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 myocardial infarction is associated with complex neuroendocrine changes, including release of arginine vasopressin, norepinephrine, and epinephrine, and activation of the renin-angiotensin system. Arginine vasopressin levels are maximal on admission, and subsequently fall even in patients in whom left ventricular failure develops. Plasma levels of norepinephrine and epinephrine are at their highest on admission and return to the normal range in patients with uncomplicated infarction, but they remain significantly elevated in patients in whom left ventricular failure or late ventricular arrhythmias develop. In contrast to catecholamines and arginine vasopressin, plasma renin and angiotensin levels are within normal limits on admission in patients without complications but increase by the third day. Patients with left ventricular failure already have increased plasma levels of renin and angiotensin on admission, but further marked and persistent increases occur over the following days. All of the aforementioned hormones may interact to cause systemic or coronary vasoconstriction, which may have short-term adverse hemodynamic consequences. Furthermore, increased afterload may result in infarct expansion and left ventricular dilatation, which will impair left ventricular function still further. Interruption of the cycle of vasoconstriction and worsening left ventricular failure by angiotensin converting enzyme inhibitors may reduce the incidence of heart failure after myocardial infarction.
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PMID:Neuroendocrine changes in acute myocardial infarction. 306

Despite recent advances, problems in the treatment of acute myocardial infarction still remain. In the earliest stages of the syndrome thrombolysis holds substantial if not absolute promise but many patients present too late for it to be effective. In these latter individuals and those in whom thrombolysis was not successful, the major mortality risk is concentrated in those with left ventricular failure. Many drugs, including diuretics, vasodilators, ACE inhibitors and positive inotropes, singly or in combination, may be used to manipulate the circulation and correct partially or completely the abnormal circulatory profile. Despite such haemodynamic efficacy the impact of drug therapy on the high morbidity and mortality risk of patients with acute myocardial infarction complicated by left ventricular failure is still unknown.
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PMID:Left ventricular failure complicating acute myocardial infarction--problems and potential of nonthrombolytic therapy. 306 18

Therapy combining vasodilators and inotropic agents is considered to be one of the most powerful means of improving cardiac function in patients with congestive heart failure (CHF). The vasodilators enhance the effectiveness of inotropic agents by providing a reduction in preload and/or afterload. Inotropic drugs with different mechanisms of action, such as digitalis glycosides, ephedrine, dopamine, dobutamine, ibopamine, terbutaline, salbutamol, pirbuterol, prenalterol, amrinone, and milrinone, have been tested in combination with vasodilators with a predominant effect on preload (nitrates, molsidomine), with a predominant effect on afterload (hydralazine, nifedipine), or with a balanced action on both arterial and venous beds (nitroprusside, prazosin, captopril), showing positive results. The problem of the combination of digitalis glycosides and vasodilators with different sites of action has been considered by our group. In 42 patients with CHF, digoxin (DIG, 0.01 mg/kg intravenously) was tested in combination with molsidomine (MLS, 4 mg sublingually) (12 patients), a nitrate-like agent with a predominant vasodilating action on the capacitance vessels, nifedipine (NFP, 10 mg sublingually) (22 patients), a Ca2+ antagonist drug with a predominant action on the resistance vessels, and captopril (CPT, 25 mg orally) (8 patients), an ACE inhibitor with a balanced effect on both preload and afterload. The combination DIG plus MLS caused a reduction in left ventricular filling pressure (LVFP) greater than that achieved with either agent alone. The hemodynamic improvement was obtained without side effects, in spite of the striking fall in preload. We stress that this investigation was performed on patients with CHF following acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Combination of positive inotropic and vasodilating substances in congestive heart failure. 315 99

The clinical course and biochemical, radioimmune and electrophysiologic findings were assessed in 421 patients with acute myocardial infarction involving heart rhythm and conductivity disorders and 49 patients with acute myocardial infarction, free of cardiac electrical instability. The studies were carried out during arrhythmias and after they were controlled, prior to treatment, at the peak of antiarrhythmic effect of medication, and after a continuous treatment course. Heart rhythm disorders related to acute myocardial infarction were accompanied with a marked response on the part of blood free fatty acids, sympatho-adrenal and kallikrein-kinin activity and carboxycathepsin. Metabolic and neurohumoral changes were eventually reversed and tended to normalize as soon as the sinus rhythm was restored by treatment.
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PMID:[Pathogenetic mechanisms of the development of cardiac rhythm disorders in the acute period of myocardial infarction]. 337 48

