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

The time course of the changes in ventricular fibrillation threshold (VFT) was determined in 28 dogs by means of electrical stimulation, triggered from the R wave, with DC square wave pulse series (of 140 ms duration) inserted into the vulnerable period of the cardiac cycle. After acute coronary occlusion there was a sudden decrease in the VFT followed by a slow increase such that 30 min after the ligation pre-occlusion values of VFT were reached. The magnitude of the decrease in VFT depended upon the collateral blood supply. There were no other changes in VFT during the remaining course of the experiment. Following slow coronary occlusion the first arrhythmic phase was not detectable. Any decreases in VFT that occurred were smaller and of shorter duration than those occurring after acute occlusion and were independent of the extent of the collateral blood supply.
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PMID:Time course of changes in ventricular fibrillation threshold in myocardial infarction: characteristics of acute and slow occlusion with respect to the collateral vessels of the heart. 94 34

Groups of dogs were exercised immediately before, and immediately after occlusion of the left anterior descending coronary artery. Coronary occlusion by a staged procedure resulted in a low mortality and rare ventricular ectopic beats. The combination of simultaneous exercise with coronary occlusion reproducibly provoked ventricular fibrillation (VF). Exercise before and after occlusion frequently produced ventricular tachycardia but no VF. The risk of major arrhythmias was related to the peak heart rate resulting from the exercise.
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PMID:Coronary occlusion before, during, and after strenuous exercise. 95 22

We have previously demonstrated that atropine pretreatment increases the incidence of fatal ventricular arrhythmias induced by left anterior descending coronary artery (LAD) occlusion. The purpose of the present study was to determine whether the deleterious effect of atropine also applies to arrhythmias induced by right coronary artery (RCA) occlsusion. Occlusion of the RCA resulted in ventricular arrhythmias in all 20 animals studied, followed by ventricular fibrillation in three animals (15 per cent). Right coronary occlusion also resulted in bradycardia (-30.3 +/- 5.1 beats per minute) and hypotension (-23.1 +/- 4.9 mm. Hg). Pretreatment of 15 animals with atropine caused no significant increase in the incidence of ventricular fibrillation (i.e., 20 per cent). In addition, atropine pretreatment had no effect on the fall in heart rate and hypotension associated with RCA ligation. Sectioning the vagus nerves produced results similar to atropine pretreatment with the exception that a significant portion of the bradycardia was prevented. These results indicate that the increase in deaths after atropine observed in animals undergoing experimental LAD occlusion in not demonstrated with RCA occlusion. The results also indicate that the potential for deleterious effects of atropine in acute infarction might depend on the anatomic location of the involved myocardium.
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PMID:Coronary occlusion site as a determinant of the cardiac rhythm effects of atropine and vagotomy. 99 81

The influence of site of acute myocardial infarction on heart rate, blood pressure, cardiac output, total peripheral resistance (TPR), cardiac rhythm, and mortality was determined in 58 anesthetized cats by occlusion of either the left anterior descending (LAD), left circumflex or right coronary artery. LAD occlusion resulted in immediate decrease in cardiac output, heart rate, and blood pressure, an increase in TPR, and cardiac rhythm changes including premature ventricular beats, ventricular tachycardia, and occasionally ventricular fibrillation. The decrease in cardiac output and increase in TPR persisted in the cats surviving a ventricular arrhythmia. In contrast, right coronary occlusion resulted in a considerably smaller decrease in cardiac output. TPR did not increase, atrioventricular condition disturbances were common, and sinus bradycardia and hypotension persisted in the cats recovering from an arrhythmia. Left circumflex ligation resulted in cardiovascular changes intermediate between those produced by occlusion of the LAD or the right coronary artery. Mortality was similar in each of the three groups. We studied the coronary artery anatomy in 12 cats. In 10, the blood supply to the sinus node was from the right coronary artery and in 2, from the left circumflex coronary artery. The atrioventricular node artery arose from the right in 9 cats, and from the left circumflex in 3. The right coronary artery was dominant in 9 cats and the left in 3. In conclusion, the site of experimental coronary occlusion in cats is a major determinant of the hemodynamic and cardiac rhythm changes occurring after acute myocardial infarction. The cardiovascular responses evoked by ligation are related in part to the anatomical distribution of the occluded artery.
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PMID:Site of myocardial infarction. A determinant of the cardiovascular changes induced in the cat by coronary occlusion. 100 Jul 78

