Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electrocardiographic (ECG) findings of pulmonary embolism (PE) include S1Q3T3 pattern, right bundle-branch block, right-axis deviation, and T-wave inversion in medial precordial leads. We report other uncommon ECG changes associated with various symptoms during recurrent PE as documented by computed tomography (CT) scans in a single patients. An 83-year-old woman was admitted with PE secondary to deep venous thrombosis in the left leg. During episodes of chest pain, ECG showed QTc prolongation (480 ms) with new T-wave inversion in leads III, aVF, and V1-V3, and ST-segment depression in leads V5-V6. Despite adequate anticoagulant therapy, recurrent episodes of PE occurred in the hospital. When the patient experienced sudden chest tightness, ECG showed a new S-wave notch in lead V1 and clock-wise rotation with sinus tachycardia. She also experienced transient syncope with hypotension. At this time, ECG showed transient atrioventricular junctional rhythm followed by sinus arrest, and CT scan showed a new massive embolus in the main pulmonary trunk with right ventricular dilatation, as demonstrated by echocardiography. The mechanism responsible for QTc prolongation with ST-T changes, the S-wave notch in lead V1 with clockwise rotation, or atrioventricular junctional rhythm with sinus arrest during PE may be associated with myocardial ischemia, acute right ventricular overload, or vagal reflex, respectively.
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PMID:Uncommon electrocardiographic changes corresponding to symptoms during recurrent pulmonary embolism as documented by computed tomography scans. 982 4

Combined oral contraceptives (OCs) have been implicated with an increased risk of a number of illnesses, particularly vascular conditions such as stroke, ischemic heart disease, venous thrombosis, and peripheral vascular disease. This study assessed the balance of risk of serious illness among a cohort of OC users followed for up to 28 years. Data from the Royal College of General Practitioners' Oral Contraception Study were examined to determine the rate of such conditions during 335,181 woman-years of observation for ever-users and 228,727 woman-years for never-users. The rates were standardized for age, parity, social class, and smoking. Results of the study indicated that in comparison with never-users, ever-users had a small increased risk of any serious disease. Ever-users had an excess risk of cerebrovascular disease, pulmonary embolism, and venous thromboembolism, and reduced risk of ovarian and endometrial cancer. The increased risk was seen only in younger women; by the age of 50, ever-users had the same risk as never-users. The risk appeared to be confined to women using OCs containing 50 mcg or more of estrogen. In conclusion, past users of higher-dose OCs can be reassured that the small increased risk of serious disease seen during current use does not persist after stopping and that latent effects do not appear later in life. Currently available OCs containing less than 50 mcg of estrogen, accompanied by the progestogen, levonorgestrel, or norethisterone acetate, do not appear to be associated with an increased net risk of serious disease.
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PMID:The risk of serious illness among oral contraceptive users: evidence from the RCGP's oral contraceptive study. 1019 18

