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)

The incidence and the direct cause of syncope in ventricular tachycardia (VT) among patients with old myocardial infarction (OMI, n = 48), dilated cardiomyopathy (DCM, n = 18) and no evidence of heart disease (IVT, n = 43) were compared. The presence or absence of syncope in each patient was surveyed by a standardized questionnaire and a variety of electrocardiographic parameters for aggravating arrhythmias were measured. Syncope occurred in 19 of 43 OMI patients (40%), in 5 of 18 DCM patients (28%) and 6 of 43 IVT patients (14%) and significantly more often in OMI than IVT (p less than 0.01). Ventricular fibrillation (VF) was confirmed in 14 of the 19 OMI patients with syncope, in 3 of the 5 DCM patients with syncope and 1 of 6 IVT patients with syncope. The incidence of VF was significantly higher in OMI than in IVT (p less than 0.01). Mean VT cycle lengths (VTRR'm) in OMI patients with and without syncope were 0.35 +/- 0.07 sec and 0.42 +/- 0.10 sec, respectively (p less than 0.05). VTRR'ms in DCM patients with and without syncope were 0.43 +/- 0.10 sec and 0.42 +/- 0.10 sec, respectively (NS). VTRR'ms in IVT patients with and without syncope were 0.27 +/- 0.04 sec and 0.41 +/- 0.10 sec, respectively (p less than 0.01). The results show that the high frequency of VT rate was the main cause of syncope in IVT, while VF was the main cause of syncope in OMI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of ventricular tachycardia with respect to syncope in patients with old myocardial infarction, dilated cardiomyopathy and no overt heart disease. 170 81

M-mode echocardiograms were recorded from 62 giant breed dogs without historical, clinical, electrocardiographic and roentgenologic signs of heart disease, from six dogs with asymptomatic dilated cardiomyopathy (DCM, NYHA class I), and 13 dogs with symptomatic DCM (NYHA class III-IV). There was a general trend that several echocardiographic parameters were significantly in control Great Danes as compared to Newfoundlands and Irish Wolfhounds. There were substantial differences in left ventricular size both in systole and diastole and in systolic indices of the left ventricle between the control group, the asymptomatic dogs and symptomatic dogs with DCM (P = 0.0001). There was also a significant decreased in the interventricular septum thickness (P = 0.0001) and left ventricular free wall thickness in systole (P = 0.002) and diastole (P = 0.005) between the three groups. Furthermore, the left atrial/aortic ratio was significantly different between the three groups (P = 0.0001). It was concluded that this study established echocardiographic reference values in giant breed dogs which may be useful in the study of heart diseases in giant breed dogs.
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PMID:M-mode echocardiographic diagnosis of dilated cardiomyopathy in giant breed dogs. 877 4

The purpose of this study was to estimate the risk of heart diseases in pregnancy. A total of 594 patients with heart diseases treated at the National Cardiovascular Center between 1982 and 1993 were evaluated. The heart diseases were classified into eight categories: congenital heart disease with or without pulmonary hypertension (8 cases (1%) and 219 cases (37%), respectively), mitral valve prolapse (38 cases (6%)), valvular heart disease with or without valve replacement (9 cases (2%) and 54 cases (9%), respectively), arrhythmia (222 cases (37%)), cardiomyotitis (15 cases (3%)) and miscellaneous (29 cases (5%)). Maternal risk was estimated from the incidence of maternal mortality and artificial preterm delivery. Maternal death within two years after delivery was observed in 7 cases (1.2%): 4 cases with cardiomyotitis (3 DCM and 1 HCH), 2 cases with heart disease with pulmonary hypertension (1 PPH and 1 PDA), and a single case with valvular heart disease with aortic valve replacement. Artificial preterm delivery was carried out in 32 cases (5.4%), most frequently in cases with congenital heart disease with pulmonary hypertension (6/8, 75%) which follows cardiomyotitis (4/15, 27%) and cases with valvular heart disease with valve replacement (2/9, 22%). Fetal risk was measured by the incidence of fetal death, fetal growth retardation and congential heart disease of the fetus. IUFD because of maternal heart disease was observed in 4 cases: two cases with valvular heart disease with valve replacement, a single case with Marfan's syndrome and a single case with DCM. Fetal growth retardation was observed in 59 cases, most frequently in cases with congenital heart disease with pulmonary hypertension and cases with valvular heart disease with valve replacement (3/8 (38%) and 3/9 (33%), respectively). Neonatal congenital heart disease was found in 8 of 228 neonates (3.5%) whose mothers also had congenital heart disease. It is therefore suggested that intensive medical care be recommended in pregnancies complicated with congenital heart disease with pulmonary hypertension or with valvular heart disease with valve replacement, which increase both maternal and fetal risk, and in pregnancies complicated with cardiomyotitis which significantly increases the maternal risk.
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PMID:[Analysis of maternal and fetal risk in 594 pregnancies with heart disease]. 893 9

