EFFECTIVE INVERSION OF LEFT HEART REMODELING BY PHENYLALANINE IN ESSENTIAL HYPERTENSION

Objective The aim is to ascertain whether phenylalanine (Phe) can inverse the left heart"remodeling" in patients with essential hypertension. Methods The changes of echocardiographic variables werecompared aler 3,6 and 9 months of observation between the Phe intervention group (Phe 1g/d+amiloride complex1 tablet/d, 20 cases) and control group (placebo 1g/d+amiloride complex 1 tablet/d, 20 cases) with eitherinterventricular septum and (or) post- wall thickness≥12mm, and were carried on further to compare incross- over trial. Results (1) Phe improved elfectively the left heart and systolic dyslunction; while theimprovement, also shown in control group due to the concurrent use of diuretic antihypertensive drug-amiloridecomplex, was much less evident than that in Phe group. (2) The disturbed left heart structure and systolic functionwere improved prominently while placebo was crossed over to Phe, and the improvement decreased afer Phe wascrrossed over to placebo. (3) The changes almost attained to its peak level after 6 months and not improved furtherat 9 months. (4) The differences seen between above 2 groops could not be eoplained by their diverse drops of bloodpressure. Conclusion Phe does exert an indopendent inverse effect on cardiac "remodeling", which mightimplicate an important clinical oplication upon the prevention and control of essential hypertension and itscomplications.

Effect of Different Styles of Coronary Heart Disease and Its Risk Factors on Cardiac Remodeling and Dysfunction

Objectives To evaluate the effect of different styles of coronary heart disease （CHD）, different regions of acute myocardial infarction （AMI）, its risk factors and branches of coronary stenosis on left ventricular remodeling and dysfunction by applying echocardiography. Methods 251 patients with CHD and 96 patients without CHD （NoCHD） were verified by selective coronary angiography. CHD patients were divided into stable angina pectoris （SAP） 26, unstable angina pectoris（UAP） 53, acute myocardial infarction （AMI） 140 and old myocardial infarction （OMI） 30 based on clinical situation, cTnT, cardiac enzyme and ECG. AMI patients were further divided into subgroups including acute anterior myocardial infarct （Aa,n = 53）, acute inferior myocardial infarction （Ai, n=54） and Aa＋Ai （n=33） based on ECG. Cardiac parameters： end-diastolic interventricular septum thickness（IVSd）, end-diastolic left ventricular internal diameter （LVd）, left ventricular mass （LM）, end-diastolic left ventricular volume （EDV）, end-systolic left ventricular volume （ESV） and left ventricular ejection fraction（LVEF） were measured by ACUSON 128XP/10 echocardiography. Multiples linear regression analyses were performed to test statistical associations between LVEF and the involved branches of coronary stenosis, blood pressure, lipids, glucose and etc after onset of myocardial infarction. Results EDV and ESV were increased and LVEF decreased on patients with AMI,OMI and UAP （P〈0.05-0.0001）. LM was mainly increased in patients with OMI （P〈0.01） and LVd was mainly enlarged in patients with AMI. EF was significantly decreased and EDV, ESV, LM and LVd were remarkably increased in AMI patients with Aa and Aa＋Ai. With the multiple linear regression analyses by SPSS software, we found that LVEF was negatively correlated to the involved branches of coronary stenosis as well as to systolic blood pressure after onset of myocardial infarction while there was no significant correlation between LVEF and other factors. LVEF was significantly decreased, and LVd and LM increased in AMI patients with antecedent hypertension, compared to patients without hypertension （P〈0.001）. Conclusions Effects of different styles of CHD and different regions of AMI on left ventricular remodeling and cardiac function are different. Myocardial infarction, especially Aa and Aa＋Ai, is one of the most important causes of left ventricular remodeling and cardiac dysfunction. Multiple vessel stenosis and systolic blood pressure at the onset of myocardial infarction reduce LVEF in AMI patients. Antecedent hypertension may accelerate the effect of AMI on cardiac remodeling and dysfunction. Therefore primary and secondary preventions of CHD are critical for protecting heart from remodeling and dysfunction.

