心室晚电位阳性与急性心肌梗死的相关因素

本文对 80例急性心肌梗死 (ＡＭＩ)后住院观察 (≤ 8Ｗ )病人心室晚电位 (ＶＬＰ)的检出率以及ＶＬＰ有关的临床因素进行分析。1　资料与方法80例ＡＭＩ中男 64例 ,女 1 6例 ,均为我院 1 997～ 2 0 0 1年住院患者。年龄 39～92 (61 5± 9 4)岁。广泛前壁 2 2例 ,前(间 )壁 2 7例 ,下壁 31例。 70例为首次ＡＭＩ,另 1 0例伴有陈旧性梗死史。均无束支阻滞。检测前均未停用任何药物 ,包括抗心律失常药。采用美国ＡＲＴ 1 2 0 0型信号平均ＥＣＧ(ＳＡ -ＥＣＧ)。ＶＬＰ阳性标准 :①ＱＲＳ≥ 1 2 0ｍｓ;②Ｖ40 ≤ 2 0 μＶ ;③Ｄ40 ≥ 40ｍｓ。…     

心肌梗死后的心室重构

在急性心肌梗死(acute myocardial infarction，AMI)后发生的左心室的进行性扩张和外形改变，这种现象被称为“梗死后心室重构”，包括心室容积、形状、室壁厚度、心肌结构和超微结构等方面的改变。目前认为AMI后发生慢性心力衰竭的主要病理基础是心室重构。预防AMI后的心室重构是预防心力衰竭不容忽视的一个重要环节。     

小剂量多巴酚丁胺核素心室造影对陈旧性心肌梗死存活心肌的评估

目的：探讨应用小剂量多巴酚丁胺负荷试验与核素心室造影相结合的方法评估存活心肌的意义。方法：采用静态核素心室造影及小剂量多巴酚丁胺测定３５例陈旧性心肌梗死患者的左心室射血分数、右心室射血分数及局部心室壁运动的变化。结果：静态核素心室造影示平均左心室射血分数为４９．９±１６．５％，右心室射血分数为５１．０±７．２％，心室壁运动异常节段８７个（４１．４％）。给予多巴酚丁胺后平均左心室射血分数为５７．９±１９．２％（Ｐ＜０．０１），右心室射血分数为６１．９±６．１％（Ｐ＜０．０５），静态核素心室造影时８７个心室壁运动异常节段中有４８个（５５．２％）节段心室壁运动恢复正常或改善。结论：多巴酚丁胺核素心室造影是可供临床检测存活心肌安全、可靠的无创性方法。     

心室前向电力增大218例分析探讨

通过对218例心室前向电力增大者的分析表明,水平面QRS环移向右前或最大向量> 90°,均有右室肥大等明确病变;而移向左前且最大向量< 90°者,无明确病变,对有心血管病症状者,考虑多由中隔支阻滞所致。QRS主体环前移与左室或右室前方游离壁传导障碍或右束支阻滞无明确关系。中隔支阻滞时水平而QRS环多呈逆钟向运行,可能由于传导延缓的加重,少数改作“8”字形或顺钟向运行,而当中隔支完全阻滞时则可无前向移位。中隔支阻滞并不增加更严重的心室内传导阻滞出现的可能性。     

存活心肌的磁共振研究

心肌梗死后存活心肌的诊断可以预测功能受损心肌在血运重建后的功能恢复。存活心肌检测方法很多,磁共振成像提供了不同的方法观察存活心肌。本文综述了磁共振延迟增强成像及舒张末期室壁厚度和小剂量多巴酚丁胺负荷磁共振成像在诊断存活心肌方面的进展。     

存活心肌—发生机制,检出手段及临床意义

存活心肌的含意为在急性心肌梗塞（ＡＭＩ）后期，将完全闭塞或严重狭窄的梗塞相关动脉（ＩＲＡ）再通后，原梗塞区无收缩功能或收缩功能异常的心肌节段可逐渐恢复功能。这种血流复灌后可恢复的心肌被称为“存活心肌”。在心肌血运重建的时代，对冠心病伴左心功能不全的病...     

