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)

We report a case of a 50-year-old woman with traumatic dissection of the right common carotid artery secondary to attempted suicidal hanging. Initial examination showed marks of strangulation on the neck, facial edema, and multiple conjunctival petechiae accompanied by difficulty in breathing and loss of consciousness. She gradually recovered except for her left upper limb weakness. Rehabilitation, with a diagnosis of left brachial plexus injury, was started. Two years later, she occasionally felt numbness of the left upper extremity. On her second admission, a bruit was heard on the right side of her neck. Neurological examination did not reveal any change. CT scan showed atrophic changes. Angiography demonstrated approximately 80% stenosis of the right common carotid artery which was thought to be responsible for the attacks of numbness. Right carotid endarterectomy was performed. Histological findings revealed dissection of the medial layer of the arterial wall. Complaints of numbness disappeared postoperatively, and angiography showed good patency at a follow-up examination. We conclude that the stenosis of the common carotid artery was not due to atherosclerosis but due to the dissection as a result of hanging.
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PMID:[A case of common carotid artery stenosis due to hanging]. 144 93

A 66-year-old-man with carotid stenosis complicated by coronary disease is reported. He suffered from mild motor weakness on the right side and speech disturbance. Radiological examination revealed 90% stenosis at the cervical portion of the left internal carotid artery, and two-vessel coronary disease. In order to prevent intraoperative cardiac stroke, initial percutaneous coronary angioplasty (PTCA), was performed and the subsequent carotid endarterectomy (CEA) was performed successfully. Preoperative symptoms gradually improved and he was discharged as ambulatory. Because atherosclerosis is always systemic, patients with carotid artery disease should be examined for coronary disease. We recommend greater use of coronary angiography and, when a lesion is found, the use of PTCA, which is a safer method in terms of preventing intraoperative cardiac stroke of CEA than any other method.
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PMID:[Carotid stenosis complicated by coronary disease; a case report]. 159 37

Weakness in the musculotendinous barrier of the abdominal wall leads to inguinal herniation. Fiber degeneration by increased metabolism has been described recently as a causative factor. In previous investigations heightened elastase was detected in abdominal aneurysms. In order to investigate a possible relationship between hernias and abdominal aneurysms, patients scheduled for infrarenal aneurysm repair were examined for history of inguinal hernia. The prevalence of inguinal hernias (n = 49; 41%, p less than .001) in 119 patients with abdominal aneurysms was significantly elevated, compared to 81 patients with aortic occlusive disease (n = 15; 18.5%) and 298 patients with coronary artery disease (n = 54; 18.1%). Additionally, the number of patients with recent hernia repair (n = 19; 16%) or still awaiting repair (n = 11; 9%) was very high in the patient group with abdominal aortic aneurysms. Smoking habits were not different among all groups. We conclude that the prevalence of inguinal hernias in patients with abdominal aortic aneurysms is high compared with those with peripheral arterial occlusive disease or coronary atherosclerosis. These findings indicate a systemic fiber degeneration.
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PMID:High coincidence of inguinal hernias and abdominal aortic aneurysms. 159 30

This is a clinical report of a rare case of Charcot-Marie-Tooth disease associated with dilated cardiomyopathy. A seventy-seven-year-old Japanese male first visited our outpatient clinic with a ten-year history of muscular weakness in his bilateral lower extremities and gait disturbance characterized by classical features of peroneal muscular atrophy and inverted champagne bottle legs. Biopsy findings of the m. quadriceps femoris and the n. gastrocnemius revealed clustered atrophy of myofibrils and segmental demyelinization mingled with remyelinization. Because of his other problem of dilated cardiomyopathy, he had been treated with salt restriction, digitalis, diuretics and vasodilators, until his third hospitalization, when he developed terminal stage of severe congestive heart failure. Despite our intensive cardiac care, the patient died because of profound pump failure. Autopsy findings disclosed a remarkably dilated left ventricular chamber and an increased total heart weight of 600 grams. Grossly, the cross sectional view of the left ventricle revealed diffuse, but not homogenous fibrosis that was most prominent in the posterior wall. On light microscopic examination, the left ventricular myocardium revealed diffusely scattered muscular degeneration interlaced with fibrosis. Although large epicardial coronary arteries revealed only mild intimal atheromatous thickening, most of the small intramuscular coronary arteries were free from atherosclerosis. Neither diabetic nor amyloid lesions could be detected. It has been well known that cardiomyopathy is often associated with various forms of muscular dystrophy and Friedreich's ataxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Charcot-Marie-Tooth disease associated with dilated cardiomyopathy: an autopsy case report]. 204 12

