Marked ST Depression Research Articles

546 DETECTION OF INFECTIVE ENDOCARDITIS COMPLICATION: USEFULNESS OF ELECTROCARDIOGRAM

Abstract We report the case of an abscess complication of infective endocarditis detected by electrocardiogram (ECG). A 51-year-old man was admitted to the Emergency Department for fever (39 C°) and asthenia from few days. About 2 months earlier he had undergone cardiac surgery for aortic valve replacement with biological valve for severe aortic stenosis. Vital signs included low blood pressure and high respiratory rate; he was also pyretic. On cardiac auscultation he had a systolic murmur on aortic focus. He underwent blood gas analysis, which showed an increase in serum lactate, ECG, which detected a I grade atrioventricular block, and blood sampling, which showed severe increases in white blood cells, C-reactive protein and procalcitonin. Chest x-ray was normal. An echocardiogram was therefore performed: thickened and hyperechogenic cusps of the aortic biological prosthesis were detected; masses, with character of mobility at the level of the left coronary cusp (maximum size of 1.4×1cm) were also described; there was also a slight increase in transprosthetic gradients and mild valve insufficiency. The first diagnostic hypothesis was therefore that of infective endocarditis (IE), further supported by a recent odontogenic procedure for dental abscesses to which the patient would have undergone a few weeks after heart surgery (possible IE according to the Duke modified criteria). Blood cultures were performed on three samples and empirical antibiotic therapy was initiated until Streptococcus mitis was isolated (definite IE according to the Duke modified criteria) and thus Ceftriaxone was started. During hospitalization in the cardiology ward the patient presented dysarthria and left hemiplegia. A cerebral angio-computed tomography and neurological consultation were conducted and an ischemic stroke of thromboembolic origin from biological valve endocarditis was diagnosed. However, in view of the extensive ischemic hypodensity, acute reperfusion treatment was not indicated. The patient therefore underwent cardiac surgery consultancy but, due to his severe comorbidities and expired clinical conditions, there was no indication for cardiac surgery. After few days, during daily ECG recording, left main coronary artery (LMCA) stenosis-like ECG modifications were detected, with ST elevation in lead aVR in addition to marked ST depression in leads V3 through V6 and in peripherals leads (Fig.). A troponin sample was immediately taken, which would have been increased. He immediately underwent new echocardiogram which revealed a new periprosthetic abscess across left coronary cusp. Given the course of LMCA through the abscess, we believe that the acute coronary syndrome that has occurred to the patient may be due either to a compression of the LMCA by the periprosthetic abscess or to embolization of abscess material in the le LMCA. It was not possible to perform coronary angiography neither to perform cardiac surgery as the patient died a few hours later due to septic shock.

Intermittent chest pain with marked ST depression after 13years of aortic valve replacement.

An 80-year-old woman who underwent aortic valve replacement with a 19-mm Medtronic Hall prosthetic valve in 1993 was admitted because of intermittent chest pain. Electrocardiography on admission revealed non-specific changes, but electrocardiography during chest pain revealed significant ST depression. Coronary angiography revealed no significant stenosis. Echocardiography revealed intermittent severe aortic regurgitation and incomplete closure of the prosthetic valve in diastole. An urgent operation was performed, and abnormal pannus formation was observed at the left ventricular side of the prosthetic valve. In this case, intermittent diastolic valvular sticking caused severe aortic regurgitation and induced serious myocardial ischemia.

A case of marked ST depression and myocardial injury as a result of disulfiram–ethanol reaction

We report a case of a 50-year-old man with intractable hypotension, which led to ischemic electrocardiogram (ECG) changes and myocardial injury due to relative myocardial ischemia as a result of a disulfiram-ethanol reaction. This is the first report that assessed cardiac function during hypotension and ischemic ECG changes by emergency coronary angiography, left ventriculography, and right heart catheterization. This case indicates that disulfiram potentially has fatal side effects due to a disulfiram-ethanol reaction.

