Time of regression of the Q wave in patients with myocardial infarction]

A rate of Q wave regression was assessed in 72 patients with ischaemic heart disease, including 46 patients after the infarction of the inferior wall and 26 patients after anterior wall infarction. All patients were followed-up for two years. Complete regression of Q wave was noted in 19 patients (41.3%) after inferior wall infarction and in one patient (3.8%) after anterior wall myocardial infarction. Partial regression of Q wave was seen in 9 patients (19.6%) after inferior wall, and in 2 patients (7.6%) of patients with anterior wall myocardial infarction. It seems that the regression of Q wave in ECG does not improve prognosis in these patients. Six out of 10 deaths which occurred in the followed up group of patients involved those in whom no electrographic features of the past myocardial infarction were seen.     

Usefulness of three additional electrocardiographic chest leads (V7, V8, and V9) in the diagnosis of acute myocardial infarction.

Additional electrocardiocardiographic chest leads (V7, V8, and V9) were used in 117 persons consecutively admitted to a coronary care unit. Among the 46 (39%) with a proven acute myocardial infarction the electrocardiograms (ECGs) of 9 (20%) showed ST-segment elevation or abnormal Q-waves, or both, in the three additional leads. In six of the nine, such changes were associated with signs of anterolateral or inferior wall infarction (in three each) on the standard 12-lead ECG, but in the other three (7% of the 46) electrocardiographic changes diagnostic of acute myocardial infarction were found only on the additional chest leads; the last three had characteristic changes in serum enzyme concentrations. This study showed that additional chest leads are helpful in detecting myocardial injury of necrosis in areas of the heart not properly reflected on the standard 12-lead ECG.     

Radionuclide diagnosis of right ventricular myocardial infarction

The diagnostic capacities of 99mTc-pyrophosphate plane myocardial scintigraphy versus 99mTc-pyrophosphate single photon emission computed tomography (SPECT) were compared. Recording right precordial ECG leads showed that 26 patients had right ventricular myocardial infarction (MI)-typical changes as ST-segment evaluation, followed by abnormal Q wave. Plane scintigraphy indicated a characteristic inclusion of 99mTc-pyrophosphate into the right ventricular myocardium in 18.8% of the patients with acute lower MI and in one of 38 patients with acute MI of the anterior left ventricular wall. SPECT revealed a characteristic inclusion of 99mTc-pyrophosphate into the right ventricular myocardium much more frequently than did plane myocardial scintigraphy--in 34% of cases. Right ventricular myocardial inclusion of 99mTc-pyrophosphate was found in 50% of the patients with acute lower MI, including all 9 patients with positive 99mTc-pyrophosphate myocardial scintigraphy. Thus, the sensitivity of SPECT in the diagnosis of right ventricular MI is somewhat higher than that of precordial ECG and more than thrice higher than that of plane scintigraphy.     

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.     

THE Q WAVE IN L III AND aVF OF THE ELECTROCARDIOGRAM—A Vectorcardiographic Analysis With the Use of the Frank System

Seventy-three consecutive patients with a Q wave in Lead III and aVF in the electrocardiogram were studied. Vectorcardiograms were recorded with the use of the Frank system.In 32 cases the ECG''s were compatible with the diagnosis of an inferior myocardial infarction based on a Q wave in Lead III and/or aVF greater than 0.04 second duration and greater than 25 per cent of the amplitude of the R wave. In this group, there were 16 patients with coronary disease and the VCG confirmed the electrocardiographic diagnosis of an infarction in 14 cases. In 13 of the other 16 cases without history of coronary disease the VCG did not suggest the presence of an infarction.In all 17 cases with questionable electrocardiographic diagnosis of an inferior infarction, and without history of coronary disease, the VCG denied the presence of an infarction. In 18 cases with small Q III or Q aVF the VCG''s were within normal limits. In two cases with normal Q III and Q aVF the VCG''s did not detect the presence of an infarction in both cases.The vectorcardiographic diagnosis of an inferior myocardial infarction was based on the superior orientation (at or above 360 degrees) of the 10, 20, 25 and 30-msec vectors in the frontal plane, superior displacement of the maximum QRS vector and clockwise rotation. In the left sagittal plane the 10, 20, 25 and 30-msec vectors were oriented at or above 180 degrees with the loop rotating counterclockwise.The data presented suggest that vectorcardiography is a useful adjunct to electrocardiography in the diagnosis of an inferior myocardial infarction.     

