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At least 37 records · Page 2Linked to original sources
PubMed1993

[Synchronized coronary vein retroperfusion for identification of myocardium with chronic ischemic disorders of wall movement ("hibernating myocardium")].

UNLABELLED: ECG-synchronized retroperfusion (SRP) via the coronary sinus has been recently demonstrated to efficiently deliver arterial blood to ischemic myocardium in an experimental setting and during PTCA. To assess the potential of SRP for identifying hibernating myocardium by improved contractile function resulting from retrograde delivery of oxygen, 10 patients (M/F = 9/1; age 56 +/- 9 years) with ischemic wall motion abnormalities, but, according to ECG-criteria, no transmural infarction in the territory of a totally occluded LAD, underwent 30 min of SRP at a flow rate of 145-250 ml/min prior to mechanical recanalization. Serial digital ventriculograms were obtained before, after 30 min of SRP and, finally, after successful PTCA at follow-up of 28 +/- 4 days. RESULTS: Wall motion analysis revealed improved global and regional contractile function in seven of 10 patients, which was maintained after successful PTCA. Continuous SRP over 30 min resulted in an improvement of global and segmental systolic function. Left ventricular ejection fraction (LVEF) increased from 53 +/- 8% to 58 +/- 5% with 30 min of SRP (p < 0.03) and significant improvement in regional function was detected in the anterobasal, apical and inferior segment of the left ventricular circumference (p < 0.05). CONCLUSION: An improved contractile response to retrograde delivery of oxygen by SRP appears to document the reversibility of myocardial hibernation. Thus, ECG-synchronized SRP via the coronary sinus has the potential to unmask viable myocardium likely to completely recover from contractile dysfunction after successful antegrade recanalization. Moreover, continuous SRP procedure over 30 min was safe and had no hazardous side-effects.

Adult↗
PubMed1996

Transplantation of fetal myocardial tissue into the infarcted myocardium of rat. A potential method for repair of infarcted myocardium?

BACKGROUND: Unlike skeletal myocytes, mammalian adult cardiomyocytes cannot regenerate after injury. A possible strategy to increase viability and augment ventricular function after myocardial injury is fetal myocardial tissue transplantation. The engrafted fetal cells are a potential source of growth factors and can be used for cardiomyocyte-based gene therapy. The purpose of our study was to test the feasibility and efficiency of fetal cardiomyocyte transplantation into a model of myocardial infarction. METHODS AND RESULTS: We subjected rats after myocardial infarction to three protocols of therapy. In the first protocol, tissue fragments of cultured human fetal ventricles were injected into the scar 7 to 24 days after infarction. The rats were treated with intraperitoneal injections of 12.5 mg.kg-1.d-1 cyclosporine. In the second protocol, fragments of cultured fetal rat ventricles were injected into the scar 9 to 17 days after infarction. A third group of animals with myocardial infarction was treated with injection of saline into the scar (control). After 7 to 65 days post-transplantation, hearts were harvested and processed for electron microscopy and alpha-actin immunohistochemistry. Toluidine blue staining and electron microscopy revealed the presence of engrafted human and rat cardiomyocytes in the infarcted myocardium up to 14 and 65 days after transplantation, respectively. The morphology was similar to that of cultured fetal cardiomyocytes. The engrafted fetal tissues were also stained positive for alpha-actin, which is unusual for the adult rat myocardium. Examination of control hearts detected infarcted tissue only, and alpha-actin staining was limited to vessel walls. CONCLUSIONS: Fetal cardiomyocyte tissue can be implanted and survive in the infarcted myocardium. This experimental approach may provide a therapeutic strategy for cardiomyocyte-based gene therapy for introduction of therapeutic proteins into myocardial infarction.

Actins↗
PubMed1993

Altered electrical and metabolic response of reperfused myocardium to ischaemia after recovery from preceding ischaemia: evidence for ischaemia sensitised myocardium.

