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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Current management of myocardial contusion is based on experience with ischemic heart disease, but the mechanism responsible for cardiac dysfunction may be quite different. The purpose of this study was to characterize the pathophysiology of myocardial contusion in a controlled animal model. Sprague-Dawley rat hearts were prepared on a standard Langendorff apparatus, and myocardial function (DP, + dP/dT, - dP/dT) measured via a left ventricular balloon. Bipolar atrial and ventricular leads were placed to define conduction changes. Coronary sinus effluent was sampled for pO2, pH, creatine phosphokinase (CPK), and lactic dehydrogenase (LDH). The hearts were freeze-clamped to measure phosphocreatine (PC) and adenosine triphosphate (ATP). Myocardial contusion was produced by a single blow with a weighted pendulum. Hearts were divided into control (n = 5), moderate impact--Group I (n = 5), and major impact--Group II (n = 5). Group I sustained a 25% decrease in function after an impact of 78 +/- 5 mJoules/gm, and Group II a 50% deficit after 87 +/- 7 mJoules/gm. Impact resulted in complete electrical arrest, followed by sequential ventricular, atrial, and AV nodal recovery; recovery time correlated directly with degree of injury. Coronary flow at 2 min postinjury was decreased (p less than 0.05) in Group I (12.8 +/- 0.8 ml/min) and Group II (11.5 +/- 1.3) compared to control (17.2 +/- 0.5), and returned to baseline levels at 20 min. LDH and CPK levels were twice as high in Group II as in Group I. The PC/ATP ratio in Group II increased from 1.63 at baseline to 2.54 (p less than 0.05) at 25 min, confirming ischemic reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Graded experimental myocardial contusion: impact on cardiac rhythm, coronary artery flow, ventricular function, and myocardial oxygen consumption. 317 98

The author discusses the results of examination conducted by means of continuous ECG recording for many hours, intracardiac electrography, and programmed electric stimulation of the heart in patients with ischemic heart disease and arrhythmias. It was established that ventricular extrasystoles, including the so-called precursors of ventricular fibrillation, are recorded in most patients suffering from chronic ischemic heart disease and acute myocardial infarction, in 66 and 95% of those examined, respectively. The article gives the electrophysiological criteria of the diagnosis of sino-atrial, atrial, nodal atrio-ventricular, supraventricular in additional paths of stimulation conduction, and ventricular paroxysmal tachycardia.
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PMID:[New study methods and their significance for the diagnosis of heart rhythm disorders]. 616 Feb 79

Information on the prevalence of ECG abnormalities in patients with acute pancreatitis together with pertinent simultaneous laboratory data have been missing. This prospective study was undertaken in order to clarify these points. 54 patients with 72 acute attacks of pancreatitis were examined. 31 patients (57%) had transient ECG abnormalities. The ECG changes consisted mainly of unspecific T-wave changes (25 cases) and accelerated atrial or nodal rhythms (8 cases). The ECG changes were more common in patients with biliary etiology (80%) than in patients with alcoholic etiology (49%), probably partly due to the higher age of the patients with biliary disease. The laboratory data did not give any clue to the cause of the ECG changes. The authors believe that the ECG changes may be due to underlying ischemic heart disease unmasked by the stress of acute pancreatitis, and/or imbalance of the autonomous nervous system.
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PMID:Transient ECG changes during acute attacks of pancreatitis. 616 2

The specialized conduction system of the heart is responsible for both congenital and acquired disorders of cardiac rhythm. Sinoatrial disorders may result from disruption of nodal cells and takeover by subsidiary pacemaker cells. AV block may occur congenitally or result from the ravages of ischemic heart disease. Clinically overt or concealed accessory pathway conduction via various types of bypass tracts are responsible for the genesis of many supraventricular arrhythmias. Anatomohistologic correlations provide the analytic basis for many disturbances of rhythm.
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PMID:Anatomopathology of the normal and abnormal AV conduction system. 620 43

1) In canine experiment, the averaging of high right atrial electrical activity revealed the pre-A preceding the atrial deflection, which was proven to be a part of the electrical activity of sinus nodal region. 2) The pre-A was obtained in 114 (75%) of 153 clinical cases. 3) The mean pre-A interval was 18 +/- 4 msec in control group, and was prolonged in cases with sick sinus syndrome, ischemic heart disease and myocarditis. 4) The significant correlation existed between the pre-A interval and the SACT by Strauss' method (r = 0.80, p < 0.01). 5) The pre-A obtained by averaging technique is relatively simple, safe and reliable method, and is useful for evaluating the sino-atrial function.
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PMID:Clinical significance of the pre-atrial electrical activity recorded by the catheter electrode in high right atrium. 740 Dec 81

Adenosine is a purine nucleoside found in every cell of the human body. In addition to its well-established role in cellular metabolism, extracellular adenosine exerts pronounced effects on the cardiovascular system. These effects, mediated by specific cell surface receptors, include a negative chronotropic effect on cardiac pacemakers, a negative dromotropic effect on atrioventricular nodal conduction, an antiadrenergic effect, and a vasodilatory effect on blood vessels. In addition, adenosine can attenuate platelet aggregation and neutrophil activation and alter cardiac metabolism. Its electrophysiologic effects on atrioventricular nodal conduction constitute the rationale for the use of adenosine as an antiarrhythmic drug for the acute management of paroxysmal reentrant supraventricular tachycardias involving the atrioventricular node, as well as for its use as a diagnostic tool in broad complex tachycardias and in preexcitation. The antiadrenergic action of adenosine explains its potential use in the acute management of catecholamine-dependent ventricular tachycardias. Several of the other effects of adenosine suggest the use of this compound as well as its analogues as cardioprotective agents in the setting of myocardial ischemia (occlusion then reperfusion of coronary vessels, cardioplegia, coronary angioplasty, thrombolysis, and so forth).
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PMID:Mechanisms of action and therapeutic potential of adenosine and its analogues in the treatment of cardiac arrhythmias. 750 14

