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

A detailed pathological study was made in 10 patients dying up to 13 months after aortocoronary saphenous vein bypass grafting for coronary atherosclerosis. The coronary arteries and vein grafts were investigated by injection with a radio-opaque mass, radiography, dissection, and histology. The report is to some extent historical since the patients died during a period when the operation was first being introduced into two cardiothoracic hospitals. About 80 operations were performed during the time the 10 deaths occurred, a mortality of 12-5 per cent (including cases followed up to 13 months after operation). Seven of the patients were operated on for intractable angina and 3 with a view to aneurysmectomy. All the patients selected for operation were severely disabled despite medical treatment. The main cause of death was extremely severe coronary artery disease and its effects on the left ventricle; in one case, over two-thirds of the left ventricle had been destroyed by infarction before operation. Other causes or contributing causes of death were pulmonary embolism, myocardial infarction complicating angiography (ostial stenosis), and cerebral damage. Ten of the 14 vein grafts (71%) were patent at necropsy. A free flow of injection medium usually occurred between patent grafts and coronary arteries. Thrombosis of a graft was thought to have contributed to death in 3 patients, but not in a fourth who died of pulmonary embolism. Since thrombosis of grafts was usually secondary to poor run-off blood into severely atheromatous coronary arteries, this was also an indirect effect of the advanced coronary arterial disease. In one case, thrombosis followed severe chronic intimal thickening of a graft in place for 13 months. The study of these deaths emphasizes that in some patients the pathological changes in the coronary arteries and left ventricle are too severe for them to benefit from surgery. Vein grafts cannot be expected to distribute blood effectively through grossly narrowed coronary arteries. In addition, when a large part of the left ventricle is infarcted or scarred, it is almost certain that improving the blood supply by grafting will not result in significant regeneration of cardiac muscle. Since the time when this study was made, there have been few deaths among the many vein graft operations subsequently carried out in the hospitals involved. The two most important factors thought responsible for the improvement are the selection of cases more suitable for surgery by continued improvement of diagnostic techniques, and also the employment of more radical surgical procedures in the form of coronary endarterectomy and the insertion of more grafts per patient.
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PMID:Pathology of hearts after aortocoronary saphenous vein bypass grafting for coronary artery disease, studied by post-mortem coronary angiography. 108 91

CK-isoenzymes were measured in 31 patients hospitalised for suspected myocardial infarctions who had an increase in serum creatine kinase (CK) above 50 U/l. Of 26 patients with definite evidence of myocardial infarction, MB-isoenzyme--specific for myocardial necrosis--was demonstrated in 24. MB-isoenzyme was no longer detectable in two patients hospitalised 48 hours after the onset of symptoms. In the remaining five patients only MM-isoenzyme was found, the elevated CK activity in three patients having been due to an intramuscular injection, and in two others due to pulmonary embolism. Measurement of CK isoenzymes proved of great diagnostic value in three patients with sudden circulatory arrest of, at first, unknown cause after successful resuscitation. Acute myocardial infarction was proven by the presence of MB-isoenzyme. In one of these patients an additional BB-isoenzyme was seen, possibly due to concomitant cerebral ischaemia. In all other patients (with angina, after cardioversion, or after major surgical operations) only MM-isoenzyme was detected. MB-CK-isoenzyme was found to be a highly specific, as well as sensitive, indicator of myocardial necrosis. This being a rather difficult method, its use is not justified in the routine diagnosis, but in doubtful instances its value can hardly be overestimated.
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PMID:[The diagnostic value of CK-isoenzymes in suspected acute myocardial infarction (author's transl)]. 124 17

The authors examined the records of all patients referred for right heart catheterization between 1963-84 because of persistent dyspnoea after one or more episodes of pulmonary emboli. Patients with a history of congestive heart failure, angina, restrictive or obstructive pulmonary disease that could explain their symptoms were excluded. Catheterization was performed 15.8 +/- 24 months after the first suspected episode of pulmonary embolism. Seven of the 29 patients included had resting pulmonary hypertension (PH). All of these had an alveolo-arterial oxygen difference (AaDO2) greater than 25 mmHg. Twenty patients of the group, taken as a whole, had an AaDO2 greater than 25 mmHg. Information was available from 1 month to 5 years later in 6/9 patients with an AaDO2 less than 25 mmHg. In all of them dyspnoea improved or resolved. Information was available in 15/20 patients with AaDO2 greater than 25 mmHg. Three of 8 patients without PH but with an increased AaDO2 on the initial catheterization developed PH within 2 years. Dyspnoea increased in 1 of the remaining five. Four patients who initially had PH developed right heart failure 6 months-3 years later. In the remaining 3, dyspnoea was stable in 1, increased in 1 and one patient died with autopsy evidence of multiple pulmonary emboli. Abnormal oxygenation predicts the presence or subsequent development of PH in patients who are chronically dyspnoeic after pulmonary embolism.
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PMID:AaDO2 as a predictor of pulmonary hypertension resulting from pulmonary emboli. 191 74

