Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
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An 86-year-old man with previous normal renal function was hospitalized because of renal insufficiency. He had a long history of atherosclerotic heart disease, mild hypertension and pulmonary embolism, requiring anticoagulant therapy. In view of the normal-sized kidneys and absence of casts in the urinary sediment, a diagnosis of atheroembolic renal disease was made. The patient's renal function deteriorated, but he refused hemodialysis. Death occurred within a few weeks. At autopsy, severe aortic atherosclerosis was observed and atheroembolic renal disease was confirmed as the cause of renal failure. Occasionally, renal failure can be the sole manifestation of spontaneous atheroembolic disease. This possibility should be considered if the physician is called upon to establish the diagnosis when renal insufficiency develops in atherosclerotic patients.
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PMID:"Spontaneous" atheroembolic disease as a cause of renal failure in the elderly. 46 53

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

Individuals with homocystinuria have been found to suffer from several types of inherited enzymatic deficiencies. Experiments indicated that vascular changes were subsequent to the metabolic effects of homocysteine derivatives in the tissues. Experimental studies in animals showed that homocysteine thiolactone, methionine, homocysteic acid, and homocystine cause fibrous arteriosclerotic plaques, arterial thrombosis or venous thrombosis with pulmonary embolism. The type which develops depends on the particular homocystine derivative, the dose, and the route of administration. The use of oral contraceptives causes similar alterations in nutrient metabolism. This fact suggests the possibility of increased risk of atherosclerosis, thrombosis, and embolism among long-term oral contraceptive users. Pyridoxine supplementation may reduce the risk. Further research is needed to assess the degree of risk involved.
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PMID:Homocystine, atherosclerosis and thrombosis: implications for oral contraceptive users. 109 78

Arteriosclerotic plaques were found in the aorta and arteries of rabbits given homocysteine thiolactone, methionine or homocysteic acid, both parenterally and in a synthetic diet. Animals given large doses of parenteral methionine or homocysteine thiolactone died of pulmonary embolism and pulmonary infarct. Pyridoxine prevented thrombosis and pulmonary embolism but did not prevent arteriosclerotic plaques. These findings and previous work, showing a new matabolic pathway for sulfate ester synthesis from methionine, the somatotrophic activity of homocysteic acid, and control of cellular growth and intercellular matrix synthesis by homocysteine derivatives, suggest a theory to explain aspects of the pathogenesis of arteriosclerosis.
Atherosclerosis
PMID:Homocysteine theory of arteriosclerosis. 119 72

Cardiovascular diseases account for approximately 50% of deaths in patients on chronic haemodialysis. Therefore we prospectively studied 54 consecutive patients on dialysis for the presence or absence of ventricular late potentials (LP). LP, i.e. low-amplitude potentials in the terminal part of the QRS complex, have been shown to be highly indicative of life-threatening arrhythmias and sudden death. The results were correlated with echocardiographic studies and the clinical outcome during a follow-up period of 18 months. Fifty patients were suitable for evaluation (29 males, 21 females; mean age 55 years; mean time on dialysis 32 months; coronary artery disease present in 5) Our analysis revealed LP in seven of 50 patients only. Left ventricular hypertrophy, i.e. mean wall diameter > 12 mm, was present in 78%, a compromised left ventricular function, i.e. shortening fraction < 28%, was found in 28% of the patients. With respect to echocardiographic parameters, patients with and without LP were similar. During follow-up, sudden cardiac death was observed in three of 11 patients deceased. LP were detectable in one of the three only. From the remaining six patients with LP, four are still alive, and two patients died due to atherosclerosis and pulmonary embolism. Our data underline the crucial role of sudden cardiac death in dialysis patients. Ventricular late potentials, however, are of no prognostic relevance with respect to identification of dialysis patients at risk of sudden death.
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PMID:Ventricular late potentials in haemodialysis patients and the risk of sudden death. 133 75

