Late Ventricular Dysrhythmias after Myocardial Infarction

Serious ventricular dysrhythmias occurred in hospital after discharge from a coronary intensive care unit in 11 out of 142 patients with myocardial infarction. Previous rhythm changes, hypotension, and left ventricular failure were common findings; only one of these patients had an uneventful previous course. Four patients were resuscitated and left hospital; six were resuscitated but died at varying periods up to eight days after the event; one patient could not be resuscitated. Recent coronary occlusion or further myocardial infarction was demonstrated in 7 of these 11 patients and presumably accounted for the dysrhythmia.     

Changes in Left Ventricular Wall Movement after Acute Myocardial Infarction Measured by Reflected Ultrasound

Serial measurements of left ventricular posterior wall movement were made in eight patients with acute myocardial infarction by an ultrasound technique. Maximum posterior wall velocity and excursion were decreased during the first 36-hour period after infarction. In two patients a reduction in posterior wall velocity was associated with an increased pulmonary artery pressure and as the pressure returned towards normal the posterior wall motion also improved. It is suggested that this method provides a convenient, non-invasive bedside assessment of left ventricular function after acute myocardial infarction.     

Pericarditis after Acute Myocardial Infarction

Fifty-two (6·8%) of 779 patients admitted to a coronary monitoring unit with acute myocardial infarction developed a pericardial friction rub. A diagnosis of postmyocardial infarction syndrome was made in three of these.The course of the 52 patients with pericarditis was compared with that of a consecutive series of 100 patients without pericarditis. As a group those with pericarditis manifested a longer period of pyrexia, a greater rise in serum enzymes, and a higher incidence of major arrhythmias and of radiological pulmonary oedema. The Peel prognostic index, however, did not differ significantly in the two groups. The hospital mortality of the pericarditis group was not significantly different from that of the 727 non-pericarditis patients. No specially adverse features were found in a follow-up of the pericarditis group.Though the presence of a pericardial rub in the first few days after a myocardial infarction may be a sign of extensive myocardial damage and is associated with a relatively high incidence of ventricular fibrillation, it does not appear to influence the hospital mortality of patients treated in a monitoring unit.     

Lignocaine Therapy after Acute Myocardial Infarction

Thirty-five patients with ventricular dysrhythmias and seven with other dysrhythmias after acute myocardial infarction were treated with intravenous lignocaine.Satisfactory initial suppression of ventricular ectopic beats was achieved in 27 (82%) of 33 patients after either a 50-mg. bolus or a 50-mg. bolus followed by a 100-mg. bolus of intravenous 2% lignocaine. Continuous suppression of ventricular ectopic beats was accomplished in 21 (78%) of these 27 patients by continuous intravenous lignocaine infusions of 1 to 2 mg. per minute. Recurrence of ventricular ectopic beats occurred in four patients despite lignocaine infusion rates of up to 6 mg. per minute. Six patients with ventricular ectopic beats developed ventricular fibrillation despite satisfactory initial suppression of their dysrhythmia by lignocaine. In three of them ventricular fibrillation supervened while they were receiving a lignocaine infusion and two subsequently died. Unheralded ventricular fibrillation occurred in three other patients between four and seven days after completing the full course of lignocaine therapy.Toxic effects of lignocaine were minimal in patients receiving 1 to 2 mg. per minute.     

Lignocaine Therapy for Ventricular Ectopic Activity after Acute Myocardial Infarction: A Double-blind Trial

The effectiveness of intravenous lignocaine in suppressing ventricular ectopic activity after acute myocardial infarction was examined in a double-blind trial in 82 patients. Whereas suppression of unifocal ventricular ectopics was achieved by lignocaine in 90% of patients, other forms of potentially more dangerous ectopic activity (multifocal or R-on-T ectopics) seemed more resistant to therapy. Cessation of ectopic activity was also observed in about one-third of the patients in the control group. The incidence of ventricular tachycardia and fibrillation and the mortality during and after the trial period were similar in the lignocaine-treated and control groups, whether or not the initial ventricular ectopics had been suppressed.This study provides no evidence to support the routine use of intravenous lignocaine in the management of ventricular ectopic activity after acute myocardial infarction.     

Integrative Pathway-Centric Modeling of Ventricular Dysfunction after Myocardial Infarction

Background

A significant proportion of myocardial infarction (MI) patients undergo complex, coordinated perturbations at the molecular level that may eventually drive the occurrence of ventricular dysfunction and heart failure. Despite advances in the elucidation of key processes implicated in this condition, traditional methods relying on gene expression data and the identification of individual biomarkers in isolation pose major limitations not only for improving prediction power, but also for model interpretability. Mechanisms underlying clinical responses after MI remain elusive and there is no biomarker with the capacity to accurately predict ventricular dysfunction after MI. This calls for the exploration of system-level modeling of ventricular dysfunction in post-MI patients. Within this discovery framework key perturbations and predictive patterns are characterized by the integrated biological activity levels observed in pathways, rather than in individual genes.

