Atherosclerotic Vascular Changes Research Articles

Reduced myocardial flow reserve relates to increased carotid intima-media thickness in healthy young men

Increased carotid artery wall thickness and lipoprotein oxidation are key early events in atherosclerosis. To test the hypothesis that reduced myocardial flow reserve is a marker of subclinical atherosclerosis, we examined the relationships between flow reserve and carotid artery intima-media thickness (IMT) in young men free from coronary heart disease. Basal and dipyridamole stimulated coronary blood flow was measured using positron emission tomography (PET) in 55 healthy men aged 36±4 years. Myocardial flow reserve was calculated as the ratio of stimulated flow to basal flow. The mean carotid artery IMT was measured using high-resolution ultrasound. Oxidised LDL was measured as baseline LDL diene conjugation. Myocardial flow reserve decreased across the quartiles of increasing IMT ( P=0.006), and was 5.2±1.9 in the lowest quartile for IMT and 3.7±1.2 in the highest ( P=0.04, I vs. IV quartile). In univariate analysis, oxidised LDL correlated inversely with flow reserve ( r=−0.35, P=0.01) and directly with IMT ( r=0.51, P<0.001). The association between flow reserve and IMT remained significant ( P≤0.01) in multivariate regression model including age, blood pressure, left ventricular mass, ox-LDL, total cholesterol, HDL-cholesterol and triglycerides as covariates. These data support the concept that reduced myocardial flow reserve reflects subclinical atherosclerosis in asymptomatic subjects, and suggest that increased lipoprotein oxidation is directly related to early structural and functional atherosclerotic vascular changes.

Arteriosclerosis in the influx and intravisceral arteries of the liver, kidney and lung of WHHL rabbits.

We performed a histopathological investigation on arteriosclerotic development in the influx and intravisceral arteries of the liver, kidney and lung of male WHHL rabbits. In the influx arteries of these organs, we observed severe atherosclerotic vascular lesions with high-grade luminal stenosis. In the intravisceral arteries of the liver and kidney, no arteriosclerotic lesions were observed. However, in the intrapulmonary arteries, we recognized severe atherosclerotic vascular changes with high-grade stenosis or total obstruction of the lumen in some middle to large sized pulmonary arteries. These observations indicate that the development of arteriosclerosis in parenchymatous organs differs, and that some organs are predisposed to arteriosclerosis formation.

Effect of Lp(a) on the early functional and structural changes of atherosclerosis.

Epidemiologic studies have shown a significant relationship between elevated plasma levels of Lp(a) and increased risk of cardiovascular events; however, the mechanisms by which elevated Lp(a) levels produce this increased risk are not known. To test the hypothesis that high Lp(a) levels might contribute to the development of subclinical atherosclerosis, we examined the influence of Lp(a) levels on early functional and structural atherosclerotic vascular changes. Flow-mediated (endothelium-dependent) and nitrate-mediated (smooth muscle-dependent) arterial dilations were measured by high-resolution ultrasound in 241 normal healthy subjects (aged 15 to 69 years; 116 men). In addition, carotid artery intima-media thickness was measured by ultrasound in 71 subjects. Plasma Lp(a) was measured using a 2-sided immunoradiometric assay (cohort median, 10 mg/dL; interquartile range, 3.9 to 24.4 mg/dL). In these subjects, there were no significant relationships between Lp(a) and arterial endothelial function, smooth muscle responses, or carotid wall thickness (P>0.25). By contrast, other lipid risk factors, such as LDL-cholesterol and LDL-cholesterol/HDL-cholesterol ratio, were significantly correlated with abnormal arterial function and structure (P</=0.01). These data suggest that elevated Lp(a) levels do not confer cardiovascular risk by contributing to the early functional or structural changes of atherosclerosis.

Hyperhomocysteinaemia and associated disease.

An elevated plasma homocysteine level may result from various environmental and genetic factors. Herediatary causes of severe hyperhomo-cysteinaemia are very rare and usually lead to disease in childhood or adolescence. Common pathology consists of early atherosclerotic vascular changes, arterioocclusive complications and venous thrombosis. Mildly elevated genetically determined plasma homocysteine levels are observed in 5% of the general population. In the last two decades research has shown mild hyperhomocysteinaemia to be linked to an increased risk of premature atherosclerosis, pregnancies complicated by neural tube defects and early pregnancy loss, and venous thrombosis. Homozygosity for thermolabile MTHFR deficiency has been identified as one important genetic factor, which expression is modified by dietary folate intake. Although mild hyperhomocysteinaemia can easily be treated by vitamin supplementation the beneficial effects of such treatment remains to be shown.