The Significance of Ventricular Premature Beats in the Diagnosis of Septal Infarction

Two hundred and twenty electrocardiograms containing premature ventricular beats were reviewed. Twenty of these contained premature ventricular beats of a myocardial infarction pattern, that is, one consisting of a significant Q wave followed by an R wave. A review of the case histories of these 20 patients disclosed that all 20 had angina pectoris and/or myocardial infarction. Postmortem examinations were performed in seven, and the presence of myocardial infarction was verified. In three instances, only the premature ventricular beat disclosed the myocardial infarction pattern while the normally conducted beats did not. In these three cases the postmortem examination confirmed the presence of septal infarction.     

New Insights into the Circadian Rhythm of Acute Myocardial Infarction in Subgroups

The aim of this study was to determine the existence of the circadian rhythm (CR) in the onset of acute myocardial infarction (AMI) in different patient subgroups. Information was collected about 41,244 infarctions from the database of the ARIAM (Analysis of Delay in AMI) Spanish multicenter study. CR in AMI were explored in subgroups of cases categorized by age, gender, previous ischemic heart disease (PIHD), outcome in coronary care unit, infarction electrocardiograph (ECG) characteristics (Q wave or non‐Q wave), and location of AMI. Cases were classified according to these variables in the different subgroups. To verify the presence of CR, a simple test of equality of time series based on the multiple‐sinusoid (24, 12, and 8 h periods) cosinor analysis was developed. For the groups as a whole, the time of pain onset as an indicator of the AMI occurrence showed a CR (p<0.0001), with a morning peak at 10:10 h. All the analyzed subgroups also showed CR. Comparison between subgroups showed significant differences in the PIHD (p<0.01) and infarction ECG characteristics (p<0.01) groups. The CR of the subgroup with Q‐wave infarction differed from that of non‐Q wave subgroup (p<0.01) when the patients had PIHD (23% in Q wave infarction vs. 39.2% in non‐Q wave). AMI onset followed a CR pattern, which is also observed in all analyzed subgroups. Differences in the CR according to the Q/non‐Q wave infarction characteristics could be determined by PIHD. The cosinor model fit with three components (24, 12, and 8 h periods) showed a higher sensitivity than the single 24 h period analysis.     

New insights into the circadian rhythm of acute myocardial infarction in subgroups

The aim of this study was to determine the existence of the circadian rhythm (CR) in the onset of acute myocardial infarction (AMI) in different patient subgroups. Information was collected about 41,244 infarctions from the database of the ARIAM (Analysis of Delay in AMI) Spanish multicenter study. CR in AMI were explored in subgroups of cases categorized by age, gender, previous ischemic heart disease (PIHD), outcome in coronary care unit, infarction electrocardiograph (ECG) characteristics (Q wave or non-Q wave), and location of AMI. Cases were classified according to these variables in the different subgroups. To verify the presence of CR, a simple test of equality of time series based on the multiple-sinusoid (24, 12, and 8 h periods) cosinor analysis was developed. For the groups as a whole, the time of pain onset as an indicator of the AMI occurrence showed a CR (p<0.0001), with a morning peak at 10:10 h. All the analyzed subgroups also showed CR. Comparison between subgroups showed significant differences in the PIHD (p<0.01) and infarction ECG characteristics (p<0.01) groups. The CR of the subgroup with Q-wave infarction differed from that of non-Q wave subgroup (p<0.01) when the patients had PIHD (23% in Q wave infarction vs. 39.2% in non-Q wave). AMI onset followed a CR pattern, which is also observed in all analyzed subgroups. Differences in the CR according to the Q/non-Q wave infarction characteristics could be determined by PIHD. The cosinor model fit with three components (24, 12, and 8 h periods) showed a higher sensitivity than the single 24 h period analysis.     

