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)

In addition to the underlying pathophysiological processes that cause myocarditis and dilated cardiomyopathy, structural, biochemical, neurohormonal and haemodynamic influences and interrelations promote progression of the heart failure syndrome. Independent of their symptomatic benefits, diuretics, digitalis, ACE inhibitors, PDE inhibitors and dopamine agonists exert specific influences on factors that retard or accelerate progression of congestive heart failure (CHF). Important factors that indicate or promote progression of CHF are discussed here, with special emphasis on therapeutic options. Interference with baroreceptor function (digitalis, ACE inhibitors), the RAA system (ACE inhibitors), the sympathetic nerve system (dopamine agonists, ACE inhibitors, digitalis) can potentially retard progression of CHF, while other therapeutic options, such as PDE inhibitors and diuretics, might accelerate progression of left ventricular dysfunction and CHF.
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PMID:Therapeutic alternatives in dilated cardiomyopathy--a review of current options. 168 Jun 88

Infectious heart diseases in childhood are--with less than 1% of hospital admissions--rare, but serious diseases. Among several causes of myocarditis in our region virus myocarditis plays the most important role. Besides of the acute course an autoimmune mediated chronic myocarditis and the transition to dilated cardiomyopathy are observed. The patho-histological assessment depends also on subjective influences. Clinical diagnosis is based on cardiac symptoms (Adams-Stokes, congestive heart failure, LV-dilatation), ECG-changes with increased enzyme levels and positive virus-serology or endomyocardial biopsy. Immunoserology and -histology as well as in-situ-hybridization can support diagnosis, echocardiography and eventually heart catheterization exclude other causes. In respect to therapy, ACE-inhibitors are a substantial improvement of conventional therapy of heart failure, while immunosuppressive therapy of chronic myocarditis has to assessed.
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PMID:[Myocarditis in childhood]. 202 60

To date, there is no universally accepted therapy for viral myocarditis. We investigated the effect of the angiotensin converting enzyme inhibitor captopril on both early and late phases of coxsackievirus murine myocarditis. Mice were infected with coxsackievirus B3 and were divided into two main protocols. Mice in the early treatment protocol (n = 30) were treated on day 1 after infection with either captopril or saline through day 6 of infection and euthanized on day 6 of infection. In the late treatment protocol, mice (n = 60) were treated starting on day 10 of infection through day 30 of infection with either captopril or saline. Mice were killed on days 20 and 30 of infection. In the early treatment protocol, heart weight was 67 +/- 14 mg in the captopril-treated group versus 98 +/- 17 mg in the control group (p less than 0.0001). The degree of inflammation, necrosis, and dystrophic calcification assessed with a semiquantitative histological score was significantly less in the captopril-treated group. The degree of pathological involvement determined by planimetry of histological sections was 8.1 +/- 7.2% for the captopril-treated group versus 22.5 +/- 10.0% for the saline-treated group (p less than 0.0001). In the late treatment protocol, captopril also caused a reduction in heart weight as compared with controls at day 20 (116 +/- 21 mg in captopril-treated group vs. 166 +/- 34 mg in controls, p less than 0.0001) and also at day 30 (136 +/- 23 mg in captopril-treated group vs. 185 +/- 48 mg in controls, p less than 0.004). On days 20 and 30 of infection, the degree of inflammation, necrosis, and dystrophic calcification was similar in both groups. We conclude that captopril is beneficial in acute coxsackievirus B3 murine myocarditis because it reduces heart weight and necrosis when administered early and reduces heart weight when administered in a delayed manner.
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PMID:Beneficial effects of captopril in acute coxsackievirus B3 murine myocarditis. 217 9

Recent evidence suggests that the most common form of idiopathic cardiomyopathy in our altitudes, the dilated cardiomyopathy (DCM), is a post-infectious autoimmune disease which is triggered by virus infections. In animal experiments, the development of the coxsackie virus B3 myocarditis to a congestive cardiac insufficiency resembling the clinical picture of DCM was demonstrated. In mice, species-dependent varying disease courses could be observed, which point to a genetically different behaviour of the animals' immunological reactions, either humoral or T-cell mediated immune reactions being responsible. In comparison with non-DCM patients, patients with DCM and chronic myocarditis exhibit significantly higher coxsackie virus antibody titres. Obviously, also a differently long viral persistency in the cardiac muscle plays a role, as enterovirus-specific RNA was detected in myocardial biopsies from patients with DCM. Along with myocardial fibroses, endomyocardial biopsies in DCM frequently reveal mononuclear cellular infiltrates, which, however, only in 20-25% of the cases may be regarded as chronic persisting myocarditis. The clinical and paraclinical findings in DCM and in the so-called latent cardiomyopathy are presented. In congestive heart failure, the best therapeutic results are achieved by the ACE inhibitors, along with vasodilator agents, digitalis glycosides and diuretics. Ultima ratio is the orthotopic heart transplantation, as it is only this intervention that will be able to improve the primarily bad prognosis decisively. Whether the treatment with immunosuppressive drugs exerts an influence upon the prognosis, has thus far remained an open question.
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PMID:[Dilated cardiomyopathy--heart muscle disease of unknown origin or an autoimmune disease? New aspects of etiology, pathogenesis and clinical practice]. 268 30