Methodology/Principal Findings

Here we report an integrative approach to identifying pathways related with ventricular dysfunction post MI with potential prognostic and therapeutic value. We found that a diversity of pathway-level perturbations can be profiled in samples of patients with ventricular dysfunction post MI, most of which represent major reductions of gene expression. Highly perturbed pathways included those implicated in antigen-dependent B-cell activation and the synthesis of leucine. By analyzing patient-specific samples encoded with information derived from highly-perturbed pathways, it is possible to visualize differential prognostic patterns and to perform computational classification of patients with areas under the receiver operating characteristic curve above 0.75. We also demonstrate how the integration of the outcomes generated by different pathway-based analysis models may improve ventricular dysfunction prediction performance.

Significance

This research offers an alternative, comprehensive view of key relationships and perturbations that may trigger the emergence or prevention of ventricular dysfunction post-MI.     

A Panel of 4 microRNAs Facilitates the Prediction of Left Ventricular Contractility after Acute Myocardial Infarction

Background

Prediction of clinical outcome after acute myocardial infarction (AMI) is challenging and would benefit from new biomarkers. We investigated the prognostic value of 4 circulating microRNAs (miRNAs) after AMI.

Methods

We enrolled 150 patients after AMI. Blood samples were obtained at discharge for determination of N-terminal pro-brain natriuretic peptide (Nt-proBNP) and levels of miR-16, miR-27a, miR-101 and miR-150. Patients were assessed by echocardiography at 6 months follow-up and the wall motion index score (WMIS) was used as an indicator of left ventricular (LV) contractility. We assessed the added predictive value of miRNAs against a multi-parameter clinical model including Nt-proBNP.

Results

Patients with anterior AMI and elevated Nt-proBNP levels at discharge from the hospital were at high risk of subsequent impaired LV contractility (follow-up WMIS>1.2, n = 71). A combination of the 4 miRNAs (miR-16/27a/101/150) improved the prediction of LV contractility based on clinical variables (P = 0.005). Patients with low levels of miR-150 (odds ratio [95% confidence interval] 0.08 [0.01–0.48]) or miR-101 (0.19 [0.04–0.97]) and elevated levels of miR-16 (15.9 [2.63–95.91]) or miR-27a (4.18 [1.36–12.83]) were at high risk of impaired LV contractility. The 4 miRNA panel reclassified a significant proportion of patients with a net reclassification improvement of 66% (P = 0.00005) and an integrated discrimination improvement of 0.08 (P = 0.001).

Conclusion

Our results indicate that panels of miRNAs may aid in prognostication of outcome after AMI.     

Ventricular Aneurysm Following Myocardial Infarction

Cineradiographic examination appears to be the best method for the study of cardiac pulsations. Fifty consecutive patients, who had sustained transmural myocardial infarction at least six months previously, were studied by this technique. Thirty-six had some abnormality of pulsation and eight had dynamic ventricular aneurysm. Six of the eight had suffered severe infarct. Functional recovery in those with aneurysm was not as complete as in the rest of the group. Two made a poor functional recovery, two a fair recovery, and four a moderately good recovery. Clinically, there were no systemic emboli in the patients with dynamic aneurysms. Five of the 50 had persistent ST-segment elevation and “coving” of the T waves; three of these patients had aneurysms. There was no good correlation between the electrocardiographic site of the infarct and the site of the abnormal pulsation.     

Advanced Heart Block During Acute Myocardial Infarction Treated with an Electrode Pacing Catheter

The mortality rate is high from advanced atrioventricular block associated with acute myocardial infarction. There is reason to believe that if in these patients the hearts are electrically paced with an endocardial pacing catheter, the mortality rate can be considerably decreased. Five patients in second- and third-degree heart block associated with acute myocardial infarction were paced with a considerable lowering of the expected mortality rate. Twenty-three cases from the literature are also presented and discussed. A silastic bipolar electrode catheter was used in these five cases. Four of the five cases returned to normal sinus rhythm within the first 10 days. The average duration of pacing was 6.7 days. It is the opinion of the author that second- and third-degree heart block associated with acute myocardial infarction should have a pacing catheter introduced at the earliest possible moment for continuous or demand endocardial pacing.     

