N-乙酰半胱氨酸对心肌梗死心室重构的影响

目的:观察N-乙酰半胱氨酸(NAC)对急性心肌梗死(AMI)左室重构的影响.方法:比较常规治疗组(对照组)和常规治疗基础上加用NAC组(实验组)的超声指标、氨基末端脑钠肽(NT-proBNP)和严重心脏不良事件(MACE).结果:实验组术后3个月左室舒张末容积、左室收缩末容积、心室重构发生率、NT-proBNP、MACE发生率显著低于术前和对照组(P<0.05),左室球形指数和左室射血分数显著高于术前和对照组(P<0.05).结论:NAC可能通过降低NT-proBNP水平而显著改善AMI心室重构.     

急性心肌梗塞后左室舒张功能影响因素的探讨

为探讨急性心肌梗塞（ＡＭＩ）左室舒张功能的变化及影响因素，我们用脉冲多普勒超声心动图测量了７２例ＡＭＩ患者的左室舒张功能，并用多元逐步回归对其影响因素进行了分析。结果表明，７２例病人中Ｅ／Ａ＜１者４１例，占５６．９％。ＡＭＩ后左室舒张功能除受年龄影响外，梗塞面积的大小直接影响左室舒张功能，但与梗塞部位无关，梗塞前心绞痛可减轻梗塞后左室舒张功能的损害，是通过减小梗塞面积而实现的。溶栓治疗可以改善心肌梗塞后的左室舒张功能。     

Neurohormonal effects of early treatment with enalapril after acute myocardial infarction and the impact on left ventricular remodelling

Plasma neurohormones were sequentially analysed in 98 patientswith acute myocardial infarction randomized to treatment withenalapril or placebo for 4–6 months. Plasma angiotensinconverting enzyme activity was rapidly suppressed by enalapril,but unaffected by placebo (P = 0.0001). No significant differenceswere found in the plasma levels of angiotensin II, aldosterone,atrial natriuretic peptide, noradrenaline, adrenaline or dopaminebetween the two treatment groups. Among patients with infarctsize above median, plasma angiotensin II increased during head-uptilt at one month in the placebo group, but not in the enalaprilgroup. Left ventricular end-diastolic volume (LVEDV) and leftventricular endsystolic volume (LVESV) were evaluated by echocardiographyin 28 patients (placebo 15, enalapril 13) and changes in leftventricular volumes between baseline and 4–6 months werecalculated. Only in the placebo group was a positive correlationfound between plasma levels of noradrenaline at day 5–7and the subsequent increase in LVEDV (r = 0.78, P = 0.005) andLVESV (r = 0.75, P = 0.008). The same trend was found for angiotensinII, adrenaline and dopamine levels at days 5–7 and thesubsequent increase in left ventricular volumes. In the placebogroup a negative correlation was found between plasma aldosteroneat days 5–7 and the subsequent increase in left ventricularejection fraction (r = –0.77, P = 0.006) during the studyperiod. Although circulating neurohormones were not significantlyinfluenced by enalapril treatment, it is concluded that enalaprilmay influence the relationship found between sustained neurohormonalactivation and left ventricular remodelling after acute myocardialinfarction.     

A case-control study of melatonin receptor type 1A polymorphism and acute myocardial infarction in a Spanish population

Coronary artery disease (CAD) is a complex disease with genetic and environmental determinants. Although a large number of genetic polymorphisms involved in the pathogenesis of atherosclerosis have been identified, there is still no evidence of a genetic association with CAD. As melatonin might play a role in the pathogenesis of atherosclerosis through its anti-inflammatory and antioxidant properties, we tested whether the expression of six single nucleotide polymorphisms (SNPs) of the melatonin receptor differs in acute myocardial infarction (AMI) patients with acute myocardial infarction (n = 300) compared with healthy age- and sex-matched controls (n = 250). Finally, only MEL1A receptor SNP rs28383653 was selected because of Hardy-Weinberg equilibrium (χ(2) = 0.49). The distribution of genotype frequencies for this SNP showed that the unfavourable CT genotype was significantly more frequent in patients with AMI than in controls (4.5% versus 1.3%; P = 0.006). Multivariable analysis showed a significantly higher frequency of the unfavourable CT genotype in AMI patients with peripheral arteriopathy (28% versus 10%; P = 0.01). This finding suggests a synergism effect between the unfavourable genotype (CT) of the MELIA receptor SNP and the vascular disease in this subgroup of patients. To our knowledge, this is the first study to report an association between a genetic polymorphism of the melatonin receptor 1A and CAD.     