A 42-year-old woman was transferred to our hospital for evaluation of bradycardia with a complete atrioventricular block. Her pulse was 41 regular beats/min with blood pressure 166/92 mmHg. There were no skin lesions, edema, or lymphadenopathy. The white blood cell count was 6300/mm3. The serum glutamic oxaloacetic transaminase was 21 IU and creatine phosphokinase was 34 IU. C-reactive protein was negative. The level of serum angiotensin converting enzyme was slightly increased at 25.8 IU/l/37.0 degrees C (normal range: 7-24.0). Chest radiography showed congestive heart failure with a cardiothoracic ratio of 54%. There was no bilateral lymphadenopathy or fibrous changes during her clinical course. The coronary arteries were completely normal angiographically. Left ventriculograms revealed slight hypokinesis and dilatation (end-diastolic volume index of 112 ml/m2, ejection fraction of 53%). Left ventricular end-diastolic pressure was slightly abnormal at 16 mmHg. Two right and two left ventricular endomyocardial biopsies were performed. Right ventricular biopsy demonstrated edematous tissue and a slight mononuclear cell infiltration with little fibrosis. Left ventricular specimens showed an extensive area of fibrosis, with large, multinucleated giant cells with an asteroid body and chronic inflammation without epithelioid cells. The less affected areas of another specimen showed mild interstitial fibrosis and degenerative myocytes with vacuolation, and some multinucleated myocytes without an asteroid body were present. This case was diagnosed as cardiac sarcoidosis rather than idiopathic giant cell myocarditis. The patient has been implanted with a permanent pacemaker.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocarditis with multinucleated giant cells detected in biopsy specimens. 338 73

Acute infectious myocarditis in childhood has a very poor initial outcome, but the long-term outlook is relatively good for the survivors. This retrospective study was based on cases of acute myocarditis admitted to two hospital departments with different modes of recruitment. Firstly, a polyvalent paediatric intensive care unit where 12 children (mean age 12 months) were admitted during the acute phase of myocarditis. The initial symptoms were non-specific and misleading, the diagnosis being established at autopsy in 9 cases. Only 4 children presented with typical cardiac failure. The clinical signs were hepatomegaly, sinus tachycardia, cardiomegaly, ECG ST-T wave changes and biological signs of multiple organ failure. Left ventricular function was very poor with a fractional shortening of only 17%. The causal agent was usually viral. The clinical course was marked by a high early mortality (11/26, 42%) within 23 hours of hospital admission. Secondly, a paediatric cardiology unit where 81 children (mean age 15 months) were followed up after acute infectious myocarditis. Thirteen cases were taken from our first series and were included for long-term follow-up; 76.5% had premonitory signs of infection and 71% were in cardiac failure, Classes III or IV, during the hospital admission. The causal agent was identified in 30 cases (37%) and was usually a virus (22 cases). Treatment was classical (association of digitalis, diuretics, angiotensin converting enzyme inhibitors, anticoagulants and beta-sympathomimetics when necessary).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute infectious myocarditis in children. Apropos of 2 series from Lyon]. 764 88

Hypertension is the commonest cardiovascular disease in Africans occurring in more than 15% of the adult population in some studies. It occurs in the lower as much as in the higher socio-economic groups. Recent studies have confirmed earlier findings that essential hypertension in Africans is characterised by volume loading, low plasma renin activity, high salt taste threshold, high urinary sodium and low potassium excretion and high plasma aldosterone. The commonest complication of hypertension in Africans is congestive cardiac failure followed by cerebrovascular accidents. Coronary heart disease is rare. Even in the absence of overt heart failure and compounding factors like obesity, alcoholism, cigarette smoking, diabetes mellitus and myocarditis, evidence of abnormal left ventricular morphology and function is often present in newly diagnosed patients with moderate or severe hypertension. Response to monotherapy with beta-blockers or ACE inhibitors is usually poor but is good with thiazide diuretics or calcium channel blockers. The diuretics are an essential component of a two or three drug regime containing other classes of antihypertensive drugs. Cost of drugs is the most important determinant of compliance with drug treatment and consequently the likelihood of progression of the diseases to more severe forms in long term follow-up.
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PMID:Hypertension in Africa and effectiveness of its management with various classes of antihypertensive drugs and in different socio-economic and cultural environments. 826 3