This investigation focused on whether apoptosis can be observed in some heart diseases. Apoptosis was examined immunochemically using monoclonal antibodies such as p53, Bcl-2 and cyclin E, A, and B1 in parallel with flow cytometry. Left ventricular myocardium was obtained at autopsy from 40 patients with acute myocarditis (AM; N = 10, 6 males, 4 females, mean age 56 +/- 13 years), chronic myocarditis (CM; N = 10, 5 males, 5 females, mean age 48 +/- 16 years), dilated cardiomyopathy (DCM; N = 10, 7 males, 3 females, mean age 60 +/- 11 years), and no heart disease (Cont; N = 10, 5 males, 5 females, mean age 63 +/- 14 years). Cell cycle analysis of myocytes by flow cytometry revealed that the relative content of G2M phase in acute myocarditis was far higher than those in other heart diseases (AM, 12.3 +/- 3.7%; CM, 5.2 +/- 4.5%; DCM, 6.3 +/- 4.0%; Cont, 3.4 +/- 1.8%; Mean +/- SD). Expression of p53 was observed mainly in myocytes from chronic myocarditis. Expression of Bcl-2, on the other hand, was detected in myocytes from acute myocarditis. Results suggest that apoptosis may play some role in the repairing process of myocardial inflammation.
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PMID:Stress signal to survival and apoptosis. 1041 52

Although enteroviruses have long been considered the most common cause of inflammatory heart muscle diseases, parvovirus B19 (PVB19) is emerging as a new and important candidate for myocarditis and dilated cardiomyopathy with inflammation (DCMi) and without inflammation (DCM). We investigated left ventricular endomyocardial biopsy specimens from 110 patients with suspected inflammatory heart disease for the presence of PVB19, Coxsackie virus (CVB), and adenovirus (Ad2) genome by polymerase chain reaction. Diagnosis of myocarditis (36 patients), DCM (18 patients), DCMi (13 patients), and perimyocarditis (12 patients) was made by immunohistochemical and histopathological investigation of endomyocardial biopsy specimens. A control group consisting of patients with arterial hypertension was also investigated. Prevalence of the PVB19 genome in endomyocardial biopsy specimens was highest in patients with DCMi (3 of 13) and patients with myocarditis (7 of 36); in patients with DCM and perimyocarditis, prevalence was 3 of 13 and 2 of 12, respectively. In patients with resolved myocarditis, no PVB19 DNA was detected; in patients with no inflammation and controls, prevalence was only 4% and 7%, respectively. CVB-RNA was detected in endomyocardial biopsy specimens from 3 of 37 patients with myocarditis; Ad2-DNA was found in 1 patient with DCM and 1 patient with perimyocarditis. These findings suggest an association of the PVB19 genome in endomyocardial biopsy specimens of adults with the development of DCM, DCMi, and chronic myocarditis more frequently than previously expected. PVB19 should therefore be recognized as a potential cardiotropic pathogen in patients of all ages.
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PMID:Prevalence of the parvovirus B19 genome in endomyocardial biopsy specimens. 1279 25

