心肌灌注断层显像对心肌梗塞诊断的价值

本文对50例心肌梗塞（急性、陈旧性心梗39例,无Q波型心梗11例）的99mTc-MIBI心肌灌注断层显像结果同平面心肌显像,心电图及核素心室造影进行对比研究,结果:心肌灌注断层显像诊断心梗灵敏度98％、平面心肌显像90％、心电图78％。多病灶检出率心肌断层76％、平面心肌显像25％、心电图20％。11例无Q波型心梗10例显像示局部放射性缺损。13例同时行核素心室造影,3例LVEF正常,均为一个室壁段梗塞。10例LVEF在34％以下,梗塞的室壁段在3个以上,其中5例呈现形态失常经心室核素造影示局部室壁瘤形成;还有2例为5个室壁段梗塞,梗塞体积占左室体积45％,均在二周内死亡。表明:心肌灌注断层显像以它生理学基础和三维图像显示特点提高诊断心梗灵敏度和多病灶检出率。定位直观、准确。为无Q波型心梗是否穿壁与非穿壁问题提供无创性检测手段。梗塞范围大小估价和形态学变化对心功能评价、疗效判定、预后估价、室壁瘤诊断有其重要临床意义。     

碎裂QRS波对心肌缺血及心肌梗死的诊断价值

目的分析心电图碎裂QRS波对急性心肌缺血及陈旧性心肌梗死的诊断价值。方法选择10例心电图出现碎裂QRS波患者,应用心肌核素断层显像技术识别心肌缺血及心肌瘢痕。结果10例患者行心肌核素灌注显像,静息与负荷结果显示,7例心电图碎裂QRS波与无灌注的心肌瘢痕有关;1例碎裂QRS波显示急性心肌大范围灌注不良,提示心肌缺血;1例碎裂QRS波为跨越冠状动脉供血支配导联分布,1例碎裂QRS波无心肌灌注缺损。结论心电图碎裂QRS波对急性心肌缺血和/或陈旧性心肌梗死的诊断有重要作用。     

陈旧性心肌梗塞体表的差电位图

本文通过临床研究陈旧性心肌梗塞(下简称心梗)的差电位图表现与核素心血管造影及心肌灌注断层显像结果进行对照。80例陈旧性心梗分为前壁、下后壁、前壁 下后壁心梗三组。差电位田显示,心室兴奋早中期,前壁及下后壁心梗组的负区部位、范围及出现时间与心梗后电位丧失区域对应。前壁 下后壁心梗组负区意义难定。差电位图平均负区面积百分比与核素心血管造影所示左室相位分布的标准差及半定量计分法测定的局部相位延迟呈正相关,与左室射血分数之间为负相关。与33例心肌灌注断层显像缺损体积呈正相关。     

心电图R波递增不良诊断前壁心肌梗死756例分析

目的探讨心电图R波递增不良(PRWP)诊断前壁心肌梗死(MI)的价值。方法回顾性分析2000—2006年本院核医学科连续进行的三磷酸腺苷(ATP)负荷心肌核素灌注断层显像(MPI)检查病例的心电图,排除前壁Q波MI或前壁导联异常q波、束支阻滞、预激综合征、心室肥厚、心房颤动、心室起搏心电图、MPI图像质量差的病例及MPI诊断为基底部下壁MI的病例,应用心电图PRWP的常规诊断标准Marquette、Zema、Warner和Depace以及10种新的诊断标准对药物负荷MPI检查前卧位标准12导联心电图进行分析,将多个标准诊断的心电图PRWP同药物负荷MPI前壁MI检出结果进行比较。结果符合入选标准的病例756例,常规标准心电图PRWP的检出率为2.0%～18.0%,MPI检出前壁MI43例中,常规标准心电图PRWP检出率为14.0%～48.8%,常规标准心电图PRWP病例中前壁MI检出率为15.4%～40.0%。常规及新诊断标准中的A、B、C、D、E、H、I、J标准诊断的心电图PRWP阳性组前壁MI检出率显著高于心电图PRWP阴性组,但上述标准的正确诊断指数(Youden指数)为0.11～0.51。结论心电图PRWP诊断前壁MI价值有限。     

