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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent multicentre studies evaluating the therapeutic value of calcium antagonists in reducing the incidence of cardiovascular complications after myocardial infarction (secondary prevention) and in retarding the development of atherosclerosis in coronary artery disease (tertiary protection) are reviewed. The prognosis of patients after acute myocardial infarction can be improved not only by interventional measures such as aortocoronary bypass surgery or percutaneous transluminal catheter angioplasty, but also by various drugs. Numerous studies have shown that beta-blockers and platelet aggregation inhibitors can reduce mortality and reinfarction rates. Calcium antagonists in secondary prevention trials after acute myocardial infarction, however, have produced variable results. Whereas the Secondary Prevention Reinfarction Israeli Nifedipine Trial (SPRINT) [Israeli SPRINT Study Group 1988] with nifedipine showed no beneficial effect of the drug, studies with verapamil in the Danish Verapamil Infarction Trial II (DAVIT II) [Danish Study Group on Verapamil in Myocardial Infarction 1990] and diltiazem in the Multicentre Diltiazem Postinfarction Trial (MDPIT) [Multicenter Diltiazem Postinfarction Trial Research Group 1988] as secondary prevention have demonstrated improvements in survival and cardiovascular complications, but these improvements were restricted to patients without heart failure. In view of the ability of calcium antagonists to reduce atheroma progression in coronary artery disease in animal models, the antiatherosclerotic effects of these agents in clinical studies have generally been disappointing. In the International Nifedipine Trial on Antiatherosclerotic Therapy (INTACT) [Lichtlen et al. 1990], however, nifedipine treatment was associated with a 28% reduction in new lesion development, but did not affect the development of severe lesions. Similar results have been obtained with nicardipine.
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PMID:Secondary and tertiary prevention with calcium antagonists in coronary artery disease. 137 87

Postinfarction cardiac rupture (PCR) up to the present accounts for approximately 20 percent of autopsy infarcted cases, ranking only behind arrhythmias and cardiac failure in the frequency of AMI complications. We re-examined our observations of a previous anatomo-clinical study of 96 patients who underwent autopsy after death from AMI. Sixteen patients had rupture of the free wall of the left ventricle at the site of infarction. All the patients with rupture showed the following statistically significant characteristics (p less than 0.01) if compared to those without rupture: cardiac hypertrophy (heart weight 390 to 1020 gm; mean: 627.5 +/- 201 gm; left ventricular wall thickness 18 mm to 29 mm; mean: 25.17 +/- 3.6 mm), sudden death (6 cases) without premonitory symptoms or with symptoms of less than an hour's duration or reappearance of chest pain not improved by opiates before late death, that occurred 240 to 660 minutes from chest pain, recorded electrocardiograms showing sinus rhythm with unchanged ST-segment (12 cases), atrioventricular block (2 cases) and junctional rhythm (2 cases). Hypertension pre-existing to the infarction was seen in 6 cases with rupture versus 9 cases without rupture (p less than 0.01). Blood pressure, heart weight and wall thickness of the left ventricle are the most increased parameters in the patients with PCR. Preventive measures against these factors can reduce PCR.
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PMID:Postinfarction cardiac rupture in the nineties: do we know determinating factors? 163 89

The impact of postinfarction angina pectoris on the course of myocardial infarction (MI) was studied in the hospital setting in 359 patients who had sustained large MI, 247 of them being followed for a year after their discharge. In the group of patients with postinfarction angina pectoris, the course of the disease was found to be more severe in hospital and during a year-follow-up after MI. They more frequently developed acute and chronic heart failure, rhythm and conduction disturbances, recurrent MI. A statistic relationship was not established between the development of postinfarction angina and late fatality. Postinfarction angina was demonstrated to increase a risk for an unfavorable course of a postinfarction period. No significant difference was found in the prognostic significance of the time angina occurred following MI.
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PMID:[Post-infarction stenocardia (clinical and prognostic significance)]. 204 41