3-D MRI assessment of regional left ventricular systolic wall stress in patients with reperfused MI

The goal of this study was to assess the regional variations of end-systolic wall stress in patients with reperfused Q wave acute myocardial infarction (AMI), with the use of a three-dimensional (3-D) approach. Fifteen normal volunteers and fifty patients with reperfused AMI underwent cardiac MRI that used a short-axis fast-gradient-echo sequence. The end-systolic wall stress was calculated with the use of the Grossman formula with the radius and the wall thickness defined with a 3-D approach using the tridimensional curvature. The mean wall stress was significantly increased at each level of the short-axis plane only in patients with anterior AMI. When calculated at a regional level in patients with anterior AMI, wall stress significantly increased in anterior sector as well as normal sector. In patients with inferior AMI, wall stress significantly increased only in inferior and lateral sectors. In conclusion, the quantification of regional wall stress by cardiac MRI is better with the 3D approach than other methods for precise evaluation in patients with AMI. Despite early reperfusion, the wall stress remained high in patients with anterior AMI.     

Early identification of patients at low risk of death after myocardial infarction and potentially suitable for early hospital discharge.

OBJECTIVES--To find (a) whether data available shortly after admission for acute myocardial infarction can provide a reliable prognostic indicator of survival at 28 days, and (b) whether such an indicator might be used to identify patients at low risk of death and suitable for early discharge. DESIGN--Retrospective analysis of data collected on patients admitted to a coronary care unit for acute myocardial infarction. A validation sample was selected at random from these patients. SETTING--Coronary care units in Perth, Western Australia. SUBJECTS--6746 patients aged under 65 and resident in the Perth Statistical Division who during 1984-92 were admitted to a coronary care unit with symptoms of myocardial infarction. MAIN OUTCOME MEASURES--Sensitivity and specificity of several models for predicting survival at 28 days after myocardial infarction, and detailed performance characteristics of a particular model. RESULTS--Patients with a pulse rate of 100 beats/min or less, aged 60 or under, and with symptoms typical of myocardial infarction, no past history of myocardial infarction or diabetes, and no significant Q wave in the admission electrocardiogram had a very high chance of survival at 28 days (99.2%). These patients made up one third of all patients studied. CONCLUSION--The prognostic index identifies patients very soon after admission who are at low risk of death and potentially eligible for early discharge from hospital or the coronary care unit. Computing the index does not need complex cardiac investigations.     

Clinical observations and echocardiographic features of mural thrombi in the left ventricle during myocardial infarction]

The incidence and changes in the mural thrombi in left ventricle in ECHO-2D in the acute myocardial infarction as well as relationship between clinical parameters and echocardiographic indices of the left cardiac ventricle contractability asynergy and dynamics of changes in mural thrombi have been investigated. The studies included 137 consecutive patients (98 males and 39 females) treated for the acute myocardial infarction. Patients' age ranged from 35 to 87 years (mean 62 years). Infarction of the anterior and/or lateral wall was diagnosed in 67 patients, and infarction of the inferior and/or posterior wall in 70 patients. Mural thrombi were diagnosed in 42 (31%) patients. Eighteen thrombi (43%) were liquefied during hospitalization. Comparative analysis of patients in whom mural thrombi underwent liquefaction in the hospital and a group of patients with myocardial infarction and persisting mural thrombi showed that return of left ventricle movements with subsequent contractability facilitate liquefaction of mural thrombi. Higher mortality rate in the group of patients with myocardial infarction with mural thrombi is due to extension of the infarction accompanied by marked asynergy of left ventricular contractions which does not decrease in sequential examinations, and increasing congestive heart failure.     

Syndrome X: case report.

Transmural myocardial infarction occurred in a 48-year-old woman with syndrome X -- atypical angina pectoris and angiographically normal coronary arteries. Before the infarction her electrocardiogram had been normal at rest but showed ischemia after exercise. Angiography 3 months after infarction revealed a normal coronary tree but hypokinesia of the posterior left ventricular wall.     