ECG variations in patients pre- and post-local anaesthesia and analgesia

To determine the incidence of ECG abnormalities in a healthy adults undergoing a surgical extraction of third molar teeth pre-and post-operatively and to study the effect of local anaesthetics, surgical stress and analgesics on cardiac rhythm. One hundred and ninety-eight healthy adult patients taking part in a clinical trial of analgesics were randomly selected for this study. All patients required the removal of at least one impacted mandibular wisdom tooth under local anaesthetic. An ECG was taken at a screening visit and repeated post-operatively 30 minutes after analgesia was given. The effects of analgesia were also monitored to ascertain whether any changes were related to pain experience or the analgesic itself. ECG abnormalities were detected in 44 patients at the screening visit. Of these patients, 20 showed rsR complex patterns, seven showed non-specific ST elevation, six patients had an abnormal P wave axis, three patients presented with single atrial premature beats and three patients showed a short PR interval. Other minor abnormalities were occasionally seen. The results recorded were of minimal clinical significance and the numbers are in line with previous research. Post-operative abnormalities were seen in 60 patients. Nineteen patients showed rsR complex patterns, sinus arrhythmias were seen in 11 individuals, seven patients showed non-specific ST elevation and six patients had an abnormal P-wave axis. Other minor abnormalities were occasionally seen. Although the results were not statistically significant, some of the patients did show clinically relevant abnormalities which necessitated referral to a cardiologist. These included: marked ST elevation; marked ST depression and one case of Right Bundle Branch Block (RBBB).

Multi-vessel coronary artery spasm

A 69-year-old male, a chronic smoker with history of hypertension, presented with chest pain. Electrocardiogram showed marked ST-depression over antero-lateral leads (Panel A). Echocardiogram showed inferior wall hypokinesia. Troponin level was elevated confirming the diagnosis of non-ST-elevation myocardial infarction. He was treated with aspirin, clopidrogel, low molecular heparin, and glycoprotein 2b/3a inhibitors. Coronary angiography the following day (Panel C) showed non-obstructive diffusely diseased vessels over …

Common Carotid Dissection

Patient 1 was a 58-year-old man who was brought to the emergency department after he collapsed in the kitchen. On arrival, the patient was comatose and did not react to pain stimuli. He was hypotensive (blood pressure 70/50 mm Hg), and ECG showed sinus tachycardia (120/min) with left bundle-branch block. Tests for troponin T were negative, and his D-dimer level was 3771 μg/L (normal range: 0 to 190 μg/L). Because of tachypnea and developing respiratory insufficiency, intubation became necessary. A massive pulmonary embolism was initially suspected. Patient 2 was a 47-year-old man who suddenly collapsed with aphasia, right-sided hemiparesis, and progressive loss of consciousness. After intubation and during transportation to the emergency department, he was hypertensive, but on arrival he became hypotensive (blood pressure 80/60 mm Hg). An ECG showed sinus tachycardia (127/min) and marked ST depression in V5 and V6. Tests for troponin T were negative, and his D-dimer level was 212 μg/L. Cerebral …

Marked Reversible ST-T Abnormalities Induced by Cardiac Compression From a Retrosternal Gastric Tube Used to Reconstruct the Esophagus After Tumor Resection A Case of a Diabetic Patient and Mini-Review of 7 Reported Patients

A 69-year-old male patient with type 1 diabetes mellitus had been under treatment at our outpatient clinic since the age of 65. He had previously undergone surgery for esophageal cancer at the age of 55; the excised portion of the esophagus was replaced by a retrosternal gastric tube. He was admitted to our hospital for suspected pneumonia on April 8, 2004. An electrocardiogram (ECG) on admission showed marked ST depression in leads V1 and V2, and prominent negative T waves in leads I and aVL; however, the T waves unexpectedly flattened after 2 minutes and the ST depression resolved after about 4 hours. On January 7, 2005, we performed a deep breathing test to analyze the effects of movements of the thoracic wall and intrathoracic structures on the ECG. In this test, deep inspiration induced ST depression reaching 0.5 mV in leads V1 to V3; this resolved on switching to deep expiration. ECG changes together with chest computed tomography images supported the concept that the ST-T abnormalities were induced by cardiac compression caused by expansion of the gastric tube between the sternum and heart. We have reviewed 7 other similar reported cases.

