Implanting a valve that will reduce left ventricular mass is critical in aortic stenosis. Regression of left ventricular hypertrophy in 46 aortic valve replacement (AVR) patients receiving a St. Jude Medical (SJM) valve was assessed by serial electrocardiographic and echocardiographic studies during the preoperative, immediate, and late postoperative periods. The patients were divided into three groups according to valve size; 19 mm group (n=9), 21 mm group (n=20), and 23+mm group (n=17). There was no surgical mortality. The NYHA functional class improved from an average of 2.2+/-0.8 preoperatively to 1.3+/-0.5 post-operatively. Left ventricular muscle mass index (LVMI) regression failed to reach statistical significance in the 19 mm group, whereas in the other two groups a steady decrease in the LVMI occurred with follow up. ECG findings were less remarkable showing insignificant differences in voltage among the three groups (p=0.000). In conclusion, the current data suggest that the 19 mm SJM valve may not result in satisfactory left ventricular muscle mass regression despite adequate function, even in small patients. Therefore, additional procedures to accommodate a larger valve may be warranted in the aortic annulus smaller than 21 mm.
Adult ; Aged ; Aortic Valve/ultrasonography ; Aortic Valve Stenosis/surgery* ; Aortic Valve Stenosis/complications ; Echocardiography ; Electrocardiography ; Female ; Follow-Up Studies ; Heart Valve Prosthesis* ; Human ; Hypertrophy, Left Ventricular/prevention & control* ; Hypertrophy, Left Ventricular/etiology ; Hypertrophy, Left Ventricular/diagnosis ; Male ; Middle Age ; Multivariate Analysis ; Postoperative Period ; Remission Induction ; Risk Factors ; Treatment Outcome

OBJECTIVETo explore whether the Astragalus injection (AI) has effect for reversing left ventricular hypertrophy and myocardial fibrosis induced by renal vascular hypertension in rats.

METHODSThirty male SD rats were randomized equally into three groups: the AI group, the control group and the sham-operated group. All rats, except those in the sham-operated group, were established into the hypertension models by two kidney one clip (2K1C) operation. Blood pressure was measured before operation and every 4 weeks after operation. AI intervention was given to rats in the AI group starting from the 4th week of experiment at dose of 8 g/kg by peritoneal injecting once a day for 8 weeks, while for rats in the other 2 groups, equal volume of normal saline was given instead. All rats were sacrificed 12 weeks after operation by cervical breaking. And indexes including left ventricular mass index (LVMI), left ventricular wall thickness (LVWT), inter-ventricular septal thickness (IVST), left ventricular diameter (LVD), cardiomyocytes diameter (CCD), collagen volume fraction (CVF), and peri-vascular volume collagen area (PVCA) in rats were measured.

RESULTSBlood pressure was not different in the three groups before operation (P>0.05), whereas it rose in the control group and the AI group 4, 8 and 12 weeks after operation correspondingly, showing no difference between the two groups, but significantly higher than that in the sham-operated group (P<0.05). The related indexes in the sham-operated group, control group and AI group were: LVMI, 2.71 +/- 0.24, 3.42 +/- 0.26, 3.13 +/- 0.23, respectively; LVWT (mm), 2.25 +/- 0.42, 4.26 +/- 0.48, 3.28 +/- 0.36; IVST (mm), 2.13 +/- 0.38, 3.98 +/- 0.32, 3.02 +/- 0.28; and LVD (mm), 3.76 +/- 0.29, 2.18 +/- 0.27, 2.82 +/- 0.20 respectively. Comparisons showed that LVMI, LVWT and IVST were significantly higher, but LVD was significantly lower in the control group than those in the sham-operated group (P<0.05); LVMI, LVWT and IVST were significantly lower but LVD was significantly higher in the AI group than those in the control group (P<0.05). CCD, CVF and PVCA in the three groups (in the fore-mentioned order) were: CCD (microm), 14.54 +/- 2.25, 19.56 +/- 2.53, 16.58 +/- 2.46; CVF(%), 3.83 +/- 1.40, 11.21 +/- 2.96, 7.83 +/- 1.67; PVCA (%), 15.71 +/- 3.85, 30.58 +/- 6.25, 21.76 +/- 4.36, respectively. These indexes showed that CCD, CVF, PVCA in the control group were significantly higher than those in the sham-operated group (P<0.05); and those were significantly lower in the AI group than in the control group (P<0.05).

