PubMed HealthSearch

SEARCH · PubMed Health

Results for “Myocardial Infarction”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Submaximal exercise testing after acute myocardial infarction: myocardial scintigraphic and electrocardiographic observations.

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.

Adult

Pulmonary infarction, myocardial infarction, and acute disseminated intravascular coagulation.

Pulmonary and myocardial damage are frequently cited as manifestations of disseminated intravascular coagulation (DIC), but rarely as causes. Three elderly cases of severe DIC due to pulmonary and myocardial infarction are reported. All three patients died. Necropsy showed extensive pulmonary emboli in each case with large pulmonary infarcts in cases 1 and 2 and a ventricular aneurysm containing thrombus in cases 2 and 3. Early diagnosis and treatment of pulmonary embolism requires a high degree of clinical suspicion but may prevent progression to the irreversible stage of severe DIC.

Aged

[Non-Q wave myocardial infarction. Recurrent myocardial infarction, unstable angina and arrhythmia in 8-year observation].

UNLABELLED: The contradictory views on long term clinical course of patients after non-Q wave myocardial infarction (NQMI) as compared with those after Q wave myocardial infarction (QMI)--induced us to undertake a comparative study of both types of myocardial infarction during a 8 year follow-up. The study was carried out in 400 patients (pts) with NQMI (mean age 51) and 485 pts with QMI (mean age 53). Both groups were compared. We have analysed the following parameters: the dynamics of ischaemic heart disease (unstable angina, reinfarction, arrhythmias, mortality) and coronary arteriography. During 8 year observation unstable angina and arrhythmias, were statistically more frequent in pts after NQMI. Recurrent myocardial infarction occurred in 196 (49%) of pts after NQMI and only in 87 pts (18%) after QMI (p less than 0.001). However, the difference in mortality between both groups was not significant (37% vs 39% respectively). Coronary angiography was performed at 1-6 months after myocardial infarction. In 65% of pts after NQMI detected lesions were limited to proximal part of one or two coronary arteries. CONCLUSION: NQMI is characterized by unstable long-term clinical course, and that is why pts with NQMI should be recommended for early coronary angiography and revascularization.

Adult

Surgery for impending myocardial infarction, acute evolving myocardial infarction, and complications of myocardial infarction.

Post-infarction ventricular aneurysm, ventricular septal defect, and mitral insufficiency are all potentially amenable to surgical intervention. In each instance the results of operation and the prognosis following operation depend largely on the extent of infarction, the status of the residual myocardium, and the interval between infarction and operation. When the residual myocardium exhibits good contractility, the results are usually good. When early operation is performed in the face of a deteriorating clinical course and with poorly contracting residual myocardium, the mortality rates are extremely high. In an effort to increase the efficiency of the residual myocardium, concomitant coronary bypass surgery should be performed whenever possible. In this difficult group, more recent supportive measures such as the intra-aortic balloon pump may be particularly helpful when utilized both before and after operation. The surgical indications and results of coronary bypass surgery in impending or acute evolving myocardial infarction are not as well defined, but it is evident that myocardial revascularization may be useful in carefully selected patients.

Acute Disease

Rectilinear scanning in the detection of acute myocardial infarction.

Myocardial scintigraphy with phosphate bone scanning agents is a new and very useful development in the detection of acute myocardial infarction. Initial experience using a rectilinear scanner is described in 50 consecutive patients admitted to hospital because of suspected myocardial infarction. The routine dose was 15 mCi/5 mg, 99Tcm stannous pyrophosphate intravenously with anterior, left anterior oblique, and lateral scans obtained 45-90 minutes after injection. There was only one false negative scan in 17 patients with proven acute myocardial infarction and that was 16 days after onset. There was no proven false positive investigation in seven patients in which fresh myocardial infarction could be definitely excluded, or in a further 11 cases in which it could be excluded with reasonable confidence. Myocardial scintigraphy was considered helpful in resolving the diagnostic problem in 27 out of 29 equivocal cases. It is concluded that myocardial scintigraphy with a rectilinear scanner is a highly accurate and safe procedure in the detection of acute myocardial infarction. The optimum scanning time is two to six days after onset of suspected infarction, when a diagnostic accuracy approaching 100 per cent can be expected.

Adult

Myocarditis with microabscess formation caused by Listeria monocytogenes associated with myocardial infarct.

Myocardial infarction complicated by bacterial infection is rare. The present case is an instance in which the infecting organism, Listeria monocytogenes, is also rare--an instance not previously reported. The clinical findings were fever without localized infection, severe atherosclerotic heart disease, a myocardial infarct of indeterminate age, and a left ventricular aneurysm. Additional electrocardiographic findings include left bundle branch block, intraventricular conduction defect, and multiple episodes of ventricular tachycardia, all of which may be associated with myocardial infarction and none of which is specific for suppurative myocarditis. Myocardial enzyme abnormalities were absent. Listeria monocytogenes was identified from blood cultures on the day following the patient's death. This case illustrates the difficulty in diagnosing suppurative myocarditis complicating myocardial infarction and the dire consequence of such infection. A review of the literature is included.