Unfavourable left ventricular remodelling in patients with dobutamine-inducible ischaemia after acute myocardial infarction.

AIMS: Aim of the study was to assess the role of early inducible ischaemia for determining left ventricular remodelling in patients with acute myocardial infarction. METHODS AND RESULTS: In 179 consecutive patients with first myocardial infarction the occurrence of new wall motion abnormalities during dobutamine stress echocardiography at discharge was related to the left ventricular volume changes at 6 months. Left ventricular end-diastolic and end-systolic index volumes (mL/m(2)) were echocardiographically detected at discharge and at 6 months and the relative changes were calculated. The study population consisted of 105 patients without and 74 patients with inducible ischaemia; of these, 46 patients had > or =4 ischaemic segments. At 6 months, the end-diastolic index volume increased in patients with inducible ischaemia compared to patients without (+7.5+/-11.2 vs -0.1+/-10.2 mL/m(2); P=0.0049) and final mean end-diastolic volume was greater in patients with inducible ischaemia than without (70.8+/-16.0 vs 61.1+/-17.0 mL/m(2); P=0.0012). The end-systolic volume increased at 6 months in patients with inducible ischaemia and it decreased in patients without (+2.8+/-8.6 vs -1.4+/-7.8 mL/m(2); P=0.021). At the multivariate analysis, inducible ischaemia in > or =4 segments (odds ratio=6.43), the wall motion score index at the peak of dobutamine infusion (odds ratio=1.14) and the end-systolic index volume at discharge (odds ratio=1.06) were independent predictors of subsequent left ventricular end-diastolic index volume increase > or =15 mL/m(2). CONCLUSION: In patients with first myocardial infarction the presence and the severity of inducible ischaemia, as detected by dobutamine stress echocardiography at discharge, indicates an unfavourable left ventricular remodelling.     

肝细胞生长因子对急性心肌梗死后左室重构的预测作用

目的: 探讨血清肝细胞生成因子(HGF)对急性心肌梗死(AMI)后早期左室重构的预测价值。方法: 36例AMI患者入院时及发病7 d测定血清HGF水平;AMI其中的26例分别于发病后7~10 d及发病后3个月行超声心动图检查,3个月时左室舒张末期容积指数（LVEDVI）与7~10 d时比增加≥5 ml/m2定义为左室重构组(n=11),对两组血清HGF值进行比较。结果: AMI患者入院时血清HGF浓度较对照组明显升高［(809±288)ng/L vs.(620±162)ng/L,P<0.01］,7 d时升高更显著［(1 607±1 355)ng/L,P<0.01］。发病7 d时血清HGF浓度在左室重构组较非左室重构组升高［(2 216±1 522)ng/L vs.(1 176±593)ng/L,P<0.05］,而入院时两组浓度则无显著差异。结论: AMI时血清HGF浓度升高,AMI后7 d时增高的血清HGF可能预示心室重构。     

血管内超声参数与非ST段抬高型急性心肌梗死患者冠状动脉病变及左心室功能的关系

[目的]探究血管内超声(IVUS)参数与非ST段抬高型急性心肌梗死(NSTEAMI)患者冠状动脉病变及左心室功能的相关性。[方法]选取2016年6月—2021年12月佛山市三水区人民医院收治的90例NSTEAMI患者为研究对象,根据冠状动脉病变支数分为单支病变组(42例)和多支病变组(48例)。分析NSTEAMI患者冠状动脉病变加重的独立预测因素,构建列线图预测模型并进行评价。采用Pearson检验分析斑块负荷、偏心指数、重构指数、纤维帽厚度与左心室射血分数(LVEF)间的相关性。采用受试者工作特征(ROC)曲线分析IVUS参数变化对NSTEAMI患者冠状动脉病变加重的预测价值。[结果]血清胱抑素C(CysC)>1.54 mg/L(OR=2.115,95%CI:1.377～3.047)、高敏C反应蛋白(hs-CRP)>34.25 mg/L(OR=1.342,95%CI:1.128～2.412)、斑块负荷>60%(OR=1.399,95%CI:1.232～2.405)、偏心指数>6.99(OR=1.357,95%CI:1.035～2.164)、重构指数>0....     