The definition of proper patient selection criteria remains a prominent item in constant need of attention. While the concept of gathering evidence in order to determine practice continues to be hopelessly ambiguous, it can never be emphasized too much that these univariate results are just a first foray into analysing predictors of survival; all following results should be regarded and interpreted in this perspective. HEART TRANSPLANT SURVIVAL: The 3-year survival rate for heart transplant recipients under age 16 was 83% versus 72% for adult recipients. Acutely retransplanted adult heart recipients had a 3-year survival rate of 36% compared with 72% for recipients of a first heart allograft. Patients suffering from DCM had the best survival rates at 3 years (74%) compared with patients suffering from CAD (70%) or from another end-stage heart disease (67%). With advancing age of the adult recipient, the mortality risk increased. Patients aged 16-40 had a 3-year survival rate of 77%, compared with 74%, 70% and 61% for transplant recipients aged 41-55, 56-65 and over age 65, respectively. The 3-year survival rates for adult recipients transplanted with an heart allograft from a donor aged under 16 or between 16-44 were 78% and 74%, compared with 66% and 63% for donors aged 45-55 and over 55, respectively. The 3-year survival rates for recipients of hearts with cold ischemic times under 2 hours, 2-3, 3-4, 4-5, 5-6 and more than 6 hours were 74%, 75%, 70%, 65%, 54% and 40%, respectively. Transplanting a female donor heart into a male recipient was associated with the worst prognosis: the 3-year survival rates were 73%, 71%, 66% and 76%, respectively, for the donor/recipient groups male/male, male/female, female/male and female/female, respectively. When the donor-to-recipient body weight ratio was below 0.8, the 3-year survival rate was 64%, compared to 72% for weight-matched pairs and 74% for patients who received a heart from an oversized donor (p=0.004). Better survival rates were obtained for better HLA-matched transplants. The 3-year survival rates were 75%, 89%, 78%, 78%, 69%, 72%, and 71% for HLA-A,-B,-DR zero, 1, 2, 3, 4, 5 and 6 mismatched groups, respectively (p=0.04). Survival was significantly associated with the CMV serologic status of the donor and recipient; the 3-year survival rates were: D+/R+, 71%; D+/R-, 69%; D- R-, 76%; and D-/R+, 76% (p=0.04). Patients in an ICU had a 3-year survival rate of 62%, compared to 72% for patients in a general ward and 74% for outpatients (p<0.0001). Patients that were on a VAD and there-upon transplanted had a 3-year survival rate of 65%, compared to 73% for patients without a VAD (p=0.004). Being on a ventilator was a major risk factor for death after transplantation; patients on ventilator support at the time of the transplant had a 3-year survival rate of 52% compared to 73% for the other patients (p<0.0001). LUNG TRANSPLANT SURVIVAL: The 3-year survival rate for children (73%) appeared to be better than the adult rate (61%; p=0.8). Adult lung transplant survival was significantly worse in the case of a repeat lung transplant; a 3-year retransplant survival rate of 42% was obtained compared with 61% for first transplants (p=0.049). With respect to the underlying end-stage lung disease, no statistically significant difference in long-term survival could be detected in this cohort. The 3-year survival rates were: 62% for COPD/Emphysema, 70% for CF, 58% for IPF, 64% for Alpha-1 ATD and 56% for PPH (p=0.2). Our data demonstrated no effect of the recipient's age on long-term lung transplant survival, except for 2 senior patients in this cohort. At 3-years the survival rates for recipients aged 16-40, 41-55 and 56-65 were 65%, 60% and 62%, respectively (p=0.05). The 3-year survival rates for transplants performed with lungs from donors aged under 16, 16-44, 45-55 and over 55 was 57%, 64%, 55% and 62%, respectively (p=0.1) No association between the duration of cold ischemic time and 3-year survival was observed; under 3 hours, 3-4, 4-5, 5-6 and over 6 hours of ischemia resulted in 3-year survival rates of 53%, 59%, 64%, 68% and 57%, respectively (p=0.2). Early posttransplant outcome tended to be better for gender-matched transplants, while transplanting a female donor lung into a male recipient was associated with the worst prognosis. The 3-year survival rates were 65% for male/male, 63% for male/female, 48% for female/male and 61% for female/female (p=0.009). No effect of donor-to-recipient weight match was observed in this Eurotransplant cohort; when the donor-to-recipient weight ratio was below 0.8, the 3-year survival rate was 57%, compared with 59% for weight-matched pairs and 64% for patients who received a lung from an oversized donor (p=0.5). Long-term survival after lung transplantation was influenced by HLA matching. The 3-year survival rates were 100%, 68%, 70%, 65%, 54% and 55% for the HLA-A,-B,-DR 1, 2, 3, 4, 5 and 6 mismatched groups, respectively (p=0.06). A donor CMV+ and recipient CMV- match was a risk factor for long-term mortality, with 3-year survival rates of 56% for D+/R+, 55% for D+/R-, 71% for D-/R- and 62% for D-/R+ transplants (p=0.046). En-bloc transplantation of both lungs yielded worse early results, but the 3-year survival rates for patients who underwent single (60%), bilateral sequential double lung (63%) and en-bloc double lung transplantation (56%) were not different (p=0.2). Ventilator dependency was associated with a significantly reduced survival at 3 years. Patients on a ventilator support at the time of the transplant had a 3-year survival rate of 48% compared with 63% for other patients (p=0.006).
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PMID:Three-year survival rates for all consecutive heart-only and lung-only transplants performed in Eurotransplant, 1997-1999. 1538