Aged

[Biochemical characteristics of uncomplicated and complicated healing of experimental myocardial infarcts].

Myocardial infarction was simulated in experiments with 138 dogs showing normal, high, and low responses. The kinetics of creatine kinase as a marker of necrotic processes in myocardial infarction was shown to accelerate with hyperreactivity and to slow down with hyporeactivity. The kinetics of ů-glutamyl transpeptidase as a marker of reparative processes in myocardial infarction was characterized by delayed and slower evolution in hyper- and hyporeactivity. The kinetics of dienic conjugates, cyclic nucleotides (cAMP, cGMP) and immunoreactive insulin was also determined largely by the body's reactivity and the types of experimental myocardial infarction healing and was closely related to that of enzymatic markers of necrotic processes.

Adrenocorticotropic Hormone

Small animal model for myocardial infarction.

Myocardial infarctions were produced in rats by electro-cauterization of the left anterior descending artery, and the extent of myocardial damage was measured by serial serum levels of creatine phosphokinase activity utilizing spectrophotometric analysis. All animals were also evaluated for myocardial damage by electrocardiographic wave alterations. A correlation between myocardial infarct size and serum creatine phosphokinase was demonstrated. Significant arrhythmias and death occurred only in experimental groups where myocardial infarction had been produced. This small animal model offers a quick, inexpensive, and simple method for screening therapeutic agents that alter infarct size.

Animals

Drug-induced myocardial ischemia and acute myocardial infarction.

Myocardial infarction generally occurs in the presence of known risk factors and identifiable coronary artery disease. Atypical presentations due to therapeutic and illicit drug use are documented, however, and lead to the consideration of alternative pathophysiologic rationales for myocardial infarction. This article discusses central nervous system stimulants and other drugs that have the potential for myocardial damage and their nursing implications.

Amphetamines

[Painless myocardial ischemia. Comparison of 2 groups of patients with a positive exercise test after myocardial infarction].

Myocardial ischemia usually presents with chest pain, the characteristics of which are well known. However, anginal pain may be absent during true ischemia, an entity known as painless or silent myocardial ischemia. Does this type of ischemia have special clinical, angiographic or ergometric characteristics after posterior myocardial infarction (MI)? In order to answer this question 183 consecutive patients with recent posterior MI who had undergone coronary angiography and who had positive exercise stress tests on bicycle ergometers were separated into two groups depending on whether they had experienced at least one episode of pain after the acute phase of myocardial infarction or during the exercise stress test (Group S: 83 patients, average age 54 +/- 10 years) or not (Group A: 100 patients, average 54 +/- 8 years). The following parameters were commoner in Group A: cigarette smoking, heart rate and load developed during exercise stress testing provoking electrical signs of ischemia, single vessel disease on coronary angiography, long-term medical treatment. On the other hand, the following parameters were statistically more frequent in Group S: hypercholesterolemia, preinfarction angina, degree of ST depression during exercise testing, reperfusion of the distal vessels of the occluded artery responsible for the infarct by a collateral circulation, triple vessel disease and surgical treatment. However long-term follow-up (average 3 years) shows that mortality and recurrence of MI are similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiocardiography

Potential precipitating factors of the onset of myocardial infarction.

Myocardial infarction (MI) usually results from thrombotic coronary artery occlusion at the site of a ruptured atherosclerotic plaque. The factors responsible for triggering MI are not known but conditions that increase serum catecholamines may be involved. Accordingly, the authors prospectively evaluated the presence of factors that may increase catecholamines immediately prior to MI in 186 patients. Myocardial infarction was documented by a rise in serum CK-MB. There were 149 men and 37 women, aged 57 +/- 12 (mean +/- SD) years. All patients were interviewed within 72 hours of admission concerning strenuous physical activity, emotional stress, and assumption of the upright posture immediately prior to the onset of symptoms. Seventy-five (40%) patients had one or more of these factors immediately prior to the onset of MI chest pain. Fourteen (8%) experienced acute emotional upset; 28 (15%) were involved in strenuous physical activity; and 39 (21%) had suddenly changed position. In the latter group, 18 changed from being supine for more than 1 hour to standing; three rose from supine to sitting; and 18 changed from prolonged sitting (greater than 60 minutes) to standing. The conclusion is that a potential triggering factor is present in many patients immediately prior to the onset of MI. A sudden change in position is the most frequent potential trigger, typically occurring the morning after awakening from sleep.

Circadian Rhythm

Nucleic DNA and RNA in cardiac muscle cell of experimental myocardial infarct.