The effects of unipolar and bipolar stimulation on ventricular fibrillation threshold were studied during acute occlusion of the left anterior descending coronary artery in 13 anesthetized dogs. Values for ventricular fibrillation threshold were determined by delivering trains of rapid bipolar or unipolar pulses (100/sec) during the vulnerable period. The mean threshold value was found to be 13.0 ma for bipolar, 13.9 ma for unipolar anodal and 21.0 ma for unipolar cathodal stimulation. Ventricular fibrillation threshold was significantly lower (P less than 0.01) with both unipolar anodal and bipolar stimulation than with unipolar cathodal stimulation. In these animals, the first premature beats induced by the rapid stimuli occurred significantly earlier with unipolar anodal and bipolar stimulation than with unipolar cathodal stimulation. The effect of competition of unipolar or bipolar pacing stimuli with normally conducted ventricular beats was also studied in a group of 16 dogs. Repeated trials of competitive pacing during coronary occlusion showed that the incidence of ventricular fibrillation was significantly greater (P less 0.05) with bipolar pacing (36 percent) than with unipolar cathodal pacing (15 percent). These results indicate that bipolar pacing is potentially more dangerous than unipolar cathodal pacing and suggest that the incidence of pacemaker-induced ventricular fibrillation might be further reduced by the use of unipolar cathodal stimulation during acute myocardial infarction.
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PMID:Effects of unipolar cathodal and bipolar stimulation on vulnerability of ischemic ventricles to fibrillation. 110 45

Fibrillation threshold (FS) were determined in 27 mongrel dogs by direct electrical stimulation of the myocardium by 50 Hz AC impulses of 0.20-0.28 sec during the vulnerable period. The FS is the current which just suffices to produce ventricular fibrillation. Sinus rhythm was restored 10 sec after onset of ventricular fibrillation by defibrillation. Determinations of FS were carried out for each animal repeatedly before and 3 min after acute ligation of the circumflex ramus respectively the descendens ramus of the left coronary artery. Post mortem selective coronary angiography was performed in all cases and the extent of spontaneous collateral vessels was estimated by the rate of retrograde contrast radiography of the ligated coronary artery. The FS fell appreciably following acute ligation of both the circumflex ramus and the sescendens ramus. Beside the size of the ligated area (the circumflex ramus supplies a larger area of the myocardium in the dog than the ramus descendens) the extent of collateral supply was the determining factor for the reductions of the FS: Following coronary ligation of the circumflex ramus the FS fell on the average from 24.0 mA to 4.1 mA if no collateral vessels were detectable; in the animals with well developed collaterals the FS was reduced from 24.8 to only 14.1 mA. After acute occlusion of the descendens ramus the FS fell from 27.9 mA to 11.5 mA in the group with not sufficient collateral supply and from 31.2 mA to only 21.5 mA in the group with well developed collaterals. The comparison of the different decreases of the FS after coronary occlusion clearly shows that the influence of the in size differing ischemic areas on the decrease of the FS is particularly evident if no collateral vessels are existent. If collateral vessels are well developed this difference is not significant. These results demonstrate that the influence of well developed collaterals on the decrease of the FS after coronary occlusion exceeds the dependence on the size of the ischemic area.
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PMID:[Influence of spontaneous collaterals on the fibrillation threshold of the heart following acute coronary occlusion]. 113 Jan 25

The influence of vagal stimulation and/or beta-adrenergic receptor blockade on the heart rate, blood pressure, contractile force, and cardiac rhythm was evaluated in chloralose-anesthetized cats subjected to occlusion of the anterior descending coronary artery. Occlusion performed in 25 control animals produced significant decreases in heart rate (minus 22.9 plus or minus 4.4 beats per minute), blood pressure (minus 19.2 plus or minus 2.4 mm. Hg), and contractile force (minus 21.6 plus or minus 6.3 per cent). Death due to ventricular fibrillation occurred in five out of 25 animals. Coronary occlusion performed in the presence of vagal nerve stimulation resulted in similar decreases in blood pressure, whereas the decreases in contractile force were significantly greater than in control animals. In addition, the time to onset of the arrhythmias occurring in the vagus-stimulated group was increased. Death due to ventricular fibrillation was similar to control animals (i.e., two of seven, or 28 per cent). Blockade of beta-adrenergic receptors with propranol (0.75 mg. per kilogram) resulted in the usual decreases in rate, pressure, and force with occlusion but the duration of arrhythmias was shortened. The incidence of ventricular fibrillation was not different from that of the control animals. The combination of propranolol and vagal stimulation also failed to confer protection against ventricular fibrillation. Propranolol was observed to prevent the large decrease in contractile force seen with vagal stimulation. These results suggest that: (1) increasing vagal tone above the level existing after acute myocardial infarction does not decrease mortality, (2) propranolol pretreatment does not affect the incidence of ventricular fibrillation induced by coronary occlusion, (3) the duration of the arrhythmia after coronary occlusion is effectively shortened with propranolol, and (4) cardiac beta-adrenergic receptors do not appear to be involved in the decreases in heart rate, blood pressure, and contractile force seen with coronary occlusion.
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PMID:Effect of autonomic neural influences on the cardiovascular changes induced by coronary occlusion. 113 Feb 69

