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At least 577 records · Page 32Linked to original sources
PubMed2003

Aspirin does not adversely affect survival in patients with stable congestive heart failure treated with Angiotensin-converting enzyme inhibitors.

BACKGROUND: Experimental studies and retrospective analyses of mortality trials with angiotensin-converting enzyme inhibitors (ACE-Is) have suggested that aspirin may reduce the beneficial effect of these drugs. The aim of this study was to assess a possible detrimental effect of aspirin on survival in stable patients with left ventricular systolic dysfunction who had congestive heart failure and had been treated with ACE-Is. METHODS AND RESULTS: We performed a retrospective analysis in 755 consecutive stable patients with left ventricular systolic dysfunction. A Cox regression model was used to select independent predictors of survival and to test for a possible interaction between aspirin and ACE-Is with an adjustment to differences in clinical characteristics in subgroups of patients. Of the 755 patients, 328 (43.4%) had proven ischemic cardiomyopathy, 693 patients (91.8%) were receiving ACE-Is, and 317 patients were receiving aspirin (mean [+/- SD] dose, 183 +/- 65 mg/d; 74% of the patients receiving < or = 200 mg/d). During a median follow-up period of 1,996 days, there were 273 cardiac-related deaths, 14 urgent transplantations, 71 nonurgent transplantations, and 46 noncardiac-related deaths, and 3 patients were lost to follow-up. The cardiovascular mortality rates were 11.5% and 19.0%, respectively, at 1 and 2 years. There were no interactions among aspirin, ACE-Is, and survival in the overall population (p = 0.21), or in subgroups of patients with ischemic cardiomyopathy (p = 0.41) or with nonischemic cardiomyopathy (p = 0.74). CONCLUSIONS: In this population of stable patients with left ventricular systolic dysfunction, our retrospective analysis did not demonstrate any interaction between the use of aspirin and survival in patients receiving ACE-Is.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

Semirigid or flexible mitral annuloplasty rings do not affect global or basal regional left ventricular systolic function.

BACKGROUND: Previous studies have revealed that rigid mitral annuloplasty rings may be associated with left ventricular (LV) systolic dysfunction, but whether ring type affects regional systolic function at the base of the LV, in the region near the mitral annulus, is unclear. We tested the hypothesis that rigid fixation of the mitral annulus results in significant regional systolic dysfunction at the base of the LV. METHODS AND RESULTS: Twenty-six adult male sheep underwent placement of 13 miniature tantalum markers into the LV epicardium and around the mitral annulus to allow calculation of LV volume and regional epicardial area. Group I (n = 7) sheep served as controls; animals randomized to groups II (n = 11) and III (n = 8) underwent mitral annuloplasty with either a semirigid or flexible ring, respectively. After a 7- to 10-day recovery period, animals were studied in a closed-chest, sedated, autonomically blocked state. Global LV systolic function (end-systolic elastance and preload recruitable stroke work) were not significantly different among the 3 groups (P = 1.0, ANOVA). Regional systolic function at the base of the LV (fractional area shrinkage [FAS] of 4 epicardial areas) at comparable LV preload and afterload was similar in the 4 basal areas (P = 0.223, MANOVA). With the use of load-insensitive indexes (slope and area intercept of the end-systolic pressure-regional area relationship and regional stroke work-end-diastolic area relationship), regional systolic function also was not different between groups at baseline or with inotropic stimulation in any basal region (P > 0.05, MANOVA). Furthermore, neither annuloplasty ring perturbed the regional pattern of basal LV systolic function. CONCLUSIONS: Postoperative LV systolic function, both globally and in the region of the base of the LV (near the mitral annulus), was not altered with either semirigid or flexible ring fixation of the mitral annulus.

Animals↗
PubMed2006

Cardiogenic shock in a young female with multiple sclerosis.

A 24-year-old patient with no previous cardiovascular illness or symptoms, was admitted in profound cardiogenic shock related to severe left ventricular systolic dysfunction, accompanied by multiple sclerosis (MS) exacerbation. Initially the patient required mechanical ventilation, inotropic support, and intra-aortic balloon counter-pulsation along with invasive haemodynamic monitoring. Within a few days of high dose corticosteroid therapy patients left ventricular systolic dysfunction returned almost completely to normal, and this was accompanied by dramatic clinical improvement. We review the current literature on the relation between MS and left ventricular systolic dysfunction and heart failure.