Emergency coronary angioplasty in patients with severe left ventricular dysfunction or cardiogenic shock after acute myocardial infarction

Emergency percutaneous transluminal coronary angioplasty (PTCA) was performed during an acute myocardial infarction (AMI) after either systemic or intracoronary thrombolytic therapy in six patients with severe ischaemic left ventricular dysfunction or cardiogenic shock, among 37 patients (17%) who were treated with PTCA during AMI over a 13-month period. Thrombolytic therapy with streptokinase (1.5 x 10 Units) was initiated after a mean (+/- SD) time delay of 5.5 +/- 1.3 h from the onset of symptoms. The infarct-related artery was found to be occluded (TIMI grade 0-1) in three patients and partially reperfused (TIMI grade 2) in the remaining patients at baseline coronary angiography. Intracoronary administration of urokinase (100-200,000 Units) was ineffective in those patients failing systemic thrombolysis and resulted in only a slight increase of residual lumen in three patients. The coronary artery could be opened by a guidewire mechanical technique in patients with persistent coronary artery occlusion and coronary dilation could be done in all patients. The mean percentage diameter stenosis of the infarct-related vessel was reduced from 98.8 +/- 2% to 27 +/- 11% (P less than 0.005). After the procedure, left ventricular ejection fraction increased from 27 +/- 8% to 41 +/- 7% (P less than 0.02), systemic blood pressure and cardiac index increased respectively from 86 +/- 10 to 126 +/- 14 mmHg (P less than 0.005) and from 2.2 +/- 0.6 to 3.3 +/- 0.6 (P less than 0.01). Left ventricular end-diastolic pressure decreased from 26 +/- 8 to 18 +/- 3 mmHg (P less than 0.05). Severe mitral regurgitation was relieved in one patient.(ABSTRACT TRUNCATED AT 250 WORDS)     

Spontaneous recovery of left ventricular function following acute anterior myocardial infarction

Four patients with acute anterior wall myocardial infarction showing spontaneous and marked improvement in systolic left ventricular function are described. All 4 patients showed abnormal Q waves and severe wall motion abnormalities soon after acute infarction. In all 4 patients, at least some regeneration of R-wave forces occurred and the regional wall motion in the involved area of the left ventricle improved dramatically without coronary angioplasty or surgical revascularization during the intervening period. The improvement in left ventricular function was attributed to spontaneous increase in nutrient flow to the involved area. It is concluded that Q waves and severe wall motion abnormalities do not necessarily indicate irreversible scar formation.     

Early ventricular fibrillation in patients with acute myocardial infarction: correlation with coronary angiographic findings

To define coronary angiographic characteristics of patientsexperiencing early primary ventricular fibrillation (VF) inthe acute phase of myocardial infarction we studied 266 consecutivepatients without clinical evidence of heart failure. Twenty-sixpatients (group 1) experienced early (< 12 h from the onsetof symptoms of myocardial infarction) primary VF whereas 240patients (group 2) with the same clinical characteristics servedas an appropriately matched cohort. All patients were catheterizedbefore or soon after hospital discharge (1 to 8 weeks afterthe acute event). There was no significant difference in left ventricular ejectionfraction between the two groups of patients (39.6±6%vs 36.9±8%, P = ns). Patients with early VF had a significantlygreater number of diseased vessels than those without VF (3.38±1.05vs 2.03±1.25. P <0.001) and a higher coronary arteriographicGensini score (29.31±4.80 vs 20.16±4.14, P <0.001).The left anterior descending coronary artery was identifiedas the infarct-related vessel in 53.6% of group 1 vs 44.5% ofgroup 2 patients (P <0.05). The mean maximal serum creatinekinase values were not significantly different (1897±1062vs 1426 ±839 IU.l–1, P=ns) between the two groups. These data indicate that patients with early primary VF in thesetting of acute myocardial infarction may have more extensivecoronary artery disease than similar patients without VF. Aworse prognosis could be anticipated for these patients on thebasis of worse coronary anatomy. A more aggressive therapeuticapproach with routine coronary angiography before hospital dischargecould reasonably be justified for patients with early primaryVF complicating acute myocardial infarction.     

