Asymptomatic myocardial ischemia

The concept, physiopathology, epidemiology, diagnostic procedures, prognosis and treatment of asymptomatic myocardial ischemia are reviewed. Hypotheses given to explain the absence of pain in the presence of myocardial ischemia are analyzed; Cohn's classification of asymptomatic myocardial ischemia is described and complemented with other clinical entities of painless myocardial ischemia. Prevalence of asymptomatic myocardial ischemia in different groups of patients is also discussed as well as the most important characteristics of diagnostic procedures. Finally the prognosis of asymptomatic myocardial ischemia is analyzed and the present therapeutic possibilities are discussed.     

Assessment of myocardial viability by using newly developed myocardial SPECT imaging.

Thallium myocardial imaging has been widely available for the detection of myocardial ischemia and assessment of myocardial viability in coronary artery diseases. However, myocardial imaging using SPECT and gamma-emitting radiopharmaceuticals has been developed for accurate evaluation of myocardial infarction and ischemia. The present study was undertaken to clinically evaluate myocardial necrosis, metabolism and sympathetic nerve activity. In this study, myocardial fatty acid metabolism was assessed using 123I-BMIPP, myocardial sympathetic neural activity was assessed using 123I-MIBG and myocardial necrosis was assessed using 111-In-antimyosin Fab. Dual energy SPECT using these new agents and thallium gives precise characterization of myocardial viability in coronary artery disease.     

Clinical features of early myocardial rupture of acute myocardial infarction

We assessed the clinical features of patients with myocardial rupture within 48 to 72 hours, defined as early myocardial rupture, after percutaneous coronary intervention (PCI) for ST-segment elevation acute myocardial infarction (STEMI). Six patients (4 men, 66 ± 13 years) with early myocardial rupture were identified from 1252 consecutive patients undergoing PCI for STEMI. We evaluated the degree of microvascular reperfusion using thrombolysis in myocardial infarction (TIMI) myocardial perfusion (TMP) grade and a resolution of sum of ST-segment elevation in a 12-lead electrocardiogram (ECG). Time from PCI to myocardial rupture was 11 ± 7 hours. All patients showed TMP grade 0 or 1 and an increase in sum of ST-segment elevation after PCI (1.9 ± 0.5 vs 2.5 ± 0.7 mV; P = .032), suggesting severely failed reperfusion at the level of microcirculation as the common feature to develop early myocardial rupture after PCI for STEMI.     

Evaluation of myocardial infarction by radioisotope myocardial imaging with special reference on thallium-201 myocardial perfusion imaging

One hundred and three patients with myocardial infarctions were studied with 201-thallium chloride and/or 99m-technetium pyrophosphate myocardial imaging and were followed-up for an average of 23 months. There were 24 false negative cases with 201-thallium chloride, but no deaths or serious complications occurred during the follow-up period in these false negative cases. There were six patients with widened QRS complexes (more than 0.12 seconds) without bundle branch blocks and in three of them myocardial infarction was not identified by electrocardiography. However, there were large myocardial perfusion defects in the anterior-inferior wall of the left ventricle. All of this group of patients died suddenly during the follow-up period. The incidence of complications and mortality rose sharply in patients whose myocardial perfusion defects detected by thallium-201 were larger than 40% of the entire left ventricle. The myocardial infarction areas measured by 99m-technetium pyrophosphate were 28.5 +/- 9.8 cm2 in non-survivors and 16.5 +/- 1.7 cm2 in survivors. In addition, ten patients with acute myocardial infarction were studied by double scan methods with thallium-201; myocardial perfusion defect areas were reduced from 29 +/- 3% of the entire left ventricle to 19 +/- 4% by nitrate administration, indicating that there were reversibly ischemic areas in acute myocardial infarction which could be transiently reduced by nitrate. Thus, the study suggests the possibility of decreasing myocardial perfusion defects in the early phase of acute myocardial infarction, leading to a better long term prognosis for the patients.     

