颈交感干离断对急性心肌梗死大鼠左室重构的影响

目的 探讨颈交感干离断(TCST)对急性心肌梗死大鼠左室重构的影响.方法 健康清洁级成年雄性SD大鼠64只,体重230～250 g,随机分为4组(n=16):假手术组(S组)、心肌梗死组(MI组)、左TCST组(LT组)、右TCST组(RT组).采用结扎左冠状动脉前降支的方法 制备急性心肌梗死模型.S组只穿线不结扎左冠状动脉前降支,分离颈交感干,不离断;MI组制备心肌梗死模型,随后分离颈交感干,不离断;LT组和RT组在心肌梗死模型制备成功后,分别实施左、右侧TCST.于TCST后第4周,每组随机选取8只大鼠,称重,随后处死,取左心室组织,称量,计算左心室质量指数(左心室质量/体重),并采用体视学三维形态定量分析左室重构情况,测定左心室心肌细胞体积密度(V_v)、心肌组织总体积(V_t)和心肌细胞总体积(V_c),采用RT-PCR测定心肌c-fos mRNA的表达水平.结果 与S组比较,其余各组左心室质量指数增加,心肌c-fos mRNA表达上调,左心室V_t和V_c增大,MI组和LT组左心室V_v增大(P<0.01),RT组左心室V_v差异无统计学意义(P>0.05);与MI组比较,LT组左心室质量指数增加,心肌c-fos mRNA表达上调,左心室V_t和V_c增大(P<0.05或0.01),左心室V_v差异无统计学意义(P>0.05),RT组左心室质量指数降低,心肌c-fos mRNA表达下调,左心室V_v、V_t和V_c减小(P<0.05或0.01);与LT组比较,RT组左心室质量指数降低,c-fos mRNA表达下调,左心室V_v、V_t和V_c减小(P<0.05).结论 右侧TCST可下调心肌梗死大鼠心肌c-fos mRNA的表达,一定程度上抑制左室重构;而左侧TCST可进一步诱导c-fos mRNA表达,促进左室重构的发展.     

心室重塑中基质金属蛋白酶和组织抑制酶的表达

目的 观察大鼠心肌梗死后基质金属蛋白酶-2，9(MMP-2，9)和组织金属蛋白酶抑制剂-1(TIMP-1)的变化规律。方法 结扎SD大鼠冠状动脉前降支建立心肌梗死模型。分为对照组(n=20)、心肌梗死组(Ⅰ组，n=48)，酶谱法测定心肌梗死后MMP-2，9活性蛋白的表达规律，Western blotting进一步确定所消化条带酶的属性。结果正常心肌中无活性MMP-9的存在。MMP-2蛋白水平在心肌梗死后第1、2周活性增强、表达增加，MMP-9第1、2、4周活性增强、表达增加，TIMP-1蛋白含量减少。结论 心肌梗死后心肌组织内MMP-2，9的活性增高和蛋白含量增加，TIMP-1蛋白含量减少，是心室重塑机制重要组成部分。MM-9在心肌梗死后心室重塑过程中可能具有特殊的地位。     

Giant left ventricular pseudo-false aneurysm following myocardial infarction

We report a successful surgical ease of giant left ventricular pseudo-false aneurysm in a 63-year-old man. The abnormality of the inferior wall of the left ventricle was discovered incidentally by abdominal ultrasonography for health examination at another hospital. Transthoracic echocardiography and left ventriculography revealed a giant false aneurysm (74×75×40 mm) in the inferior wall of the left ventricle with a large orifice (70×58 mm). Repair of the aneurysm was performed under arrested heart, closing the large orifice with a Hemashield patch. Postoperative pathological examination proved that the wall of the aneurysm had myocardial tissue. The microscopic results strongly suggested that this aneurysm was a pseudo-false aneurysm.     

Self-limiting left ventricular wall rupture following myocardial infarction

Abstract   A left ventricular posterior–inferior free wall rupture without pseudo aneurysm following inferior myocardial infarction was identified in a 40-year-old male patient. Coronary angiography of the patient demonstrated a total occlusion of the circumflex artery. Repair of the rupture was performed during an elective surgery carried out 15 days after the infarction. We approved to discuss this rarely encountered clinical case with the cases in the literature.     