螺内酯抑制急性前壁心肌梗死患者的左室重构

目的探讨急性前壁心肌梗死患者口服螺内酯对于左室重构的影响。方法将急性前壁心肌梗死患者随机分为两组。对照组30例,接受血管紧张素转换酶抑制剂、β-受体阻滞剂、抗血小板、调脂药物等常规处理。螺内酯组30例,在常规治疗基础上加用螺内酯（40mg,每日1次）。随访1年,并检测脑钠尿肽（BNP）及超声心动图以评价左室功能和左室容积。结果6和12月时螺内酯组血清BNP水平明显低于对照组[（355±74）ng/Lvs（418±77）ng/L,P<0.05和（316±72）ng/Lvs（389±67）ng/L,P<0.05],且12月时螺内酯组较对照组左室舒张末期内径（LVEDD）、左室收缩末期内径（LVESD）明显缩小[LVEDD:（49±6）mmvs（53±5）mm,P<0.05;LVESD:（37±5）mmvs（40±4）mm,P<0.05]。结论螺内酯可抑制急性前壁心肌梗死患者左室重构。     

急性心肌梗死后择期冠脉介入治疗对左室重构和心功能的影响

目的探讨急性心肌梗死（AMI）后择期经皮冠状动脉介入（PCI）治疗对左心室重构和心功能的影响。方法112例AMI患者,分为PCI组和药物治疗组,PCI组于发病后1～2周内行PCI治疗,所有患者于发病后1～2周时、4周和24周时行超声心动图（UCG）检查,观察左心室收缩末容积指数（LVESVI）、左心室舒张末容积指数（LV-EDVI）和左室射血分数（LVEF）。结果行PCI治疗后,血管再通率为100%,术后4周和24周的LVESVI、LVEDVI和LVEF均明显优于术前,与药物治疗组比较有显著性差异（P<0.05）。结论AMI后择期PCI治疗能够有效抑制左心室重构,改善心功能。     

The acute effects of intravenous nisoldipine on left ventricular function within 24 h after acute myocardial infarction.

Nisoldipine is a calcium antagonist with potent coronary vasodilating effects in patients with chronic stable angina pectoris. We studied the acute effects of nisoldipine in six patients within 24 h (mean 14 +/- 4 h) after the onset of myocardial infarction. Nisoldipine was administered as a 4.5 micrograms kg-1 intravenous bolus over 3 min followed by intravenous infusion of 0.2 microgram kg-1 min-1 during 60 min. Radionuclide angiography, cardiac output and intra-arterial blood pressure measurements were performed before and during nisoldipine. Left ventricular ejection fraction increased from 48.3 +/- 10.3% to 55.3 +/- 11.8% (P = 0.034) during nisoldipine infusion. Regional wall motion score changed during nisoldipine infusion from 3.3 +/- 2.5 to 1.8 +/- 2.6 (P = 0.027). Cardiac output increased from 5.5 +/- 1.0 to 7.3 +/- 1.3 l min-1 (P = 0.0001). Heart rate increased from 78 +/- 12 to 88 +/- 11 beats.min-1 (P = 0.004). Mean arterial blood pressure decreased from 91.7 +/- 20.2 to 78.7 +/- 13.1 mmHg (P = 0.038). The rate-pressure product did not change significantly during nisoldipine infusion. It is concluded that nisoldipine improves global and regional left ventricular function in patients with acute myocardial infarction within the first 24 h. Our findings suggest that this effect is achieved without increasing myocardial oxygen demand.     

Role of aldosterone in mid- and long-term left ventricular remodelling after acute myocardial infarction: The REMI study

Aims

Whether aldosterone levels after myocardial infarction (MI) are associated with mid- and long-term left ventricular (LV) remodelling in the era of systematic use of renin–angiotensin system inhibitors is uncertain. We prospectively investigated the relationship between aldosterone levels and mid- and long-term LV remodelling in patients with acute MI.