Potential prevention of myocardial rupture resulting from acute myocardial infarction

The clinical characteristics of 30 cases of myocardial rupture resulting from acute myocardial infarction were analyzed. Predisposing factors of myocardial rupture appeared to be the following (1) age 60 years or older, (2) female, (3) no previous history of angina or myocardial infarction, (4) hypertension on admission, (5) persistent or recurrent chest pain, (6) physical activity and/or emotional unrest, (7) less than 10 days since the onset of myocardial infarction. From 1979 to 1982, we tried to eliminate these risk factors in the acute stage of myocardial infarction, of which hypertension appeared to be the most important and main correlating factor. The incidence of myocardial rupture before elimination of risk factors was 31.2% (26 of 84 patients) which was reduced to 8.8% after elimination. In the years 1981 and 1982, only two cases of myocardial rupture were found in each year, 4.3% and 5.6% of MI patients, respectively.     

Anaerobic myocardial abscess following myocardial infarction

An anaerobic myocardial abscess due to Bacteroides fragilis developed in a 60-year-old man when he had an acute myocardial infarction while recuperating from surgery for a paracolonic abscess. Anaerobic bacteremia is a common event and may lead to infection in areas of low oxygen tension far removed from the original portal of entry.     

Silent myocardial ischemia and its relationship to acute myocardial infarction

The preceding review indicates that silent myocardial ischemia has definite prognostic implications in both symptomatic and asymptomatic patients with coronary artery disease. Patients surviving an acute myocardial infarction are at a particularly high risk if they show evidence of myocardial ischemia. At present, many noninvasive diagnostic modalities are available to the physician for the evaluation of symptomatic and silent myocardial ischemia in such patients. Because as many as 30 per cent of patients may become asymptomatic after myocardial infarction, physicians must be aggressive in evaluating their patients for the presence of silent myocardial ischemia. The presence of silent ischemia would help identify those patients at high risk of postinfarction complications. Future use of currently available therapeutic modalities directed toward treatment of total ischemic burden on the myocardium may help lower morbidity and mortality in these patients by reducing the risk of subsequent cardiac events.     

CTRP9在心肌梗死后心肌重构中的作用研究进展

心肌梗死后的心肌重构是一个复杂的病理过程,严重影响患者预后。CTRP9是近年来新发现的脂肪因子,大量研究表明CTRP9可抑制心肌梗死后心肌重构,本文就CTRP9对心肌梗死后心肌重构的相关研究作一综述。     

Endothelin and myocardial ischemia

Summary Endothelin is a potent vasoconstrictor with a wide range of effects on the heart. Changes in myocardial and circulating levels of endothelin have been described in various experimental models of myocardial ischemia, and in humans with acute myocardial infarction and different forms of angina pectoris. The role played by endothelin in the different states of myocardial ischemia is unclear. However, myocardial damage has been shown to be reduced in several experimental models of myocardial infarction by administering agents that block the action of endothelin. The aim of this review article is to present the current literature concerning the interaction between endothelin and the various forms of myocardial ischemia, and to explore the significance of such interactions.     

QT dispersion and myocardial viability in patients after acute myocardial infarction

