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)

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

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

The diagnosis of acute myocarditis in children is based on histological criteria. Often viral in origin, it results in acute left ventricular dysfunction, the clinical manifestations of which are very variable. The potential severity of the disease is maximal in its initial phase, justifying rapid and intensive treatment. Long-term outcome is relatively good although there is a risk of chronic left ventricular dysfunction. This retrospective study is based on 11 cases of acute myocarditis admitted to the paediatric unit of Clermont-Ferrand University Hospital between February 1989 and March 1999. The initial symptoms were non-specific. Echocardiography was the key diagnostic procedure. Half of the patients had severe cardiac failure requiring admission to the intensive care unit. Four cases presented with a severe complication: two embolic events, one syncopal atrioventricular block and one cardiac arrest. The cardiac treatment was classical (digitalis, diuretics, angiotensin converting enzyme inhibitors, anticoagulants). The aetiology was established in 3 cases (toxoplasmosis, haemolytic and uraemic syndrome, Kawasaki) and a viral cause was suspected in 6 other cases (adenovirus in 3 cases, herpes virus, RSV and enterovirus in 1 case). There were no deaths in the acute phase. The long-term outcome was globally good: complete regression in 8 cases, 1 chronic left ventricular dysfunction and 2 late deaths due to intractable cardiac failure. This short series illustrates the often misleading presentation of acute myocarditis in childhood, the value of systematic investigation in the hope of a specific treatment becoming available in the near future for the often viral aetiology.
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PMID:[Acute myocarditis in children. Study of 11 clinical cases]. 1085 55

Viral infection of the heart is relatively common and usually of little consequence. It can, however, lead to substantial cardiac damage and severe acute heart failure. It can also evolve into the progressive syndrome of chronic heart failure. Recent studies have gone some way towards unravelling the complex mechanisms underlying the heart muscle damage that occurs after viral infection. These studies have lent support to both immune and viral mediated (independent of an immune response) cardiac damage. Acute myocarditis can present in various ways, and it may be a cause of sudden death in an otherwise healthy young adult. New treatments for viral heart disease are awaited. In the meanwhile, the haemodynamic support of patients with acute left ventricular failure caused by myocarditis should be aggressive, to allow for the possibility of spontaneous recovery. Contemporary trials of treatment in chronic heart failure secondary to dilated cardiomyopathy support the use of angiotensin converting enzyme inhibitors, beta adrenoceptor blockers, and spironolactone in such patients.
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PMID:Viral myocarditis and dilated cardiomyopathy: mechanisms, manifestations, and management. 1112 85

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 angiotensin converting enzyme inhibitor captopril prevents myosin-induced experimental autoimmune myocarditis. Captopril inhibits production of angiotensin II and increases bradykinin signaling, among other actions. To test whether captopril inhibits disease through blockade of angiotensin signaling, we tested the ability of losartan, an angiotensin II receptor blocker, to prevent myosin-induced myocarditis. A/J mice immunized with the heavy chain of cardiac myosin in complete Freund's adjuvant develop acute myocarditis by day 21 post-immunization, consisting of severe focal inflammation, necrosis and fibrosis. Administration of losartan (250 mg/L in the drinking water) or captopril (75 mg/L in the drinking water) significantly reduced inflammation, necrosis and fibrosis in myosin-immunized mice. The heart weights and the heart weight-to-body weight ratios were also significantly reduced in both treatment groups. However, whereas captopril reduced myosin-specific delayed-type hypersensitivity, losartan did not. Both captopril-treated mice and losartan-treated mice showed a decrease in myosin-specific autoantibody production. Because losartan treatment significantly reduced myocarditis, fibrosis and autoantibody production in EAM, it is likely that prevention of angiotensin II receptor stimulation is a major mechanism underlying the inhibition of myosin-induced myocarditis by captopril.
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PMID:Comparison of angiotensin converting enzyme inhibition and angiotensin II receptor blockade for the prevention of experimental autoimmune myocarditis. 1758 93

The leading cause of acute myocardial infarction (AMI) in patients with coronary heart disease is plaque rupture. Between 6% and 12% of AMI patients have angiographically normal coronary arteries. However, new procedures have demonstrated the limits of coronarography and challenged the existence of this situation. Angiograms may fail to detect minimal lesions whereas, in many cases, intravascular sonography reveals small atherosclerotic plaques. With the development of intravascular sonography and multislice computed tomography, the prevalence of myocardial infarction with normal coronary arteries has fallen to about 1%. Myocardial infarction with normal coronary arteries may be due to coronary vasospasm, hypercoagulable states, intense sympathetic stimulation, non atherosclerotic coronary disease, alcohol or cocaine abuse, and systemic diseases. In a series of 1205 AMI patients, we found no significant coronary disease in 45 patients, but intravascular sonography showed minimal intracoronary plaque in 21 of these cases. The 24 patients without significant lesions were young, had no risk factors for AMI without a prodrome, low peak creatine release, a small reduction in the left ventricular ejection fraction after thrombolysis or angioplasty, and good outcome at 26 months. The mechanisms of AMI in these 24 patients were coronary spasm, myocardial bridge, a prothrombotic state, contraceptive pill usage, and drug or alcohol abuse. The diferential diagnoses of these cases of AMI are acute myocarditis and stress cardiomyopathy, and apical left ventricular ballooning. Initial management is the same as for "conventional" AMI, including pain relief nitrates, antiplatelet agents, heparin, thrombolysis or angioplasty in the acute phase, and ACE inhibitors. Patients with spasm should receive calcium antagonists rather than beta-blockers. The prognosis of these patients is better than that of patients with atherosclerotic lesions. They nonetheless need close follow-up and strict secondary prevention measures, including smoking cessation and prevention of dyslipidemia and diabetes.
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PMID:[Myocardial infarction with "angiographycally normal coronary arteries" myth or reality?]. 1822 36