CONCLUSIONAI intervention can reverse the left ventricular hypertrophy and myocardial fibrosis induced by renal vascular hypertension in rats.

Animals ; Astragalus Plant ; Blood Pressure ; Drugs, Chinese Herbal ; therapeutic use ; Hypertension, Renal ; drug therapy ; Hypertrophy, Left Ventricular ; prevention & control ; Injections ; Male ; Phytotherapy ; Rats ; Rats, Sprague-Dawley

Chronic treatment with Salvia Miltiorrhiza preventing left ventricular hypertrophy (LVH) and its possible mechanism--inhibiting the action of cardiac aldosterone in spontaneously hypertensive rats (SHR) were investigated. Normotensive Wistar-kyoto (WKY) rats and SHRs were used. Part of SHRs was treated with Salvia Miltiorrhiza for 12 weeks. Systolic blood pressure (SBP) and left ventricular mass index were measured. Sections of heart tissue were stained with HE method and VanGieson method. Collagen volume fraction was determined in the left ventricle by automatically quantitative morphometry. Cardiac aldosterone concentration was measured by radioimmunoassay. The results indicated that compared with WKY rats, SHRs exhibited higher SBP, left ventricular collagen volume fraction, and aldosterone concentration (all P < 0.05). After the treatment with Salvia Miltiorrhiza, SBP, left ventricular collagen volume fraction, and aldosterone concentration in SHR were decreased as compared with control group (P < 0.05) except SBP. It was concluded that chronic treatment with Salvia Miltiorrhiza could prevent left ventricular hypertrophy in SHR, significantly inhibit collagen compositions in left ventricle. The mechanism was probably related with the inhibition of the cardiac aldosterone action.
Aldosterone ; metabolism ; Animals ; Drugs, Chinese Herbal ; pharmacology ; Hypertension ; metabolism ; physiopathology ; Hypertrophy, Left Ventricular ; metabolism ; prevention & control ; Male ; Myocardium ; metabolism ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Salvia miltiorrhiza

BACKGROUND: It is absolutely necessary to evaluate cardiac function on starting and during hemodialysis in patients with end stage renal disease. In this study, we tried to determinate the changes of cardiac function associated with hemodialysis. METHODS: Twenty patients with end stage renal disease, who had been in a hemodialysis program from February, 1997 to August, 1999 in Pusan National University Hospital, were enrolled. They were examined with echocardiography and gated blood pool scintigraphy on starting hemodialysis and after follow-up. The data were analyzed by paired t-test. RESULTS: The patients were 46.2 +/- 16.8 years old and male to female ratio was 8 : 12. The underlying diseases were diabetes mellitus (n=10), hypertension1), glomerulonephritis2) and others1). The duration of symptoms associated with end stage renal disease and underlying diseases was 3.4 2.6 years and the duration of hemodialysis was 13.8 7.0 months. The LVEDID, LVESID and RVC decreased significantly (-6.10, -7.80 and -20.00%, respectively, p < 0.05) with no significant changes for LAD, IVS, PWT and EF (p > 0.05). In ten cases associated with diabetes, LVEDID decreased (-7.90%, p < 0.05). In twelve cases associated with cardiac diseases, LVEDID and LVESID decreased (-8.60 and -10.50%, respectively, p < 0.05). In four cases associated with diabetes without cardiac diseases, LAD decreased (-5.10%, p 0.05) and in four cases associated with cardiac diseases without diabetes there were no significant changes in cardiac dimensions and EF. In seven cases associated with diabetes and cardiac diseases, LVEDID decreased (-10.50%, p < 0.05). The EF on gated blood pool scintigraphy decreased (-0.9%, p < 0.05) as a whole while it increased (5.90%, p < 0.05) in the cases associated with diabetes and cardiac diseases. CONCLUSION: During the early hemodialysis stage of end stage renal disease, we found a change of concentric left ventricular hypertrophy and relatively preserved left ventricular function. Furthermore, we can expect that adequate hemodialysis - with dry weight as low as possible - may prevent progression to eccentric left ventricular hypertrophy and dilated cardiomyopathy.
Adult ; Aged ; Cardiomyopathy, Congestive/prevention & control ; Diabetic Nephropathies/pathology/physiopathology/therapy ; Echocardiography ; Female ; Gated Blood-Pool Imaging ; Heart/*physiopathology ; Human ; Hypertrophy, Left Ventricular/prevention & control ; Kidney Failure, Chronic/pathology/*physiopathology/*therapy ; Male ; Middle Age ; Myocardium/pathology ; *Renal Dialysis ; Ventricular Function, Left

OBJECTIVETo investigate the impact of 1, 25-(OH)2D3 on left ventricular hypertrophy (LVH) in type 2 diabetic rats.

