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In the study of cardiac toxicology cholesterol journal articles best atorvastatin 5mg, the manifestations of cardiac toxicity in human patients and animal models are critical parameters serving as indices of cardiac toxicity lowering cholesterol tlc diet cheap 10mg atorvastatin with amex. These manifestations are expressed in the forms of cardiac arrhythmia cholesterol medication affect kidneys generic 10mg atorvastatin with mastercard, hypertrophy cholesterol quotes cheap atorvastatin 5mg without prescription, and heart failure. These abnormal changes reflect myocardial functional alterations resulting from both acute and chronic cardiac toxicity. Although some changes, such as cardiac hypertrophy, was viewed as a compensatory response to hemodynamic changes in the past, more recent studies suggest that cardiac hypertrophy is a maladaptive process of the heart in response to intrinsic and extrinsic stresses (van Empel et al. Cardiac hypertrophy is a risk factor for sudden cardiac death and has a high potential to progress to overt heart failure. Therefore, a distinction between compensatory and maladaptive responses is critical for treatment of patients with toxicologic cardiomyopathy. Cardiac Arrhythmia Cardiac rhythms under physiological conditions are set by pacemaker cells that are normally capable of developing spontaneous depolarization and responsible for generating the cardiac rhythm, the so-called automatic rhythm. A cardiac rhythm that deviates from the normal automatic rhythm is called cardiac arrhythmia, often manifested in the form of tachycardia (fast heart rate). There are several classes of tachycardia, including sinus tachycardia, atrial tachycardia, ventricular tachycardia, and torsade de pointes (TdP) (a life-threatening ventricular tachycardia). In addition, subclasses such as atrial fibrillation, atrial flutter, and accelerated idioventricular rhythm provide further description of the manifestations of arrhythmia. Recognition of chronic cardiac toxicity in the pathogenesis of cardiomyopathy is of clinical relevance, and this knowledge can be used to prevent and treat patients with toxicologic cardiomyopathy. Myocardial Degeneration and Regeneration Myocardial degeneration is the ultimate response of the heart to toxic exposure, which can be measured by both morphological and functional degenerative phenotypes. However, myocardial degeneration should not be considered an irreversible toxic response. In the past, the heart has been considered incapable of regenerating, so that cardiac injury in the form of cell loss or scar tissue formation was considered permanent damage to the heart. However, evidence now indicates myocardial regeneration and recovery from cardiomyopathy. Cardiac toxic responses or damage are now divided into reversible and irreversible. Myocardial Degenerative Responses Myocardial cell death, fibrosis (scar tissue formation), and contractile dysfunction are considered as degenerative responses, which can result in cardiac arrhythmia, hypertrophy, and heart failure. If acute cardiac toxicity does not affect the capacity of myocardial regeneration, the degenerative phenotype is reversible. Both acute and chronic toxic stresses can lead to irreversible degeneration, depending on whether or not the cardiac repair mechanisms are overwhelmed. Both apoptosis and necrosis occur in the process of myocardial cell death, which will be discussed in the next section. Myocardial cell death is accompanied by hypertrophy of the remaining cardiac myocytes so that in the hypertrophic heart, the total number of cardiac myocytes is reduced but the size or volume of individual cells is increased. During myocardial remodeling after cell death, not only is there an increase in the size of cardiac myocytes, but also cardiac fibrosis occurs. The activities of these enzymes are altered during the processes of fibrogenesis and fibrinolysis. Under toxic stress condition, the imbalance between fibrogenesis and fibrinolysis leads to enhanced fibrogenesis and excess collagen accumulation- fibrosis. Toxic Effect on Myocardial Regeneration the mainstay of cardiac medicine and therapy has centered on the concept that the heart is a terminally differentiated organ and that cardiac myocytes are incapable of proliferating. Thus, cell death would lead to a permanent loss of the total number of cardiac myocytes. However, this view has been challenged recently due to the identification of cardiac progenitor cells (Anversa et al. These cells are characterized and proposed to be responsible for cardiac repair because these cells can make myocytes and vascular structures. These cells possess the fundamental properties of stem cells, therefore, they are also called cardiac stem cells. They are self-renewing, clonogenic, and multipotent, as demonstrated by reconstitution of infarcted heart by intramyocardial injection of cardiac progenitor cells or the local activation of these cells by growth factors.

