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

Cardiogenic shock is a frequent and threatening complication in the course of acute myocardial infarction. Besides the well known causes (left ventricular failure, acquired interventricular defect, papillary muscle rupture, free wall rupture) other less frequent mechanisms recognize a functional substrate. The recognition of such mechanisms makes us to revert to the treatments with completely different prognostic implications. In our Coronary Care Unit we encountered, in a period of 12 months, 4 patients who presented clinical, electrocardiographic and/or echographic signs and symptoms of acute myocardial infarction, with different degrees of heart failure up to cardiogenic shock. Only 1 patient showed a severe stenosis of the left anterior descending coronary artery and a significant creatine kinase reduction. Left ventriculography, performed at admission, was unable to disclose the true mechanism of clinical presentation. Only a thorough echographic examination disclosed the presence of a dynamic left ventricular outflow tract obstruction as the cause of heart failure culminating in cardiogenic shock. Once recognized, pathophysiological treatment (administration of beta-blockers and withdrawal of vasodilators, inotropic drugs and intra-aortic balloon pump) led to a dramatic improvement, with an almost complete left ventricular function recovery. Left ventricular outflow tract obstruction is a mechanism that can lead to severe heart failure as a complication of an acute myocardial infarction. Conversely such a mechanism can be precipitated by other causes (hypotension, hypovolemia, especially in hypertensive patients) and can mimic an acute myocardial infarction. Its incidence is not negligible: in our Coronary Care Unit it accounted for about 15% of all cases of myocardial infarction requiring inotropic support. An accurate echocardiographic examination is mandatory even after coronary angiography, and always permits the physician to select the appropriate therapy.
 ...
PMID:Dynamic left ventricular outflow tract obstruction: an unusual mechanism mimicking anterior myocardial infarction with cardiogenic shock. 1121 4

Spontaneous recanalization (SR) occurs after the onset of acute myocardial infarction (AMI), but its clinical significance in the reperfusion era remains uncertain. We evaluated the determinants and prognostic significance of SR in 196 consecutive patients with AMI who underwent primary angioplasty at our institution. The study population was divided into 2 groups according to the presence (group I, n = 44) or absence (group II, n = 152) of SR (Thrombolysis In Myocardial Infarction [TIMI] anterograde > or = 2 flow on the preintervention angiogram). The primary end point was the occurrence, within 6-weeks after AMI, of death, nonfatal reinfarction, and congestive heart failure. Baseline characteristics were similar between the 2 groups. Peak levels of creatine kinase were lower in group I than in group II (2,500 +/- 1,800 vs 4,000 +/- 2,900 U/L, respectively, p < 0.05). The rate of TIMI flow grade 3 after intervention was higher in group I than in group II (93.2% vs 79.6%, respectively, p < 0.05), and patients in group I had a faster corrected TIMI frame count than those in group II (22.7 +/- 12.4 vs 30.3 +/- 22.8, respectively, p < 0.05). Preinfarction angina (odds ratio [OR] 2.18, 95% confidence interval [CI] 1.10 to 4.33, p < 0.05), heavy thrombi (OR 0.10, 95% CI 0.01 to 0.74, p < 0.05), and good angiographic collaterals (OR 0.12, 95% CI 0.02 to 0.89, p < 0.05) were independent predictors of SR. Death, reinfarction, and severe arrhythmia were not different between the 2 groups. However, heart failure occurred more frequently in group II than in group I (15.1% vs 2.3%, respectively, p < 0.05). The primary end point was also significantly lower in group I than in group II (4.5% vs 18.4%, respectively, p < 0.05). In conclusion, SR in AMI is associated with faster coronary flow, smaller infarct size, and a better clinical outcome after primary angioplasty.
 ...
PMID:Determinants and prognostic significance of spontaneous coronary recanalization in acute myocardial infarction. 1130 84

