We report herein a case of benign cardiac schwannoma in the interatrial septum. A 42-year-old woman was transferred from a clinic because of cardiomegaly as determined by chest X-ray. A transthoracic echocardiography and chest computed tomography examination revealed a huge mass in the pericardium compressing the right atrium, superior vena cava (SVC), left atrium, and superior pulmonary vein. To confirm that the tumor originated from either heart or mediastinum, cine magnetic resonance imaging was performed, but the result was not conclusive. To facilitate surgical planning, we used 3D printing. Using a printed heart model, we decided that tumor resection under cardiopulmonary bypass (CPB) through sternotomy would be technically feasible. At surgery, a huge tumor in the interatrial septum was confirmed. By incision on the atrial roof between the aorta and SVC, tumor enucleation was performed successfully under CPB. Pathology revealed benign schwannoma. The patient was discharged without complication. 3D printing of the heart and tumor was found to be helpful when deciding optimal surgical approach.
Adult ; Atrial Septum/pathology/surgery ; Cardiomegaly/*etiology/radiography ; *Cardiopulmonary Bypass ; Female ; Heart Atria/pathology ; Heart Neoplasms/pathology/*surgery ; Humans ; Magnetic Resonance Imaging, Cine ; Neurilemmoma/*pathology/surgery ; *Printing, Three-Dimensional ; Sternotomy ; Treatment Outcome ; Vena Cava, Superior/pathology

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

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

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

OBJECTIVETo compare the effects of amlodipine, benidipine and nifedipine on myocardial hypertrophy and evaluate the underlying mechanism.

METHODSMyocardial hypertrophy model was created by transverse aortic constriction (TAC) in C57 BL/6 mice, and plasma catecholamine concentrations were measured 7 days after surgery to confirm the sympathetic activation. The 3 drugs were administered in TAC mice for 7 days and cardiac hypertrophy was evaluated according to the heart-to-body weight ratio (HW/BW). Effects of those drugs on the protein synthesis stimulated by phenylephrine in cultured neonatal cardiac myocytes were also examined.

RESULTSHW/BW and plasma concentrations of catecholamine were significantly increased in TAC mice one week after surgery in comparison with to sham-operated mice. One week after TAC, the HW/BW ratio was significantly lower in the amolodipine but not nifedipine-treated group than in the TAC group. Administration of nifedipine via minipump infusion for one week did not decrease HW/BW ratio. Treatment with amlodpine or benidipine, but not nifedipine, decreased the neonatal rat myocyte protein synthesis induced by phenylephrine stimulation.

CONCLUSIONAntihypertrophic effect of DHEs on myocardium is dependent on their potential of blocking N-type calcium channel, and the underlying mechanism involves the sympathetic inhibition.

Amlodipine ; pharmacology ; therapeutic use ; Animals ; Calcium Channel Blockers ; pharmacology ; therapeutic use ; Calcium Channels, N-Type ; drug effects ; Cardiomegaly ; drug therapy ; etiology ; Dihydropyridines ; pharmacology ; therapeutic use ; Disease Models, Animal ; Male ; Mice ; Mice, Inbred C57BL ; Nifedipine ; pharmacology ; therapeutic use

OBJECTIVETo investigate the molecular mechanism of tanshinone II A (TSN) for preventing left ventricular hypertrophy (LVH) by studying the expressions of angiotensin I type 1 receptor (AT1R), transforming growth factor beta1 (TGF-beta1) and intracellular signal protein gene (Smads gene) in the hypertrophic myocardium of hypertensive rat models induced by pressure over-loading.

METHODSSD rat model of LVH was established by abdominal aorta constriction. The model animals were randomly divided into 4 groups 4 weeks after modeling, the untreated model control group (C1), the two tested groups (T1 and T2) treated respectively with high (20 mg/kg) and low (10 mg/kg) dose of TSN II A per day via intraperitoneal injection, and the positive control group (C2) treated with 10 mg/kg of Valsartan per day by gastric perfusion, with 8 animals in each group. Besides, 8 SD rats managed with sham operation were set up as the sham-operated control group (C3) After an 8-week treatment, the caudal arterial pressure, left ventricular mass index (LVMI), myocardial fiber dimension (MFD, by pathologic examination with HE staining) in rats were measured. Meanwhile, mRNA expression of AT1R, protein expression of TGF-beta1 and activity of Smad-3, 4, 7 in the ventricular tissue were detected by RT-PCR analysis and Western blotting respectively.

RESULTS(1) Blood pressure in Group T1 and T2 was unchanged after treatment, which was significantly higher than that in Group C2 and C3 (P < 0.01, P < 0.05). (2) LVMI and MFD in Group T1, T2 and C2 were higher than that in Group C3 (P < 0.01), but remarkably lower than that in Group C1 (P < 0.01). (3) Levels of AT1R, TGF-beta1 and Smad-3 expression increased significantly in the model rats (P < 0.01), but they were down-regulated in Group T1 and C2, and the TGF-beta1 regulating effect in the C2 was more potent than that in Group T1 and T2 (P < 0.05). (4) Protein expression of Smad-7 was up-regulated in Group T1, T2 and C2 obviously (P < 0.01), and the effect in Group T1 was superior to that in C2 (P < 0.05).

CONCLUSIONThe myocardial hypertrophy inhibition effect of TSN II A is a blood pressure independent process, and it may be related to the inhibition of AT1R mRNA expression and blocking of TGF beta1/Smads signal pathway.

