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PubMed1983

[Diagnostic possibilities of myocardial scintigraphy using T1-201 in acute myocardial infarction].

Myocardial scintigraphic investigation using 201T1 was performed in 36 patients with suspected acute myocardial infarction and 11 clinically normal controls. The scintigrams were assessed visually and using a computer program for semiquantitative assessment of 201T1 distribution across the myocardium. The control subjects' scintigrams show a comparatively even myocardial distribution of the label. Patients with acute myocardial infarction were divided into 2 groups: those with large-focal (28) and small-focal (8) infarctions. All the patients from the large-focal group showed perfusion defects in their scintigrams. Clinical and autopsy diagnoses coincided in all the cases, and the vital scintigraphic pattern correlated with the posthumous localization of the myocardial infarction. However, the method of myocardial scintigraphy with 201T1 in acute myocardial infarction is of low specificity. To improve the differential diagnosis of myocardial infarction, repeated scintigraphy is needed.

Adult↗
PubMed1976

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↗
PubMed1996

Sympathetic reinnervation after acute myocardial infarction.

Myocardial infarction produces sympathetic denervation of the necrotic myocardium and noninfarcted myocardium apical to the injury. Proof of sympathetic reinnervation after myocardial infarction has, however, remained elusive. In this study, we investigated whether cardiac sympathetic reinnervation occurs in men recovering from myocardial infarction. I-123 metaiodobenzylguanidine (MIBG), I-123 paraphenylpentadecanoic acid, and Tc-99m sestamibi scintigraphic imaging were conducted in 13 men 3 and 12 months after a first myocardial infarction to determine the extent of denervated myocardium, the size of the infarct, and the size of the myocardium with reduced perfusion, respectively. A defect was determined as regional uptake of < or = 30% of the maximal myocardial activity. The size of the MIBG defect was not significantly different between 3 and 12 months after infarction (17 +/- 8% and 18 +/- 8% of left ventricular mass, respectively). There was also no significant change in the extent of viable but denervated myocardium at 3 and 12 months (average 9 +/- 6% and 10 +/- 5%, respectively). MIBG activity of the infarct zone (expressed as a percentage of MIBG activity of the myocardium with normal perfusion) did not change (17 +/- 13% and 20 +/- 16%), whereas MIBG activity of the periinfarct zone increased during follow-up (32 +/- 11% and 41 +/- 14%, p < 0.01). This was associated with an increase in periinfarct I-123 paraphenylpentadecanoic acid activity (40 +/- 11% and 48 +/- 9%, p < 0.05), but not Tc-99m sestamibi activity (48 +/- 10% and 48 +/- 11%). In conclusion, we did not observe sympathetic reinnervation in the infarct zone between 3 and 12 months after myocardial infarction. However, MIBG activity of the periinfarct zone increased, suggesting partial reinnervation, and this was associated with a recovery of myocardial metabolic activity of the periinfarct zone.

3-Iodobenzylguanidine↗
PubMed1983

How reliable is myocardial imaging in the diagnosis of acute myocardial infarction?

Myocardial scintigraphic techniques available presently allow a sensitive and relatively specific diagnosis of acute myocardial infarction when they are used correctly, although every technique has definite limitations. Small myocardial infarcts (less than 3 gm.) may be missed, and there are temporal limitations in the usefulness of the scintigraphic techniques. The development of tomographic methodology that may be used with single-photon radionuclide emitters (including technetium and thallium-201) will allow the detection of relatively small abnormalities in myocardial perfusion and regions of myocardial infarction and will help to provide a more objective interpretation of the myocardial scintigrams. The use of overlay techniques allowing simultaneous assessment of myocardial perfusion, infarct-avid imaging, and radionuclide ventriculograms will provide insight into the relevant aspects of the extent of myocardial damage, the relationship of damage to myocardial perfusion, and the functional impact of myocardial infarction on ventricular performance.

Animals↗
PubMed1987

Elevated levels of the rapid inhibitor of plasminogen activator (t-PAI) in acute myocardial infarction.

Myocardial infarction is frequently caused by acute coronary thrombosis. A previous study in patients three years after myocardial infarction has shown twice as high concentrations of the rapid inhibitor of plasminogen activator (t-PAI) as in healthy controls. The present study involves 29 patients with acute onset of myocardial infarction. Already on admission the mean concentration of t-PAI was 16.5 +/- 7.4 units/ml as compared to 7.5 +/- 2.3 in healthy controls. It is presently unknown if moderately elevated t-PAI levels contribute to a delay of the spontaneous thrombolysis of the coronary occlusion, thus promoting the development of myocardial infarction.