Cardiac troponin levels are regarded as the most specific of currently available biochemical markers of myocardial damage. Elevated levels of troponin have been previously reported in patients with left heart failure, reflecting small areas of undetected myocardial cell death. The aim of this study was to compare the levels of the cardiac troponin I (cTnI) in patients with left- and right-sided heart failure. Cardiac troponin I levels were studied with immunochemical methods in patients with right heart failure (n = 17) resulting from chronic obstructive pulmonary disease, ischemic left heart failure (n = 23), and nonischemic left heart failure (n = 18) who were admitted to departments of cardiology and chest diseases. Also, cTnI levels were measured in 32 healthy subjects as control group. Protein markers of myocardial injury (cTnI and myoglobin) in patients with left and right heart failure were collected approximately 12 to 36 hours after onset of obvious symptoms. Serum creatine kinase MB band was determined on admission and thereafter twice a day during the first 3 days. Elevated levels of serum cTnI were found in patients with nonischemic (0.83 +/- 0.6 ng/mL, p<0.01) and ischemic left heart failure (0.9 +/- 0.5 ng/mL, p<0.01) when compared to healthy subjects, whereas serum cTnI levels in patients with right heart failure due to chronic obstructive pulmonary disease were not significantly different from those of control subjects (0.22 +/- 0.1 vs 0.16 +/- 0.1 ng/mL, p>0.05). In addition, creatine kinase MB band and myoglobin levels were not significantly different between patient and healthy groups. The mean of cTnI levels in ischemic and even nonischemic left heart failure were increased compared to the mean of values in healthy individuals but without significant creatine kinase MB band and myoglobin elevations. But cTnI levels were not increased in patients with right heart failure due to chronic obstructive pulmonary disease. These data indicate that the cTnI levels are abnormal in left heart failure but not in cor pulmonale.
 ...
PMID:Cardiac troponin I levels in patients with left heart failure and cor pulmonale. 1138 82

Diabetes increases both the incidence of cardiovascular disease and complications of myocardial infarction and heart failure. Studies using diabetic animals have shown that changes in myocardial sodium transporters result in alterations in intracellular sodium (Na(i)) homeostasis. Because the changes in sodium homeostasis can be due to increased entry of Na+ via the electroneutral Na+-K+-2Cl- cotransporter (NKCC), we conducted experiments in acute diabetic hearts to determine if 1) net inward cation flux via NKCC is increased, 2) this cotransporter contributes to a greater increase in Na(i) during ischemia, and 3) inhibition of NKCC limits injury and improves function after ischemia-reperfusion. These issues were investigated in perfused type I diabetic and nondiabetic rat hearts subjected to ischemia and 60 min of reperfusion. A group of diabetic and nondiabetic hearts was perfused with 5 microM of bumetanide, an inhibitor of NKCC. Flux via NKCC, Na(i), and ATP was measured in each group with the use of radiotracer 86Rb, 23Na, and 31P nuclear magnetic resonance spectroscopy, respectively, whereas ischemic injury was assessed by measuring creatine kinase release on reperfusion. Cation flux via NKCC, as measured by 86Rb uptake, was significantly increased in diabetic hearts. Inhibition of NKCC significantly reduced ischemic injury in diabetic hearts, improved functional recovery on reperfusion, attenuated the ischemic rise in Na(i), and conserved ATP during ischemia-reperfusion. Parallel studies in nondiabetic hearts showed that NKCC inhibition was not cardioprotective. These findings demonstrate that flux via NKCC is increased in type I diabetic hearts and that inhibition with bumetanide attenuates changes in Na(i) and ATP during ischemia and protects against ischemic injury. The data suggest a therapeutic role for pharmacological agents that inhibit flux via NKCC in diabetic patients with myocardial ischemia.
 ...
PMID:Protection of ischemic myocardium in diabetics by inhibition of electroneutral Na+-K+-2Cl- cotransporter. 1145 52

Cardiac troponin I levels are frequently above normal values in several disease states in which myocardial necrosis is not a prominent aspect, particularly in pulmonary embolism, heart failure, liver cirrhosis, septic shock, renal failure and arterial hypertension. Sub-clinical myocardial necrosis has been postulated to be the cause of the phenomenon. Studies performed so far have not included pathological data to confirm this hypothesis. Increased troponin I plasma levels may be the result of myocardial strain, especially the type of strain that accompanies some forms of cardiac dilatation or hypertrophy. Troponin I may act as a marker of myocardial strain, either acute (in pulmonary embolism, septic shock and acute heart failure) or chronic (in chronic cardiac, renal and hepatic failure, as well as in arterial hypertension). The apparent paradox of elevated levels of troponin I without elevated levels of creatine kinase in several disease states might be solved if troponin I could be released from myocardial cells without the disruption of myocardial cell plasma membranes. Precise pathological studies are needed to elucidate whether increased troponin I with normal CK is associated with myocyte death, and, if so, with necrosis or with apoptosis.
 ...
PMID:Cardiac troponin I in systemic diseases. A possible role for myocardial strain. 1158 28