MYOCARDIAL INFARCTION FOLLOWING CAROTID ENDARTERECTOMY

Myocardial infarction has been the major cause of mortality following operation for cerebrovascular insufficiency. In our institution, a clinical diagnosis of coronary artery disease was made in 37 of 125 (29.6%) consecutive male patients having carotid endarterectomy. Six of these 37 patients developed postoperative myocardial infarction. In contrast, none of the 88 patients without coronary artery disease developed myocardial infarction. A more recently treated group of 20 patients who had undergone carotid artery surgery and had previously undergone coronary artery bypass for angina did not develop postoperative myocardial infarction. These data suggest that in patients with both coronary artery and carotid artery disease, prior or concomitant coronary artery bypass should be considered. Myocardial infarction has been the leading cause of early and late death following operation for cerebrovascular insufficiency.(1) DeBakey(2) found operative mortality in patients having surgery for cerebrovascular insufficiency directly related to the incidence of coronary artery disease. An increased operative mortality due to reinfarction has been found in patients recovering from recent myocardial infarction.(3) Cooley(4) found that in patients having aortocoronary bypass there was no increased operative mortality 30 days after myocardial infarction and this may apply to patients having carotid endarterectomy. Subendocardial postoperative infarction associated with minor T wave changes and slight enzyme elevation had a better prognosis than did transmural infarction causing significant Q waves, sequential ST and T wave changes and marked enzyme elevations.(5) The purpose of this study was to document our experience with myocardial infarction in patients undergoing carotid artery operation for clinical coronary artery disease. Consideration of the role of saphenous vein bypass in those patients with coronary artery disease was the background for this review even though the evidence that myocardial infarction can be prevented with saphenous vein bypass operation is only preliminary at the present time.(6)     

Study protocol to investigate the effects of testosterone therapy as an adjunct to exercise rehabilitation in hypogonadal males with chronic heart failure

Background

Most studies on risk factors for development of coronary heart disease (CHD) have been based on the clinical outcome of CHD. Our aim was to identify factors that could predict the development of ECG markers of CHD, such as abnormal Q/QS patterns, ST segment depression and T wave abnormalities, in 70-year-old men, irrespective of clinical outcome.

Methods

Predictors for development of different ECG abnormalities were identified in a population-based study using stepwise logistic regression. Anthropometrical and metabolic factors, ECG abnormalities and vital signs from a health survey of men at age 50 were related to ECG abnormalities identified in the same cohort 20 years later.

Results

At the age of 70, 9% had developed a major abnormal Q/QS pattern, but 63% of these subjects had not been previously hospitalized due to MI, while 57% with symptomatic MI between age 50 and 70 had no major Q/QS pattern at age 70. T wave abnormalities (Odds ratio 3.11, 95% CI 1.18–8.17), high lipoprotein (a) levels, high body mass index (BMI) and smoking were identified as significant independent predictors for the development of abnormal major Q/QS patterns. T wave abnormalities and high fasting glucose levels were significant independent predictors for the development of ST segment depression without abnormal Q/QS pattern.

Conclusion

T wave abnormalities on resting ECG should be given special attention and correlated with clinical information. Risk factors for major Q/QS patterns need not be the same as traditional risk factors for clinically recognized CHD. High lipoprotein (a) levels may be a stronger risk factor for silent myocardial infarction (MI) compared to clinically recognized MI.     

Early exercise testing after treatment with thrombolytic drugs for acute myocardial infarction: importance of reciprocal ST segment depression.

OBJECTIVE--To investigate the clinical importance of reciprocal ST depression induced by exercise testing early after acute myocardial infarction in patients treated with thrombolysis. DESIGN--Prospective observational study. SETTING--District general hospital in London. SUBJECTS--202 patients (170 men) aged 33-69 with acute myocardial infarction treated with thrombolysis. MAIN OUTCOME MEASURES--All patients underwent exercise testing and coronary arteriography. ST depression induced by exercise was classified as either reciprocal (associated with ST elevation) or isolated (occurring on its own). The relation between reciprocal ST depression and the following end points was studied: characteristics of the infarct, left ventricular ejection fraction, extent of coronary artery disease on arteriography, and presence of angina induced by exercise. RESULTS--Reciprocal ST depression occurred almost exclusively in Q wave infarctions and was associated with a lower overall ejection fraction than isolated ST depression. It tended to be associated with persistent occlusion of the coronary artery related to the infarct and did not indicate remote ischaemia due to multivessel coronary disease. Unlike isolated ST depression, reciprocal ST depression was not associated with angina induced by exercise. CONCLUSIONS--Reciprocal ST depression induced by exercise is usually associated with extensive Q wave infarctions and persistent occlusion of the artery related to the infarct. It does not seem to indicate reversible ischaemia and should not be used as a non-invasive marker of multivessel disease in the assessment of requirements for further investigation soon after acute myocardial infarction.     