The effects of increased and decreased cardiac sympathetic tone and coronary occlusion on ventricular fibrillation were determined in 14 open chest dogs anesthetized with sodium pentobarbital. Heart rate was kept constant by pacing the right atrium at cycle lengths of 500 msec. Ventricular fibrillation threshold was measured by delivering 350 msec trains of constant current stimuli with a frequency of 100 hertz and 2 msec duration. The minimal current of the train that induced fibrillation was taken as the ventricular fibrillation threshold. In seven animals, the effects of stellate stimulation were studied. Ventricular fibrillation threshold was measured during control periods, after 2 minutes of cornoary occlusion, after 2 minutes of stellate stimulation and after 2 minutes of stellate stimulation and coronary occlusion. Coronary occlusion alone decreased ventricular fibrillation threshold an average of 35 percent of control valvues and stellate stimulation alone decreased the threshold an average of 42 percent of control values. The combination of both these interventions decreased ventricular fibrillation threshold an average of 63 percent of control values. The effects of stellate ablation were studied in seven animals. Ventricular fibrillation threshold was measured during control periods, and during coronary occlusion before and after stellate ganglionectomy. Stellectomy increased the threshold an average of 31 percent above control values. After stellectomy, coronary occlusion decreased ventricular fibrillation threshold by only 11 percent of control values, a value 26 percent higher than the threshold during coronary occlusion before stellectomy. These findings may have therapeutic implications for the management of arrhythmias in patients with acute myocardial infarction or some forms of central nervous system disease.
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PMID:Influence of sympathetic tone on ventricular fibrillation threshold during experimental coronary occlusion. 114 97

The adrenergic neurohumors, when present locally in the myocardium in high concentrations, can produce a variety of cardiac arrhythmias which may develop into ventricular fibrillation (VF). Of particular importance are the arrhythmias observed immediately after experimentally induced acute myocardial infarction (AMI). Fatal VF, often seen to occur after acute coronary occlusion in the canine heart, may be related to the release of endogenous catecholamines, and a similar phenomenon might be responsible for sudden coronary death (SCD) in man. If adrenergic amines play a vital role in the development of arrhythmias and VF in response to acute myocardial ischemia, then it is conceivable that pharmacological means may be undertaken in an attempt to prevent the release of the adrenergic neurotransmitter or to prevent its arrhythmogenic actions by specific blockade of cardiac beta-adrenergic receptors. Drugs that have a central site of action and are capable of producing a decrease in sympathetic outflow might also play a valuable role in the prevention of arrhythmias and SCD. While the activity of the autonomic nervous system can modify the type and severity of arrhythmias resulting from AMI, existing pharmacological agents have little to offer in preventing the potential adverse effects of adrenergic stimulation without compromising the level of consciousness or cardiovascular function through the removal of adrenergic support to the heart. It would seem more beneficial to direct drug therapy at the electrophysiological defect in the myocardium in an effort to prevent arrhythmias and fatal VF. While currently available antiarrhythmic agents fail to achieve the desired effect, the recent evidence dealing with the quaternary ammonium derivatives of propranolol, lidocaine, and bretylium provides some hope for the future development of drugs with antiarrhythmic as well as antifibrillatory properties which may provide a therapeutic approach to the prevention of SCD.
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PMID:Pharmacological modification of arrhythmias after experimentally induced acute myocardial infarction. Drugs acting on the nervous system. 118 77

In a comparative study in pigs the extent of myocardial infarction has been estimated following a temporary three hour coronary occlusion and following a permanent coronary ligation. For evaluation of the cellular injury the infarct size has been determined by a histochemical staining procedure and correlated with serum enzyme studies (creatine phosphokinase, alpha-hydroxybutyric dehydrogenase) in the surviving animal. No significant difference could be detected between the two experimental groups and the extent of cellular damage was similar. A strict linear correlation was found between the serum enzyme activity plotted logarithmically and the morphological infarct size. Likewise the incidence of ventricular fibrillation depended on the extent of cellular injury. Myocardial revascularization does not appear to benefit a pig heart subjected to an acute coronary occlusion lasting three hours or more. Revascularization may even be harmful by creating a haemorrhagic infarct, as found in all the animals submitted to a transient coronary occlusion.
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PMID:Effects of myocardial revascularization following acute coronary occlusion in pigs. 125 10


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