Seven related Quarter Horse foals that died by 7 weeks of age were examined for glycogen branching enzyme (GBE) deficiency. Clinical signs varied from stillbirth, transient flexural limb deformities, seizures, and respiratory or cardiac failure to persistent recumbency. Leukopenia (5 of 5 foals) as well as high serum creatine kinase (CK; 5 of 5), aspartate transaminase (AST; 4 of 4), and gamma glutamyl transferase (GGT; 5 of 5) activities were present in most foals, and intermittent hypoglycemia was present in 2 foals. Gross postmortem lesions were minor, except for pulmonary edema in 2 foals. Muscle, heart, or liver samples from the foals contained abnormal periodic acid Schiff's (PAS)-positive globular or crystalline intracellular inclusions in amounts proportional to the foal's age at death. Accumulation of an unbranched polysaccharide in tissues was suggested by a shift in the iodine absorption spectra of polysaccharide isolated from the liver and muscle of affected foals. Skeletal muscle total polysaccharide concentrations were reduced by 30%, but liver and cardiac muscle glycogen concentrations were normal. Several glycolytic enzyme activities were normal, whereas GBE activity was virtually absent in cardiac and skeletal muscle, as well as in liver and peripheral blood cells of affected foals. GBE activities in peripheral blood cells of dams of affected foals and several of their half-siblings or full siblings were approximately 50% of controls. GBE protein in liver determined by Western blot was markedly reduced to absent in affected foals, and in a half-sibling of an affected foal, it was approximately one-half the amount of normal controls. Pedigree analysis also supported an autosomal recessive mode of inheritance. The affected foals have at least 2,600 half-siblings. Consequently, GBE deficiency may be a common cause of neonatal mortality in Quarter Horses that is obscured by the variety of clinical signs that resemble other equine neonatal diseases.
 ...
PMID:Glycogen branching enzyme deficiency in quarter horse foals. 1181 63

C-C chemokines are essential factors in the recruitment and activation of leukocytes from the circulation into inflamed tissue and may play a role in ischemia-induced myocardial injury and left ventricular remodeling after acute myocardial infarction (AMI). We investigated the kinetics of three major C-C chemokines, macrophage chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1 alpha (MIP-1 alpha), and regulated on activation normally T cell expressed and secreted (RANTES), in the sera of AMI patients and correlated the findings with the severity of the disease. Serum levels of C-C chemokines were determined in 35 AMI patients by ELISA assays serially during the first week of hospitalization and 1 month after hospital admission. Patients (n = 18) with uncomplicated AMI (Killip class I) were classified as group A, patients (n = 17) with AMI complicated by heart failure manifestations (Killip classes II and III) were classified as group B, and 15 age-matched and sex-matched volunteers were used as healthy controls. A sustained increase in serum C-C chemokines was observed in both AMI groups during the 7-day hospitalization period. Peaks of these inflammatory factors were significantly higher in group B than in group A (MCP-1, 295 +/- 11 vs. 203 +/- 9 pg/ml, p < 0.01; MIP-1 alpha, 30 +/- 1 vs. 24 +/- 2 pg/ml, p < 0.05; RANTES, 32 +/- 2 vs. 16 +/- 1 ng/ml, p < 0.01) and healthy controls (MCP-1, 125 +/- 7 pg/ml, p < 0.001; MIP-1 alpha, 14 +/- 1 pg/ml, p < 0.001; RANTES, 12 +/- 1 ng/ml, p < 0.001). In group B, significant correlations were found between the peak of MCP-1 and the peak of C-reactive protein levels (r = 0.55, p < 0.02) as well as wedge pressure (r = 0.40, p < 0.05). In the same group, the peak of MIP-1 alpha levels was also significantly correlated with the peak of serum creatine kinase-myocardial band (MB) (r = 0.51, p < 0.04) and left ventricular ejection fraction (LVEF) (r = -0.45, p < 0.05). After 1 month, AMI patients (n = 14) with severe left ventricular dysfunction (LVEF < or = 35%) exhibited significantly higher levels of C-C chemokines (all p < 0.05) than the other AMI patients (n = 21) (LVEF > 35%). A significant correlation was found between MIP-1 alpha levels and left ventricular end-diastolic diameter (r = 0.47, p < 0.03) in this patient population. In conclusion, we have detected a significant elevation of major C-C chemokines during the course of AMI, with the highest levels in patients with AMI complicated by heart failure manifestations and severe left ventricular dysfunction. The elevation of these chemotactic inflammatory factors may actively contribute to the pathophysiology of the disease and the subsequent left ventricular remodeling.
 ...
PMID:Serum profiles of C-C chemokines in acute myocardial infarction: possible implication in postinfarction left ventricular remodeling. 1191 5

