Morphological Changes In Myocardium Research Articles

DOPAMINE EFFECT ON CARDIAC REMODELING IN EXPERIMENT

Aim. To study morphologic changes in myocardium of Wistar rats caused by single and long term dopamine administration. Methods. In acute study dopamine 10 mkg/kg was administrated to 15 rats by a single intraperitoneal injection. The material was taken in 2, 6, 24 hours and in 1 month after drug administration. In chronic study dopamine 10 mkg/kg was administrated to 15 rats 3 times a day by intraperitoneal injections during 2 weeks. The material was taken just after the drug administration was stopped and in 1 month of animals keeping without stress and drug influences. Control group included 15 rats comparable with experimental animals in age and weight. They were keeped without stress and drug influences. Morphometric parameters of left and right ventricles were evaluated as well as density of cardiomyocytes, collagen, vessels and volume of extracellular space. Results. The enlargement of cardiac fibrosis is found both in acute, and in chronic study. In acute study cardiac fibrosis was located mainly in a right ventricle. In chronic study cardiac fibrosis was located in both ventricles, but also mainly in a right one. Conclusion. Significant morphological «asynchronism» of the left and right ventricles remodeling requires elaboration of methods of myocardium protection and cardiac function control during dopamine administration.

Cardioprotective effect of amlodipine in oxidative stress induced by experimental myocardial infarction in rats

The present study investigated whether the administration of amlodipine ameliorates oxidative stress induced by experimental myocardial infarction in rats. Adrenaline was administered and myocardial damage was evaluated biochemically [significantly increased serum aspertate aminotransferase (AST), lactate dehydrogenase (LDH) and malondialdehyde (MDA) levels of myocardial tissue] and histologically (morphological changes of myocardium). Amlodipine was administered as pretreatment for 14 days in adrenaline treated rats. Statistically significant amelioration in all the biochemical parameters supported by significantly improved myocardial morphology was observed in amlodipine pretreatment. It was concluded that amlodipine afforded cardioprotection by reducing oxidative stress induced in experimental myocardial infarction of catecholamine assault.

Short- and long-term changes in myocardial function, morphology, edema, and infarct mass after ST-segment elevation myocardial infarction evaluated by serial magnetic resonance imaging

Knowledge of the natural course after an ST-elevation myocardial infarction (STEMI) treated according to guidelines is limited because comprehensive serial magnetic resonance imaging (MRI) of systolic left ventricular function, edema, perfusion, and infarct size after STEMI has not been undertaken. The aim of this study was to evaluate effects of therapy for STEMI on left ventricular function and perfusion and to test the hypothesis that myocardial perfusion by MRI predicts recovery of left ventricular function. Cine MRI, edema, first-pass perfusion, and late enhancement imaging were performed in 58 patients at day 2 and at 1 and 6 months after successful primary percutaneous coronary stent intervention for STEMI. Ejection fraction increased 6.3% during the first month (P < .001) and 1.9% from 1 to 6 months (P < .06), indicating a maximal recovery very early after the infarction. The systolic wall thickening in the infarct area almost doubled (P < .001), the perfusion of infarcted myocardium increased approximately 50% (P = .02), and perfusion improved in 72% of patients. Edema decreased with a mean of 2 segments (P < .001) during the first month and another 2.5 segments from 1 to 6 months (P < .001). Infarct size decreased to 1 month (P = .01) and was unchanged from 1 to 6 months (P = .5). Baseline perfusion did not predict improvement in ejection fraction (r = 0.2, P = .2) but did predict regional systolic function (P = .03). Left ventricular function, perfusion, and infarct mass recovered substantially after STEMI, with the main part of the change within the first month. First-pass perfusion at rest appeared to predict regional ventricular recovery.

