Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heart disease is the leading cause of mortality and morbidity in the world. As such, biomarkers are needed for the diagnosis, prognosis, therapeutic monitoring and risk stratification of acute injury (acute myocardial infarction (AMI)) and chronic disease (heart failure). The procedure for biomarker development involves the discovery, validation, and translation into clinical practice of a panel of candidate proteins to monitor risk of heart disease. Two types of biomarkers are possible; heart-specific and cardiovascular pulmonary system monitoring markers. Here we review the use of MS in the process of cardiac biomarker discovery and validation by proteomic analysis of cardiac myocytes/tissue or serum/plasma. An example of the use of MS in biomarker discovery is given in which the albumin binding protein sub-proteome was examined using MALDI-TOF MS/MS. Additionally, an example of MS in protein validation is given using affinity surface enhanced laser desorption ionization (SELDI) to monitor the disease-induced post-translational modification and the ternary status of myocyte-originating protein, cardiac troponin I in serum.
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PMID:Heart disease, clinical proteomics and mass spectrometry. 1550 50

We studied 193 patients free of heart disease to determine the relation between QRS amplitude and serum albumin. Although there were no significant differences in echocardiographic indexes between the 2 groups, albumin (35.1 +/- 4.3 vs 40.1 +/- 3.2 g/L) and colloid osmotic pressure (21 +/- 4 vs 24 +/- 3 mm Hg) were significantly lower in patients with low voltages compared with those without. Moreover, there was a good relation (r = 0.78) between change in QRS amplitude and change in albumin concentration.
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PMID:Effect of serum albumin on QRS wave amplitude in patients free of heart disease. 1575 15

Mild elevations in liver chemistry tests such as alanine transaminase and aspartate transaminase can reveal serious underlying conditions or have transient and benign etiologies. Potential causes of liver transaminase elevations include viral hepatitis, alcohol use, medication use, steatosis or steatohepatitis, and cirrhosis. The history should be thorough, with special attention given to the use of medications, vitamins, herbs, drugs, and alcohol; family history; and any history of blood-product transfusions. Other common health conditions, such as diabetes, heart disease, and thyroid disease, can cause or augment liver transaminase elevations. The recent American Gastroenterological Association guideline regarding the evaluation and management of abnormal liver chemistry tests proposes a practical, algorithmic approach when the history and physical examination do not reveal the cause. In addition to liver chemistries, an initial serologic evaluation includes a prothrombin time; albumin; complete blood count with platelets; hepatitis A, B, and C serologies; and iron studies. Depending on the etiology, management strategies may include cessation of alcohol use, attention to medications, control of diabetes, and modification of lifestyle factors such as obesity. If elevations persist after an appropriate period of observation, further testing may include ultrasonography and other serum studies. In some cases, biopsy may be indicated.
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PMID:Mildly elevated liver transaminase levels in the asymptomatic patient. 1579 89

Considerable effort by clinicians and scientists focuses on the utility of biomarkers to prevent, diagnose and manage adverse cardiac events as well as provide information on a specific patient's underlying pathology. Although troponins I and T (TnI and TnT) are cardiac specific markers that yield diagnostic and prognostic value in patients with myocardial injury, troponins cannot be utilized in all clinical settings. Troponins have limited utility for the diagnosis of early ischemia and preoperative myocardial infarction. Troponin T also lacks specificity in patients with renal failure. New markers, such as ischemia modified albumin (IMA) and CD40 ligand, and new technologies, such as proteomics, are under investigation to advance our knowledge of heart disease.
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PMID:Laboratory diagnosis of acute myocardial injury. 1591 1