Serum lipoproteins in children and young adults: determinants and treatment strategies.

Serum lipoproteins are related to vascular atherosclerotic changes as seen in necropsy studies of child fatal accident victims; therefore, efforts have been made to reveal the determinants of lipoprotein metabolism in children and young adults. Recent data emphasize the adverse effects of obesity, insulin resistance and high fat intake on lipid profiles of children, and currently many lifestyle and dietary intervention studies are in progress. Detection of hereditary dyslipidemias in childhood is presently hampered by diagnostic problems. However, with the advent of efficient tools for genetic mapping, early diagnosis of common genetic dyslipidemias will probably be possible in the near future.

Modulation of endothelial function: strategy for long-term cardiovascular protection.

Calcium antagonists primarily affect the cellular interactions of endothelial cells, smooth muscle cells, monocytes and thrombocytes, which are important in the early phases of the development of atherosclerosis. The protective effect of calcium antagonists on the vascular system appears to be low at later stages, which include increased matrix formation and central necrosis of atherosclerotic plaques. Present evidence indicates that calcium antagonists may be useful prophylactic agents at an early stage in the development of atherosclerotic vascular changes.

«Essential» phospholipids in diabetes mellitus. Review of the results all over the world

The purpose of the review is to evaluate the results obtained with the use of EPL (essential phospholipids) for the treatment of diabetes mellitus in the light of modern scientific knowledge, as well as to highlight the role of lipostabil in the treatment of diabetes mellitus. Since some studies did not set as their primary task the study of the effect of EPL on serum lipids and lipoproteins, and diabetes-specific parameters, such as blood glucose concentration, glycated hemoglobin (HbA1c), ketonemia, as well as possibilities, were put on the forefront. development of late complications (atherosclerotic vascular changes or retinopathy), then the evaluation of these studies was carried out in accordance with the measured parameters.&#x0D; The most important studies were analyzed. Since the beginning of the 90s, interest in the use of lipostabil in the treatment of diabetes has grown markedly. This interest was reflected in a double blind study by R. Kirsten et al., Completed in 1993. To date, there are data on 650 patients with insulin-dependent and non-insulin-dependent diabetes mellitus; one study is mainly related to diabetic retinopathy. The duration of therapy ranged from 14 days to 39 months, in most studies - several months. In some cases, lipostabil was used only orally, in others, simultaneously with intravenous administration, or therapy began with intravenous administration of the drug and continued with the use of oral capsules. The treatment of EPL was initially carried out on the background of only a diet, and then in combination with oral antidiabetic drugs or insulin.

Absence of clinically overt atherosclerotic vascular disease and adverse changes in cardiovascular risk factors in 70 patients with insulinoma.

Hyperinsulinemia has been assumed to contribute to the pathogenesis of atherosclerosis. To assess the reliability of such claim we planned a retrospective study on a cohort of patients with pancreatic insulin producing neoplasm. A correlation was sought between fasting insulin plasma levels and the metabolic profile emerging from those parameters known to be cardiovascular risk factors, i.e. plasma triglycerides and cholesterol, insulin resistance, hypertension. Special attention was paid to the duration of disease, because the time exposure to hyperinsulinemia could play an important role in developing cardiovascular disease. Seventy patients, 41 females and 29 males, aged 44.9 +/- 1.96 yr (range 15-80), with surgically proved insulinoma were included in the study. Chronic exposure to hyperinsulinemia was documented through the measurement of insulin plasma levels either in the fasting state or post-prandially, resulting in 44.7 +/- 3.28 and 149.9 +/- 12.22 microU/ml, respectively. Fasting glycemia in average was 45.3 +/- 1.34 mg/dl. Plasma triglycerides and cholesterol concentrations were 136.3 +/- 7.93 and 195.8 +/- 5.18 mg/dl, respectively, their distribution overlapping that anticipated for the general population. No correlation arose between the degree of hyperinsulinemia and the lipidic profile. Preoperative blood pressure was 136.9 +/- 2.87 mmHg, systolic and 81.9 +/- 1.32 mmHg, diastolic. Hypertension was present in 5 (7.1%) out of 70 patients and persisted after tumor removal. A condition of insulin resistance (M = 4.06 +/- 0.4 mg/kg min vs 7.41 +/- 0.21) was documented through the euglycemic hyperinsulinemic clamp technique in 20 patients and showed a positive and significant correlation with fasting insulinemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Association of DOCA hypertension with induction of atherosclerosis in rats with short-term diabetes mellitus