We sought to measure plasma endothelin-1 (ET-1) concentrations in normal dogs and to compare them with those measured in dogs with acquired heart disease with or without pulmonary edema. A sandwich enzyme-linked immunosorbent assay kit was validated and used to measure ET-1 immunoreactivity in plasma samples obtained from 32 normal dogs and 46 dogs with either dilated cardiomyopathy (DCM, n = 27) or degenerative valvular disease (CDVD, n = 19) with (n = 30) or without (n = 16) overt congestive heart failure (CHF). Plasma ET-1 concentrations (geometric mean, 95% confidence interval of geometric mean) were 1.17 (1.04-1.32) fmol/mL in the 32 normal control dogs, 1.25 (0.981-1.60) fmol/mL in 16 dogs with DCM (n = 9) or CDVD (n = 7) without CHF, and 2.51 (2.10-3.01) fmol/mL in 30 dogs with DCM (n = 18) and CDVD (n = 12) with CHE Plasma immunoreactivity of ET-1 was significantly higher in dogs with CHF in comparison with normal dogs (P < .001) and dogs with heart disease without CHF (P < .001). No significant difference was found between normal dogs and dogs with heart disease but without CHF (P > .05). Significant correlations were between plasma ET-I concentrations and left atrial:aortic ratio (P < .0001, r2 = .39), left ventricular internal dimension at end-diastole indexed to aortic diameter (P < .0001, r2 = .30) or body surface area (BSA) (P = .0071, r2 = .10), and left ventricular internal dimension at end-systole indexed to aortic diameter (P = .0003, r- = .17) or BSA (P = .0008, r2 = .15).
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PMID:Plasma endothelin-1 immunoreactivity in normal dogs and dogs with acquired heart disease. 1563 67

