Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ectopic origin of the right coronary artery from the left sinus of Valsalva is an infrequent coronary anomaly. The right coronary artery then passes between the aorta and pulmonary artery. We report two such cases with chest pain suggestive of angina pectoris in the absence of atherosclerosis, as demonstrated by selective coronary arteriography. A technique for selectively catheterizing the ectopic right coronary artery is described.
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PMID:Anomalous origin of the right coronary artery from the left sinus of Valsalva with associated chest pain: report of two cases. 100 Jun 28

The clinical, roentgenologic and laboratory findings in 124 patients with dissecting aneurysm of the aorta are reported. In 53 patients the dissection occurred in the ascending aorta ("proximal" dissection), and in 71 patients the site of origin was the descending thoracic aorta ("distal" dissection). Certain distinct clinical differences between the groups were apparent. Although hypertension was an important predisposing factor, it was significantly more common in distal dissection, as was atherosclerosis. Back pain and hypertension on hospital presentation characterized patients with distal dissection. Conversely patients with proximal dissection were younger and had a significantly higher incidence of Marfan's syndrome, cystic medial necrosis, anterior chest pain, pulse deficits, neurologic compromise, aortic insufficiency and congestive heart failure. In both groups, syncope appeared to correlate well with the occurrence of cardiac tamponade. Chest roentgenograms almost always showed an abnormal aortic contour. Aortic angiography, when performed, was usually confirmatory of the diagnosis.
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PMID:The clinical recognition of dissecting aortic aneurysm. 102 Jul 50

A comparison of cold pressor response with coronary arteriography and left ventriculography was made in 26 consecutive patients having chest pain suggesting coronary heart disease. Patients with normal coronary arteriograms and normal left ventriculograms showed normal cold pressor responses. Patients with coronary atherosclerosis and normal left ventricular performance showed an exaggerated cold pressor response, whereas patients with severe coronary atherosclerosis and poor left ventricular performance did not exhibit an exaggerated cold pressor response. In patients with inferior wall myocardial infarction having dyskinesia or akinesia of the inferior wall, the cold pressor response was not impaired. In contrast, patients with anterior wall myocardial infarction and dyskinesia or akinesia of the anterior wall showed a marked impairment of the left ventricular performance and no exaggeration of the cold pressor response.
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PMID:Correlation of cold pressor response with coronary atherosclerosis and left ventricular performance. 105 63

A review of 120 patients who had a discharge diagnosis of intermediate coronary syndrome showed 12 patients with documented transient ST elevation during spontaneous rest pain consistent with Prinzmetal's angina. Coronary arteriography showed severe proximal occlusive coronary atherosclerosis in nine of the patients, and normal or minimal disease in the other three patients. In two of these three, there was documented coronary arterial spasm with reproduction of symptoms during arteriography. Although a shorter history of chest pain, presence of an old myocardial infarction and a positive finding on electrocardiogram treadmill test tended to predict the patients with severe occlusive coronary artery disease, these methods were inadequate to select candidates for arteriography. All patients responded well to nitroglycerine while in the hospital. Five of the nine patients with coronary artery disease had coronary bypass operations, with two excellent, two fair and one poor result. One of the three patients with normal findings on coronary arteriograms died with refractory ventricular arrhythmia six months after study. The other two have had good-to-moderate relief of symptoms on long-acting vasodilators and propranolol. Current concepts of the syndrome of Prinzmetal's angina and ST elevation are reviewed. It appears that this syndrome has a wide spectrum of clinical presentations and coronary arteriographic anatomies.
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PMID:Prinzmetal's angina Clinical and anatomic aspects. 114 90

The concentrations of individual phospholipids and of cholesterol have been determined in plasma samples taken from 77 apparently healthy individuals, and from 76 male patients presenting with atherosclerotic diseases. Significant differences in the relative and absolute concentrations of lysolecithin were found between different populations. In healthy individuals the plasma levels of lysolecithin were lower in women than in men and lower in the younger age groups studied. The relative and absolute concentrations of plasma lysolecithin were lower in men suffering from chronic ischaemic heart disease and peripheral arterial disease when compared with age-matched healthy male subjects. The lowest levels of plasma lysolecthin were, however, associated with patients suffering from acute myocardial infarction or acute myocardial ischaemia studied within 48 hr of the onset of chest pain. In a further study, significantly decreased relative concentrations of lysolecithin were found in blood platelets and erythrocytes as well as in plasma of patients suffering from chronic ischaemic heart disease. The results are discussed in terms of a possible thrombo-protective role for plasma lysolecithin in man.
Atherosclerosis
PMID:Plasma concentrations of lysolecithin and other phospholipids in the healthy population and in men suffering from atherosclerotic diseases. 115 68