Myocardial infarction was produced in dogs, and the changes in nucleic acid synthetic activity were investigated quantitatively by microspectrophotometer in the myocardial cells as time progressed. DNA value, immediately after infarction, was greatly increased in comparison to that of the control group. At two weeks after infarction the value had increased to the highest level. After this point the value decreased, and, in 12 weeks, the mean value was back to the control level. Changes in RNA followed a pattern similar to DNA changes. The mechanism of the repair process of myocardial infarction was investigated.

Animals

[Site and type of acute myocardial infarct in relation to myocardial infarct size--dynamics of global ejection fraction in acute myocardial infarct].

By the ejection fraction global (EFg) statements concerning the remaining function of the myocardium in acute myocardial infarction and thus individually concerning the prognosis (classification of risk groups) become possible. For the valuation of the dynamics of the EFg in a period up to 6 months after an acute myocardial infarction the EFg was multifariously controlled. Only patients with first myocardial infarction in localization on the anterior wall and Q-wave showed a significant dynamics of the EFg between the measurements acute and third week as well as acute and 6th month (absolutely 5.2%). --In re-infarction/Q-wave this could be confirmed also for the localization of the posterior wall in the period acute till third week. For the localization on anterior and posterior wall a dynamics of the EFg could also be calculated for the period acute and 6th month. Thereby the absolute increase of the EFg was between 4.0 and 4.6%. The dynamics of the EFg in the region of the anterior wall was 5.2% for the first infarction and only 4% for the reinfarction. Thus it is below the dynamics of the EFg in an effective thrombolytic therapy.

Angina Pectoris

Qualitative and quantitative comparison of amounts of narrowing by atherosclerotic plaques in the major epicardial coronary arteries at necropsy in sudden coronary death, transmural acute myocardial infarction, transmural healed myocardial infarction and unstable angina pectoris.

The amounts of narrowing of the 4 major (left main, left anterior descending, left circumflex and right) epicardial coronary arteries by atherosclerotic plaques were compared in 4 subsets of coronary patients. Of the 129 patients studied at necropsy, an average of 2.7 of the 4 arteries was narrowed greater than 75% in cross-sectional area at some point (0.7/4 in controls), and the group with unstable angina pectoris (3.2/4) had more narrowing than did the groups with sudden coronary death (2.8/4), acute myocardial infarction (2.7/4) and healed myocardial infarction (2.3/4). Each of the 4 major epicardial coronary arteries was divided into 5-mm long segments and a histologic section was prepared and stained by the Movat method of each of the 6,461 segments in the 129 patients and in the 1,849 segments in the 40 control subjects. In the 129 patients, 35% of the 5-mm segments were narrowed 75 to 100% in cross-sectional area (3% in controls) and the group with unstable angina had the highest percent (48%) of segments severely narrowed compared to the groups with sudden coronary death (36%), acute myocardial infarction (34%) and healed myocardial infarction (31%). Thus, of the 4 subsets of patients with fatal coronary artery disease studied at necropsy, those with unstable angina pectoris had the most severe and extensive coronary atherosclerosis.

Angina Pectoris

Scan analysis in myocardial infarction.

Myocardial scans with 99mTc-labelled phosphates are reported to be useful in the diagnosis of acute myocardial infarction. A retrospective survey of 205 patients referred for 99mTc-phosphate bone scanning and with no evidence of recent heart disease revealed an occurrence of 10% of false positive images, that is to say, uptake of phosphate in non-infarcted myocardium. These striking findings stress the need for critical assessment of the usefulness of this diagnostic technique.

Etidronic Acid

Rehabilitation after a myocardial infarction.

Myocardial infarction is only one event in a chronic and progressive disease. A well-planned convalescence is part of the long-term promotion of a healthy and enjoyable lifestyle and provides the best possible prognosis.

Exercise

Myocardial uptake of antimyosin antibody compared with serum myosin light chain I levels in patients with myocardial infarction.

Myocardial accumulation of In-111-antimyosin (InAM) was evaluated in comparison with circulating serum myosin light chain I (LCI) level at the time of InAM injection. Seventeen consecutive patients were studied at various stages ranging from 6 days to 34 days after myocardial infarction (MI). The infarct area was positive for InAM uptake in all patients (100%), and significant myocardial uptake was observed in 14 patients (82.4%). The intensity of InAM uptake correlated with the infarct location shown by ECG and CAG. In contrast, 12 patients (70.6%) had normal or undetectable serum myosin LCI levels, with 5 being normal (0.42-2.5 ng/ml) and 7 undetectable (0.42 ng/ml or less). Only 5 patients (29.4%) had elevated serum myosin LCI levels at the time of InAM injection, and this elevation was slight, ranging from 3.4 to 4.5 ng/ml (mean: 3.75 ng/ml). Among patients with undetectable, normal, and elevated serum myosin LCI levels, there was no significant correlation between InAM uptake and the serum myosin LCI level. Thus, even after the serum myosin LCI level has decreased to normal, InAM can still bind to cardiac myosin in patients with MI, presumably until there is complete recovery from the hibernating myocardium due to ischemic damage.

Adult