The group of idiopathic inflammatory myopathies encompasses polymyositis, dermatomyositis and inclusion body myositis. These diseases share the following features: progressive muscle weakness, an increase in serum creatine kinase activity and the presence of mononuclear cell infiltrates in the muscle biopsy. Polymyositis, dermatomyositis and inclusion body myositis are differentiated on the basis of the distribution of muscle weakness, and specific histopathological features. Many specialties may see these patients as the clinical presentation can vary widely and may be atypical, requiring further diagnostic procedures. A 40-year-old man with a heliotrope rash and periorbital oedema, but no muscle involvement, was diagnosed with dermatomyositis sine myositis. He was successfully treated with corticosteroids but died later of cardiac failure. A 72-year-old man with a pulmonary malignancy subsequently developed the clinical features of dermatomyositis. Steroid therapy diminished the complaints but he died of pulmonary embolism. A 54-year-old woman with the clinical features of inclusion body myositis did not have rimmed vacuoles in her muscle biopsy specimen and was initially erroneously diagnosed with polymyositis, for which she was treated with corticosteroids, but without beneficial effect.
 ...
PMID:[Three patients with divergent presentations of idiopathic inflammatory myopathy]. 1203 18

Critical pathways are predefined protocols that define the crucial steps in evaluating and treating a clinical problem to improve quality of patient care, reduce variability and enhance efficiency. Critical pathways have proliferated for a variety of diagnoses, including evaluation of patients with chest pain, a common and costly complaint. This review will outline the development, implementation, and assessment of critical pathways using as a paradigm our experience with a pathway for patients presenting to the Emergency Department with acute chest pain who are at low risk of myocardial ischemia. The goals of the pathway were to expedite evaluation of low-risk patients and reduce admission rates among these patients and in the cohort overall without compromising outcomes. The pathway was developed by a multidisciplinary team in an iterative process that considered published literature, as well as the experience and consensus of local opinion leaders. Patients at least 30 years old presenting to the Emergency Department of an urban teaching hospital who were pain-free without heart failure or ischemic changes on EKG, but who were not considered appropriate for discharge by the treating physician, were eligible for the critical pathway. The pathway involved one set of creatine kinase-MB enzymes drawn at least 4 hours after pain, a 6 hour observation period after the last episode of pain and exercise testing. Outcomes during evaluation and admission rates were assessed. Clinical outcomes at 7 days and 6 months after evaluation and patient satisfaction at 7 days were also measured. Of 1363 patient visits, 145 (10.6%) were triaged by the pathway: 131 (90.3%) were discharged, 14 (9.7%) were admitted. The overall admission rate decreased from 63% (2898/4595) to 60% (819/1363) [p < 0.05] in comparison to a cohort studied prior to pathway implementation. Pathway patients reported low rates of subsequent cardiac procedures. No deaths or myocardial infarctions were recorded. At 7 days, only 2 respondents (2%) reported going to an Emergency Department since their evaluation. Most respondents (83%) rated their care as very good or excellent. Critical pathways designed to enhance efficiency, reduce variability, and improve the quality of care are becoming increasingly common. Our pathway for evaluation of patients with chest pain at low risk of myocardial ischemia was feasible and safe and was associated with a decline in absolute admission rates. Because of the possibility of concomitant secular trends and the effects of a changing medical environment, further rigorous research on the efficacy of individual pathways is needed.
 ...
PMID:Critical pathways for patients with acute chest pain at low risk. 1210 86

Myocardial contrast echocardiography is a promising diagnostic tool for detecting microvascular integrity. Multiple experimental laboratories have shown that diagnostic combined microbubble contrast and ultrasound exposure can cause vessel rupture and myocardial damage in laboratory animals. This study investigated the phenomenon of contrast ultrasonically induced myocardial damage in human beings. Twenty consecutive patients (mean age of 60 +/- 12 years, 14 men) underwent contrast echocardiography with intravenous Optison using a mechanical index of at least 1.4 (Vivid Five System (GE, Vingmed Ultrasound, Horton, Norway). Creatine kinase (CK), creatine kinase-isoenzyme MB (CK-MB); CK-MB mass, myoglobin, and troponin I were measured before and 2, 4, 8, and 24 hours after contrast echocardiography. There was no significant correlation concerning the response to contrast echocardiography for any pair of parameters at any time after the intervention. Only in 2 patients were there higher values for troponin I before and after contrast echocardiography without an increase of myoglobin, CK, or CK-MB mass and activity. These values were therefore interpreted as false positive because of renal failure and severe heart failure. The use of contrast echocardiography is without demonstrated risk of myocardial damage even in patients with different cardiologic entities.
 ...
PMID:Does contrast echocardiography with Optison induce myocardial necrosis in humans? 1237 50


<< Previous 1 2 3 4 5 6 7 8 9 10