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PubMed1996

Intraarterial pressure measurements during angiographic evaluation of peripheral vascular disease: techniques, interpretation, applications, and limitations.

Many operative and percutaneous procedures are available for the treatment of occlusive disease involving the lower-extremity arterial system. Peripheral vascular disease involving the aorta and lower-extremity vessels usually is attributable to atherosclerosis. The lower-extremity arterial supply is divided segmentally into the inflow (aortoiliac) and outflow (femoropopliteal and tibioperoneal) vessels. Given the length of the lower-extremity vascular system, the propensity for multifocal disease, and the possibility of a nonvascular cause for a patient's symptoms, both localization of disease in arterial segments and determination of the hemodynamic impact of diseased sites are important for judicious treatment planning. This review focuses on the use of intraarterial pressure measurement as an adjunct to angiography and intravascular intervention in evaluating the significance of arterial occlusive disease in lower-extremity arteries.

Angiography↗
PubMed2000

Is an atherogenic lipoprotein profile in the fetus a prerequisite for placental vascular disease?

OBJECTIVE: To measure the blood apolipoprotein A-1 and apolipoprotein B in the fetal circulation in normal pregnancy and in pregnancy with evidence of vascular disease in the fetal umbilical placental circulation defined in the antenatal period by Doppler ultrasound study. DESIGN: An observational study to compare fetal plasma apolipoprotein levels in normal and complicated pregnancy. SETTING: A university hospital tertiary referral obstetric unit. SAMPLES: Umbilical vein blood was collected at delivery from 22 normal fetuses delivered by elective caesarean section for non fetal reasons and 30 fetuses with evidence of umbilical placental vascular disease identified antenatally by Doppler ultrasound study. METHODS: Plasma apolipoprotein A-1 and B were determined using an enzyme-linked immunosorbent assay (ELISA) methods. MAIN OUTCOME MEASURES: Fetal plasma levels of apolipoprotein A-1 and B were measured. RESULTS: There was a significantly lower level of fetal plasma apolipoprotein A-1 in placental insufficiency [placental insufficiency vs normal pregnancy, median 0.30 g/L (interquartile range 0.24, 0.39 g/L) vs 0.35 g/L (0.31, 0.42 g/L), P = 0.045]. In contrast, the levels of fetal plasma apolipoprotein B in placental insufficiency [0.20 g/L (0.17, 0.26 g/L)] were significantly increased compared with normal pregnancy [0.16 g/L (0. 14, 0.20 g/L), P = 0.03]. The ratio of fetal plasma apolipoprotein B to A-1 was also substantially higher in placental insufficiency [0.68 (0.55, 0.83)] than in normal pregnancy [0.45 (0.36, 0.60), P = 0.0003]. CONCLUSIONS: Our study has demonstrated that levels of fetal plasma apolipoprotein A-1, apolipoprotein B and the ratio of apolipoprotein B to A-1 were altered in the fetuses who are victims of umbilical placental insufficiency in the same direction as in adults associated with a high risk of atherogenesis.

Adult↗
PubMed1996

Pathology of acute and chronic ischaemic neuropathy in atherosclerotic peripheral vascular disease.

The peripheral nerve pathology in ischaemic limbs with atherosclerotic peripheral vascular diseases (PVD) is difficult to ascertain because of the limited number of reports. In addition, it has been debated whether chronic ischaemia per se could cause morphological abnormalities in peripheral nerves. In this prospective study, we examined pathological findings in the sural, saphenous, deep peroneal, superficial peroneal and tibial nerves, taken from seven acutely and nine chronically ischaemic amputated legs in which ischaemia was due to non-diabetic severe PVD. For morphological comparison, nerves were also taken from amputated legs without ischaemic disease and those in which PVD was associated with diabetes. In acutely ischaemic nerves, pathological changes were dependent upon the duration of ischaemia. Axonal degeneration of both myelinated and unmyelinated nerve fibres (MFs and UMFs) with occluded vessels was prominent, if acute ischaemia was present for > 24 h. Focal lesions, a hallmark of acute ischaemic neuropathy, were seen in both acute and chronic PVD nerves. Chronic PVD nerves also revealed considerable variations in the density of MFs between the fascicles of individual nerves and between the nerves of individual subjects: demyelination and remyelination, endoneurial oedema particularly at the subperineurial region, swollen endothelial cells, various but infrequent axonal changes, and relative preservation of UMFs were also seen. All pathological changes found in acute and chronic PVD nerves, except for a high rate demyelinated and remyelinated nerve fibres, have been described in experimental models of acute ischaemic/reperfusion injury. Demyelination could be induced by chronic ischaemia. Thus, pathological alterations in chronic ischaemic neuropathy may be due to the combined effects of acute ischaemia/reperfusion and chronic hypoxia.

