ST-segment elevation due to myocardial invasion of lung cancer mimicking ST elevation myocardial infarction: A case report

Introduction:When a cancer patient presents with ST-segment elevation on an electrocardiogram (ECG), several causes including acute myocardial infarction (MI) should be considered. Myocardial metastasis is one of the rare causes of ST-segment elevation in cancer patients and its clinical silence makes it difficult to diagnose.Patient concerns:A 78-year-old man with lung cancer presented to the emergency room for chest pain. ECG revealed ST-segment elevation in inferior and lateral leads.Interventions:After emergent coronary angiography, percutaneous coronary intervention (PCI) on proximal right coronary artery was performed.Outcomes:Even 7 days after PCI, ST-segment elevation in inferior and lateral leads still existed. Cardiac markers continued to be within the normal range.Diagnosis:We found evidence of metastasis of lung cancer on the inferolateral wall of the myocardium by trans thoracic echocardiogram and positron emission tomography (PET)/computed tomography (CT). We diagnosed myocardial metastasis as the cause of ST-segment elevation in the patient.Conclusion:Myocardial metastasis is one of the differential diagnosis of ST-segment elevation in cancer patients. Periodic ECG is necessary for lung cancer patients and rapid cardiac work-up is recommended when ST-segment elevation is newly discovered.     

Relationship between ST-segment elevation and local tissue flow during myocardial ischaemia in dogs.

The relationship between electrocardiographic ST-segment changes and local tissue flow recorded from idential sites in the myocardium was determined by inserting platinum electrodes into the left ventricular wall of anaesthetized dogs. Local myocardial blood flow was measured during graded coronary constriction by recording tissue hydrogen desaturation rate. In the detection of ischaemic ST-segment elevation, intramural recordings proved to be more sensitive than corresponding epicardial recordings. Significant ST-segment elevation could only be detected by reducing local myocardial flow below 50% of control; by further reduction ST-segment elevation increased in proportion to the reduction in myocardial flow. Thus, significant myocardial ischaemia might exist without electrocardiographic alterations.     

Precordial mapping of ST-segment elevation and Q waves following anterior myocardial infarction. The effects of established beta-blocking drugs.

The electrocardiographic (ECG) signs of ST-segment elevation and the development of Q was using 72-lead precordial surface mapping, and the release of creatine kinase (CK) activity has been studied in 47 patients with uncomplicated anterior myocardial infarction. These findings were compared with a further nine patients who had acute myocardial infarction but were receiving long-term beta-blocking drugs. It was found that ST-segment elevation and Q waves had rapidly changing and different natural histories and that beta-blocking drugs altered the natural history of ST-segment changes but had no effect on the pattern and time course for the loss of electrically active myocardium. There was a close relationship between the precordial area of ST-segment elevation at 2--3 h and the final development of Q waves in the patients with uncomplicated anterior myocardial infarction. No similar relationship could be found in those on beta-blocking drugs. The pattern of changes in plasma CK and its MB isoenzymes activity were similar for both groups. The relationship between early ST-segment elevation and the final area of Q waves may prove useful in clinical practice. This may not apply where beta-blocking drugs are commenced before the initial recording of ST-segment elevation.     

Ventricular Tachycardia Associated with Radiation-Induced Cardiac Sarcoma

Cardiac tumors can lead to distinct electrocardiographic changes and ventricular arrhythmias. Benign and malignant cardiac tumors have been associated with ventricular tachycardia. When possible, benign tumors should be resected when ventricular arrhythmias are intractable. Chemotherapy can shrink malignant tumors and eliminate arrhythmias.We report the case of a 52-year-old woman with breast sarcoma whom we diagnosed with myocardial metastasis after she presented with palpitations. The initial electrocardiogram revealed sinus rhythm with new right bundle branch block and ST-segment elevation in the anterior precordial leads. During telemetry, hemodynamically stable, sustained ventricular tachycardia with right ventricular localization was detected. Images showed a myocardial mass in the right ventricular free wall. Amiodarone suppressed the arrhythmia.To our knowledge, this is the first report of ventricular tachycardia associated with radiation-induced undifferentiated sarcoma. We discuss the distinct electrocardiographic changes and ventricular arrhythmias that can be associated with cardiac tumors, and we review the relevant medical literature.     