心肌梗死后心室晚电位检测结果的分析

目的：探讨心肌梗死后心室晚电位（VLP）的阳性率。方法：采用泰安市医疗仪器研究所研制的SXG－7000VLP记录仪，x、y、z正交心电图双极导联，检测心肌梗死（MI）后3小时至1年不等患的心室晚电位。结果：80例MI患VLP阳性29例，阴性30例。AMI44例中VLP阳性15例（34．1％），陈旧性心肌梗死（OMI）36例中阳性14例（38．8％），前壁MI28例中阳性5例（17．8％），下壁MI 47例中阳性24例（51．0％）。结论：相比较而言，以急性心肌梗死，下壁心肌梗死的心室晚电位阳性率为高。     

存活心肌的识别与乏氧心肌显像的研究进展

冠心病 (CHD)心肌梗死和严重心肌缺血后在病变区还有没有功能可逆的存活心肌直接关系到血运重建治疗或再灌注后心室功能障碍能否改善及其治疗方法的有效性。临床识别和评价存活心肌的基础是缺血 ,但存活心肌共有的特点即 :收缩功能障碍 ,心肌血流灌注减低 (冬眠心肌 )或不低 (顿抑心肌 ) ,心肌细胞代谢存在 ,细胞膜完整性存在 ,具有潜在的收缩储备 对正性肌力药物有收缩增强反应。基于这些特点 ,主要方法有 :核素心肌显像包括1 8F标记 (fluoro deoxyglucose ,FDG)的PET显像 ,2 0 1 Tl和99mTc MIBI的SPECT显像。小剂量多巴酚丁胺单…     

老年急性心肌梗死冠脉介入术后心肌显色分级无复流现象对心肌存活及心功能的影响

目的探讨急性心肌梗死（AMI）患者直接经皮冠状动脉成形术后的无复流现象对心肌梗死后心肌存话及心功能的影响。方法直接PCI患者132例，应用心肌显色分级（MBG）方法将患者分为无复流组（MBG0～1级）和有复流组（MBG2～3级），于PCI后即行左心室造影，测定心室容积、舒张末压和室壁运动积分（WMS）；平衡法核素心室造影，测定心脏收缩功能、舒张功能和收缩同步性参数；AMI后6个月随访时重复行心室造影和核素心室造影及主要恶性心脏事件（MACE）的发生率。AMI后1W时行静息及硝酸甘油介入^99mTc—MIBI SPECT，以极坐标靶心图定量法测定缺血范围记分（ES）和缺血程度记分（SS）。结果AMIPCI后6个月随访时，无复流组LVESVI、LVEDVI、WMS和LVEDP均较有复流组明显增高（P均〈0．05）；核素心室造影参数比较，无复流组LVEF、PER和PFR各参数均较有复流组明显降低（P均〈0．05）。急性心肌梗死PCI后1W硝酸甘油介入后，有复流组Es较无复流组降低37．73％（P〈0．05），有复流组SS较无复流组降低24．24％（P〈0．05）。相位分析示无复流组左室收缩同步性参数PS和PSD亦高于有复流组（P〈0．05）。在6个月随访期内，无复流组MACE发生率明显高于有复流组。结论MBG可准确判定直接PCI后的无复流现象，反映梗死相关区域的心肌存活，预示着心脏功能的恢复和临床预后。     

急性心肌梗死后心室重塑--心肌细胞凋亡的意义

急性心肌梗死 (AMI)后的心室重塑是指心肌梗死后心室大小、形态、结构和功能的变化过程 ,包括 :梗死区心肌坏死产生膨出、非梗死区心肌肥大、间质纤维化、心室壁增厚扩张并导致整个心室的进行性扩张、变形和收缩功能降低。近年来研究发现 ,心肌细胞凋亡也是导致心肌细胞数量减少的重要原因 ,在心室重塑中起重要作用 ,本文将就这方面的研究进展进行综述。细胞凋亡的基本概念　　细胞凋亡又称程序性细胞死亡 ,是由基因控制的细胞主动死亡形式。其主要特征为细胞皱缩、细胞膜完整并发泡、细胞器完整、染色质固缩和凋亡小体形成。细胞凋亡在正…     

生存和心室肥大试验

标 题１．生存和心室肥大试验的基本原理、设计和基本特征 ２．卡托普利对心肌梗死后左室功能不全患者病死率和患病率的影响：生存和心室肥大试验的结果 ３．心肌梗死后２年的心血管死亡和左心室重构,基本的预报因子和长期应用卡托普利的结果：来源于生存和心室 肥大试验的资料作 者１．Ｍｏｙｅ　ＬＡ,等 ２．Ｐｆｅｆｆｅｒ ＭＡ,等 ３．Ｓｔ．Ｊｏｈｎ Ｓｒｔｔｏｎ Ｍ,等 参考文献 １．Ａｍ Ｊ Ｃａｒｄｉｏｌ,１９９１,６８：７０Ｄ～７９Ｄ ２．Ｎ Ｅｎｇｌ Ｊ Ｍｅｋ,１９９２,３２７：６６９～６７７ ３．Ｃｉｒｃｕｌａｔ…     

Two-year time course and significance of neurohumoral activation in the Survival and Ventricular Enlargement (SAVE) Study

