Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anthracyclines, found to be efficacious in the treatment of a broad spectrum of pediatric malignancies, are cardiotoxic and may lead to heart failure even a long time after successful treatment of cancer. It is thought that subtle abnormalities can progress to the more permanent myocardial disease, resulting in cardiomyopathy which may progress to congestive heart failure. There are some precipitating factors leading to the sudden onset of cardiac symptoms such as increase in afterload or preload. We describe a young patient with congestive heart failure treated with doxorubicin (cumulative mean dose 420 mg/m2) in infancy because of pelvic sarcoma in whom the appearance of symptoms was related to pulmonary embolism. Four years before hospital admission, the patient presented echocardiographic abnormalities such as left ventricular fractional shortening and thickness reduction and he was treated with ACE-inhibitors. The myocardial ischemia, which is present in pulmonary embolism, probably worsened the left ventricular systolic function and caused congestive heart failure.
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PMID:[Heart failure in a subject treated with anthracyclines in childhood: myocardial dysfunction is not always the only reason of it]. 1534 97

Afterload reduction is useful for treating and preventing adult congestive heart failure outside the realm of anthracycline toxicity. Afterload reducers are commonly used as treatment for acute heart failure associated with anthracyclines. However, the use of afterload reduction for the prevention of anthracycline associated late cardiomyopathy remains a controversial area, with strong opinions expressed concerning the potential risks and benefits of such an approach. This article will define "afterload" and the tools utilized to measure afterload. The study will then describe the theory for the use of afterload reduction in patients with anthracycline exposure who show signs of anthracycline cardiotoxicity, and will present data from the ACE-Inhibitor After Anthracyclines (AAA) Trial to help answer the question, "Should an afterload reducer be used to aid in preventing late anthracycline cardiotoxicity?" Finally, recommendations for future research will be presented.
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PMID:Role of afterload reduction in the prevention of late anthracycline cardiomyopathy. 1579 84

The fact that anthracyclines are cardiotoxic seriously narrows their therapeutic index in cancer therapy. The cardiotoxic risk increases with the cumulative dose and may lead to congestive heart failure (CHF) and dilated cardiomyopathy in adults and in children. The prevention of anthracycline-induced cardiotoxicity is particularly important in children who can be expected to survive for decades after being cured of their malignancy. Attempts to reduce anthracycline cardiotoxicity have been directed towards: (i) decreasing myocardial concentrations of anthracyclines and their metabolites by dose limitation and schedule modification; (ii) developing less cardio-toxic analogs; and (iii) concurrently administering cardioprotective agents to attenuate the effects of anthracyclines on the heart. As regards schedule modification, avoidance of anthracycline peak levels may reduce the pathologic and clinical cardiotoxicity, although this has not always been observed. The analogs of doxorubicin, such as idarubicin and epirubicin, have similar cardiotoxicity to that of doxorubicin when given in amounts of equivalent myelotoxicity. Liposomal anthracyclines are a new class of agents that may permit more specific organ targeting, thereby producing less systemic and cardiac toxicity, but more studies are required to assess the advantages, if any, of these preparations over classical anthracyclines. The cardioprotective agent, dexrazoxane, an iron chelator, is highly effective and provides short-term cardioprotection to most patients receiving even the most intensive doxorubicin-containing regimens. Its long-term benefits remain to be determined. In addition, data remain insufficient to make specific recommendations regarding current use of dexrazoxane in children. It is thought that subtle abnormalities, related to anthracycline treatment in childhood, can develop into more permanent myocardial disease resulting in cardiomyopathy, which may progress to CHF. As regards the therapy of patients with anthracycline cardiotoxicity, two different situations have, therefore, to be considered: (i) if the patient presents with cardiac abnormalities, such as a reduction in fractional shortening at echocardiogram, without cardiac symptoms; and (ii) if the patient has CHF. In the presence of CHF, recovery with digitalis-diuretic therapy alone seldom occurs, and in patients who have refractory hemodynamic decompensation, heart transplantation is indicated. In patients with CHF, therapy with ACE inhibitors induces improvement in left ventricular structure and function, but this improvement is transient. Randomized clinical trials are, therefore, necessary to determine the effects of ACE inhibitors in mild-to-moderate left ventricular dysfunction. The beneficial effects of beta-adrenoceptor antagonists (beta-blockers) on cardiac function in heart failure due to anthracyclines seem comparable with those observed in other forms of heart failure with systolic dysfunction. Many drugs are available to treat children with CHF due to anthracycline treatment, but they are only palliative.
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PMID:Anthracycline-induced cardiotoxicity in children with cancer: strategies for prevention and management. 1587 28