Gallopamil is a methoxy derivative of verapamil. As is typical of the phenylalkylamine class of calcium antagonists, it acts on the vascular system, and on the heart and its nodal structures. In the treatment of stable angina pectoris, gallopamil is at least as effective as nifedipine and diltiazem, though apparently better tolerated than nifedipine. Typical of calcium antagonists there is little or no tolerance to the antiischaemic effects of gallopamil. Preliminary studies indicate that gallopamil, like other calcium antagonists, has cardioprotective potential. However, further investigation is required to explore the clinical relevance of the improved myocardial regional perfusion and free fatty acid utilisation in reversibly ischaemic regions, and the potential of delayed ischaemia during angioplasty that is observed during gallopamil administration. Gallopamil is well tolerated, exhibiting a low propensity for causing cardiovascular and gastrointestinal adverse effects, thus making it a suitable alternative to other calcium antagonists for the treatment of patients with ischaemic heart disease.
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PMID:Gallopamil. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in ischaemic heart disease. 751 Jun 24

Heart block induced by exercise or associated with symptomatic, chronic bifascicular block can progress to high-grade atrioventricular (AV) block and sudden death. The authors describe a case of exercise-induced AV block in a patient with chronic bifascicular block. Thirty seconds of ventricular asystole were observed during exercise treadmill testing. Myocardial ischemia was ruled out, and the cause was determined to be distal AV nodal block. The pathophysiology, diagnosis, and treatment of distal AV nodal block are reviewed. The role of exercise treadmill testing and electrophysiologic studies in distal AV block are outlined in a diagnostic and therapeutic strategy.
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PMID:Exercise-induced complete heart block in a patient with chronic bifascicular block. 781 13

Calcium channel antagonists can reduce calcium overload induced by myocardial ischemia and thereby protect against malignant arrhythmias. However, these drugs may also adversely affect cardiac contractile function. Mibefradil is a new calcium antagonist that can inhibit cardiac calcium current without reducing myocardial force development. The effects of mibefradil on the inducibility of arrhythmias both before and during ischemia were therefore evaluated in animals with healed infarctions. First, a 2-min coronary occlusion was made during the last minute of exercise (n = 48): 25 animals had ventricular fibrillation (susceptible), whereas 23 did not (resistant). On a subsequent day, programmed electrical stimulation (PES, 8 paced beats followed by two extrastimuli) induced ventricular tachycardia in 19 of 25 susceptible animals but in none of the resistant animals (chi square = 24.6, P < .001). Verapamil (n = 14), diltiazem (n = 13) and mibefradil (n = 14) elicited significant dose-dependent decreases in refractory period and in the Q-Tc interval (except mibefradil) yet failed to prevent PES-induced arrhythmias. Diltiazem and verapamil also increased P-R interval and reduced the maximum rate of change of left ventricular pressure, whereas mibefradil did not. However, all three drugs abolished arrhythmias induced by PES during ischemia. In contrast, lidocaine suppressed PES-induced arrhythmias but failed to prevent ischemically induced arrhythmias. Thus mibefradil can prevent ischemically induced ventricular fibrillation without adverse actions on either A-V nodal conduction or contractile function. These data further suggest that calcium entry may play a critical role in the initiation of ventricular fibrillation during ischemia, whereas other factors must be responsible for the extrasystoles induced by PES.
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PMID:The effects of mibefradil, a novel calcium channel antagonist on ventricular arrhythmias induced by myocardial ischemia and programmed electrical stimulation. 866 18

Ischemic heart disease (IHD) and systemic hypertension commonly coexist in a large number of patients, and the presence of hypertension is a risk factor for worsening IHD. A monotherapy that would effectively treat both is thus an attractive idea, and calcium antagonists have been evaluated in this role. Calcium antagonists exert therapeutic effects through a combination of actions, including systemic and peripheral vasodilation, negative inotropy, and reduced nodal conduction. In randomized, double-blind clinical trials, verapamil compares favorably with propranolol in the alleviation of angina and hypertension. Both diltiazem and nifedipine, as well as long-acting diltiazem, are also effective in treating the combined condition. In addition, each of these drugs enhances exercise tolerance and favors compliance with calcium antagonist therapy. Recent questions regarding the safety of this class of drug have tempered the enthusiasm for their use as first-line therapy in cardiovascular disease. In particular, short-acting dihydropyridine derivatives, including nifedipine and isradipine, may increase cardiovascular morbidity and mortality because of reflex sympathetic stimulation. The results of appropriately controlled, prospective clinical trials will provide more definitive conclusions. For now, we must be cautious in the use of calcium antagonist monotherapy for combined IHD and hypertension.
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PMID:Use of calcium antagonists in patients with ischemic heart disease and systemic hypertension. 918 65


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