急性心肌梗死后左心室重构及其防治

本文简述了急性心肌梗死后左心室重构的发生机制、时间、后果、影响因素及防治措施等     

Left ventricular dyssynchrony acutely after myocardial infarction predicts left ventricular remodeling.

OBJECTIVES: We sought to identify predictors of left ventricular (LV) remodeling after acute myocardial infarction. BACKGROUND: Left ventricular remodeling after myocardial infarction is associated with an adverse long-term prognosis. Early identification of patients prone to LV remodeling is needed to optimize therapeutic management. METHODS: A total of 178 consecutive patients presenting with acute myocardial infarction who underwent primary percutaneous coronary intervention were included. Within 48 h of intervention, 2-dimensional echocardiography was performed to assess LV volumes, LV ejection fraction (LVEF), wall motion score index, left atrial dimension, E/E' ratio, and severity of mitral regurgitation. Left ventricular dyssynchrony was determined using speckle-tracking radial strain analysis. At 6-month follow-up, LV volumes, LVEF, and severity of mitral regurgitation were reassessed. RESULTS: Patients showing LV remodeling at 6-month follow-up (20%) had comparable baseline characteristics to patients without LV remodeling (80%), except for higher peak troponin T levels (p < 0.001), peak creatine phosphokinase levels (p < 0.001), wall motion score index (p < 0.05), E/E' ratio (p < 0.05), and a larger extent of LV dyssynchrony (p < 0.001). Multivariable analysis demonstrated that LV dyssynchrony was superior in predicting LV remodeling. Receiver-operating characteristic curve analysis demonstrated that a cutoff value of 130 ms for LV dyssynchrony yields a sensitivity of 82% and a specificity of 95% to predict LV remodeling at 6-month follow-up. CONCLUSIONS: Left ventricular dyssynchrony immediately after acute myocardial infarction predicts LV remodeling at 6-month follow-up.     

Left ventricular remodeling after myocardial infarction in antecedent hypertensive patients.

Antecedent hypertension adversely affects mortality and heart failure after myocardial infarction (MI). In addition, accelerated ventricular remodeling is a contributor to the increased mortality observed after MI. The purpose of this study was to assess the relationship of antecedent hypertension to ventricular remodeling after MI. Ninety-four patients presenting with a first acute MI who were treated with reperfusion therapy within 12 h of their symptom onset were enrolled in this study. All of them underwent left ventriculography immediately after reperfusion therapy and again at 6 months after the occurrence of MI. Patients were divided into two groups: a hypertensive group and a normotensive group. End-diastolic volume index (EDVI), end-systolic volume index (ESVI), and ejection fraction (EF) values in the acute phase were compared to those at 6 months after acute MI in either group. The hypertensive group showed a significant increase in both EDVI and ESVI after 6 months, whereas the normotensive group did not. In addition, there was no change in EF in the hypertensive group, whereas EF increased significantly after 6 months in the normotensive group. As a result, the percent changes in ESVI and EF were significantly different between the hypertensive group and normotensive group. The results demonstrated that antecedent hypertension interacts with ventricular cavity dilatation after MI.     

Left ventricular remodeling in patients with stress hyperglycemia after acute myocardial infarction

Background To investigate the association between left ventricular remodeling and stress hyperglycemia (SH) inpatients with acute anterior wall myocardial Infarction. Methods Patients with acute anterior myocardial infarction and a successful primary percutaneous coronary intervention (PCI) were enrolled and divided into two groups according to the presence or absence of SH. Patients with diabetes mellitus were excluded. Echocardiographic studies were performed on discharge and at 6 month follow-up. Left ventricular (LV) ejection fractions (EF), LV end-diastolic volume (EDV) and LV end-systolic volume (ESV) were obtained at baseline and at 6 month. Differences between changes of ESV (ΔESV) and changes of EDV (ΔEDV) in the two groups as well as EF improvement rate (ΔEF %) over six month were obtained. Correlation between SH and LV remodeling was investigated. Results (1) At baseline, the level of hemoglobin A1c was significantly higher in SH group (6.9±1.4 vs 6.2±0.8 P=0.04). Other baseline characteristics, including peak serum creatine kinase MB and LV function, were similar between two groups; (2) EF increased significantly over 6 months in both group with SH((41.1±7.2)% vs (52.7±8.4)%, P=0.02) and group without SH. ((43.6±8.7)% vs (54.5±9.3)%, P=0.03) (3) Only in SH group, EDV increased significantly at 6 month (139.6±26.7 vs 126.1±26.7 P=0.04); (4) There was a weak correlation between ΔEDV and the level of fasting plasma glucose on admission.(Pearson's r=0.35, P0.01). Conclusions (1) Previous glucose metabolism disorder is at least partially responsible for hyperglycemia on admission; (2) Given successful primary PCI within recommended time interval, left ventricular function improved regardless of whether SH is present or not; (3) The degree of glucose metabolic dysfunction on admission is weakly associated with the remodeling process in 6 months     