We investigated the effect of deoxycorticosterone acetate (DOCA)-induced hypertension on plasma lipid and cholesterol levels and the development of vascular atherosclerotic changes in male Wistar rats injected with streptozotocin (STZ) or saline (CON). Rats given STZ alone demonstrated a mild hyperlipidemia and hypercholesterolemia without any change in blood pressure. One week of DOCA administration was without effect on blood pressure in CON and STZ groups, but at 3 and 6 wk caused a significant and similar elevation in both groups. This DOCA-induced elevation in blood pressure appeared to be associated with the increase in plasma lipid and cholesterol levels seen in both CON and STZ groups at 3 and 6 wk, although the elevation in lipid and cholesterol levels was significantly more pronounced in the STZ rats. Both CON and STZ groups injected with DOCA developed significant pathological changes in all vessels under investigation. However, the degree of atherosclerosis appeared, from a semiquantitative analysis, to be worse in the thoracic aortas and renal arteries of the STZ group. Neither normotensive group developed any atherosclerosis. It is concluded that hypertension is associated with atherosclerosis in normal rats and rats with short-term STZ-induced diabetes mellitus, although the higher plasma lipid and cholesterol levels of the latter group may potentiate the degree of vascular damage.

Binocular interaction in lesions of the visual pathways:III. Retrochiasmal lesions

The presumed cause of anterior ischemic optic neuropathy is atherosclerotic vascular changes. Small-vessel occlusive vascular disease most likely causes occlusion of one or more posterior ciliary arteries, compromising blood flow to the optic nerve head and choroid. We present the case of a 59-year-old black man with cholesterol emboli within the retinal vasculature combined with a clinical picture of anterior ischemic optic neuropathy and choroidal nonperfusion demonstrated by i.v. fluorescein angiography. We believe this is evidence that, in a rare case, embolic phenomena may be the cause of anterior ischemic optic neuropathy.

Impotence in diabetic men

Studies relating to pathogenetic mechanisms resulting in importance in diabetic subjects have been reviewed. Erectile dysfunction was reported to occur in 50 to 75 percent of diabetic patients and the prevalence appeared to increase with age. Contributions of vascular, endocrine, and neurologic system alterations result in this disturbing condition, but a detailed analysis of all the parameters was not found in any individual study. In our review of 301 veterans presenting to a sexual dysfunction clinic, the clinical and hormonal alterations in the diabetic patients closely resemble those seen in nondiabetic impotent subjects. Atherosclerotic vascular changes play an important predisposing role in the development of impotence. A difference exists between the prevalences of associated medical conditions in diabetic patients taking insulin, compared with those receiving oral agents or receiving dietary management. The high prevalence of impotence in diabetic patients seems to be due to the high prevalence of its vascular complications. Considering the availability of useful therapeutic approaches, it is mandatory to evaluate all diabetic men for the presence of impotence.

Effect of vitamin E and ticlopidine on platelet aggregation in Fabry's disease.

Thromboembolism, increased platelet aggregation and high plasma concentration of beta-thromboglobulin were observed frequently in hemizygotes and heterozygotes of Fabry's disease. The administration of vitamin E and ticlopidine could improve the increased platelet aggregation in this disease. The platelet activation, probably induced by vascular endothelial damages, would accelerate atherosclerotic and thromboembolic vascular changes. Antiplatelet therapy will be effective for the prevention of these vascular complications in this disease.

Effects of noise exposure and hypercholesterolemia on auditory function in the New Zealand white rabbit.

An association between hypercholesterolemia and high-frequency hearing loss has been suggested previously. Most data have been epidemiologic, and only recently have experimental studies appeared supporting this observed association. It is unclear whether this hearing loss is related solely to hypercholesterolemia or if it is a consequence of cholesterol-induced vascular changes. The New Zealand White rabbit was used to study the auditory effects of noise, hypercholesterolemia, and the combination of both. Auditory function was evaluated with far-field monitoring of click-evoked auditory brain stem responses by comparing latency/intensity functions and absolute click-evoked thresholds. Hypercholesterolemia was maintained for only 3 weeks, theoretically eliminating atherosclerotic vascular changes as a mechanism contributing to observed changes. Auditory function was unchanged after 3 weeks of hypercholesterolemia. Also, the changes observed after noise exposure were comparable between the normal and the hypercholesterolemic groups. We conclude that if hypercholesterolemia contributes to high-frequency hearing loss, the pathophysiology is related to cholesterol-induced vascular changes, not solely to hypercholesterolemia.