Reciprocal change in ST segment in acute myocardial infarction: correlation with findings on exercise electrocardiography and coronary angiography.

The clinical relevance of reciprocal changes in the ST segment occurring at the time of acute myocardial infarction was studied prospectively in 85 consecutive uncomplicated cases. Reciprocal depression of the ST segment was defined as depression of 1 mm or more in electrocardiogram leads other than those reflecting the infarct. All patients underwent maximal, symptom limited treadmill stress testing two weeks after the infarct and coronary angiography six weeks after infarction. Forty six patients had inferior, 34 anterior, and five true posterior infarction. Of the 51 patients with reciprocal changes, 45 (88%) developed exercise induced ST segment depression in areas remote from the infarction zone. At angiography all 45 patients were shown to have stenoses greater than 70% in at least two major vessels. Four patients had negative exercise electrocardiograms and were sequently shown to have single vessel disease subtending their infarct, and the remaining two patients had a false negative treadmill test result. Of the 27 patients without reciprocal changes, 21 (78%) had negative treadmill stress test results associated with single vessel coronary disease. Five had positive stress test results and multivessel coronary disease, and one had a false negative stress test result. The remaining seven patients had ST segment elevation without Q wave formation in the reciprocal areas and were assessed separately. Of these, six had positive stress test results and multivessel coronary disease and one had a negative stress test result and single vessel coronary disease to the infarct area. Twenty one patients with anterior infarcts (62%) and 27 with inferior infarcts (59%) had reciprocal changes. No differences emerged in the relation between infarct site, reciprocal change, and presence of additional coronary disease. At follow up of the 51 patients with reciprocal changes in the ST segment 36 had become symptomatic, of whom 29 had undergone coronary artery bypass surgery. By contrast, only four of the 27 patients without reciprocal changes in the ST segment had developed symptoms, and two of these had undergone coronary revascularisation. Reciprocal ST segment depression at the time of acute myocardial infarction may identify patients with severe coronary disease who are at risk of subsequent cardiac events and appears to be as reliable as results of early postinfarction treadmill stress testing in predicting the underlying coronary anatomy. When the electrocardiogram does not show reciprocal changes treadmill testing provides valuable additional information.     

A longitudinal study on BIO14.6 hamsters with dilated cardiomyopathy: micro-echocardiographic evaluation

Background

Acute myocarditis may mimic myocardial infarction, since affected patients complain of "typical" chest pain, the ECG changes are identical to those observed in acute coronary syndromes, and serum markers are increased. We describe a case series of presumptive myocarditis with ST segment elevation on admission ECG.

Methods and Results

From 1998 to 2009, 21 patients (20 males; age 17-42 years) were admitted with chest pain, persistent ST segment elevation, serum enzyme and troponine release. All but one patients had fever and flu-like symptoms prior to admission. No abnormal Q wave appeared in any ECG tracing, and angiography did not show significant coronary artery disease. Patients remained asymptomatic at long term follow-up, except 2 who experienced a late relapse, with the same clinical, electrocardiographic and serum findings as in the first clinical presentation.

Conclusion

Presumptive myocarditis of possible viral origin characterized by ST elevation mimicking myocardial infarction, good short term prognosis and some risk for recurrence is relatively frequent in young males and appears as a distinct clinical condition.     

Electrocardiograms Corresponding to the Development of Myocardial Infarction in Anesthetized WHHLMI Rabbits (Oryctolagus cuniculus), an Animal Model for Familial Hypercholesterolemia