Predictors of Sudden Cardiac Death during Extracardiac Surgical Interventions

The paper presents the currently available data in the literature on sudden cardiac death (SCD), including its definition, epidemiology, etiology, risk factors, predisposition to the development of SCD, the ways of assessing the risk of SCD. It outlines myocardial morphological changes in the development of SCD, the pathogenesis of the major links of the origin of ventricular fibrillation in myocardial ischemia, and the mechanisms responsible for the development of SCD. A relationship has been established between coronary heart disease and the risk of developing SCD. Particular attention is given to the topicality of the problem of SCD to inpatients: at the stages of anesthetic management during extracardiac surgical interventions. Emphasis is placed on the importance of preoperative meticulous examination of the patients. A number of the drugs that are most frequently used in anesthesiology and negative affect the myocardium and systemic hemodynamics are listed, which is extremely important to patients having initially cardiovascular diseases. The detection of the predictors of SCD in the preop-erative period and the methods of studying the patients, among which scale, instrumental, and biochemical methods being emphasized, feature in the paper. Recommendations to improve the quality of perioperative management and to increase the safety of anesthetic maintenance are listed.

Iron chelation-afforded cardioprotection against chronic anthracycline cardiotoxicity: A study of salicylaldehyde isonicotinoyl hydrazone (SIH)

Pyridoxal-derived aroylhydrazone iron chelators have been previously shown as effective cardioprotectants against chronic anthracycline cardiotoxicity. In this study we focused on a novel salicylaldehyde analogue (salicylaldehyde isonicotinoyl hydrazone, SIH), which has been recently demonstrated to possess marked and dose-dependent protective effects against oxidative injury of cardiomyocytes. Therefore, in the present study the cardioprotective potential of SIH against daunorubicin (DAU) cardiotoxicity was assessed in vitro (isolated rat ventricular cardiomyocytes; DAU 10 μM, 48 h exposure) as well as in vivo (chronic DAU-induced cardiomyopathy in rabbits; DAU 3 mg/kg, i.v. weekly, 10 weeks). In vitro, SIH (3–100 μM) was able to partially, but significantly decrease the LDH leakage from cardiomyocytes. In vivo, SIH co-administration was capable to reduce (SIH dose of 0.5 mg/kg, i.v.) or even to completely prevent (1.0 mg/kg, i.v.) the DAU-induced mortality. Moreover, the latter dose of the chelator significantly improved the left ventricular function (LV d P/d t max = 1185 ± 80 kPa/s versus 783 ± 53 kPa/s in the DAU group; P < 0.05) and decreased the severity of the myocardial morphological changes as well as the plasma levels of cardiac troponin T. Unfortunately, further escalation of the SIH dose (to 2.5 mg/kg) resulted in a nearly complete reversal of the protective effects as judged by the overall mortality, functional, morphological as well as biochemical examinations. Hence, this study points out that aroylhydrazone iron chelators can induce a significant cardioprotection against anthracycline cardiotoxicity; however, they share the curious dose–response relationship which is unrelated to the chemical structure or the route of the administration of the chelator.

Eccentric cardiac hypertrophy was induced by long‐term intermittent hypoxia in rats

It is unclear whether cardiac hypertrophy and hypertrophy-related pathways will be induced by long-term intermittent hypoxia. Thirty-six Sprague-Dawley rats were randomly assigned into three groups: normoxia, and long-term intermittent hypoxia (12% O(2), 8 h per day) for 4 weeks (4WLTIH) or for 8 weeks (8WLTIH). Myocardial morphology, trophic factors and signalling pathways in the three groups were determined by heart weight index, histological analysis, Western blotting and reverse transcriptase-polymerase chain reaction from the excised left ventricle. The ratio of whole heart weight to body weight, the ratio of left ventricular weight to body weight, the gross vertical cross-section of the heart and myocardial morphological changes were increased in the 4WLTIH group and were further augmented in the 8WLTIH group. In the 4WLTIH group, tumour necrosis factor-alpha(TNFalpha), insulin-like growth factor (IGF)-II, phosphorylated p38 mitogen-activated protein kinase (P38), signal transducers and activators of transcription (STAT)-1 and STAT-3 were significantly increased in the cardiac tissues. However, in the 8WLTIH group, in addition to the above factors, interleukin-6, mitogen-activated protein kinase (MEK)5 and extracellular signal-regulated kinase (ERK)5 were significantly increased compared with the normoxia group. We conclude that cardiac hypertrophy associated with TNFalpha and IGF-II was induced by intermittent hypoxia. The longer duration of intermittent hypoxia further activated the eccentric hypertrophy-related pathway, as well as the interleukin 6-related MEK5-ERK5 and STAT-3 pathways, which could result in the development of cardiac dilatation and pathology.