METHODSType 2 diabetic mellitus (DM) model rats were established by intraperitoneally injecting with 30 mg/kg streptozotocin. After 8 weeks, 19 male rats were identified as diabetic with left ventricular hypertrophy (LVH) by ultrasound examination, and randomly assigned into three groups: untreated (DM-LVH, n=7), treated with insulin (DM-LVH+INS, n=6), and treated with 1, 25-(OH)2D3 (DM-LVH+VD, n=6). Healthy male rats were used as the controls group (n=6). The fasting blood glucose and the insulin level were determined weekly. The left ventricular mass index, myocardial collagen content, collagen volume fraction, and 1, 25-(OH)2D3-receptor level were determined by 4 weeks later.

RESULTSIn the DM-LVH model group, the insulin level was significantly decreased compared with the non-diabetic control group (P<0.05), whereas the blood glucose, left ventricular mass index, myocardial collagen content, collagen volume fraction, and 1, 25-(OH)2D3-receptor expression were significantly increased (all P<0.05). In the DM-LVH+INS and DM-LVH+VD groups, the insulin levels were significantly increased compared with the DM-LVH model group (P<0.05), whereas the other parameters were significantly decreased (all P<0.05).

CONCLUSION1, 25-(OH)2D3 could reverse LVH in diabetic rats and that the mechanism may involve stimulating insulin secretion and reducing blood glucose via direct up-regulation of 1, 25-(OH)2D3-receptor expression.

Animals ; Blood Glucose ; analysis ; Calcitriol ; therapeutic use ; Diabetes Mellitus, Experimental ; blood ; complications ; Diabetes Mellitus, Type 2 ; blood ; complications ; Hypertrophy, Left Ventricular ; prevention & control ; Insulin ; blood ; Male ; Rats ; Rats, Wistar ; Receptors, Calcitriol ; analysis ; Streptozocin

BACKGROUND: Increased aortic stiffness measured by pulse wave velocity (PWV) and left ventricular hypertrophy (LVH) are independent risk factors of cardiovascular events in hypertensive patients. We have conducted a prospective study to examine the effects of the angiotensin II receptor antagonist (irbesartan) on PWV and LVH in hypertensive patients. METHODS: A total of 52 untreated hypertensive patients (age:53.3+/-8.0 yrs) were enrolled; they had no evidence of associated cardiovascular complications. Blood pressure, heart rate, aortic PWV and left ventricular mass index (LVMI) by 2-D echocardiography were measured at baseline and after irbesartan treatment (150 mg or 300 mg/day) at 12 weeks and 24 weeks. RESULTS: Blood pressure was significantly decreased after 12 weeks and 24 weeks of treatment compared to baseline (SBP: 134.6+/-13.3 mmHg, 134.0+/-11.0 mmHg vs 163.7+/-13.8 mmHg p<0.001, DBP: 86.0+/-10 mmHg, 83.07 mmHg vs 102.4+/-9.6 mmHg p<0.001, respectively) without significant change in heart rate. LVMI decreased at 12 weeks and at 24 weeks after treatment compared to baseline (from 145.5+/-35.1 g/m2 at baseline to 137.5+/-35.4 g/m2 at 12 weeks, p=0.017 and 135.3+/-35.4 g/m2 at 24 weeks, p=0.008). Aortic PWV was decreased after irbesartan treatment at 12 weeks (from 9.6+/-2.8 m/sec to 8.7+/-3.1 m/sec at 12 weeks, p=0.064) and at 24 weeks (from 9.6+/-2.9 m/sec to 7.7+/-2.1 m/sec at 24 weeks, p=0.007). CONCLUSIONS: Long-term treatment with irbesartan may reduce arterial stiffness and regression of LVH in hypertensive patients. The pleiotropic effects of irbesartan, further decreasing PWV without change of BP between 12 and 24 weeks of treatment, may have favorable vascular effects on arterial stiffness and LVH.
Tetrazoles/*therapeutic use ; Prospective Studies ; Middle Aged ; Male ; Hypertrophy, Left Ventricular/*prevention & control ; Hypertension/*drug therapy/pathology/physiopathology ; Humans ; Female ; Biphenyl Compounds/*therapeutic use ; Aorta/*drug effects/physiopathology ; Angiotensin II Type 1 Receptor Blockers/*therapeutic use ; Aged ; Adult