"Mycotic" aneurysm was originally described by Osler in 1885. It occurs in a normal or atherosclerotic artery from septic emboli in patients with infective endocarditis. However, now the term "mycotic" aneurysm is applied to all cases of aneurysms caused by any organisms. From September 1988 to November 1990, four cases of ruptured mycotic aneurysm were diagnosed at our institute. Three were males and one was a female; they were elderly with atherosclerosis of the aorta. The diagnosis was established by computed tomography (CT) scan, bacteriology or operative findings. Two of the patients underwent emergency operation; only one survived. In general, the diagnosis of mycotic aneurysm is based on the classical features of fever, abdominal or chest pain, positive blood culture and a pulsatile mass. Because the clinical manifestations are often variable, a patient may present with chronic sepsis (esp. Salmonella sp) of unknown origin with deterioration to a fatal outcome from the aneurysmal rupture, which is a rare cause of retroperitoneal abscess or pericardial effusion. The principles of management, including high clinical suspicion, an accurate diagnosis by imaging studies (arteriography or CT scan), prolonged effective antibiotic therapy, arterial ligation or wide excision of the infected lesion, intraoperative Gram's stain and culture, extra-anatomic bypass grafting through clean tissue planes, and prolonged postoperative follow-up, are indispensable to reduce morbidity and mortality.
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PMID:Mycotic aneurysm rupture: report of four cases. 136 21

Leucocyte elastase may be involved in the structural modification observed in the atherosclerotic process. Therefore, we tested the usefulness of leucocyte elastase plasma level determination as a marker for atherosclerosis. Plasma levels of elastase were determined by ELISA in 100 consecutive patients (mean age 56 +/- 9.8 years) admitted to hospital for coronary angiographic investigation of chest pain. Eighty-seven patients had evidence of atherosclerosis, and 13 patients had normal coronary vessels. No significant difference in leucocyte elastase was found between the 2 groups, nor was there any relationship between elastase levels and the severity of atherosclerosis. However, relationships between plasma leucocyte elastase levels and various lipid fractions (Apo AI, LDL) and daily tobacco consumption were found. Leucocyte elastase may thus play a role not only by direct modification of the vessel wall, but also indirectly via risk factors such as dyslipoproteinemia and leucocyte toxicity.
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PMID:Evaluation of plasmatic leucocyte elastase levels in coronary artery disease. 137 65

A 29-year-old man with congenital protein C deficiency and acute myocardial infarction is reported. Four hours after the onset of chest pain, he was treated intravenously with tissue-type plasminogen activator. Subsequent coronary angiography revealed only slight stenosis of the left anterior descending coronary artery without any atherosclerosis. The propositus, his brother, and his mother, showed low levels of both protein C activity and antigen, while plasma thrombomodulin levels were normal. His grandfather had died from acute myocardial infarction at 38 years of age. We investigated several other risk factors for arterial thrombosis, including factor VII, fibrinogen, heparin cofactor II, lipoprotein (a), and anticardiolipin antibodies. No other haemostatic abnormalities apart from factor VII hyperactivity were detected in this family. To study the effects of protein C and factor VII on procoagulant activity, prothrombin time was measured after the addition of activated protein C and factor VII to protein C-deficient plasma. The prothrombin time ratio decreased along with an increase in the factor VII level. It also decreased with a decrease in the activated protein C level. These findings indicated that the procoagulant activity of factor VII was enhanced by low protein C levels, suggesting that concomitant factor VII hyperactivity may cause acute myocardial infarction in patients with protein C deficiency.
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PMID:Congenital protein C deficiency and myocardial infarction:concomitant factor VII hyperactivity may play a role in the onset of arterial thrombosis. 144 May 17

A 57-year-old man developed anginalike chest pain for the first time but there was no objective evidence of an infarct (i.e., EKG and serum enzymes were normal). After 12 days the pain increased, but EKG and serum enzymes remained normal ("preinfarct," crescendo, unstable, or accelerated angina). At this time a cardiac catheterization showed 90% occlusion of the left anterior descending (LAD) coronary artery. On the 17th day after the onset of pain, severe pain recurred together with an abnormal EKG and the patient was taken immediately to the laboratory where a total occlusion of the LAD was now found and he was treated with intracoronary streptokinase. The artery remained open for only a short time, and balloon angioplasty was performed. However, the patient died 12 hours after onset of the last episode of severe pain. A very early acute myocardial infarct was diagnosed at autopsy together with severe coronary atherosclerosis especially of the LAD which had disruption of atherosclerotic plaques and microscopic evidence of embolization.
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PMID:Very early acute myocardial infarct treated with streptokinase and balloon angioplasty. 153 26

A 63-year-old man was admitted with an acute anteroseptal myocardial infarction. Coronary angiography performed 3 hours after the onset of chest pain revealed 99% stenosis of the proximal left anterior descending coronary artery (LAD) with delayed filling and intraluminal thrombus distal to the stenosis. After the intracoronary injection of isosorbide dinitrate, the delayed filling disappeared and a subsequent intracoronary urokinase partially dissolved the thrombus. Repeat coronary angiography in the chronic phase disclosed 75% stenosis of the LAD and disappearance of the thrombus. Intracoronary acetylcholine provoked a coronary spasm at the stenotic site of the LAD, concomitantly with chest pain and ST-segment elevation in the anterior leads. The present case demonstrated that coronary spasm plays an important role in thrombus formation and acute myocardial infarction. To date, the concept has been postulated that a dynamic interaction between atherosclerosis, platelet aggregation and spasm may work to cause coronary thrombosis and subsequently lead to acute myocardial infarction. Our report shed light on the importance of coronary spasm in the pathogenesis of myocardial infarction.
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PMID:[Coronary spasm-induced acute myocardial infarction associated with intracoronary thrombosis]. 156 86


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