Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cocaine abuse may lead to serious cardiac complications, including myocardial ischemia and infarction, myocarditis, cardiomyopathy and arrhythmias. With concomitant use of alcohol and cocaine, cocaethylene is produced by hepatic transformation. Cocaethylene is now thought to be primarily responsible for the deaths that occur among cocaine abusers. Treatment of cardiovascular complications focuses on cocaine-induced ischemia, hypertension and arrhythmias. The use of thrombolytic agents in myocardial infarction remains controversial. Concurrent detoxification with bromocriptine and norepinephrine is recommended.
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PMID:Cardiovascular complications of cocaine abuse. 846 3

The preoperative assessment of the high risk patient undergoing noncardiac surgery has traditionally been based on history, physical examination, and preoperative testing. We propose a method of assessing preoperative risk based on the presentation of coronary artery disease, exercise tolerance, and extent of the surgical procedure. Since this is an evolving field, as new information and perioperative management techniques become available, the preoperative evaluation of the high risk patient will change. We have presented one approach based on our interpretation of data from the current anesthesiology and cardiology literature. In the patient with a recent MI, the predischarge symptom-limited stress test and the electrocardiographic classification can be used to better stratify risk. In the patient with angina, testing should be reserved for those patients who are candidates for coronary revascularization or alternative surgical procedures. In the patient at risk of but without overt symptoms of coronary artery disease, the number of clinical risk factors can determine the probability of coronary artery disease in the individual patient. The decision to perform preoperative revascularization should be based on its anticipated improvement of both the short- and long-term prognosis of the patient considering the risk of such procedures. The objective assessment of LVEF should be performed in patients with a poor exercise tolerance with either a high risk of perioperative ischemia or a suspicion of cardiomyopathy.
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PMID:Preoperative cardiac evaluation for noncardiac surgery: a functional approach. 155 27

Since mitochondria occupy a pivotal position in energy metabolism, mitochondrial dysfunction is directly linked with disturbances in cellular function. Mitochondria possess their own DNA, which codes 13 subunits of the mitochondrial energy transducing system; the other subunits are coded by nuclear DNA. Recent advances in gene technology, especially the polymerase chain reaction (PCR), permit us to analyze mitochondrial DNA mutations in a small quantity of tissue. We devised rapid and accurate methods to detect mitochondrial DNA mutations, i.e., the primer shift PCR method and the PCR-Southern method. We also developed a method to determine DNA sequences directly without cloning. Using these methods, we revealed that multiple mitochondrial DNA mutations exist in the myocardium of patients with cardiomyopathy. One mutation was based on the following directly repeated sequence: 5'-CATCAACAACCG-3'. This sequence exists in both the ATPase6 gene and the D-loop region, and pseudo-recombination occurs at that directly repeated sequence resulting in a 7.4 kbp deletion. Accordingly, some subunits of the mitochondrial energy transducing system can not be biosynthesized by these deleted mitochondrial DNA, and energy transduction is substantially depleted. Even without reduction of blood supply, mitochondrial DNA mutations can induce a chronic ischemia-like state in the myocardium, which might be a factor in the genesis of cardiomyopathy.
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PMID:Mitochondrial DNA mutations and disturbances of energy metabolism in myocardium. 174 73

Experimental studies have demonstrated that myocardium reperfused after reversible ischemia exhibits prolonged depression of contractile function ("stunning"). Despite the multiplicity of clinical situations in which myocardial stunning would be expected to occur, investigation of this phenomenon in humans has been hindered by several major problems, including the limited accuracy of the methods available to measure regional left ventricular function, the inability to quantify regional myocardial blood flow during acute ischemia, the difficulty in establishing with certainty, the beginning and end of an ischemic episode, and the uncontrolled influence of variables (such as preload, afterload, adrenergic tone, and inotropic therapy) that have a major impact on postischemic dysfunction. The main problem is to discern whether a reversible defect of contractility is caused by stunning, silent ischemia, or hibernation (i.e., chronic ischemia). This differential diagnosis requires the simultaneous measurement of regional myocardial function and flow, which thus far has not been generally possible. Despite these limitations, however, numerous clinical observations suggest that stunning does occur in various settings in which the myocardium is exposed to transient ischemia, including coronary angioplasty, exercise-induced angina, angina at rest (unstable or variant), acute myocardial infarction with early reperfusion, open-heart surgery, and cardiac transplantation. Recognition of this entity is important, amongst other reasons, because it is likely to cause significant morbidity and because it is potentially correctable with inotropic therapy or even preventable with antioxidant therapy. In addition, the appreciation of the phenomenon of myocardial stunning should allow the clinician to assess the efficacy of reperfusion therapy with greater accuracy and to recognize that patients should not be denied mechanical revascularization solely because of an abnormal left ventricular wall motion. Perhaps the most intriguing clinical implication of the concept of myocardial stunning is the possibility that in patients who exhibit frequent episodes of ischemia in the same territory, the myocardium may not be able to fully recover between episodes and thus may remain reversibly depressed for prolonged periods of time, or even chronically, which could account for some cases of "ischemic cardiomyopathy." Our understanding of myocardial stunning in humans is still relatively crude and will not significantly improve until studies are performed that measure simultaneously regional myocardial perfusion and function (so that stunning can be differentiated from silent ischemia and hibernation). Future important areas of research should also include the elucidation of whether stunning can become chronic and the evaluation of therapies (such as antioxidant treatments) designed to prevent this contractile abnormality.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical relevance of myocardial "stunning". 175 33