Abnormal serum angiotensin converting enzyme (ACE) activity has been reported in various human lung disorders and in laboratory animals with acute lung injuries. To test the value of serum ACE activity as an indicator of lung damage and its assistance in diagnosis or prognosis, 328 serum samples were obtained from 108 hospitalized patients with lung disease and 26 normal subjects. When patients were clinically grouped by disease entity, only the sarcoidosis group showed elevated mean serum ACE. Significantly increased serum ACE was found in 17 patients with various lung diseases (15% of hospitalized patients) 12 of whom also had concomitant liver disease. It is hypothesized that the liver may play a role in the normal metabolism of ACE being released by lung endothelial injury. Significantly low levels were seen in many acute and chronic lung injuries; specifically the groups with chronic obstructive lung disease, lung cancer, acute pneumonia, aspiration pneumonitis, gram-negative sepsis, acute myocardial infarction, and congestive heart failure. Serial measures of ACE in 71 patients with lung injuries showed that significantly decreasing levels over successive days were associated with a very high mortality. A single ACE measurement did not predict the presence or extent of lung injury, or aid in diagnosis or prognosis, but serial levels are of value prognostically.
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PMID:The value of serial serum angiotensin converting enzyme determinations in hospitalized patients with lung disease. 609 28

Structural remodeling of the left ventricular (LV) myocardium develops in a time-dependent fashion following acute myocardial infarction and may be an integral component in the transition toward overt heart failure. Globally, the remodeling process is characterized by progressive LV enlargement and increased chamber sphericity. At the cellular level, the remodeling process is associated with myocyte slippage, hypertrophy, and accumulation of collagen in the interstitial compartment. In the present study, we examined the effects of early, long-term monotherapy with the angiotensin converting enzyme (ACE) inhibitor, enalapril, on the progression of LV remodeling in dogs with LV dysfunction (ejection fractions 30-40%) produced by multiple sequential intracoronary microembolizations. Dogs were randomized to 3 months oral therapy with enalapril (n = 7) or to no treatment (n = 7). In untreated dogs, LV end-systolic volume index (ESVI), end-diastolic volume index (EDVI) and chamber sphericity increased significantly during the 3 months follow-up period. In contrast, in dogs treated with enalapril ESVI, EDVI and chamber sphericity remained essentially unchanged. Treatment with enalapril attenuated myocyte hypertrophy and the accumulation of interstitial collagen in comparison to untreated dogs. These data indicate that early treatment with ACE inhibitors can prevent the progression of LV remodeling in dogs with LV dysfunction. Afterload reduction, inhibition of direct action of angiotensin-II and possibly the decrease in bradykinin degradation elicited by ACE inhibition may act in concert in preventing the progression LV chamber remodeling.
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PMID:Ventricular remodeling: insights from pharmacologic interventions with angiotensin-converting enzyme inhibitors. 749 55

Depressed baroreflex sensitivity (BRS) after acute myocardial infarction (AMI) is considered an indication of decreased vagal and/or increased sympathetic tone. To determine the effect of angiotensin converting enzyme inhibitors (ACEI) on BRS after AMI we studied 27 patients with a first Q wave AMI, no signs of heart failure and no history of arterial hypertension or diabetes mellitus. An additional group of 10 patients with the same clinical characteristics served as controls. On the 5th day after the onset of AMI, three consecutive boluses of phenylephrine were given intravenously and baseline BRS was taken as the mean slope of the linear regression lines of RR intervals over systolic blood pressure. QT interval was also measured and corrected according to Bazett's formula (QTc). Consequently, a single oral dose of captopril 50 mg or placebo was given to treatment or control group patients, respectively; BRS and QTc were reassessed 1 h later. One hour after captopril administration BRS increased from 5.95 +/- 2.80 to 9.14 +/- 3.46 ms.mmHg-1 (P < 0.0001); QTc increased from 414 +/- 46 to 425 +/- 46 ms (P < 0.0001), systolic blood pressure decreased from 125 +/- 19 to 115 +/- 15 mmHg (P = 0.0002), while heart rate did not change significantly. Baseline BRS was correlated only with age (r = -0.74, P < 0.0001). In the control group, 1 h after placebo, no difference was observed in any variable compared to baseline. Captopril appears to improve BRS immediately in the early phase of AMI.
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PMID:Acute effect of captopril administration on baroreflex sensitivity in patients with acute myocardial infarction. 749 6