Exercise-induced ST-segment changes in lead V1 identify the significantly narrowed coronary artery in patients with single-vessel disease: correlation with thallium-201 scintigraphy and coronary arteriography data

We investigated the correlation of exercise-induced ST-segment changes in lead V1, with the detection of the significantly narrowed vessel that induced ischemia during exercise in myocardial areas supplied by this vessel. We studied 198 patients who underwent exercise testing, thallium-201 scintigraphy, and coronary arteriography. The patients were divided into three groups. In group 1 (ST-segment elevation in lead V1), 84% had left anterior descending coronary artery disease (P<.001); in group 2 (ST-segment depression in lead V1), 76% had right coronary artery disease (P<.001); and in group 3 (no ST-segment changes in lead V1), there were no significant differences concerning the narrowed vessel. Thallium-201 scintigraphy data confirmed the existence of the reversible perfusion defect(s) in an area(s) of myocardium supplied by the respective coronary arteries (P<.001). Exercise-induced ST-segment elevation or depression in V1 may identify the obstructed vessel in patients with single-vessel disease and without prior myocardial infarction.     

Headache:An unusual presentation of acute myocardial infraction

Acute myocardial infarction should be diagnosed as early as possible for the appropriate management to salvage ischemic myocardium. Accurate diagnosis is typically based on the typical symptoms of angina. Headache is an unusual symptom in patients with acute myocardial infraction. We report a patient with ST-segment elevation acute myocardial infarction who presented to the emergency department complaining of severe occipital headache without chest discomfort.     

Implications of inferior ST-segment elevation accompanying anterior wall acute myocardial infarction for the angiographic morphology of the left anterior descending coronary artery morphology and site of occlusion.

Inferior ST-segment elevation during anterior wall acute myocardial infarction (AMI) due to left anterior descending (LAD) coronary artery occlusion is unusual and was not previously investigated. This study tested the hypothesis that inferior ST-segment elevation during anterior AMI predicts a specific angiographic morphology that satisfies 2 necessary conditions: (1) mass of ischemic anterior wall myocardium is relatively small, resulting in a weaker anterior injury current and less reciprocal inferior ST-segment depression; and (2) there is concomitant inferior wall transmural ischemia that further shifts the inferior ST segments upward. The study group consisted of 42 consecutive patients with anterior AMI undergoing angiography at 4.1 days (range 0 to 14). Coronary angiograms were examined for 3 features: (1) site of LAD artery occlusion (a distal obstruction implying a smaller mass of ischemic anterior wall myocardium), (2) LAD artery extension onto inferior wall of left ventricle (termed a "wrap around" vessel), and (3) collateral flow from LAD artery to inferior wall. The latter 2 features would be expected to contribute to inferior wall transmural ischemia. Acute inferior ST-segment elevation (sum of ST-segment deviation in leads II, III and aVF greater than or equal to 3.0 mm) was seen in 7 patients (16%). A greater number of LAD artery branches proximal to the site of occlusion was significantly correlated with less inferior ST-segment depression (r = 0.59, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

非心肌梗死冠心病患者运动致ST段抬高的临床意义

目的 研究运动致ST段抬高在非心肌梗死患者中发生率及其临床意义。方法 2004年6月至2006年6月共有4601例患者接受了运动平板试验,其中有15例非心肌梗死患者出现ST段抬高,对这15例患者的临床特点与冠状动脉造影结果进行分析。结果 15例（3．2‰）运动致ST段抬高患者中,男性13例,女性2例,年龄40-75岁。单支病变者6例（40％）,2支病变者6例（40％）,3支病变者3例（20％）;12例（80％）累及前降支,1例（6．6％）累及左主干,7例累及右冠状动脉,在累及前降支及左主干13例患者中有8例为重度狭窄病变（狭窄程度为90％-100％）,所有ST段抬高的导联均与病变血管的供血部位一致。结论 运动致ST段抬高在非心肌梗死患者中发生率非常低,多因冠状动脉有严重的固定性狭窄,特别是前降支,可根据出现ST段抬高的导联判断缺血心肌的部位。     