Adult↗
PubMed1979

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↗
PubMed1991

[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↗
PubMed1993

[Significance of treatment of early forms and prevention of heart failure. Value of ACE inhibitors in therapy after myocardial infarct].

Myocardial infarction has become the most important condition causing congestive heart failure. Several treatment regimens compete with each other in the early and later post myocardial infarction phase focussing on different pathophysiologic mechanisms. In this review emphasis is put on absolute risks and absolute risk reductions in patients with left ventricular dysfunction after myocardial infarction. In the first year mortality is still as high as 10% and the major risks are sudden unexpected death, reinfarction, and congestive heart failure. In the following years sudden death and development of congestive heart failure become less prominent, while a considerable risk of reinfarction persists. Thrombolysis and beta-blockade are the most important drugs in the acute infarction phase leading to a marked reduction in one year mortality. In the first year after infarction beta-blockade has an established place in the prevention of sudden death; revascularization and aspirin are established in reinfarction prophylaxis. However, since most drugs lower 1 year mortality by 0.5 to 2% only, drugs like ACE inhibitors that influence more than one risk, i.e. sudden death and reinfarction as well as deterioration of pump dysfunction might play a more important role in the therapeutic strategy after myocardial infarction. A supplementation by one or two drugs aiming at the individually estimated leading risks might be the best choice in patients with left ventricular dysfunction today.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Risk of stroke during long-term anticoagulant therapy in patients after myocardial infarction.

Myocardial infarction survivors have an increased risk of stroke, which is reduced with long-term anticoagulant therapy. However, an estimated 10-times increase in risk of bleeding during such treatment has been reported. We evaluated the risk of stroke in patients after a myocardial infarction and examined the relationship of the risk of intracranial hemorrhage or cerebral infarction and the intensity of anticoagulant therapy. The study population consisted of 3,404 post-myocardial infarction patients who took part in a randomized, double-blind, placebo-controlled trial. Patients were randomized to treatment with anticoagulants (international normalized ratio range, 2.8-4.8) or matching placebo. Mean follow-up was more than 3 years. The incidence of stroke analyzed on "intention-to-treat" was 0.7 per 100 patient-years in the anticoagulant patients against 1.2 in placebo, a hazard ratio of 0.60, with 95% confidence interval of 0.40 to 0.90. In the anticoagulation group, 15 patients had cerebral infarction and 17 an intracranial bleeding, 3 of which occurred after withdrawal of treatment. In the placebo group, the numbers were 43 and 2. Of the 14 intracranial bleeds during anticoagulation, 6 occurred at an international normalized ratio between 3.0 and 4.0 and 8 at greater than 4.0. These results confirm that long-term anticoagulant therapy substantially reduces the risk of stroke in post-myocardial infarction patients. The increased risk of bleeding complications associated with anticoagulant therapy is offset by a marked reduction in ischemic events. The risk of intracranial bleeding is directly related to the intensity of anticoagulant treatment.

Adult↗
PubMedDate not supplied

Decreased expression of cardiac sarcoplasmic reticulum Ca(2+)-pump ATPase in congestive heart failure due to myocardial infarction.

Myocardial infarction in rats induced by occluding the left coronary artery for 4, 8 and 16 weeks has been shown to result in congestive heart failure (CHF) characterized by hypertrophy of the viable ventricular myocardial tissue. We have previously demonstrated a decreased calcium transport activity in the sarcoplasmic reticulum (SR) of post-myocardial infarction failing rat hearts. In this study we have measured the steady state levels of the cardiac SR Ca(2+)-pump ATPase (SERCA2) mRNA using Northern blot and slot blot analyses. The relative amounts of SERCA2 mRNA were decreased with respect to GAPDH mRNA and 28 S rRNA in experimental failing hearts at 4 and 8 weeks post myocardial infarction by about 20% whereas those at 16 weeks declined by about 35% of control values. The results obtained by Western blot analysis, revealed that the immunodetectable levels of SERCA2 protein in 8 and 16 weeks postinfarcted animals were decreased by about 20% and 30%, respectively. The left ventricular SR Ca(2+)-pump ATPase specific activity was depressed in the SR preparations of failing hearts as early as 4 weeks post myocardial infarction and declined by about 65% at 16 weeks compared to control. These results indicate that the depressed SR Ca(2+)-pump ATPase activity in CHF may partly be due to decreased steady state amounts of SERCA2 mRNA and SERCA2 protein in the failing myocardium.

