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)

The purpose of this retrospective study was to consider impaired renal function in patients with severe congestive heart failure after converting enzyme inhibition and to emphasize the characteristics of this population. The study concerned 26 patients (pts), 72.5 +/- 8.1 years old, with a severe congestive heart failure (NYHA Class IV). Before treatment serum creatinine was slightly increased and the introduction of angiotensin converting enzyme inhibitor (ACEI) - Captopril 58.9 +/- 17.3 mg/j or enalapril 9.2 +/- 4.4 mg - impaired renal function from 132.0 +/- 50.7 mumol/l to 183.5 +/- 139.3 mumol/l (n = 26; p less than 0.05). Patients were separated in 3 groups: in group I; 15 pts, serum creatinine remained unchanged under ACEI in despite of the significant decrease of blood pressure (BP); from 140.7 +/- 24.0/82.5 +/- 13.4 to 120.3 +/- 12.8/71.8 +/- 8.7 mmHg (p less than 0.01). The cause of heart failure was an ischemic heart disease (IHD) in 15 patients (chi 2 test, p less than 0.05), a dilated cardiomyopathy in 4 pts and an aortic or mitral valvular regurgitation in 2 pts. In contrast renal function was significantly impaired in group II; serum creatinine increased from 120.8 +/- 25.2 to 189.0 +/- 80.7 mumol/l under ACEI. BP remained unchanged 136.9 +/- 29.0/78.1 +/- 4.9 and 118.7 +/- 13.6/75.6 +/- 7.6 mmHg respectively before and after treatment. There was 4 pts with dilated cardiomyopathy, 4 pts with mitral or aortic valvular regurgitation and only one with IHD. The introduction of an ACEI in two pts--group III--with severe tricuspid regurgitation induced an acute and reversal renal failure (serum creatinine at 600 mumol/l).
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PMID:[Renal insufficiency and treatment of persistent cardiac insufficiency with converting enzyme inhibitor]. 273 17

Vasodilator therapy of heart failure has through the last 5-10 years become a well established treatment. Traditionally these drugs have been classified after their primary site of action on the vascular beds. Thus drugs primarily acting on the arteriolar bed are called afterload-reducing agents and are exemplified by hydralazine. Drugs primarily acting on the venous bed have been called preload-reducing reducing agents and the typical example is nitroglycerin. Other drugs, like prazosin, act on both the arteriolar and venous vascular beds. The classification is, however, not as sharp as originally believed since preload- and afterload-reducing activities mix with each other. Treatment with vasodilators for chronic heart failure has mainly been advocated in patients with valvular regurgitation, ischemic heart disease and various types of dilated cardiomyopathies. It seems appropriate today to put some questions concerning vasodilator therapy for heart failure. Among such questions are: When in the natural history of congestive heart failure should vasodilator therapy be commenced? How effective is long-term administration of vasodilating drugs? May vasodilator therapy decrease mortality in congestive heart failure? What about the efficacy of new vasodilating drugs compared to more traditional ones? In the review of vasodilating drugs besides ACE inhibitors, these questions will be addressed.
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PMID:Aspects on "traditional" vasodilators in the treatment of chronic heart failure. 352 22

A 57-year-old man with a cough and increasing exertional dyspnoea for the past 6 weeks was found on examination to have a loud systolic murmur and cardiomegaly with pulmonary congestion. Echocardiography revealed congenitally corrected transposition of the great arteries (cTGA: atrioventricular and ventriculoarterial discordance): a morphologically right ventricle with a tricuspid valve on the left, a morphologically left ventricle with bicuspid a-v valve on the right, the aorta arising ventrally from the left-sided (morphologically right) ventricle. The tricuspid valve showed an Ebstein-like anomaly with obvious regurgitation. Transoesophageal and contrast echocardiography defined valvar anatomy, attachment of the great arteries and cardiac chambers to the venous and arterial circulations, as well as absence of a left to right shunt. Angiography revealed a coronary anatomy typical for cTGA. The exertional dyspnoea responded to diuretics and low doses of ACE inhibitor. Follow-up monitoring of the valvar regurgitation and appropriate endocarditis prophylaxis were recommended. As the haemodynamics in cTGA is normal, in the absence of additional anomalies, it is a congenital cardiac defect which can, though rarely, present first in adulthood. Life expectancy depends on the nature of any additional defects and the degree of commonly associated tricuspid valve regurgitation. As this case demonstrates, echocardiography can largely define the anomalies.
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PMID:[Congenitally corrected transposition of the great vessels in adulthood. The value of noninvasive study methods]. 807 3