The correlation between presenting ST-segment depression and the final size of acute myocardial infarcts in patients with acute coronary syndromes

The use of reperfusion therapy in patients with ST elevation acute coronary syndromes had been established. However, reperfusion therapy is usually considered contra-indicated in those with ST depression, despite the knowledge that regional posterior infarction is typically indicated by ST depression maximal in leads V 1 to V 3 and nonregional subendocardial infarction is typically indicated by marked ST depression maximal in other leads. This study of patients with non-ST-elevation acute coronary syndromes investigates the quantitative relationship between presenting ST depression and final QRS changes in both of these subgroups. The final QRS score was significantly higher (2.44 points) than that of a control group with not ST depression, (1.55 points) in the group with maximal ST depression in V 1 to V 3 ( P=0.04). However, in the entire population, there was a highly significant correlation ( P=.003) between the sum of the presenting ST depression and the final QRS score. Trials of reperfusion therapy will be required to determine if such evolution to electrocardiogram documented acute myocardial infarction can be prevented in patient with marked ST depression acute coronary syndromes.

Epicardial ST depression in acute myocardial infarction.

The presence of electrocardiographic ST depression in acute infarction remains controversial and poorly explained. A combined animal and modeling study was performed to evaluate the source of ST changes in acute infarction. In anaesthetized sheep, small infarcts showed uniform ST elevation over the infarction whereas larger infarcts showed marked ST depression over the normal myocardium in addition to the ST elevation. These findings were replicated by bidomain models of the heart. A hollow sphere was used to model a gradually increasing infarct, and this showed that there was a decrease in the ratio of ST elevation to ST depression as the infarct was increased. The current flowing out of the heart must be identical to the current flowing back into the heart. This means that any infarction will produce ST depression as well as ST elevation, the ratio between the two being related to the size of the infarction. Small infarction is associated with a small region of ST elevation and minor ST depression of the remaining myocardium, and as the infarct region increases, the amplitude of the epicardial ST elevation falls and the amplitude of the ST depression increases. Infarction size is proportional to both the height of the ST depression on the epicardium and the strength of the epicardial ST segment dipole.

Surgery for left main spasm. Is it indicated?

A 38-year-old Chinese man presented with chest pain associated with loss of consciousness and a witnessed generalized seizure. An electrocardiogram (ECG) done soon after the seizure showed a junctional rhythm and anteroseptal ST elevation of 2 mm with marked inferolateral ST depression of 3 mm. Peak creatinine kinase (CK) was 870 U/l with an MB fraction of 43 U/l. Exercise treadmill test was abnormal with 3 mm inferolateral ST depression at peak exercise. A computed tomographic scan of the head and electroencephalogram were normal. Coronary angiography showed 75% narrowing of the left main coronary artery with normal left anterior descending and circumflex coronary arteries. There was ventricularization of the pressure tracing and the patient experienced chest pain with ST segment depression in leads II and Vl which were the monitoring leads. The blood pressure, however, remained normal. The luminal narrowing increased to 90% (Fig. 1) following the second injection of contrast. Buccal nitroglycerine spray was administered with good symptomatic relief, and reinjection

Acute infarction of the left ventricular papillary muscle: electrocardiographic pattern and recognition of its location.