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After emergency use of an intramuscular antipsychotic or benzodiazepine cholesterol in eggs and chicken discount atorvastatin 5mg mastercard, pulse cholesterol medication safe during pregnancy cheap 10 mg atorvastatin mastercard, blood pressure cholesterol test particle size 40 mg atorvastatin with visa, temperature and respiration are monitored cholesterol test how long to fast buy atorvastatin 40mg line, and pulse oximetry (for oxygen saturation) if consciousness is lost. Clinicians are now becoming reluctant to use this heavily sedating preparation other than for patients who have previously responded well to it, and never use it for neuroleptic-naive patients. Amobarbital and paraldehyde have a role in emergencies only when antipsychotic and benzodiazepine options have been exhausted. Consequently some 75% of patients experience extrapyramidal symptoms shortly after starting the drug or increasing its dose (acute effects), or some time after a particular dose level has been established (tardive effects). Parkinsonian symptoms result in the classical triad of bradykinesia, rigidity and tremor. Both dystonias and parkinsonian symptoms are believed to result from a shift in favour of cholinergic rather than dopaminergic neurotransmission in the nigrostriatal pathway (see p. Akathisia is a state of motor and psychological restlessness, in which patients exhibit persistent foot tapping, moving of legs repetitively and being unable to settle or relax. A strong association has been noted between its presence in treated schizophrenics and subsequent suicide. Differentiating symptoms of psychotic illness from adverse drug effects is often difficult: druginduced akathisia may be mistaken for agitation induced by psychosis. Adverse drug effects can be the final straw in compromising already fragile compliance, leading to relapse. When atypical antipsychotics first came to prominence in the mid-1990s much was made of their lower propensity to cause several of the most troublesome side-effects of classical antipsychotics, especially extrapyramidal motor effects. However, while these problems are encountered less frequently, atypical drugs have a range of troublesome metabolic side-effects which had not been reported in the previous era of classic antipsychotics. Thus, to understand the current position relating to the pros and cons of atypical antipsychotics, it is necessary first to describe the side-effect profile of classical antipsychotic drugs. Tardive dyskinesia affects about 25% of patients taking classical antipsychotic drugs, the risk increasing with length of exposure. It was originally thought to be a consequence of up-regulation or supersensitivity of dopamine receptors, but a more recent view is that oxidative damage leads to increases in glutamate transmission. Patients display a spectrum of abnormal movements from minor tongue protrusion, lip-smacking, rotational tongue movements and facial grimacing, choreoathetoid movements of the head and neck, and even to twisting and gyrating of the whole body. Remission on discontinuing the causative agent is less likely than are simple dystonias and parkinsonian symptoms. Dose ranges are not specified as they are extremely wide and drugs are normally increased from low starting doses. The chlorpromazine equivalent dose concept is of less value for atypical antipsychotics because minimum effective doses (min. Alternatively, an atypical antipsychotic can provide rapid improvement while retaining control of psychotic symptoms. Atypicals, particularly at high doses, can cause extrapyramidal effects, so this strategy is not always helpful. Clozapine, which does not appear to cause tardive dyskinesia, may be used in severe cases where continuing antipsychotic treatment is required and symptoms have not responded to other medication strategies. If the classical antipsychotic is continued, tardive dyskinesia remits spontaneously in around 30% of patients within 1 year, but the condition is difficult to tolerate and patients may be keen to try other medications even where evidence suggests that the success rates for remission are limited. These include vitamin E, benzodiazepines, b-blockers, bromocriptine and tetrabenazine. Atypical antipsychotics Having considered the side-effect profile of classical antipsychotic agents, the adverse effects of atypical antipsychotics can be viewed as those shared with classical agents and those unique to one or more atypical agents. Extrapyramidal effects occur less frequently than with classical agents (there is less blockade of dopamine D2 receptors in the nigrostriatal pathway) but do occur with high doses of risperidone and olanzapine. Tardive dyskinesia is much less common with all of the atypical agents than with classical drugs. Anticholinergic (antimuscarinic) effects are most likely with clozapine and olanzapine. Adverse effects relating to prolactin stimulation are also rare, with the exception of risperidone and amisulpride (for which galactorrhea is as common as with classical drugs). Atypicals have also been implicated as causing metabolic disorders especially diabetes mellitus and hyperlipidaemia. Obesity, impaired glucose tolerance and hyperlipidaemia, along with hypertension, are all features of metabolic syndrome.