Collagen is the major extracellular matrix protein in the heart and represents a crucial target for anti-remodeling and cardioprotective therapy. Collagen quantity and quality have been shown to be regulated under various physiological and pathologic conditions. Excessive deposition of collagen, leading to cardiac fibrosis, is a major determinant of cardiac dysfunction and arrhythmogenecity associated with sudden death. Serological markers of collagen turnover were proven as a noninvasive reliable tool for monitoring from a distance cardiac tissue repair and fibrosis, both in experimental and clinical conditions. Some markers of collagen synthesis and degradation were shown to have a prognostic significance in myocardial infarction, cardiomyopathy and heart failure, and were reported as independent predictors of mortality. Aldosterone represents the end-product of the renin angiotensin aldosterone system and may play a role in cardiac collagen deposition independent of its effect on blood pressure. Production of aldosterone is mainly regulated by angiotensin II and is activated in the failing human ventricle in proportion to heart failure severity. Circulating or locally produced aldosterone stimulates fibrillar collagen accumulation in the heart directly via mineralocorticoid receptors or, indirectly, modifying angiotensine II receptors number and/or function. The use of mineralocorticoid receptor antagonists counters collagen deposition, even when used on top of classical RAAS inhibitors, such as ACE inhibitors and angiotensine II receptor blockers. There is now accumulating evidence from experimental and clinical studies showing antifibrotic and cardioprotective effect for aldosterone antagonists, spironolactone and eplerenone. In chronic heart failure and post myocardial infarction patients, aldosterone receptor blockade benefit was associated with decreased serum levels of collagen synthesis marker PIIINP (procollagen type III amino-terminal peptide), without affecting collagen degradation. Understanding various autocrine/paracrine mechanisms involved in extracellular matrix remodeling in heart failure represents a major challenge, essential for developing new cardioreparative and cardioprotective strategies.
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PMID:Effect of MR blockade on collagen formation and cardiovascular disease with a specific emphasis on heart failure. 1594 94

Cardiomyopathies are defined as diseases of the myocardium associated with cardiac dysfunction. They are classified as dilated cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy. Dilated cardiomyopathy is characterized by dilatation and impaired contraction of the ventricles. Hypertrophic cardiomyopathy is characterized by ventricular hypertrophy, which is usually asymmetric. Restrictive cardiomyopathy is characterized by restrictive filling and reduced diastolic function, with normal systolic function and wall thickness. Except for cardiac failure, sudden death from arrhythmia is the leading cause of death among cardiomyopathy patients. ACE inhibitors and beta blockers are effective medicine for cardiac failure patients. However sudden death rate of cardiomyopathy patients is still high. Implantable cardioverter-defibrillator could save many cardiomyopathy patients from sudden death according to a lot of trials.
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PMID:[Idiopathic cardiomyopathy]. 1600 75

A 15-year-old, neutered male, domestic shorthair presented with dyspnea. Unclassified cardiomyopathy was diagnosed. Treatment resulted in a profound bradycardia, which was attributed to the administration of a beta-adrenergic blocker. The pathogenesis of unclassified cardiomyopathy is discussed and the side effects of beta-adrenergic blockers and angiotensin converting enzyme inhibitors are reviewed.
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PMID:Unclassified cardiomyopathy in a geriatric cat. 1623 54

Pheochromocytoma may infrequently lead to dilated cardiomyopathy, which may reverse partially or completely after treatment. Progressive dyspnea, palpitations, and paroxysmal attacks of severe hypertension leading to cardiac failure had developed in a 25-yr-old woman. Chest radiography and echocardiography revealed a massive 4-chamber dilatation of the heart with an ejection fraction of 12%. Twenty-four-h urinary vanillylmandelic acid and metanephrine levels were elevated. Magnetic resonance imaging detected a large mass lesion in the right adrenal gland. Oral glucose tolerance testing revealed diabetes mellitus. Medical drug therapy with alpha-blocker, angiotensin converting enzyme inhibitor, beta-blocker, digoxin, and diuretic rapidly improved her cardiac condition. Repeat echocardiogram showed that the left ventricular function had improved substantially. The clinical condition of excess catecholaminemia (and thus, arterial hypertension and the abnormality of the glucose metabolism) subsided with complete resolution of the congestive heart failure following the surgical removal of the tumor. Evaluation for medullary thyroid carcinoma (MTC) revealed an elevated calcitonin level demonstrated by fine needle aspiration biopsy. There were no biochemical evidences for primary hyperparathyroidism. Multiple endocrine neoplasia 2 (MEN 2A) syndrome was diagnosed. An overwhelming secretion of catecholamine might cause severe cardiomyopathy and impair glucose metabolism, as evidenced by the improvement of both conditions following the medical treatment of catecholaminemia and surgical resection of the tumor.
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PMID:Severe reversible dilated cardiomyopathy in a patient with multiple endocrine neoplasia 2A syndrome. 1669 5

