Cardiomegaly ; Humans ; Signal Transduction

This study introduced the deep researches on the diagnosis of left ventricular hypertrophy by electrocardiogram (ECG) and cardiac ultrasound as well as treatment of the left ventricular hypertrophy due to hypertension including drug therapy and non drug therapy
Hypertrophy, Left Ventricular ; Cardiomegaly ; hypertension

Animals ; Cardiomegaly ; Constriction ; Heart ; Mice

A Kinase Anchor Proteins ; Cardiomegaly ; metabolism ; Humans

Left ventricular remodeling index (LVRI) was assessed in patients with hypertensive heart disease (HHD) and coronary artery disease (CAD) by real-time three-dimensional echocardiography (RT3DE). RT3DE data of 18 patients with HHD, 20 patients with CAD and 22 normal controls (NC) were acquired. Left ventricular end-diastolic volume (EDV) and left ventricular end-diastolic epicardial volume (EDVepi ) were detected by RT3DE and two-dimensional echocardiography Simpson biplane method (2DE). LVRI (left ventricular mass /EDV) was calculated and compared. The results showed that LVRI measurements detected by RT3DE and 2DE showed significant differences inter-groups (P<0.01). There was no significant difference in NC group (P>0.05), but significant difference in HHD and CAD intra-group (P<0.05). There was good positive correlations between LVRI detected by RT3DE and 2DE in NC and HHD groups (r=0.69, P<0.01; r=0.68, P<0.01), but no significant correlation in CAD group (r=0.30, P>0.05). It was concluded that LVRI derived from RT3DE as a new index for evaluating left ventricular remodeling can provide more superiority to LVRI derived from 2DE.
Cardiomegaly/etiology ; Cardiomegaly/pathology ; Cardiomegaly/*ultrasonography ; Coronary Artery Disease/pathology ; Coronary Artery Disease/*ultrasonography ; Echocardiography, Three-Dimensional/*methods ; Hypertension/*complications ; Hypertension/ultrasonography ; Ventricular Remodeling/*physiology

Roentgenograms of the chest were reviewed from 122 childrens with acute glomeruloneph ritis. Abnormalities were found in 110 roentgenograms. These included cardiomegaly in 82(67.2%), prominent pulmonary vasculature in 98(80.3%), pleural effusion in 35(28.6%), pulmonary edema in 24(19.6%), and pulmonary consolidation in 20(16.3%). The roentgen findings in the chest, although not pathognomic, may have diagnostic values occasionally.
Cardiomegaly ; Child* ; Humans ; Pleural Effusion ; Pulmonary Edema ; Thorax*

We report an extremely specific case of Pendred's syndrome, originally described with an association of thyroid organification defect and hearing impairment; normal-sized thyroid, severe hypothyroidism manifested by profoundly retarded physical and mental development, cardiomegaly and severe hypochromic & microcytic anemia associated with asymmetrical septal hypertrophy.
Adolescent* ; Anemia* ; Cardiomegaly ; Hearing Loss ; Humans ; Hypertrophy* ; Hypothyroidism ; Thyroid Gland

OBJECTIVETo find the characteristic parameters from electrocardiogram (ECG) which is most related to pathological progress, surface ECG was performed in mice at 2, 5, 9 and 13 week post surgery.

METHODSElectrocardiogram recordings: The mice were anaesthetized with tribromoethanol (250 mg/kg, i.p.). Lead II surface ECG were acquired by using the Biopac System MP150 at a rate of 5 kHz.

RESULTS(1) No arrhythmia was observed in Sham and 2-week Band mice. Spontaneous arrhythmias were observed in ECG recordings, with an incidence of 15%, 28% and 63% in 5-, 9- and 13-week Band mice, respectively. Tachyarrhythmias, such as frequent premature ventricular extrasystole, bigeminy, trigeminy, and paroxysmal tachycardia were found. (2) Analysis of ECG recordings revealed a significant prolongation of QT and QTc intervals. Compared with age-matched Sham mice, the increment in QT and QTc intervals was 20.4%, 32.7%, 49.7%, 61.0% and 27.1%, 32.1%, 43.9%, 59.1% at 2, 5, 9 and 13 week, respectively (P < 0.01). (3) The characteristic change in electrocardiogram was on the J wave. The amplitude of J wave was upward in Sham mice, and it was significantly flattened or inverted in Band mice. (4) Except that RR interval at 2 week showed a slight decrease, there was no significant change in PR interval and RR interval in Band mice.

CONCLUSIONIn the present study, we found that the increase incidence of spontaneous arrhythmias, prologation of QT interval and changes in the amplitude of the J wave in the surface ECG during progression of mouse cardiac hypertrophy and failure, and the progressive pattern indicated that a gradual aggravation of the ventricular repolarization delay in this mouse model.

Tricuspid regurgitation(TR) with normal heart structure during fetal life is a frequent functional phenomenon with a prevalence of six to seven percent. Isolated severe congenital TR, however, is an uncommon cause of neonatal congestive heart failure, cyanosis and massive cardiomegaly. We experienced a case of severe transient neonatal TR presented as massive cardiomegaly during fetal life which was normalized in the postnatal period.
Cardiomegaly* ; Cyanosis ; Heart ; Heart Failure ; Prevalence ; Tricuspid Valve Insufficiency*

Cardiac hypertrophy contributes an increased risk to major cerebrovascular events. However, the molecular mechanisms underlying cerebrovascular dysfunction during cardiac hypertrophy have not yet been characterized. In the present study, we examined the molecular mechanism of isoproterenol (ISO) -evoked activation of Ras/Raf/MAPK pathways as well as PKA activity in cerebral artery of rabbits, and we also studied whether the activations of these signaling pathways were altered in cerebral artery, during ISO-induced cardiac hypertrophy compared to heart itself. The results show that the mRNA level of c-fos (not c-jun and c-myc) in heart and these genes in cerebral artery were considerably increased during cardiac hypertrophy. These results that the PKA activity and activations of Ras/Raf/ERK cascade as well as c-fos expression in rabbit heart during cardiac hypertrophy were consistent with previous reports. Interestingly, however, we also showed a novel finding that the decreased PKA activity might have differential effects on Ras and Raf expression in cerebral artery during cardiac hypertrophy. In conclusion, there are differences in molecular mechanisms between heart and cerebral artery during cardiac hypertrophy when stimulated with beta2 adrenoreceptor (AR), suggesting a possible mechanism underlying cerebrovascular dysfunction during cardiac hypertrophy.
Cardiomegaly* ; Cerebral Arteries* ; Heart* ; Isoproterenol ; Rabbits ; RNA, Messenger