Aged, 80 and over ; Cardiomegaly ; etiology ; pathology ; Cerebrovascular Disorders ; etiology ; Humans ; Hypertension ; complications ; pathology ; Proteinuria ; etiology ; pathology

Cardiac autophagy dramatically increases in heart failure induced by sustained pressure overload. However, it has not yet been addressed if enhanced autophagy plays a role in protecting myocardium or mediating progression from compensative hypertrophy to heart failure. The aim of the present study was to detect autophagic flux of cardiomyocytes from 20-week transverse abdominal aortic constriction (TAC) rats. Fasting rats were used as the positive control for detecting cardiac autophagy. Echocardiography was applied to find the changes of cardiac structure and function. Immunofluorescent histochemistry and Western blot were used to analyze the related biomolecular indexes reflecting cardiac autophagic flux. After the previous methods for detecting cardiac autophagy were confirmed, the autophagic flux in cardiomyocytes of rats subjected to 20-week TAC was examined. The results showed that fasting had no obvious influence on parameters of cardiac structure in rats, including interventricular septal wall thickness and left ventricle posterior wall thickness, but heart rate, diastolic left ventricle internal dimension, fractional shortening of left ventricle dimension, ejection fraction and mitral inflow velocity decreased in rats after fasting for 3 d. Meanwhile, positively stained particles of LC3 and cathepsin D, but not ubiquitin and complement 9, distributed within cardiomyocytes of 3-day fasting rats, indicating augmented autophagic flux. Compared with sham rats, 20-week TAC rats did not show any changes of LC3, cathepsin D, ubiquitin and complement 9 in myocardium detected by immunofluorescent histochemistry. In addition, protein levels of LC3, cathepsin D and p62 in myocardium of TAC rats did not changed. These results reveal the unchanged autophagic flux in cardiomyocytes at middle or late phase of cardiac hypertrophy in TAC rats, implying a balance between inhibition of hypertrophy and activation of pressure load stress on autophagy.
Animals ; Aorta ; pathology ; Autophagy ; Cardiomegaly ; physiopathology ; Constriction ; Heart ; physiopathology ; Myocardium ; pathology ; Myocytes, Cardiac ; cytology ; Rats

OBJECTIVETo study the morphologic classification and its clinical significance of giant left atrium (GLA) combined with mitral valvular disease.

METHODSBetween January 1993 and December 1999, a total of 62 consecutive patients with mitral valvular disease, whose preoperative left atrial endodiastolic volume index >/= 300 ml/m(2) or endosystolic diameter >/= 6.0 cm, were enrolled as research candidates. Morphologically, GLA was classified by Q Hierarchical cluster analysis according to the right or left side cardiothoracic ratio of the left atrium (r- or l-LATR) on an anteroposterior chest roentgenogram and the ratio of the distant diameter of the left main bronchus to the approximate diameter of the left main bronchus (LBDd/Dp) or to the trachea (LB/TR) on an left anterior oblique chest roentgenogram.

RESULTSAccording to r-LATR and l-LATR, the morphology of GLA was classified clinically into three types: type L (l-LATR >/= 0.6 and r-LATR < 0.58), type R (r-LATR >/= 0.58 and l-LATR < 0.6) and type B (r-LATR >/= 0.58 and l-LATR >/= 0.6). According to LBDd/Dp and LB/TR, GLA in type L and B was further classified into two subtypes, respectively: left posterior downward type (L(I) and B(I)), in which LBDd/Dp is equal or exceeds 0.38 or LB/TR is equal or exceeds 0.33, and left posterior upward type (L(II) and B(II)), in which LBDd/Dp is less than 0.38 or LB/TR less than 0.33.

CONCLUSIONThe morphologic classification of GLA may represent the main pathophysiological changes of GLA and might be a guideline for the selection of the optimal plication procedures of GLA in patients with valve diseases.

Adolescent ; Adult ; Cardiomegaly ; pathology ; Female ; Heart Atria ; pathology ; Humans ; Male ; Middle Aged ; Mitral Valve Insufficiency ; pathology ; Mitral Valve Stenosis ; pathology

Animals ; Apoptosis ; Cardiomegaly ; metabolism ; pathology ; Glycogen Synthase Kinase 3 ; metabolism ; Mice ; Mice, Transgenic ; Myocytes, Cardiac ; cytology

OBJECTIVETo see the change of capillary of heart in Athlete's Heart, so that to discover the mechanism of pathologic change.

METHOD18 male SD rats were separated randomly into control group (without any exercise), aerobic exercise group (swimming for 75 min every day), and overload group (swimming for 180 min with 5% weight of its body every day). After 5 days per week, 12 weeks, exercise training stopped and heart of rats were observed under Transmission Electron Microscope.