Aged↗
PubMed2001

Role of aminothiols as a component of the plasma antioxidant system and relevance to homocysteine-mediated vascular disease.

Hyperhomocysteinaemia is considered to be an independent risk factor for vascular disease. Elevated plasma homocysteine may pose an oxidative stress, leading to the development of vascular damage. A component of this effect may be a disturbance of the extracellular aminothiol redox state. The relative contributions of plasma total homocysteine (tHcy) and plasma total cysteine (tCys) to the total antioxidant capacity (TAOC) of plasma was established in subjects with normal and elevated plasma tHcy. A total of 10 subjects with severe hyperhomocysteinaemia (due to inherited metabolic defects), 13 of their heterozygous parents and 72 normal healthy subjects were recruited to the study. The mean plasma tHcy in the patients was 91.8 micromol/l, compared with 13.2 micromol/l in the parents and 14.7 micromol/l in healthy control subjects. Plasma tCys and plasma TAOC were significantly lower in the subjects with severe hyperhomocysteinaemia compared with the parents and healthy control subjects (P<0.05). In blood samples from subjects with a normal tHcy, a positive correlation was observed between tCys and tHcy (P=0.0001). In contrast, in blood samples with tHcy >or=20 micromol/l, plasma tCys was negatively correlated with tHcy (P=0.0001). In samples with tHcy >or=20 micromol/l, tHcy was inversely correlated with TAOC (P=0.0001), whereas tCys was positively associated with TAOC (P=0.0001). Multiple regression analysis revealed that tCys was the most important independent determinant of TAOC in the patient and control groups when the effects of tHcy and several factors known to influence TAOC, such as urate, were taken into account. Thus hyperhomocysteinaemia may pose an oxidative stress not only through the direct cytotoxicity of homocysteine, but also from an associated fall in plasma cysteine.

Adolescent↗
PubMed1998

Renal vascular disease in the elderly.

The aging of Western societies is causing a progressive increase in the number of patients over 65 starting dialysis. The EDTA Registry shows that in 1995 this section of the population represented nearly 45% of patients under dialysis, and the percentage is even higher in the USRDS at 48%, 20% of whom are over 75. These changes have not only been quantitative, but have also modified the causes of end-stage renal disease (ESRD). Diabetic nephropathy (DN) and renal vascular disease (RVD) account for more than 50% of all these causes, reaching 66% according to the latest USRDS calculations. According to these numbers, RVD represents 29% of all causes, the incidence varying with the age group, and has become the main cause of ESRD in the elderly (38% of all cases). Until a few years ago, RVD was synonymous with hypertension, but as the population ages, the range of diseases in this group is increasing. The main RVDs that cause ESRD in the elderly are: hypertensive RVD (nephrosclerosis), atheromatous RVD (either as ischemic atherosclerotic nephropathy or as atheroembolism), and acute occlusion of renal arteries (either bilateral or unilateral in single-kidney patients). The diagnosis of nephrosclerosis in the absence of histological confirmation is a presumed clinical diagnosis, made in most cases by exclusion, and is therefore clearly overestimated. On the other hand, atheromatous RVD is an underdiagnosed disease that is often overlooked. The prevalence, natural history, diagnosis and prognosis are discussed in this report.

Aged↗
PubMed2003

Predictive value of noninvasively determined endothelial dysfunction for long-term cardiovascular events in patients with peripheral vascular disease.

OBJECTIVES: The goal of this study was to prospectively examine the long-term predictive value of brachial-artery endothelial dysfunction for future cardiovascular events. BACKGROUND: Brachial-artery endothelial function is impaired in individuals with atherosclerosis and coronary risk factors. The prospective relation between endothelial function determined by brachial-artery ultrasound and long-term cardiovascular risk is unknown. METHODS: We examined brachial-artery endothelial function using ultrasound in 199 patients with peripheral arterial disease before elective vascular surgery. Patients were prospectively followed with an average follow-up of 1.2 years after surgery. RESULTS: Thirty-five patients had an event during follow-up, including cardiac death (5 patients), myocardial infarction (17 patients), unstable angina (10 patients), or stroke (3 patients). Preoperative endothelium-dependent flow-mediated dilation (FMD) was significantly lower in patients with an event (4.4 +/- 2.8%) compared with those without an event (7.0 +/- 4.9%, p < 0.001), whereas endothelium-independent vasodilation to nitroglycerin was similar in both groups. In a Cox proportional-hazards model, independent predictors of events included age (p = 0.003), more invasive surgery (surgery other than carotid endarterectomy, p = 0.02), and impaired brachial-artery endothelial function (p = 0.002). Risk was approximately nine-fold higher in patients with FMD <8.1% (lower two tertiles) compared with those in the upper tertile (odds ratio 9.5; 95% confidence interval 2.3 to 40). CONCLUSIONS: Impaired brachial-artery endothelial function independently predicts long-term cardiovascular events in patients with peripheral arterial disease. The findings suggest that noninvasive assessment of endothelial function using brachial-artery FMD may serve as a surrogate end point for cardiovascular risk.