Adult↗
PubMed1995

[Hypertrophic cardiomyopathy: spontaneous course].

Hypertrophic cardiomyopathy is a relatively rare (prevalence approximately 0.2%), primary myocardial disorder with an autosomal pattern of inheritance, characterized by mostly asymmetric left ventricular hypertrophy with myocyte and myofibrillar disarray. To date, about 34 mutations of the beta-cardiac myosin heavy chain gene have been described and shown to have prognostic implications. The disease has an annual mortality rate of 3%, related to both sudden cardiac death and progressive systolic dysfunction. Not only diastolic but also progressive systolic dysfunction with cavity dilatation occurs in a minority of patients with severe hypertrophy during the long-term course. Sudden death often occurs in young, asymptomatic or mildly symptomatic patients. The degree of hypertrophy and the presence of a pressure gradient are of little prognostic significance. Nonsustained ventricular tachycardia is associated with a poor prognosis in the presence of a history of syncope.

Adolescent↗
PubMed2001

[Echocardiography in storage and neuromuscular disorders].

Storage disorders and neuromuscular disorders may lead to cardiac involvement which can be visualized by echocardiography. In storage disorders like hypothyroidism, haemochromatosis, amyloidosis, mucopolysaccharidosis and Fabry's disease, myocardial thickening and systolic dysfunction can be found. In amyloidosis, atrial enlargement and abnormal texture of the myocardium are additional findings. In advanced haemochromatosis all cardiac chambers may be dilated. In hypothyroidism and amyloidosis, a pericardial effusion can be present. In haemochromatosis and amyloidosis, a restrictive filling pattern may be detected using Doppler-sonography. Mucopolysaccharidosis and Gaucher's disease may lead to aortic and mitral stenosis. In neuromuscular disorders like glycogenosis, mitochondriopathy and myotonic dystrophy, myocardial thickening and systolic dysfunction are found, in spinal muscular atrophy myocardial thickening and in muscular dystrophy Becker/Duchenne systolic dysfunction. An abnormal myocardial texture may be present in glycogenosis, isolated left ventricular abnormal trabeculation (ILVAT) in mitochondriopathy, myotonic dystrophy and muscular dystrophy Becker/Duchenne. Using Doppler-sonography an impaired relaxation of the left ventricle may be detected in mitochondriopathy, myotonic dystrophy and spinal muscular atrophy. Most of these echocardiographic findings are unspecific and may be overlooked, especially if the storage or neuromuscular disorder is yet unknown. Establishing a correct diagnosis is important, since healing or functional improvement is possible in many of these disorders.

Amyloidosis↗
PubMed1988

Critical analysis of cineangiographic criteria for diagnosis of arrhythmogenic right ventricular dysplasia.

Biplane 30-degree RAO and 60-degree LAO RV selective cineangiography was performed in 21 patients with significant ventricular arrhythmias (ventricular tachycardia in 14, salvos in three, and complex PVCs in seven) and a high presumption of arrhythmogenic RV dysplasia (ARVD), and in a control group of 10 presumed normal individuals. Comparing the two series revealed the lack of specificity of some angiographic images usually reported as suggestive signs of ARVD, such as slow dye evacuation of RV during the levophase and deep fissuring in the anterior wall with a "pile of plates" image. Inversely, localized morphologic and contraction abnormalities in the RV free wall were more sensitive and specific signs for diagnosis of ARVD; these were localized akinetic or dyskinetic bulges sometimes giving a true image of aneurysm (90%), wide and deep fissuring of the apex or of the inferior wall (33%), and large areas of akinesia. By order of frequency, these abnormalities were found on the apex in 71%, on the inferior wall in 52%, on the anterior wall in 48%, in the subtricuspid area in 38%, and on the pulmonary infundibulum in 33%. These localized lesions can suffice for the diagnosis of RV dysplasia in the absence of associated pathologies, such as ischemic heart disease or congenital defects. Usually a global RV systolic dysfunction is associated in ARVD, as confirmed by greater RV volumes (134 +/- 26 vs 79 +/- 10 ml/m2 for RVEDV, p less than 0.001; 76 +/- 34 vs 32 +/- 6 ml/m2 for RVESV, p less than 0.001), and lower RV ejection fraction (58 +/- 18% vs 47 +/- 8%, p less than 0.001) in the ARVD group compared to controls. Nevertheless, normal RV volumes and ejection fraction can be observed in some localized forms with mono- or bisegmental lesions in which RV systolic dysfunction is absent or moderate, and extensive forms with multiple segmental lesions where RV systolic dysfunction is constant and often severe. Six out of 21 patients in the ARVD group exhibited obvious global or segmental LV dysfunction, indicating the possibility of biventricular forms, as previously reported in other publications.

