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)

Speculations about development of tolerance to the inotropic effect of digitalis have been engendered since studies in various in vitro systems and tissues not representative of the heart have shown up-regulation of sodium potassium adenosine triphosphatase (Na,K-ATPase) when exposed to digitalis. Moreover the digitalis receptor (i.e., Na,K-ATPase) concentration in the normal, vital human left ventricle has not been previously determined. On this basis, digitalis receptor concentration was quantified in the left ventricle of explanted hearts from subjects without heart disease and from patients with end-stage heart failure who had received digitalis therapy. This was performed using vanadate-facilitated 3H-ouabain binding to intact tissue samples giving values of 728 +/- 58 (n = 5) and 467 +/- 55 pmol/g wet weight (n = 6) (mean +/- SEM) (p < 0.005), respectively. However, some of the digitalis receptors may have retained digoxin before 3H-ouabain binding and thus may have escaped detection. To eliminate this effect of retained digoxin, samples were exposed to prolonged washing in buffer containing excess digoxin antibody, a method recently shown to clear digoxin from receptors and allow subsequent complete digitalis receptor quantification by 3H-ouabain binding. After washing in digoxin specific antibody, specific digitalis receptor concentration was 760 +/- 58 pmol/g (n = 5) and 614 +/- 47 pmol/g (n = 6) wet weight in samples of the normal and failing hearts, respectively (p < 0.08). Thus, digitalization was associated with occupancy of digitalis receptors in the failing human heart of 24% (p < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:No adaptation to digitalization as evaluated by digitalis receptor (Na,K-ATPase) quantification in explanted hearts from donors without heart disease and from digitalized recipients with end-stage heart failure. 838 May 32

Sheathed microfilariae (mean length 278 +/- 10 microns SEM; mean width 7.2 +/- 0.8 microns) were detected in the blood of 7/14 housed camels (Camelus dromedarius). Microfilaraemic camels of either sex were inappetent, lethargic, reluctant to move and exhibited weakness in the hind limbs; some remained in sternal recumbency. Cardiac disorders, orchitis and skin nodules were conspicuously absent. The microfilariae showed a biphasic pattern in the blood that peaked at 20:00 and plateaued between 04:00 and 06:00. Adult filarial worms were recovered from the mesenteric and femoral arteries. Marked clinical improvement within 1-2 weeks was seen in three camels treated at 10:00 with a single subcutaneous injection of 0.2 mg/kg of ivermectin. These camels became amicrofilaraemic 2-5 days after treatment and remained so for the length of the observation period (133 days). Treatment of two camels at the time of high microfilaraemia (06:30) resulted in adverse reaction and death.
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PMID:An outbreak of cameline filariasis in the Sudan. 848 44

Changes in the circulating volume associated with haemodialysis result in modification of left ventricular loading conditions. To determine the influence of haemodialysis on Doppler indices of left ventricular filling, 12 patients (mean age 40.8 +/- 2.7 (SEM) years) with renal insufficiency but without overt heart disease were studied by Doppler-echocardiography immediately before and after haemodialysis. Haemodialysis resulted in a decrease in body weight from 68.0 +/- 3.8 kg to 65.0 +/- 3.7 kg (P < 0.01). Heart rate and blood pressure did not change significantly during haemodialysis. Left ventricular diastolic dimension (M-mode) decreased from 53.5 +/- 1.1 mm to 49.5 +/- 1.9 mm (P < 0.05), whereas the shortening fraction did not change. Haemodialysis elicited marked changes in the early diastolic rapid filling wave (E wave) recorded by pulsed Doppler at the level of the mitral annulus. Peak velocity of the early rapid filling phase (peak E) decreased significantly from 95.3 +/- 8.2 cm.s-1 to 63.0 +/- 5.7 cm.s-1 (P < 0.001) and mid-diastolic deceleration of transmitral velocity decreased from 437.3 +/- 54.2 cm.s-2 to 239.7 +/- 54.4 cm.s-2 (P < 0.01). The peak filling velocity during atrial contraction (peak A) did not change (79.7 +/- 6.3 cm.s-1 vs 74.1 +/- 4.7 cm.s-1; P = NS). The ratio peak E/peak A decreased from 1.19 +/- 0.06 to 0.85 +/- 0.04 (P < 0.01) during haemodialysis. The results provide further evidence for the pronounced preload-dependence of Doppler indices of left ventricular diastolic function.
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PMID:Effect of altered loading conditions during haemodialysis on left ventricular filling pattern. 850 59