胸段硬膜外阻滞对心肌梗塞兔左心室实质早期重构的影响

目的探讨胸段硬膜外阻滞对心肌梗塞兔左心室实质早期重构的影响。方法成年健康新西兰兔60只,随机分为3组（n=20）：假手术组（S组）、心肌梗塞组（MI组）和胸段硬膜外阻滞组（TEB组）。结扎冠状动脉左前降支制备心肌梗塞模型,S组和MI组硬膜外注射0.9%生理盐水0.5 ml/kg,2次/d,持续4周;TEB组于硬膜外注射0.1%罗哌卡因0.5 mg/kg,2次/d,持续4周。给药4周后处死动物,称取左室重量,计算左室重量指数;制备心肌组织切片,观察病理学;测量心肌细胞直径;RT-PCR法检测心肌转化生长因子-β1（TGF-β1）mRNA和β-肌球蛋白重链（β-MHC）mRNA的表达水平。结果3组左室重量指数差异无统计学意义（P〉0.05）;与S组比较,MI组和TEB组细胞直径增加,MI组TGF-β1 mRNA和β-MHC mRNA表达均增加,TEB组TGF-β1表达增加（P〈0.05或0.01）;与MI组比较,TEB组细胞直径减少,TGF-β1 mRNA和β-MHC mRNA表达均降低（P〈0.05或0.01）;TEB组心肌组织病理学损伤较MI组轻。结论胸段硬膜外阻滞可一定程度上抑制心肌梗塞兔左心室实质早期重构,其机制与下调心肌梗塞导致的TGF-β1 mRNA和β-MHC mRNA表达增加有关。     

Repair of ventricular septal defect and left ventricular aneurysm following myocardial infarction

A successful simultaneous surgical repair of rupture of the interventricular septum and left ventricular aneurysm resulting from myocardial infarction is described. Very few similar cases have been described in the literature and in none was angiocardiography performed before operation. Preoperative angiocardiographic examination to demonstrate a ventricular aneurysm is of major importance in all cases of rupture of the interventricular septum following myocardial infarction. The right heart approach with injection of contrast material into the main pulmonary artery is shown to be the method of choice for this purpose.     

Matrix metalloproteinase inhibition modifies left ventricular remodeling after myocardial infarction in pigs

BACKGROUND: Global and regional shape changes that occur within the left ventricular wall after myocardial infarction have been termed infarct expansion. A potential mechanism for this postinfarction remodeling is activation of the matrix metalloproteinases. Accordingly, the present study examined the effects of matrix metalloproteinase inhibition on left ventricular global geometry after myocardial infarction in pigs. METHODS: Myocardial infarction was created in pigs by means of occlusion of the first and second obtuse marginal branches of the circumflex coronary artery, resulting in a uniform left ventricular free wall infarct size of 21% +/- 2%. At 5 days after infarction, the pigs were randomized to undergo broad-spectrum matrix metalloproteinase inhibition (n = 9; PD166793, 20 mg. kg(-1). d(-1) by mouth) or myocardial infarction alone (n = 8). Ten pigs served as noninfarction control animals. Left ventricular end-diastolic area, determined by means of echocardiography, was measured 8 weeks after infarction. RESULTS: Left ventricular end-diastolic area increased in both the myocardial infarction plus broad-spectrum matrix metalloproteinase inhibition and myocardial infarction only groups compared to reference control animals (3.7 +/- 0.2 cm(2)), but was reduced with broad-spectrum matrix metalloproteinase inhibition compared to myocardial infarction alone (4.5 +/- 0.2 vs 4.9 +/- 0.2 cm(2), respectively; P <.05). Regional radial stress within the infarct region increased in both infarction groups when compared to values obtained from reference control animals (599 +/- 152 g/cm(2)), but was attenuated in the myocardial infarction plus broad-spectrum matrix metalloproteinase inhibition group compared to the myocardial infarction alone group (663 +/- 108 vs 1242 +/- 251 g/cm(2), respectively; P <.05). Similarly, regional myocardial stiffness increased in both the myocardial infarction plus broad-spectrum matrix metalloproteinase inhibition and the myocardial infarction only groups compared with that observed in reference control animals (14 +/- 1 rkm, P <.05) but was lower with broad-spectrum matrix metalloproteinase inhibition than with myocardial infarction alone (42 +/- 6 vs 68 +/- 10 rkm, respectively; P <.05). CONCLUSIONS: Matrix metalloproteinase inhibition reduced postinfarction left ventricular dilation, reduced regional myocardial wall stress, and modified myocardial material properties. These unique findings suggest that increased myocardial matrix metalloproteinase activation after infarction contributes directly to the left ventricular remodeling process.     