ST-segment elevation during dobutamine stress testing predicts functional recovery after acute myocardial infarction

OBJECTIVES: The aims of this study were (1) to assess the relation between ST-segment elevation and wall motion response occurring during dobutamine testing and (2) to evaluate the usefulness of stress-induced ST-segment elevation for predicting functional recovery after acute myocardial infarction. BACKGROUND: Clinical significance of stress-induced ST-segment elevation after acute myocardial infarction remains controversial. According to previous studies, it may reflect a larger infarcted area, depressed left ventricular function, left ventricular aneurysm, stress-induced dyskinesia, residual myocardial ischemia, or viability in the affected region. Whether transient ST-segment elevation occurring during dobutamine testing may predict functional recovery is unknown. METHODS AND RESULTS: We studied 38 patients who underwent dobutamine stress testing early (5 +/- 2 days) after a first acute myocardial infarction. Dobutamine was infused at increasing doses from 5 to a maximum of 40 microg/kg per minute, with the addition of up to 1 mg of atropine if the target rate could not be reached by dobutamine alone. Twelve-lead electrocardiography and cross-sectional echocardiography were continuously monitored throughout the test. Dobutamine-induced ST-segment elevation was defined as a new or worsening >/=1 mm elevation, 80 ms after J point, in >/=2 infarct-related leads. Quantitative angiography was available in all patients before hospital discharge. Follow-up resting echocardiography was recorded in all patients 12 to 18 months after the acute event. ST-segment elevation was observed in 20 of the 38 patients. There were no significant differences between patients with and those without dobutamine-induced ST-segment elevation in age, site of infarction, peak level of total creatine kinase enzyme, and use of thrombolytic therapy, angioplasty, or both. Persistent akinesis without change during dobutamine stress testing was more frequently observed in patients without ST elevation (P <. 05). A biphasic response during dobutamine testing was more frequently observed in patients with ST-segment elevation (P =.01). Multivariate analysis selected 2 independent variables associated with ST-segment elevation: a biphasic response during dobutamine stress (chi-square = 7.3; P =.007) and the minimal lumen diameter of the infarct-related vessel at quantitative angiography (chi-square = 5.5; P <.02). Functional recovery was demonstrated in 26 patients. Sensitivity of ST-segment elevation for the prediction of functional recovery was 69%, specificity 83%, positive predictive value 90%, and accuracy 74%. Two independent variables predicting functional recovery were selected: dobutamine-induced ST-segment elevation (chi-square = 9.1; P =.003) and a biphasic response during stress (chi-square = 6.15; P =.013). CONCLUSIONS: Dobutamine-induced ST-segment elevation in the infarct-related leads is an ancillary sign of viable myocardium in jeopardy. It has a high specificity and an acceptable sensitivity for the prediction of functional recovery after acute myocardial infarction.     

非急性心肌梗死性ST段抬高研究进展

心电图是决策急性心肌梗死再灌注治疗时机的基石.但ST段抬高型心肌梗死不是引起ST段抬高的惟一原因.ST段抬高的最常见原因为左室肥厚、左束支阻滞、早期复极以及室壁瘤.这些情况可能被误诊为ST段抬高型心肌梗死,而引起不应该的溶栓治疗或急诊冠状动脉造影.因此,要熟悉非急性心肌梗死性ST段抬高的心电图线索才有助于与真正的急性心肌梗死相鉴别.     