Cardiac dysfunction and heart failure are associated with abnormalities in the subcellular distribution and amounts of oligomeric muscle LIM protein

Prolonged hemodynamic overload results in cardiac hypertrophy and failure with detrimental changes in myocardial gene expression and morphology. Cysteine-rich protein 3 or muscle LIM protein (MLP) is thought to be a mechanosensor in cardiac myocytes. Therefore, the subcellular location of MLP may have functional implications in health and disease. Our hypothesis is that MLP becomes mislocalized after prolonged overload, resulting in impaired mechanosensing in cardiac myocytes. Using the techniques of biochemical subcellular fractionation and immunocytochemistry, we found MLP exhibits oligomerization in the membrane and cytoskeleton of cultured cardiac rat neonatal myocytes. Nuclear MLP was always monomeric. MLP translocated to the nucleolus in response to 10% cyclic stretch at 1 Hz for 48 h. This was associated with a threefold increase in S6 ribosomal protein (P < 0.01; n = 3 cultures). Adenoviral overexpression of MLP also resulted in a twofold increase in S6 protein, suggesting that MLP can activate ribosomal protein synthesis in the nucleolus. In ventricles from aortic-banded and myocardially infarcted rat hearts, nuclear MLP increased by twofold (P < 0.01; n = 7) along with a significant decrease in the nonnuclear oligomeric fraction. The ratio of nuclear to nonnuclear MLP increased threefold in both groups (P < 0.01; n = 7). In failing human hearts, there was almost a complete loss of oligomeric MLP. Using a flag-tagged adenoviral MLP, we demonstrate that the COOH terminus is required for oligomerization and that this is a precursor to stretch sensing and subsequent nuclear translocation. Therefore, reduced oligomeric MLP in the costamere and cytoskeleton may contribute to impaired mechanosensing in heart failure.

SUPRAVENTRICULAR RHYTHM DISTURBANCES TREATMENT WITH ANTIARHYTHMIC DRUG III CLASS NIBENTAN IN PATIENTS WITH ISCHEMIC HEART DISEASE (EXPERIMENTAL, CLINICAL AND MORPHOLOGICAL EVIDENCES)

Aim. To evaluate antiarhythmic efficiency of Nibentan (Verofarm, Russia), antiarrythmic drug III class, in supraventricular rhythm disturbances (SRD) relief in patients with ischemic heart disease (IHD). To assess morphological changes of myocardium in IHD with SRD. To specify inotropic characteristics of nibentan in experiment. Material and methods. 55 patients with IHD with different SRD were studied. 41 patients had heart failure (HF) of III functional class.14 other patients suffered acute myocardial infarction (AMI). SRD relief was achieved with 1% solution of nibentan in dose of 0.125 mg/kg patient's weight. After sinus rhythm recovery all patients received sotalol 80 mg twice a day to prevent SRD relapses. In vitro on myocardium of 10 healthy rats and 10 sliced myocardium strips of IHD patients (obtained during surgical intervention) changes in myocardium contraction intensity were assessed with PowerLab plant (ADInstruments, Australia) as a reaction on nibentan in doses of 4, 6 and 8 mkM. These doses correspond to doses of 0.125, 0.2 and 0.250 mg/kg, which are recommended for clinical practice. Histological study of autopsy materials of atrium myocardium of IHD patients with and without SRD was carried out. Phase-contrast and luminescent microscopy was also used. Results. Nibentan treatment lead to sinus rhythm recovery in 92.67% of HF patients. In 3 patients with persistent auricular fibrillation the drug was inefficient. Nibentan therapy did not result in blood pressure reduction. Heart rate decreased in 26.5%. Nibentan recovered sinus rhythm in 85.7% of AMI patients. Sinus rhythm didn't recover in 2 patients with persistent auricular fibrillation. Experimental studies revealed that myocardium contraction intensity in healthy rats increased at nibentan 4 and 6 mkM, and decreased at nibentan 8 mkM. Myocardium contraction intensity in IHD patients was decreasing while nibentan dose was growing. Histological study of auricular myocardium in IHD patients with SRD compared to myocardium in IHD patients without SRD, showed predominance of the following characteristics: fibrolipomatosis, focal and diffusive fibrosis and sclerosis, chaotic allocation of cardiac cells, muscular-elastic hyperplasia of vascular intima, contractile degeneration (at phase-contrast microscopy). Conclusion. Nibentan in bolus i.v. administration in dose of 0.125 mg/kg is effective drug for SRD relief in patients with IHD with HF and in patients with AMI. It doesn't affect BP significantly. According to data of experiments dose of nibentan 0.125mg/kg is optimal for inotropic function of myocardium. More significant histological changes in auricular myocardium can be the reason of SRD.