急性心肌梗死患者心肌顿抑发病机制探讨

心肌顿抑也称缺血后心肌功能障碍,为持续数小时、数天、甚至数周的心肌细胞可逆性损伤。可见于急性冠脉综合症早期再灌注、心脏移植、心脏瓣膜置换等心脏外科大手术术后,应激性心肌病、心脏骤停、心肺复苏、主动脉狭窄、高血压性心脏病、房颤转复。心肌梗死后发生心肌顿抑是导致心梗死亡、心衰再住院的重要病因,但目前其发病机制尚不明确。有关心肌顿抑的研究已经由器官细胞水平,深入到分子基因水平。具体而言,心肌顿抑的发病机制包括：缺血再灌注导致的心肌细胞直接损伤、心肌细胞兴奋收缩脱偶联、线粒体及内质网损伤、血管内皮细胞功能障碍及微循环痉挛、能量代谢障碍、氧自由基损伤、钙超载理论、炎性介质释放理论、心肌顿抑的基因组学机制等。目前,广为接受的是氧自由基理论和钙超载理论。前者认为心肌梗死时,心肌组织氧自由基产生增多,清除障碍,导致心肌细胞结构受伤和功能障碍;后者认为心肌梗死时,心肌细胞酸中毒,细胞膜通透性增加,钙内流增多,同时,钙库重吸收钙障碍,导致钙超载,引起心肌细胞破坏、肌钙蛋白溶解,导致心功能障碍。阐明心肌顿抑发病机制,指导心梗治疗,有助于完善救治策略,改善预后。     

Financial Stress and Outcomes after Acute Myocardial Infarction

Background

Little is known about the association between financial stress and health care outcomes. Our objective was to examine the association between self-reported financial stress during initial hospitalization and long-term outcomes after acute myocardial infarction (AMI).

Materials and Methods

We used Prospective Registry Evaluating Myocardial Infarction: Event and Recovery (PREMIER) data, an observational, multicenter US study of AMI patients discharged between January 2003 and June 2004. Primary outcomes were disease-specific and generic health status outcomes at 1 year (symptoms, function, and quality of life (QoL)), assessed by the Seattle Angina Questionnaire [SAQ] and Short Form [SF]-12. Secondary outcomes included 1-year rehospitalization and 4-year mortality. Hierarchical regression models accounted for patient socio-demographic, clinical, and quality of care characteristics, and access and barriers to care.

Results

Among 2344 AMI patients, 1241 (52.9%) reported no financial stress, 735 (31.4%) reported low financial stress, and 368 (15.7%) reported high financial stress. When comparing individuals reporting low financial stress to no financial stress, there were no significant differences in post-AMI outcomes. In contrast, individuals reporting high financial stress were more likely to have worse physical health (SF-12 PCS mean difference −3.24, 95% Confidence Interval [CI]: −4.82, −1.66), mental health (SF-12 MCS mean difference: −2.44, 95% CI: −3.83, −1.05), disease-specific QoL (SAQ QoL mean difference: −6.99, 95% CI: −9.59, −4.40), and be experiencing angina (SAQ Angina Relative Risk = 1.66, 95%CI: 1.19, 2.32) at 1 year post-AMI. While 1-year readmission rates were increased (Hazard Ratio = 1.50; 95%CI: 1.20, 1.86), 4-year mortality was no different.

Conclusions

High financial stress is common and an important risk factor for worse long-term outcomes post-AMI, independent of access and barriers to care.     

Depression and Anxiety after Acute Myocardial Infarction Treated by Primary PCI

AimsThe main objective of the study was to find out prevalence of depression and anxiety symptoms in the population of patients with AMI with ST-segment elevation (STEMI), treated with primary PCI (pPCI). Secondary target indicators included the incidence of sleep disorders and loss of interest in sex.ConclusionsPatients with STEMI treated by primary PCI have relatively low overall prevalence of symptoms of depression and anxiety. A significant decrease in mental stress was observed before discharge from the hospital, but in a period of one year after pPCI, prevalence of both symptoms was gradually increasing, which should be given medical attention.     