Left ventricular pseudoaneurysm after myocardial infarction

In this report, a case of a left ventricular (LV) pseudoaneurysm due to a previous myocardial infarction, which was repaired successfully, is described. A 62-year-old man, with a history of acute anterior wall myocardial infarction 6 months previously, was admitted with the complaints of acute dyspnea and palpitation. Echocardiography revealed an LV aneurysm, and ventriculography showed ventricular dysfunction and an LV pseudoaneurysm. Coronary angiography showed total occlusion of the proximal segment of the left anterior descending artery with a very thin lumen and insufficient retrograde filling. Under cardiopulmonary bypass and beating heart, the pseudoaneurysm was resected and the defect on the ventricular free wall was closed by the remodeling ventriculoplasty method of Dor. Histopathologic examination of the resected material confirmed the diagnosis of pseudoaneurysm. The postoperative course of our patient was uneventful. He was discharged on the ninth postoperative day.     

Effects of early captopril administration on infarct expansion, left ventricular remodeling and exercise capacity after acute myocardial infarction

In a double-blind study, 99 patients (82 men, age range 40 to 75 years) with acute myocardial infarction (AMI) were randomly assigned to receive captopril or placebo. Treatment began within 24 hours of admission. Serial echocardiographic measurements of endocardial segment lengths and left ventricular (LV) volumes, and ejection fractions were obtained. The 2 groups were matched at baseline except for an excess of previous AMI in the placebo group (13 of 50 vs 2 of 49 patients, p = 0.002). The increase in anterior segment length, from baseline to 2 months, was significantly less in the captopril than in the placebo group (2.8 +/- 1.6 vs 10.4 +/- 2.4mm, 95% confidence interval [CI] -13.5 to -1.7, p = 0.01). The increase in posterior segment length was also less in the captopril group, but the difference was not significant (3.2 +/- 1.2 vs 7.0 +/- 1.8mm, 95% CI -8.0 to 0.5, p = 0.08). Fewer patients in the captopril group demonstrated increases in segment length greater than 2 standard deviations of the measurement error (14 of 70 [20%] vs 29 of 72 [40%] patients, p = 0.009). In patients with anterior AMI, the infarct-containing anterior segment length increased by 4.5 +/- 2.3 mm in the captopril versus 12.4 +/- 3.1 mm in the placebo group (95% CI -15.7 to -0.2, p = 0.046), and fewer patients in the captopril group demonstrated infarct expansion (6 of 20 [30%] vs 13 of 21 [62%] patients, p = 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular performance after acute myocardial infarction

Current knowledge concerning the major hemodynamic features of acute myocardial infarction has been reviewed and discussed in relation to present concepts of cardiac pathophysiology. The physical examination provides a great deal of information and new, noninvasive methods promise to supplement the bedside appraisal of left ventricular function. Direct hemodynamic methods of serially monitoring patients with acute myocardial infarction are finding increasing application and recently have added considerably to our understanding of this condition. Certain limitations in the use of the central venous pressure, pulmonary arterial pressure, and cardiac output in appraising left ventricular function have become apparent, but together with direct catheterization of the left ventricle such hemodynamic studies have now provided limited correlations between the clinical picture and various hemodynamic patterns. It is becoming increasingly clear that most of these features, including cardiogenic shock, probably reflect varying degrees of left ventricular failure. These initial findings and interpretations will require confirmation, however, and so far insufficient objective data are available concerning the natural history of acute myocardial infarction and its responses to various forms of therapy. The aims of investigations now being carried in specialized Myocardial Infarction Research Units and other cardiovascular research centers, are to gain such further understanding of the pathophysiology of this disease and to aid in its clinical management by developing accurate indirect monitoring techniques as well as new forms of therapy.     