OBJECTIVETo investigate the changes in renin angiotensin system (RAS) in hypertrophied myocardium of spontaneous hypertensive rat (SHR), and the effect of Banxia Baizhu Tianma Decoction (BBTD) on the changes in haemodynamic parameters and mRNA of signaling molecules of RAS at different periods.

METHODSFifty-four male SHRs of 6 weeks old were randomly and equally divided into three groups: the untreated control group, the test group, and the positive control group, and they were treated respectively with distilled water, BBTD and captopril by dissolving in equal volume of water administrated via gavage for 18 weeks. Besides, 18 age matched Wistar-Kyoto (WKY) rats treated with distilled water were allocated in a normal control group. Rats were managed in batches at their age of 18, 24, and 32 weeks old. Rat's hemodynamic parameters were measured through carotid artery catheterization, myocardial pathology was observed, and their mRNA expressions of angiotensin (AGT), angiotensin-converting (ACE) and angiotension-converting 2 (ACE2) were determined by Real-time PCR.

RESULTSCompared with WKY rats, the arterial pressure and left ventricular mass index (LVMI)in SHR were significantly higher at 18, 24 and 32 weeks respectively (P < 0.01); average cycle rate showed in electrocardiogram was higher (P < 0.05), though the blood stream was similar; mRNA expressions of AGT and ACE in heart tissue were markedly higher (P < 0.01), but that of ACE2 at 18 and 24 weeks were lower (P < 0.01). Compared with untreated SHR, arterial pressure at 18 and 24 weeks was lower (P < 0.05); cardiac muscle structure was improved; LVMI at 24 weeks was improved (P < 0.05); the mRNA expressions of AGT and ACE were suppressed but that of ACE2 increased at 18, 24,and 32 weeks significantly in the test group after BBTD treatment (P < 0.05).

CONCLUSIONSChanges in RAS in the hypertrophied myocardium of SHR may be one of the molecular mechanisms for hypertension leading to left ventricular hypertrophy. BBTD can improve the hemodynamic parameters, regulate RAS, so as to lower the arterial pressure.

Animals ; Drugs, Chinese Herbal ; pharmacology ; Hemodynamics ; drug effects ; Hypertension ; complications ; physiopathology ; Hypertrophy, Left Ventricular ; etiology ; physiopathology ; prevention & control ; Male ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Renin-Angiotensin System ; drug effects

OBJECTIVETo investigate the effects and mechanisms of Shexiang Baoxin Pill (SBP) on myocardial fibrosis in spontaneous hypertensive rats (SHR).

METHODSSHR of 12 weeks old were divided into the SBP group, the control group (treated with benazepril) and the model control group. The effects on such indexes as systolic blood pressure (SBP), left ventricular mass (LVM), left ventricular mass index (LVMI), content of myocardial collagen (MC) in left ventricle, extracellular matrix fibronectin (FN), laminin (LN), cardiac fibroblast (cFb) and transforming growth factor-beta1 (TGF-beta1) were determined after 12 weeks of treatment.

RESULTSSBP had no marked pressure depressive effect, but had the effect similar to that of benazepril in reducing the level of LVM, LVMI and content of MC (P < 0.05), as well as the content of LN, FN in myocardium, cFb count and TGF-beta1 expression (P < 0.05).

CONCLUSIONSBP can prevent and treat myocardial fibrosis, whose action is independent of its hypotensive effect. The mechanism may be associated with such factors as the decrease of MC synthesis in left ventricle and the deposition of extracellular matrix.

Animals ; Collagen ; biosynthesis ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Fibrosis ; prevention & control ; Hypertension ; drug therapy ; pathology ; Hypertrophy, Left Ventricular ; prevention & control ; Male ; Myocardium ; pathology ; Phytotherapy ; Random Allocation ; Rats ; Rats, Inbred SHR ; Transforming Growth Factor beta ; biosynthesis ; genetics ; Transforming Growth Factor beta1

AIMTo investigate the preventive and reversional effect of praeruptorum caumarin compound on left ventricular hypertrophy in renovascular hypertensive rats (RHR) and its mechanism.