Adult↗
PubMedDate not supplied

[Current approaches to intraoperative diagnosis and treatment of low cardiac output during cardiosurgical operations].

The paper deals with the development of a diagnostic and therapeutic algorithm of intraoperative heart failure during cardiosurgical operations on the basis of evaluation of systolic and diastolic functions of the left and right ventricles. The study included 101 patients with low cardiac output in the postperfusion period. All the patients suffered from coronary heart disease and they underwent myocardial revascularizing operations under extracorporeal circulation. In all the patients, in addition to traditional hemodynamic parameters (heart rate, blood pressure, central venous pressure), the functional status of the left and right ventricles was evaluated by transesophageal Doppler echocardiography (TED echoCG) and the thermodilution technique using a Swan-Ganz catheter having a prompt thermistor. Evaluating the diastolic and diastolic functions of the right and left ventricles makes it possible to identify 2 types of left and right ventricular failure: 1) that due to systolic dysfunction and 2) that due to concomitance of systolic and diastolic dysfunctions. Dobutrex (5-7.5 microg/kg/min) should be used in right ventricular systolic dysfunction. Amrinone (5-10 microg/kg/min) should be given to patients with concomitance of systolic and diastolic dysfunction; in this situation, a combination of dobutrex and nitroglycerin (100-150 ng/kg/min) may be used. The drugs of choice in impaired left ventricular systolic function are epinephrine (30-100 ng/kg/min), dopamine (5-10 microg/kg/min), or dobutrex (5-7.5 microg/kg/min). Their combination with sodium nitroprusside can enhance the efficiency of therapy. In patients with left ventricular failure caused by systolic and diastolic dysfunction, epinephrine, dopamine, or dobutrex may be combined with amrinone (5-10 microg/kg/min) or nitroglycerin (100-150 ng/kg/min).

Amrinone↗
PubMed2002

Myocardial stiffness is determined by ventricular fibrosis, but not by compensatory or excessive hypertrophy in hypertensive heart.

OBJECTIVES: Diastolic dysfunction that determines symptoms and prognosis in patients with systolic dysfunction causes heart failure even in the absence of systolic dysfunction. Our recent studies have suggested that myocardial stiffening is likely to play a crucial role in triggering deleterious cardiac disorder. This study investigated differential contribution of left ventricular (LV) hypertrophy and fibrosis to myocardial stiffening in the pressure-overloaded heart. METHODS: Dahl-Iwai salt-sensitive rats fed on high-salt diet since 7 weeks transit to congestive heart failure at 20 weeks following development of hypertension, LV hypertrophy and fibrosis, and 20 such rats were divided into three groups: rats treated with angiotensin II type 1 receptor antagonist from 8 weeks (n=7), rats treated with calcineurin inhibitor from 8 weeks (n=6), and untreated rats (n=7). RESULTS: Administration of angiotensin II type 1 receptor antagonist and calcineurin inhibitor did not affect blood pressure and allowed the development of compensatory hypertrophy. However, in contrast to the untreated rats, additive and excessive LV hypertrophy was not observed in either of the treated rats. The blockade of angiotensin II kept LV hydroxyproline content, a ratio of type I to type III collagen mRNA levels, collagen solubility and myocardial stiffness constant at the normal level; however, the calcineurin inhibition failed. CONCLUSIONS: Myocardial stiffening may be attributed to progressive collagen accumulation, collagen phenotype shift and enhanced collagen cross-linking, but not to either compensatory LV hypertrophy or LV hypertrophy that progresses from the compensatory stage.

Analysis of Variance↗
PubMed1988

Appropriateness of digoxin use in medical outpatients.