Chest pain can arise from cardiovascular or noncardiovascular causes. Among the latter are the skin, the chest wall, intrathoracic structures, or subdiaphragmatic organs. The problem to attribute the chest discomfort to either the heart or extracardiac organs arises because the heart, pleura, aorta, and esophagus are all supplied by sensory fibers from the same spinal segments. In contrast to the diseases mentioned above, angina pectoris in sensu strictu is defined as chest pain or discomfort of cardiac origin that arises because of temporary imbalance between myocardial oxygen supply and demand. The metabolic oxygen requirements of the myocardium are essentially dictated by myocardial contraction since only a fraction of the consumed oxygen is needed by the quiescent heart. Therefore, the factors that primarily influence myocardial oxygen consumption include heart rate, the force of cardiac contraction, and myocardial wall tension, as determined by pressure (afterload), volume (preload), and wall thickness. Extracoronary diseases, e.g. hypertensive heart disease, aortic stenosis or cardiomyopathies, can influence these factors and induce angina pectoris (Figure 1). On the other hand, different diseases influencing the oxygen supply, e.g. anemia, can cause angina pectoris, too. In addition, the modulation of the coronary tone by mediators and cytokines can cause angina, coronary spasm being one example. The neurophysiological substrate of angina pectoris are ganglia which are present within the heart, particularly in epicardial fat. The sympathetic nervous system is the main conveyer of afferent pain fibers from the heart and pericardium, but many fibers may travel by the vagus and the phrenic nerves. Therefore, multiple thoracic structures may cause similar pain syndromes in the distressed patient. The blood supply of intrinsic cardiac ganglia arises primarily from branches of the proximal coronary arteries. Adenosine, among a number of substances, can modulate the activity generated by cardiac afferent nerve endings and intrinsic cardiac neurones. During myocardial ischemia adenosine is released in large quantities into the interstitial space. Given as an intravenous bolus to healthy volunteers or to patients with ischemic heart disease and angina pectoris, adenosine provokes angina pectoris-like pain, which is similar to habitual angina pectoris with regard to quality and location. But other mediators (e.g. bradykinin, histamine, prostaglandins, potassium, lactate) can be involved in the development of angina pectoris, too. As most emphasis should be given to the most serious causes first, the cardiologist has to consider ischemic cardiac disease in the differential diagnosis of nearly every case of acute chest pain. The differential diagnosis contains several causes of nonischemic cardiac chest pain. Dissecting aortic aneurysm may cause severe anterior chest pain that can be mistaken for myocardial infarction. Patients frequently will note the sudden onset of the pain rather than the relatively slower onset of ischemic pain. Furthermore, they feel as a tear and describe it as the most severe pain they have ever had. Pericarditis can be characterized as a sharp precordial knife-like pain that is often increased by lying down, breathing, swallowing, or any other thoracic motion. Radiation of pericardial pain is often relieved by sitting up or leaning forward. It may involve the shoulders, upper back, and neck because of the irritation of the diaphragmatic pleura. Acute pulmonary embolism is associated with severe chest pain. It may mimic acute myocardial infarction. Pulmonary embolism should be suspected when dyspnea or tachypnea seems to be disproportionate to the severity of the chest pain. Diffuse esophageal spasm is the extracardiac condition that is confused most often with ischemic cardiac chest pain. This pain presents as a deep thoracic pain that may be present over most of the thorax. It may extend down the anterome
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PMID:[Angina pectoris in extracoronary diseases]. 1037 99

Physicians face a therapeutic dilemma in patients with acute hemorrhagic stroke requiring long-term, high-intensity anticoagulants because this treatment increases the risk of intracranial hemorrhage (ICH) 8- to 11-fold. We retrospectively studied 15 patients with ICH which occurred under anticoagulation with phenprocoumon, with an international norrmalized ratio (INR) of 2.5-6.5 on admission. Hemispheric, thalamic, cerebellar, intraventricular, or subarachnoid hemorrhage without aneurysm occurred. Absolute indications for anticoagulation were double, mitral, or aortic valve replacement, combined mitral valve failure with atrial fibrillation and atrial enlargement, internal carotid artery-jugular vein graft, frequently recurring deep vein thrombosis with risk of pulmonary embolism, and severe nontreatable ischemic heart disease. As soon as the diagnosis of ICH was established, INR normalization was attempted in all patients by administration of prothrombin complex, fresh frozen plasma, or vitamin K. After giving phenprocoumon antagonists (and neurosurgical therapy in four patients) heparin administration was started. Nine patients received full-dose intravenous and six low-dose subcutaneous heparin. The following observations were made: (a) All patients with effective, full-dose heparin treatment with a 1.5- to 2-fold elevation in partial thromboplastin time after normalization of the INR were discharged without complication. (b) Three of four of the patients with only incomplete correction of the INR (> 1.35) experienced relevant rebleeding within 3 days (all patients with an INR higher than 1.5), two of whom were on full-dose heparin. (c) Three of seven of the patients with normalized INR and without significant PTT elevation developed severe cerebral embolism. Although our data are based on a retrospective analysis, they support treatment with intravenous heparin (partial thromboplastin time 1.5-2 times baseline value) after normalization of the INR in patients with an ICH and an urgent need for anticoagulation.
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PMID:Managing the therapeutic dilemma: patients with spontaneous intracerebral hemorrhage and urgent need for anticoagulation. 1078 17