Methods and results

Plasma aldosterone was measured in 119 patients successfully treated by primary percutaneous coronary angioplasty for a first acute ST-elevation MI (STEMI) 2–4 days after the acute event. LV volumes were assessed by cardiac magnetic resonance (CMR) and transthoracic echocardiography (TTE) in the same timeframe and 6 months later. LV assessment was repeated by TTE 3–9 years after MI (n = 80). The median aldosterone level at baseline was 23.1 [16.8; 33.1] pg/ml. In the multivariable model, higher post-MI aldosterone concentration was significantly associated with more pronounced increase in LV end-diastolic volume index (TTE: β ± standard error [SE]: 0.113 ± 0.046, p = 0.015; CMR: β ± SE: 0.098 ± 0.040, p = 0.015) and LV end-systolic volume index (TTE: β ± SE: 0.083 ± 0.030, p = 0.008; CMR: β ± SE: 0.064 ± 0.032, p = 0.048) at 6-month follow-up, regardless of the method of assessment. This result was consistent also in patients with a LV ejection fraction (LVEF) >40%. The association between baseline plasma aldosterone and adverse LV remodelling did not persist at the 3–9-year follow-up evaluation.

Conclusion

Aldosterone concentration in the acute phase was associated with adverse LV remodelling in the medium term, even in the subgroup of patients with LVEF >40%, suggesting a potential role of the mineralocorticoid system in post-MI adverse remodelling. Plasma aldosterone was no longer associated with LV remodelling in the long term (NCT01109225).     

Coronary collateral development after acute myocardial infarction

In 31 patients without a history of preinfarction angina, coronary collateral circulation to the completely obstructed coronary artery was evaluated by coronary angiography during a convalescent period of their first myocardial infarction. Collateral visualization (collateral index) was found to be significantly greater in patients with involvement of the right coronary artery (2.1 +/- 1.1, SD) than in those with obstruction of the left anterior descending coronary artery (1.2 +/- 1.0, p less than 0.05). The time interval from the onset of symptoms of acute myocardial infarction to angiographic evaluation did not affect the extent of collateral visualization or the degree of coronary artery disease. These findings indicate that the collateral vessels develop after acute myocardial infarction regardless of the extent of coronary artery disease and accomplish the proliferative process within one month. It is also suggested that the collateral visualization is dependent on the size of perfusion territory of the infarct-related coronary artery.     

Coronary collaterals and left ventricular function early after acute transmural myocardial infarction

The coronary collateral circulation and ventricular function,segmental wall motion and infarct size, were investigated fromhemodynamic and angiographic data in 126 patients with acutetransmural myocardial infarction and complete obstruction ofa major coronary vessel. The patients were divided into twogroups: 74 with obstruction of the right coronary artery and52 with obstruction of the left anterior descending artery.The collateral circulation was rated as absent, poor, fair oradequate: two weeks after infarction, collateral vessels wereobserved in only 27% (poor 15.4%, fair 5.8%, adequate 5.8%)of the patients with an anterior myocardial infarction and inonly 35% (poor 13.5%, fair 16.4%, adequate 4.5%) of the patientswith an inferior myocardial infarction. In both groups of patients, the presence of collateral vesselshad no significant influence on the following parameters: leftventricular performance (left ventricular end-diastolic pressure,left ventricular enddiastolic volume, ejection fraction andmean velocity of fiber shortening), extent of abnormally contractingsegment and segmental wall motion. After anterior myocardialinfarction, there was an insignificant trend to lesser myocardialdamage in patients with coronary collaterals. Thus, coronary collaterals are infrequent in patients with acutetransmural myocardial infarction and total obstruction of acoronary vessel; in these patients we conclude that the collateralshave no effect either on left ventricular function or on thesize of the infarction.     

急性心梗心电图QRS波终末变形与左室功能变化的研究

目的探讨急性心肌梗死患者心电图QRS波终末变形情况与左心室功能变化的关系。方法根据入院心电图将急性心梗患者分成QRS终末变形阳性(QRS+)组(n=22)与QRS终末变形阴性(QRS-)组(n=46),于经皮冠状动脉介入术后2周与6个月时行超声心动图检查。结果术后6个月时QRS-组左心室舒张末期容积指数(LVEDVI)、左室收缩末期容积指数(LVESVI)及室壁活动异常积分(VWMA)明显小于QRS+组p<0.05),而左室射血分数(LVEF)显著高于QRS+组(p<0.05)。结论心电图QRS终末变形可作为急性心梗后左室重构和左室功能变化的预测因子之一。     

Simultaneous assessment of segmental and global left ventricular function by two-dimensional echocardiography in acute myocardial infarction