心肌桥患者~(99)Tc~m-MIBI运动负荷心肌血流灌注断层显像的特点

目的 总结和分析冠状动脉心肌桥患者99Tcm-MIBI运动负荷心肌血流灌注断层显像的特点.方法 回顾2003年至2009年经冠状动脉造影证实的冠状动脉心肌桥患者17例,分析其~(99)Tc~m-MIBI运动负荷心肌血流灌注断层显像放射性分布特点.结果 17例心肌桥患者中有12例患者出现异常心肌血流灌注断层影像.6例收缩期壁冠状动脉受压狭窄＜50%的患者中有2例患者出现异常心肌血流灌注断层影像,表现为可逆性缺损和反向再分布.4例收缩期壁冠状动脉受压狭窄50%～75%的患者中有3例患者出现异常心肌血流灌注断层影像,表现为可逆性缺损、部分可逆性缺损、固定缺损、反向再分布.7例收缩期壁冠状动脉受压狭窄75%～100%的患者心肌血流灌注断层影像异常率为100%,表现为可逆性缺损、部分可逆性缺损、固定缺损、反向再分布.结论 冠状动脉心肌桥患者可以导致心肌血流灌注断层显像异常.收缩期壁冠状动脉受压75%～100%心肌桥患者均出现异常心肌血流灌注断层显像.     

心电图R波递增不良诊断前壁心肌梗死的价值

R波递增不良(PRWP)是临床广泛应用的心电图(ECG)术语,是等位性Q波表现之一,常用于提示或怀疑陈旧性前壁心肌梗死(MI)。ECG PRWP除见于前壁MI外,还可见于心室肥厚、束支阻滞及导联位置误放等,ECGPRWP诊断标准尚不统一,其诊断前壁MI的价值有限。     

R波递增不良诊断前壁心肌梗死价值研究

目的研究心电图R波递增不良在临床对前壁心肌梗死的临床诊断价值。方法研究时间为2008年1月~2014年12月,对象选择为2400例心电图检查中均出现R波递增不良的患者,根据病变的不同将其分为器质性病变组(1400例)和非器质性病变组(1000例),分别在不同的标准下进行前壁心肌梗死的诊断。结果分别参照Wamer、Depace、Zema、Marquette四种常规诊断标准,器质性病变组诊断率平均在30.0%~45.0%,非器质性病变组诊断率平均在3.0%~9.0%,器质性病变组诊断率高于非器质性病变组,组间具有显著统计学差异(p0.05)。以超声心动图检查结果为标准,心电图R波递增不良与前壁心肌梗死具有显著相关性(p0.01)。结论临床对前壁心肌梗死的诊断标准不一,心电图R波递增不良可对前壁心肌梗死进行诊断,但诊断率不高,在临床使用中具有一定的局限性。     

硝酸甘油介入99mTc-MIBI静息态心肌断层显像估测冠心病存活心肌的临床意义

目的：探讨含服硝酸甘油（ Ｎ Ｔ Ｇ）介入９９ｍ Ｔｃ甲氧基异丁基异晴（ Ｍ Ｉ Ｂ Ｉ）心肌断层显像在心肌存活估测中的价值。方法：５４ 例冠心病患者,其中陈旧性心肌梗死（ Ｏ Ｍ Ｉ）、不稳定型心绞痛（ Ｕ Ａ）、稳定型心绞痛（ Ｓ Ａ）各１８ 例。先行静息态９９ｍ Ｔｃ Ｍ Ｉ Ｂ Ｉ心肌断层显像,４８ ｈ 后在静脉注入９９ｍ Ｔｃ Ｍ Ｉ Ｂ Ｉ前 ５ ｍ ｉｎ 舌下含服 Ｎ Ｔ Ｇ ０．５ ｍ ｇ,然后再行静息态心肌断层显像。结果：５４ 列患者静息态心肌断层显像有１６８ 个节段放射性分布异常, Ｎ Ｔ Ｇ 介入后有７１ 个节段灌注改善（４２．３％ ）。 Ｕ Ａ 组有８ 个心肌节段为不可逆性灌注缺损, Ｓ Ａ 组无不可逆性灌注缺损的心肌节段。结论：含服 Ｎ Ｔ Ｇ 能明显改善静息态９９ｍ Ｔｃ Ｍ Ｉ Ｂ Ｉ时心肌存活的检测效果,对判断病情和指导治疗有一定价值。     