瑞舒伐他汀对兔心肌梗死后心室重构及细胞凋亡的影响

目的：观察瑞舒伐他汀对新西兰大白兔心肌梗死后左室重构及心肌细胞凋亡的影响。方法：45只雄性新西兰大白兔随机分成三组,即：假手术组（S,n=15）,心肌梗死对照组（MI,n=15）,心肌梗死瑞舒伐他汀干预组（R,n=15）。MI组和R组大鼠结扎左冠状动脉前降支建立AMI模型。心肌梗死对照组及假手术组术后24h灌等量的生理盐水．．瑞舒伐他汀干预组于术后24h直接灌胃法给药,给药剂量以10mg／kgtd计算。干预2周后,进行心脏超声测定,随即处死新西兰大白兔、取出心脏,观察病理组织形态,并通过Westernblot方法检测Bcl-2,Bax在心肌梗死边缘区的蛋白表达。结果：①心脏超声检测表明干预组左室舒张末内径（LVEDD）、左室收缩末内径（LVESD）较心肌梗死对照组降低而左室射血分数（LVEF）较心肌梗死对照组增高。②干预组心肌梗死边缘区Bax表达与心肌梗死对照组比较未见统计学差异,而Bcl一2表达高于心肌梗死对照组。结论：瑞舒伐他汀上调Bcl一2的表达,改善心室重构。     

瑞舒伐他汀对兔心肌梗死后心室重构及细胞凋亡的影响

目的:观察瑞舒伐他汀对新西兰大白兔心肌梗死后左室重构及心肌细胞凋亡的影响。方法:45只雄性新西兰大白兔随机分成三组,即:假手术组(S,n=15),心肌梗死对照组(MI,n=15),心肌梗死瑞舒伐他汀干预组(R,n=15)MI组和R组大鼠结扎左冠状动脉前降支建立AMI模型。心肌梗死对照组及假手术组术后24h灌等量的生理盐水。瑞舒伐他汀干预组于术后24h直接灌胃法给药,给药剂量以10mg/kg*d计算。干预2周后,进行心脏超声测定,随即处死新西兰大白兔、取出心脏,观察病理组织形态,并通过Western blot方法检测Bcl-2,Bax在心肌梗死边缘区的蛋白表达。结果:①心脏超声检测表明干预组左室舒张末内径(LVEDD)、左室收缩末内径(LVESD)较心肌梗死对照组降低而左室射血分数(LVEF)较心肌梗死对照组增高②干预组心肌梗死边缘区Bax表达与心肌梗死对照组比较未见统计学差异,而Bcl-2表达高于心肌梗死对照组。结论:瑞舒伐他汀上调Bcl-2的表达,改善心室重构     

猪急性心肌梗死模型发生心室颤动的相关因素分析

目的探讨猪冠状动脉前降支(LAD)结扎后发生室颤的特点及其相关因素,以期提高猪急性心肌梗死模型的成活率。方法57只小型猪开胸结扎心脏LAD不同位点,对室颤和体重、性别、术前心率、术前左室射血分数(LVEF)、开胸径路(旁正中/肋间)、手术时间、结扎百分位点、术后心率、术后发生室早或短阵室速等因素进行单因素相关分析和Logistic回归分析,进而对室颤的发生时间、室颤前心电图特点等进行评价。结果57例动物手术过程发生室颤18例,死亡11例。室颤均发生在结扎冠脉后35 min内,高峰时间为结扎冠脉后5 min和20 min;心率快于160 bpm或慢于60 bpm时容易诱发室颤。与非室颤组动物比较,室颤组动物的结扎位点高,术后最快心率>60 bpm的动物较多,短阵室速发生率高(P<0.01)。Logistic回归分析显示结扎位点过高是急性心肌梗死后发生室颤唯一的独立危险因素。结论结扎位点过高是猪急性心肌梗死后发生室颤的最重要危险因素;冠脉结扎后30 min内应该严密心电监护,特别注意结扎冠脉后5 min和20 min二个时间点、>160 bpm或<60 bpm二种心率、以及短阵室速等先兆事件。     

T波峰-末间期对急性心肌梗死并发室性心律失常的预测价值

目的:探讨T波峰-末间期(Tp-Te间期)和Tp-Te间期离散度(Tp-Ted)对急性心肌梗死并发室性心律失常的预测价值。方法:选择我院2013年5月至2014年5月收治的140例确诊急性ST段抬高型心肌梗死(STEMI)患者,按照心律失常类型分为室性心动过速组,室性早搏组以及无室性心律失常组。分析并比较各组患者心电图Tp-Te间期及Tp-Ted的变化情况。结果:急性期FPG、Tp-Te、Tp-Ted高于恢复期,差异有统计学意义(P0.05);急性期与恢复期之间TG、CHOL、LDL-C、K+、Na+水平差异无统计学意义(P0.05)。无室性心律失常组与室性心动过速组及室性早搏组比较,Tp-Te和Tp-Ted更低,差异有统计学意义(P0.05);室性早搏组和室性心动过速组比较,Tp-Te和Tp-Ted更低,差异有统计学意义(P0.05)。结论:Tp-Te间期和Tp-Ted可用于区分急性心肌梗死患者室性心律失常类型。