We measured plasma concentrations of adrenomedullin (AM), a novel bioactive peptide with potent vasodilator activity, in 21 patients with chronic congestive heart failure due to various heart diseases and compared them to levels in age- and sex-matched healthy subjects to examine the pathophysiological role of plasma AM in heart failure. In addition, the relationship between plasma AM and other hormones known to control the cardiovascular system was examined in these patients. The plasma AM level in the patients with heart failure was significantly (P < 0.01) higher than that in the control subjects (mean +/- SEM, 2.94 +/- 0.15 fmol/mL; n = 16), with a significantly (P < 0.05) higher concentration in patients in class III or IV (11.82 +/- 1.81 fmol/mL; n = 5) of the New York Heart Association functional classification than in those in class I or II (8.74 +/- 0.44 fmol/mL; n = 16). There were no significant correlations between plasma AM and catecholamine levels, whereas the plasma AM level was significantly correlated with the concentrations of plasma atrial natriuretic peptide (r = 0.58; P < 0.01), brain natriuretic peptide (r = 0.47; P < 0.05), and PRA (r = 0.77; P < 0.01) in the patients. Thus, the plasma AM concentration increased in proportion to the severity of heart failure along with the hormones known to modulate the development of congestive heart failure. The present findings suggest a possible role for AM as a circulating hormone participating in the defense mechanism against further deterioration of congestive heart failure in patients with heart disease.
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PMID:Plasma adrenomedullin concentration in patients with heart failure. 855 Jul 49

To investigate the regulation of endothelin-1 (ET-1) production, cardiac catheterization was performed in young patients with congenital heart disease (27 +/- 5 months old, mean +/- SEM), and plasma levels of ET-1 in the inferior vena cava were measured by a sandwich-enzyme immunoassay. Plasma ET-1 levels of age-matched healthy controls were 1.55 +/- 0.07 pg/ml (n = 6). In patients with atrial septal defect [without pulmonary hypertension (PH)] who had volume but not pressure overload to the pulmonary circulation (PC), plasma ET-1 levels were significantly lower than in controls. In patients with PH due to ventricular septal defect (VSD) who had both volume and pressure overload to PC, the levels were significantly higher than in controls. In patients with PH and severe pulmonary congestion due to pulmonary venous stenosis (PVS), plasma ET-1 levels were significantly higher than in those with VSD, suggesting that ET-1 production is also augmented by pulmonary congestion. The present findings suggest that ET-1 production is increased by pressure overload to PC but decreased by volume overload to PC.
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PMID:Influence of pulmonary blood pressure and flow on endothelin-1 production in humans. 858 35

An insertion(I)/deletion(D) polymorphism in the angiotensin I-converting enzyme (ACE) gene seems to be associated with clinical heart disease in patients with diabetes mellitus. It is not known whether increased atherosclerosis or other factors among individuals with certain ACE-gene subtypes form the basis for the increased prevalence of heart disease among these subjects. We measured, at autopsy, the extent of macroscopically visible aortic atherosclerosis in 22 diabetic and 39 non-diabetic subjects and determined the ACE-genotype of all individuals by the polymerase chain reaction. The percentage of aortic surface area covered with atherosclerotic lesions was 29 +/- 8 (n = 6), 71 +/- 7 (n = 9), and 65 +/- 7 (n = 5) in the II-, ID-, and DD-genotype subgroups, respectively, among diabetes patients (mean +/- SEM) (2 p < 0.01, when comparing values from the ID and DD groups to the II group). The values were 37 +/- 9 (n = 11), 40 +/- 5 (n = 14) and 37 +/- 6 (n = 11) in the II-, ID-, and DD-genotypes in the non-diabetic group. There were no differences in sex ratio or age in any of the ACE-gene subtypes. The previously described relationship between heart disease and the ACE-gene polymorphism in diabetes could thus be founded in an increased extent of atherosclerosis among patients with the ID- and DD-ACE-gene subtypes. Patients with diabetes have several alterations in the composition of the collagenous components in the arterial wall. We also analysed for associations between total collagen and type IV and type V collagen content in the aortic vessel wall and the ACE-gene subtypes. We were, however, not able to disclose correlations between the polymorphism and any of these parameters. In conclusion, our data show an association between the ACE-I/D polymorphism and the degree of aortic atherosclerosis in diabetes; however, we did not observe correlations between the polymorphism and data concerning arterial collagenous components.
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PMID:Aortic atherosclerosis in diabetes mellitus is associated with an insertion/deletion polymorphism in the angiotensin I-converting enzyme gene. No relation between the polymorphism and aortic collagen content. 878 65