OBJECTIVE: The aim was to examine electrical and metabolic responses of myocardium to ischaemia after recovery from preceding ischaemia. METHODS: In 23 open chest dogs (5 min occlusion group), the left anterior descending coronary artery was occluded three times in the following order: 2 min occlusion (Trial 1) followed by 15 min reperfusion; then 5 min occlusion followed by 90 min reperfusion and 2 min occlusion (Trial 2). In 15 control dogs, the 2 min occlusion was performed twice at a 110 min reperfusion interval; the former occlusion was also referred to as Trial 1 and the latter as Trial 2. The dogs were monitored by epicardial surface ECG, while regional myocardial function was estimated by sonomicrometry. Continuous measurements of myocardial tissue PCO2, pH, and extracellular K+ concentration were made concurrently. RESULTS: Both trial occlusions produced a biphasic change in R wave amplitude characterised by a transient initial decrease succeeded by an increase with ST elevation. This biphasic change in R wave amplitude was indistinguishable between Trial 1 and Trial 2 in the control group. By contrast, in the 5 min group, the R wave amplitude initially decreased to a greater degree in Trial 2 than in Trial 1. More rapid contractile failure was also noticed in Trial 2, suggesting the possible involvement of mechanically induced electrical changes in the genesis of decreased R wave amplitude. After 45-60 s of occlusion, however, the R wave amplitude increased to a level much beyond the initial amplitude in Trial 1 [124.9(SEM 8.4)% at 120 s], whereas this level of increase was not observed in Trial 2 [106.5(7.8)%, p < 0.05 v Trial 1]. There was also reduced elevation of the ST segment in Trial 2: 3.6(0.8) mV v 6.5(0.8) mV in Trial 1 at 120 s (p < 0.05). This reduction in ST elevation was concomitant with decreased changes in PCO2, pH, and extracellular K+ concentration in Trial 2. These reduced changes in the ST segment and the metabolic variables were absent in the control group. CONCLUSIONS: These altered electrical responses of the myocardium may be the result of more rapid early contractile failure and attenuated metabolic changes during ischaemia occurring after recovery from preceding ischaemia.

Animals↗
PubMed1982

Myocardial kinetics of thallium-201 after dipyridamole infusion in normal canine myocardium and in myocardium distal to a stenosis.

The purpose of the present study was to define myocardial and blood thallium-201 (Tl-201) kinetics after infusion of dipyridamole in normal canine myocardium and in myocardium distal to a coronary artery stenosis. Miniature radiation detector probes were implanted in the left ventricle in 39 open-chest dogs. A balloon constrictor was placed around the proximal left circumflex coronary artery. Electromagnetic flow probes were positioned proximally around both the left circumflex and left anterior descending coronary arteries. In five control dogs (group 1) the balloon occluder was not inflated; in 12 dogs (group 2) a mild stenosis was created such that resting flow was not reduced, yet the hyperemic response after 10 s of total occlusion was partially attenuated; in nine dogs (group 3) a moderate stenosis was created such that resting flow was not reduced, yet the hyperemic response was completely eliminated; and in 13 dogs (group 4) a severe stenosis was created such that resting flow was reduced. After intravenous dipyridamole (0.08 mg/kg . min-1 x 4 min), 1.5 mCi Tl-201 was injected intravenously and probe counts were collected continuously for 4 h. The mean 4-h fractional myocardial Tl-201 clearance for nonstenotic zones was 0.35, 0.27 for group 2 stenotic zones, 0.19 for group 3 stenotic zones, and 0.05 for group 4 stenotic zones (P less than 0.0001). After reaching peak activity, myocardial Tl-201 activity cleared biexponentially with a final decay constant lambda 2 = 0.0017 +/- 0.0001 min-1 (SE) for nonstenotic zones, 0.0011 +/- 0.0001 min-1 for group 2 stenotic zones, and 0.0006 +/- 0.0001 min-1 for group 3 stenotic zones (P less than 0.01). Group 4 stenotic zone Tl-201 clearances were negligible (decay constant essentially zero). Blood Tl-201 activity decayed triexponentially with a final blood lambda 3 = 0.0018 +/- 0.0001 min-1, which was almost identical to the final myocardial lambda 2 decay constant. Thus, the rate of myocardial Tl-201 clearance can distinguish between coronary stenoses of graded hemodynamic severity. These results may be applicable to quantitative techniques for determining myocardial Tl-201 clearance rates on serial clinical images after dipyridamole administration.

Animals↗
PubMed1996

Force pattern of hypoxic myocardium applied to oxygenated muscle preparations: comparison with effects of regional ischemia on the contraction of non-ischemic myocardium.

