardial infarction are taken as representative, the basal ECG can in no way differentiate the diagnosis; on the other hand tests on the bicycle ergometer appear to have a good indicative value. Coronary arteriography shows the sharply isolated character of the stenosis of the trunk which is part of the picture of diffuse coronary disease, and the frequency (2 cases out of 3) of total coronary occlusion. The haemodynamic findings are even more variable and unpredictable, and bear no relationship to the degree of trunk stenosis, to the index of the lesion, and to the number of occlusions. However, joint analysis of the index of the lesion and of the degree to which the coronary circulation is compensated or de-compensated allows a better interpretation of the haemodynamic picture.
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PMID:[Stenosis of the trunk of the left coronary artery. Contribution of coronary arteriography and hemodynamic correlations. Apropos of 34 cases]. 41 68

Etiology of the negative chronotropic response to coronary artery occlusion was studied in chloralose-anesthetized monkeys. One-minute occlusion of the circumflex (CIRC) coronary artery resulted in marked negative chronotropic responses and consistent alterations in atrial electrograms. These responses were dependent on interruption of flow to a small proximal CIRC branch, and postmortem examination revealed that it perfused the sinus node region. The negative chronotropic response was not dependent on any apparent neural reflexes because it was not affected by autonomic blockade. Coronary artery occlusion in anesthetized monkeys can result in significant decreases in heart rate and changes in atrial electrical activity when flow to the pacemaker region is interrupted. We suggest that (1) rhesus monkeys may be suitable for study of the sick sinus syndrome, and (2) atropine-resistant bradycardia and atrial arrhythmias observed in postinfarction patients may be due to sinus node artery blockade.
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PMID:Etiology of the negative chronotropic responses to transient coronary artery occlusion in the anesthetized rhesus monkey. 41 26

This study was designed to determine whether quantitative alterations in ultrasonic attenuation are associated with myocardial changes occurring after acute ischemic injury. Five hundred seventeen regions of myocardium from 41 dogs were studied in vitro at five intervals after coronary occlusion: 15 min, 1 h, 6 h, 24 h, 3 days, and 6 wk. Quantitative indices of ultrasonic attenuation were determined from the measured frequency dependence of the ultrasonic attenuation coefficient characterizing each myocardial region over the range 2-10 MHz. Independent definition of regions of ischemic injury was provided by either creatine kinase depletion or colloidal carbon dye distribution. Results of this study indicate that ischemic myocardial regions investigated 15 min to 24 h after coronary occlusion demonstrated ultrasonic attenuation significantly decreased from nonischemic regions (P less than 0.05). In contrast, ultrasonic attenuation was significantly increased in zones of ischemia or infarction investigated at 3 days and 6 wk after coronary occlusion (P less than 0.05 and P less than 0.01, respectively). These results indicate that altered attenuation of transmitted ultrasound by myocardium in vitro is an early manifestation of ischemia.
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PMID:Changes in ultrasonic attenuation indicative of early myocardial ischemic injury. 42 Mar 17

Transmembrane potentials and ultrastructure of subendocardial Purkinje and ventricular muscle fibers, isolated 1, 3, 5, 6, 14, and 24 h after coronary occlusion were investigated. Action potentials were recorded from progressively fewer layers of muscle cells as the age of the infarct increased. At 14 h little viable muscle remained. The decrease in the number of electrophysiologically viable muscle fibers correlated with structural evidence that the infarct moved with time toward the endocardial surface until only viable Purkinje fibers remained. Purkinje and surviving ventricular muscle fibers demonstrated a progressive decrease in resting potential, action potential amplitude, and Vmax and a progressive increase in action potential duration. Spontaneous diastolic depolarizations were found in Purkinje fibers only in 24-h infarcts and occasionally in cells deep to the endocardial surface, which may have been muscle cells. We hypothesize that during the first 24 h after coronary occlusion arrhythmias originate near the interface of infarcted and ischemic myocardium. As this interface moves toward the endocardium, this site of origin of arrhythmias moves with it until the Purkinje network is reached.
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PMID:Time course of infarct growth toward the endocardium after coronary occlusion. 42 Mar 19