低HDL血症の病態に関する研究

We have proposed the new classification of hypo-high density lipoproteinemia based on the plasma lipoprotein profile, especially HDL cholesterol (HDL-C)/LDL-C ratio. In hypo-high density lipoproteinemia Type I, HDL-C/LDL-C ratio is low and in Type II, it is normal or high. Furthermore, there are two subtypes in Type I: Type Ia and Type Ib. In Type Ia, LDL-C is not high and in Type Ib, its level is high. Among these types of hypo-high density lipoproteinemia, clinical characteristics, severity of atherosclerotic vascular changes and the necessity for drug therapy to increase HDL level are probably different. It has been indicated that HDL2 was metabolically more variable and has more efficient antiatherogenic function than HDL3. However, we have found that HDL3 concentrations could vary in certain states such as hypo-high density lipoproteinemia of liver cirrhosis. The purpose of the present study was to investigate the characteristics of plasma lipoprotein composition of hypo-high density lipoproteinemia in the aged group and address ourselves to the question which subfraction of HDL2 and HDL3 was responsible for low levels of HDL in the aged hypo-high density lipoproteinemia. Thirty one subjects whose mean age was 67±14 years were studied. Subjects with diabetes mellitus, or dysfunction of thyroid, liver or kidney were excluded from the present study. Lipoprotein fraction was isolated by sequential ultracentrifugation. In eight subjects, HDL-C level was lower than 45mg/100ml and plasma lipoprotein composition of this hypo-high density lipoproteinemic group (hypo-HDL group) was compared to normal HDL-C levels group (normal-HDL group) and younger (20-50 years old) normal controls. In hypo-HDL group, HDL-C/LDL-C ratio was significantly lower than that of controls (0.39±0.009 vs 0.57±0.17, P<0.01), although LDL-C did not show significant difference. We classified these eight subjects into the types of hypo-high density lipoproteinemia using 0.35 and 150mg/100ml as cut off values for HDL-C/LDL-C ratio and LDL-C level, respectively. There were two Type Ia, one Type Ib, and five Type II. Lipids composition of HDL2 and HDL3 were investigated. In hypo-HDL group, HDL2-C level was significantly lower than those of other two groups (hypo-HDL group, 14±4mg/100ml, normal-HDL group, 18±6mg/100ml, p<0.05, control, 18±4mg/100ml, p<0.05). Also HDL3-C level was significantly lower than that of controls (21±2 vs 25±4mg/100ml, P<0.02). HDL2-triglyceride (TG), HDL2-phospholipid (PL) and HDL3-PL were significantly lower than those of controls. HDL2-PL was significantly lower than that of normal HDL group. The data presented suggest the heterogeneity of hypo-high density lipoproteinemia in the aged in terms of types of hypo-high density lipoproteinemia. Low HDL-C levels in the aged were due to low levels of both HDL subfraction, HDL2 and HDL3.