RESULTSIn aerobic exercise group, the capillary cavities in heart expand, the walls of capillary become thick; the number of mitochondrion increases; endothelium cells become active in growth. However, after overload exercise, the walls of capillary cockle and protuberances appear. The mitochondrion swell and the cristae become disorder. Most of endosomes expand and their number increases. The karyons become abnormity in shape and uniformity in electronic density, besides the nuclear envelope cockle. The basilar membranes become thick and unclear.

CONCLUSIONAfter exercise training, both physical and pathologic changes in heart capillary are found. In suitable exercises group, the capillaries change physically; the pathologic changes are becoming visible after overload exercise however.

Animals ; Capillaries ; ultrastructure ; Cardiomegaly ; etiology ; pathology ; Male ; Physical Conditioning, Animal ; adverse effects ; Physical Endurance ; Rats ; Rats, Sprague-Dawley ; Sports

OBJECTIVETo map and compare the right atrium in patients with AF to those with atrioventricular nodal reentrant tachycardias (AVNRT, as control group) and to investigate the anatomical and electrophysiological abnormality of the right atrium in AF.

METHODSThe anatomy and electrophysiology of right atrium and cavotricuspid isthmus were evaluated in 20 patients with AF (16 M/4 F, mean age 55.9 +/- 10.68 years) and 26 patients with AVNRT (9 M/17 F, mean age 47.50 +/- 19.56 years) during coronary sinus pacing at 600 ms prior to ablation with electro-anatomical mapping system. Right atrial volume (RAV), the length and width of cavotricuspid isthmus (IsL, IsW), unipolar and bipolar voltage in the right atrium (UniV-RA, BiV-RA) were measured and compared between patients with AF and those with AVNRT.

RESULTSRAV, IsL, IsW, UniV-RA, and BiV-RA were 143.22 +/- 40.72 vs 104.35 +/- 21.06 ml, 39.31 +/- 8.10 vs 32.42 +/- 9.77 mm, 30.54 +/- 7.48 vs 23.15 +/- 6.61 mm, 1.96 +/- 1.24 vs 1.53 +/- 0.91 mv and 1.47 +/- 1.47 vs 1.29 +/- 1.12 mv in AF and AVNRT respectively.

CONCLUSIONThe right atrial volume is larger; both the length and width of cavotricuspid isthmus are greater. Unipolar and bipolar voltages in the right atrium are higher in AF than in AVNRT, suggesting that the enlarged right atrium, increased length and width of cavotricuspid isthmus, and concomitant atrial hypertrophy are important substrates for initiation and perpetuation of typical AF.

Adult ; Aged ; Atrial Flutter ; etiology ; pathology ; physiopathology ; Cardiomegaly ; complications ; Female ; Heart Atria ; pathology ; physiopathology ; Humans ; Male ; Middle Aged ; Tachycardia, Atrioventricular Nodal Reentry ; pathology ; physiopathology

OBJECTIVETo explore the pathogenic changes of myocardial apoptosis in heart hypertrophy during hypertension and evaluate the anti-apoptosis effect of Valsartan.

METHODSThirty spontaneously hypertensive rats (SHRs) were divided into two groups: 15 treated with Valsartan (20 mg x kg(-1) x d(-1)) (SHR + Valsartan group), the others with placebo (SHR + placebo group), with 15 normal Wistar rats as control. Systolic blood pressure was measured by the tail-cuff method. The observation period was from 8 to 16 weeks of age. Cardiac apoptosis was evaluated by a Terminal Deoxynucleotidyl Transferase-Mediated dUTP-biotin Nick End Labeling (TUNEL) assay.

RESULTSMean blood pressure values were 127 +/- 2 mm Hg in controls, 163 +/- 6 mm Hg in the SHR + Valsartan group and 193 +/- 7 mm Hg in the SHR + placebo group at 16 weeks of age, whereas the blood pressure in 8-week-old SHR and Wistar rats were 175 +/- 3 mm Hg and 125 +/- 5 mm Hg, respectively. The ratio of the heart weight over body weight declined in Wistar (3.07 +/- 0.03 mg/g) and SHR + Valsartan groups (3.22 +/- 0.19 mg/g) compared with the SHR + placebo group (4.02 +/- 0.31 mg/g) (P < 0.05). The density of TUNEL-positive cells in Wistar and SHR +/- Valsartan groups was 23.3 +/- 3.3 nuclei/HPF and 35.0 +/- 1.3 nuclei/HPF, both of which were significantly less than that of the SHR + placebo group (116.7 +/- 11.3 nuclei/HPF).