BACKGROUND: In recent years QT dispersion (QTd) in post-infarct patients was estimated in many studies, but still little is known about its association with the presence of dysfunctional but viable myocardium. AIM: We investigated the relation between dispersion of QT interval and myocardial viability in patients after acute myocardial infarction (AMI). MATERIAL AND METHODS: In 52 patients (mean age 67.2+/-11.7) treated thrombolytically because of AMI 12-lead ECG and low dose-high dose dobutamine echocardiography was performed on 14th day after treatment. QTd and regional myocardial contractility were estimated three times: at baseline, low dose dobutamine (LDD) (10-15 microg/kg per min) and high dose dobutamine (HDD) infusion (up to 40 microg/kg per min). RESULTS: Patients with viable myocardium had lower baseline QTd than patients with only necrosis in infarct zone. Significant increase in QTd was shown during LDD and HDD both in patients with and without myocardial viability. During infusion of HDD QTd was significantly higher in patients with myocardial ischemia. The greatest percentage increase of QTd at HDD was shown in patients with biphasic response to dobutamine infusion i.e. with myocardial viability evidenced at LDD and myocardial ischemia at HDD. CONCLUSION: Patients with preserved myocardial viability had lower QTd values compared to those with similar left ventricular dysfunction but caused only by post-infarction necrosis. Ischemia evoked on 14th day after AMI was accompanied by greater increase in QTd in patients with myocardial viability in infarct region than in patients without. It may be one of the reasons of greater risk of serious ventricular arrhythmias in such patients during myocardial ischemia.     

Spontaneous changes in thallium-201 myocardial perfusion imaging after myocardial infarction

To examine regional myocardial perfusion after myocardial infarction, 26 patients underwent exercise electrocardiographic testing with thallium-201 myocardial perfusion imaging 3 weeks and 3 months after infarction. At 3 weeks, 9 of 26 patients (35%) had myocardial ischemia by exercise electrocardiographic testing, whereas 18 of 26 (69%) had ischemia by thallium-201 imaging. The thallium-201 scintigrams were scored by dividing each image, in 3 views, into 5 segments, using a 5-point scoring scheme. The exercise thallium-201 score was 44.3 ± 1.2 and increased to 47.3 ± 1.2 in the redistribution study (p < 0.001). Three months after infarction, although there was a significantly greater rate-pressure product which would predict a larger ischemic defect and a decrease in the stress thallium-201 score, the stress score was improved (48.3 ± 1.1, p < 0.001). The redistribution score was similar, that is, 48.9 ± 1.0. The improvement in thallium-201 myocardial perfusion was associated with a loss of stress-induced ischemia in 8 patients (30%). These results indicate that spontaneous improvements in thallium-201 myocardial perfusion imaging may occur after myocardial infarction.     

心肌缺血预适应对急性心肌梗死影响的观察

目的:探讨心肌缺血预适应对急性心肌梗死(AMI)临床表现及其预后的影响。方法:根据AMI前有无心绞痛发作分为预缺血组和无预缺血组,分组观察AMI患者血清肌酸磷酸激酶(CPK)峰值,住院期间并发症(心衰、心源性休克、严重心律失常),以及住院期间心性病死率。结果:预缺血组血清CPK峰值明显低于无预缺血组(P<0.05),住院期间心源性休克及严重心律失常发生率明显低于无预缺血组(P<0.05)。结论:心肌缺血预适应可减轻心肌坏死程度,缩小梗死面积,并减少AMI并发症的产生。     

Impact of normalized myocardial perfusion after successful angioplasty in acute myocardial infarction

OBJECTIVES: We sought to evaluate and validate the ability of the angiographic myocardial blush grade to risk stratify patients after successful angioplasty in acute myocardial infarction (AMI). BACKGROUND: Although epicardial Thrombolysis In Myocardial Infarction (TIMI)-3 flow is restored in >90% of patients undergoing primary percutaneous coronary intervention (PCI), normal myocardial perfusion may be present less frequently and may detrimentally impact survival. METHODS: A cohort of 173 consecutive patients undergoing intervention within 24 h of AMI onset were studied. High-risk features of this population included failed thrombolysis in 39%, cardiogenic shock in 17% and saphenous vein graft culprit in 11% of patients. RESULTS: Despite the restoration of TIMI-3 flow in 163 (94.2%) patients, myocardial perfusion, as evidenced by normal contrast opacification of the myocardial bed subtended by the infarct artery (myocardial blush), was normal in only 29.4% of patients with TIMI-3 flow following PCI, and in no patient with TIMI 0 to 2 flow. In patients in whom TIMI-3 flow was restored, survival was strongly dependent on the myocardial perfusion grade; one-year cumulative mortality was 6.8% with normal myocardial blush, 13.2% with reduced myocardial blush and 18.3% in patients with absent myocardial blush (p = 0.004). CONCLUSIONS: Abnormal myocardial perfusion is present in most patients following primary or rescue PCI in AMI, despite restoration of brisk epicardial coronary flow. In high risk patients achieving TIMI-3 flow after intervention, the myocardial blush score may be used to stratify prognosis into excellent, intermediate and poor survival. Further study is warranted to examine whether adjunctive mechanical or pharmacologic strategies can further improve myocardial perfusion and survival of patients with acute myocardial infarction undergoing intervention.     