Aims To describe the temporal evolution of neurohumoral activationin survivors of myocardial infarction with left ventriculardysfunction who are initially asymptomatic and to relate thisto prognosis. Methods and Results Patients in the neurohumoral substudy (n=534)of the Survival and Ventricular Enlargement (SAVE) study hadtheir neurohormones measured at baseline, 3, 12 and 24 monthspost-infarction, were followed 38±7 months and had thesevalues related to prognosis. All patients had a left ventricularejection fraction 40% early post-infarction. Atrial natriureticpeptide, aldosterone, norepinephrine and plasma renin activitydecreased progressively over time. Patients with events hada persistent increase in these neurohormones with those dyingwithin the first 24 months of follow-up having the greatestincrease. Treatment with captopril affected only plasma reninactivity (increase) and aldosterone (decrease). For patientswho remained asymptomatic for the first 3 months post-infarction(n=471), by multivariate analyses (all neurohormones togetherwith non-neurohumoral risk factors), 3-month plasma atrial natriureticpeptide and aldosterone were the most closely related to thedevelopment of severe heart failure or to the combined end-points(cardiovascular death, myocardial infarction, or severe heartfailure). No neurohormone was related to recurrent myocardialinfarction or to cardiovascular mortality. When the last neurohormonemeasured prior to an event was considered along with non-neurohumoralrisk factors (adjusted univariate), atrial natriuretic peptide,aldosterone, norepinephrine and epinephrine were associatedwith prognosis indicating that a time-dependent analysis identifieda closer relationship between neurohormones and events thanthat identified by 3-month values. However, by multivariateanalyses atrial natriuretic peptide was the only neurohormoneassociated with an event, being associated with the developmentof severe heart failure (P<0·001) and the combinedend-points (P=0·022). However, when neurohormones werecon-sidered as binary variables, activated or non-activated(defined as >1·96SD above the mean of age-matched controls),an association between activation of norepinephrine prior torecurrent myocardial infarction (P<0·001) and combinedend-points (P<0·01) and between activation of aldosteroneand severe heart failure (P<0·05) was identified. Conclusions Neurohumoral activation decreases pro-gressivelypost-infarction, but only in patients with a good prognosis.In patients with a left ventricular ejection fraction 40% andasymptomatic post-infarction plasma atrial natriuretic peptideat 3 months, aldosterone levels appeared to be the neurohormonesmost closely associated with prognosis. Increased levels ofatrial natriuretic peptide, aldosterone and norepinephrine appearto be temporally most closely associated with events.     

Additive Beneficial Effects of Beta-Blockers to Angiotensin-Converting Enzyme Inhibitors in the Survival and Ventricular Enlargement (SAVE) Study

Objectives. This study assessed whether treatment with a beta-adrenergic blocking agent in addition to the use of the angiotensin-converting enzyme (ACE) inhibitor captopril decreases cardiovascular mortality and morbidity in patients with asymptomatic left ventricular dysfunction after myocardial infarction (MI) and whether the presence of neurohumoral activation at the time of hospital discharge predicts the effects of beta-blocker treatment in these patients.Background. Both beta-blockers and ACE inhibitors have been shown to have beneficial effects in patients with left ventricular dysfunction but no overt heart failure after MI. These patients often have persistent neurohumoral activation at the time of hospital discharge, and one would expect that patients with activation of the sympathetic nervous system derive the most benefit from treatment with beta-blockers. However, beta-blockers are underutilized in this high risk group of patients, and it is unknown whether their beneficial effects are additive to those of ACE inhibitors.Methods. We performed a retrospective analysis of data from the Survival and Ventricular Enlargement (SAVE) study and its neurohumoral substudy. The relations between beta-blocker use at the time of randomization and neurohumoral activation and the subsequent development of cardiovascular events were analyzed by use of Cox proportional hazards models controlling for covariates.Results. After adjustment for baseline imbalances, beta-blocker use was associated with a significant reduction in risk of cardiovascular death (30%, 95% confidence interval [CI] 12% to 44%) and development of heart failure (21%, 95% CI 3% to 36%), but the reduction in recurrent MI (11%, 95% CI 13% to 31%) was not significant. These reductions were independent of the use of captopril. Beta-blockers were not found to have a greater effect in patients with neurohumoral activation at the time of hospital discharge.Conclusions. The beneficial effects of beta-blocker use at the time of hospital discharge in patients with asymptomatic left ventricular dysfunction after MI appear to be additive to those of captopril and other interventions known to improve prognosis. Neurohumoral activation at the time of hospital discharge fails to identify those patients who will derive the greatest benefit from treatment with beta-blockers.(J Am Coll Cardiol 1997;29:229–36)     

