Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among one hundred and five consecutive patients with pre-excitation (PE) syndrome studied during a 10-year period, eight had an associated hypertrophic cardiomyopathy (HC) (7.62 per cent), eight had a coronary heart disease (7.62 per cent) and nine had a hypertensive heart disease (8.57 per cent). Of the eight patients with HC, four had an asymmetrical form (three of them with an obstructive component), and four a symmetrical form. Seven of these patients had a Wolff-Parkinson-White (WPW) type of PE and the remainder a Lown-Ganong-Levine type of PE. The incidence of paroxysmal tachycardias in the total group was 56.2% (61/105) and in the patients with associated HC was 62.5% (5/8). One of these latter patients had a concomitant brady-tachy syndrome and a severe obstructive form of HC. He was surgically treated (septal myomectomy and section of accessory atrioventricular pathway). The ECGs and VCGs of the seven patients with the HC-WPW type of PE association showed the coexistence of incomplete left bundle branch block of left ventricular hypertrophy patterns. The eight patients with associated HC were closely followed up from two to seven years (total follow-up period 435 patient/months). One of them died suddenly during the 40th month of follow-up. This study suggests that: 1) HC-PE association is not infrequent; 2) the incidence of paroxysmal tachycardias in the subgroup is quite similar to that presented in isolated PE; and 3) the electrocardiographic and vectorcardiographic changes in the HC-WPW type of PE association are highly specific.
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PMID:Pre-excitation syndrome and hypertrophic cardiomyopathy. 668 36

Myocardial glucose metabolism has been shown to be heterogeneous in patients with hypertrophic cardiomyopathy (HCM). We tested the hypothesis that myocardial glucose metabolism differs between patients with HCM and those with hypertensive heart disease (HHD) associated with asymmetrical septal hypertrophy. We studied 12 patients with HCM, 7 HHD patients associated with asymmetrical septal hypertrophy using 18F 2-deoxyglucose (FDG) and positron emission tomography. We calculated % FDG fractional uptake in the inter-ventricular septum and posterolateral wall. Heterogeneity of FDG uptake was evaluated by % interregional coefficient of variation of FDG fractional uptake in each wall segment. In both the interventricular septum and posterolateral wall, % FDG fractional uptake was not significantly different between the two groups. The % interregional coefficient of variation for both interventricular septum (10.6 +/- 1.6 vs. 4.1 +/- 0.5, p < 0.01) and posterolateral wall (5.9 +/- 0.7 vs. 3.8 +/- 0.5, p < 0.05) was significantly larger in patients with HCM than in HHD patients associated with asymmetrical septal hypertrophy. Echocardiography demonstrated that the degree of asymmetrical septal hypertrophy was similar between the two groups. These results suggest that myocardial glucose metabolism may be more heterogeneous in patients with HCM compared to HHD patients associated with asymmetrical septal hypertrophy, although the left ventricular shape is similar. The difference in the heterogeneity might have resulted from differences in the pathogeneses of the two diseases.
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PMID:Myocardial glucose metabolism is different between hypertrophic cardiomyopathy and hypertensive heart disease associated with asymmetrical septal hypertrophy. 926 31

Although echocardiography is a useful diagnostic tool in hypertrophic cardiomyopathy (HCM), it is sometimes difficult to differentiate it from hypertensive heart disease (HHD): some patients with HCM show symmetrical hypertrophy, whereas patients with HHD sometimes show asymmetrical septal hypertrophy. We used a radioiodinated long-chain fatty acid tracer to visualize the altered myocardial fatty acid metabolism of HCM and HHD. Carnitine is the essential substance for the beta-oxidation of long-chain fatty acids. We recently reported that serum free carnitine levels in HCM were elevated and that they were significantly correlated with the severity of myocardial fatty acid metabolic disorder. Therefore, we investigated serum carnitine levels in patients with HCM and HHD, which can contribute to the differentiation of each other. We studied 56 patients with HCM and 20 patients with essential hypertension. Serum free carnitine levels were significantly higher in patients with HCM than those with HHD (HCM 52.5+/-9.5 nmol/mL, HHD 46.6+/-6.4 nmol/mL, P<0.01), but they showed no statistical difference between patients with HHD and normal subjects. Serum acylcarnitine levels were significantly lower in patients with HCM than those with HHD (HCM 10.1+/-4.0 nmol/mL, HHD 14.5+/-4.9 nmol/mL, P<0.0005), although they did not differ between patients with HHD and normal subjects. Scintigraphic analyses with a long-chain fatty acid analog revealed that myocardial tracer uptake was much reduced in patients with HCM compared with that in patients with HHD (quantitative analysis: HCM 2.11+/-0.12, HHD 2.22+/-0.17, P<0.05; semiquantitative analysis: HCM 13.6+/-6.3, HHD 2.0+/-1.5, P<0.0001). In conclusion, the differences in serum carnitine levels between HCM and HHD reflect altered myocardial fatty acid metabolic impairment, and the levels can help to distinguish these 2 diseases.
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PMID:Can serum carnitine levels distinguish hypertrophic cardiomyopathy from hypertensive hearts? 1094 80