急性ST段抬高心肌梗死直接经皮冠脉介入治疗对QT离散度的影响

目的 探讨直接经皮冠脉介入治疗(PCI)对急性ST段抬高心肌梗死患者QT离散度(QTd)的影响。方法 选择48例成功实施了直接PCI术的急性ST段抬高心肌梗死患者为治疗组，选择6例直接急诊PCI术失败未能行早期再灌注的急性ST段抬高心肌梗死患者为对照组，分别记录术前半小时与术后即刻、术后3小时、术后6小时、术后24小时、第3天、第7天的十二导联心电图，计算各时期的QTd。结果 急性ST段抬高心肌梗死直接PCI治疗后6小时QTd即明显下降(P＜0．01)，术后24小时下降至高峰，此后维持稳定。治疗组术后6小时以后QTd较对照组有显著下降(P＜0．01)。结论 直接PCI术治疗急性ST段抬高心肌梗死，可使患者QTd明显缩短。     

Electrocardiographic ST-segment elevation and changes in the regional work of the left ventricle during coronary angioplasty

This study evaluated the reduction in regional work of the left ventricle caused by acute myocardial ischemia during coronary angioplasty, and correlated it with ST-segment elevation. Regional work of the left ventricular myocardium, which is derived from a stress-strain loop, is a useful index of the function of a diseased heart. However, the effects of transient ischemia on the regional work of the myocardium have not been fully elucidated. The subjects consisted of 25 patients who had proximal left anterior descending artery stenosis with normal wall motion and without collateral circulation. The patients were classified as showing ST-segment elevation > or = 0.2 mV (group A, 10 patients), or ST-segment elevation < 0.2mV (group B, 15 patients) during coronary angioplasty. Group A showed a greater reduction in the regional work of the interventricular septum than group B. Regional work recovered to the baseline level 30 s after balloon deflation in group B, but took 40 s in group A. A greater ST elevation during balloon inflation was associated with a greater, prolonged reduction of work performance in the ischemic region and a greater concomitant increase in the opposite nonischemic region.     

Nonischemic ST-segment elevation induced by negative inotropic agents.

The present study investigated whether regional ventricular dyskinesia (ie, systolic bulging) is a direct cause of ST-segment elevation in canine hearts in vivo. Regional ventricular dyskinesia was induced in 33 anesthetized open-chest dogs by injection of negative inotropic agents into the left anterior descending coronary artery (LAD) without disruption of coronary blood flow. Regional myocardial contraction was assessed in terms of the percent systolic shortening (%SS) and percent systolic bulging (%bulging), which were measured using ultrasonic crystals. The ST-segment elevation of the LAD-perfused area was measured with a unipolar electrode. Lidocaine, a sodium channel blocker, nicorandil, a potassium channel opener, propranolol, a beta-adrenergic blocker, or verapamil, a calcium channel blocker, was administered by intracoronary injection during maximal vasodilation induced by adenosine. All drugs induced dose-dependent ST-segment elevation in association with a parallel reduction in %SS and a parallel increase in %bulging. The absence of myocardial ischemia was confirmed by the absence of NADH fluorescence. It was concluded that regional ventricular dyskinesia had an important role in ST-segment elevation not associated with myocardial ischemia.     

The effects of isoprenaline on epicardial ST-segment elevation, lactate production, and myocardial blood flow following coronary artery ligation.

Isoprenaline was infused at low and high rates into anaesthetized dogs after ligation of the left anterior descending coronary artery, the resultant changes in epicardial ST-segment elevation being compared with lactate production and myocardial blood flow in the infarcting myocardium. Although ST elevation was increased at both infusion rates, there was no change in the arterial-local coronary venous difference of lactate concentration nor in myocardial blood flow at the centre of the infarct. The results suggest that the relationship between epicardial ST-segment elevation and other indices of ischaemic myocardial injury is complex and requires further evaluation.     