An analytical and clinical evaluation of cardiac troponin I (cTnI) on the IMMULITE system is presented. The assay results were compared with those of the Stratus II and the Dimension RxL-HM. A between-run imprecision CV < 20% was found at a cTnI concentration of 0.23 microg/L (functional limit of detection). On the basis of a reference study including 215 patients without ischemic heart disease (97.5th percentile: 0.294 microg/L) and 36 patients clinically classified as having stable angina pectoris (<0.22 microg/L) a preliminary cutoff level of 0.3 microg/L was defined. Assay linearity, sample stability, influence of sample material and method comparison studies were performed. In patients with Duchenne's disease, chronic hemodialysis treatment, pulmonary embolism, coronary artery bypass surgery and minimally cardiac surgery the cTnI results of the IMMULITE agreed better with the Dimension RxL-HM than with the Stratus II data. Of 142 samples from patients with unstable angina 67 samples were classified as cTnI positive with the IMMULITE, 76 with the Dimension RxL-HM, and 62 with the Stratus II. In conclusion, the new assay is sensitive for the determination of cTnI and easy to perform within 45 min.
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PMID:Comparison of diagnostic performance of cardiac troponin I on the IMMULITE system with other automated troponin I assays in minor myocardial damage. 1138 9

We assessed the diagnostic usefulness of helical CT scan of the thorax in the setting of chronic thromboembolic pulmonary hypertension by prospectively comparing the results of helical CT scan to those of the pulmonary angiogram (gold standard). We studied 40 patients with diagnosis of pulmonary hypertension of diverse etiology (mean age: 40.7 +/- 12 y.o.; mean systolic pulmonary artery pressure: 91 +/- 33 mmHg)). Thirty of these patients fulfilled the diagnostic criteria of chronic thromboembolic pulmonary hypertension and the other ten were used as controls. Diagnosis in control patients included: primary pulmonary hypertension (4); patent ductus arteriosus (2); atrial septal defect (1); rheumatic valve disease (1); ischemic heart disease (1); and acute pulmonary embolism (1). Both helical CT scan and pulmonary angiogram were part of the routine diagnostic work up of these patients, and were, performed and interpreted almost simultaneously (within one week) by a different group of investigators in a blind manner. Only the diagnostic accuracy of the method regarding central (major arteries) vascular lesions was evaluated. Helical CT scan had an overall sensitivity of 100% (29/29), and a specificity of 91% (10/11). Positive predictive and negative predictive values were 96.6% (29/30) and 100% (10/10), respectively. Overall diagnostic accuracy was 97.5% (39/40). We conclude that helical CT scan of the thorax is an excellent alternative approach for the diagnosis of major arteries lesions in the setting of chronic thromboembolic pulmonary hypertension.
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PMID:[Helical computerized tomography of the thorax in the diagnosis of unresolved chronic pulmonary thromboembolism]. 1153 96

The electrocardiographic findings associated with pulmonary embolism have been well described in the medical literature for over 50 years. These abnormalities include changes in rhythm, QRS axis, and morphology, particularly in the QRS and T waves. Such findings may reflect hemodynamic changes, such as right heart strain, as well as myocardial ischemia associated with the disease. Although certain findings may correlate with the severity of pulmonary embolism, the overall utility of the electrocardiogram is limited due to the variable presence, frequency, and transient nature of most of the abnormalities associated with the disease.
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PMID:Electrocardiographic manifestations: pulmonary embolism. 1160 81