Clinical findings in fifteen dogs with tricuspid valve dysplasia are described. Thirteen dogs had loud systolic heart murmurs. Eleven of them hat a palpable precordial thrill over the same location. In 14 dogs, right heart enlargement was suspected on thoracic radiographs and electrocardiography. Right atrial dilation was seen echocardiographically in all dogs. Fourteen dogs had additional right ventricular dilatation, some with hypertrophy as well. Doppler echocardiography revealed tricuspid valve regurgitation. Seven dogs remained free of clinical symptoms to date. If symptoms of decompensation develop with tricuspid dysplasia, diuretics, ACE inhibitors and eventually positive inotrope drugs are indicated. Antiarrhythmic drugs may become necessary in cases of supraventricular tachyarrhythmias.
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PMID:[Tricuspid valve dysplasia in fifteen dogs]. 1085 Jan 63

This review has been focused on the new insights in the pathophysiology of mitral and aortic regurgitation and on the role of ACE-inhibitor therapy in children with chronic volume overload due to left-sided valvular lesions. Recent clinical studies show that these drugs have favorable effects when administered orally in chronic mitral and aortic regurgitation. Interestingly, the beneficial effects of ACE-inhibition regard the basic anatomic, hemodynamic and adaptive pathologic conditions related to volume overload, namely, the regurgitant orifice area and volume and ventricular remodeling. The heart is a plastic structure, constantly being altered in size, shape and composition in response to chronic volume overload. Thus, modulation of cardiac plasticity by ACE-inhibition raises the possibility of using new therapeutic strategies specifically designed to prevent and/or antagonize the mechanical disadvantages secondary to volume overload-induced cardiac remodeling. The beneficial effects of ACE-inhibition have also been observed in growing children with asymptomatic valvular regurgitation; thus, it appears that the unloading therapy has the potential of influencing the natural history of both mitral and aortic regurgitation and possibly delays surgical valve repair or replacement. These data justify early inhibition of the renin-angiotensin system in children with left ventricular volume overload due to mitral and aortic regurgitation.
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PMID:New insights in the pathophysiology of mitral and aortic regurgitation in pediatric age: role of angiotensin-converting enzyme inhibitor therapy. 1125 36

Optimal management of pregnancies for patients with acquired heart disease requires exact knowledge of the hemodynamic influence of pregnancy-related cardiovascular adaptation processes on the heart disease. Maternal and fetal risks must be carefully considered and mutually weighed. Critical time periods, during which closely networked, interdisciplinary support for the patient is essential, are primarily during the 30th to 32nd week of pregnancy. This is the period in which maximum increases in heart rate, cardiac output, and plasma volume are observed. The peripartal phase represents another critical period. Owing to the mechanically related fixation of cardiac output, stenotic valvular diseases are generally tolerated much poorer than are valvular insufficiency defects. Therapeutic objectives are reduction in heart rate and--in cases of pulmonary-venous congestion--decrease in preload. Vaginal deliveries are possible with slight to moderate valvular stenosis; cesarean section is to be preferred in more severe cases. In patients with valvular insufficiency and normal left ventricular function pregnancy is usually well tolerated. Reduction in regurgitation is even often observed owing to pregnancy-induced decrease in peripheral vascular resistance. Since ACE inhibitors and AT1 antagonists are contraindicated during pregnancy, afterload reduction can be achieved by a combination of hydralazin and nitrates, or calcium antagonists. Peripartal cardiomyopathy is rare and is associated with a high degree of maternal mortality (25-50%). Apart from the necessary consideration of pregnancy-related contraindications, therapeutic principles do not differ from those for other forms of heart failure. Most patients exhibiting hypertrophic obstructive cardiomyopathy satisfactorily pass through their pregnancies. Individual cases have been described, however, of both pregnancy-related cardiac decompensation as well as sudden death. Aortal and coronary-arterial dissections represent rare, life-endangering complications for mother and fetus: these developments can occur among predisposed patients as a result of the hormonal and hemodynamic adaptation processes during pregnancy. Close interdisciplinary collaboration and tightly networked support for patients are the prerequisite for successful management of high-risk pregnancies involving maternal heart disease.
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PMID:[Pregnancy risks in acquired heart diseases]. 1137 39

