OBJECTIVETo compare the results of echocardiographic evaluation of pressure overload-induced cardiac remodeling in mice using different ultrasound machines.

METHODSEighteen C57 BL/6 mice were randomly divided into the sham-operated and the transverse aortic constriction (TAC) groups (n=9). Eight weeks after the operation, the cardiac function of TAC group was evaluated using Siemens ultrasonic instrument with 15L8 probe and the differences between the awake and anesthetized states were compared. The heart rate, left ventricular (LV) dimensions, systolic and diastolic functions were measured in both sham-operated and TAC groups using the Siemens ultrasonic instrument and a high-resolution ultrasonic imaging system for small animals (Vevo 770).

RESULTSCompared with the mice in wakefulness, the anesthetized mice showed significantly decreased heart rate and LV fractional shortening (P<0.001) and markedly increased LV end diastolic diameter and LV end systolic diameter (P<0.05). Both machines sensitively detected the cardiac remodeling of TAC mice in comparison with the sham-operated group. Compared with Siemens machine, Vevo 770 provided a higher resolution of 2D and M mode echocardiography with clearer Doppler frequency image of the mitral valve flow for evaluation of the LV diastolic function.

CONCLUSIONBoth machines are suitable for evaluating cardiac remodeling induced by pressure overload independent of anesthesia, though anesthesia depresses cardiac function. Vevo 770 is optimal to evaluate LV diastolic function in mice.

Animals ; Echocardiography ; instrumentation ; Hypertrophy, Left Ventricular ; diagnostic imaging ; Male ; Mice ; Mice, Inbred C57BL ; Ventricular Remodeling ; physiology

OBJECTIVEThe clinical diagnosis and treatment of ischemia mitral regurgitation (IMR) remained difficult because of its unclear mechanisms. This paper reviews studies on the mechanisms of IMR during the last 20 years, and discusses the relevance of the various mechanisms.

DATA SOURCESData used in this review were mainly from CNKI and Pubmed in English. The search terms were "ischemia mitral regurgitation mechanism", "myocardial infarction" AND "mitral regurgitation".

STUDY SELECTIONArticles were selected if they involved mechanisms of IMR.

RESULTSIMR is one of the common complications of coronary artery disease. But currently, the clinical diagnosis and treatment of IMR remained difficult because of its unclear mechanisms.

CONCLUSIONSFor now, dominating theory of ischemic mitral regurgitation mechanisms are left ventricular remodeling, imbalance of leaflet tethering and the closing force, left ventricular dysfunction, changes in spatial structure of the annulus and the dyssynchrony of the left ventricular electromechanical activity.

Animals ; Humans ; Mitral Valve Insufficiency ; etiology ; Myocardial Ischemia ; complications ; Papillary Muscles ; physiology ; Systole ; Ventricular Dysfunction, Left ; complications ; Ventricular Remodeling

OBJECTIVETo evaluate wave intensity (WI) on left ventricular (LV) performance in the different hypertensive remolding hearts.

METHODS105 hypertensive and 98 control subjects were underwent noninvasive evaluation of carotid arterial wave intensity, LV structure and function.

RESULTS(1) There were increasing trends in the levels of blood pressure, LV end-diastolic diameter and LV mass index in the control, normal geometry group, concentric remodeling group, concentric and eccentric hypertrophy group. LV ejection fraction increased in the concentric hypertrophy group and decreased in the eccentric hypertrophy group in which mid-wall fractional shortening showed a decreasing trend. LV diastolic filling pressure presented increased progression accompanied by LV remodeling (P < 0.05). (2) Transient acceleration wave intensity (W1) in hypertensive subjects were higher than that in the control (P < 0.05). Transient deceleration wave intensity (W2) was lower than that in the control (P < 0.05). (3) W1 in the concentric hypertrophy group was higher and lower in the eccentric hypertrophy, compared with that in the control group, normal geometry group and concentric remodeling group (P < 0.05). W2 was lower in concentric hypertrophy group and eccentric hypertrophy group than that in the control, normal geometry group and concentric remodeling group (P < 0.05).

CONCLUSIONWI is a noninvasively obtained, clinically useful parameter for evaluation of LV performance.