STUDY OF MORPHOLOGICAL CHANGES OF HEART IN VIRAL MYOCARDITIS CAUSED BY REPETITIVE INFECTION OF CVB_3m

Objective To investigate the morphological changes of heart in viral myocarditis caused by repetitive infection of CVB3m. Methods 4-week-old mice were infected four times intraperitoneally with a timedependent dose and killed at the 10th, 30th and 60th day after the final infection respectively, then we examined the heart changes and collagen hyperplasia by HE, VG stain and 1HC. Results Heart damage appeared very serious at the tenth day, even there were small necrotic foci at the day of 30th, but we could not see any injury of heart 2 months later after final infection. Collagen turned up at the tenth day and there was much more collagen in heart and increased PCVA, CVF index at the sixtieth day. The 1HC of collagen demonstrated the collagen I hyperplasia was much obvious compared to collagen Ⅲ. Conclusion It strongly indicated that repetitive infection of CVB3m could lead to heart fibrosis and ventricular remodeling, which resulted in decreased systolic and diastolic function of heart.

Effects of Qili Qiangxin capsule on lung structural remodeling in heart failure rats after myocardial infarction and its mechanism

Objective To observe the effect of Qili Qiangxin Capsule(QQC)in improving lung structural remodeling on heart failure(HF)rats after myocardial infarction(MI)and to study its possible mechanism.Methods The proximal left anterior descending branch of coronary artery was ligated using a terylene suture to establish

Combined effects of ramipril and angiotensin Ⅱ receptor blocker TCV116 on rat congestive heart failure after myocardial infarction

Background Congestive heart failure (CHF) is a major cause of morbidity and mortality worldwide and angiotensin convertingenzyme inhibitor (ACEI) is the cornerstone in its treatment However, CHF continues to progress despite this therapy, perhaps because of production of angiotensin Ⅱ (Ang Ⅱ) by alternative pathways The present study was conducted to examine the combined effects of a chronic ACEI, ramipril, and a chronic Ang Ⅱ type 1 receptor blocker, TCV116, on rat CHF after myocardial infarction (MI) Methods Congestive heart failure was caused by MI in rats, which was induced by ligating the left anterior descending coronary artery The experiment protocol included shamoperated rats (Sham), MIcontrol rats (MIcontrol), MI rats treated with ramipril 3 mg/kg (MIramipril) or TCV116 2 mg/kg (MITCV116) per day, half dosage (MI1/2R&T) or full dosage (MIR&T) combination of the two At 22 weeks, cardiac hemodynamic parameters such as mean arterial pressure (MAP), left ventricular systolic pressure (LVSP), maximal rate of left ventricule pressure development and decline (LV dP/dtmax) and left ventricular end diastolic pressure (LVEDP), and cardiac morphometric parameters such as heart weight (HW), left ventricular weight (LVW) and left ventricular cavity area (LVCA) were measured, mRNA expressions of cardiac molecule genes such as β myosin heavy chain (βMHC), Btype natriuretic peptide (BNP), transforming growth factorβ1 (TGFβ1), collagen I and Ⅲ were quantified with reverse transcription polymerase chain reaction (RTPCR) in the surviving septum myocardium, and survival rates were calculated Results There were no significant differences in MI sizes (%) among each MI related experimental groups (33±13, 34±14, 33±13, 35±13 and 33±14 for MIcontrol, MIramipril, MITCV116, MI1/2R&T and MIR&T, respectively, no statistical significance for all) Compared with shamoperated rats, MI rats without therapy showed significant increases in morphometric parameters as well as in mRNA expressions of cardiac molecule genes (P<001); while their hemodynamic parameters were significantly impaired (P<001), and in terms of spontaneous deaths survival rate shortened (P<005) Compared with MI rats without therapy, MI rats treated with each single drug showed significant attenuation of mRNA expressions of cardiac molecule genes (P<001); while their hemodynamic parameters were significantly improved (P<005 or P<001), and in terms of spontaneous deaths survival rate prolonged (P<005) Both half and full dosage combined treatments exerted more powerful effects on improvement of cardiac phenotypic changes and on attenuation of βMHC, BNP mRNA expressions (P<005 vs monotherapy); while LVEDP was further lowered (P<005 vs monotherapy) However, the total death in MI rats with full dosage combined treatment was more though there were no significant differences when compared with other treatmentsConclusions The results suggest that treatment with appropriate dosage combination of a chronic ACEI and a chronic ARB may further improve cardiac remodeling and cardiac function after MI