Mitral regurgitation is a common valvular abnormality that can result in substantial morbidity. Primary care physicians should maintain a high index of suspicion for this disorder, especially in patients with symptoms of heart failure. The paramount concern is early identification of patients with mitral regurgitation and prompt referral to a cardiologist when symptoms occur or if evidence of ventricular enlargement or reduction in ejection fraction is found. Echocardiography is an invaluable tool in determining the severity of regurgitation, the integrity of the mitral valve apparatus, the extent of left ventricular enlargement, and the ejection fraction. Although no standard medical treatment has been established for mitral regurgitation, use of ACE inhibitors is appropriate. Patients presenting with severe, acute mitral regurgitation from papillary muscle rupture should be evaluated for ischemia and treated expediently. The preferred operative procedure in patients with severe mitral regurgitation and left ventricular dysfunction is mitral valve repair, if possible, or mitral valve replacement with posterior chordal preservation, if feasible.
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PMID:Native mitral valve regurgitation. Proactive management can improve outlook. 1178 16

8 patients suffering transposition of the great arteries (d-TGA) aged from 8-17 years (mean 12.6 years) after Senning procedure performed were analyzed. Right atrium and right ventricle enlargement was detected in all patients. Small jet tricuspid valve regurgitation was confirmed in 5 patients, significant tricuspid valve insufficiency in 3 patients. 4 patients had presented with tricuspid valve, aorta valve and mitral valve insufficiency. In one patient insignificant pulmonary artery stenosis had been diagnosed. Chronic cardiac failure (NYHA III/IV) has been diagnosed in 2 patients, other patients from the analyzed group are in good clinical condition. All patients but 2 were diagnosed with arrhythmia using 24-hour Holter ECG. In 2 patients sinus node dysfunction was noted. Also supraventricular extrasystole, ventricular extrasystole, supraventricular tachycardia, ventricular salve, paroxysmal atrial fibrillation were described. No drug therapy in 4 patients is needed, one is treated with ACE-inhibitors, one with diuretic drugs. 2 patients suffering cardiac failure had been treated with 4 drugs, also temporary with intravenous dopamine. One death had been noted, caused by serious arrhythmia. One patient had been qualified for heart transplantation, there is no further data regarding this case. Senning procedure can be considered high risk for various problems, so patients who underwent this type of correction should be carefully observed.
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PMID:[Long-term results of valvular condition and clinical state in patients operated with the Senning method]. 1572 58

A subset of patients with mitral valve disease has a marked rise in pulmonary vascular resistance (PVR) that is disproportionate to elevations in pulmonary venous pressure. Termed a "hyperactive" pulmonary vasculature, the elevation in PVR falls promptly and dramatically in response to mitral valve replacement. We report a 55-year-old man with progressive, exertional dyspnea of several months' duration who had signs of congestive heart failure (CHF) with moderate mitral valvular regurgitation and aortic stenosis by echocardiographic interrogation. These lesions in combination, together with his CHF and disproportionate elevation in pulmonary artery systolic pressure (90 mm Hg) and PVR (527 dyne x s x cm(-5)), raised the prospect of valvular replacement. There followed a normalization of PVR and marked improvement in his symptoms and signs of CHF in response to pharmacologic management with an ACE inhibitor, loop diuretic, and aldosterone receptor antagonist to negate any further consideration of surgery.
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PMID:A hyperactive pulmonary vasculature in response to chronic mitral regurgitation. 1757 Sep 95

Severe mitral regurgitation (MR) confers a poor prognosis, in particular for patients with heart failure. Based on the results of the Euro Heart Survey, a large proportion of patients with mitral regurgitation is not referred to surgery and many other patients are rejected for cardiac surgery due to the high surgical risk or co-pathologies. Improving ventricular function with ACE inhibitors, beta-blockers and CRT may reduce mitral regurgitation, but for most patients a mechanical intervention is ultimately preferable. Mitral valve surgery is invasive and requires a long recovery period; therefore, less invasive and effective approaches are highly desirable, particularly in high risk patients. Therefore, new techniques have been recently developed to treat MR with percutaneous approach. The MitraClip device (Abbott Vascular, Menlo Park, CA) is used to treat both functional and degenerative mitral valve regurgitation. Its safety and efficacy has been initially tested in the Endovascular Valve Edge-to-Edge REpair Study (EVEREST), while MitraClip has been compared to surgery in the EVEREST II randomized trial. Besides EVEREST trials, safety and efficacy of the device as well as its health economic value is under evaluation in ongoing registries. Although the field of catheter based management of MR is at an early stage, initial clinical results have demonstrated that catheter based approaches can reduce MR, suggesting there is a great deal of potential for clinical benefit to patients with MR.
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PMID:Clinical trial experience with the MitraClip catheter based mitral valve repair system. 2150 2


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