Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Coronary insufficiency is a pathophysiologic state that can initiate lethal cardiac arrhythmias in the absence of myocardial necrosis. Patients with suspected coronary insufficiency should be monitored until they are stabilized and a diagnosis is confirmed. 2. Early and adequate intravenous antiarrhythmic prophylaxis with lidocaine to raise the fibrillation threshold in the setting of coronary insufficiency can prevent primary ventricular fibrillation. Classic "warning arrhythmias" are not predictive of ventricular fibrillation. Their persistence during adequate antifibrillatory prophylaxis does not indicate therapeutic failure. 3. The isoenzyme of creatine phosphokinase, CPK-MB, is an extremely sensitive and specific indicator of myocardial necrosis if measured serially during the 24 hours following the onset of symptoms suggesting coronary insufficiency. It may prove most useful in eliminating the false positive diagnosis of myocardial infarction in difficult clinical cases. 4. The management of heart failure in myocardial infarction requires an understanding of the relationship between ventricular preload and the cardiac output. The treatment of clinical manifestations of an elevated ventricular preload in asymptomatic patients is not justified and may be detrimental. In symptomatic patients, however, judicious manipulation of ventricular preload should be the first therapeutic consideration, and an optimal filling pressure should be achieved and maintained when other determinants of the cardiac output are manipulated. 5. Indications for the prophylactic insertion of a temporary transvenous pacing electrode for heart block associated with myocardial infarction must be individualized. Most authorities agree that prophylactic pacing may be justified in patients with evidence of new infranodal block involving two of the three fascicles. Patients with bifascicular block who progress to complete heart block transiently may benefit from permanent transvenous pacemaker insertion before discharge. 6. Hospitalized patients with persistent pain of suspected cardiac origin but without evidence of myocardial infarction can be studied safely with coronary angiography. A small percentage will be normal or have diffuse disease that is inoperable. Of those with operable disease, short-term mortality appears to be similar for medical and surgical therapy. 7. Patients with an uncomplicated myocardial infarction may be safely discharged from thehospital by day 7-10. 8. Experimental evidence indicates that modification of infarct size is possible. Application of these concepts to human subjects presently is limited by the absence of a proved method of measuring infarct size in vivo in humans.
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PMID:The management of acute coronary insufficiency. 32 38

The dependence between the severity of cardiac insufficiency and the size of the necrotic lesion of the heart muscle, measured according to the area of 99m Tc-pyrophosphate cumulation and the rate of liberation of the isoenzyme MV creatine phosphokinase into the blood, was studied in 77 patients with myocardial infarction in the acute period of the disease. It was demonstrated that the severity of left ventricular insufficiency is directly dependent on the size of necrosis of the heart muscle. Not only the size of the necrotic focus but also the state of the contractility of the other parts of the myocardium is an important factor determining the origin and severity of cardiac insufficiency.
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PMID:[Size of myocardial necrosis and left ventricular insufficiency in acute myocardial infarct]. 49 84

The effects of acute myocardial infarction on the pharmacokinetics of digoxin were studied. Digoxin, 0.75 mg, was given orally to 12 patients with left-sided cardiac failure due to acute myocardial infarction and to 9 healthy control subjects. Serum concentration of digoxin in the first 4 hours and the area under the serum concentration-time curve in the first 12 hours after administration of the drug were lower in patients with infarction than in control subjects (P less than 0.01). The 24 hour area under the concentration curve, the amount excreted in urine and the renal clearance did not differ between the groups. The 24 hour area under the concentration curve correlated with the predigoxin pulmonary capillary wedge pressure and with heart rate (P less than 0.01). The decrease of renal clearance of digoxin was related to the serum activity of MB isoenzyme of creatine kinase (P less than 0.001). Morphine reduced and delayed the peak serum concentrations of digoxin (P less than 0.001). Thus, the absorption of oral digoxin was slower and the peak concentrations remained lower in patients with acute myocardial infarction than in healthy control subjects. However, the total amount of digoxin absorbed was unchanged.
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PMID:Pharmacokinetics of digoxin in patients with acute myocardial infarction. 49 14

