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

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

AIMTo identify the expression of proteins in cardiomyocytes in rats with left kidney artery coarctation.

METHODS16 male SD rats were separated into 2 groups (n=8): 2 kidney 1 Clip group (2K1C) and sham operation group (SO). The postoperational 8th week, after examination by normal doppler and tissue doppler echocardiography, the extracted proteins from cardiomyocytes were isolated by two-dimensional gel electrophoresis with staining. The gel images were acquired by scanner and 2-DE analysis software. Different spots observed on two 2D gels were selected and identified by matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF-MS).

RESULTSOverall, 21 protein spots showed significant difference, and 14 out of which were identified.

CONCLUSIONKidney artery coactation-induced cardiac hypertrophy displays different expression of proteins in cardiomyocytes.

Animals ; Cardiomegaly ; etiology ; metabolism ; Constriction ; Male ; Proteome ; analysis ; metabolism ; Proteomics ; methods ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Renal Artery ; physiopathology

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

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

The function of the transplanted heart will be affected by acute allograft rejection, chronic rejection, high blood pressure and so on, which may induce the reconstruction of the left ventricle and the increase of left ventricular mass (LVM), and eventually lead to left ventricular hypertrophy that will significantly affect the prognosis of heart transplantation (HT). The purpose of this study was to dynamically monitor the changes of left ventricular geometric patterns after HT using two-dimensional echocardiography and to understand the remodeling process and its possible influencing factors. The left ventricular internal diameter, interventricular septal wall thickness, posterior wall thickness at end diastole were measured and the relative wall thickness (RWT), left ventricular mass, left ventricular mass index were calculated respectively in 34 HT patients and 34 healthy volunteers by two-dimensional echocardiography. The type of left ventricular geometry was identified based on the echocardiographic determination of LVM index (LVMI) and RWT. The HT patients were divided into three groups according to the time length after surgery: A (3 months postoperatively), B (6 months postoperatively) and C (12 months postoperatively). We compared the parameters of left ventricle between HT group and normal control group, and explored the risk factors causing the increase of LVM. The results showed that 4 patients (16%) in group A had concentric remodeling. Nine patients (34.62%) in group B had reconstruction, including 5 cases of concentric remodeling, 2 cases of concentric hypertrophy and 2 cases of eccentric hypertrophy. The hypertrophy incidence rate was 15.4% in group B. 15 patients (62.5%) had reconstruction in group C, including 9 cases of concentric remodeling, 5 cases of concentric hypertrophy, and 1 case of eccentric hypertrophy. The prevalence of hypertrophy was 25%. Multivariate analysis showed that hypertension and acute rejection history were the risk factors that resulted in left ventricular hypertrophy. It is concluded that the left ventricular remodeling occurs following cardiac transplantation at an early stage and the incidence of left ventricular hypertrophy increases with survival time. In this study, the one-year prevalence of left ventricular hypertrophy was 25% after surgery. Hypertension and acute rejection history are risk factors that can predict the left ventricular hypertrophy.
Adult ; Cardiomegaly ; diagnostic imaging ; etiology ; Case-Control Studies ; Echocardiography ; Female ; Heart Transplantation ; adverse effects ; Heart Ventricles ; diagnostic imaging ; Humans ; Male ; Middle Aged ; Postoperative Period ; Ventricular Remodeling

OBJECTIVEThis study is to see the pathologic change of cardiac myocyte in Athlete's Heart, and explore the mechanism of the pathologic change.

METHODSFifteen male SD rats were separated randomly into control group (without any exercise), aerobic exercise group (Ae group, swimming for 75 min every day), and overloading exercise group (Oe group, swimming for 180 min with a loading of 5 percent of body weight every day). After 5 days per week for 12 weeks, swimming stopped, the rat hearts were prepared to specimens and examined under Transmission Electron Microscope.

RESULTSThe Ae group, the number and volume of mitochondria increased, and the membrane of mitochondria remained entire. Few of dense bodies were found in cytoplasm. The nucleus envelopes of expansion nucleus appear as dentition. These changes were considered as the adaptation to exercises. At the same time, some pathologic changes of the cardiac myocytes similar to senescence also appeared, such as mitochondria expanse, the crista disorder or disappearance, unclear mitochondria membrane, many dense bodies in cytoplasm, nucleus disfiguration and chromatin collection at edge.

