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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relation between global and regional left ventricular function and electrocardiographic signs of ischemia at rest and during submaximal supine exercise was studied in 27 patients 2 to 3 weeks after acute myocardial infarction. Dynamic myocardial scintigraphy was performed at rest and during submaximal exercise utilizing an in vivo method of labeling red blood cells with technetium-99m pertechnetate. Gated radionuclide blood pool scintigrams were obtained in a modified left anterior oblique, and in some patients also in the right anterior oblique projection, to measure left ventricular ejection fraction and segmental wall motion. Electrocardiographic monitoring of heart rate and rhythm was provided during the exercise. The submaximal exercise test was terminated when the patient's heart rate reached 125 beats/min or if angina, malignant ventricular ectopy or electrocardiographic evidence of myocardial ischemia developed before this rate was reached. The data demonstrate that patients with a recent anterior myocardial infarct, in contrast to patients with a recent inferior or nontransmural infarct, manifest a significant reduction in left ventricular ejection fraction with submaximal exercise. Of the eight patients with an anterior infarct, seven had segmental wall motion abnormalities at rest. Four of these eight manifested more severe abnormalities with submaximal exercise; three had abnormalities at rest that did not change with exercise. Four of the eight had a positive electrocardiographic response during exercise (two were taking digoxin). Of these four, only two had more marked wall motion abnormalities with effort. Of the 13 patients with an inferior infarct, 11 had apparently normal wall motion in the modified left anterior oblique projection at rest, including 2 who manifested segmental wall motion abnormalities with submaximal exercise; the 2 remaining patients had wall motion abnormalities at rest that, on exercise, became more marked in one and were unchanged in one. Four of the 13 had a positive electrocardiographic response with exercise (one was taking digoxin); only one of these had a detectably more severe wall motion abnormality with exercise. Of the six patients with a nontransmural infarct, four had no identifiable wall motion abnormalities at rest; in one of these, an abnormality developed with exercise. The remaining two patients had wall motion abnormalities at rest; in one, a positive electrocardiographic ischemic response developed with exercise. Patients with an anterior infarct appear to have a different functional ventricular response to submaximal exercise at the time of hospital discharge than patients with an inferior or nontransmural infarct. To identify ischemic responses with submaximal exercise in these patients one should ideally use both electrocardiographic monitoring and dynamic myocardial scintigraphy.
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PMID:Submaximal exercise testing after acute myocardial infarction: myocardial scintigraphic and electrocardiographic observations. 35 68

We review the hemodynamic effects and clinical usefulness of five natural and synthetic catecholamines. Their actions are best understood by an appreciation of the relative ability of each catecholamine to activate alpha, beta 1 and beta 2 adrenergic receptors in the myocardium and peripheral vasculature. Epinephrine, the first catecholamine isolated, is shown to have little useful role in the therapy of acute myocardial infarction. L-norepinephrine has powerful alpha and moderate beta 1 effects. It is the catecholamine of choice in the initial treatment of cardiogenic shock associated with acute myocardial infarction. Isproterenol markedly increases myocardial contractility and heart rate by beta 1 stimulation, while simultaneously decreasing peripheral vascular resistance and, therefore, arterial pressure through its action on beta 2 receptors. It increases cardiac output, but its metabolic costs are high in the presence of ischemia. Its role in the therapy of acute myocardial infarction has largely been supplanted by more selective agents. Dopamine causes slightly less vasoconstriction than l-norepinephrine and slightly less myocardial stimulation than isoproterenol. In low doses, it increases renal and mesenteric blood flow by activation of a non-adrenergic receptor. Tachycardia and associated metabolic deterioration render it a second-line drug in the treatment of severe cardiogenic shock. Dobutamine, a new synthetic catecholamine, has primarily beta 1 activity. It increases myocardial contractility with little effect on heart rate or peripheral vascular resistance. It is ineffective in cardiogenic shock, but may eventually be shown to have a role in the treatment of left ventricular failure uncomplicated by severe hypotension.
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PMID:Use of catecholamines in acute myocardial infarction. 39 85