OBJECTIVE: To examine the basis for local wall motion abnormalities commonly seen in patients with ischemic heart disease, computer-controlled isolated muscle studies were carried out. METHODS: Force patterns of physiologically sequenced contractions (PSCs) from rat left ventricular muscle preparations under well-oxygenated conditions and during periods of hypoxia and reoxygenation were recorded and stored in a computer. Force patterns of hypoxic-reoxygenating and oxygenated myocardium were applied to oxygenated and hypoxic-reoxygenating myocardium, respectively. RESULTS: Observed patterns of shortening and lengthening closely resemble those obtained from ischemic and non-ischemic myocardial segments using ultrasonic crystals in intact dog hearts during coronary occlusion and reperfusion, and are similar to findings reported in angiographic studies of humans with coronary artery disease. CONCLUSION: The current study, demonstrating motions of oxygenated isolated muscle preparations which are similar to those in perfused segments of intact hearts with regional ischemia, supports the concept that the multiple motions of both ischemic and non-ischemic segments seen in regional myocardial disease can be explained by interactions of strongly and weakly contracting muscle during the physiologic cardiac cycle.

Animals↗
PubMedDate not supplied

Detection of viable myocardium with p-iodophenyl-9-(R,S)-methylpentadecanoic acid in ischemic rat myocardium.

BACKGROUND: The methyl-branched free fatty acid analog 15-(p-iodophenyl)-9-(R,S)-methylpentadecanoic acid (9MPA) is metabolized more rapidly than 15-(p-iodophenyl)-3(beta)-(R,S)-methylpentadecanoic acid. This study investigates whether myocardial ischemic injury to beta-oxidation and viable myocardium can be detected with the use of 9MPA in a rat myocardial ischemia model. METHODS AND RESULTS: In the acute study the left coronary arteries were occluded for 15 or 45 minutes and then reperfused; the rats were killed after 2 hours. Iodine 125 and iodine 123 9MPA was injected 60 minutes (delayed images) and 3 minutes (early images), respectively, before the rats were killed. In the subacute study the left coronary arteries were either occluded for 45 minutes and then reperfused or occluded and not reperfused. One week later, I-125 and I-123 9MPA was injected 60 minutes and 3 minutes, respectively, before the rats were killed. The distribution of 9MPA was examined with the use of dual-tracer autoradiography. In the acute study the delayed images showed a higher uptake in viable regions at risk than in normal areas and nonviable regions. In the subacute study a difference in uptake between viable regions at risk and normal areas was visible on the early images, but this difference disappeared on the delayed images. CONCLUSIONS: 9MPA is a useful tracer for detecting viable regions of ischemic myocardium during acute and subacute disease stages.

Animals↗
PubMed2002

[Acute focal dystrophy of the myocardium with hibernating or stunned myocardium].

Opportunities of clinical, laboratory and device diagnosis of acute focal dystrophy (AFD) with hibernating or stunned myocardium are postulated. Myocardial AFD belongs to intermediate coronary syndrome and is a clinico-morpho-functional manifestation of one of the acute coronary syndromes in ischemic heart disease. Differentiation of hibernating with stunned myocardium is made after myocardial revascularization. 230 coronaroventriculographies have been made, of them 72 were urgent with balloon angioplasty and stenting.

Acute Disease↗
PubMed1977

Pathology of acute ischemic myocardium. Special references to (I) evaluation of morphological methods for detection of early myocardial infarcts, and (II) lipid metabolism in infarcted myocardium.

Morphological changes of early myocardial infarction within 24 hours after the onset of the acute attack were described together with a review of the literatures. For the practical purpose in detecting very early infarcts, enzymatic histochemistry is the most reliable method. Other methods previously reported such as wavy pattern of the muscle fibers and fuchsinophilia are still controvertial. Lipid metabolism in the infarcted myocardium of dogs was studied both morphologically and biochemically. Up to 3 hours, after the coronary ligation, the tissue lipids accumulated in the necrotic areas with a rise of triglyceride, but later than 6 hours the lipids decreased and were lost from the necrotic tissue, while the surrounding living cells were accumulated with neutral lipids. Serum free fatty acids were elevated in the coronary sinus blood in 6 hours after the ligation. Linolic acids were contained in high proportion in both coronary venous blood after 6 hours, and normal myocardial phospholipid. These results may lead to another possible factor in addition to catecholamine activity to elevate serum FFA in acute myocardial infarction that fatty acids may be released partly from tissue phospholipid and once ever accumulated triglyceride.