Is there an Optimal Training Intensity for Enhancing the Maximal Oxygen Uptake of Distance Runners?

The maximal oxygen uptake (V-dotO(2max)) is considered an important physiological determinant of middle- and long-distance running performance. Little information exists in the scientific literature relating to the most effective training intensity for the enhancement of V-dotO(2max) in well trained distance runners. Training intensities of 40-50% V-dotO(2max) can increase V-dotO(2max) substantially in untrained individuals. The minimum training intensity that elicits the enhancement of V-dotO(2max) is highly dependent on the initial V-dotO(2max), however, and well trained distance runners probably need to train at relative high percentages of V-dotO(2max) to elicit further increments. Some authors have suggested that training at 70-80% V-dotO(2max) is optimal. Many studies have investigated the maximum amount of time runners can maintain 95-100% V-dotO(2max) with the assertion that this intensity is optimal in enhancing V-dotO(2max). Presently, there have been no well controlled training studies to support this premise. Myocardial morphological changes that increase maximal stroke volume, increased capillarisation of skeletal muscle, increased myoglobin concentration, and increased oxidative capacity of type II skeletal muscle fibres are adaptations associated with the enhancement of V-dotO(2max). The strength of stimuli that elicit adaptation is exercise intensity dependent up to V-dotO(2max), indicating that training at or near V-dotO(2max) may be the most effective intensity to enhance V-dotO(2max) in well trained distance runners. Lower training intensities may induce similar adaptation because the physiological stress can be imposed for longer periods. This is probably only true for moderately trained runners, however, because all cardiorespiratory adaptations elicited by submaximal training have probably already been elicited in distance runners competing at a relatively high level.Well trained distance runners have been reported to reach a plateau in V-dotO(2max) enhancement; however, many studies have demonstrated that the V-dotO(2max) of well trained runners can be enhanced when training protocols known to elicit 95-100% V-dotO(2max) are included in their training programmes. This supports the premise that high-intensity training may be effective or even necessary for well trained distance runners to enhance V-dotO(2max). However, the efficacy of optimised protocols for enhancing V-dotO(2max) needs to be established with well controlled studies in which they are compared with protocols involving other training intensities typically used by distance runners to enhance V-dotO(2max).