PURPOSE: Digoxin is the third most commonly prescribed drug, yet limited information exists about its use in outpatients. Therefore, 242 medical outpatients receiving digoxin at our hospital were studied to evaluate the appropriateness of its use, defined by: (1) current or past supraventricular arrhythmias and/or (2) left ventricular systolic dysfunction (ejection fraction less than 45 percent). PATIENTS AND METHODS: Charts of 242 patients receiving digoxin were obtained. The patients were divided into groups based upon their physician's stated indication for digoxin therapy. Patients with only a clinical diagnosis of congestive heart failure (CHF) underwent echocardiography or radionuclide angiography to quantify left ventricular systolic function. Those with documented supraventricular arrhythmias and/or those with confirmed left ventricular systolic dysfunction were classified as appropriate candidates for digoxin. RESULTS: Ninety-five percent of patients received digoxin for appropriate indications; 75 percent had confirmed supraventricular arrhythmias (27 percent also had CHF) and 20 percent with normal sinus rhythm had documented systolic dysfunction. However, physicians had difficulty in the clinical assessment of left ventricular function; 18 percent of patients with sinus rhythm and CHF by the Framingham scoring system and 20 percent of those with supraventricular arrhythmias and CHF had preserved systolic function. An S3 was present in 15 percent of patients with preserved ejection fraction and CHF and in 69 percent with low ejection fraction; hypertension was significantly more common in the former group. Noninvasive assessment of systolic function was obtained in 97 percent of patients independent of this study, yet some patients without supraventricular arrhythmias and with documented preservation of systolic function continued to receive the drug. CONCLUSION: Noninvasive assessment of left ventricular function, which appears to have become routine, is of value in the appropriate utilization of digoxin, since clinicians' assessment of left ventricular function may be inaccurate. Physicians also do not always discontinue digoxin therapy when indicated.

Aged↗
PubMed2003

Portable echocardiography: an innovative tool in screening for cardiac abnormalities in the community.

AIMS: Heart failure is placing an increasing burden on society. This has led to calls for echocardiographic-based programmes to screen for left ventricular systolic dysfunction and other cardiac abnormalities. Echocardiography using new fully portable echocardiography devices would allow community-based cost-effective screening programmes once validated. This study was undertaken to evaluate this further in both high and low-risk subjects. METHODS AND RESULTS: 562 consecutive subjects attending a community-based heart failure screening programme, some at high-risk and some at low-risk of cardiac abnormalities, underwent echocardiography by both portable and traditional echocardiography machines. An 'eyeball' estimate of left ventricular ejection fraction was made on the portable device and compared to a quantitative measure of ejection fraction on the traditional machine. Qualitative measures of valvular regurgitation and quantitative measures of left ventricular hypertrophy were also compared. An estimate of ejection fraction was possible in 97% of cases using portable echocardiography. It gave a sensitivity, specificity and negative predictive value in diagnosing left ventricular systolic dysfunction of 96%, 98% and 99.6%, respectively. Inter-observer variability gave a mean difference in ejection fraction of 2%, and 95% limits of agreement of -8% to +12%. All cases of moderate or severe valvular regurgitation and 29 of 31 cases of significant left ventricular hypertrophy were correctly identified as abnormal on the portable device. CONCLUSIONS: Thus, echocardiography performed by experienced sonographers using these new fully portable devices is an accurate and reproducible technique for detecting left ventricular systolic dysfunction, left ventricular hypertrophy and valvular regurgitation in both high-risk and low-risk members of the community. Its very high negative predictive values would allow their use in future community-based screening programmes.

Adult↗
PubMed2002

Management of heart failure in primary care (the IMPROVEMENT of Heart Failure Programme): an international survey.

BACKGROUND: Heart failure is a prevalent condition that is generally treated in primary care. The aim of this study was to assess how primary-care physicians think that heart failure should be managed, how they implement their knowledge, and whether differences exist in practice between countries. METHODS: The survey was undertaken in 15 countries that had membership of the European Society of Cardiology (ESC) between Sept 1, 1999, and May 31, 2000. Primary-care physicians' knowledge and perceptions about the management of heart failure were assessed with a perception survey and how a representative sample of patients was managed with an actual practice survey. FINDINGS: 1363 physicians provided data for 11062 patients, of whom 54% were older than 70 years and 45% were women. 82% of patients had had an echocardiogram but only 51% of these showed left ventricular systolic dysfunction. Ischaemic heart disease, hypertension, diabetes mellitus, atrial fibrillation, and major valve disease were all common. Physicians gave roughly equal priority to improvement of symptoms and prognosis. Most were aware of the benefits of ACE inhibitors and beta blockers. 60% of patients were prescribed ACE inhibitors, 34% beta blockers but only 20% received these drugs in combination. Doses given were about 50% of targets suggested in the ESC guidelines. If systolic dysfunction was documented, ACE inhibitors were more likely and beta blockers less likely to be prescribed than when there was no evidence of systolic dysfunction. INTERPRETATION: Results from this survey suggest that most patients with heart failure are appropriately investigated, although this finding might be as a result of high rates of hospital admissions. However, treatment seems to be less than optimum, and there are substantial variations in practice between countries. The inconsistencies between physicians' knowledge and the treatment that they deliver suggests that improved organisation of care for heart failure is required.