Activation of the sympathetic nervous system is an important factor in the genesis of ventricular arrhythmias in patients with impaired ventricular function. Such patients have an appropriate substrate that is capable of generating rhythm abnormalities, which may be related to enhanced automaticity, triggered automaticity, and reentrant mechanisms; all three mechanisms are markedly potentiated by the action of catecholamines. Additionally, the sympathetic nervous system can provoke the development of hypokalemia and ischemia (which can independently lead to the occurrence of rhythm disturbances), and catecholamines may negate the beneficial electrophysiological actions of antiarrhythmic drugs. A substantial amount of experimental data implicates the sympathetic nervous system as a potent stimulus for ventricular tachyarrhythmias and sudden cardiac death, especially in the setting of myocardial ischemia. Two important mechanisms that have been identified include 1) enhanced sympathetic outflow from the central nervous system and 2) nonuniform myocardial denervation resulting in beta-receptor up-regulation and catecholamine hypersensitivity in the infarct zone. Disruption of sympathetic neural innervation of the heart and the use of beta-blocking agents may reduce the occurrence of sudden death and improve survival in animal models of arrhythmias and in some subsets of patients, including those with the long QT syndrome, a recent myocardial infarction, and perhaps those with a cardiomyopathy. The mechanism of this beneficial effect remains to be defined.
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PMID:Role of the sympathetic nervous system in the genesis of ventricular arrhythmia. 1461 4

A sharp and unusually high increase in the serum of glutamic-oxalacetic and glutamic-pyruvic transaminase and of lactic-dehydrogenase accompanied the terminal events, acute pulmonary edema with cardiogenic shock, in 2 patients suffering from chronic congestive heart failure caused by dilatative myocardiopathy. Experimental and clinical data raises the possibility that the considerable enzymic increase may be due to the combined effect of chronic stasis and acute ischemia on the liver.
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PMID:[Acute hepatic ischemia and cardiogenic shock in patients with dilated cardiomyopathy]. 208 28

The high-amplification signal-averaged ECG (SAECG) allows the detection and analysis of late potentials (LP), which are related to a higher risk of severe ventricular arrhythmias in patients with myocardial disease and coronary artery disease. Because of excessive noise, this technique is usually performed at rest and occasionally immediately after interruption of exercise. Until now, however, it has not been used during exercise. The authors relate in this paper the method and results of the SAECG recorded at rest and during a standard stress test on 30 patients with a recent first myocardial infarction (day 10-14), in good condition, without ECG evidence of significant residual ischemia or bundle branch block. The SAECG was recorded during the steady state of a standardized stress test when a heart rate (HR) corresponding to 80% of the maximal HR was reached during a first test. Three patients had three criteria for LP, three others had two criteria, and two had only one. It has been impossible to analyze the SAECG during exercise because of excessive noise. One patient out of 30 in our study, 21 subjects had normal SAECG at rest and during exercise. None of the 6 patients with more than 1 abnormal criterion at rest became normal during the stress test despite a decrease of the duration criteria in all and an increase of the amplitude (root mean square) the terminal 40 ms (RMS40), as opposed to the 2 patients with just one positive criterion at rest (RMS 40 less than 25 muV) who became normal during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Detection of late potentials on the averaged QRS signal recorded at rest and during a standardized stress test after acute myocardial infarction. 209 Jul 32