Effects on Reperfusion Injury of Adding Diltiazem to Tepid Blood Cardioplegia

Although the present techniques of myocardial preservation for limiting ischemia/reperfusion injury in open heart operations yield excellent results for most patients, certain subgroups of patients with advanced coronary artery disease present a challenge in terms of intraoperative safety. In a prospective, randomized, controlled study, we assessed the myocardial protective effects of a total dose of 150 +/- 150 = 300 microg/kg diltiazem added to induction and terminal (reperfusion) doses of tepid blood cardioplegia. We determined the myocardial morphological (ultrastructural) and enzymatic (serum assays for the cardiospecific isoenzyme of creatine kinase [CK-MB]) changes and functional recovery (atrioventricular [AV]-node recovery time and postoperative need for inotropic support) in patients undergoing elective coronary artery bypass operations. The determinations were made with respect to values for control patients, who received the same cardioplegia but without the addition of diltiazem. The mean isoenzyme CK-MB levels and semiquantitative ultrastructural score values of the diltiazem group were significantly less than those of the control group. Although AV-node recovery time was significantly prolonged (P < .05), this factor did not have major clinical impact. We concluded that the addition of 150 +/- 150 microg/kg diltiazem to the induction and terminal doses of tepid cardioplegia enhanced myocardial protection in elective aortocoronary bypass surgery in high-risk patients and presented no significant additional operative risk.

Chronobiological and morphofunctional aspects of arterial hypertension under circumpolar conditions

Introduction. Nowadays the problem of population health in the northern areas is of great importance. While evaluating human adaptation to the extreme geoecological northern conditions the state of the cardiovascular system can be used as an index of effective compensatory adaptation. Study design. The data on 24-hour BP monitoring, data of echocardiography and heliogeophysical factors in different periods of ontogenesis in 317 patients, living in the north of the Tyumen region, were analysed to estimate the morphofunctional and chronobiological peculiarities of arterial hypertension. Results. Considerable disorders of haemodynamic circadian rhythms, manifesting either insufficient decrease of BP at night are revealed in the examined subjects. Above 42.2% of such patients have myocardial hypertrophy. Insufficient night decrease of BP is typical for the examined patients, with coupling of the indices of haemodynamic and current geomagnetic activity. The peculiarities of heliogeophysical factors at early ontogenesis of the examined subjects with an increased variability and decreased circadian index of BP are defined using multivariate analysis. Conclusion. Thus, a combination of disorders of temporary haemodynamic organisation with the morphological changes of myocardium and peculiarities of biogeophysical coupling of the examined is shown. This anthropoecological approach can be used for the diagnostics and treatment of arterial hypertension under conditions of the northern ecosystem.

Chronic oral administration of raw garlic protects against isoproterenol-induced myocardial necrosis in rat

Wistar albino rats (150–200 g) were fed raw garlic homogenate orally in three different doses (125, 250, 500 mg/kg/day) for 30 days. Isoproterenol (85 mg/kg, s.c. 2 doses at 24-h interval, animals sacrificed after 24 h of last injection) induced myocardial necrosis in control rats and after 30 days of garlic feeding. Myocardial oxidative stress was evident following isoproterenol administration by reduction in myocardial superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities along with a rise in plasma thiobarbituric acid reactive substances (TBARS). Myocardial necrosis was evident from the light microscopic and ultrastructural changes, along with a rise in plasma lactate dehydrogenase (LDH). Significant preservation of myocardial SOD activity was observed in all the garlic-fed rats. However, there was no significant change in myocardial reduced glutathione level and GPx activity in any of the treated groups. Significant reduction in plasma TBARS and LDH levels was observed in the 500 mg/kg garlic treated group. Isoproterenol-induced myocardial morphological changes were least in the 250 and 500 mg/kg garlic treated groups. The results suggest that chronic oral administration of raw garlic offered protection against isoproterenol-induced myocardial necrosis and associated oxidative stress.

Ets-1 and Ets-2 transcription factors are essential for normal coronary and myocardial development in chicken embryos.

