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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum myoglobin was determined by radioimmunoassay in 20 cases of sudden and unexpected death resulting from acute coronary occlusion. There was consistent elevation of myoglobin 2 h after death, with peaking at 3 h. No comparable elevation of serum myoglobin level was noted in patients who had succumbed to pulmonary embolism, ruptured aortic aneurysm, or subarachnoid or intracerebral hemorrhage. Thus, determination of serum myoglobin seems useful in confirming or establishing acute coronary occlusion as the cause of sudden and unexpected death.
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PMID:Determination of serum myoglobin level after death in the diagnosis of sudden coronary artery occlusion. 74 96

Causes of death of 260 tumorous patients autopsied in 1974 were analyzed. Most common causes were inflammation and tumorous and non-tumorous organ insufficiencies; the others, in order of decreasing incidence, massive tumorous dissemination, infarct and haemorrhage. Pneumonia was predominating over the inflammatory causes although peritonitis and sepsis were also not rarely encountered. Death due to inflammation occurred most frequently in cases of myeloid-lymphoid, urogenital and gastro-intestinal tumours and in postoperative states. The incidence of insufficiencies due to tumorous or non-tumorous origin differed but slightly. Of the various organ insufficiencies, massive hepatic metastases, occlusion of the biliary duct and cardiac failure were the most common. In cases of tumors of the small pelvis, compression of the ureters led most often to death. Massive dissemination was observed most of all in breast and ovarian carcinomas. Myeloid-lymphoid tumors led to death through extensive organ infiltration in about one thirds of the cases. After hearth infarction, venous thrombosis was often followed by pulmonary embolism, however, coronary occlusion was also not rare. Death due to haemorrhage originated from acute or chronic ulcers of the gastrointestinal tract or from vascular invasion of tumors in the head and neck regions or from thrombocytopaenia induced by cytostatics.
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PMID:[Causes of death in cancer patients]. 92 45

A case of a 53-year-old male with acute myocardial infarction complicated by cardiac arrest is presented. Due to neurological complications which were transient, the patient was not selected for primary angioplasty. Three days later his condition significantly improved and the patient was transferred to internal ward were he developed cardiogenic shock due to a massive pulmonary embolism. Thrombolysis and low molecular weight heparin were effective and the patient did well during subsequent hospitalisation period. Coronary angiography was performed 4 weeks from hospital admission and revealed a total left main coronary occlusion with good collateral circulation from the right coronary artery. Finally, the patient underwent successful CABG.
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PMID:[Complete occlusion of the left main coronary artery complicated by cardiac arrest and acute massive pulmonary embolism with a favourable outcome--a case report]. 1650 71

Pulmonary embolism (PE) is an uncommon and often overlooked cause of ST-segment elevation on the electrocardiogram (ECG). Emergent echocardiography has been cited as a means to rapidly distinguish acute myocardial infarction from PE. However, both of these conditions can present with focal wall motion abnormalities. We report a case of a 51-year-old asymptomatic male who presented to our emergency department with anterior ST-segment elevation and right-heart strain on an ECG. The clinical diagnosis of ST elevation myocardial infarction was in doubt, and an echocardiogram was obtained while the patient was in the emergency department. Although a focal area of hypokinesia was observed on echocardiography, cardiac catherization did not demonstrate any evidence of acute coronary occlusion. A computed tomographic angiogram of the chest was subsequently obtained, which demonstrated evidence of submassive pulmonary emboli. Our case highlights the limited utility of emergent echocardiography in cases of ST-segment elevation.
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PMID:Asymptomatic pulmonary embolus masquerading as acute anteroseptal myocardial infarction. 2132 1

Patient history, physical examination, 12-lead electrocardiogram (ECG) and cardiac biomarkers are key components of an effective chest pain assessment. The first priority is excluding serious chest pain syndromes, namely acute coronary syndromes (ACSs), aortic dissection, pulmonary embolism, cardiac tamponade and tension pneumothorax. On history, the mnemonic SOCRATES (Site Onset Character Radiation Association Time Exacerbating/relieving factor and Severity) helps differentiate cardiac from non-cardiac pain. On examination, evaluation of vital signs, evidence of murmurs, rubs, heart failure, tension pneumothoraces and chest infections are important. A 12-lead ECG should be interpreted within 10 minutes of first medical contact, specifically to identify ST elevation myocardial infarction (STEMI). High-sensitivity troponins improve the rapid rule-out of myocardial infarction (MI) and confirmation of non-ST elevation MI (NSTEMI). ACS (STEMI and NSTEMI/unstable anginapectoris (UAP)) result from acute destabilisation of coronary atheroma with resultant complete (STEMI) or subtotal (NSTEMI/UAP) thrombotic coronary occlusion. The management of STEMI patients includes providing urgent reperfusion: primary percutaneous coronary intervention(PPCI) if available, deliverable within 60 - 120 minutes, and fibrinolysis if PPCI is not available. Essential adjunctive therapies include antiplatelet therapy (aspirin, P2Y12 inhibitors), anticoagulation (heparin or low-molecular-weight heparin) and cardiac monitoring.
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PMID:Approach to chest pain and acute myocardial infarction. 2730 59