Inverted T waves produced by myocardial ischemia are classically narrow and symmetric. T-wave inversion (TWI) associated with an acute coronary syndrome (ACS) is morphologically characterized by an isoelectric ST segment that is usually bowed upward (ie, concave) and followed by a sharp symmetric downstroke. The terms coronary T wave and coved T wave have been used to describe these ischemic TWIs. Prominent, deeply inverted, and widely splayed T waves are more characteristic of non-ACS conditions such as juvenile T-wave patterns, left ventricular hypertrophy, acute myocarditis, Wolff-Parkinson-White syndrome, acute pulmonary embolism, cerebrovascular accident, bundle branch block, and later stages of pericarditis.
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PMID:Electrocardiographic T-wave inversion: differential diagnosis in the chest pain patient. 1860 29

Medicolegal (coroner's) autopsies are an important source of epidemiological data. A large proportion of them comprise sudden natural deaths and an analysis of such cases has never been undertaken at the University Hospital of the West Indies, the only teaching hospital in Jamaica. In a retrospective study, 841 cases of sudden natural deaths comprising 51.3% of the medicolegal autopsies conducted over the 15-year period, January 1983 to December 1997, were analyzed. There were 459 males and 382 females (M:F ratio = 1.2:1); 35 patients (4.1%) were less than 1 year of age, and the mean age of the remainder was 53.7+/-21.8 years. The peak age group was the seventh decade accounting for 21.9% of cases. The most common causes of death were cerebrovascular accidents (13.6%), pneumonia (9.4%), pulmonary embolism (7.4%), ischaemic heart disease (7.0%) and diabetes mellitus (6.1%). These findings contrasted with those from developed countries in which ischaemic heart disease is the commonest cause of sudden death. Hypertension was associated with the majority of cases of cerebrovascular accident and congestive cardiac failure (78.1 and 61.9%, respectively). Sickle cell disease represented one of the 10 most common causes of death accounting for 2.5% of cases. Documentation of autopsy-based data such as these is important in the planning of medical services in a developing country.
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PMID:Causes of sudden natural death in Jamaica: a medicolegal (coroner's) autopsy study from the University Hospital of the West Indies. 1224 80

Although positive troponin-I (TnI) assays have been reported in patients with pulmonary embolism (PE), TnI levels in patients with suspected PE have not been evaluated systematically. The purpose of this study was to evaluate the diagnostic utility of TnI measurements in patients with suspected PE. Consecutive patients with suspected PE were identified in whom nuclear ventilation/perfusion (V/Q) scans were performed and TnI levels were measured. TnI levels in patients with and without positive V/Q scans were compared by use of t tests. After categorizing TnI levels as positive (TnI-pos, > or = 0.40 ng/mL) or negative, chi-square tests were used to relate these values to V/Q scan results. Separate comparisons were made for subjects with high-probability V/Q scans (V/Q-high, > or = 90% likelihood of PE) and intermediate- or high-probability V/Q scans (V/Q-pos, > or = 50% likelihood of PE). The mean TnI level in the 10 subjects with V/Q-high scans was 0.39 +/-0.79 ng/mL. The mean TnI level in the 81 subjects without V/Q-high scans was 0.36 +/-0.66 ng/mL (p=0.89). TnI levels did not differ between the 22 V/Q-pos subjects and the 69 subjects with negative V/Q scans (p = 0.86). A positive TnI in the setting of V/Q-pos had a sensitivity of 32%, specificity of 71%, positive predictive value of 26%, and a negative predictive value = 77% (chi-square = 0.06, p = 0.80). Elevated TnI levels are not associated with positive V/Q scans. The TnI assay is not a useful test in patients suspected of having PE, unless used to exclude myocardial ischemia or infarction.
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PMID:Diagnostic utility of cardiac troponin-I levels in patients with suspected pulmonary embolism. 1236 67


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