CONCLUSIONAfter exercise training, some pathologic changes of cardiac myocyte also occur with physiological changes. With the raise of exercise intension, the pathologic changes become more obvious, even appearance of cardiac myocyte death.

Animals ; Cardiomegaly ; etiology ; pathology ; Exercise Tolerance ; Male ; Microscopy, Electron ; Mitochondria, Heart ; ultrastructure ; Myocardial Contraction ; Myocytes, Cardiac ; ultrastructure ; Rats ; Rats, Sprague-Dawley ; Swimming

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 study the effect of Sanhuang Jiangtang recipe (SJR) on renin-angiotensin system in local myocardium in diabetic rats.

METHODSRats were made into diabetes model by intraperitoneally administering of streptozocin, and medicated through gastrogavage with SJR (50 g/kg), gliclazide (20 mg/kg), captopril (15 mg/kg) and nitrendipine (30 mg/kg) respectively, for successive 8 weeks, started from 2 weeks after modeling. Levels of fasting blood sugar (FBS), serum insulin (Ins), heart/body weight ratio (H/BW), myocardial angiotensin II (Ang II), angiotensin converting enzyme (ACE) and aldosterone (ALD) were determined. And the mRNA expression of type I angiotensin receptor (AT1R) in myocardium were detected by RT-PCR assay.

RESULTSAs compared with those in the normal rats, levels of FBS, H/BW, Ang II, ACE, ALD and AT1R mRNA expression were higher (all P < 0.05) and level of serum Ins was lower (P < 0.01) in the model rats. SJR, gliclazide, captopril and nitrendipine could slightly reduce the blood sugar level in model rats, but with no increase of serum Ins. All the four drugs could reduce H/BW, Ang II, ACE and AT1R mRNA expression. SJR and captopril could also decrease the ALD content in myocardium.

CONCLUSIONCardiac hypertrophy has been induced in 10 weeks after diabetic modeling. Activation of local myocardial RAS is related to the genesis of diabetic cardiomyopathy. SJR, gliclazide, captopril and nitrendipine could antagonize the genesis of diabetic cardiomyopathy, the mechanism is related to the inhibition of RAS activation in local myocardium.

Animals ; Cardiomegaly ; etiology ; prevention & control ; Diabetes Mellitus, Experimental ; complications ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Hypoglycemic Agents ; pharmacology ; therapeutic use ; Male ; Myocardium ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley ; Renin-Angiotensin System ; drug effects

To get insights into the principles of gene expression changes during cardiac hypertrophy, three rat cardiac hypertrophy models were prepared, i.e., suprarenal abdominal aortic stenosis (SRS), arterial-vein fistula (AVF) and continuous jugular vein infusion of norepinephrine (NEi). The cardiac function and structure were analyzed by echocardiograph as well as histological examination. Total RNA of left ventricles was extracted and gene expression profiles were analyzed by cDNA microarray. SRS and NEi induced concentric cardiac hypertrophy and AVF induced eccentric hypertrophy in rats, among which NEi caused obvious cardiac fibrosis. The changes of gene expression profiles were compared comprehensively across different pathologic cardiac hypertrophy models. While gene expression profiles of different cardiac hypertrophy models compared with pairs, parts of the genes involved were found overlapped, and mostly the gene expression changed in the same direction between two models, but some of them changed in the opposite directions. Expression levels of 19 genes were found changed across all cardiac hypertrophy models, and genes relatively regulated in a specific model was also found when comparison of all the three models was carried out. Novel clues for further study might derive from the results mentioned above, and some genes might be the marker genes of cardiac hypertrophy or the targets of therapy.
Animals ; Aorta, Abdominal ; surgery ; Arteriovenous Shunt, Surgical ; Cardiomegaly ; etiology ; genetics ; Constriction ; Gene Expression Profiling ; Male ; Myocytes, Cardiac ; drug effects ; metabolism ; Norepinephrine ; Oligonucleotide Array Sequence Analysis ; Oligonucleotide Probes ; Random Allocation ; Rats ; Rats, Wistar ; Venae Cavae ; surgery