Orthotopic heart transplantation has become an accepted therapy for adult patients with end-stage heart disease. In newborns and infants, this procedure is still controversial because of the unknown long-term results and the lack of donor organs. Since March 1988, we have performed orthotopic heart transplantation in 11 infants and children with hypoplastic left heart syndrome (n = 6), cardiomyopathy (n = 4), or congenital endocardial fibroelastosis (n = 1). The smallest infant was 3 days old and weighed 2,650 g. Four of 15 potential donors had to be refused for various medical reasons, and 4 were transferred to our hospital for organ retrieval. Seven hearts were procured remotely. We accepted weight mismatches up to 105% between donor and recipient. There were three perioperative deaths, two in patients 5 and 17 days old with hypoplastic left heart syndrome and 1 in a 2-year-old patient with a dilated cardiomyopathy. All 3 patients had drug-resistant right heart failure. A 2-year-old girl with a dilated cardiomyopathy died 2 months after transplantation owing to severe pulmonary embolism originating from the superior vena cava. The remaining 7 patients are alive and well between 1 month and 31 months after transplantation. Angiographic follow-up has not revealed signs of graft atherosclerosis at 2 years.
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PMID:Pediatric heart transplantation for congenital heart disease and cardiomyopathy. 206 37

These recommendations for secondary prevention of clinical coronary cardiopathy are the result of a symposium attended by 46 experts belonging to the councils on arteriosclerosis, clinical cardiology, epidemiology, and prevention and rehabilitation of the International Society and Federation of Cardiology. Secondary prevention of coronary cardiopathy refers to measures designed to prevent deterioration or death in patients with clinical manifestations of coronary cardiopathy. Such measures in addition to drugs include health actions that may improve the status of various coronary risk factors: the patient's life style should stress maintenance of proper weight, regular physical exercise, reduction of saturated fats and cholesterol in the diet, and elimination of smoking and excessive alcohol consumption. It is considered reasonable to control hypertension through the most innocuous means possible, but findings of the few existing controlled studies of effects of treatment of hypertension in coronary cardiopathy are complex. Drug treatment may be necessary for most patients, but nondrug measures should be added when possible. Various proofs including results of some controlled studies justify the recommendations for reducing elevated levels of serum cholesterol and low density lipoprotein cholesterol through dietary measures. Optimum plasma cholesterol levels are 5.2 mmol/1 or less, and the upper limit is 5.7 mmol/1. The rules for secondary prevention are the same for diabetics as for nondiabetics, but some special precautions are necessary in diabetics. Habitual and vigorous physical activity has been associated with a decline in the incidence of coronary cardiopathy in different population studies, although there has been no demonstration that exercise can alter the progression of atherosclerosis or improve collateral circulation. Stress should be recognized as a risk factor and included in secondary prevention, but the concept that stress is the key risk factor in coronary events is in conflict with a large body of scientific evidence. Oral contraceptives (OCs) tend to increase boood pressure and weight as well as serum triglyceride levels, and to reduce glucose tolerance and high density lipoprotein cholesterol in some formulations. OCs also affect the integrity of the vascular endothelium and alter blood coagulation, fibrinolysis, and platelet function. These thrombogenic changes are intensified with age, especially after 35, and with smoking. OCs are innocuous in women under 35 with no history of venous or arterial disease or pulmonary embolism and who have normal blood pressure and serum cholesterol levels. Patients using OCs should control their blood pressure and weight and be alert to any symptoms of thrombotic episodes. The risk/benefit ratio of longterm estrogen treatment in meno- and postmenopausal women with coronary cardiopathy has not yet been established. Apart from 1 study in primates, there is no evidence that vasectomy should be considered either indicated or contraindicated for coronary patients. Beta blockers, platelet function inhibitors, anticoagulants, and other drugs are under active study for secondary prevention of coronary cardiopathy.
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PMID:[Recommendations for secondary prevention of the clinical coronary cardiopathy]. 285 11

Between 1982 and 1987, 32 patients with severe aortorenal atherosclerosis had simultaneous aortic and bilateral renal revascularization. All patients were hypertensive. Eighteen patients (56%) had renal insufficiency with a mean serum creatinine (SC) of 2.8 mg/dl. Nine patients had an aortic aneurysm; the remaining 23 patients had aortoiliac occlusive disease of varying severity. Aortic reconstruction was done with either a straight (six patients) or bifurcated (26 patients) Dacron graft. Renal revascularization was accomplished with either bypass (60 arteries) or transaortic endarterectomy (four arteries). One patient died of pulmonary embolism (operative mortality rate 3%). Beneficial blood pressure response was achieved in 28 of 31 survivors, (90%). Among the 18 patients with renal insufficiency, mean SC was 2.80 +/- 1.18 mg/dl preoperatively and 1.65 +/- 0.48 mg/dl postoperatively (p less than 0.001). Among eight patients with severe renal dysfunction before surgery (SC greater than 3 mg/dl), mean SC was 3.90 +/- 0.85 mg/dl before and 1.79 +/- 0.69 mg/dl after operation (p less than 0.001). In follow-up extending to 58 months (mean 27.6 months), five late deaths occurred; cumulative survival was 94% at 2 years and 60% at 4 years. There were no instances of worsening hypertension; one patient had deteriorating renal function. These results indicate that severe aortorenal atherosclerosis can be managed with simultaneous aortic reconstruction and bilateral renal revascularization at low operative risk. In addition, there can be high expectation of significant and persisting benefit in both hypertension and renal dysfunction after operation.
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PMID:Simultaneous aortic reconstruction and bilateral renal revascularization. Is this a safe and effective procedure? 274 98