Cardiac transplantation has become a successful therapy for end-stage heart disease. However, increased bone loss has been observed in heart transplant recipients, sometimes being responsible for osteoporotic fractures. Glucocorticoids cause dose-related bone loss, particularly in the first 6-12 months of use, but cyclosporine might play a role as well. The evolution of bone mineral density (BMD) and biochemical parameters was prospectively assessed in 24 patients (mean age 52 years) from cardiac transplantation. All patients received cyclosporin A (CsA) and prednisone, the latter at decreasing dosage. The mean current daily dose of CsA was 321 mg and serum levels of CsA were constant. All patients received calcium (500 mg day-1) and vitamin D (1000 U day-1) for prevention of bone loss. BMD (gcm-2) was measured in 17 patients at the lumbar spine, femoral neck and total hip with dual energy X-ray absorptiometry every 6 months. Spinal BMD as well as neck and total hip BMD decreased at 6 and 12 months after transplantation, being statistically significant at the three sites: -5.6 and -3.4% for the lumbar spine, -9.3 and -8.5% for the femoral neck, -4.8% and -6.0% for the total hip respectively. Parathyroid hormone (PTH) and osteocalcin (BGP) increased by 90% and 800% respectively between pretransplantation values and 18 months after transplantation. BGP levels measured every 2 months from transplantation increased continuously from 8.7 micrograms L-1 (mean +/- SEM) before transplantation to 31.3 +/- 10.1 (P < 0.05) at 4 months, to 59.1 +/- 8.8 (P < 0.01) at 6 months and to 72.2 +/- 9.9 (P < 0.01) at 18 months (Kruskal-Wallis analysis: P < 0.0001). PTH showed a biphasic pattern with an initial decrease from 39.3 +/- 4.1 ng L-1 at baseline to 22.0 +/- 2.8 ng L-1 at 2 months, but increasing thereafter to 45.9 +/- 5.7 at 6 months and 74.2 +/- 8.9 at 18 months (Kruskal-Wallis analysis: P < 0.001). These variations represent a glucocorticoid-induced osteoporosis. In summary, cardiac transplant patients lose bone immediately after transplantation at the spine and the hip. Later on, the loss in BMD discontinues at all sites of the skeleton, but predominantly at the spine, and a few patients still lose bone at the hip. This is probably a result of the high bone turnover either due to secondary hyperparathyroidism or induced by cyclosporin A.
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PMID:Cyclosporine induces high bone turnover and may contribute to bone loss after heart transplantation. 886 16

This retrospective study analyses the clinical presentation, surgical management and early outcome of 174 patients (mean age +/- SEM: 73 +/- 15 yrs) admitted for critical limb ischaemia. 145 (84%) had tissue loss at admission: toe gangrene or ischaemic ulcer in 77, and gangrene extending beyond the forefoot in 68. 87 primary limb amputations and 107 revascularisations were performed at iliofemoral (n = 20), suprapopliteal (n = 22) or infrapopliteal level. The postoperative mortality rate was 14% in the "Amputation" group and 9% in the "Revascularisation" group but the difference was not statistically significant. Infective complications were comparable in both groups, although 5 of 14 deaths after amputation were directly related to infection and all deaths after revascularisation resulted from cardiovascular complications. The early limb salvage rate after revascularisation was 82%. 19 secondary limb amputations were performed for bypass failure. Patients in whom primary amputations were required were older (p < 0.03) and had significantly higher rates of heart disease and nonambulatory status (respectively, 24 vs 17%, p < 0.05; and 37 vs 13%, p < 0.001) than patients in whom revascularisation was performed. Ischaemic rest pain and tissue loss confined to digit gangrene or ischaemic ulcer occurred more frequently than extensive gangrene in the "Revascularisation" group (p < 0.0001), while extensive gangrene extending beyond the forefoot occurred more frequently than ischaemic rest pain and tissue loss in the "Amputation" group (p < 0.0001). Late presentation of patients and enhanced tissue loss are probably the reasons for the higher primary amputation rate in our patients compared to that observed elsewhere. In patients amenable to revascularisation (56%), arterial reconstruction for critical limb ischaemia improves the chances of limb salvage.
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PMID:Surgical management of critical limb ischaemia in the French West Indies. 986 59