METHODSThe two-kidney-one-clip (2K1C) RHR model was used. The blood pressure, wet weight of the left ventricle, surface area of myocardial cells, resting [Ca2+]i level and Na+, K(+)-ATPase, Ca2+, Mg(2+)-ATPase activity of myocardial membrane and mitochondria were measured.

RESULTSPraeruptorum caumarin 30 mg.kg-1.d-1 was given ig for 9 weeks from the 6th or 9th week after operation in the preventive or regressive group. The blood pressure, left ventricle wet weight and area of myocardial cells of the preventive and regressive group were significantly reduced than that of the LVH group. The resting [Ca2+]i of the both praeruptorum caumarin treated groups (121 +/- 13, 133 +/- 9 nmol.L-1) were lower than that of the LVH group (158 +/- 7 nmol.L-1). The KCl-induced [Ca2+]i elevation was decreased more significantly in preventive and regressive group than that of the hypertrophic myocytes. The activity of Na+, K(+)-ATPase and Ca2+, Mg(2+)-ATPase increased by 40% and 93% in the preventive group, 28.4% and 48.8% in regressive group than that of the LVH group.

CONCLUSIONPraeruptorum caumarin was shown to prevent and reverse hypertrophy of LVH by lowering [Ca2+]i and increasing the ATPase activity.

Animals ; Apiaceae ; chemistry ; Ca(2+) Mg(2+)-ATPase ; metabolism ; Calcium ; metabolism ; Cell Separation ; Coumarins ; isolation & purification ; pharmacology ; therapeutic use ; Disease Models, Animal ; Hypertension, Renovascular ; complications ; metabolism ; pathology ; prevention & control ; Hypertrophy, Left Ventricular ; etiology ; metabolism ; pathology ; Mitochondria ; enzymology ; Myocytes, Cardiac ; drug effects ; metabolism ; Plants, Medicinal ; chemistry ; Rats ; Rats, Sprague-Dawley ; Sodium-Potassium-Exchanging ATPase ; metabolism

OBJECTIVEPrevious study showed that the signaling pathway of dual-specificity tyrosine-phosphorylated and regulated kinase 1A (Dyrk1A)-alternative splicing factor (ASF)- alternative splicing of Ca(2+)/calmodulin-dependent protein kinase IIδ (CaMKIIδ) is related to myocardial hypertrophy. The aim of present study was to determine the effect and related mechamism of metoprolol on pressure overload induced myocardial hypertrophy.

METHODSPressure overload-induced hypertension was induced by coarctation of suprarenal abdominal aorta in rats. Rats were randomly divided into sham-operated control, hypertension and hypertension plus metoprolol (30 mg×kg(-1)×d(-1)) groups (n = 10 each). Blood pressure, the left ventricular weight to body weight ratio and cardiomyocytes area were measured, the protein expression of Dyrk1A and ASF were determined by Western blot and mRNA expression of alternative splicing of CaMKIIδ was detected by RT-PCR.

RESULTSFour weeks after coarctation, cardiac hypertrophy was evidenced in rats of hypertensive group, and the protein expression of Dyrk1A was significantly upregulated, while the expression of ASF was significantly downregulated, the mRNA expression of CaMKIIδ A and B were significantly upregulated and mRNA expression of CaMKIIδ C was significantly downregulated compared to those in sham-operated control rats (all P < 0.05). Treatment with metoprolol effectively attenuated cardiac hypertrophy and reversed pressure overload induced changes on Dyrk1A and ASF, and alternative splicing of CaMKIIδ (all P < 0.05).

CONCLUSIONMetoprolol attenuates pressure overload-induced cardiac hypertrophy possibly through modulating Dryk1A-ASF-CaMKIIδ signaling pathways.

Animals ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; metabolism ; Hypertrophy, Left Ventricular ; prevention & control ; Male ; Metoprolol ; pharmacology ; Myocytes, Cardiac ; drug effects ; Nuclear Proteins ; metabolism ; Protein-Serine-Threonine Kinases ; metabolism ; Protein-Tyrosine Kinases ; metabolism ; RNA-Binding Proteins ; metabolism ; Rats ; Rats, Sprague-Dawley ; Serine-Arginine Splicing Factors ; Signal Transduction ; drug effects