Effects of sevoflurane and propofol on left ventricular diastolic function in patients with pre-existing diastolic dysfunction

Background. The effects of anaesthetics on left ventricular(LV) diastolic function in patients with pre-existing diastolicdysfunction are not well known. We hypothesized that propofolbut not sevoflurane will worsen the pre-existing LV diastolicdysfunction. Methods. Of 24 randomized patients, 23 fulfilled the predefinedechocardiographic criterion for diastolic dysfunction. Theyreceived general anaesthesia with sevoflurane 1 MAC (n=12) orpropofol 4 µg ml^–1 (n=11). Echocardiographic examinationswere performed at baseline and in anaesthetized patients underspontaneous breathing and under positive pressure ventilation.Analysis focused on peak early diastolic velocity of the mitralannulus (E_a). Results. During spontaneous breathing, E_a was higher in thesevoflurane than in the propofol group [mean (95% CI) 7.0 (5.9–8.1)vs 5.5 (4.7–6.3) cm s^–1; P<0.05], reflectingan increase of E_a from baseline only in the sevoflurane group(P<0.01). Haemodynamic findings were similar in both groups,but the end-tidal carbon dioxide content was more elevated inthe propofol group (P<0.01). During positive pressure ventilation,E_a was similarly low in the sevoflurane and propofol groups[5.3 (4.2–6.3) and 4.4 (3.6–5.2) cm s^–1, respectively]. Conclusions. During spontaneous breathing, early diastolic functionimproved in the sevoflurane but not in the propofol group. However,during positive pressure ventilation and balanced anaesthesia,there was no evidence of different effects caused by the twoanaesthetics.     

Doxycycline ameliorates ischemic and border-zone remodeling and endothelial dysfunction after myocardial infarction in rats.

BACKGROUND: Although matrix metalloproteinase (MMP) activity increases, endothelial function decreases after myocardial infarction (MI). The antibiotic doxycycline inhibits MMP activity in vitro. The role of doxycycline-mediated MMP inhibition in endothelial function is unclear. HYPOTHESIS: Doxycycline ameliorates endothelial dysfunction, in part, by inhibiting MMP activity. METHODS: We subjected Sprague-Dawley male rats to MI by ligating the left anterior descending arteries. We subjected another group of rats to sham surgery. We administered doxycycline in drinking water (0.67 mg/ml) to both groups 2 days before surgery: the sham group underwent sham surgery and received doxycycline therapy, and the MI group underwent MI and received doxycycline therapy (n = 6 in each group). After 4 weeks, we anesthetized rats and prepared left ventricular rings from infarcted-ischemic (I), non-infarcted near-infarcted (NI), and sham surgery hearts with and without doxycycline treatment. RESULTS: The MMP-2 activity increased significantly in I and NI hearts, and we observed a selective increase in MMP-9 activity only in I hearts, when compared with other groups (p < 0.05), measured by zymography. Cardiac inhibitor of metalloproteinase decreased only in I hearts (p < 0.05 vs other groups), measured by Western analysis, and doxycycline treatment reversed this decrease. Contractile response of rings to acetylcholine was attenuated in the I group, suggesting nitric oxide-mediated dysfunction, and was reversed by doxycycline. The response to nitroprusside was attenuated in I hearts and ameliorated by doxycycline, suggesting cardiomyocyte dysfunction. Bradykinin induced relaxation in rings from sham surgery hearts and from NI hearts, but induced paradoxic contraction in rings from I hearts. Treatment with doxycycline reversed the paradoxic contraction. CONCLUSION: Results suggest a protective action of doxycycline in the ischemic heart, possibly because of additional pharmacologic actions such as metalloproteinase inhibition.     

Improved functional results following myocardial revascularization in patients with left ventricular dysfunction

Between February 1978 and October 1982, 40 patients with preoperative ejection fraction (EF) of 0.35 or less underwent aortocoronary bypass. An average of 3.1 saphenous vein grafts per patient were inserted and revascularization was considered complete in 33 (82%) of the subjects in the group. Mean follow-up period was 29 months (range 12-65 months). Early mortality was 5% (2 patients) and there were seven late deaths (3 cardiac and 4 non-cardiac). The five-year cardiac actuarial survival rate was 74% +/- 13% (+/- SEM). Angina has improved in 29 (94%) of the 31 long-term survivors with 23 (74%) being totally asymptomatic. Twenty-two of the long-term survivors performed an exercise test at the end of their follow-up period. These tests revealed that bypass surgery in such patients results in significantly enhanced myocardial oxygen consumption with concomitant increase in effort level and duration. The exercise ability is probably directly related to the degree of revascularization.     