Coronary occlusion and pulmonary embolism are responsible for the majority of cases of out-of-hospital cardiac arrest (OHCA). Despite previous favourable results of pre-hospital fibrinolysis in cases of OHCA, the benefit could not be confirmed in a large controlled study using the fibrinolytic tenecteplase. For reteplase (r-PA), there are hardly any data regarding pre-hospital fibrinolysis during ongoing resuscitation. The present study reported results using r-PA therapy in a German physician-supported Emergency Medical Services system. The data of OHCA patients who received pre-hospital fibrinolytic treatment with r-PA after an individual risk/benefit assessment were retrospectively analysed. To assess the effectiveness of this approach, the rate of patients with a return of spontaneous circulation (ROSC) was compared with the corresponding figure that was calculated with the help of the RACA (ROSC after cardiac arrest) score. The RACA algorithm predicts the probability of ROSC based on data from the German Resuscitation Registry. Further outcome data comprised hospital discharge rate and neurologic status at discharge. From 2001 to 2009, 43 patients (mean age, 58.5 years; 65.1% male; 58.1% ventricular fibrillation) received r-PA. Of these, 20 patients (46.5%) achieved ROSC, compared to a probability of 49.8% according to the RACA score (P=0.58). A total of 8 patients (18.6%) were discharged alive, including 5 (11.2%) with a good neurological outcome. For the analysed small patient collective, pre-hospital r-PA did not offer any benefits with regard to the ROSC rate. Further analyses of larger patient numbers on a nationwide registry basis are recommended.
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PMID:Outcome of out-of-hospital cardiac arrest after fibrinolysis with reteplase in comparison to the return of spontaneous circulation after cardiac arrest score in a geographic region without emergency coronary intervention. 2841 15

Troponin is a specific cardiac infarction isoform (TnIc, TnTc) and its determination is used for the diagnosis of myocardial infarction even with normal Electrocardiography. The increase of cardiac troponins occurs in a variety of clinical situations without an acute coronary syndrome (ACS), cardiologists and emergency physicians are often confronted with positive troponins that are difficult to interpret. Few data exist about the occurrence, the clinical characteristics and the predictive value in case of absence of ACS. The objective of this study is to present the main extracardiac causes responsible of the increase of TnIc. We present some clinical cases that illustrate this diagnostic problem. A troponin elevation is observed in myopericarditis, renal failure, heart failure, pulmonary embolism, septic shock, rhabdomyolysis, stroke and others where there is a myocardial damage unrelated to coronary occlusion. Many cases of false positives, which raise the possibility of analytical interferences, must be identified.
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PMID:Troponin elevation in other conditions than acute coronary syndromes. 2875 Dec 86

Wellens' syndrome represents critical occlusion of the proximal left anterior descending coronary artery. Electrocardiographic changes similar to Wellens' wave are not exceptional to acute coronary occlusion and can also be seen in cardiac and non-cardiac conditions, such as left ventricular hypertrophy, persistent juvenile T wave, bundle branch blocks, cerebral haemorrhage, pulmonary oedema, pulmonary embolism, pheochromocytoma, Takotsubo syndrome, digitalis and cocaine-induced coronary vasospasm. Cocaine-induced pseudo-Wellens' syndrome should be considered as one of the differentials, since cocaine is used frequently by young adults and can cause left anterior descending coronary vasospasm mimicking Wellens' syndrome. Initiation of the beta-blocking agent in pseudo-Wellens' syndrome as a part of acute coronary syndrome management can be disastrous. We illustrated a case of cocaine-induced pseudo-Wellens' syndrome presented with typical chest pain associated with Wellenoid ECG.
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PMID:Cocaine-induced pseudo-Wellens' syndrome: a Wellens' phenocopy. 2924 35

Computed tomography angiography is frequently used for double rule out of obstructive coronary artery disease and pulmonary embolism in patients presenting to the emergency department with acute chest pain, but it is rare to see concomitant acute coronary occlusion and pulmonary embolism on the same computed tomography angiography scan.
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PMID:Double Rule In: Concomitant Acute Coronary Occlusion and Pulmonary Embolism. 3185 79