ST-segment depression during acute myocardial infarction (AMI) is known to herald serious hemodynamic complications. Since the mechanism of this dependence is not clear, we reinvestigated the old concept of papillary muscle infarction (PMI) as a cause of marked ST depression. Autopsies and morpho-electrocardiographic cor-relations were performed in 53 patients with AMI involving one or both left ventricular papillary muscles, and in 10 patients with AMI, but without acute PMI. ST-segment depression > or = 1 mm in at least two leads (mean 3.6 +/- 2.2 mm) was found in 46 (86.8%) patients with, and in one without acute PMI. Thus, the sensitivity and specificity in selecting patients with acute PMI from among those with AMI were 86.8 and 90%, respectively, with an overall accuracy of diagnosis of acute PMI in the course of AMI of 87.3%. Among 26 patients with ST elevation consistent with diagnosis of AMI, ST depression, recorded in 22 patients, was insignificantly greater than in 24 of 27 patients without ST elevation: 4.1 +/- 2.9 versus 3.1 +/- 1.2 mm. Localization of ST depression in the limb leads allowed recognition of which papillary muscle suffered from acute infarction: ST depression in the inferior leads was seen only in patients with anterolateral PMI, whereas in leads I and/or a VL it was seen only in cases with posteromedial PMI. This rule was also valid in patients without concomitant ST elevation. Patients with acute PMI show marked ST-segment depression. Its location in the limb leads allows recognition of which papillary muscle has undergone necrosis. This cause of marked ST depression in patients with AMI may explain the high mortality in this particular group.

Two year Cottbus reinfarction study with 30 mg aspirin per day

All 701 heart infarction patients admitted to 15 hospitals in the district of Cottbus between 1981 and 1983 were randomly administered 30, 60 or 1000 mg aspirin daily according to the territorial affiliation of their local hospitals. The physical and drug therapy during the 2 years follow-up was highly standadized; deviations — as far as they occurred — were documented. Lower all-cause mortality was statistically demonstrated in patients over 60 and a lower fatal reinfarction rate in patients over 50 as well as in men. Deaths and fatal reinfarctions were significantly lower among patients with a history of angina pectoris, marked ST-depression, with an infarction location except for the posterior wall and among hypercholesterolemic patients. The preventive effect of 60 mg aspirin daily was less than that of 30 mg in comparison to the 1000 mg group. Side effects were seen in 4 and 8% (first and second year), respectively, of the patients administered 30 mg aspirin as opposed to 22 and 17% in patients allocated 1000 mg. We conclude that the optimum dose of aspirin for preventing reinfarctions could be as low as 30 mg daily.

Prognostic significance of ST potentials determined by body surface mapping in inferior wall acute myocardial infarction

Electrocardiographs body surface mapping on admission to coronary care has been shown to predict prognosis in a previous study of 100 patients with inferior wall acute myocardial infarction (AMI). A further 98 patients with first inferior wall AMI were now studied by body surface mapping on admission to coronary care to confirm that both the spatial distribution or map pattern of ST-segment potentials and the precise measurement of the maxima and minima are of prognostic significance. Each ST-segment map was compared by correlation coefficient to the average map pattern of the 4 groups derived in a previous study and placed in the group with the highest correlation coefficient. Analysis of these groups against outcome confirmed that the group dominated by a large area of marked anterior ST depression was associated with a high rate of complications and a significantly lower survival free of coronary artery bypass grafting (p < 0.01). Patients in this group had more extensive and severe coronary artery disease than patients in the other groups. Increasing values of maximal ST depression correlated with mortality and complication rates. The extent by which the magnitude of ST-segment depression exceeded the magnitude of ST-segment elevation correlated with mortality and incidence of left ventricular failure. The results confirm the findings of the original study. Body surface mapping is of prognostic significance in inferior wall AMI.