低HDL血症の病態に関する研究

Recent evidences from population surveys suggest that a decrease in HDL-cholesterol (HDL-C) is associated with an increased risk of atherosclerotic cardiovascular diseases. When we evaluate atherogenecity of plasma lipoprotein profile, we must consider not only HDL level, but also other lipoprotein levels especially LDL level. The purpose of the present study was to investigate the characteristics of plasma lipoprotein compositions of hypo-high density lipoproteinemia without severe hypertriglyceridemia higher than 300mg/100ml. In sixty six subjects with cerebrovascular disease (CVD), thyroid dysfunction, or other disorders who seemed to have low HDL levels, concentrations of plasma cholesterol (P-Chol), LDL-cholesterol (LDL-C), HDL-C and HDL-C/LDL-C ratio were studied. Lipoprotein fractions were isolated by sequential ultracentrifugation as previously reported. HDL-C level (mean±SD) was 48±12.6mg/100ml, and significantly lower than that of seventy five normal controls (<0. 53.5±9.7mg/100ml, p 01), indicating that subjects studied in the present study include many hypo-high density lipoproteinemic patients. There were no significant differences in other factors such as P-Chol, plasma triglyceride (P-TG), LDL-C level and HDL-C/LDL-C ratio between patients in the present study and normal controls. There were significant positive correlations between HDL-C and P-Chol levels (p<0.01), and also between HDL-C and LDL-C levels (p< 0.05). Furthermore, in seventeen subjects whose HDL-C levels were lower than 40mg/100ml (group of hypo-high density lipoproteinemia: group A), P-Chol level(mean±SD) was significantly lower than that of forty nine other subjects (group B) whose HDL-C levels were higher than 40mg/100ml (129±31.5 vs. 196±67.0mg/100ml, p<0.01). LDL-C of group A was also significantly lower than that of group B (82±27.4 vs. 130± 65.0mg/100ml, p<0.01).However, there was no significant difference in HDL-C/LDL-C ratio between two groups. These findings suggest that in hypo-high density lipoproteinemic patients, there was a group of patients whose P-Chol and LDL-C levels are low, and therefore, HDL-C/LDL-C ratio is normal. From these observations, we propose to subdivide hypohigh density lipoproteinemia into two groups; Type I and Type II. In hypo-high density lipoproteinemia Type I, HDL-C/LDL-C ratio is low, and in Type II, it is normal or high. Furthermore, there may be two subtypes in Type I: Type Ia and Ib. In Type Ia, LDL-C level is not high, and in Type Ib, its level is high. Among these types of hypo-high density lipoproteinemia, clinical charcteristics, severity of atherosclerotic vascular changes and the necessity for drug therapy to increase low HDL level are probably different. Key-point of these differences may exist in HDL-C/LDL-C ratio. We tried to classify thirty subjects of the present study whose HDL-C were lower than 45mg/100ml, into these types and subtypes using 0.35 of HDL-C/LDL-C ratio, 150mg/100ml of LDL-C level as cut points. There were nine Type Ia, four Type Ib and seventeen Type II. Seven of nine (78%), three of four (75%) and seven of seventeen (41%) of patients were CVD in Type Ia, Ib and II, respectively. Type Ib had one familial hypercholesterolemia. Type II consisted of many patients with hyperthyroidism. As far as the pathogenesis of low HDL level are concerned, a significant negative correlation was found only in patients with hypo-high density lipoproteinemia between HDL-C and P-TG (p<0.001), despite exclusion of severe hypertriglyceridemia. Therefore, one of the causes of low HDL level seems to be due to decrease of HDL production from triglyceride-rich lipoprotein.

Platelet aggregation in relationship to plasma catecholamines in patients with hypertension

Plasma catecholamine concentration and platelet aggregation were studied in 22 patients with uncomplicated primary hypertension and 13 age-matched normotensive, healthy subjects at rest and in some during isometric handgrip exercise. The effect of norepinephrine (NE) infusion upon platelet aggregation was also examined. Plasma catecholamine concentration was slightly higher in the hypertensive than the normotensive group, but the difference was not significant. However, platelet aggregation to ADP was significantly greater in the hypertensive than the normotensive subjects. Exercise increased significantly both catecholamines and aggregation in both groups. Platelet aggregation was correlated with age ( r = 0.62, P < 0.01) and plasma NE ( r = −0.34, P < 0.05 for the total group of subjects). The infusion of NE increased significantly plasma NE and platelet aggregation and there was an inverse correlation between NE increase and threshold decrease ( r = −0.69, P < 0.05). Thus, plasma catecholamines are important determinants of platelet aggregation. However, in our study, uncomplicated primary hypertension was not associated with abnormal plasma catecholamine concentration. It is likely that the observed abnormal platelet aggregability to ADP represents a secondary phenomenon, possibly related to more advanced atherosclerotic vascular changes in hypertensive than normotensive subjects.

Platelet lipid peroxides as determinant of platelet survival and sympathetic stimulation in patients with hypertension

The platelet lipid peroxidation technique was used to determine platelet survival time in 10 patients with uncomplicated essential hypertension and 10 age-matched normotensive and healthy subjects. Mean platelet survival time was 7.3 ± 0.65 days in the hypertensive group and 9.6 ± 0.82 days in the normotensive group ( P < 0.05). However, shortened survival time was observed in four hypertensive and in two normotensive subjects. It is possible that the significant decrease in survival time found in the hypertensive group might reflect more advanced atherosclerotic vascular changes than in the normotensive group. Posture change affects lipid peroxides, probably via the catecholamines.