A 69-year-old man with no remarkable medical history was admitted to the intensive care unit in septic shock due to severe community-acquired pneumonia. Twelve hours later he developed electrocardiographic abnormalities with ST elevation in leads II, III, aVF, V5, and V6 in the absence of chest pain and the presence of dyspnea, agitation, and hypertension. Serial measurements of cardiac enzymes were also elevated. Acute coronary syndrome was suspected. A cardiac ultrasound revealed left ventricular dilation with akinesia and systolic dysfunction (ejection fraction, 40%). Emergency catheterization revealed normal coronary arteries, suggesting a probable diagnosis of acute myocarditis. From the fourth day, the patient was progressing favorably. Findings in a follow-up ultrasound were consistent with the onset of dilated myocardiopathy, and angiotensin converting enzyme inhibitors were prescribed. All serology and microbiological studies were negative. Fifteen days after admission the patient was discharged to home after clinical, radiologic and analytic recovery.
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PMID:[Myocarditis in the differential diagnosis of acute coronary syndrome]. 1682 73

The discovery of a new angiotensin II (Ang II) pathway generated by mast cell chymase has highlighted new biological functions for Ang II that is not related to the classic renin-angiotensin system (RAS). The conversion of Ang I to II occurs not only via the plasma angiotensin converting enzyme (ACE) or tissue ACE but also via chymase produced in the mast cells of humans, monkeys, dogs, and hamsters. The conversion by chymase has been especially found in morbid tissues following the migration of mast cells. The newly discovered functions of chymase are discussed in this review. During the vascular narrowing that occurs after vein grafting or balloon injury in dogs, chymase activity and Ang II concentrations along with intimal proliferation are significantly increased and chymase inhibitors completely suppressed these increase, though ACE inhibitors are ineffective. Similar results have also been confirmed in the dog arteriovenous fistula stenosis model. In both human and animal aneurysmal aortas, chymase activity is significantly increased, and chymase inhibitor has been shown to prevent the development of aneurysms in dogs. Chymase is activated in diseased hearts, and chymase inhibitors reduce both the mortality rates after acute myocardial infarction and the cardiac fibrosis that leads to the development of cardiomyopathy in hamsters. Chymase is also a pro-angiogenic factor, since the injection of chymase strongly facilitates angiogenesis in hamsters. We propose that chymase inhibitors are effective in the prevention of multiple cardiovascular disorders, especially at the local event level without any effect on the systemic blood pressure.
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PMID:Pathological roles of angiotensin II produced by mast cell chymase and the effects of chymase inhibition in animal models. 1683 49

Aim. To assess role of 24 hour heart rate variability (HRV) for prognosis of patients with chronic heart failure (CHF) and systolic dysfunction in the era of wide use of b-adrenoblockers. Material. Patients (n=135) with symptomatic CHF and ischemic (68%) or nonischemic cardiomyopathy (32%) with systolic left ventricular (LV) dysfunction and sinus rhythm (age 52+/-11.9 years; 42, 40 and 18% with NYHA class II, III and IV, respectively; mean LV ejection fraction 30.1+/-6.7%) At study entry 89 and 78% of patients received angiotensin converting enzyme inhibitors and b-adrenoblockers, respectively. Methods. Holter ECG monitoring with HRV temporal and spectral analysis. Results. During average follow-up of 2.4 years 60 patients (44.4%) died of cardiac causes (92.3% of all deaths). Other deaths were due to surgical pathology (n=1) and stroke (n=2). All standard HRV values with the exception of high frequency power were lowered, this lowering correlated with functional severity of heart failure. According to multifactorial analysis the following characteristics were independent predictors of all cause death: NYHA class III-IV (RR=1.9, 95% confidence interval 1.1-9.6, p=0.002), and SDNN value 90 ms (RR=1.5, 95% confidence interval 1.2-2.5, p=0.001). Conclusion. In CHF parameters of HRV are lowered compared to normal values and correlate with functional heart failure severity. NYHA class III-IV and lowered HRV (SDNN 90 ms) allow to identify patients with high risk of death.
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PMID:[Heart rate variability in chronic heart failure and its role in prognosis of the disease.]. 1731 Sep 56


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