Mutations in the lamin A/C gene seem to be important aetiological factors in familial DCM. Heart disease caused by lamin A/C gene mutations is characterised by conduction system disorders with the need for permanent pacemaker implantations, atrial fibrillation, severe heart failure, and increased risk for sudden cardiac death. We described an asymptomatic 28-year-old man with a R190W lamin A/C gene mutation and mild left ventricular enlargement and near normal left ventricular ejection fraction who suffered from sudden cardiac death during sleeping. His electrocardiogram did not show conduction system disease and the most remarkable finding was a progressive decrease in voltage, which may be a marker of disease progression. The case study's mother had a similar phenotype to this and also had died suddenly. Sudden cardiac death in some lamin A/C gene mutations may occur even before the development of severe left ventricular dysfunction and implantable cardioverter-defibrillator should be early considered.
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PMID:Sudden death in a patient with lamin A/C gene mutation and near normal left ventricular systolic function. 1744 30

MicroRNAs are recently discovered regulators of gene expression and are becoming increasingly recognized as important regulators of heart function. Genome-wide profiling of microRNAs in human heart failure has not been reported previously. We measured expression of 428 microRNAs in 67 human left ventricular samples belonging to control (n = 10), ischemic cardiomyopathy (ICM, n = 19), dilated cardiomyopathy (DCM, n = 25), or aortic stenosis (AS, n = 13) diagnostic groups. miRNA expression between disease and control groups was compared by ANOVA with Dunnett's post hoc test. We controlled for multiple testing by estimating the false discovery rate. Out of 428 microRNAs measured, 87 were confidently detected; 43 were differentially expressed in at least one disease group. In supervised clustering, microRNA expression profiles correctly grouped samples by their clinical diagnosis, indicating that microRNA expression profiles are distinct between diagnostic groups. This was further supported by class prediction approaches, in which the class (control, ICM, DCM, AS) predicted by a microRNA-based classifier matched the clinical diagnosis 69% of the time (P < 0.001). These data show that expression of many microRNAs is altered in heart disease and that different types of heart disease are associated with distinct changes in microRNA expression. These data will guide further studies of the contribution of microRNAs to heart disease pathogenesis.
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PMID:Altered microRNA expression in human heart disease. 1784 2

Interleukin-1 (IL-1) is a potent regulator of cell proliferation, inflammation, and contraction of cardiovascular cells. It has been proposed that the IL-1/IL-1ra (IL-1 receptor antagonist) ratio influences these functions. Other members of the IL-1 family and the related caspase-1 also contribute to regulation of IL-1-mediated functions. We determined the mRNA expression of caspase-1, caspase-3, IL-1alpha , IL-1beta , IL-18, IL-1 receptor type I (IL-1-RI), and IL-1ra in left ventricle tissue of hearts from patients with ischemic or dilated cardiomyopathy (ICM or DCM) and in control tissues from unused donor transplant hearts in RT-PCR experiments. We show that the expression of caspase-1, caspase-3, IL-1beta , and IL-1-RI mRNA was not different between patients and control tissues. Furthermore, we did not find detectable amounts of IL-1alpha mRNA in any of these adult myocardial tissues. On the other hand, expression of IL-18 RNA was lower in myocardium of both patient groups compared with control hearts. Furthermore, IL-1ra mRNA expression was significantly lower in tissues of DCM patients compared with ICM patients and controls. This was in line with a trend towards lower IL-1ra protein levels in myocardial tissues of DCM patients. In contrast with the adult tissues discussed above, which did not express IL-1alpha mRNA, commercially available human fetal tissue expressed IL-1alpha mRNA. On the other hand IL-1beta mRNA was present in fetal and in adult human heart tissue. Our data provide evidence for an altered ratio of IL-1/IL-1ra in DCM patients. This dysregulation may contribute to pathogenesis and/or progression of heart disease by modulating the otherwise balanced IL-1-mediated functions in cardiovascular cells.
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PMID:Altered interleukin-1 receptor antagonist and interleukin-18 mRNA expression in myocardial tissues of patients with dilatated cardiomyopathy. 1794 66


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