Aged↗
PubMed1993

Effects of lisinopril on cardiorespiratory, neuroendocrine, and renal function in patients with asymptomatic left ventricular dysfunction.

OBJECTIVE: To determine the cardiac, renal, and neuroendocrine effects of lisinopril in men with untreated, symptom free left ventricular systolic dysfunction. DESIGN: A randomised, double blind cross over trial with six week treatment periods to compare lisinopril (10 mg/day) and matching placebo. SETTING: Hospital outpatient department. PATIENTS: Patients with pronounced systolic dysfunction on cross sectional echocardiography due to myocardial infarction at least six months previously, without angina and with no or minimal breathlessness. Eighteen men were identified of whom 15 completed the study. INTERVENTIONS: Lisinopril (10 mg) or placebo given once daily by mouth. MAIN OUTCOME MEASURES: Primary: oxygen consumption at peak exercise. Secondary: resting cardiac function as measured by radionuclide ventriculography and echocardiography, renal function estimated radioisotopically, and plasma indices of neuroendocrine activity. RESULTS: Compared with placebo, lisinopril increased (mean (SD)) peak oxygen consumption during exercise (19.8(3.1) ml/kg/min v 21.4(3.2) ml/kg/min; p < 0.003). Lisinopril did not improve indices of cardiac function at rest. It reduced plasma concentrations of angiotensin II (median values 7 pg/ml to 5 pg/ml; p < 0.02), aldosterone (median values 113 pg/ml to 66 pg/ml; p < 0.05) and atrial natriuretic peptide (median values 69 pg/ml to 40 pg/ml; p < 0.04), but noradrenaline and antidiuretic hormone concentrations did not change. Renal blood flow increased and glomerular filtration rate declined. CONCLUSIONS: Even before the onset of heart failure lisinopril improves the cardiopulmonary response to exercise in patients with systolic ventricular dysfunction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2002

Congestive heart failure: what should be the initial therapy and why?

Left ventricular systolic dysfunction is associated with neurohormonal activation which contributes to progressive ventricular remodeling and worsening clinical heart failure. Renin-angiotensin-aldosterone and sympathetic nervous systems are activated, not only in patients with clinically overt heart failure, but also in patients with asymptomatic or minimally symptomatic left ventricular systolic dysfunction. Activation of the angiotensin and adrenergic systems produces deleterious effects on systemic and coronary hemodynamics, promotes myocyte hypertrophy and fibroblast growth, and myocyte necrosis and apoptosis. Thus, therapy of heart failure should consist of pharmacologic agents not only to relieve symptoms but also to prevent and attenuate ventricular remodeling and progressive heart failure, thereby improving prognosis. In patients who are symptomatic, ACE inhibitors along with digitalis and diuretics as initial therapy (triple therapy) have the greater potential to improve exercise tolerance and decrease the incidence of treatment failure compared with diuretics alone or a combination of diuretics and digitalis. Diuretics alone should not be considered for long-term therapy as plasma renin activity, angiotensin II, aldosterone, norepinephrine and vasopressin levels may increase. ACE inhibitors decrease mortality in patients with heart failure resulting from left ventricular systolic dysfunction. The results of presently available studies indicate that angiotensin II receptor blockers (ARBs) do not provide any advantage over ACE inhibitors regarding survival benefit but may be better tolerated. Long-term adrenergic inhibition with the use of ss-adrenoceptor antagonists added to ACE inhibitors is associated with attenuation of ventricular remodeling, improvement in ventricular function and clinical class and survival of patients with symptomatic systolic left ventricular failure. Thus, initial pharmacotherapy for systolic heart failure should consist of: maximal tolerated dosages of ACE inhibitors;ARBs if ACE inhibitors are not tolerated because of intractable cough or angioedema;adequate dosages of hydralazine and isosorbide dinitrate if ACE inhibitors or ARBs are not tolerated; relatively low dosages of digoxin (serum concentrations of < or = 1.0 ng/dl) if not contraindicated; and diuretics to relieve congestive symptoms. Addition of spironolactone to ACE inhibitors can result in a significant reduction in the risk of sudden death in patients with symptomatic severe heart failure. Myocardial infarction resulting from ischemic heart disease is the most common cause of systolic left ventricular failure and the therapeutic modalities with potential to reduce the risks of myocardial infraction, such as risk factor modification, adequate control of diabetes and hypertension, antiplatelet agents and lipid-lowering agents, should also be included in the initial therapy.