The increase in sympathetic nervous system activity noted in heart failure of several etiologies has beneficial effects in the short term; in the long term, though, it may be detrimental. This provides a rationale for use of beta-blocker therapy in patients with cardiac myopathies of various etiologies. Postinfarction trials in patients with ischemic heart disease have suggested that beta blockade provides a substantial mortality benefit, and beta blockers are accepted as first-line therapy for hypertrophic cardiomyopathy. The use of beta-blocking drugs for dilated cardiomyopathy (DCM), however, is currently investigational. Early trials reporting benefits in functional class, exercise capacity, and myocardial function stimulated further interest in this application of beta blockade. Recent studies comparing metoprolol with placebo or standard treatment have shown promising improvements in functional class and exercise capacity. The patients who will benefit most from beta-blocker therapy in DCM may be those with a high resting heart rate and a short duration of symptoms and, perhaps, feminine gender. Marked structural abnormality on cardiac biopsy (eg, fibrosis) may suggest a poor response to treatment. A multicenter controlled study of metoprolol in dilated cardiomyopathy is in progress. If the outcome is favorable, beta-blocker therapy in DCM may become an accepted, rather than an experimental, treatment.
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PMID:Treatment of cardiac myopathies with beta blockers. What do we know, where do we go from here? 289 53

Quantification of heart failure is possible with hemodynamic parameters such as cardiac output and filling pressure at rest and during exercise. These parameters can easily but invasively be achieved by floating catheter measurements. In our experience, the risk of this method is low but existent. In greater than 20 000 patients with chronic diseases no death occurred in connection with the procedure; 26 patients developed ventricular fibrillation or ventricular tachycardias which made defibrillation necessary in 10 of these patients. In three patients asystolia demanded resuscitation. Hemoptysis did not occur. In the acute stage of a disease, e.g. in the acute myocardial infarction, the risk may be higher, especially if the catheter remains in the circulation for longer periods. The possibilities and limitations of the method will be discussed for the following patient groups: (1) Patients with acute myocardial infarction, (2) Postinfarction patients, (3) Patients with cardiomyopathies, (4) Patients with valvular heart disease.
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PMID:Does exercise testing with invasive measurements of cardiac output and pressure really contribute? 684 Jan 19

Myocardial infarction evokes major physiological changes because of the acute loss of functional cardiac tissue, resulting in more or less severe symptoms of congestive heart failure. In addition, general well-being of patients, their quality of life, is reduced. This includes anxiety/depression, loss of interest in environment and social interactions, sexual problems, and sleep disturbances. Postinfarction treatment is aimed mainly at improving life expectancy, whereas less attention is paid to the quality of that life. The aim of the present study was to determine behavioral changes after myocardial infarction in a (otherwise proven as clinically relevant) rat model for heart failure after myocardial infarction. We have chosen for behavioral tests based upon certain aspects of quality of life in patients. Anxiety/depression, interest in environment, and mobility, tested in an open field, revealed that infarcted rats are more anxious (as inferred from a higher preference for the safe corner area and less visits to the middle area), have less interest in a new environment [as indicated by less exploratory behavior and a longer time before they go into the new area (free exploration)], and showed less mobility (as indicated by reduced distance walked and less time spent on walking). In a test on social interaction, infarcted rats spent less time on social behavior and displayed even somewhat more walking away, suggesting active avoidance of social interaction. The observed behavioral changes in infarcted rats match very well with the aspects of reduced quality of life in postinfarct patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Behavioral changes following chronic myocardial infarction in rats. 797 12

Postinfarction ventricular septal defect (PIVSD) remains a surgical challenge resulting in devastating mortality rates. We present our 10-year experience in surgical management of this catastrophic complication of acute myocardial infarction. During a decade (1987-1996) 14 patients with PIVSD were treated surgically in our department. There were 10 men and 4 women, ranging in age from 51 to 78 years. The rupture occurred within the first 4 days after the infarction in most cases (n = 10). Eight patients were supported perioperatively by intraaortic balloon counterpulsation (IABP). In all cases the surgical technique included infarctectomy and ventricular septum reconstruction with synthetic patches. Coronary artery bypass grafting was synchronously performed in four patients. Seven patients died perioperatively (mortality rate 50%) due to heart failure and to multiple organ failure. The most frequent complications were low cardiac output syndrome, hemorrhage, and respiratory and renal insufficiency. The PIVSD needs urgent surgical intervention with the patient hemodynamically stable after cardiac catheterization. Long-term results are favorable for survivors.
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PMID:Surgical repair of postinfarction ventricular septal defect: 10-year experience. 984 65

