Studies of Male Survivors of Myocardial Infarction: IX. Mortality Experience and Insurability

The mortality of a group of Canadians who survived myocardial infarction for at least three months was compared with the mortality of medically selected lives insured in Canada at standard rates. The results were expressed as the ratio of the actual deaths incurred in the infarction group to the deaths expected according to the insured table. There were 120 men, approximately 25 in each decade from the fourth to the eighth inclusive, with no condition other than coronary disease which might affect survival. The severity and number of infarcts did not influence selection.Calculating from the date of entry into the study the mortality ratio after 10 years was 530%. Calculating from the date of first infarction, the mortality ratio from 0 to five years was 980%, from six to 10 years 510% and after 10 years 320%. The mortality ratio was greatest in the fourth decade, 9400%, and decreased progressively: fifth, 2400%; sixth, 1300%; seventh, 400%; eighth, 230%. In the younger groups the high mortality ratios were due to the small number of expected deaths at young ages, not to an increase in the absolute number of actual deaths. In each age group the mortality ratio decreased with time but remained substantially increased even after 10 years. The mortality experience of this coronary group was worse than that of more rigidly selected, insured coronary groups.     

Studies of Male Survivors of Myocardial Infarction: XII. Relation of Serum Lipids and Lipoproteins to Survival Over a 10-Year Period

The relation of serum cholesterol and standard S_t lipoproteins to survival over a 10-year period was studied in a “good risk” group of 120 men, aged 31 to 83, who had survived myocardial infarction by at least three months. All subjects were free of other disorders that might affect survival and were not receiving therapy to alter their serum lipids.Ten-year survival from time of entry into the study was 35%. Age had no important influence on survival. Neither the level of the serum cholesterol nor of the lipoprotein fractions related to survival. Mode of coronary death, whether infarctional or sudden, was also unrelated to serum cholesterol.Although the incidence and age of onset of CHD is influenced by serum lipid levels, survival subsequent to infarction is not. Apparently serum lipids affect the rate of atherogenesis in the long silent preclinical stage, but in the short clinical stage other factors determine survival. This suggests that therapy to lower serum lipids, based on a specific diagnosis of the type of hyperlipoproteinemia, should be started early in life before clinical disease occurs.     

Peeling off the Mask: Pseudo Myocardial Infarction Pattern on Electrocardiogram During AICD Implantation

Lead induced transient right bundle branch block is not uncommon during pacemaker implantation. We describe a patient with old anterior wall myocardial infarction with severe left ventricular dysfunction presenting with recurrent ventricular tachycardia who developed transient right bundle branch block and pseudomyocardial infacrction pattern during AICD implantation.Key words: Pseudo Myocardial Infarction, AICD implantation     

The Pathogenesis of Human Myocardial Infarction

Coronary arteriography, dissection of the coronary arteries and histopathological examination of the heart were carried out in 150 autopsies to study the effect of coronary narrowing and occlusion, of the presence of collaterals, and of coronary artery predominance on the development of myocardial infarction. The thrombosis rate was related to the severity of coronary sclerosis. The development of collaterals was not enhanced by coronary sclerosis and occlusion, and collaterals did not protect the myocardium against reinfarction. Coronary occlusion was regularly demonstrable in recent myocardial infarct cases. The association of atrial and posterior ventricular infarcts was explained by occlusion of their common arterial branch. The interdependence between coronary sclerosis, thrombosis and myocardial infarction in human autopsy material emphasizes the importance of mural coronary artery disease in the genesis of coronary occlusion and myocardial infarction, and it is at variance with statistical data and experimental results.     

Structural Composition of Myocardial Infarction Scar in Middle-aged Male and Female Rats: Does Sex Matter?

The present study was designed to determine whether the structural composition of the scar in middle-aged post–myocardial infraction (MI) rats is affected by the biological sex of the animals. A large MI was induced in 12-month-old male (M-MI) and female (F-MI) Sprague-Dawley rats by ligation of the left coronary artery. Four weeks after the MI, rats with transmural infarctions, greater than 50% of the left ventricular (LV) free wall, were evaluated. The extent of LV remodeling and fractional volumes of fibrillar collagen (FC), myofibroblasts, vascular smooth muscle (SM) cells, and surviving cardiac myocytes (CM) in the scars were compared between the two sexes. The left ventricle of post-MI male and female rats underwent a similar degree of remodeling as evidenced by the analogous scar thinning ratio (0.46 ± 0.02 vs. 0.42 ± 0.05) and infarct expansion index (1.06 ± 0.07 vs. 1.12 ± 0.08), respectively. Most important, the contents of major structural components of the scar revealed no evident difference between M-MI and F-MI rats (interstitial FC, 80.74 ± 2.08 vs. 82.57 ± 4.53; myofibroblasts, 9.59 ± 1.68 vs.9.56 ± 1.15; vascular SM cells, 2.27 ± 0.51 vs. 3.38 ± 0.47; and surviving CM, 3.26 ± 0.39 vs. 3.05 ± 0.38, respectively). Our data are the first to demonstrate that biological sex does not influence the structural composition of a mature scar in middle-aged post-MI rats.     