Effect of antecedent systemic hypertension on subsequent left ventricular dilation after acute myocardial infarction (from the Survival and Ventricular Enlargement trial)

Whether antecedent systemic hypertension influences the risk of subsequent left ventricular (LV) dilation in patients after an acute myocardial infarction with LV systolic dysfunction is unclear. We assessed echocardiographic evidence of ventricular remodeling from baseline (mean +/- SD 11 +/- 3 days) to 2 years after an acute myocardial infarction in 122 hypertensive (defined as a history of treated hypertension, baseline systolic blood pressure > or =140 or baseline diastolic blood pressure > or =90 mm Hg) and 334 nonhypertensive patients in the Survival and Ventricular Enlargement echocardiographic substudy. Compared with nonhypertensives, baseline heart size, defined as the sum of the average short- and long-axis LV cavity areas, was similar (70.1 +/- 11.9 vs 68.8 +/- 11.2 cm(2), p = 0.33 at end-diastole; 50.1 +/- 11.3 vs 48.8 +/- 10.8 cm(2), p = 0.31 at end-systole), but short-axis LV myocardial area (24.7 +/- 4.3 vs 25.7 +/- 5.0 cm(2), p = 0.043) and wall thickness (1.15 +/- 0.16 vs 1.21 +/- 0.17 cm, p = 0.004) at end-diastole were greater among hypertensives. The myocardial infarct segment lengths were similar in the 2 groups (p = 0.22). Although LV cavity areas increased significantly in the 2 groups from baseline to 2 years (p < or =0.001), the increase was significantly greater in hypertensives than in nonhypertensives (+5.6 +/- 11.5 vs +2.2 +/- 10.7 cm(2), p = 0.005 at end-diastole; +6.23 +/- 12.75 vs +2.94 +/- 11.4 cm(2), p = 0.012 at end-systole). There was no concomitant difference in the change in LV myocardial area or LV wall thickness between the 2 groups (p >0.30). After adjusting for known confounders, antecedent hypertension was associated with a doubling of the risk of LV dilation (50.8% vs 37.7%, odds ratio 2.09, 95% confidence interval 1.27 to 3.45, p = 0.004). This association was not modified by diabetes mellitus, myocardial infarct segment length, or captopril use (all p values for interaction >0.10). We conclude that antecedent hypertension is associated with subsequent LV dilation in patients after acute myocardial infarction with LV systolic dysfunction.     

The sleep apnea cardiovascular endpoints (SAVE) trial: Rationale and start-up phase

THE SLEEP APNEA CARDIOVASCULAR ENDPOINTS (SAVE) STUDY (CLINICAL TRIALS REGISTRATION NUMBER: NCT00738170) is an academic initiated and conducted, multinational, open, blinded endpoint, randomised controlled trial designed to determine whether treatment of obstructive sleep apnea (OSA) with continuous positive airways pressure (CPAP) can reduce the incidence of serious cardiovascular events in patients with established cardiovascular disease. The answer to this question is of major importance to populations undergoing ageing and lifestyle changes all over the world. The SAVE study brings together respiratory, sleep and cardiovascular clinician-scientists in a unique interdisciplinary collaborative effort with industry sponsors to conduct the largest and most ambitious clinical trial yet conducted in the field of sleep apnea, with a global recruitment target of 5000 patients. Following its launch in Australia and China in late 2008, SAVE has now entered a phase of international expansion with new recruitment networks being established in New Zealand, India and Latin America. This article describes the rationale for the SAVE study, the considerations behind its design, and progress thus far in establishing the recruitment network. The report emphasises the important role that Chinese sleep and cardiovascular investigators have played in the start-up phase of this landmark international project.     

Enlargement of epididymal adipocytes in relation to hyperinsulinemia in obese hyperglycemic mice (ob-ob)

The diameters of epididymal fat cells of 12–17-day-old obese and normal littermates were compared following operative removal of the epididymal fat body. The animals were kept alive and checked for obesity at an age of 6 wk. Fat cells of the genetically obese mice began their fast growth between day 12 and day 14. At this age, it is possible to identify on the basis of fat-cell diameters three classes, representing +/+, ob/+, and $\text{ob}\text{ob}$, respectively, which shows that the ob allel is incompletely dominant. Measurements of the plasma-insulin concentration revealed that hyperinsulinemia, which is characteristic for the obese hyperglycemic syndrome, is not manifested before the beginning of the fourth week. Since hyperinsulinemia becomes evident at a later stage in development than the rapid increase in growth rate of the fat cells, it seems that the insulin resistance and the hyperinsulinemia cannot be the primary cause of the enlargement of the epididymal adipocytes.