Neutrophil-induced coronary microvascular barrier dysfunction is an important pathophysiological event in heart disease. Currently, the precise cellular and molecular mechanisms of neutrophil-induced microvascular leakage are not clear. The aim of this study was to test the hypothesis that rho kinase (ROCK) increases coronary venular permeability in association with elevated endothelial tension. We assessed permeability to albumin (P(a)) in isolated porcine coronary venules and in coronary venular endothelial cell (CVEC) monolayers. Endothelial barrier function was also evaluated by measuring transendothelial electrical resistance (TER) of CVEC monolayers. In parallel, we measured isometric tension of CVECs grown on collagen gels. Transference of constitutively active (ca)-ROCK protein into isolated coronary venules or CVEC monolayers caused a significant increase in P(a) and decreased TER in CVECs. The ROCK inhibitor Y-27632 blocked the ca-ROCK-induced changes. C5a-activated neutrophils (10(6)/ml) also significantly elevated venular P(a), which was dose-dependently inhibited by Y-27632 and a structurally distinct ROCK inhibitor, H-1152. In CVEC monolayers, activated neutrophils increased permeability with a concomitant elevation in isometric tension, both of which were inhibited by Y-27632 or H-1152. Treatment with ca-ROCK also significantly increased CVEC monolayer permeability and isometric tension, coupled with actin polymerization and elevated phosphorylation of myosin regulatory light chain on Thr18/Ser19. The data suggest that during neutrophil activation, ROCK promotes microvascular leakage in association with actin-myosin-mediated tension development in endothelial cells.
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PMID:Involvement of ROCK-mediated endothelial tension development in neutrophil-stimulated microvascular leakage. 1617 66

This study investigated mortality in 568 individuals from the Goessel Mennonite community in rural central Kansas. There were three main objectives to this research: 1) characterize mortality trends within a biologically well-defined Mennonite community; 2) determine what biochemical, morphological, and physiological risk factors could be related to all-cause mortality, stratified by age and sex; and 3) compare these results to previously described variables that were associated with both biological age and mortality in this population. Mortality data were obtained from three sources: Kansas Vital Records, the Social Security death index, and church records. In total, 221 (39%) individuals were found to have died in this population between January 1980-June 2002. Analogous to the larger US population, the three leading causes of death in this community were heart disease, cancer, and stroke, accounting for 60% of all deaths. Besides advancing age, the greatest biological risk factor in this population was decreased amounts of albumin in men (relative risk, 2.47), potentially indicating underreported cases of either chronic kidney disease or frailty syndrome for males. Cox proportional hazard models demonstrated that increased amounts of total cholesterol may provide a protective effect for elderly individuals. We conclude, based on the previously described heritability of both albumin (h(2) = 0.40) and total cholesterol (h(2) = 0.50) in this population, that underlying genetic factors associated with both chronic degenerative diseases and biological aging may have important implications for understanding mortality patterns in this community.
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PMID:Biological aging and Cox hazard analysis of mortality trends in a Mennonite community from south-central Kansas. 1663 24

Kawasaki disease (KD) is an acute febrile vasculitic syndrome of unknown etiology that preferentially affects the coronary artery. Interleukin-10 (IL-10) is a key proinflammatory cytokine, and a polymorphism near the major transcriptional start site of the IL-10 gene was shown to influence IL-10 production in vitro. This study investigated the association of the IL-10 promoter polymorphism with KD and its clinical parameters in Korean children. A total of 194 children with congenital heart disease (CHD) and 95 children with KD were included in this study. IL-10 (-627 A/C) polymorphism genotypes were determined using the single-base extension method. There was no difference in the allele frequencies of IL-10 (-627 A/C) polymorphism between CHD children and KD children. KD children with one or two copies of the IL-10 (-627C) allele showed significantly lower albumin levels (p = 0.020) and higher frequencies of early coronary artery aneurysm [62.22% versus 37.78%, adjusted odds ratio (aOR) = 3.50, 95% confidence interval (CI): 1.50-8.16] compared with KD children with the common IL-10 (-627A) allele. These findings suggest that the IL-10 (-627 A/C) promoter polymorphism might be a genetic marker for the risk of early coronary artery complication in KD.
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PMID:The IL-10 (-627 A/C) promoter polymorphism may be associated with coronary aneurysms and low serum albumin in Korean children with Kawasaki disease. 1741 67