The aim of this study was to determine whether features indicative of myocardial ischemia occur in the electrocardiograms (ECG) in myocardial infarction-prone Watanabe heritable hyperlipidemic (WHHLMI) rabbits, an animal model for human familial hypercholesterolemia. ECG were recorded in 110 anesthetized WHHLMI rabbits (age, 10 to 39 mo) by using unipolar and bipolar limb leads with or without chest leads. We noted the following electrocardiographic changes: T wave inversion (37.4%), ST segment depression (31.8%), deep Q wave (16.3%), reduced R wave amplitude (7.3%), ST segment elevation (2.7%), and high T wave (1.8%). These ECG changes resembled those in human patients with coronary heart disease. Histopathologic examination revealed that the left ventricular wall showed acute myocardial lesions, including loss of cross-striations, vacuolar degeneration, coagulation necrosis of cardiac myocytes, and edema between myofibrils, in addition to chronic myocardial lesions such as myocardial fibrosis. The coronary arteries that caused these ECG changes were severely stenosed due to atherosclerotic lesions. Ischemic ECG changes corresponded to the locations of the myocardial lesions. Normal ECG waveforms were similar between WHHLMI rabbits and humans, in contrast to the large differences between rabbits and mice or rats. In conclusion, ischemic ECG changes in WHHLMI rabbits reflect the location of myocardial lesions, making this model useful for studying coronary heart disease.Abbreviations: CHD, coronary heart disease; ECG, electrocardiogram; WHHL, Watanabe heritable hyperlipidemic; WHHLMI, myocardial infarction-prone Watanabe heritable hyperlipidemicCoronary heart disease (CHD) is prevalent in developed countries, including the United States.^16,24 Although potent compounds (for example, statins to inhibit cholesterol synthesis) have been developed to reduce the public health burden of this disease, CHD remains a leading cause of death, and further efforts are needed to reduce associated morbidity and mortality.²⁵ In evaluating the therapeutic effects of CHD interventions, the electrocardiogram (ECG) is an essential tool for examining myocardial function.³⁹In humans, various ischemic ECG changes occur in association with myocardial ischemia and infarction, such as high T wave, ST segment elevation, emergence of the deep Q wave, reduction of R wave amplitude, resolution of ST segment elevation, and T wave inversion.^21,39 In addition, ST segment depression is a typical change observed with subendocardial ischemia.^2,7In the study of myocardial ischemia, animal models that show ECG waveforms comparable to those of human patients with CHD play an important role. This similarity is important not only for assessing the effects of agents for the treatment of CHD but also for assessing adverse effects of newly developed agents on cardiac function. Although ECG have been used to study myocardial ischemia in several species including pigs, dogs, rabbits, rats, and mice,^{3,9,10,14,18,23} most of these studies used coronary ligation models. These models do not fully reflect the events that occur during myocardial ischemia caused by atherosclerotic coronary stenosis, which is seen typically in patients with CHD.The Watanabe heritable hyperlipidemic (WHHL) rabbit⁴⁰ and the myocardial infarction-prone WHHL (WHHLMI) rabbit³³ are animal models for the study of human myocardial ischemia. WHHLMI rabbits spontaneously develop hypercholesterolemia due to a deficiency of receptors for low-density lipoproteins and manifest severe coronary atherosclerosis and myocardial infarction. Importantly, lipoprotein metabolism in WHHL and WHHLMI rabbits resembles that in humans.^28,30 Using these advantages of the WHHL and WHHLMI models, we and others have been studying the effects of hypocholesterolemic and antiatherosclerotic agents on coronary atherosclerosis.^29,32,34 However, ECG were not examined in these studies. Because the rabbit heart is electrophysiologically similar to the human heart,^27,38 using ECG to monitor myocardial function in the WHHLMI rabbit may be valuable.In the present study, we examined whether ECG changes observed in WHHLMI rabbits reflect myocardial ischemia and whether those changes correspond to ECG features in human patients with CHD.     

心肌梗塞面积无损计测数学模型

本文根据生物电学电极化理论,引入心肌梗塞向量,定量地描述心肌梗塞面电偶层源的形成,运用电动力学源场关系,首次建立计测心肌梗塞面积的理论数学模型.此数学模型计测方法简易,所需导联电极数少,而测得信息较多,属于无损伤非侵入性,便于临床推广应用.经动物实验验证,本数学模型计测所得心肌梗塞面积与组织化学染色切片实测面积,两者极显著正相关,心前壁与前间壁心肌损伤r=0.96(n=12,P<0.01);侧壁、后壁、下壁心肌坏死r=0.93(n=10,P<0.01).在临床上,与ECT相对照,r=0.91(r=14,P<0.01),极显著相关.