Aged ; Blood Flow Velocity ; physiology ; Carotid Artery, Common ; physiopathology ; Case-Control Studies ; Female ; Humans ; Hypertension ; physiopathology ; Male ; Middle Aged ; Pulsatile Flow ; physiology ; Ventricular Function, Left ; physiology ; Ventricular Remodeling

PURPOSE: Coronary flow reserve (CFR) in the non-infarcted myocardium is often impaired following acute myocardial infarction (AMI). However, the clinical significance of CFR in the non-infarcted myocardium is not fully understood. The objective of the present study was to assess whether a relationship exists between CFR and left ventricular remodeling following AMI. MATERIALS AND METHODS: We enrolled 18 consecutive patients undergoing coronary intervention. Heart function was analyzed using real-time myocardial contrast echocardiography at one week and six months after coronary angioplasty. Ten subjects were enrolled as the control group and were examined using the same method at the same time to assess CFR. Cardiac troponin I (cTnI) levels were routinely analyzed to estimate peak concentration. RESULTS: CFR was 1.55+/-0.11 in the infarcted zone and 2.05+/-0.31 in the remote zone (p<0.01) at one week following AMI. According to CFR values in the remote zone, all patients were divided into two groups: Group I (CFR <2.05) and Group II (CFR >2.05). The levels of cTnI were higher in Group I compared to Group II on admission (36.40 vs. 21.38, p<0.05). Furthermore, left ventricular end diastolic volume was higher in Group I compared to Group II at six months following coronary angioplasty. CONCLUSION: Microvascular dysfunction is commonly observed in the remote myocardium. The CFR value accurately predicts adverse ventricular remodeling following AMI.
Aged ; Coronary Angiography ; Coronary Circulation/physiology ; Female ; Humans ; Male ; Middle Aged ; Myocardial Infarction/*physiopathology/radiography ; Myocardium/*pathology ; Ventricular Remodeling/*physiology

PURPOSE: Coronary flow reserve (CFR) in the non-infarcted myocardium is often impaired following acute myocardial infarction (AMI). However, the clinical significance of CFR in the non-infarcted myocardium is not fully understood. The objective of the present study was to assess whether a relationship exists between CFR and left ventricular remodeling following AMI. MATERIALS AND METHODS: We enrolled 18 consecutive patients undergoing coronary intervention. Heart function was analyzed using real-time myocardial contrast echocardiography at one week and six months after coronary angioplasty. Ten subjects were enrolled as the control group and were examined using the same method at the same time to assess CFR. Cardiac troponin I (cTnI) levels were routinely analyzed to estimate peak concentration. RESULTS: CFR was 1.55+/-0.11 in the infarcted zone and 2.05+/-0.31 in the remote zone (p<0.01) at one week following AMI. According to CFR values in the remote zone, all patients were divided into two groups: Group I (CFR <2.05) and Group II (CFR >2.05). The levels of cTnI were higher in Group I compared to Group II on admission (36.40 vs. 21.38, p<0.05). Furthermore, left ventricular end diastolic volume was higher in Group I compared to Group II at six months following coronary angioplasty. CONCLUSION: Microvascular dysfunction is commonly observed in the remote myocardium. The CFR value accurately predicts adverse ventricular remodeling following AMI.
Aged ; Coronary Angiography ; Coronary Circulation/physiology ; Female ; Humans ; Male ; Middle Aged ; Myocardial Infarction/*physiopathology/radiography ; Myocardium/*pathology ; Ventricular Remodeling/*physiology

OBJECTIVETo study whether Ca(2+)-activated Cl(-) current (I(to2)) contributes to the functional remodeling of the failing heart.

METHODSThe cardiac myocytes were isolated enzymatically from rapidly pacing-induced failing canine hearts (HF) at room temperature. Patch-Clamp whole cell recording technique was employed to record the I(to2). The Cl(-) transport blocker 4, 4'-diisothiocyanostilbene-2, 2'-disulfonic acid (DIDS, 200 micromol) was used to isolated the I(to2). The relations of I(to2) to L-type Ca(2+) current (I(Ca-L)) and to the membrane voltage under the constant intracellular [Ca(2+)]i were evaluated in HF and the normal hearts.

RESULTSWe found that the current density of I(to2) was significantly decreased in HF cells compared with the controls. At membrane voltage of 20 mV, for example, the I(to2) density was (3.02 +/- 0.54) pA/pF in control cells (n = 7) vs. (1.31 +/- 0.25) pA/pF in HF (n = 8) cells, P < 0.05. While the averaged I(Ca-L) density did not show difference between two groups. The time constant of current decay of I(to2) was similar in both types of cells. However, in intracellular Ca(2+) clamped mode with 100 micromol [Ca(2+)]i, I(to2) density was increased significantly in HF cells at membrane voltage of +30 mV or higher.