Effects of Statin Therapy on Clinical Outcomes of Survivors of Acute Myocardial Infarction with Severe Systolic Heart Failure

Objective

Large randomized trials have failed to show a beneficial effect of statin treatment in chronic HF. The investigators tried to evaluate the long-term effects of statin therapy in patients with new onset heart failure (HF) following acute myocardial infarction (AMI).

Methods

Between January 2008 and December 2011, a total of 13,616 AMI patients were enrolled in the Korea Acute Myocardial Infarction Registry (KAMIR) which was a prospective, multi-center, nationwide, web-based database of AMI in Korea. From this database, we studied 1,055 patients with AMI who had newly developed severe acute HF [left ventricular ejection fraction ≤ 40%] and were discharged alive. The patients were divided into two groups, a statin group (n = 756) and a no-statin group (n = 299). We investigated the one-year major adverse cardiovascular events (MACEs), including all-cause mortality, MI, and any revascularization of each group. We then performed a propensity-score matched analysis.

Results

In the original cohort, one-year MACEs were similar between the two groups (16.5% vs. 14.7% in the statin or no-statin groups; p = 0.47). Propensity-score matching yielded 256 pairs, and in that population we observed comparable results in terms of MACEs (18.0% vs. 12.5% in the statin or no-statin groups, p = 0.11) and mortality (5.1% vs. 3.5% in the statin or no-statin groups, p = 0.51). Cox-regression analysis revealed that statin therapy was not an independent predictor for occurrence of a MACE [Hazard ratio (HR) 1.11, 95% CI 0.79–1.57, p = 0.54] or all-cause mortality (HR 1.42, 95% CI 0.75–2.70, p = 0.28).

Conclusion

Statin therapy was not associated with a reduction in the long-term occurrence of MACEs or mortality in survivors of AMI with severe acute HF in this retrospective cohort study.     

CC类趋化因子亚家族与心肌梗死的研究进展

CC类趋化因子亚家族是趋化因子家族中成员最多、研究最广泛的一大类细胞因子,其主要功能参与炎症细胞激活、迁移、粘附等病理生理过程。大量研究表明,CC类趋化因子亚家族成员参与了心肌梗死后病理过程的各个阶段。其中研究最为深入的为单核细胞趋化蛋白-1（monocyte chemoattractant protein-1,MCP-1）及其受体CC趋化因子受体2（CC chemokine receptor 2,CCR2）,在心肌梗死后炎症期、增殖期及疤痕愈合期都发挥了重要作用从而影响梗死后心室重构。近年来,CC类趋化因子亚家族其他成员亦被逐渐揭示参与了心肌梗死的发展。本文结合以往大量文献将对CC类趋化因子亚家族在心肌梗死各个阶段中尤其是梗死后各期对于心室重构的影响进行综述,以期为今后的实验研究提供方向及疾病的预防和治疗提供药物靶点。     

心肌酶和红细胞形态学参数与心肌梗死的相关性研究

目的:研究红细胞形态学参数对心肌梗死患者诊断作用及其与心肌酶谱的相关性。方法:选取40例心肌梗死患者,40例稳定型心绞痛组患者,40例健康对照组人群。对比分析稳定性心绞痛、急性心肌梗死(入院1h内)和对照组红细胞形态学参数(MCV、MCH、MCHC、RDW)、及心肌酶谱(CK-MB、c Tn I)。分析心肌梗死不同时间MCV、MCH、MCHC、RDW变化趋势。结果:稳定性心绞痛、心肌梗死组1 h内MCV、RDW明显高于正常对照组,差异有统计学意义(P0.05);稳定性心绞痛、心肌梗死组1 h内MCHC、MCH低于对照组,差异有统计学意义(P0.05)。心肌梗死组MCV、RDW在发病后1 h、24 h、48 h、7 d水平逐渐升高,各时间点间差异有统计学意义(P0.05)。心肌梗死组发病后1 h、24 h、48 h、7 d、14 d MCHC、MCH水平逐渐降低,各时间点间差异有统计学意义(P0.05)。RDW和CK-MB、c Tn I呈正相关性(P0.05)。RDW对心肌梗死诊断的灵敏度最高达到93.4%,特异度为69.7%,RDW对急性心肌梗塞的诊断临界值为14.04%。结论:RDW对心肌梗死的诊断具有较高的敏感性,可用于临床早期诊断心肌梗死,为临床诊断提供一新的诊断标准。     