冠状动脉造影正常的心肌梗塞患者核素心肌灌注显像

目的 :分析冠状动脉造影正常的心肌梗塞患者核素心肌灌注显像表现。　　方法 :回顾总结了 18例冠状动脉造影正常的心肌梗塞患者 99m锝 -甲氧基异丁基异腈 (99m Tc- MIBI)静息心肌断层显像。　　结果 :18例心肌梗塞患者心肌灌注显像均显示异常 ,12例有节段性缺损 ,6例未见缺损但可见心肌节段性稀疏。心肌灌注显像对心肌梗塞的定位与心电图 Q波比较 ,显示病变部位更明确。　　结论 :心肌灌注显像提供了冠状动脉造影正常的心肌梗塞患者心肌损伤部位及程度。     

急性心肌梗死的心电图分类与诊断

临床对急性心肌梗死的诊断一直沿用WHO的标准,即典型的胸痛症状、心肌酶学升高和心电图特征性的动态演变,这3个条件中满足2个即可诊断。尽管心电图在心梗极早期诊断、多支血管病变的冠状动脉定位等方面有一定的局限性,但由于其具有特异性和敏感性较高、无创、便捷、可多次重复等优点,在心梗的分类和诊断中仍具有不可忽视的重要地位。1.急性心肌梗死的心电图分类急性心肌梗死的心电图分类历经透壁性心梗和非透壁性心梗(20世纪80年代前)、Q波心梗和非Q波心梗(80年代),到近年随着再灌注治疗的临床应用已演变为ST段抬高型心梗和非ST段抬高型…     

Electrocardiographic poor R-wave progression: analysis of multiple criteria reveals little usefulness

Background

Poor or reverse R-wave progression (PRWP) is a common statement on electrocardiogram (ECG) interpretations, but its value in diagnosing anterior myocardial infarction (MI) is disputed. We assessed the accuracy of PRWP criteria in diagnosing anterior MI.

Methods

We searched MEDLINE (1960-1998) and found 3 criteria for PRWP. We included a modified version of the Marquette Muse system's criteria and multiple novel criteria. We interpreted resting ECGs of consecutive patients undergoing pharmacologic stress tests with dual isotope gated single photon emission computed tomography. Subjects with Q-wave anterior MI, bundle branch block, or Wolf-Parkinson-White syndrome were excluded. We established whether patients met the PRWP criteria. A nuclear cardiologist blinded to PRWP classifications reviewed the scintigrams. χ² Methods were used for statistical analysis.

Results

Inclusion criteria were met by 122 subjects. The standard PRWP criteria were met in 15% to 42% of ECGs. Of subjects meeting PRWP criteria, 2% to 9% had anterior MI and 27% to 33% had anterior MI or ischemia. These proportions were similar to those expected by chance. The performance of PRWP criteria did not improve when subjects with electrocardiographic left ventricular hypertrophy were excluded or when more stringent criteria for right precordial R-wave amplitude were tested.

Conclusions

In our study of patients undergoing cardiac stress tests, only a small percentage of patients who met various criteria for PRWP (a proportion no different than would be expected by chance) had anterior MI. Conclusions about the presence of anterior MI solely on the basis of PRWP have little usefulness.     

Correlation between non-reversible thallium-201 myocardial perfusion defect and ECG criteria in the diagnosis of apical myocardial infarction