There is a complex network of collagen throughout the heart. It is composed of a hierarchy of fibrils and fibers ranging from 10 nm to 2-3 microns in diameter. This network can be broken down by ischemia, adriamycin administration, or disulfide administration in laboratory animals. Following loss due to coronary artery ligation, the ischemic area begins bulging within 3 h. General loss of portions of the collagen matrix is induced by intravenous oxidizing glutathione, and results in marked diffuse ventricular dilatation. Generalized collagen loss in the ventricles, as induced by disulfide administration or adriamycin infusion, persists for 6 months at which time evidence of some replacement is visible, and evidence of diffuse fibrosis is present. In humans, cardiac dilatation occurs in a variety of disease states without overstretch of sarcomeres. This presumes rearrangement of the muscle bundles, which can only occur with marked alterations of the collagen matrix. Ventricular dilatation, associated with viral myocarditis or puerperal cardiomyopathy, may persist for months, suggesting the collagen loss, as with the experimental animals, takes many months to repair. The cardiac dilatation may ameliorate, or, in some patients, deteriorate into heart failure. The animal experiments with loss of the collagen matrix, ventricular dilatation, and failure to replace the matrix for many months provide an explanation for persistent cardiac dilatation in various human diseases.
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PMID:Myocardial connective tissue alterations. 209 Dec 28

We performed exercise thallium-201 myocardial scintigraphy in 32 patients with angina pectoris to study the incidence of perfusion defects, who had no significant organic stenosis on coronary angiography. None of them had myocardial infarction or cardiomyopathy. Thallium-201 myocardial scintigraphy and 12-lead ECG recording were performed during supine bicycle ergometer exercise. Perfusion defects in thallium-201 scintigrams in SPECT images were assessed during visual analysis by two observers. In the coronary angiograms obtained during intravenous infusion of nitroglycerin, the luminal diameter of 75% stenosis or less in the AHA classification was regarded as an insignificant organic stenosis. Myocardial perfusion defects in the thallium-201 scintigrams were detected in eight (25%) of the 32 patients. Six of these eight patients had variant angina documented during spontaneous attacks with ST elevations in standard 12-lead ECGs. Perfusion defects were demonstrated at the inferior or inferoposterior regions in six patients, one of whom had concomitant anteroseptal defect. The defects were not always accompanied by chest pain. All but one patient demonstrating inferior or inferoposterior defects showed ST depression in leads II, III and aVF on their ECGs, corresponding to inferior wall ischemia. The exception was a case with right bundle branch block. Thus, 25% of the patients with angina pectoris, who had no evidence of significant organic stenosis on their coronary angiograms, exhibited exercise-induced perfusion defects in their thallium-201 scintigrams. Coronary spasms might have caused myocardial ischemia in these patients.
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PMID:[Exercise-induced thallium-201 myocardial perfusion defects in angina pectoris without significant coronary artery stenosis]. 209 48

Calcium ions are important in many aspects of normal cardiac function as well as in the response to certain pathologic states. The contribution that myocardial calcium influx makes to the cardiac action potential and the pharmacologic efficacy of compounds designated as calcium channel blockers is examined with respect to current knowledge regarding the structure and characteristics of cardiac sarcolemmal calcium channels. Once intracellular, calcium provides the link between cardiac electrical activity and actual mechanical shortening of cardiomyocytes through a complex interaction of regulatory and structural contractile proteins. This is followed by calcium clearance from the cytosol; the mechanisms by which this occurs are manipulated by drugs such as the digitalis glycosides to enhance myocardial contractility. The importance of intracellular 'second messengers' (eg, cyclic AMP) in constituting a final common pathway for the effects of certain cardiotonic agents is defined. The significance of abnormal calcium homeostasis under conditions of heart failure, myocardial infarction, ventricular fibrillation and cardiomyopathy is examined. The role of calcium in the mediation of myocardial damage under conditions of ischemia and secondary to a phenomenon known as 'the calcium paradox' is discussed. The finding that neonatal hearts are more vulnerable to ischemic contracture than adult hearts may be partially explained by differences between neonatal and adult myocardial calcium handling. Understanding of the interactions that exist between the calcium ion and the cardiomyocyte requires a sound knowledge of this essential partnership by both the physiologist and the practising physician.
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PMID:Calcium and the heart: an essential partnership. 217 38


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