The high number of patients with advanced heart failure despite optimal medical therapy and the limited availability of radical therapeutic solutions (including heart transplantation) increase the interest in alternative surgical procedures. In this paper, the correction of secondary mitral valve regurgitation, left ventriculectomy, and aneurysmectomy/ventriculoplasty will be reviewed. Secondary mitral valve regurgitation worsens both symptoms and prognosis in patients with left ventricular dysfunction of ischemic and non-ischemic etiology. Its correction, mostly by conservative repair, can be performed with an acceptable perioperative risk in patients with compensated heart failure. Concomitant correction of mitral insufficiency is advisable in patients with significant regurgitation undergoing revascularization surgery. On the other hand, data regarding the improvement in clinical and objective parameters after mitral valve surgery in patients with severe mitral regurgitation and idiopathic or ischemic cardiomyopathy who are unsuitable for revascularization are discordant. In view of its feasibility and presumed efficacy, partial left ventriculectomy or the Batista operation seemed attractive but the expectations were not met: success cannot be predicted in individual patients, the initial improvement may be of short duration, and the peri and postoperative mortalities are relevant. Postinfarction surgical reconstruction and reshaping of the left ventricle is performed mostly together with revascularization surgery; the surgical experience, indications and results reported in various studies are however discordant. In conclusion, multicenter cooperation including randomized studies or registries is worthwhile in order to define the role of surgery of the mitral valve and left ventricle in patients with advanced heart failure.
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PMID:[Refractory heart failure. Surgery of the left ventricle and mitral insufficiency]. 1240 37

Infarct-induced heart failure is usually associated with cardiac hypertrophy and decreased -adrenergic responsiveness. However, conflicting results have been reported concerning the density of L-type calcium current (I Ca(L)), and the mechanisms underlying the decreased -adrenergic inotropic response. We determined I Ca(L) density, cytoplasmic calcium ([Ca2+]i) transients, and the effects of -adrenergic stimulation (isoproterenol) in a model of postinfarction heart failure in rats. Left ventricular myocytes were obtained by enzymatic digestion 8-10 weeks after infarction. Electrophysiological recordings were obtained using the patch-clamp technique. [Ca2+]i transients were investigated via fura-2 fluorescence. -Adrenergic receptor density was determined by [ H]-dihydroalprenolol binding to left ventricle homogenates. Postinfarction myocytes showed a significant 25% reduction in mean I Ca(L) density (5.7 0.28 vs 7.6 0.32 pA/pF) and a 19% reduction in mean peak [Ca2+]i transients (0.13 0.007 vs 0.16 0.009) compared to sham myocytes. The isoproterenol-stimulated increase in I Ca(L) was significantly smaller in postinfarction myocytes (Emax: 63.6 4.3 vs 123.3 0.9% in sham myocytes), but EC50 was not altered. The isoproterenol-stimulated peak amplitude of [Ca2+]i transients was also blunted in postinfarction myocytes. Adenylate cyclase activation through forskolin produced similar I Ca(L) increases in both groups. -Adrenergic receptor density was significantly reduced in homogenates from infarcted hearts (Bmax: 93.89 20.22 vs 271.5 31.43 fmol/mg protein in sham myocytes), while Kd values were similar. We conclude that postinfarction myocytes from large infarcts display reduced I Ca(L) density and peak [Ca2+]i transients. The response to -adrenergic stimulation was also reduced and was probably related to -adrenergic receptor down-regulation and not to changes in adenylate cyclase activity.
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PMID:Impaired beta-adrenergic response and decreased L-type calcium current of hypertrophied left ventricular myocytes in postinfarction heart failure. 1271 84

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and is a frequent complication of acute myocardial infarction (MI). AF occurs in 5% to 10% of patients who have received fibrinolysis. Post-MI AF is more common in older patients, in patients with heart failure, and after more extensive infarction. Postinfarction prognosis is worse among patients complicated by AF--indeed, mortality and morbid events including stroke, thromboembolism, and heart failure are increased in this group. It is unclear as to whether AF directly reduces survival or merely demarcates patients at higher overall risk. Despite its frequent occurrence and deleterious influence on outcomes, randomized data regarding management of AF after acute MI are scarce. This review summarizes recent data charting the incidence of AF after acute MI and describes features associated with its occurrence. Clinical sequelae and current principles in treatment are also discussed.
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PMID:Atrial fibrillation post-myocardial infarction: frequency, consequences, and management. 1603 38


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