Right ventricular diastolic dysfunction in patients with left ventricular hypertrophy: analysis of right ventricular myocardial relaxation using two-dimensional speckle tracking imaging

Background  Although several previous studies have suggested the presence of right ventricular (RV) diastolic dysfunction in patients with hypertrophic cardiomyopathy (HCM) and those with hypertensive left ventricular hypertrophy (HT-LVH), the mechanisms are still unclear. This study aimed to clarify the relationship between the RV global diastolic dysfunction in these patients and the regional myocardial diastolic function, including synchronicity of the interventricular septum and RV free wall. Methods  In 20 age-matched patients with HT-LVH, 20 patients with HCM and 22 control subjects without pulmonary hypertension, RV isovolumic relaxation time (IRT_R) was measured using continuous-wave Doppler echocardiography. The early diastolic peak strain rate (E _SR) and time from QRS to E _SR (T–E _SR) were measured in the apical, mid-ventricular and basal segments of the interventricular septum and RV free wall using two-dimensional speckle tracking imaging (2DST). Results  IRT_R was more prolonged both in HT-LVH and in HCM than in the controls. The averaged septal E _SR was reduced both in HT-LVH and in HCM (P < 0.0001, respectively), but the averaged RV free wall E _SR was decreased only in HCM (P = 0.0007). E _SR averaged for six septal and RV free wall segments was correlated with IRT_R (r = −0.46, P = 0.0001). Neither intergroup difference nor correlation with IRT_R was observed in a coefficient of variation of T–E _SR for the six segments. Conclusions  RV global diastolic function is impaired in patients with HT-LVH and HCM due to relaxation abnormalities, not an asynchrony, of the myocardium surrounding the RV cavity. The detection of RV free wall relaxation abnormality using 2DST may be useful to differentiate HCM from HT-LVH.     

Management of ventricular aneurysms following myocardial infarction

Aneurysmectomy is the most effective form of therapy for patients with symptomatic aneurysms of the left ventricle following myocardial infarction. Operation should not be undertaken less than 2 months following myocardial infarction unless there is severe hemodynamic derangement. Circulatory assist devices, such as the intra-aortic balloon pump, have been of particular help in this group of severely ill patients. Results of elective aneurysmectomy performed 2 months or more following myocardial infarction are quite good, with the long-term outlook for the patient generally depending on the function of the uninvolved myocardium and the status of the remaining coronary circulation. When ventricular irritability results in life-threatening arrhythmia, aneurysmectomy must often be performed. The results in this group of patients have been somewhat disappointing, but newer techniques of localizing irritable foci may result in the development of more effective surgical procedures.

---

Résumé La résection de l'anévrisme est la thérapeutique la plus efficace chez les malades qui présentent, après infarctus du myocarde, des symptomes d'anévrisme ventriculaire gauche. L'opération ne doit pas être faite avant le 2ème mois post-infarctus, sauf s'il existe de graves troubles hémodynamiques. Dans ce groupe de malades graves, les méthodes d'assistance circulatoire, comme la contrepulsion aortique, sont très utiles. La résection de l'anévrisme donne de très bons résultats lorsqu'on peut attendre un minimum de 2 mois après l'infarctus pour opérer le malade. Le pronostic à long terme dépend, en général, de l'état fonctionnel du myocarde restant et de la qualité de la circulation coronaire. Lorsqu'une irritabilité ventriculaire entraîne des arythmies menaçantes, il faut parfois réséquer l'anévrisme. Dans ce groupe de malades, les résultats sont médiocres. Mais les nouvelles techniques de localisation des foyers d'irritation vont peut-être conduire à des interventions plus efficaces.

     

Sexual dysfunction following myocardial infarction in the male

Sexual activity does not always correlate with the severity of myocardial damage or the extent of any complications. The general objective of management is to restore sexual activities to approximately pre-infarct levels and, generally, it is better to introduce sexual activities sooner rather than later. Special investigations may be necessary to determine whether the penile arteries are involved in generalized arteriosclerosis, which may contribute to sexual problems. The pelvic steal test is simple and improves the diagnostic value of a penile blood pressure measurement. Counselling procedures are the mainstay of treatment, but cardiovascular drugs, antidepressants and anxiolytic drugs may all have a part to play. A crucial influence is the attitude of the sexual partner. Reassurance concerning future re-infarction is of paramount importance.     