Left ventricular intra-myocardial dissection after myocardial infarction

Left ventricular (LV) intra-myocardial dissection or dissecting hematoma is a rare complication of myocardial infarction that could occur in the acute phase, during remodeling process and even after coronary revascularization. LV intra-myocardial dissection has a high mortality, and the best management strategy remains controversial. Here, we present a case of dissection of left ventricle late after anterior myocardial infarction diagnosed by multimodality imaging.     

Increased afterload aggravates infarct expansion after acute myocardial infarction

After acute transmural myocardial infarction, the heart may undergo major remodeling characterized by thinning and dilation of the infarct zone and overall enlargement of the heart. The effect of increased left ventricular pressure on infarct expansion and the extent to which it alters postinfarction remodeling were studied in a rat model. Rats with either aortic banding or a sham operation and a survival period of 3 weeks were further randomized to sham thoracotomy or left coronary ligation. Surviving rats were killed 7 days later and the hearts were fixed in diastole for morphologic analysis. Hearts with aortic banding had a mean peak to peak gradient of 20.7 +/- 4.9 mm Hg across the aortic band at death and a significantly thicker heart than that of the comparison group without an aortic band. Infarct size, as a percent of total left ventricular mass, at the time of death was less in the group with aortic banding, yet infarct expansion was more marked. However, when original infarct size was estimated taking into account the effects of aortic banding, scar formation, infarct expansion and infarct-induced hypertrophy, it was found to be similar in both infarct groups (45.50 +/- 4.2 versus 47.90 +/- 3.1%). Infarct expansion, as measured by cavity dilation and infarct thinning, occurred in both infarct groups but was greater in the group with aortic banding.(ABSTRACT TRUNCATED AT 250 WORDS)     

心肌梗死后左室重构发病机制进展

急性心肌梗死(AMI)是威胁人类健康的重大疾病,心肌梗死(MI)后30 min,部分心肌细胞即发生不可逆的坏死,因此,MI有效救治的时间窗极为短暂,许多患者不能够得到及时有效的治疗,使得MI后心力衰竭(HF)的发生率仍然居高不下。最新调查研究表明,MI后1年HF的发生率约为14.2%。因MI后HF再次入院的患者,1年死亡率高达为45.5%。MI后HF的主要原因是部分心肌细胞坏死,左室重构,心脏扩张,继而引发HF。目前,MI后左室重构的机制尚未完全阐明。本文介绍了AMI后左室重构的发病机制主要进展。     

Prevention of left ventricular remodeling after myocardial infarction

Opinion statement Postinfarction left ventricular remodeling begins early after acute myocardial infarction and may continue for months to years afterward. Early re-establishment of flow in the occluded artery is associated with smaller left ventricular cavity volumes and reduced remodeling. Acute percutaneous coronary intervention (PCI) or thrombolytic therapy (for patients more than 1 hour away from a catheterization facility) as early as possible after symptoms is critical. Late reperfusion (PCI more than 12 hours after infarction) may prove useful, and this will be determined by the results of ongoing clinical trials. Recurrent MI is reduced by antiplatelet agents (aspirin in most patients) and by 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors. Intravenous nitroglycerin may limit early (initial 24 hours) dilatation following infarction, but long-term use in asymptomatic patients is not efficacious. Betaadrenergic receptor antagonists and angiotensin-converting enzyme (ACE) inhibitors have independent efficacy in attenuating the early and late phases of remodeling. The combined use of a beta-blocker and an ACE inhibitor has greater efficacy than either agent alone, provided they are tolerated hemodynamically. Although angiotensin II receptor antagonists have similar efficacy to ACE inhibitors and have fewer side effects, the angiotensin II receptor blockers should be reserved for patients intolerant to ACE inhibitors. In patients requiring diuretic therapy, spironolactone is preferred because of its salutary properties regarding extracellular matrix remodeling, specifically in reducing fibrosis. Surgical revascularization with or without associated mitral valve repair is useful in selected patients with severe ischemic mitral regurgitation or hibernating myocardium. New therapies directed at modulating the remodeling process may focus on manipulating the components of the extracellular matrix to reduce the deleterious impact of this process.