BACKGROUND: ECG identification of apical myocardial infarction (MI) is controversial and lacks of accuracy. Our aim was to investigate the sensitivity of different proposed ECG criteria in the presence of apical perfusion defects assessed with SPECT analysis. METHODS: One hundred twenty-four (98 M, 26 F) out of 1500 patients with suspected coronary artery disease, showed apical perfusion defect not reversible at rest and after reinjection at tomographic SPECT analysis during thallium-201 scintigraphy. RESULTS: In the group of 29 patients presenting wide isolated apical perfusion defect (wAPD) Q waves in anterior segments with definition of antero-septal MI was prevalent (51.7%), while few patients (41.3%) presented the ECG criteria of apical MI as proposed in the literature. In 19 of the 25 patients with partial isolated apical perfusion defect (pAPD), the absence of Q wave was clearly prevalent. Fifty patients had a wAPD partially extended in surrounding regions, as anterior or septal, inferior or lateral myocardial segments, in these patients, the site of Q wave location was more variable, with prevalent Q wave in anterior leads, but with more incidence of Q waves in leads II III aVF, especially in patients with associated perfusion defect in inferior segments. Substantially, the same finding resulted in the 20 patients showing a pAPD extended in surrounding myocardial segments. CONCLUSION: In conclusion, the low diagnostic sensitivity of the ECG criteria of identification of apical MI is clearly demonstrated by our analysis carried out using SPECT perfusion scintigraphy, with ECG findings of anterior/anterior-septal myocardial necrosis in the patients with wAPD.     

The effect of the Q wave infarct on left ventricular electromechanical function

OBJECTIVE: To assess the nature of left ventricular (LV) electrical and mechanical dysfunction in Q compared to non-Q anterior myocardial infarction (MI). SUBJECTS: We used ECG and echocardiography to study 54 unselected patients, age 57+/-15 years, 32 male, with old (>6 months after) anterior MI (39 Q and 15 non-Q), confirmed by enzyme rise and regional wall motion abnormality, and compared them with 21 normals of similar age. METHODS: Analysis of resting LV minor and long axis function and 12-lead surface electrocardiogram. RESULTS: Only 10% of normals did not have a normal septal Q wave compared with 46% of non-Q wave MI and 84% Q wave MI (P<0.001). All patients with Q wave MI had a scarred anteroseptal wall but none of the non-Q wave MI. LV minor axis dimensions were increased only with Q wave MI: 6.0 +/- 0.9 vs. 4.9 +/- 0.5 cm at end-diastole and 4.5 +/- 1.1 vs. 3.3 +/- 0.5 cm at end-systole and fractional shortening was reduced 27 +/- 8 vs. 33 +/- 3% (P<0.001 for all). Total left ventricular long axis amplitude of motion was reduced at the left, septal and posterior sites only in Q wave MI but was not different from controls in non-Q wave MI. The onset of long axis shortening was delayed by 20 ms at the left and septal sites in non-Q wave MI and by an additional 20 ms at the three sites in Q wave MI. Peak long axis shortening rate was reduced in the two patient groups, with the same distribution as post-ejection shortening (greater than 1 mm), which occurred in 21% of patients with non-Q wave MI and 76% of patients with Q wave MI (P<0.001). In diastole, the onset of long axis lengthening was delayed by 20 ms at the left and septal sites in non-Q wave MI and at the three sites in Q wave MI (P<0.001). Peak long axis lengthening rate was reduced with a similar distribution in the two patient groups. CONCLUSION: Patients with Q wave MI have an increased LV dimension and reduced FS, whereas patients with non-Q wave MI appear to have morphologically normal LV minor axis dimensions and fractional shortening apart from the anterior wall hypokinesis. In the latter, however, long axis function shows significant systolic and diastolic disturbances affecting the anteroseptal and lateral walls. The absence of conduction disturbances in non-Q wave MI suggests intrinsic myocardial dysfunction that may be reversible.     

Prognostic significance of location and type of myocardial infarction: independent adverse outcome associated with anterior location