One hundred fifty seven consecutive octogenarians (mean age +/- standard deviation, 82.4 +/- 1.9 years) underwent coronary artery bypass grafting with hypothermia (mean temperature, 21.8 degrees +/- 1.8 degrees C), hyperkalemic cardioplegia, and cardiopulmonary bypass in a 9-year period. Sixty-six percent were male. Preoperatively, 115 patients (73%) were in New York Heart Association functional class IV, with the remainder being in either class III (23%) or class II (4%). Twenty percent of the patients had major complications including postoperative hemorrhage (15), sepsis (9), cerebrovascular accident (6), third-degree heart block (5), renal failure requiring dialysis (1), and pulmonary embolism (1). The 30-day or in-hospital mortality rate was 7.0%. Mean total hospital stay was 26.1 +/- 17.9 days. One-year and 5-year actuarial survival rates were 85% and 62%, respectively. Higher mortality was seen to be associated with New York Heart Association class IV, left ventricular ejection fraction less than 0.40, and lesser values for cardiac output and cardiac index. At the 6-month postoperative follow-up, 73% of the survivors reported that their general health had improved as compared with before operation. This experience demonstrates that for select octogenarians with unmanageable angina pectoris, coronary artery bypass grafting is an effective therapeutic option.
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PMID:Morbidity and mortality after coronary artery bypass in octogenarians. 203 31

Cohorts of diabetic (n = 121) and non-diabetic (n = 584) patients were prospectively followed for up to ten years after having suffered from a stroke. All but six of the diabetic patients had Type 2 (non-insulin-dependent) diabetes mellitus. The diabetic patients had more risk factors associated with stroke: heart failure (p less than 0.001) and angina pectoris (p less than 0.001), than the non-diabetic patients. Neither body mass index nor blood pressure levels differed between the groups at admission. Haematocrit levels were higher in the diabetic group (p less than 0.01). The diabetic patients were more commonly afflicted by cerebral embolism and to a lesser extent by transient ischaemic attacks than the non-diabetic patients. When calculated by log-rank tests, the diabetic group had an increased risk of death (p less than 0.001), recurrent stroke (p = 0.001), and of myocardial infarction (p = 0.001) after the initial stroke. Autopsy-verified causes of death between the groups did not differ significantly, although half of all deaths during the period one to six months after stroke were caused by pulmonary embolism in the diabetic group. Thus, diabetes increases the risk of death after a stroke, and it also increases among stroke survivors the risk of recurrent stroke and myocardial infarction.
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PMID:Prognosis after stroke in diabetic patients. A controlled prospective study. 234 37

A 78-year-old woman, suffering from acute massive pulmonary embolism, was successfully treated with transvenous pulmonary embolectomy by catheter. This patient had been suffering from oppressive chest sensations during exercise, and diagnosed and treated as angina pectoris at a nearby clinic. She consulted our hospital complaining that her chest pains were increasing in frequency. She was admitted to our hospital on July 7, 1988, for coronary angiography (CAG), which she underwent on July 8 by the right femoral approach. After the CAG, she was ordered to rest in bed overnight, with the right inguinal region compressed. 18 hours later, the compression was removed and she was allowed to walk. Soon after she walked to the toilet, she complained of chest discomfort and fell into shock (systolic blood pressure was 60 mmHg). An ECG examination showed a right bundle branch block and an inverted T wave in lead V1-3. An echocardiography showed normal contraction of the left ventricle, but an enlargement of the right ventricle and a flattened interventricular septum. An analysis of arterial blood gas showed hypoxia (Pao2 52.5 mmHg, Paco2, 30.9 mmHg). Acute pulmonary embolism was suspected. 240,000 units of urokinase were administered intravenously, and pulmonary angiography was performed immediately. It revealed that the bilateral pulmonary arteries were almost completely obstructed. Although 720,000 units of urokinase were infused into the pulmonary artery, the obstruction did not improve. At that time, we performed a transvenous pulmonary embolectomy. We used a Judkins R 4 guiding catheter for PTCA made by USCI. The catheter was inserted into the pulmonary artery and clots were aspirated with a syringe.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of acute massive pulmonary embolism successfully treated with transvenous pulmonary embolectomy by catheter]. 261 14

There are 2 striking differences in the practice of medicine in the US and in the UK: 1) in the former, there is a great emphasis on private medicine, and 2) in the US there is a much higher incidence of litigation, whereas in the UK, family planning services are free, and litigation in this area is almost unknown. British medical opinion agrees with the US on the following oral contraceptive contraindications: 1) cancer of the breast, ovary, uterus, vagina, or cervix; 2) coronary thrombosis, pulmonary embolism, deep vein thrombosis, angina pectoris, or stroke; and 3) unusual or unexplained vaginal bleeding. Both countries agree that it is inadvisable to give the combined pill over the age of 45, and over the age of 35 in smokers. The UK agrees with 75% of the routines adopted by US doctors on a patient's 1st visit for oral contraceptives. However, a patient who becomes amenorrheic while taking the pill is not regarded as lightly in the UK as she would be in the US; she is closely monitored. If 1 of 4 risk factors (age 35 or over, hypertension, obesity, or smoking) is evident, a patient in the UK is closely supervised while taking the pill. If more than 2 risk factors are present, a UK doctor may advise against the pill. Since the 1960s the media have both praisd and condemned the pill. There is no doubt that, in the field of contraceptive advice, the US and the UK lead the way, and a closer liaison between the 2 medical professions is essential to reassure patients.
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PMID:Contraceptive advice: how the English differ from the Americans. 309 Feb 54