The effect of isoproterenol infusion on regional myocardial perfusion and tissue oxygenation during acute myocardial infarction was investigated in anesthetized dogs. Measurements of regional flow with radioactive microspheres and myocardial lactate and adenosine triphosphate from analysis of myocardial biopsies were compared in normal, marginal, and infarcted tissue in dogs with a ligated coronary artery. After 10 minutes of isoproterenol 0.15 microgram/Kg./minute, flow was unchanged in the marginal and infarcted regions, and, although rises occurred in most dogs, changes were inconsistent in the normal regions. In the marginal regions, tissue lactate rose by 5.6 mumoles/g (97 per cent) and adenosine triphosphate fell by 2.4 mumoles/g (46 per cent) after isoproterenol. No consistent changes occurred in the normal or infarcted regions of the dogs given isoproternol or in any regions of control dogs given saline. It is concluded that beta-adrenergic stimulation with isoproterenol increases tissue ischemia in experimental acute myocardial infarction.
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PMID:Effect of isoproterenol on regional myocardial perfusion and tissue oxygenation in acute myocardial infarction. 42 73

A 65-year-old woman with an acute myocardial infarction, as judged by serial enzyme changes, developed transitory Q waves in leads V2 to V4 and leads 2, 3, and aVF during an attack of pain in the chest. These Q waves were not present 12 hours later. It is suggested that these changes represent a focal block in the septal fibers of the left bundle-branch system. This defect could underlie the transient right precordial Q waves seen in myocardial infarction or ischemia, as well as the fixed Q waves of many patients without septal infarction at autopsy.
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PMID:Transient focal septal block. 43 30

Concurrent viral infection and myocarditis presumably indicate viral myocarditis. The electrocardiographic and pathologic changes developing during acute infection may, however, result from changes not produced by the infection itself, eg, fever, tachycardia, ischemia, potassium depletion, vitamin deficiencies, drugs. This qualification should be remembered in the evaluation of all alleged virus myocarditis. Viral infection seems to prefer the very young. Its localization in the heart is favored by general or local hypoxia, perhaps thus explaining a predilection for the subendocardium. It may be influenced by the strain of the organism or by the hormonal or immunologic state of the host. Intrauterine infection of the fetus with rubella, mumps, and perhaps coxsackievirus can induce congenital cardiac defects. The role of virus infection in precipitating acute myocardial infarction deserves further study. The value of treatment, including steroids, nonsteroidal immunosuppressive agents, and "antiviral" agents is not yet established.
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PMID:Virus myocarditis: a critique of the literature from clinical, electrocardiographic, and pathologic standpoints. 46 41

This study was conducted to determine whether low level exposure to carbon monoxide would increase myocardial ischemia associated with acute myocardial infarction. An hour after coronary artery ligation, eleven anesthetized dogs underwent five sequential respiratory exposures to 5,000 ppm carbon monoxide, producing mean blood carboxyhemoglobin levels of 4.9% to 17.0%. Ischemia, as indicated by the amount of S-T segment elevation in epicardial electrocardiograms, increased significantly at the lowest carboxyhemoglobin level and increased further with increasing carbon monoxide exposure. These changes occurred in the absence of altered heart rate, blood pressure, left atrial pressure, cardiac output, or blood flow to ischemic myocardium. Flow to non-ischemic myocardium increased with carbon monoxide exposure, the percentage increase being approximately double the increase in carboxyhemoglobin level. Thus, low level exposure to carbon monoxide can significantly augment ischemia in acute myocardial infarction, apparently through a reduction in oxygen supplied to ischemic tissue. The data suggest that hypoxia induced by carbon monoxide exposure is more severe than can be accounted for by a simple reduction in oxygenated hemoglobin.
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PMID:Augmentation of myocardial ischemia by low level carbon monoxide exposure in dogs. 47 72