In the development of a functional myocardium and formation of the coronary vasculature, epicardium-derived cells play an essential role. The proepicardial organ contributes to the developing coronary system by delivering mural cells to the endothelium-lined vessels. In search of genes that regulate the behavior of (pro)epicardial cells, the Ets-1 and Ets-2 transcription factors stand out as strong candidates. In the present study, the hypothesis that Ets transcription factors have a role in proper coronary and myocardial development was tested via antisense technology, by targeting Ets-1 and Ets-2 mRNAs to downregulate protein expression in chicken embryos. The results suggest that hereby the development of the coronary system is hampered, primarily by defects in the process of epithelial-mesenchymal transformation of the mesothelia of the primary and secondary heart fields. This was indicated by a lack of periarterial and epicardial mesenchyme, of peripheral coronary smooth muscle cells, and changes in myocardial morphology. A defect in myocardial perfusion caused by the absence of one or both coronary ostia seems to be "solved" by the development of numerous small fistulae connecting the ventricular lumen with the subepicardially located coronary vessels. The presence of coronary vascular aberrations in the antisense-Ets phenotype enabled us for the first time to study abnormal coronary development in a model that is not lethal to the embryo.

Evaluation of cardiac troponin I and T levels as markers of myocardial damage in doxorubicin-induced cardiomyopathy rats, and their relationship with echocardiographic and histological findings

Background: Cardiac troponins I (cTnI) and T (cTnT) have been shown to be highly sensitive and specific markers of myocardial cell injury. We investigated the diagnostic value of cTnI and cTnT for the diagnosis of myocardial damage in a rat model of doxorubicin (DOX)-induced cardiomyopathy, and we examined the relationship between serial cTnI and cTnT with the development of cardiac disorders monitored by echocardiography and histological examinations in this model. Methods: Thirty-five Wistar rats were given 1.5 mg/kg DOX, i.v., weekly for up to 8 weeks for a total cumulative dose of 12 mg/kg BW. Ten rats received saline as a control group. cTnI was measured with Access® (ng/ml) and a research immunoassay (pg/ml), and compared with cTnT, CK-MB mass and CK. By using transthoracic echocardiography, anterior and posterior wall thickness, LV diameters and LV fractional shortening (FS) were measured in all rats before DOX or saline, and at weeks 6 and 9 after treatment in all surviving rats. Histology was performed in DOX-rats at 6 and 9 weeks after the last DOX dose and in all controls. Results: Eighteen of the DOX rats died prematurely of general toxicity during the 9-week period. End-diastolic (ED) and end-systolic (ES) LV diameters/BW significantly increased, whereas LV FS was decreased after 9 weeks in the DOX group ( p<0.001). These parameters remained unchanged in controls. Histological evaluation of hearts from all rats given DOX revealed significant slight degrees of perivascular and interstitial fibrosis. In 7 of the 18 rats, degeneration and myocyte vacuolisation were found. Only five of the controls exhibited evidence of very slight perivascular fibrosis. A significant rise in cTnT was found in DOX rats after cumulative doses of 7.5 and 12 mg/kg in comparison with baseline ( p<0.05). cTnT found in rats after 12 mg/kg were significantly greater than that found after 7.5 mg/kg DOX. Maximal cTnI (pg/ml) and cTnT levels were significantly increased in DOX rats compared with controls ( p=0.006, 0.007). cTnI (ng/ml), CK-MB mass and CK remained unchanged in DOX rats compared with controls. All markers remained stable in controls. Analysis of data revealed a significant correlation between maximal cTnT and ED and ES LV diameters/BW ( r=0.81 and 0.65; p<0.0001). A significant relationship was observed between maximal cTnT and the extent of myocardial morphological changes, and between LV diameters/BW and histological findings. Conclusions: Among markers of ischemic injury after DOX in rats, cTnT showed the greatest ability to detect myocardial damage assessed by echocardiographic detection and histological changes. Although there was a discrepancy between the amount of cTnI and cTnT after DOX, probably due to heterogeneity in cross-reactivities of mAbs to various cTnI and cTnT forms, it is likely that cTnT in rats after DOX indicates cell damage determined by the magnitude of injury induced and that cTnT should be a useful marker for the prediction of experimentally induced cardiotoxicity and possibly for cardioprotective experiments.

Inhibition of doxorubicin chronic toxicity in catalase-overexpressing transgenic mouse hearts.