We have recently detected accumulation of lysophosphoglycerides, catabolites of phospholipids, in ischemic myocardium early after coronary occlusion. In the present study we delineated effects of selected concentrations of albumin-bound lysophosphatidyl choline (LPC) comparable to those accompanying ischemia in vivo on action potentials of isolated canine Purkinje fibers. Lysophosphoglycerides induced concentration-dependent (0.75-3.0 mM) decreases in resting membrane potential, overshoot of phase 0, maximal velocity of upstroke (Vmax) of phase 0, and action potential duration. The highest concentrations (2.0-3.0 mM) induced fractionation of the action potential into several components, unresponsiveness to external stimulation, and enhanced automaticity at normal and reduced membrane potentials. LPC induced a rightward shift in the membrane response curve, a 40-fold prolongation of conduction time, and an increase in the ratio of effective refractory period to action potential duration such that the effective refractory period persisted beyond action potential duration, resulting in postrepolarization refractoriness. These electrophysiological alterations were entirely reversible after 70 minutes of perfusion without LPC, with the exception of a persistent depression in the Vmax of phase 0. Lysophosphatidyl ethanolamine (LPE) elicited alterations in action potentials indentical to those elicited by LPC. Furthermore, LPC (3.0 mM) induced comparable alterations in action potentials recorded from isolated rabbit papillary muscles. Since lysophospholipids accumulate early after myocardial ischemia, and since concentrations equivalent to those occurring in vivo induce electrophysiological alterations resembling those seen in ischemic myocardium in vivo, lysophosphoglycerides may be of major importance as biochemical mediators of malignant dysrhythmia induced by ischemia.
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PMID:Potential arrhythmogenic electrophysiological derangements in canine Purkinje fibers induced by lysophosphoglycerides. 42 75

The major goal of this investigation was to determine if activation of cardiac receptors during coronary artery occlusion could inhibit efferent renal sympathetic nerve activity. In nine chloralose anesthetized dogs with only carotid (n = 3) or with sinoaortic (n = 6) baroreceptors operative, anterior descending coronary artery (LAD) occlusion resulted in a small decrease in mean arterial pressure (-9.8+/-5.1 mm Hg, NS) and in a significant (P < 0.05) increase in renal nerve activity (24.0+/-4.1%). In these dogs, circumflex coronary artery (Cx) occlusion resulted in greater hypotension (-18.4+/-4.0 mm Hg), and yet no change (1.1+/-9%) in renal nerve activity was noted. Changes in left atrial pressure during LAD and Cx occlusion were not different. In seven dogs with carotid sinus denervation, coronary occlusions resulted in decreases both in arterial pressure and in renal nerve activity which were consistently greater during Cx occlusion. The responses to coronary occlusion in six dogs after sinoaortic deafferentation were similar to those observed with only carotid sinuses denervated. In all experiments, vagotomy abolished the difference in the blood pressure responses and the decreases in renal sympathetic nerve activity during Cx occlusion. Vagotomy also abolished the decrease in nerve activity during LAD occlusion in dogs with carotid or sinoaortic denervation. These data show that Cx occlusion and, to a lesser degree, LAD occlusion resulted in reflex withdrawal of renal sympathetic nerve activity mediated by left ventricular receptors with vagal afferents. The reflex withdrawal of renal nerve activity during Cx occlusion occurred in spite of hypotension and the presence of functioning sinoaortic baroreceptors.
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PMID:Reflex inhibition of renal sympathetic nerve activity during myocardial ischemia mediated by left ventricular receptors with vagal afferents in dogs. 42 60