Emergency coronary bypass grafting for evolving myocardial infarction. Effects on infarct size and left ventricular function

Emergency aorta-coronary bypass grafting was performed early in the course of evolving myocardial infarction in 48 patients. The time interval between the onset of symptoms and reperfusion was 169 +/- 80 minutes. Quantitative assessment of postoperative thallium 201 myocardial scans in 19 patients revealed a significant salvage of myocardium after surgical reperfusion: The size of the residual infarction was less than 50% of that in a matched, medically treated, prospective control group (n = 39) (p less than 0.05). Postoperative equilibrium-gated radionuclide blood pool studies (technetium 99m) showed an enhanced recovery of regional and global ejection fraction after operation as compared to after medical treatment (p less than 0.05). Ultrastructural evaluation of biopsy specimens obtained during the operation delineated subendocardial necrosis in the majority of cases (72%), but subepicardial necrosis was found in only 6% of instances. Q-wave abnormalities were observed on the postoperative electrocardiogram in 50% of cases. Operative mortality was 0% in low-risk patients (i.e., hemodynamically stable condition, n = 26) and 18% in high-risk patients (i.e., cardiogenic shock including total electromechanical dysfunction, n = 22). Survival rate at 18 months was 92% +/- 4%, and 95% +/- 4% of the survivors were event free. It is concluded that early surgical reperfusion of evolving myocardial infarction limits infarct size significantly, enhances functional recovery, and may be a lifesaving operation in patients having cardiogenic shock associated with unsuccessful resuscitation.     

Impact of pre-existing left ventricular dysfunction on kidney transplantation outcomes: implications for patient selection

Background

End-stage kidney disease patients with decreased left ventricular ejection fraction (EF) are often denied kidney transplantation (KT) for fear of poor graft and patient survival.

Methods

We retrospectively studied all patients who underwent KT at our center between 2001 and 2005 to determine the impact of low EF on outcomes post KT. Low EF was defined as <50% EF by noninvasive cardiac imaging. Follow-up was for 1 year post KT. Outcomes assessed included hospitalization for congestive heart failure (CHF), cardiac events, and renal allograft and patient survival.

Results

Among 254 patients, 37 had low EF (study group) and 217 had normal EF (≥50%; control group). Post KT, the low EF group had a significantly higher rate of hospitalization for CHF. No significant difference was noted in the rate of cardiac events, graft loss, GFR, and all cause death at 12 months post KT.

Conclusion

Patients with low EF should not be excluded from transplantation, given favorable outcomes.     

Left ventricular remodeling after experimental myocardial cryoinjury in rats

The standard coronary ligation, the most studied model of experimental myocardial infarction in rats, is limited by high mortality and produces unpredictable areas of necrosis. To standardize the location and size of the infarct and to elucidate the mechanisms of myocardial remodeling and its progression to heart failure, we studied the functional, structural, and ultrastructural changes of myocardial infarction produced by experimental myocardial cryoinjury.The cryoinjury was successful in 24 (80%) of 30 male adult CD rats. A subepicardial infarct was documented on echocardiograms, with an average size of about 21%. Macroscopic examination reflected closely the stamp of the instrument used, without transition zones to viable myocardium. Histological examination, during the acute setting, revealed an extensive area of coagulation necrosis and hemorrhage in the subepicardium. An inflammatory infiltrate was evident since the 7th hour, whereas the reparative phase started within the first week, with proliferation of fibroblasts, endothelial cells, and myocytes. From the 7th day, deposition of collagen fibers was reported with a reparative scar completed at the 30th day. Ultrastructural study revealed vascular capillary damage and irreversible alterations of the myocytes in the acute setting and confirmed the histological findings of the later phases. The damage was associated with a progressive left ventricular (LV) remodeling, including thinning of the infarcted area, hypertrophy of the noninfarcted myocardium, and significant LV dilation. This process started from the 60th day and progressed over the subsequent 120 days period; at 180 days, a significant increase in LV filling pressure, indicative of heart failure, was found.In conclusion, myocardial cryodamage, although different in respect to ischemic damage, causes a standardized injury reproducing the cellular patterns of coagulation necrosis, early microvascular reperfusion, hemorrhage, inflammation, reparation, and scarring observed in myocardial infarction with a late evolution toward heart failure. This model is therefore suitable to study myocardial repair after injury.