To determine the relative prognostic significance of location (anterior or inferior) and type (Q wave or non-Q wave) of infarction, the hospital course and follow-up outcome (mean duration 30.8 months) of 471 patients with a first infarction were analyzed. Analyses were performed grouping the patients according to infarct location (anterior, n = 253; inferior, n = 218), infarct type (Q wave, n = 323; non-Q wave, n = 148), and both location and type (inferior non-Q wave, n = 85; inferior Q wave, n = 133; anterior non-Q wave, n = 63; and anterior Q wave, n = 190). Patients with anterior infarction had a substantially worse in-hospital and follow-up clinical course compared with those with inferior infarction, evidenced by a larger infarct size (21.2 versus 14.9 g Eq/m2 creatine kinase, MB fraction [MB CK], p less than 0.001), lower admission left ventricular ejection fraction (38.1 versus 55.3%, p less than 0.001) and higher incidence of heart failure (40.7 versus 14.7%, p less than 0.001), serious ventricular ectopic activity (70.2 versus 58.9%, p less than 0.05), in-hospital death (11.9 versus 2.8%, p less than 0.001) and total cumulative cardiac mortality (27 versus 11%, p less than 0.001). Patients with Q wave infarction similarly experienced a worse in-hospital course compared with patients with non-Q wave infarction, evidenced by a larger infarct size (20.7 versus 12.7 MB CK g Eq/m2, p less than 0.001), lower admission left ventricular ejection fraction (43.7 versus 50.6%, p less than 0.001), and a higher incidence of heart failure (31.9 versus 21.6%, p less than 0.05) and in-hospital death (9.3 versus 4.1% p less than 0.05). However, there was no increased rate of reinfarction or mortality in hospital survivors with non-Q wave infarction compared with those with Q wave infarction, and total cardiac mortality was similar (16 versus 21%, p = NS). To evaluate the role of infarct location and type independent of infarct size, patients were grouped according to quartile of infarct size, and outcome was reanalyzed within each group. Patients with anterior infarction demonstrated a lower left ventricular ejection fraction on admission and after 10 days than did patients with inferior infarction, even after adjustment for infarct size, as well as a higher incidence of congestive heart failure and cumulative cardiac mortality.(ABSTRACT TRUNCATED AT 400 WORDS)     

ST segment shifts are poor predictors of subsequent Q wave evolution in acute myocardial infarction. A natural history study of early non-Q wave infarction

Acute ST segment elevation is regarded generally as the sine qua non of evolving Q wave myocardial infarction (MI) because such electrocardiographic (ECG) injury is believed to be a marker of transmural ischemia and a forerunner of transmural necrosis. Alternatively, ST segment depression with or without T wave inversion is viewed as the dominant ECG feature of non-Q wave MI. However, this hypothesis has not been assessed prospectively in an acute MI population. We analyzed 2,304 serial ECGs at study entry (admission), day 2, day 3, and predischarge (mean, 10.2 +/- 2 days) from 576 patients with creatine kinase MB confirmed acute non-Q wave MI to determine what percentage of patients with early ST segment elevation culminated in subsequent Q wave development. Of this group, 187 patients (32%) exhibited 1 mm or greater ST segment elevation in two or more contiguous entry ECG leads. Of those patients whose non-Q wave MI could be localized on the basis of diagnostic admission ST segment shifts, the prevalence of early ST segment elevation was 43% (187 of 439). The sum total mean (+/- SD) peak ST segment elevation by lead group (anterior, inferior, lateral) was 4.0 +/- 2.4, 4.5 +/- 2.4, and 2.5 +/- 0.6 mm, respectively. Despite this, only 20% of patients with ST segment elevation (37 of 187) developed Q waves. Of 252 patients who exhibited early ST segment depression or T wave inversion or both, 39 (15%) evolved subsequent Q waves. Thus, while the prevalence of early ST segment elevation in acute evolving non-Q wave MI was higher than previously reported, 80% of patients with and 85% of patients without ST segment elevation and absent Q waves on the admission ECG did not develop subsequent Q waves during a 2-week period of observation (p = NS). In addition, when patients with ST segment elevation were compared with patients with ST segment depression or T wave inversions or both, there were no between-group differences in log peak creatine kinase (404 vs. 383 IU), reinfarction (6% vs. 8%), postinfarction angina (50% vs. 42%), or early recurrent ischemia (49% vs. 45%), defined as postinfarction angina with transient ECG changes. Thus, in patients who present with initial acute non-Q wave MI, ST segment shifts on admission are unreliable predictors of subsequent Q wave evolution and do not discriminate significant differences in postinfarction outcome. In particular, ST segment elevation during the early hours of evolving infarction is not an invariable harbinger of subsequent Q wave development.     