Catalase is an important antioxidant enzyme, which has been shown to provide cardiac protection from acute toxicity induced by doxorubicin, a most effective anticancer agent. Because cumulative dose-dependent chronic cardiomyopathy due to a long-term administration of doxorubicin is a significant clinical problem, the present study was undertaken to test the hypothesis that catalase also provides protection against doxorubicin chronic cardiotoxicity. Transgenic mice containing cardiac catalase activities of 15-, 60-, or 100-fold higher than normal and nontransgenic controls were treated with doxorubicin in a cumulative dose of 45 mg/kg in five equal iv injections (9 mg/kg every other week) over a period of 10 weeks. On the second day after the last injection, the mice were sacrificed for analysis of cardiotoxicity. As compared to nontransgenic controls, doxorubicin-reduced body weight gain was significantly inhibited in the transgenic mice. There were 15% mortality in nontransgenic mice, but no mortality was observed in transgenic mice during the course of treatment. Light microscopic examination revealed that doxorubicin-induced myocardial morphological changes were markedly suppressed in the transgenic mice in an activity-dependent fashion. Under electron microscopy, extensive sarcoplasmic vacuolization and severe disruption of mitochondrial fine structure were observed in nontransgenic cardiomyocytes, but all markedly suppressed in the transgenic mice. The results indicate that catalase elevation in the heart prevents doxorubicin chronic cardiomyopathy.

Morphological changes in myocardium in rats with different resistance to hypoxia after ligation of the coronary artery.

We studied morphological changes in the myocardium during experimental myocardial infarction in rats with different resistance to hypoxia. Microscopic examination showed that morphological changes in the ischemic zone and adjacent tissues are different in rats with high and low resistance to acute ischemia. In highly resistant rats, necrotic changes in cardiomyocytes included focal contracture and loosening. These changes were followed by the formation of focal necroses with well-defined boundaries, dense demarcation infiltrates, and pronounced hypertrophy of cardiomyocytes in the adjacent tissue. In low resistant rats, pronounced edema in the ischemia zone and numerous hemorrhages in the interstitial tissue developed in the early stage after coronary occlusion. These changes were followed by the formation of more extensive necrotic areas with diffuse boundaries, less pronounced demarcation, and irregular hypertrophy of cardiomyocytes in the surrounding tissue.

Electrophysiologic properties and ventricular fibrillation in normal and myopathic hearts

This study tests the hypothesis that moderate myocardial dysfunction is associated with altered myocardial anisotropic properties and structurally altered ventricular fibrillation (VF). Mongrel dogs were randomized to either a control group or a group that was rapidly paced at 250 beats/min until the left ventricular ejection fraction was < or = 40%. Changes in anisotropic properties and the electrical characteristics of VF associated with the development of moderate myocardial dysfunction were assessed by microminiature epicardial mapping studies. In vivo conduction, refractory periods, and repolarization times were prolonged in both longitudinal and transverse directions in myopathic animals versus controls. VF was different in myopathic versus control animals. There were significantly more conducted deflections during VF in normal hearts compared with myopathic hearts. Propagated deflection-to-deflection intervals during VF were significantly longer in myopathic hearts compared with controls (125.5 +/- 49.06 versus 103.4 +/- 32.9 ms, p = 0.009). There were no abnormalities in cell size, cell shape, or the number of intercellular gap junctions and there was no detectable change in the expression of the gap junction proteins Cx43 and Cx45. Moderate myocardial dysfunction is associated with significant electrophysiological abnormalities in the absence of changes in myocardial cell morphology or intercellular connections, suggesting a functional abnormality in cell-to-cell communication.

Morphological changes in myocardium of heat acclimated rats

Morphological changes in myocardium of heat acclimated rats

Morphological changes in myocardium from patients with coronary heart disease and cardiac hypertrophy.

Morphological changes in myocardium from patients with coronary heart disease and cardiac hypertrophy.

Morphological changes in myocardium from patients with coronary heart disease

Morphological changes in myocardium from patients with coronary heart disease