Complete regression of myocardial involvement associated with lymphoma following chemotherapy

Cardiac involvement as an initial presentation of malignant lymphoma is a rare occurrence.We describe the case of a 26 year old man who had initially been diagnosed with myocardial infiltration on an echocardiogram,presenting with a testicular mass and unilateral peripheral facial paralysis.On admission,electrocardiograms(ECG)revealed negative T-waves in all leads and ST-segment elevation in the inferior leads.On twodimensional echocardiography,there was infiltration of the pericardium with mild effusion,infiltrative thickening of the aortic walls,both atria and the interatrial septum and a mildly depressed systolic function of both ventricles.An axillary biopsy was performed and reported as a T-cell lymphoblastic lymphoma(T-LBL).Following the diagnosis and staging,chemotherapy was started.Twenty-two days after finishing the first cycle of chemotherapy,the ECG showed regression of T-wave changes in all leads and normalization of the ST-segment elevation in the inferior leads.A followup two-dimensional echo confirmed regression of the myocardial infiltration.This case report illustrates a lymphoma presenting with testicular mass,unilateral peripheral facial paralysis and myocardial involvement,and demonstrates that regression of infiltration can be achieved by intensive chemotherapy treatment.To our knowledge,there are no reported cases of T-LBL presenting as a testicular mass and unilateral peripheral facial paralysis,with complete regression of myocardial involvement.     

Altered plasma concentrations of glutamate, alanine and citrate in the early phase of acute myocardial infarction in man

Plasma levels of glutamate, alanine, free fatty acids (FFA),citrate, glucose, insulin, lactate, creatine kinase and aspartateaminotransferase were determined frequently during the first2–48 h after onset of chest pain 10 patients who developedacute myocardial infarction (AMI) and in 8 who did not (non-AMI). An initial decrease in plasma glutamate and increase in alaninewas found in AMI compared to non-AMI patients. The AMI groupshowed early, moderate rises of plasma FFA and citrate concentrations,positively related to the initial ST-segment elevation and tothe enzymatic estimated infarct size. The AMI patients werecontinuously hyperglycaemic, but their relative insulin responsei.e. plasma glucose/insulin ratio was identical to that of non-AMIpatients. Lactate values did not differ between the two groups. Via participation in the malate–aspartate shuttle andby shunting pyruvate to alanine instead of lactate, glutamateis of importance for maintaining myocardial glucose utilization.Our finding of initial low plasma glutamate concentrations afteronset of myocardial infarction suggests insufficient glutamatesupply to the ischaemic myocardium. On basis of this and animalexperiments, an external supply of glutamate might be a ‘metabolic’treatment of AMI, alternative or additional to glucose-insulin-potassiuminfusion in order to promote myocardial glucose oxidation.     

Role of myocardial ischemia and left ventricular wall motion abnormalities as contributory factors in the genesis of exercise-induced ST-segment elevation in Q-wave myocardial infarction.

In patients with a previous myocardial infarction, controversy exists regarding the significance of postexercise ST-segment elevation in the infarct-related leads. Although usually admitted to be a sign of left ventricular dysfunction or myocardial aneurysm, other studies however have related this finding to transient myocardial ischemia and to the presence of jeopardized but viable myocardium in the infarct area. The aim of the present study was to assess the significance of postexercise ST-segment elevation in Q-wave leads as a marker of transmural ischemia or left ventricular dysfunction in 36 consecutive patients, 16 with exercise-induced ST-segment elevation in infarct-related leads. Patients were evaluated by treadmill exercise testing, coronary angiography and ventriculography, thallium-201 tomographic scintigraphy and radionuclide ventriculography within 3 months of the first myocardial infarction. Sixteen patients (group I) had exercise-induced ST segment elevation and 20 (group II) postexercise inversion, no change or pseudonormalization of the T wave in infarct-related leads. The study showed no difference in infarct-related artery, vessel disease or luminal diameter stenosis in groups I and II. The overall agreement between ST shifts and myocardial perfusion in the infarct area was 30.56% with a kappa coefficient of -0.33 (p = NS). The overall agreement between ST shifts and wall motion abnormalities was 69.44% with a kappa coefficient of 0.39 (p < 0.01), stress-induced ST-segment elevation being associated with severe wall contractile disorders in 85% of the patients. In conclusion stress-induced ST-segment elevation in Q wave leads, although not a marker of wall motion abnormalities, is associated with akinesia or dyskinesia of the left ventricular wall.     