Animals↗
PubMed1997

Cardiac sympathetic denervation in patients with coronary artery disease without previous myocardial infarction.

Myocardial infarction damages sympathetic nerve fibers coursing through the infarct zone. In this study we investigated whether coronary artery disease without myocardial infarction results in sympathetic denervation. We examined 12 patients without a history of previous myocardial infarction and 19 postinfarction patients. 1-123 metaiodobenzylguanidine (MIBG) and technetium-99m sestamibi (MIBI) single-photon emission tomography were conducted at rest to determine the extent of denervated myocardium and the extent of myocardium with reduced perfusion, respectively. In addition, myocardial perfusion during exercise was assessed with MIBI. A MIBG or MIBI defect was determined as being regional uptake of < or =30% of the maximal myocardial activity. All but 1 patient without previous infarction had MIBG defects. MIBG defects (10.3 +/- 8.5% of left ventricular mass) were significantly larger than MIBI defects at rest (2.4 +/- 3.2%, p <0.001) and during exercise (4.8 +/- 6.1%, p <0.05). In multiregression analysis, the size of an MIBG defect was associated with severity of coronary stenoses (> or =90% of lumen diameter; p <0.05), but not with age, number of significant stenoses (> or =50% of lumen diameter), left main disease, functional class, left ventricular ejection fraction, angina pectoris, maximal ST depression, or mean workload during exercise test. MIBG and MIBI defects were significantly larger in patients with severe coronary stenoses than in patients with moderate stenoses (50% to 89% of lumen diameter) (16.4 +/- 8.9% vs 6.0 +/- 5.2% [p <0.05] and 5.0 +/- 3.1% vs 0.6 +/- 1.3% [p <0.001], respectively). The size of MIBG (16.1 +/- 8.9%) and MIBI defects (7.3 +/- 6.5%) at rest in postinfarction patients did not differ from patients with severe stenoses. Our study demonstrates that cardiac adrenergic tissue is very sensitive to ischemia and that regional cardiac sympathetic denervation can occur in patients with stable coronary artery disease without previous myocardial infarction.

Adult↗
PubMedDate not supplied

Myocardial abscess complicating myocardial infarction.

Myocardial abscess may occur rarely as a complication of myocardial infarction. This case report is the first demonstration of a myocardial abscess at the site of acute myocardial infarction in a 38-year-old man diagnosed by transesophageal echocardiography and color-flow imaging. Transesophageal echocardiography was crucial in the timing of surgery. Three months later the patient was well. Our patient is the first reported survivor of this uncommon complication of myocardial infarction.

Abscess↗
PubMed1997

Early apoptosis in human myocardial infarcts.

Myocardial apoptosis has previously been observed in human acute myocardial infarcts. We examined the time of appearance and extent of apoptosis in human acute myocardial infarcts, and compared these with necrotic cell death. Because nuclear internucleosomal DNA fragmentation is a hallmark of apoptosis, autopsied tissue from cases of acute myocardial infarct of varying histological ages was subjected to two tests that identify such fragmentation: in situ end-labeling (ISEL) and DNA electrophoresis on agarose gels. Both tests showed widespread apoptosis in infarcts only a few hours in age before the appearance of coagulative necrosis. No apoptosis was detected in normal myocardium. ISEL in recent infarcts was visible primarily in myocytes containing contraction bands, which occur predominantly in regions of reperfused myocardium. During the next 1 to 2 days, ISEL remained extensive but increasingly appeared in cells with morphological features of coagulative necrosis, representative of nonreperfused myocardium. In older infarcts, the incidence of apoptosis declined in myocytes, but increased in invading inflammatory cells. These data suggest that apoptosis is the early and predominant form of cell death in infarcted human myocardium, and that its appearance is accelerated in reperfused myocardium. Therapies directed at early rescue of apoptotic myocytes may, therefore, prove valuable.

Adult↗
PubMed1982

Psychologic sequelae of myocardial infarction.

Myocardial infarction should be understood not only in relation to its biologic impact but also in terms of its psychologic effect. Patients with myocardial infarction pass through identifiable dynamic phases associated with psychologic recovery and adaptation to myocardial damage. These phases consist of denial, anxiety, depression and convalescence. Some therapeutic strategies help the patient to cope with this life-threatening event. Delirium is a special problem after myocardial infarction.

Antidepressive Agents↗
PubMed1977

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↗