Both segmental and global left ventricular performance were assessed simultaneously in 29 patients with acute myocardial infarction using two-dimensional echocardiography. Comparisons were made between left ventricular wall motion versus peak CK-MB, site of infarction, and occurrence of heart failure. Two-dimensional echocardiography identified areas of dyssynergy which corresponded to electrocardiographic areas of infarction in 89% of all cases. Patients with heart failure had more dyssynergic segments, and these segments manifested more severe dyssynergy than patients without heart failure. Patients with severe global dysfunction manifested higher peak CK-MB values, and those with anterior infarction had more global dyssynergy than did those patients with inferior infarction. These observations suggest that two-dimensional echocardiography is a useful technique for localization and assessment of segmental and global dyssynergy in acute myocardial infarction. Information so derived correlates with the clinical status of patients with acute myocardial infarction, and may offer important insights into both prognosis and treatment.     

Effect of hepatocyte growth factor on left ventricular remodeling after acute myocardial infarction in canine

Background and objectives To investigate the effect of hepatocyte growth factor (HGF) on left ventricular (LV) remodeling after acute myocardial infarction (AMI). Methods AMI was produced by ligation of proximal left anterior descending coronary artery(LAD) in 12 mongrel canines. These animals were randomized into 2 groups. In HGF group (n=6), canines were injected with pcDNA3-HGF lml (about 300ug) at the margin of infarcted myocardium; in control group (n=6) canines were injected with equal volume of normal saline. Cardiac function and left ventricular remodeling were evaluated with echocardiography at 1, 4, 8 weeks after MI. LV myocardium specimens were obtained at 8 weeks and stained with hematoxylin and eosin for histological examination or with sirius red to assess the collagen content. Results Compared with control group, LVEF in HGF group was significantly higher at 4 weeks (49.61+6.66 vs 39.84+6.39; P＜0.05) and at 8 weeks (51.57+8.53 vs 40.61+7.67; P＜0.05) after AMI, while LVESV was significantly lower in HGF group than that in control group at 8 weeks after AMI (18.98+3.47 vs 25.66+5.86; P＜0.05). Posterior left ventricular wall thickness decreased significantly from 1 wk to 8 wks after AMI in control group, while remained unchanged in HGF group. Compared with control group, histological examination showed more neovascularization and less scar, and sirius red staining indicated higher volume of type Ⅲ collagen (7.10&#177;4.06% vs 3.77&#177;1.09%; P＜0.05) and lower collagen Ⅰ/Ⅲ ratio value (1.11&#177;0.52 vs 2.94&#177;2.48; P＜0.05)in HGF group. Conclusion HGF gene transfer might improve cardiac function and LV remodeling after acute myocardial infarction by stimulating angiogenesis, reducing fibrosis, and reducing myocardial scarring.     

Sustained cardiomyocyte apoptosis and left ventricular remodelling after myocardial infarction in experimental diabetes

Aims/hypothesis Diabetes is known to reduce survival after myocardial infarction. Our aim was to examine whether diabetes is associated with enhanced cardiomyocyte apoptosis and thus interferes with the post-infarction remodelling process in myocardium in rat.Methods Four weeks after intravenous streptozotocin (diabetic groups) or citrate buffer (controls) injection, myocardial infarction was produced by ligation of left descending coronary artery. Level of cardiomyocyte apoptosis was quantified by TUNEL and caspase-3 methods. Collagen volume fraction and connective tissue growth factor were determined under microscope. Left ventricular dimensions were evaluated by echocardiography and planimetry.Results The number of apoptotic cardiomyocytes was equally high in diabetic and non-diabetic rats after 1 week from infarction. At 12 weeks after infarction the number of apoptotic cells was higher in the diabetic as compared to non-diabetic rats both in the border zone of infarction and in non-infarcted area. Correspondingly, left ventricular end diastolic diameter, relative cardiac weight, connective tissue growth factor-expression and fibrosis were increased in diabetic compared with non-diabetic rats with myocardial infarction.Conclusion/interpretation Sustained cardiomyocyte apoptosis, left ventricular enlargement, increased cardiac fibrosis and enhanced profibrogenic connective tissue growth factor expression were detected after myocardial infarction in experimental diabetes. Apoptotic myocyte loss could be an important mechanism contributing to progressive dilatation of the heart and poor prognosis after myocardial infarction in diabetes.Abbreviations STZ streptozotozin - MI myocardial infarction - CTGF connective tissue growth factor - LV left ventricular - LVEDD LV end-diastolic diameter - BNP B-type natriuretic peptide