The effects of (n-3) fatty acids on the postprandial state were investigated by monitoring the alimentary responses to identical test meals fed to adults [n = 11; fasting triacylglycerol (TG) 2.55 +/- 0.24 mmol/L; mean +/- SEM] after a self-selected diet baseline period (BLP) and then after a 6-wk (n-3) fatty acid period (FOP) [ approximately 5.2 g (n-3) fatty acids] and a 6-wk control oil period (COP) administered in random order. Samples were drawn immediately prior to the test meal (time 0) and then hourly from 2 to 6 h postmeal. Postprandial plasma triacylglycerol (TG) and TG-rich lipoprotein (TRL) TG apo B48, and B100 absolute concentrations were significantly lower after FOP than after COP or BLP, while plasma cholesterol was unchanged. Normalizing the results as increments over time 0 eliminated the diet effect on all but plasma TG. Time remained a significant effect for plasma TG, TRL TG, and TRL TC. Finally, only absolute TRL B48 and absolute and incremental plasma TG concentrations displayed significant time-diet interactions. These results suggest that postprandial TRL apo B reductions are likely caused by (n-3) fatty acid suppression of both hepatic and intestinal apoB secretion/synthesis. Altered TRL metabolism, i.e. changes in postprandial TG, cholesterol, apo B48, and increase in LDL particle size, may represent an additional mechanism for the reduced heart disease risk associated with fish [(n-3) fatty acid] consumption.
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PMID:(n-3) fatty acid supplementation in moderately hypertriglyceridemic adults changes postprandial lipid and apolipoprotein B responses to a standardized test meal. 1035 76

Flavonoids are components of fruits, vegetables and wines. An abundance of flavonoids in the diet is correlated with reduced heart disease mortality, suggesting that they act as protective nutrients. However, little is known about the absorption and metabolism of flavonoids after normal foods are consumed. This study measured the levels of one abundant flavonoid, (+)-catechin, and its metabolites in plasma after five male and four female volunteers consumed 120 mL of red wine (RW) one day and de-alcoholized red wine (DRW) on a separate day. Each wine sample contained 35 +/- 1 mg catechin (mean +/- SEM). Plasma levels of catechin and its metabolite 3'-O-methylcatechin (3'MC) were determined by gas chromatography-mass spectrometry (GC-MS) of the trimethylsilylated (TMS) derivatives. Glucuronide and sulfate conjugates were determined after enzymatic hydrolysis. Before RW or DRW consumption, plasma levels of catechin, 3'MC and all conjugates were <2 nmol/L. After 1 h, average levels of catechin, 3'MC and all conjugates increased to 91 +/- 14 nmol/L (RW) and 81 +/- 11 nmol/L (DRW). At 1 h, 21 +/- 1% of the metabolites were methylated and <2% of catechin and 3'MC were unconjugated. Catechin was present as both a sulfate conjugate and a conjugate containing both glucuronide and sulfate residues. 3'MC was present primarily as a glucuronide conjugate. At every time point, catechin was present almost exclusively as metabolites, and these levels were independent of ethanol. Therefore, if flavonoids are protective nutrients, the active forms are likely to be metabolites, which are far more abundant in plasma than the forms that exist in foods.
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PMID:Catechin is present as metabolites in human plasma after consumption of red wine. 1046 Feb 1


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