The concept of "cardioprotection" with ACE inhibitors has evolved over the last decade. In the 1980s, protective benefits of ACE inhibitors in hypertension were established, regression of left ventricular hypertrophy was demonstrated, and improved ventricular function and survival in mild-to-moderate and severe congestive heart failure was documented. A further "protective" role of ACE inhibitors in coronary artery disease is emerging as more attention is focused on the concept of local tissue renin-angiotensin systems. Recent contributions to the literature describe significant benefits of ACE-inhibitor therapy in acute myocardial infarction, including suppression of ventricular arrhythmias and reduction of both early and late ventricular dilation, preservation of left ventricular function, and improved survival. All of the above effects can be considered "cardioprotective." However, as new benefits are reported in the 1990s, a broadened view of "cardiovascular protection" emerges from investigative studies in the literature. ACE inhibitors may reduce tolerance to nitrates, reduce angina in some but not all studies, and limit smooth muscle cell proliferation (and perhaps restenosis) induced by experimental balloon angioplasty. Local vascular effects may attenuate atherosclerotic changes in the arterial wall in experimental animals and may decrease the incidence of aneurysm formation in hypertensive animals. The effectiveness of ACE inhibitors in acute myocarditis, suggested by reports that captopril may reduce lesions of murine myocarditis when administered early after infection with coxsackievirus B3, requires clinical confirmation. Despite these apparently diverse "cardiovascular protective" consequences of ACE inhibitor therapy, the mechanism(s) of action of these agents remain to be elucidated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardioprotection with angiotensin-converting enzyme inhibitors: redefined for the 1990s. 843 34

Among the various anticancer drugs, used alone or in combination during courses of chemotherapy, anthracyclines (leader: doxorubicin) are responsible for direct myocardial toxicity, which can exceptionally be acute, but more often chronic with a delayed onset. This cardiotoxicity is directly proportional to the cumulative dose administered and the recommended total dose for doxorubicin is 550 mg/m2. The risk factors able to potentiate cardiotoxicity must be analysed before starting chemotherapy and follow-up by ultrasonography and/or isotope ejection fraction must be repeated before each course. The treatment of anthracycline-induced heart failure consists of digitalis alkaloids combined with angiotensin converting enzyme inhibitors. The cardiac toxicity of 5FU is currently explained by the theory of coronary spasm, based on clinical findings such as chest pain associated with ischaemic electrical modifications. The incidence of this toxicity is low, but it can be fatal. Exceptional examples include the cardiotoxicity induced by high-dose cyclophosphamide responsible for acute haemorrhagic myocarditis, potentiation of the cardiotoxic effect of anthracyclines by dacarbazine and plicamycin, and serious ventricular and supraventricular arrhythmias induced by amsacrine. Among the various cytokines used in oncology, interferon is responsible for heart failure, reversible after stopping treatment, but also for ventricular arrhythmias, or even sudden death, the pathophysiology of which still remains unclear.
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PMID:[Chemotherapy and cardiotoxicity]. 866 96

Myocarditis is a poorly understood condition and its prevalence is largely underestimated. A significant proportion of cases may be subclinical and chronic, leading to dilated cardiomyopathy, which represents the first cause of heart transplantation worldwide. Although inflammation of the myocardium can be associated with various causes, particularly viruses, myocarditis is usually idiopathic. Present evidence suggests that some 'idiopathic' and chronic 'postviral' myocarditis cases may be autoimmune, whereas others with acute self-limited disease or with persisting pathogenic virus by molecular methods may represent viral myocarditis. The major obstacle in identifying a specific therapy in myocarditis lies in the difficulty of a thorough clinical characterisation of individual patients in relation to viral and autoimmune involvement. This also explains the inconclusive results of trials of immunosuppressive drugs in myocarditis/dilated cardiomyopathy. Diagnosis is based upon endomyocardial biopsy. Management of myocarditis requires avoidance of agents that exacerbate myocarditis or depress myocardial function, and conventional therapy for heart failure (diuretics, ACE inhibitors and, if indicated, digoxin) and arrhythmias. Although at present the use of immunosuppressive therapy cannot be recommended on a routine basis, the recent Myocarditis Treatment Trial, where an aetiologically heterogeneous patient population was treated without significant adverse effects, provides some rationale for applying the same immunosuppression protocol to selected patients, e.g. those with active biopsy-proven myocarditis, unresponsive to conventional therapy, prior to transplantation, and those with idiopathic giant cell myocarditis.
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PMID:Recognition and optimum management of myocarditis. 889 64


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