This study focus on predicting factors of survival possible to modify by nursing care, and the incidence and mortality rate of nursing-home-acquired pneumonia, allocated to 1, 2 and 3 years of follow ups. The residents consisted of 156 women and 78 men living in special housing for the elderly. Data on chronic disease and medication were obtained at baseline, and activities of daily living (ADL) status, nutritional status and body temperature were assessed. The incidence of pneumonia was noted prospectively for 1 year and retrospectively for the following 2 years. Predictive factors for survival were explored by Cox hazard regression analysis. The results showed that age, functional and cognitive impairment were predictors of mortality irrespective of gender, while poor nutritional status in women and chronic obstructive pulmonary disease, heart disease and medication with sedatives in men were gender-specific predictors. ADL correlated positively with dementia and negatively with S-albumin irrespective of gender, while malnutrition correlated positively with ADL in women and positively with chronic obstructive pulmonary disease in men. To promote the quality of daily living in elderly individuals, it is of importance to improve the capabilities in daily functions and nutritional status, especially in women with functional impairment, and to prevent anxiety particularly in men. The findings also clarify that pneumonia is as common as cerebral vascular insult and heart failure as cause of death in this population.
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PMID:Gender differences in predictors of survival in elderly nursing-home residents: a 3-year follow up. 1742 10

The objective was to identify abdominal lymphatic malformations in pediatric patients with protein-losing enteropathy after palliation of complex congenital heart disease with total cavo-pulmonary connection (TCPC). In 2006, we performed complete hemodynamic and laboratory workup and thoracic and abdominal MRT screens in three patients who newly presented with symptoms of protein-losing enteropathy. All three patients, aged 3, 5, and 7 years, showed excellent TCPC hemodynamics with central venous pressures of 10-13 mm Hg. None of the patients had right-to-left overflow. All three patients showed extensive thoracic and mesenterial lymphangiomatosis. One patient died after 18 months of therapy, which included long-term parenteral nutrition, somatostatin, subcutaneous heparin injections, and frequent albumin and immunoglobulin substitution. The other two patients are in stable condition. Lymphangiomatosis might play an unknown role in the pathogenesis of protein-losing enteropathy after TCPC. It remains unclear whether lymphangiomatosis is a primary congenital disease related to the cardiac disease or if it is triggered by repeated surgery or venous congestion. The presence of lymphangiomatosis should be given diagnostic and therapeutic consideration in TCPC patients in the future.
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PMID:First description of three patients with multifocal lymphangiomatosis and protein-losing enteropathy following palliation of complex congenital heart disease with total cavo-pulmonary connection. 1932 2

We report a case of pseudocirrhosis arising in the setting of regression of liver metastases from pancreatic cancer. A 55-year-old asymptomatic woman presented to our clinic with newly diagnosed metastatic pancreatic cancer with extensive liver metastases. She underwent systemic chemotherapy with gemcitabine and oxaliplatin (GEMOX). After 8 cycles of therapy, she had a remarkable response to the therapy evidenced by decline of carcinoembryonic antigen (CEA) and CA19 by > 50% and nearly complete resolution of hepatic metastases in computed tomography (CT) scan. Shortly after, she developed increasing bilateral ankle edema and ascites, associated with dyspnea, progressive weight gain, and declining performance status. Gemcitabine and oxaliplatin were discontinued as other causes of her symptoms such as congestive heart disease or venous thrombosis were ruled out. CT scan 6 mo after the initiation of GEMOX revealed worsening ascites with a stable pancreatic mass. However, it also revealed a lobular hepatic contour, segmental atrophy, and capsular retraction mimicking the appearance of cirrhosis. She was managed with aggressive diuresis and albumin infusions which eventually resulted in a resolution of the above-mentioned symptoms as well as complete resolution of pseudocirrhotic appearance of the liver and ascites in CT scan. This case demonstrates that pancreatic cancer patients can develop pseudocirrhosis. Clinicians and radiologist should be well aware of this entity as early recognition and management can lead to a near complete recovery of liver function and much improved quality of life as illustrated in this case.
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PMID:Pseudocirrhosis in a pancreatic cancer patient with liver metastases: a case report of complete resolution of pseudocirrhosis with an early recognition and management. 1833 Sep 59


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