Atherosclerosis of the aorta and coronary vessels of the heart in cases of various diseases

The authors investigated the occurrence of atherosclerosis in “healthy” people (selected accidental deaths), in people, who died of complications due to atherosclerosis, and in some diseases: i.e. , diabetes, hypertensive disease, renal hypertension and malignant tumours. In their observations, they used the visuo-planimetric method of estimation of vascular atherosclerotic changes recommended by the WHO. In diabetics under the age of 50, extensive atherosclerosis was found in only 16 of the 38 patients. In some of these 16 cases, the duration of diabetes was over 8 years (in 8 cases). The accelerated development of atherosclerotic changes (mostly fibrous plaques) was usually observed in 1 or 2 vessels out of the 5 studied. In some instances, despite a long duration of diabetes in young people, the authors did not note any accelerated development of atherosclerotic changes as compared with the control groups. In people of 50 years of age and over, atherosclerotic changes in diabetics were as pronounced as in those who died of atherosclerosis unattended with diabetes. Hypertension of any etiology (essential, renal) involves a more pronounced atherosclerosis of the aorta than found in healthy people or those who died of complications due to atherosclerosis unattended with hypertension. The average area of atherosclerotic changes in the right coronary artery in patients with essential hypertension is larger than in persons who died of complications due to atherosclerosis but did not suffer from hypertension. The differences in the descending branch of the left coronary artery are less pronounced, although there is a tendency towards more severe lesions of this vessel in patients with essential hypertension, especially in men. In patients 30–39 years of age suffering from symptomatic renal hypertension, atherosclerosis of the aorta is more intensive than in patients with essential hypertension. There is also a tendency towards an increase in the area of atherosclerosis of the coronary arteries in patients suffering from symptomatic hypertension, especially between the ages of 30 and 39. After 40, the intensity of atherosclerosis in these two groups is essentially the same. In cases of new malignant growths, atherosclerotic changes in the aorta and coronary arteries were less prevalent than in cases of other ailments studied (diabetes, essential hypertension, symptomatic hypertension). In their prevalence, however, they differed little from atherosclerotic changes in healthy people.

Postmortem observations on the thyroid in atherosclerosis.

AbstractIn this preliminary study, an attempt was made to correlate atherosclerotic vascular changes with pathological changes in the thyroid observed post mortem in 55 patients (chiefly in the 61 to 90 year age bracket) who died of atherosclerotic disease of the coronary or other arteries. In the 55 cases, 71 per cent of the thyroids were smaller than normal, weighing from 2 to 18 grams, and 29 per cent were in the accepted normal range of 20 to 40 grams. For the purposes of this study, a small thyroid weight was considered significant only when it was 10 grams or less. The histological picture was more revealing. In one group of 24 patients the thyroids showed varying degrees of chronic lymphocytic thyroiditis, fibrosis and degenerative changes strongly indicative of impaired thyroid function. In another group of 31 patients the thyroids did not show any thyroiditis but there were several pathological changes such as great variation in the size of the acini, a reduction in their total number, atrophy of the acini, thinning and flattening of the epithelium with degeneration, swelling and desquamation of the cells, thick colloid in the follicles, and perifollicular fibrosis. The 4 patients who served as controls (age range, 51 to 76 years) showed no atherosclerosis or only slight changes and their thyroid glands were practically normal.There appeared to be a correlation between thyroid deficiency and atherosclerosis. Therefore, treatment of atherosclerosis with thyroid seems rational. If it prevents the development of hypothyroidism when given early in the course of atherosclerosis, it may help to reverse the high death rate from atherosclerotic cardiac and vascular disease.

Dissecting aneurysm of the renal artery.

The vast majority of dissecting aneurysms originate in the aorta, with the main branches involved only by extension from the aortic source. Edwards, however, expressed the opinion that local dissecting aneurysm superimposed on atheromatous changes may be associated with thrombosis of peripheral arteries and cites a case of local dissection in the popliteal artery.¹Lovitt and Corzine also report the occurrence of dissecting aneurysm in the coronary arteries.²Most dissecting aneurysms are found in relation to atherosclerotic or medial necrotic vascular changes. Careful perusal of the literature failed to reveal a case of local dissection of the renal artery without evidence of aortic involvement. <h3>Report of a Case</h3> A 47-year-old man was in apparent good health until eight hours prior to hospitalization (April 26, 1952), at which time there was the sudden onset of deep, nauseating, nonradiating, intense left flank pain. A moderate degree of shock was present