Transient myocardial ischaemia after acute myocardial infarction

The prevalence and characteristics of transient myocardial ischaemia were studied in 203 patients with recent acute myocardial infarction by both early (6.4 days) and late (38 days) ambulatory monitoring of the ST segment. Transient ST segment depression was much commoner during late (32% patients) than early (14%) monitoring. Most transient ischaemia (greater than 85% episodes) was silent and 80% of patients had only silent episodes. During late monitoring painful ST depression was accompanied by greater ST depression and tended to occur at a higher heart rate. Late transient ischaemia showed a diurnal distribution, occurred at a higher initial heart rate, and was more often accompanied by a further increase in heart rate than early ischaemia. Thus in the first 2 months after myocardial infarction transient ischaemia became increasingly common and more closely associated with increased myocardial oxygen demand. Because transient ischaemic episodes during early and late ambulatory monitoring have dissimilar characteristics they may also have different pathophysiologies and prognostic implications.     

Remodeling of myocardial interstitium in left ventricular hypertrophy and myocardial infarction

Structural and biochemical modifications of the myocardium (remodeling) occur during the development of left ventricular hypertrophy and acute myocardial infarction. An important part of this process of myocardial remodeling occurs in the interstitial compartment. The myocardial interstitium is composed mainly of fibrillar collagen. These changes are associated to modifications in ventricular function that could be deleterious and have clinical manifestations. Some salutory effects of the treatment of both conditions are related to modifications of the process of myocardial interstitial remodeling.     

Assessment of myocardial viability with myocardial contrast echocardiography

The application of noninvasive imaging techniques to assess myocardial viability has become an important part of routine management of patients with acute myocardial infarction and chronic coronary artery disease. Information regarding the presence and extent of viability may help identify patients likely to benefit from revascularization or therapy directed at attenuating left ventricular remodeling. Myocardial contrast echocardiography (MCE) is capable of defining the presence and extent of viability by providing an accurate assessment of microvascular integrity needed to maintain myocellular viability. It is especially suited for the spatial assessment of perfusion, even when myocardial blood flow is reduced substantially in the presence of severe epicardial stenoses or in a bed dependent on collateral perfusion. The routine use of MCE to evaluate viability in patients with acute and chronic coronary artery disease is now feasible with the advent of new imaging technologies and microbubble agents capable of myocardial opacification from venous injections. The utility of this technique for determining treatment strategies has not been established but is forthcoming.     

Unrecognized myocardial infarction.

This review addresses myocardial infarctions that escape clinical recognition. It focuses on the prevalence, predisposing factors, and prognosis of these unrecognized infarctions, and incorporates data from relevant epidemiologic studies, basic science investigations, and review articles. These data indicate that at least one fourth of all myocardial infarctions are clinically unrecognized. The demographic characteristics and coronary risk factor profiles of persons with previously unrecognized myocardial infarctions appear to be similar to those of persons whose infarctions are clinically detected. Impaired symptom perception may contribute to lack of recognition, but both patients' and physicians' perceptions about the risk for myocardial infarction may also play an important role. Finally, mortality rates after unrecognized and recognized myocardial infarction are similar. Given the public health implications of unrecognized myocardial infarction, future studies should address screening strategies, risk stratification after detection of previously unrecognized myocardial infarction, and the role of standard postinfarction therapies in affected patients.     