In human plasma, 11-dehydrothromboxane (TX) B2 is a major long lived metabolite (t1/2 45 min) formed from infused TXB2, the hydration product of biologically active TXA2. Plasma concentrations of TXB2 itself are readily confounded by ex vivo platelet activation and, theoretically, an enzymatic derivative of this compound, not subject to formation in whole blood, would more accurately reflect TXA2 formation in vivo. To address this hypothesis, we developed a sensitive assay for both 11-dehydro-TXB2 and TXB2, using capillary gas chromatography/negative-ion chemical ionization mass spectrometry. We established that whole blood possesses a minor capacity to form 11-dehydro-TXB2, attributable to nonenzymatic formation in erythrocytes. However, the nonenzymatic formation of 11-dehydro-TXB2 was not a practical limitation to its use as an index of TX biosynthesis. Blood was drawn from healthy volunteers (i) via an indwelling catheter at the time of insertion and at 30, 60, 90, 180, and 240 min thereafter and (ii) via separate venipunctures at 0 time and at 90 and 240 min thereafter. Plasma TXB2 drawn via the catheter at baseline (66 +/- 63 pg/ml) was substantially greater than the maximal estimate of endogenous TXB2 (1-2 pg/ml) in plasma [Patrono, C., Ciabattoni, G., Pugliese, F., Perruci, A., Blair, I. A. & FitzGerald, G. A. (1986) J. Clin. Invest. 77, 590-594] and increased in magnitude and variance over time (339 +/- 247 pg/ml at 240 min). By contrast, 11-dehydro-TXB2 did not change significantly in the sequential catheter samples or in the samples drawn by separate venipuncture. Basal plasma concentrations in volunteers were depressed by pretreatment with 325 mg of aspirin. Furthermore, the range of concentrations in patients with severe atherosclerosis in whom urinary 2,3-dinor-TXB2 was increased was significantly higher (5-50 pg/ml, P less than 0.01) than in healthy subjects (0.9-1.8 pg/ml). Concentrations of 11-dehydro-TXB2 were increased in patients who had recently suffered a pulmonary embolism to a greater extent than either the 11-dehydro-13,14-dihydro-15-keto-TXB2 or the 2,3-dinor-TXB2 metabolites in plasma. These results indicate that plasma TXB2 is readily confounded by platelet activation ex vivo. Measurement of enzymatic metabolites of TXB2 minimizes this problem. The 11-dehydro metabolite is the most appropriate analytic target to detect phasic release of TXA2 in the human circulation, such as might occur in human syndromes of platelet activation.
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PMID:11-Dehydrothromboxane B2: a quantitative index of thromboxane A2 formation in the human circulation. 346 63

To determine the relative importance of multiple interrelated factors that have been considered to contribute to pulmonary infarction, the authors performed a discriminant analysis on consecutively autopsied patients with pulmonary embolism. From the clinic records of 45 individuals, the authors tabulated the underlying illness, history of valvular or ischemic heart disease, right and left ventricular failure, sepsis, shock, malignancy, premortem functional status, and the clinician's suspicion of pulmonary embolism. At postmortem examination, the authors measured and recorded the extent of emphysema, pneumonia, neoplasia, pulmonary vascular atherosclerosis; thickness and dilatation of both cardiac ventricles; the presence of valvular heart disease; the number, diameter, and amount of occlusion of the pulmonary arteries that contained thromboemboli; the extension of the clot, the size of the infarct; the Reid-Index; and the thickness of pulmonary and bronchial arterial wall. The major determinants of infarction were as follows: poor premortem functional status, the number of lobes having emboli, left ventricular failure, and the presence of lung cancer. The authors then tested the equation generated from these patients on 21 additional patients. The discriminant function correctly classified 81% of first group and predicted the occurrence of infarction in new patients with 70% accuracy. The size of the infarct was most correlated with the use of vasodilators and the embolic burden.
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PMID:Factors associated with pulmonary infarction. A discriminant analysis study. 401 73


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