The myocardial infarct size was assessed on the basis of serial analyses of serum creatine phosphokinase (CPK) in 70 patients with first transmural myocardial infarction. Clinical symptoms of heart failure (Killip II-III) were found in patients with infarcts larger than 50 CPK-g-equ; in patients with lung oedema the infarct size averaged 104.2 CPK-g-equ. Patients without clinical and roentgenological evidence of left heart failure (Killip I) had infarct sizes always lesser than 50 CPK-g-equ, averaging 31.7 CPK-g-equ. Precordial mapping of the QRS complex in patients with anterior wall infarction revealed a significant correlation (r = 0.916) between the sum of voltages of Q waves on a 30-lead map recorded 24 hours after hospitalization and the enzymically assessed infarct size. Exact skiagraphic and auscultatory examinations of the heart and lungs, together with precordial mapping of the QRS complex, in patients with anterior wall infarct allow a relatively accurate quantification of the infarct size for prognostic classification of the patients.
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PMID:Assessment of myocardial infarct size in clinical practice. 54 93

Serum activity of creatine kinase and creatine kinase-MB have been investigated in 129 patients of various etiology in overt heart failure. Elevations in CK-MB were found in 19 patients, most frequently in patients with inflammatory heart disease. We found no correlation between CK-MB activity in serum and the severity of heart failure. CK-MB elevation in patients with chronic heart failure may be interpreted as a sign of progressive as well as regressive processes in the myocardium.
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PMID:[Determination of creatine kinase and CK-MB in heart failure (author's transl)]. 72 68

Dietary potassium depletion plus high sodium intake has been reported to elevate resting heart rate and cardiac output and to cause heart failure during exercise. We implanted aortic root electromagnetic flowmeters and aortic and pulmonary artery catheters in five splenectomized dogs condition-trained to run at 9 km/h on an 11% grade for 20 min. Postoperatively, the dogs ate a potassium-enriched diet until completion of control studies; then potassium was withdrawn. During 4 wk of depletion, skeletal muscle potassium fell from 380 +/- 22 to 311 +/- 8 meq/kg, and muscle sodium rose from 142 +/- 14 to 207 +/- 27 meq/kg (mean +/- SE). Cardiac output, aortic blood pressure, heart rate, acceleration of aortic blood flow at rest or during exercise, and the oxygen cost of exercise remained at control levels. Serum creatine phosphokinase at rest, an indicator of rhabdomyolysis, was never elevated. A 24% dietary depletion of muscle potassium in the dog did not change resting and exercise hemodynamics and exercise performance from control.
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PMID:Exercise performance and hemodynamics during dietary potassium depletion in dogs. 73 May 69

In 17 patients with coronary heart disease, hemodynamic measurements were performed before and after sublingual application of 10 mg isosorbide dinitrate (ISDN). 10 patients showed signs of heart failure with pulmonary congestion and a left ventricular filling pressure above 15 mmHg, resting hemodynamics were normal in 7 patients. Eight of the patients with left ventricular failure had sustained acute myocardial infarctions the size of which was assessed by serial determinations of serum creatine phosphokinase. Application of ISDN resulted in a significant decrease of systemic and pulmonary artery pressures and pulmonary capillary wedge and right atrial pressures of patients both with and without left ventricular failure. Cardiac index and stroke index as well as systemic and pulmonary resistances did not change significantly. ISDN did not affect left ventricular stroke work in patients with elevated filling pressures; however, a decrease of normal filling pressures was associated with a decrease of stroke work. Thus, in coronary patients with chronic congestive heart failure, sublingual application of nitrates results in a beneficial hemodynamic unloading. However, if the acute infarct size is taken into account, it can be demonstrated that hemodynamic improvement after ISDN--judged by the relation stroke work/filling pressure--becomes less pronounced with increasing infarct size.
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PMID:[Effect of sublingual isosorbide dinitrate on hemodynamics in coronary patients with and without congestive heart failure (author's transl)]. 89 50