CONCLUSIONSOur results suggest that the decrease of I(to2) density may contribute to the prolongation of the action potential in failing heart. I(to2) density abnormality may cause cardiac arrhythmia and a delayed after-depolarization. Impaired Ca(2+) handing in HF cells rather than reduced CLCA function itself may result in this abnormality.

Animals ; Calcium ; physiology ; Calcium Channels, L-Type ; physiology ; Chloride Channels ; physiology ; Dogs ; Heart Failure ; physiopathology ; Patch-Clamp Techniques ; Ventricular Remodeling ; physiology

BACKGROUNDEffect of percutaneous transluminal septal ablation (PTSA) with ethanol injection on electromechanical remodeling of left ventricule still remains unknown. This study was conducted to assess the potential significance of cardiac electromechanical mapping (CEMM) in analyzing the left ventricular remodeling before and immediately after percutaneous transseptal myocardial ablation (PTSMA) in patients with hypertrophic obstructive cardiomyopathy (HOCM).

METHODSEight patients with drug-refractory HOCM and 6 patients with hypertrophic cardiopathy (HM) without increased left ventricular outtract gradien (LVOTG) were enrolled into the present study. CEMM was undergone in patients with HOCM before and immediately after PTSA procedure, and in patients with HM.

RESULTSPTSA was successful in all patients with HOCM, LVOTG significantly decreased from (62.87 +/- 21.16) mmHg to (12.73 +/- 3.05) mmHg immediately after ablation procedure. Value of UVP in septal-base segment in HM group was higher than that in HOCM group [(22.79 +/- 2.34) mV vs (18.54 +/- 1.76) mV]. In patients with HOCM, lateral-middle and -base segments had lowest value of UVP [(15.93 +/- 1.11) mV and (15.83 +/- 1.07) mV] before PTSA. Value of UVP at posterior-middle segment decreased from (23.58 +/- 2.21) mV pre-PTSA to (18.89 +/- 1.91) mV post-procedure, PTSA led to significant increase of UVP at lateral-middle segment. Septal region in patients with HM and septal-middle, septal-base, posterior-base segments in HOCM had lower value of local linear shortening (LLS) among all patients in both HOCM and HM groups. PTSA resulted in significant reduction of LLS in anterior region and at septal-apex segment. Anterior-base and septal-middle segments in patients with HM had lowest value of local active time (LAT), and significantly differentiated from that in patients with HOCM [(-8.57 +/- 0.68) ms vs (-18.61 +/- 1.02) ms, (-6.75 +/- 0.37)ms vs (-21.90 +/- 0.96) ms, respectively]. LAT at septal-middle and -base segments in patients with HOCM was decreased significantly [(-21.90 +/- 0.96) ms vs (-13.80 +/- 1.04) ms, P < 0.002; and (-15.20 +/- 1.06) ms vs (-6.33 +/- 0.52) ms, respectively] immediately after PTSA.

CONCLUSIONSPosterior-lateral and anterior region probably played important roles in electromechanical remodeling. Significant electromechanical remodeling disassociation (uncoupling) was detected in most left ventricular regions, which would be important in differentiating of HOCM from HM, and in predicting the prognosis in patients with HOCM after PTSA procedure.

Body Surface Potential Mapping ; Cardiomyopathy, Hypertrophic ; physiopathology ; therapy ; Ethanol ; therapeutic use ; Heart Septum ; drug effects ; Humans ; Ventricular Remodeling ; physiology

OBJECTIVE: To determine the effect of stellate ganglion block on reconstruction of the left ventricle in spontaneously hypertensive rats (SHRs). METHODS: Thirty-two 10-week-old male SHRs were randomly assigned into 4 groups: a left stellate ganglion block group (group LS), a right stellate ganglion block group (group RS), a captopril group (group D) and a control group (group C). The arterial systolic blood pressure (SBP) was measured by ALC-NIBP measuring system. After 10 weeks, we observed the left ventricular mass index (LVMI), myocardial pathologic changes, and detected the endothelin (ET-1) and endothelial nitric oxide synthase (eNOS) level in the left ventricle by radioimmunoassay and the collagen protein level in the left ventricle by immunohistochemical method. RESULTS: Compared with group LS and group C, the LVMI in group RS was lowered most notably (P<0.05) and pathological changes were improved obviously. The expression of eNOS in group RS was significantly increased and ET-1 significantly decreased (P<0.05) compared with that in group C and group LS. The expression of type I collagen fibers in group RS was significantly lower and type III collagen fibers significantly higher (P<0.05) when compared with that in group C and LS. CONCLUSION Right stellate ganglion block can not only decrease the arterial pressure but also reverse the reconstruction of the left ventricle.
Animals ; Autonomic Nerve Block ; Hypertension ; physiopathology ; therapy ; Male ; Rats ; Rats, Inbred SHR ; Stellate Ganglion ; Ventricular Remodeling ; physiology