The myocardial scar, left behind by an infarct, makes up a potential substrate for complex ventricular arrhythmias due to the presence in such tissue of electrical inhomogeneity, altered refractoriness, and abnormal conduction properties, which facilitate the induction of reentrant arrhythmias and the release of abnormal automatic responses of the partially repolarised cells. The mechanism(s) by which complex ventricular arrhythmias is/are transformed into malignant arrhythmias has/have not yet been definitely proven. The observation that coronary revascularization - in patients with ischaemic heart disease surviving out of hospital cardiac arrest - improves the prognosis, indicates that transient ischaemic attacks might be the trigger of malignant ventricular arrhythmias in patients with prior myocardial infarction. Patients with large infarct scars (heart failure) have an increased incidence of complex ventricular arrhythmias, death, and ischaemic events. Antiarrhythmic medical intervention does not improve the prognosis in these patients. Intervention with ACE-inhibitors reduces the prevalence of complex ventricular arrhythmias, the incidence of death, and reinfarction, but not arrhythmic death, indicating that residual ischaemia might be the major risk variable in patients with heart failure. Ischaemia is one of several risk markers for transient supraventricular arrhythmias in patients recovering from an acute myocardial infarction (AMI). In addition, anti-ischaemic intervention in patients recovering from AMI suppresses residual myocardial ischaemia and thereby reduces major events.
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PMID:[Post-infarction, myocardial ischemia: clinical importance and risk factor]. 750 21

Acute myocardial infarction continues to be the number 1 killer in industrialised countries. While the more widespread use of thrombolytic therapy has made a dramatic impact on patient survival, changes in long-term prognosis after discharge from hospital have not improved radically and 5-year mortality remains at over 30%. The single most important determinant of survival in the long term is left ventricular function. The process of ventricular dilatation and remodelling begins early after infarction. While such changes may initially go unrecognised clinically, without intervention progressive functional impairment will ensue and the majority of patients will develop signs and symptoms of heart failure, which carries a worse prognosis than many forms of cancer. ACE inhibitors act on both the haemodynamic and neurohormonal mechanisms in heart failure. Several large-scale clinical trials have clearly demonstrated that early use of these agents in stable patients who are not hypotensive or in cardiogenic shock can reduce significantly the development of heart failure and death. A strategy for the early initiation of ACE inhibitor therapy is proposed to improve survival in AMI patients.
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PMID:Improving outcome after acute myocardial infarction: what is the role of ACE inhibitors? 754 52

In this review, we evaluate the efficacy of ACE-inhibitors for the treatment of acute myocardial infarction (AMI). Our information is based on published material and personal experience derived from extensive revision of the SMILE study. All trials with a randomized experimental design, irrespective of their primary research objective, have been included. Results are presented in terms of either hemodynamic or clinical benefit. The available evidence indicates that the mortality rate of AMI patients who undergo short- and long-term treatment with ACE-inhibitors is significantly reduced. This reduction is more evident in high risk patients, such as subjects with asymptomatic left ventricular dysfunction, congestive heart failure on admission, anterior location of the infarction. ACE-inhibitors also limit the development and progression of congestive heart failure after myocardial infarction, the onset of clinical manifestations of coronary artery disease (reinfarction, need for revascularization) and the occurrence of ventricular arrhythmias, probably by means of mechanisms involving a specific effect of these compounds. In conclusion, the available data indicate that administration of ACE-inhibitors to patients with AMI is associated with significant clinical benefit.
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PMID:[ACE inhibitors in the treatment of patients with acute myocardial infarct]. 757 15


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