Using a quantitative, computer-aided circumferential profile technique, we have shown that thallium-201 scintigrams with large defects can identify a group of patients with a high mortality after acute myocardial infarction. To determine whether high-risk thallium scintigrams predict poor survival because of a critical loss of myocardium, we correlated infarct size in 24 autopsied patients with the extent of thallium defect in three views. Of 13 patients with large defects (computer score greater than or equal to 7.0) eight (62%) had greater than 25% loss of left ventricular (LV) myocardium, but five (38%) had smaller infarcts (4--24% of LV myocardium), suggesting that part of the scintigraphic defect was related to ischemia without necrosis. Eight of the nine patients with loss greater than or equal to 25% LV myocardium had large defects. In 10 of 11 patients with small defects (computer score less than 7.0), infarcts involved less than 20% of LV myocardium. Although scintigrams with large defects predicted a critical loss of myocardium in over 60% of our patients, they included an important second group, in which the scintigraphic defect appeared to reflect a small infarct and a large surrounding area of reversibly ischemic myocardium.
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PMID:Pathologic basis of thallium-201 scintigraphic defects in patients with fatal myocardial injury. 47 82

Serial treadmill exercise testing (mean 5.5 tests/patient) was used to evaluate the prognosis of 200 males (mean age 53 years) without clinical heart failure or unstable angina pectoris 3 weeks after acute myocardial infarction (MI). Exercise-induced ischemic ST-segment depression greater than or equal to 0.2 mV 3 weeks after MI was significantly more prevalent in patients with subsequent cardiac arrest (100%) or coronary artery bypass graft surgery (64%) than in patients without subsequent events within 2 years of infarction (35%) (p less than 0.05). Exercise-induced ventricular arrhythmia on multiple tests 5-52 weeks after MI was more prevalent in patients with recurrent myocardial infarction (90%) than in patients without subsequent events (47%) (p less than 0.001). By contrast, exercise-induced ventricular arrhythmia on a single test at 3 weeks was a less powerful predictor of subsequent cardiac events. Exercise-induced ischemia 3 weeks after MI predicted early fatal events, while ventricular arrhythmia on serial testing predicted later nonfatal events.
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PMID:The prognostic significance of serial exercise testing after myocardial infarction. 49 48

This investigation was undertaken in order to experimentally reassess the value of myocardial waviness and stretching as early histological indicators of acute myocardial infarction. Twenty three dogs were subjected to periods of ischemia, from 30 minutes to 4 hours; wavy fibers were present in 87% and 91% of the ischemic and non-ischemic samples respectively. It is concluded that myocardial fiber waviness lacks significance as an indicator or early myocardial infarction, whose diagnosis remains a major challenge.
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PMID:[Experimental reevaluation of myocardial ondulations in the early histological diagnosis of myocardial infarct]. 54

The effect of verapamil on ST changes was evaluated in 10 selected patients with acute myocardial infarction admitted to the Coronary Care Unit within 8 hours after the onset of symptoms. To evaluate the extent of ischemia it has been used the magnitude and direction of the ST vector derived from X, Y and Z leads of the Frank vector system. After a control period of 2 hours, during which the changes of the ST vector magnitude were assessed, each patient received 0.1 mg/Kg verapamil intravenously, ST vector magnitude (STVM), ST azimuth (STAZ), ST elevation (STEL), heart rate, systemic blood pressure and pressure-rate product were assessed 5, 15, 30, 45, 60, 75, 90, 105 and 120 minutes after the administration of the drug. Verapamil produced a significant progressive decrease in STVM (from a mean of 254 +/- 44 muV at the end of the control period, to 139 +/- 25 muV after 2 hours; P < 0.01). Systolic blood pressure decreased significantly throughout the trial; the most significant decrease was registered immediately after the infusion of verapamil (from a mean of 134 +/- 3 mmHg to 121 +/- 3 mmHg; P < 0.001). Pressure-rate product declined slightly. No significant change in STVM was observed in 10 control patients with acute myocardial infarction examined over a 4 hours period. The apparent protective effect of verapamil in myocardial ischemia is discussed in relation to its calcium-antagonistic properties in excitable tissues.
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PMID:[Effects of acute infusion of verampil on the ST segment elevation measured with the Frank orthogonal leads in patients with acute myocardial infarct]. 54 89


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