Aromatase Inhibition Attenuates Desflurane-Induced Preconditioning against Acute Myocardial Infarction in Male Mouse Heart In Vivo

The volatile anesthetic desflurane (DES) effectively reduces cardiac infarct size following experimental ischemia/reperfusion injury in the mouse heart. We hypothesized that endogenous estrogens play a role as mediators of desflurane-induced preconditioning against myocardial infarction. In this study, we tested the hypothesis that desflurane effects local estrogen synthesis by modulating enzyme aromatase expression and activity in the mouse heart. Aromatase metabolizes testosterone to 17β- estradiol (E2) and thereby significantly contributes to local estrogen synthesis. We tested aromatase effects in acute myocardial infarction model in male mice. The animals were randomized and subjected to four groups which were pre-treated with the selective aromatase inhibitor anastrozole (A group) and DES alone (DES group) or in combination (A+DES group) for 15 minutes prior to surgical intervention whereas the control group received 0.9% NaCl (CON group). All animals were subjected to 45 minutes ischemia following 180 minutes reperfusion. Anastrozole blocked DES induced preconditioning and increased infarct size compared to DES alone (37.94±15.5% vs. 17.1±3.62%) without affecting area at risk and systemic hemodynamic parameters following ischemia/reperfusion. Protein localization studies revealed that aromatase was abundant in the murine cardiovascular system with the highest expression levels in endothelial and smooth muscle cells. Desflurane application at pharmacological concentrations efficiently upregulated aromatase expression in vivo and in vitro. We conclude that desflurane efficiently regulates aromatase expression and activity which might lead to increased local estrogen synthesis and thus preserve cellular integrity and reduce cardiac damage in an acute myocardial infarction model.     

不同性别急性心梗患者的临床特征及院内治疗预后分析

目的:观察首次确诊为急性心肌梗死(AMI)患者的临床特征并分析不同性别人群的在入院治疗及院内短期预后的差异。方法:回顾性分析2010年2月至2012年4月在沈阳军区总医院心内科初次确诊为AMI的患者271例,并按性别分为两组,其中男性组180例,女性组91例,统计其临床特征、入院后的药物和手术治疗情况,以及院内并发症及预后情况,分析总结两组患者各自的特点和差异。结果:女性患者的年龄要大于男性患者(63±14vs71±11,P0.001),且同时更易患有高血压等心血管疾病合并症(73.3%vs 58.2%,P0.05)。女性患者的发病至入院治疗时间长于男性(P0.001),且入院后行PCI治疗的比例要明显低于男性患者(67%vs 79.4%,P0.05)。初步分析结果表明,女性患者的院内死亡率高于男性(11%vs 3.3%,OR:3.11,95%CI:1.53-7.15),但排除不均衡因素的影响后,男女患者的院内死亡率无明显差异(OR:2.11,95%CI:0.68-5.12)。结论:两性AMI患者的临床特征、入院后治疗及院内短期预后均存在一定差异。根据女性患者的临床特征和院内治疗及预后的现状,应进一步加强对女性高危人群的冠心病诊治知识普及和教育,且对入院后的女性患者应采取更为积极的药物和介入手术治疗手段,以改善预后。     

Myocardial Infarction: A Five-Year Follow-up of Patients

Patients with acute myocardial infarction (2,020) admitted to coronary care units (CCU) in Utah were studied for five years. Of these, 1,641 (81.4 percent) survived to leave the hospital. The male to female ratio was 3.5:1. At four months, one year and yearly thereafter from the date of admission to CCU, patients were mailed follow-up questionnaires. Cause of death was obtained from autopsy reports and death certificates. Patients were grouped yearly by the number of cardiac symptoms reported. Of patients discharged whose cases were followed, 925 (61.9 percent) were alive after five years. Reinfarction was the major cause of death in the hospital; however, during follow-up only 36.8 percent of deaths were attributable to myocardial infarction. At follow-up after a year, fewer cardiac symptoms were reported by patients who survived to the fifth year of follow-up than by patients who did not. Women were older and showed a higher death rate during follow-up. Increasing age was found to be a determining factor in long-term mortality after acute myocardial infarction.