Neuronal intranuclear hyaline inclusion disease (NIHID) has been recognized in 14 patients. It usually occurs in the first and second decades but has been seen in the sixth. Both sexes are affected by this sporadic multisystem degenerative disorder that has involved the central and peripheral nervous systems with fibrillar and granular intranuclear inclusions. NIHID appears to be several variants of a multisystem degenerative disease as illustrated by the combination of a spontaneous, degenerative central and peripheral nervous system disorder with neuronal intranuclear inclusions and severe atherosclerotic coronary artery disease in a 23-year-old white man. Beginning at 11 years of age, this patient had experienced diffuse muscle spasms, dysarthria, dysphagia, tremors, ataxia, oculogyric crises, progressive muscle weakness, and atrophy. At autopsy, neuronal intranuclear hyaline inclusions and neuronal loss were seen in his brain, brainstem, cerebellum, spinal cord, bowel, bladder, and esophagus. These fibrillary and granular Cowdry type A and B intraneuronal inclusions were consistent with the diagnosis of NIHID associated with severe coronary atherosclerosis.
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PMID:Neuronal intranuclear hyaline inclusion disease associated with premature coronary atherosclerosis. 244 45

During our investigation of the tortuous internal carotid artery in the presence of atherosclerosis, we noted a 44% incidence of abdominal aortic aneurysm. The incidence of abdominal aortic aneurysm in the adult population is 2% to 4%, and the incidence in a group of patients with carotid atherosclerosis has been reported to be 10%. This supports an association between the tortuous internal carotid artery and the abdominal aortic aneurysm independent of other risk factors. We found no significant difference in sex, age, or other atherosclerotic risk factors between those patients with and those without an abdominal aortic aneurysm. This suggests the possibility of weakness of the arterial wall as a cause of tortuous internal carotid artery and abdominal aortic aneurysm in this group of patients. Better histologic and biochemical definition of this possible weakness is warranted. From a clinical standpoint, we feel that the high association of the two conditions should not be ignored; patients found to have a tortuous internal carotid artery should be investigated and followed up carefully for the presence or subsequent development of aneurysmal degeneration of the aorta.
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PMID:The relationship of the abdominal aortic aneurysm to the tortuous internal carotid artery. Is there one? 275 10

To determine the problem of the surgical treatment of atherosclerotic aneurysm of thoracic aorta, we reviewed our experiences with 113 consequtive patients who underwent thoracic aortic aneurysmectomy from January 1983 to December 1985. Fifty-two patients had atherosclerotic aneurysms and 61 patients had aneurysm with other etiologies. Hospital mortality was 19% in former group and was higher than in the latter group (6.5%). Especially, the mortality was the highest (50%) among the patients who required the intraoperative clamping of the arch vessels. Many complications related to atherosclerosis, such as atheroemboli, bleeding due to wall weakness and etc, was found among the patients died soon after the surgery. Also, age over 70 and renal or respiratory dysfunction were major risk factors to determine the operative death. On the other hand, asymptomatic ischemic heart disease and cerebrovascular disorders of three months after the onset were not significant determinant. It was concluded that the surgical indication should be contemplated with extreme care specifically among the patients with such risk factors.
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PMID:[Surgical treatment of atherosclerotic aneurysms of the thoracic aorta]. 280 6

Peripheral mononeuropathies may complicate distal arteriovenous fistulas for chronic renal dialysis. We observed three diabetic patients who developed pain, paresthesias, and weakness in the distribution of the median, ulnar, and radial nerves shortly after construction of proximal brachial artery-antecubital vein fistulas. EMG confirmed multiple distal nerve injuries. All three patients improved after shunt banding or ligation. Twenty additional patients with proximal shunts were examined for risk factors for brachial neuropathy. Although all patients had severe atherosclerosis and many had polyneuropathy, we identified no predictive risk factors other than diabetes.
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PMID:Brachial neuropathy after brachial artery-antecubital vein shunts for chronic hemodialysis. 303 8

Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.
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PMID:Magnesium metabolism in health and disease. 328 51

Hemodialysis patients often experience muscle weakness, cardiac arrhythmias, and hypertriglyceridemia, along with other conditions that may lead to atherosclerosis and coronary heart disease. A contributing factor in the etiology of the symptoms may be carnitine deficiency. Patients undergoing renal dialysis treatment are at risk for developing a carnitine deficiency. The small carnitine molecule can be easily lost into the dialysate. A diseased kidney may lead to a decrease in the endogenous supply of carnitine since the kidney is a major site of carnitine biosynthesis. The diet of dialysis patients may be limiting in preformed carnitine as well as in the precursors and micronutrients required for carnitine biosynthesis. Both oral and intravenous supplementation of L-carnitine have been shown to alleviate muscle weakness, reduce the incidence and severity of arrhythmias, and decrease plasma triglyceride levels, along with alleviating other complications noted in dialysis patients. Health care professionals must be aware of the possible benefits of providing carnitine supplementation for renal dialysis patients.
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PMID:Carnitine nutriture of dialysis patients. 370 Sep 27


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