Aged↗
PubMed2004

Hypercholesterolemia impairs transduction of vasodilator signals derived from ischemic myocardium: myocardium-microvessel cross-talk.

OBJECTIVE: Coronary microvessels are functionally coupled to the myocardial metabolic state. In hypercholesterolemia, the coronary vascular dysfunction extends to microvascular levels. We hypothesized that the vasodilator signal transduction from ischemic heart is impaired in the coronary microvascular wall of hypercholesterolemia. METHODS AND RESULTS: Rabbits were fed with normal chow (control group) or 2% high-cholesterol diet (hypercholesterolemia group) for 8 weeks. Coronary microvessels isolated from rabbit hearts were pressurized and gently placed on a beating canine heart. Myocardial ischemia was produced in the beating heart and the diameter of the isolated microvessel was observed using an intravital microscope with a floating objective. In control group, the isolated microvessels significantly dilated 2 minutes after the onset of ischemia, and a plateau was observed at 10 minutes. In contrast, the microvessels from hypercholesterolemia group did not dilate during ischemia. Dihydroethidium fluorescence microscopy revealed an elevated superoxide level in the microvessels of hypercholesterolemia group. The application of tiron (free radical scavenger) significantly dilated the isolated microvessels only from hypercholesterolemic animals. CONCLUSIONS: We conclude that the transduction of vasodilator signals derived from ischemic myocardium is impaired in the coronary microvascular wall of hypercholesterolemia. Enhanced oxidative stress in hypercholesterolemia may alter the microvascular function.

Acetylcholine↗
PubMed1984

[Toxic effect of carbon tetrachloride on the myocardium. II. Experimental part. A. Histochemical analysis of the rat myocardium in acute carbon tetrachloride poisoning].

The object of the study was rats myocardium. Tissue samples were examined 3, 6 and 12 hours after carbon tetrachloride treatment. The poison was administered by a gastric tube in single dose of 0.6 ml/100 g body weight. The examination carried out by the histochemical method revealed changes in the intensity of enzymatic reaction, whereas due to the Selye staining fuosynophylic fibres were found.

Acid Phosphatase↗
PubMed1984

[Toxic effect of carbon tetrachloride on the myocardium. II. Experimental part. B. Ultrastructure of the myocardium of rats in acute carbon tetrachloride poisoning].

Rat's myocardium was examined. The tissue material was collected 3, 6 and 12 hours after carbon tetrachloride administration. The poison was administered by gastric tube in single dose of 0.6 ml/100 g of body weight. Electron microscopic examination revealed a reaction of endoplasmic reticulum damage to mitochondrium and myofibrils.

Acute Disease↗
PubMed1986

Risk of myocardium adjacent to infarcted myocardium: electrocardiographic, metabolic and scintigraphic evidence within the first week of acute myocardial infarction.

Atrial pacing was carried out within 5 days of an uncomplicated acute myocardial infarction (AMI) in 28 patients to detect the existence of a menaced area. A positive pacing response (at least 1.0 mm of ST-segment shift) was observed in 23 patients (82%, group I), whereas pacing results were negative in 5 (18%, group II). Pacing-induced electrocardiographic changes involved the leads affected by AMI in patients with transmural necrosis. A well-defined thallium-201 redistribution, mostly localized near or within the AMI site, was present in 10 patients from group I (43%), in 1 from group II (20%), and in 1 of 12 comparable patients (8%) in whom pacing was not performed. During pacing, abnormal lactate metabolism was observed in 11 of 17 patients from group I (65%) and in 0 of 5 from group II (0%). A 90% or greater coronary stenosis of at least 1 artery was found in 19 of 23 patients from group I (83%) and in 1 of 5 from group II (20%); 2- to 3-vessel disease (more than 70% diameter stenosis) was present in 14 patients from group I (61%) and 1 from group II (20%). During a 15-month follow-up (range 9 to 25), effort angina developed in 9 patients from group I (39%) and in none from group II. No deaths or reinfarctions occurred in either group. Thus, very early after a first AMI, most patients have a jeopardized periinfarction area that is usually associated with a critical coronary stenosis and that heralds effort angina in a significant proportion of them.

Adult↗