Effects of afterload elevation on the ischemic myocardium in isolated, paced canine heart with partial coronary stenosis

The effect of afterload elevation on the ischemic myocardium was examined in an isolated, paced canine heart with a partial coronary stenosis. The coronary blood flow of the left circumflex coronary artery was reduced to approximately one-third of the values before stenosis. The left circumflex coronary stenosis produced a decrease in global ventricular function, a decrease in systolic shortening and deviation of the ST-segment of the epicardial electrocardiogram and an increase in myocardial carbon dioxide (CO2) tension of the ischemic region. Then, afterload elevation with constant preload decreased the myocardial CO2 tension and improved the ST-segment deviation of the ischemic myocardium. Mechanical function, estimated by the relation between mean aortic pressure and systolic shortening, also improved with elevation of mean aortic pressure. In contrast, afterload elevation combined with preload elevation did not improve ischemic injury, as estimated by myocardial CO2 tension, and did not improve ST-segment deviation or mechanical function despite an increase in left circumflex coronary flow. These results suggest that the elevation of afterload pressure under constant preload improves ischemia produced by a partial coronary stenosis due to increased coronary blood supply; however, the preload elevation counterbalances the beneficial effects of afterload elevation.     

Antithrombotische Therapie bei akutem Myokardinfarkt

Inhibition of blood coagulation is an essential cornerstone of the therapy of acute myocardial infarction. Risk stratification represents a valuable tool to adjust the intensity of anticoagulation and timing of invasive therapy according to patient risk. All patients presenting with myocardial infarction should be treated with aspirin and clopidogrel. Patients with ST-segment elevation myocardial infarction and high-risk patients with myocardial infarction without ST-segment elevation who undergo invasive therapy should be treated immediately with unfractionated heparin (alternatively enoxaparin) and a glycoprotein (GP) IIb/IIIa antagonist in the catheter laboratory. The direct thrombin antagonist bivalirudin may emerge as an attractive alternative in these patients. In low-risk patients who undergo delayed urgent elective interventional therapy the factor Xa antagonist fondaparinux may be advantageous because of its low bleeding rate. In these patients administration of unfractionated heparin is necessary for percutaneous coronary intervention.     

Relation of lateral ST-segment elevation pattern to myocardial salvage in patients with recanalized anterolateral acute myocardial infarction

BACKGROUND: Although anterior acute myocardial infarction (AMI) with ST-segment elevation in lateral leads is associated with a poor prognosis, the significance of the pattern of lateral ST-segment elevation has not been examined. HYPOTHESIS: The aim of the study was to examine the relation of the pattern of lateral ST-segment elevation to myocardial reperfusion and infarct size in patients with AMI. METHODS: We studied 111 patients who had a first AMI presenting with anterolateral ST-segment elevation and Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow of the left anterior descending coronary artery within 6 h from symptom onset. Patients were classified into two groups according to the pattern of lateral ST-segment elevation on the admission electrocardiogram: Group 1, 42 patients with equivalent or greater ST-segment elevation in lead I than in lead aVL, and Group 2, 69 patients with lesser ST-segment elevation in lead I in than in lead aVL. Left ventricular ejection fraction (LVEF) was measured by predischarge left ventriculography. RESULTS: There were no differences between the two groups in age, gender, time from onset to recanalization, culprit lesion, or collateral development. Group 1 patients had a higher probability of impaired myocardial reperfusion as indicated by a myocardial blush grade of 0 or 1 after recanalization, a higher peak creatine kinase level, and a lower LVEF than Group 2 patients (p = 0.0001, respectively). CONCLUSIONS: We conclude that equivalent or greater ST-segment elevation in lead I than in lead aVL is associated with impaired myocardial reperfusion and less myocardial salvage in patients with recanalized AMI who present with anterolateral ST-segment elevation on the admission electrocardiogram.