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Unfortunately cholesterol year score buy discount atorvastatin 10 mg line, our understanding of the toxic effects on myocardial angiogenesis is limited cholesterol levels high risk buy atorvastatin 20 mg mastercard. Cardiomyopathy was viewed not to be recoverable in the past cholesterol juice recipes buy 40 mg atorvastatin, but there is cumulative evidence that demonstrates reversibility of cardiomyopathy cholesterol ratio 1.9 good buy atorvastatin 10 mg with mastercard. The issue related to whether or not toxicologic cardiac lesions are reversible has not been explored. However, it can be speculated that there would be reversible and irreversible manifestations of the cardiac response to toxic insults. Myocardial Cell Death and Signaling Pathways Apoptosis and Necrosis Toxic insults trigger a series of reactions in cardiac cells leading to measurable changes. However, severe injuries will lead to cell death in the modes of apoptosis and necrosis. If the cell survives the insults, structural and functional adaptations will take place. The loss of cardiac myocytes is a fundamental part of myocardial injury, which initiates or aggravates cardiomyopathy. An important mode of myocardial cell loss is apoptosis, which has been demonstrated in heart failure patients (Olivetti et al. Myocardial apoptosis has been shown to play an important role in cardiac toxic effects induced by Adriamycin (Kang et al. Exposure of primary cultures of cardiomyocytes to cadmium also induces apoptosis (El-Sherif et al. At first glance, this number seems to be too insignificant to account for myocardial pathogenesis. Myocytes that undergo apoptosis are lost and may not be replaced under toxicologic conditions. Although the possibility of myocardial regeneration has been identified (Anversa et al. Adriamycin-induced cardiomyopathy is a good example for the pathogenesis resulting from both degeneration and inhibition of regeneration. Necrosis is a term that had been widely used to describe myocardial cell death in the past. Myocardial infarction, in particular, had been considered as a consequence of necrosis (Eliot et al. It is now recognized that apoptosis contributes significantly to myocardial infarction (Yaoita et al. However, the importance of necrosis in myocardial pathogenesis cannot be underestimated. The contribution of necrosis to cardiomyopathy induced by environmental toxicants and pollutants is particularly important. Apoptosis and necrosis were originally described as two distinct forms of cell death that can be clearly distinguished (Wyllie, 1994). However, these two modes of cell death can occur simultaneously in tissues and cultured cells. A downstream controller, however, may direct cells toward a programmed execution of apoptosis. If the apoptotic program is aborted before this control point and the initiating stimulus is severe, cell death may occur by necrosis (Leist et al. The specificity of this molecular probe to identify apoptosis has been confirmed by other methods such as dual labeling of TdT and caspase-3 (Frustaci et al. Proportion of apoptotic and necrotic cell death in the heart can be estimated by the combination of the above procedures. Distinguishing apoptotic myocytes from non-myocytes in the myocardium is another problem to overcome. The gold standard for identification of apoptotic cells is morphological examination by electron microscopy. Mitochondrial Control of Cell Death the role of mitochondria in myocardial response to toxicants as well as therapeutic drugs has long been a focus of investigation.

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