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

The purpose of this study is to assess the right atrial and ventricular function by radionuclide ventriculography using continuous infusion of 81mKr in normal subjects and in patients with heart disease. 1) Reproducibility of RVEF measurement by continuous infusion of 81mKr was good (interobserver; gamma = 0.97, p less than 0.001, n = 20: intraobserver; gamma = 0.97, p less than 0.001, n = 20). This method had a excellent correlation with RVEF of 99mTc first-pass technique (gamma = 0.92, p less than 0.001, n = 20). 2) RVEF was measured in 10 normal volunteers, 76 patients with myocardial infarction (OMI), 20 patients with dilated cardiomyopathy (DCM), 5 patients with arrhythmogenic right ventricular dysplasia (ARVD) and 5 patients with primary pulmonary hypertension (PPH). In OMI and DCM, their RVEF was lower than that of normal volunteers and, in ARVD and PPH, lower than that of OMI and DCM. There was a significant inverse correlation between RVEF, mean pulmonary artery pressure and right ventricular end-diastolic volume index. 3) The effect of the location of right coronary artery (RCA) lesions on RVEF during exercise was also evaluated. Ten normal volunteers and 27 patients with OMI were studied at rest and during exercise. The patients with OMI were divided into two groups: those without proximal RCA lesions (non RCA group, n = 12) and those with proximal RCA lesions (RCA group, n = 15). Although there were no significant increases of RVEF during exercise in both group, the percent change in RVEF was less in RCA group than in non RCA group. These findings suggested that proximal RCA stenosis is a major determinant of exercise RVEF. 4) To assess the right atrial function, right atrial volume curve was measured in 10 normal volunteers, 32 patients with OMI and 4 patients with PPH. The curve was clearly divided into 4 phase; filling phase (312 +/- 40 msec), early ejection phase (276 +/- 53 msec), plateau an index of right atrial reservoir function, was 0.41 +/- 0.05 and Contractile Volume/Stroke Volume (Contr. V/SV), as an index of right atrial pump function, was 0.23 +/- 0.05 in normal volunteers. In OMI and PPH, atrial reservoir function decreased and atrial pump function increased. It was concluded that radionuclide ventriculography using continuous infusion of 81mKr was useful to assess the right heart function.
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PMID:[Assessment of right atrial and ventricular function by radionuclide ventriculography using continuous infusion of 81mKr]. 206 Sep 2

We investigated whether the isovolumic relaxation time (IRT) and an interval from the start of opening to the maximal amplitude of the anterior mitral leaflet in early diastole (D-E interval) would be useful predictors of the pulmonary capillary wedge pressure (PCWP). We recorded M-mode mitral echograms and phonocardiograms in 33 patients (aged 38-70 years) with acute myocardial infarction (AMI) in the coronary care unit and in 34 patients (aged 40-75 years) with prior myocardial infarction (OMI) during cardiac catheterization. All patients underwent the insertion of a flow-directed pulmonary artery catheter to obtain the PCWP. We measured the IRT and the D-E interval from the phonocardiograms and the M-mode echograms. There was no significant correlation between the IRT and the mean PCWP (mPCWP) in patients with AMI and in patients with OMI. The D-E interval was significantly and inversely correlated with the mPCWP (r = -0.91, p <0.0001) in all patients. The regression equation was mPCWP = -0.42 x (D-E) +47.9. The D-E interval of < or = 75 ms indicated a high mPCWP (mPCWP > or = 18 mm Hg) with high sensitivity (96%) and specificity (88%). The derived equation was tested in a prospective group of 32 additional patients (aged 43-75 years). A significant correlation was observed between the predicted and measured mPCWP (r = 0.91, p <0.0001). Thus, the PCWP can be estimated by using the D-E interval derived from M-mode mitral echograms in patients in the coronary care unit and in patients with chronic heart disease.
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PMID:Estimation of pulmonary capillary wedge pressure from M-mode mitral echograms. 919 33

To study the variation and significance of plasma coagulation factor VII (FVII) in different kinds of ischemia heart disease (IHD) and examine its relation with plasma lipid and gene polymorphism. FVIIa was determined with one stage clotting assay by using a recombinant soluble tissue factor (rsTF). FVIIc was measured with one stage clotting assay. FVIIag was quantified with an enzyme-linked immunosorbent assay (ELISA). Polymorphism was analyzed with PCR-urea-polyacrylamide gel electrophoresis. Our results showed that FVIIa in stable angina (SA), unstable angina (UA), obsolete and acute myocardial infraction (OMI, AMI) patients was higher than those of normal group with the differences being significant within any two groups. FVIIag in UA, OMI and AMI was higher than those in SA and normal groups. There were positive correlations between FVIIa and serum triglycerides, FVIIa and FVIIc, FVIIc and FVIIag. FVII-323 0/10 bp polymorphism analysis was performed in 60 patients and 0/10 bp polymorphism was found in 5 cases. FVIIc and FVIIag were much lower in cases of 0/10 bp groups than those in cases of 0/0 bp groups. It is concluded that there was activation of extrinsic coagulation pathway in every kind of IHD to different extent. FVIIa was the risk factor in the development of IHD, and more sensitive in reflecting the severity of cardiovascular disease than FVIIc or FVIIag. FVIIa was higher in OMI, which may be one of the risk factors of re-infraction. Serum triglyceride may indirectly lead to the development of IHD by increasing the level of FVIIa. FVII-323 0/10 bp polymorphism was present in Chinese patients with IHD and it was correlated with the level of FVIIc, FVIIag in plasma. 10 bp allelomorphic gene was a protective factor against thrombogenesis.
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PMID:Role of coagulation factor VII in pathogenesis of ischemic heart disease. 1735 81

Heart failure arises from diverse cardiovascular diseases, including hypertension, ischemic disease and atherosclerosis, valvular insufficiency, myocarditis, and contractile protein mutations. MicroRNAs are dysregulated in heart failure, but identification of the specific microRNAs involved remains incomplete. Here, we evaluate miR-25 expression in the peripheral blood from healthy, dilated cardiomyopathy (DCM), remote infarct (OMI), hypertensive heart disease (HHD), and HHD resulting in heart failure (HHDF) using q-PCR. Interestingly, we discovered miR-25 expression in humans is initially decreased at the onset of heart failure but is later increased in end-stage heart failure. We also show that overexpression of miR-25 in normal mice causes cardiomyocyte fibrosis and apoptosis. However, inhibition of miR-25 in normal mice led to activate renin-angiotensin system (RAS) and high blood pressure, mild heart dilation. Notably, the miR-25 cluster knock-out mice was also characterized high blood pressure and no obvious cardiac function alteration. RNA sequencing showed the alteration of miR-25 target genes in angomir-treated mice, including the renin secretion signal related gene. In vitro, cotransfection with the miR-25 antagomir repressed luciferase activity from a reporter construct containing the Pde3a and Cacnalc untranslated region. In summary, miR-25 expression during different stages of heart disease, offers a new perspective for the role of miR-25 function in heart failure.
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PMID:Alteration in microRNA-25 expression regulate cardiac function via renin secretion. 2949 4