冠動脈内アラキドン酸（ＡＡ）注入による心筋虚血の発生とその予防

A Wedge-Pressure catheter was inserted to 1cm above aortic valve in ascending aorta through left common carotid artery of 36 rabbits. 1.5mg/kg of sodium arachidonate (AA) was injected into the proximal portion of ascending aorta after inflation of balloon which obstructed the ascending aorta. The inflation remained for 5 seconds, the solution was perfused into coronary arteries. 14 rabbits among the 36 rabbits were not pretreated before injection of AA, each 11 rabbits were pretreated intravenously with 10mg/kg of OKY-1580 and OKY-046 (specific inhibitors on TXA2 synthetase) respectively 3 minutes before AA injection. ECG, respiratory movement and blood pressure were recorded. Before, 3 and 60 minutes after AA, 5ml of heparinized blood was collected, added with indomethacin (10μM in final concentration) and centrifuged to collect PPP for measurement of TXB2 and 6-keto-PGF1α using radioimmunoassay (RIA). In control, 5 out of 14 cases died because of apnea. Blood pressure decreased in 5 or 6 seconds after AA, irregular respiration and arrhythmia in some 10 seconds, ST deviation in 20 seconds, apnea appeared in 30 seconds. Arrhythmia and marked ST depression appeared in all cases. Apnea was seen in 10 cases. In OKY groups, arrhythmia, ST depression and apnea were prevented significantly. In control, TXB2 values were 1.2±0.2ng/ml (mean±SE) before, 10.2±3.3 minutes after, and 1.3±0.2 60 minutes after. In OKY-046, 1580 groups, those 3 minutes after were 0.8±0.1, 1.1±0.2 respectively showing complete inhibition of TXB2. In control, 6-keto-PGF1α values were 2.1±0.4ng/ml before, 133.1±40.0 3 minutes after and 2.5±0.8 60 minutes after. In OKY-046, 1580 groups, those 3 minutes after were 41.4±7.5, 74.4±13.0 respectively also showing significant difference with that of control group. ST deviation on ECG had good correlation with the value of TXB2 (r=0.765, p<0.005), but no relation with the value of 6-keto-PGF1α. Histological findings of heart were not so severe as expected, but showed more remarkable ischemic changes in control than OKY groups. These findings clearly show that intracoronary injection of AA causes myocardial ischemic changes through TXA2, because OKY protected cardiopulmonary changes, but also suggest the important role of PGI2.

Characteristics of body surface mapping in the aged.

1) Body surface mapping was performed in 15 patients with ischemic heart disease and 5 control subjects before and after isoproterenol infusion. In ischemic heart disease, ST map developed negative areas in the left anterior chest wall extending from mid line to left axillar line after isoproterenol. This distribution on ST depression was different from that of left ventricular hypertrophy or complete left bundle branch block which spared mid anterior chest. The point of maximal ST depression corresponded to one of the conventional chest lead in 6 of 15 cases. In other 9 cases, the point of maximal ST depression was mostly located superiorly to V3-V5. epsilon ST depression correlated well with the maximal ST depression (r = 0.90) but not very well with ST depression at V5 (r = 0.70). On 201 T1 stress scan, a reversible large perfusion defect was detected in 2 out of 5 patients with marked ST depression. These findings suggested that isoproterenol induced ST map changes are useful in diagnosis of myocardial ischemia. 2) Body surface map was obtained in 16 cases with chronic pulmonary disease. The location of the maximum R and initial R was relatively inferior to that of normal controls. Relatively deep S waves were frequently observed. Pulmonary function tests correlated with the maximum R voltage but not with the deepest S. Cases with relatively high pulmonary conus voltage were proved to have right ventricular hypertrophy on 201 T1 myocardial scintigraphy or on echocardiography.

Dangers of left main coronary artery lesions: angiographic technique and evaluation.

Five hundred consecutive coronary arteriograms were reviewed to evaluate left main coronary artery lesions. This entity has been associated with a high incidence of angiographic deaths. Clinical signs claimed to be diagnostic were analyzed together with the value of various projections for making the diagnosis. Pressure damping was a vital sign, and when persistent, it required 3-5 mm to be cut from the catheter's tip for a safe study to be performed. Shallow 10-15 degrees oblique and AP projections were found to be essential for a complete evaluation of the left main trunk. Marked ST depression or hypotension during treadmill exercise testing, as well as the presence of coronary calcification were not statistically significant in anticipating this lesion. The incidence of left main lesions nearly 15% (74/500) in this series is higher than previously reported (2.4-5.9%); however, in 8% (40/500), the stenosis was 75% or greater in degree which more closely approximates to the incidence previously reported in the literature. This may be the result of the additional projections recommended, but is probably also related to the population studied. No complications occurred in this series.