The prognostic significance of first myocardial infarction type (Q wave versus non-Q wave) and Q wave location. The Multicenter Diltiazem Post-Infarction Research Group

The prognostic significance of the type of first acute myocardial infarction (Q wave versus non-Q wave) and Q wave location (anterior versus inferoposterior) was determined from a multicenter data base involving 777 placebo-treated patients who were participants in the Multicenter Diltiazem Post-Infarction Trial. There were 224 patients (29%) with a non-Q wave infarction, 326 (42%) with an inferoposterior Q wave infarction and 227 (29%) with an anterior Q wave infarction. Mean left ventricular ejection fraction was significantly (p less than 0.001) lower in patients with an anterior Q wave infarction than in the other two groups (anterior Q wave 0.39; inferior Q wave 0.52; non-Q wave 0.53). Nevertheless, the total cardiac mortality rate during the follow-up period (average 25 months per patient) was only marginally higher (p = 0.42) in the anterior Q wave group (8.4%) than in the other two groups (inferoposterior Q wave 7.1%; non-Q wave 6.3%). The total first recurrent cardiac event was somewhat higher (p = 0.08) in the anterior Q wave group (18.1%) than in the other two groups (inferoposterior Q wave 11.7%; non-Q wave 15.6%). Survivorship analyses extending over 3 years revealed that electrocardiographic classification of the type of first infarction and Q wave location did not make significant independent contributions to the risk of postinfarction cardiac death or first recurrent cardiac event, either before or after adjustment for baseline clinical variables.     

Initial ECG in Q wave and non-Q wave myocardial infarction

The initial ECGs in 440 patients admitted for suspected acute myocardial infarction were retrospectively analyzed to determine predictive values of these ECGs for acute myocardial infarction and to determine differences in the initial ECG for Q wave and non-Q wave myocardial infarction. One hundred (23%) of the study patients were diagnosed as having an acute myocardial infarction. Acute injury was seen in 47% of these patients (positive predictive value [PPV], 84%; 95% confidence interval [CI], 72% to 92%), ischemia in 15% (PPV, 39%; 95% CI, 24% to 57%), and left ventricular hypertrophy with strain in 11% (PPV, 19%; 95% CI, 4% to 29%). Forty-three patients were diagnosed as having a Q wave infarction and 50 patients as having a non-Q wave infarction. Seventy-two percent of the patients with a Q wave infarction had acute injury as the initial ECG interpretation compared with 38% in the non-Q wave infarction group (P less than .001). In contrast, only 17% of patients with Q wave infarction had an initial ECG interpretation of ischemia or strain as compared with 36% of patients with non-Q wave infarction (P = .03). Because of the relatively high incidence of acute myocardial infarction in patients admitted with an initial ECG interpretation of ischemia or left ventricular hypertrophy with strain, prospective studies must be performed to determine if selective patients with acute ST segment depression or ischemic T wave inversion in the setting of suspected acute myocardial infarction may benefit from early thrombolytic therapy.     

Isointegral analysis of body surface maps for the assessment of location and size of myocardial infarction

To estimate the location and size of myocardial infarction (MI), an isointegral mapping technique was adopted from among various body surface electrocardiographic mapping techniques. QRS isointegral and departure maps were made in 35 patients with MI. These patients were separated into 3 groups, based on the location of MI: anterior, inferior, and anterior plus inferior. The severity and location of MI were estimated by thallium-201 myocardial perfusion imaging and the degree of scintigraphic defect was represented by a defect score.

The extent of MI was expected to be reflected on the QRS isointegral maps as a distribution of negative QRS complex time-integral values. However, the extent and the location of MI were hardly detectable by the original maps. A departure mapping technique was then devised to observe the distribution of departure index on the body surface. Particular attention was given to the area where the departure index was less than −2, and this area was expected to reflect the location and size of specific abnormality of isointegral map due to MI. There were strong correlations between departure area and defect score in the anterior and inferior MI cases (r = 0.88 and r = 0.79, respectively). However, patients with anterior MI plus inferior MI showed no such correlation.

Q-wave mapping was compared with QRS isointegral mapping, and QRS isointegral mapping was found to be more accurate in the estimation of the location and size of MI than Q wave mapping. Thus, QRS isointegral mapping, especially departure mapping, is more useful and convenient for detecting the location and size of MI than methods such as isopotential and Q wave mapping.