Animals ; Cardiomegaly ; etiology ; metabolism ; Diterpenes, Abietane ; pharmacology ; Drugs, Chinese Herbal ; pharmacology ; Hypertension ; complications ; metabolism ; Myocardium ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley ; Receptor, Angiotensin, Type 1 ; metabolism ; Signal Transduction ; drug effects ; Smad Proteins ; metabolism ; Transforming Growth Factor beta1 ; metabolism

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

This experiment on rats was aimed to investigate the expression of intermedin (IMD) in hypertrophic cardiac myoctye of renal vascular hypertension induced by incomplete ligation of the left renal artery, and so to detect and compare the changes of the expression after administration of Valsartan, Amlodipine and Enalapril respectively. The criterion for standard modeling was systolic pressure > or = 140 mmHg. At 4 weeks after successful modeling, 60 SD male rats were randomly divided into 5 groups, namely the hypertrophy group, the 3 drug-treatment groups, and the sham-operation group as control. Blood pressure, left ventricular mass index (LVMI), and the left ventricular mean transverse diameter of myocardial cell (LVTDM) were investigated at the 10th week after model establishment. Gene expression of IMD mRNA was detected by reverse transcription-polymerase chain reaction (RT-PCR), and the optical density of the band was measured by use of the Gel Documentation System. The ratio of IMD mRNA to beta-actin mRNA was considered the relative amount of IMD. When compared with control, the blood pressure increased significantly in the hypertrophy group. There was no statistically significant difference between the treatment groups. No significant difference in heart rate was noted at 4 weeks after operation in all groups. LVMI and LVTDM levels were significantly higher in the hypertrophy group than in the other groups; LVMI and LVTDM levels showed no significant difference among the treatment groups but they were obviously higher than those of the Sham-operation group. The gene expression of IMD mRNA in the hypertrophy group was upregulated in the myocardium, when compared with that in the other groups. Meanwhile, although IMD mRNA in the treament groups was higher than that in the Sham-operation group, no statistically significant difference of myocardial IMD mRNA was found between the treament groups. These results suggested that, in this experiment, intracardiac IMD mRNA was upregulated and could participate in the regulation of cardiac remodeling in renal vascular hypertension-induced cardiac hypertrophy. This upregulation could improve the pathologic and physiologic process of cardiac hypertrophy, and could associate with the pressure loading or myocardia hypertrophy. However, the change did not display any difference that could be attributed to the variety of hypotensive drugs.
Adrenomedullin ; genetics ; metabolism ; Amlodipine ; therapeutic use ; Animals ; Antihypertensive Agents ; therapeutic use ; Cardiomegaly ; etiology ; metabolism ; Enalapril ; therapeutic use ; Hypertension, Renovascular ; complications ; drug therapy ; metabolism ; Male ; Myocardium ; metabolism ; Neuropeptides ; genetics ; metabolism ; RNA, Messenger ; genetics ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Tetrazoles ; therapeutic use ; Valine ; analogs & derivatives ; therapeutic use ; Valsartan

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

OBJECTIVETo investigate the effect of Yiqi Huoxue Recipe (YHR) on the cardiac function and ultrastructure during the regression of myocardial hypertrophy induced by pressure overload in rats.

METHODSThe model of myocardial hypertrophy was established by abdominal aortic banding. Eighty male Wistar rats were divided into six groups, the normal control group I (n=20), the normal control group II (n=12), the hypertension model group I (n=12), the hypertension model group II (n=12), the YHR group (n=12) and the Captopril group (n=12). The observation was carried out in the normal control group I and the hypertension model group I after 4 weeks of modeling, and the other four groups were observed after 16 weeks of modeling (12 weeks of administration). The cardiac function was measured with a multichannel biological signal analysis system, and the myocardium ultrastructure was observed by a transmission electron microscope.

RESULTS(1) Compared with the normal control group I, the systolic blood pressure and cardiac coefficient (left ventricular weight/body weight) in the model I group was higher (P<0.05, P<0.01). (2) In the YHR group, cardiac coefficient and -dp/dt(max) were lower, left ventricular systolic pressure and +dp/dt(min) were higher when compared with the model group II and the Captopril group (P<0.05 or P<0.01). In the Captopril group, only cardiac coefficient was lower when compared with the mode group II (P<0.05). (3) Compared with the normal control group II, +dp/dt(max) was higher (P<0.01) -dp/dt(max) and isovolumetric contraction time (ICT) was lower (P<0.05, P<0.01) in both the YHR group and the Captopril group. (4) Results of the myocardium ultrastructure showed edema under myocardium plasmalemma, enlarged sarcoplasmic reticulum and T tube, and significantly enlarged intercalated disc of the cardiac muscle in the model groups. In the Captopril group, the extension of sarcoplasmic reticulum and T tube as well as the pathological changes of intercalated disc were lighter, with slight edema under the myocardium plasmalemma. In the YHR group, the expansion of the sarcoplasmic reticulum was less than in the Captopril group, part of the pathological changes of intercalated discs was slightly more severe than that in the Captopril group, the dissolution of nuclear chromatin was not found, which was similar to that of the Captopril group, and no injury of the nucleus was found, either.

CONCLUSIONYHR could reverse myocardial hypertrophy in rats with abdominal aortic banding and improve the systolic and diastolic function of the left ventricle. The ultrastructure of the myocardium such as arcoplasmic reticulum, intercalated disc, and cell nucleus in abdominal aortic banding rats could be partly reversed by the recipe.

Animals ; Antihypertensive Agents ; therapeutic use ; Blood Pressure ; drug effects ; Captopril ; therapeutic use ; Cardiomegaly ; drug therapy ; etiology ; Disease Models, Animal ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Heart ; drug effects ; physiology ; Male ; Myocardium ; ultrastructure ; Phytotherapy ; Pressure ; Rats ; Rats, Wistar ; Remission Induction ; Ventricular Remodeling ; drug effects