BACKGROUNDHepatocyte growth factor (HGF) inhibits the development of pulmonary artery hypertension (PAH) by reducing pulmonary artery pressure and right ventricle (RV) hypertrophy. However, whether HGF can prevent RV remodeling via inhibiting apoptosis in RV cardiomyocytes and decreasing neurohormonal activation remains unknown.

METHODSThe PAH and subsequent RV remodeling in rats were induced by subcutaneous injection of monocrotaline (MCT). The PAH rats were transfected with adenovirus carrying HGF (Ad-HGF) via intratracheal instillation. Three weeks after transfection, the hemodynamics indexes were measured, serum levels for angiotonin II (ANG II) and brain natriuretic peptide (BNP) were determined by ELISA. Histological analysis was used to assess the RV hypertrophy and fibrosis. The cardiomyocyte apoptosis in RV was assayed by TUNEL staining. The mRNA expression of BNP, angiotensin-converting enzyme (ACE), Bax and Bcl-2 in RV was determined by reverse transcriptase polymerase chain reaction (RT-PCR), the protein expression of transforming growth factor (TGF)-β1 and tumor necrosis factor (TNF)-α in RV was determined by Western blotting.

RESULTSHGF treatment significantly decreased the mean PAH, RV systolic pressure, serum ANG II and BNP levels. HGF treatment also significantly decreased the RV hypertrophy, collagen deposition, and the number of apoptotic cardiomyocytes. Moreover, HGF treatmemt significantly decreased the expression of BNP, ACE, Bax, TGF-β1, and TNF-α, while it significantly increased the expression of Bcl-2.

CONCLUSIONSGene transfer of HGF decreases MCT-induced PAH and improves RV remodeling. This effect is mediated not only by improving the hemodynamics but also by decreasing neurohormonal activation and inhibiting cardiomyocytes apoptosis. HGF gene treatment may be an effective strategy for improving RV remodeling in MCT-induced PAH.

Animals ; Apoptosis ; genetics ; physiology ; Hepatocyte Growth Factor ; genetics ; physiology ; therapeutic use ; Humans ; Hypertension, Pulmonary ; metabolism ; therapy ; Male ; Rats ; Rats, Sprague-Dawley ; Ventricular Remodeling ; genetics ; physiology

The effects of cardiomyocyte grafting on left ventricular (LV) remodeling and function in rats with chronic myocardial infarction were evaluated using high-frequency ultrasound. Chronic myocardial infarction was induced in 50 Wister rats by ligating the left anterior descending artery. They were randomized into two groups: a trial group that received neonatal rat cardiomyocyte transplantation (n=25) and a control group which were given intramyocardial injection of culture medium (n=25). The left ventricular (LV) geometry and function were evaluated by high-frequency ultrasound before and 4 weeks after the cell transplantation. After the final evaluation, all rats were sacrificed for histological study. The results showed that 4 weeks after the cell transplantation, as compared with the control group, the LV end-systolic dimension, end-diastolic dimension, end-systolic volume and end-diastolic volume were significantly decreased and the LV anterior wall end-diastolic thickness, LV ejection fraction and fractional shortening were significantly increased in the trial group (P<0.01). Histological study showed that transplanted neonatal rat cardiomyocytes were found in all host hearts and identified by Brdu staining. It was suggested that transplantation of neonatal rat cardiomyocytes can reverse cardiac remodeling and improve heart function in chronic myocardial infarction rats. High-frequency ultrasound can be used as a reliable technique for the non-invasive evaluation of the effect of cardiomyocyte transplantation.
Animals, Newborn ; Echocardiography/*methods ; Myocardial Infarction/physiopathology ; Myocardial Infarction/*therapy ; Myocardial Infarction/ultrasonography ; Myocytes, Cardiac/*transplantation ; Random Allocation ; Rats, Wistar ; Ventricular Function, Left/*physiology ; Ventricular Remodeling