ST segment elevation, used as an index of the relative extent of myocardial ischemic injury, was measured using a single precordial lead located at the point of maximum ST elevation. ST changes were followed for two hours after acute coronary occlusion in pigs, and were compared to the sum of ST elevation recorded with an 18 lead precordial map. Some animals were subjected to Reperfusion (n = 12), others to infarct extension (n = 10), while a control group (n = 9) was followed without an ST-modifying intervention. Correlation between sigmaST and ST in the single lead was good, with a correlation coefficient of 0.844 at 360 points of comparison. Time to peak ST elevation using the single lead technique was comparable to that using the 18 lead map. Changes in the ST elevation using both techniques were similarly reduced following reperfusion, increased following extension, and followed a similar downslope pattern in the unmodified infarct group. This single lead technique offers the advantage of simplicity of use without sacrifice of accuracy. Its use can facilitate clinical studies of myocardial ischemic injury and its modification.
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PMID:The single precordial lead for ST segment monitoring: comparison with the multiple lead map. 43 52

A micro-PCO2 electrode, with dimensions of 1 x 10 mm, and a 63% response time of 14 s was inserted into the left ventricular myocardium of the pentobarbital-anesthetized dog. Continuous recordings were made of myocardial PCO2 (PmCO2), arterial PCO2 (PaCO2), and coronary sinus PCO2 (CSPCO2) during variation of respiratory rate. PmCO2 and CSPCO2 were compared at varying coronary flow. PmCO2 was similar to and closely followed changes in CSPCO2. The difference between PmCO2 and CSPCO2 was -0.52 +/- 3.63 (SD) mmHg, and PmCO2 exceeded PaCO2 by 20.69 +/- 5.12 mmHg. After coronary occlusion, PmCO2, rose promptly, but CSPCO2 was only slightly elevated until the occlusion was released, when a CO2 efflux into the coronary sinus occurred. It is concluded that the electrode measures extracellular PCO2 and that extracellular and myocardial PCO2 are essentially equal. PmCO2 rises rapidly following coronary occlusion.
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PMID:Measurement of myocardial PCO2 with a microelectrode: its relation to coronary sinus PCO2. 43 71

In order to evaluate the influence of the autonomic nervous system in the incidence and characteristics of the early arrhytmias that follows myocardial infarction, we have developed an experimental myocardial infarction in rabbits by acute occlusion of the left ventricular artery. The influence of adrenergic and cholinergic suppression over rhythm disorders and hemodynamics changes after experimental infarction in the rabbit was also studied. We found that after the acute experimental infarction in the rabbit heart, arose an early stage of rhythm disorders in 60% of the animals. In a group of animals that were injected with Practolol before coronary occlusion, the incidence of arrhythmias was 25% and in a group of animals with vagotomy prior to occlussion none of them developed rhythm disorders. It was concluded that the model is highly steemed for the study of early arrhytmias and that automatic nervous system has an important role in the incidence of such arrhythmias.
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PMID:[Role of the autonomic nervous system in early arrhythmias in acute myocardial infarct in the rabbit]. 44 30

In 16 dogs inosine was infused at 0.5 mmol/min i.v. for 5 min beginning 15 min after coronary occlusion. Tracer microspheres were used to estimate flow in subepicardium and subendocardium of nonischemic, central ischemic, and borderline ischemic muscle. Estimates of flow before occlusion, 5 min after occlusion, during inosine infusion, 30 min after infusion and 60 min after infusion were obtained. Coronary occlusion reduced flow in the central ischemic regions by 75-95%. The reduction in flow was greatest in subendocardium. In the borderline regions subendocardial flow was reduced by 30% while subepicardial flow was unaffected. The major effects of inosine were seen in nonischemic and borderline ischemic regions. Flow in borderline subendocardium returned to its pre-occlusion value, and flow in nonischemic myocardium increased by approximately 60-80%. However, only in the ischemic regions was the increase in flow sustained for the entire 60 min. In 20 dogs infarct size was determined using nitro blue tetrazolium stain. In 10 controls infarct size was 20.1%, while in 10 inosine-treated dogs infarct size was 15.2% of left ventricular weight (p less than 0.01). Thus, following coronary occlusion inosine infusion was associated with an increase in perfusion of ischemic myocardium and a reduction in infarct size.
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PMID:Effect of inosine on ventricular regional perfusion and infarct size after coronary occlusion. 44 23


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