A total of 1605 patients with myocardial infarction had been admitted to the district hospital--Sliven for 24 years. The percentage of the deceased out of them is 26.5%. The patients with cardiogenic shock were 166 (10.3%) and 131 of them died (85%). The cardiogenic shock in myocardial infarction reduced its incidence within the 5 years, from 14/4% to 5.3%, and lethality was increased from 75.5 to 91.4%. The males represented 60%. To the age of 60 proved to be 30.1% of the patients. To the age of 45-3.6%; to from 46 to 60-26.5%; from 61 to 75-51.6% and over the age of 75-18%. Angina pectoris was present in 80% in the clinic of the patients with cardiogenic shock in myocardial infarction, with irradiating pain--41%, with asthmatic manifestations--49%, with abdominal manifestations--20% and cerebral manifestations--23%. According to localization the myocardial infarction was grouped as follows: 8.4%--anteroseptal; 17.4%--anterior, 9.6%--massive anterior, 1.8--anterior-apical, 6.4%--anterior lateral, 25.3%--posterior, 9%--posterior-lateral, 5.6%--anterior-posterior, 0.6%--focal and 1% subendocardial. Hypertension proved to be a favourable factor in the development of cardiogenic shock in myocardial infarction in 21.7% as well as diabetes in 15%, rhythm disorders--in 32.2%, pulmonary embolism in 7.9% and decompensation in 14.4%.
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PMID:[Cardiogenic shock in myocardial infarct]. 371 75

Immunoreactive thromboxane B2 (i-TXB2) was measured by radio-immunoassay (RIA) in urines collected over eight hours on the day of admission in 25 patients who were admitted with the diagnosis of myocardial infarction. In 16 of the patients myocardial infarction was confirmed by ECG and plasma enzymes. Another patient presented with pulmonary embolism and the remaining eight patients had angina pectoris. A further eight hour urine collection was obtained 24 hours later from eleven of the sixteen patients with myocardial infarction. In these eleven patients myocardial infarction was associated with five fold higher urine i-TXB2 (2.72 +/- 0.48 ng/ml) at the day of admission when compared to patients admitted under the same diagnosis but found to have angina only (0.51 +/- 0.08 ng/ml, p less than 0.001). In patients with myocardial infarction the urine i-TXB2 values were reduced 24 hours later (1.58 +/- 0.27 ng/ml, p less than 0.01). One patient was followed with urine i-TXB2 from three days prior to diagnosis of myocardial infarction and to one day prior to a second infarction. In this patient i-TXB2 was highest three days prior to infarction. We conclude that this early elevation of urine i-TXB2 three days prior to diagnosis of infarction and the increased i-TXB2 in patients with myocardial infarction when compared to patients with angina suggest thromboxane is probably released from activated platelets prior to infarction. We suggest that urine i-TXB2 may be of value in the differential diagnosis between myocardial infarction and angina.
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PMID:Coronary artery thrombosis and elevated urine immunoreactive thromboxane B2. 382 90

By means of equilibrium gated radionuclide angiography (EGRA) 67 patients were studied with first inferior acute myocardial infarction (AMI) within 4 days of the onset of symptoms and 12 normal volunteers. Ejection fraction (EF) of the left ventricle (LV) and right ventricle (RV) was computed. The regional wall motion (RWM) was evaluated by parametric images of amplitude and phase (Fourier analysis). The following major in-hospital complications were diagnosed in 41 patients (61%): postinfarction angina, congestive heart failure (CHF), high-degree atrioventricular (AV) block, ventricular tachycardia or ventricular fibrillation, shock, extension of infarction, pericarditis, pulmonary embolism and acute pulmonary edema. A significant correlation between RVEF and the extent of RVRWM abnormalities and the incidence of major complications was found. In particular, the incidence of shock and CHF was significantly correlated with that of the RV disfunction, while the LVEF was generally in the normal range despite a high incidence of LVRWM abnormalities. In the patients developing high-degree AV block this correlation did not reach statistical significance; in this group, 10 of 12 patients developed other major complications. Also in 10 of 13 cases with CHF, other complications arose during the period of hospitalization. In conclusion the disfunction of the RV can identify the subgroup of patients with inferior AMI who are at high risk for developing major complications, especially shock and CHF. AV block and CHF have a severe prognostic meaning, because they occur usually in association with other major complications.
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PMID:[Right and left ventricular function and incidence of major complications in acute inferior myocardial infarct. Study by equilibrium-gated radioisotope angiography]. 383 79


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