CONCLUSIONSIn response to chronic pressure overload, cardiomyocyte-specific apoptosis contributes to the transition from compensatory hypertrophy to decompensation. Apoptosis may be effectively inhibited by Valsartan in the early stage of hypertension.

Animals ; Antihypertensive Agents ; pharmacology ; Apoptosis ; drug effects ; Cardiomegaly ; pathology ; Hypertension ; pathology ; Myocardium ; cytology ; Rats ; Rats, Inbred SHR ; Rats, Wistar ; Tetrazoles ; pharmacology ; Valine ; analogs & derivatives ; pharmacology ; Valsartan

OBJECTIVETo observe the effect of angiotensin II (Ang II) on calreticulin (CRT) expression and its association with mitochondrial dysfunction in cardiomyocytes.

METHODSPrimary neonatal rat cardiomyocytes were randomly divided into CRT siRNA group, control siRNA group, control group, Ang II+ CRT siRNA group, Ang II+ control siRNA group and Ang II group. The cell surface area, protein synthesis rate, mitochondrial membrane potential level, enzyme activities, and CRT expression were observed.

RESULTSCompared with those in the control group, the cell surface area and protein synthesis rate were both increased and mitochondrial membrane potential level and enzyme activities decreased in Ang II groups. CRT expression was significantly down-regulated in Ang II+ CRT siRNA group with increased cell surface area, protein synthesis rate, mitochondrial membrane potential level and enzyme activities as compared with those in Ang II+ control siRNA group.

CONCLUSIONAng II up-regulates CRT expression to induce mitochondrial injury, which may be an important mechanism of myocardial hypertrophy.

Angiotensin II ; pharmacology ; Animals ; Calreticulin ; metabolism ; Cardiomegaly ; Cells, Cultured ; Membrane Potential, Mitochondrial ; Mitochondria ; pathology ; Myocytes, Cardiac ; pathology ; Protein Biosynthesis ; RNA, Small Interfering ; Rats

Cardiac enlargement is an important symptom of vascular and heart disease. The cardiothoracic ratio (CTR) is an important index used to measure the size of heart. The aim of this study was to assess the relationship between aging and cardiothoracic ratio. This paper also presents an improved C-V level set method to segment lung tissue based on X-ray image, which used to automatically compute CTR. In the investigation carried out in our school, we got more than 3 120 chest radiographs from medical examination of the working population in Beijing, and we systematically studied the effects of age and gender on the CTR to obtain reference values for each group. The reference values established in this study can be useful for recording and quantifying the cardiac enlargement, so that it may be useful for calling attention to the cardiovascular diseases and the heart diseases.
Aging ; Algorithms ; Cardiomegaly ; pathology ; Heart ; diagnostic imaging ; Heart Diseases ; diagnosis ; Humans ; Lung ; diagnostic imaging ; Myocardium ; pathology ; Radiography, Thoracic ; methods ; Reference Values

To investigate the cellular mechanisms of pressure-overload cardiac hypertrophy transition to heart failure, we observed time course of changes in morphology and contractile function of cardiomyocytes in transverse abdominal aortic constriction (TAC) rats. Since TAC rats suffered higher stress, body weight had a slower growth rate compared with that of synchronous control rats. Therefore, the left ventricular to body weight ratio produced experimental bias to evaluate the degree of cardiac hypertrophy. Length and width of collagenase-isolated cardiomyocyte were directly measured. Length, width and calculated surface area of cardiomyocyte showed a progressive increase in 8-, 16-, and 20-week TAC rats. The increasing rate of surface area in cardiomyocytes was higher at the middle stage of TAC (from the eighth to sixteenth week). Due to the constraint of fibrosis formation, the increasing rate of surface area in cardiomyocytes was slower at the late stage of TAC (from the sixteenth to twentieth week). The sarcomere length of cardiomyocytes was unchanged, whereas sarcomere numbers were significantly increased in 8-, 16-, and 20-week TAC rats. Shortening amplitude of unloaded contraction in single cardiomyocyte was significantly enhanced in 1-week TAC rats, but not altered in 8-week TAC rats compared with that in the synchronous control rats. On the contrary, unloaded shortening amplitude of single cardiomyocyte was significantly reduced in 16- and 20-week TAC rats. The above results suggest that the reduced shortening amplitude may be associated with intrinsic molecular alterations in hypertrophied cardiomyocytes.
Animals ; Aorta, Abdominal ; Cardiomegaly ; etiology ; physiopathology ; Cell Enlargement ; Constriction ; Hypertension ; complications ; pathology ; physiopathology ; Male ; Myocardial Contraction ; physiology ; Myocytes, Cardiac ; pathology ; physiology ; Rats ; Rats, Sprague-Dawley