Paroxysmal hypertension in aortitis syndrome

Three patients with aortitis syndrome exhibited paroxysmal hypertension which seemed to result from baroreceptor dysfunction. All of the patients had signs of active inflammation of aortitis syndrome and stenotic carotid and subclavian arteries. During the attacks, the blood pressure rose to at least 230 mm. Hg systolic and the heart rate exceeded 100. However, with prolonged administration of steroid hormones, the attacks ceased. In two patients with dilated thoracic aortas and aortic regurgitation, the attacks of paroxysmal hypertension occurred without apparent precipitating factors and were followed by anginal pain with marked ST depression. The sympathicotonic state resulting from the disturbance of the baroreceptors was considered to be responsible for the attacks. In another patient, the attacks occurred in the course of treatment with a steroid hormone and were provoked only by voluntary micturition. This post-micturition hypertension was presumed to be an expression of abnormal overshooting following a fall in blood pressure after voiding.

Rehabilitation of cardiac patients--evaluation of cardiac function by the step test

For the rehabilitation of patients with cardiac dieases, the cardiac function and cardiac reserve were determined with oxygen consumption, modified physical fitness index, oxygen debt, oxygen pulse and ECG upon exercise loading. Method: Utilizing Master's 2-step stairs, 2-step exercise loading for 3 minutes (2-step method) was employed in 103 cases, including normal subjects, patients with coronary heart disease, valvular heart disease and hypertensive heart disease of Classes I-III of New York Heart Association (NYHA). Patients were made to step up and down the 2 steps 24 times for 3 minutes. One-step exercise loading for 10 minutes (one-step method) was used in 76 cases. Patients were made to step up one step and back down on the floor 15 times per minute for 10 minutes. Before, during and after exercise loading, oxygen consumption and blood pressure were measured and continuous ECG tracing was obtained with the use of 3 channel radioelectrocardiograph. Then, modified physical fitness index1, 2 (mPFI1, 2) were calculated from the following equation. [numerical formula] Oxygen debt and oxygen pulse were also calculated. The loading was discontinued in the one-step method when marked dyspnea, chest pain, paroxysmal tachycardia or marked ST depression (5mm) were noted.

急性肺炎患者の呼吸・循環機能

Respiratory and circulatory function tests were done on three patients with severe acute pneumonia at the height of the disease. The course of the disease was followed with these tests. From the results obtained, the occurrence of hypoxemia and electrocardiographic changes were studied.1) Pulmonary function disturbance During the height of the disease, the changes found in the pulmonary function were a decrease in lung capacity and increases in the minute ventilatory volume and oxygen consumption. The blood gas analysis during this stage showed a marked decrease in the arterial blood oxygen saturation and partial pressure with a tendency of an increase in the arterial carbon dioxide partial pressure. No remarkable difference was found in the ventilatory function distubance between a case of bronchopneumonia with widely spread pathology on X-ray and a case of lobar pneumonia with the damage limited to one lobe, but the disturbance in the blood gas was stronger in the case of bronchopneumonia.2) Electrocardiographic changes The cases of lobar pneumonia with lowered arterial blood pressure showed only low T but the two cases of bronchopneumonia had low T and marked ST depression. Sinus tachycardia was seen in all cases.3) The cause of decreased arterial blood oxygen saturation Although it is commonly thought that there should be an increase in the ineffective pulmonary blood flow in such conditions as in the present cases, it was made clear that the decrease of alveolar air oxygen partial pressure and the disturbance of alveolar diffusion are the main factors which cause the decrease in the arterial blood oxygen saturation.4) The cause of the electrocardiographic changes By referring to the results obtained by coronary catheterization studies done in our medical department, it can be considered that the cause for the electrocardiographic changes in pneumonia is a decrease in the cardiac oxygen consumption while the cardiac work increases. And, it was made clear that, although the electrocardiographic findings may be minimal especially when the arterl blood pressure is low at the same time, the state of the patient should be estimated carefully by considering the results of various other tests.