Assessment of fetal myocardial performance using myocardial deformation analysis

Conventional techniques for the assessment of cardiac function on the basis of M-mode or 2-dimensional modalities are technically difficult, load dependent, and provide information on global ventricular function only. Newer techniques, which analyze myocardial performance, such as tissue velocity, strain, and especially the less load dependent strain rate, may provide more appropriate information. Myocardial systolic and diastolic motion and performance were calculated using tissue velocity, strain, and strain rate imaging on a large cohort of normal fetuses. The assessment of myocardial performance was feasible in all 98 normal fetuses. Normal systolic and diastolic values for tissue velocity, strain, and strain rate were established. All data were highly reproducible. Tissue velocity was age dependent, whereas strain and strain rate were stable throughout gestation. All parameters were heart rate independent. In conclusion, fetal myocardial velocity, strain, and strain rate measurements are easy to obtain and reproducible, and therefore, may serve as reference data. Increases in tissue velocity throughout gestation probably reflect the growth of the fetal heart, whereas intrinsic myocardial properties as measured by strain rate do not change. In comparison with recently published myocardial performance values in children, these strain rate data suggest that fetal myocontractile properties that are already established during the second half of pregnancy remain constant throughout gestation and after birth.     

Evaluation of transmural myocardial perfusion by ultra-harmonic myocardial contrast echocardiography in reperfused acute myocardial infarction.

BACKGROUND: The transmural distribution of myocardial perfusion is important for predicting the contractile reverse of an infarcted wall in reperfused acute myocardial infarction (AMI). Evaluating transmural myocardial perfusion by myocardial contrast echocardiography (MCE) could predict the long-term recovery of left ventricular (LV) function. METHODS AND RESULTS: The study group comprised 20 consecutive patients with a first-episode anterior AMI with total occlusion of the proximal left anterior descending artery, who underwent successful percutaneous coronary intervention within 24 h of onset. MCE was performed on the 15th day after the onset, using ultraharmonic gray-scale imaging with intermittent end-systolic triggering every 4 beats or every 6 beats. Regions of interest were placed over both the endocardial and epicardial region at the mid-septal level. Regional wall motion (RWM) of the infarcted anterior wall and global LV function were assessed by 2-dimensional echocardiography and left ventriculography in both the acute and chronic phase. The transmural distribution of myocardial perfusion by MCE demonstrated a significant relation with RWM score index (r = 0.75, p = 0.0004). Recovery of RWM and LV ejection fraction (LVEF) at 6 months after reperfusion was significantly greater in the group with good perfusion of the epicardium according to MCE than in the poor perfusion group [RWM (SD/cord); -1.23+/-0.91 vs -3.51+/-0.84, p = 0.001, LVEF (%); 63.8+/-10.4 vs 47.0+/-3.4, p = 0.04]. CONCLUSIONS: Assessing the transmural distribution of myocardial perfusion by MCE can predict the long-term recovery of LV function after a reperfused AMI.     

Diagnostic possibilities of myocardial scintigraphy using T1-201 in acute myocardial infarction

Myocardial scintigraphic investigation using 201T1 was performed in 36 patients with suspected acute myocardial infarction and 11 clinically normal controls. The scintigrams were assessed visually and using a computer program for semiquantitative assessment of 201T1 distribution across the myocardium. The control subjects' scintigrams show a comparatively even myocardial distribution of the label. Patients with acute myocardial infarction were divided into 2 groups: those with large-focal (28) and small-focal (8) infarctions. All the patients from the large-focal group showed perfusion defects in their scintigrams. Clinical and autopsy diagnoses coincided in all the cases, and the vital scintigraphic pattern correlated with the posthumous localization of the myocardial infarction. However, the method of myocardial scintigraphy with 201T1 in acute myocardial infarction is of low specificity. To improve the differential diagnosis of myocardial infarction, repeated scintigraphy is needed.