Adrenergic Antagonists↗
PubMed2006

Comparison of the effect of anemia on in-hospital mortality in patients with versus without preserved left ventricular ejection fraction.

Patients with symptomatic heart failure (HF) frequently have preserved left ventricular (LV) ejection fractions (LVEFs). Although anemia is a common finding in this patient population, its prognostic role has not been well studied. This study's aim was to assess if the LVEF interferes in the association between anemia and in-hospital mortality in patients with severe HF. Consecutive patients admitted to an intensive care unit with decompensated chronic HF were prospectively enrolled. The diagnosis of HF was based on clinical criteria. Patients with LVEFs > or =45% (on echocardiography) were diagnosed as having preserved LVEFs. Multivariate analysis was performed to test the independent association between anemia and in-hospital mortality and to evaluate an interaction between anemia and systolic function. In all, 303 patients were recruited (mean age 69 +/- 13 years; 45.5% women). Preserved LVEFs were present in 34% of the population. The prevalence of anemia in this group was 58%, compared with 43% in the group with systolic dysfunction (p = 0.01). Dilated left ventricles, left bundle branch blocks, and valvular dysfunction were significantly more frequent in patients with systolic heart failure. In-hospital mortality was similar in the groups with preserved LVEFs and systolic dysfunction (p = 0.71). On multivariate analysis, anemia was independently associated with in-hospital mortality (odds ratio 2.7, 95% confidence interval 1.43 to 5.04, p = 0.002). There was no interaction between anemia and systolic function (p = 0.08 for interaction). In conclusion, anemia was an independent predictor of in-hospital mortality in symptomatic patients with severe HF, regardless of whether the patients had preserved or impaired LV systolic function.

Aged↗
PubMed1995

Congestive heart failure in dialysis patients: prevalence, incidence, prognosis and risk factors.

Cardiovascular disease is the most common cause of death in dialysis subjects. Congestive heart failure (CHF) is a common presenting symptom of cardiovascular disease in the dialysis population. Information regarding prevalence, incidence, risk factors and prognosis is crucial for planning rational interventional studies. A prospective multicenter cohort study of 432 dialysis patients followed for a mean of 41 months was carried out. Prospective information on a variety of risk factors was collected. Annual echocardiography and clinical assessment was performed. Major endpoints included death and the development of morbid cardiovascular events. One hundred and thirty-three (31%) subjects had CHF at the time of initiation of dialysis therapy. Multivariate analysis showed that the following risk factors were significantly and independently associated with CHF at baseline: systolic dysfunction, older age, diabetes mellitus and ischemic heart disease. Seventy-six of 299 subjects (25%) who did not have baseline CHF subsequently developed CHF during their course on dialysis. Compared to those subjects who never developed CHF (N = 218) multivariate analysis identified the following risk factors for the development of CHF: older age, anemia during dialysis therapy, hypoalbuminemia, hypertension during dialysis therapy, and systolic dysfunction. Seventy-five of the 133 (56%) subjects with CHF at baseline had recurrent CHF during follow-up. Independent and significant risk factors for CHF recurrence were ischemic heart disease and systolic dysfunction, anemia during dialysis therapy and hypoalbuminemia. The median survival of subjects with CHF at baseline was 36 months compared to 62 months in subjects without CHF. In this study the prevalence of CHF on starting ESRD therapy and the subsequent annual incidence was high.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed2004

Angiotensin-converting enzyme inhibitor captopril prevents volume overload cardiomyopathy in experimental chronic aortic valve regurgitation.