Serial measurements on serum creatine phosphokinase (CPK) and alpha-hydroxybutyrate dehydrogenase (HBD) activity were made in 17 patients with acute myocardial infarction. Activities of both enzymes were measured 4-hourly from less than 12 h after the onset of chest pain until CPK activity had returned to near-normal levels. Blood was then sampled twice daily for a further 4--6 days in order to follow the decline in HBD activity. Degradation rates (KD) were calculated for both enzymes, and individual figures for KD were used in order to estimate the total cumulative release of each enzyme. We found a significant correlation between the duration (r = 0.66, P less than 0.01) and magnitude (r = 0.67, P less than 0.01) of release of the 2 enzymes, comparing different patients with one another. Duration od HBD release was 11 h greater than the duration of CPK release in 9 of the 17 patients who were suffering from cardiac failure (t = 0.01, P less than 0.02). Degradation rate (KD) for HBD was on average about one quarter of that for CPK, but there was no significant correlation between KD for the 2 enzymes. KD did not appear to be reduced in patients with cardiac failure. We conclude that the release patterns of CPK and HBD after myocardial infarction are similar, and this strengthens the case for acceptance of total enzyme release as a valid index of myocardial infarct size.
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PMID:Enzyme release after myocardial infarction: comparison of serial serum alpha-hydroxybutyrate dehydrogenase with creatine phosphokinase levels. 100 39

One hundred and eleven patients with transmural (TMI) and 49 with nontransmural myocardial infarction (NTMI) underwent hemodynamic investigation within 24 hours of onset of symptoms. Patients with NTMI were subdivided into those with ST-segment or T-wave changes alone with a normal QRS complex (NTMI-A) and a group with QRS abnormalities that did not satisfy the criteria for TMI (NTMI-B). Those with TMI had a significantly higher peak creatine phosphokinase (CPK) than those with NTMI: 840 plus or minus 99 and 336 plus or minus 69, respectively, P smaller than 0.05. There was not difference in peak CPK between those with NTMI-A and B. The incidence of arrhythmias and cardiac failure, and routine hemodynamic findings except for left ventricular filling pressure were similar in those with TMI and NTMI. There was not significant difference in in-hospital mortality between those with TMI (22%) and NTMI (33%). There was however a significant difference in in-hospital mortality between those with NTMI-A (0%) and NTMI-B (27%, P smaller than 0.05). The late mortality in those surviving their initial hospitalization was also not different between those with TMI (18%) and NTMI (19%) during a mean follow-up period of 20.2 months. In contrast to the in-hospital mortality those with NTMI-A had a late mortality similar to those with NTMI-B and those with TMI.
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PMID:Hemodynamic and prognostic findings in patients with transmural and nontransmural infarction. 113 97

The status of myocardial function in rabbits subjected to cardiac catheterization and infection with Streptococcus viridans was assessed at 3 and 6 days. Sham-operated control animals as well as uninfected catheterized animals were used for comparison. Although left heart hypertrophy and interstitial edema were evident in both uninfected and infected animals, the infected animals exhibited in addition mononuclear cell infiltration and muscle degeneration as well as lung congestion and accumulation of pleural fluid. Both uninfected and infected animals has elevated levels of serum creatine phosphokinase, lactic dehydrogenase and glutamic oxaloacetic transaminase as well as electrocardiographic abnormalities such as increased amplitude of the ORS complex and flattening or inversion of the T wave. Unlike findings in the uninfected animals, the serum calcium, magnesium and sodium levels were slightly but significantly decreased and serum potassium levels were increased in the infected rabbits. Both heart rate and pulse pressure were higher in 6 day uninfected and 3 day infected animals whereas 6 day infected animals showed a decrease in heart rate. In comparison to the sham-operated control rabbits and the uninfected animals, the infected animals exhibited depression in the rates of left ventricular pressure development and relaxation as well as prolongation in time for half relaxation in situ. Relative maximal contractile element velocity extrapolated from intraventricular pressure-velocity curves was decreased by 24, 52 and 76 percent, respectively, of control values in the uninfected hearts and those with 3 and 6 days of infection. The isolated perfused hearts from infected animals also generated less contractile force and showed a decrease in the rates of contraction and relaxation, but half-relaxation time was increased. These results demonstrate myocardial dysfunction during experimental bacterial endocarditis and provide evidence that infective cardiomyopathy is associated with heart failure.
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PMID:Alterations in myocardial function during bacterial infective cardiomyopathy. 125 70


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