The efficacy of angiotensin-converting enzyme inhibitors (ACEIs) in the treatment of chronic aortic regurgitation (AR) is not well established and remains controversial. The mechanisms by which ACEIs may protect against left-ventricular (LV) volume overload are not well understood, and clinical trials performed until now have yielded conflicting results. This study was therefore performed to assess the effectiveness of two different doses of the ACEI captopril in a rat model of chronic AR. We compared the effects of a 6-month low-dose (LD) (25 mg/kg) or higher dose (HD) (75 mg/kg) treatment with captopril on LV function and hypertrophy in Wistar rats with severe AR. Untreated animals developed LV eccentric hypertrophy and systolic dysfunction. LD treatment did not prevent hypertrophy and provided modest protection against systolic dysfunction. HD treatment preserved LV systolic function and dimensions and tended to slow hypertrophy. The cardiac index remained high and similar among all AR groups, treated or not. Tissue renin-angiotensin system (RAS) analysis revealed that ACE activity was increased in the LVs of AR animals and that only HD treatment significantly decreased angiotensin II receptor mRNA levels. Fibronectin expression was increased in the LV or AR animals, but HD treatment almost completely reversed this increase. The ACE inhibitor captopril was effective at high doses in this model of severe AR. These effects might be related to the modulation of tissue RAS and the control of fibrosis.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2002

The Pediatric Randomized Carvedilol Trial in Children with Heart Failure: rationale and design.

BACKGROUND: Carvedilol is a medication with both beta-receptor and alpha-receptor blocking properties that has been approved for the treatment of heart failure in adults. Little is known about its safety, efficacy, pharmacokinetics, and dosing profile in children. METHODS: The primary objective of this study is to evaluate the efficacy of carvedilol administered twice daily for 8 months in terms of its effect compared with placebo on a composite measure of clinical outcomes in children with symptomatic systemic ventricular systolic dysfunction and heart failure. The secondary objectives are to determine the effect of carvedilol on individual components of a composite of clinical outcomes (hospitalizations for worsening heart failure, all-cause mortality and cardiovascular hospitalizations, all cause mortality, heart failure symptoms, and patient and physician global assessment); determine the effect of carvedilol on echocardiographic indices of ventricular function and remodeling; characterize the pharmacokinetics of carvedilol in pediatric patients with heart failure; characterize the effects carvedilol on neurohormonal systems; and provide data for the selection of an optimal titration schedule and daily dose of carvedilol in children with heart failure. This study will enroll 150 children between birth and 17 years of age with chronic symptomatic heart failure caused by systemic ventricular systolic dysfunction. CONCLUSION: This study will determine whether carvedilol improves symptoms in children with heart failure as a result of systemic ventricular systolic dysfunction. The study also will provide information on echocardiographic changes of ventricular performance and neurohormonal levels in children with heart failure before and after treatment with carvedilol, in addition to pharmacokinetics of carvedilol in children.

Adolescent↗
PubMed1995

Clinical characteristics and mortality of patients screened for entry into the Trandolapril Cardiac Evaluation (TRACE) study.

In mortality studies of patients after acute myocardial infarction (AMI), exclusion of patients during selection from the screened population may be important for evaluating the impact of trials, but data on patients excluded from studies are rarely presented. In the Trandolapril Cardiac Evaluation (TRACE) trial of the angiotensin-converting enzyme inhibitor trandolapril versus placebo in patients with left ventricular (LV) systolic dysfunction shortly after AMI, medical history, infarct complication, and survival were accounted for in all patients screened for entry. A total of 7,001 consecutive enzyme-confirmed AMIs were screened for entry in 27 Danish coronary care units. The 1-year mortality of all screened AMI cases was 23% (95% confidence interval 22% to 24%). The target population of the TRACE trial were patients with LV systolic dysfunction (echocardiographically determined wall motion index < or = 1.2, n = 2,606 within 6 days of AMI. The 1-year mortality of this group was 34 +/- 2%. Patients with wall motion index > 1.2 (n = 3,920) had a 1-year mortality of 12 +/- 1%. were excluded. A total of 1,749 were included in the study. The excluded and included groups had a 1-year mortality of 54 +/- 3% and 24 +/- 2%, respectively. The result of the TRACE study will be applicable to two thirds of the patients with LV systolic dysfunction; however, even with this high figure, care should be taken in extrapolating the result to the general population with reduced LV function after AMI since the group excluded from the study had a higher mortality than those who were included.

Aged↗