Aged↗
PubMed1986

[Epidemiology of vascular diseases in Italy].

The mortality rate from cardiovascular diseases was analysed for Italy as a whole and for individual regions in a sample year (1975). A distinction was made between cardiac and vascular diseases in order to assess the real incidence of the latter. The absolute number of deaths, the percentage mortality and the specific mortality quotient were studied. Deaths were also divided into age groups. Cardiovascular diseases were found to be the primary cause of death, circulatory disease the second. Among the latter, diseases of the encephalic circulation took first place. The same parameters were applied to the 1965-1983 period. Mortality due to cardiovascular disease remained constant over the period since the decrease in deaths from cardiac conditions was offset by an increase in those due to vascular disease in the strict sense. Finally the specific standardised mortality quotients per age and sex were considered in the 1970-1979 period. Mortality trends in Italy and in the individual regions were identical to those described using non-standardised indices.

Age Factors↗
PubMed1986

Inapparent pulmonary vascular disease in an ex-heroin user.

A severe pulmonary vascular derangement, usually reported in drug addicts, was diagnosed in a 28-year-old asymptomatic ex-heroin user by means of fortuitously performed pulmonary perfusion imaging. Neither physical findings nor pulmonary function tests, aroused suspicion of the diagnosis. A search for asymptomatic pulmonary vascular disease probably should be undertaken in drug addicts.

Adult↗
PubMed1975

Progressive pulmonary vascular disease after surgical correction (Mustard procedure) of transposition of great arteries with intact ventricular septum.

Severe pulmonary vascular disease developed 1 year after a Mustard operation in a 2 1/3 year old boy with transposition of the great arteries and intact ventricular septum. The possible etiologic factors responsible for the development of pulmonary vascular disease are discussed, and it is suggested that this disturbing late postoperative complication may occur more frequently than is recognized.

Cardiac Catheterization↗
PubMedDate not supplied

Microscopic structure of disturbed flows in the arterial and venous systems, and its implication in the localization of vascular diseases.

A novel technique to prepare isolated transparent natural blood vessels was developed and used to investigate the connection between blood flow and the localization of vascular diseases in man. Transparent segments of arteries and veins were prepared from dogs and humans postmortem, and the flow patterns in various regions of the circulation were studied in detail by means of flow visualization and cinemicrographic techniques. It was found that under normal physiological conditions, complex spiral secondary flows and recirculation zones form in various regions of the arterial and venous systems such as the aortic arch, aortic T-junctions, carotid artery bifurcations, the major branching sites of the intracranial cerebral arteries and venous valve pockets. Incipient saccular aneurysms were found at the flow divider of the anterior communicating-anterior cerebral artery junction where the flow directly impinged on the vessel wall. In human cerebral arteries, atherosclerotic thickenings of the vessel wall were found to be localized on the outer wall (hip) of one or both daughter vessels at bifurcations and T-junctions, and at the inner wall of arterial bends, at the very places where secondary and recirculation flows were dominant and wall shear stress was low. The results clearly indicate that there is a strong correlation between the sites of flow disturbance and the preferred sites for the genesis and development of vascular diseases clinically found in man.

Animals↗
PubMed1997

Racial differences in operation for peripheral vascular disease: results of a population-based study.

Operation for non-coronary atherosclerotic peripheral vascular occlusive disease may vary among race and gender groups. Using a state-wide registry, the authors identified all operations performed for infrarenal peripheral vascular disease over a 12-month period in a single south-eastern state. Procedures performed included reconstruction for aortoiliac (n=641) and infrainguinal (n=1129) disease and major amputation (n=1077). The incidence for patients over age 50 was calculated using census data. Operation for aortoiliac disease was significantly more likely for white patients (relative risk 3.79, 95% C.I. 2.84-5.15), but less likely for infrainguinal peripheral vascular disease (relative risk 0.64, 95% C.I. 0.56-0.73) and amputation (relative risk 0.17, 95% C.I. 0.15-0.19). Trends toward lower operative mortality in blacks with aortoiliac disease (10.6% versus 12.0%), PVD (3.2% versus 3.5%), and amputation (5.5 versus 8.7%) failed to attain statistical significance. Patient race was associated with the type and location of operation performed for peripheral vascular disease.

Aged↗
PubMed2000

Elevated levels of circulating heat shock protein 70 (Hsp70) in peripheral and renal vascular disease.

Heat shock proteins (Hsp) are families of phylogenetically conserved molecules that have a range of cytoprotective and intracellular functional roles. Reactivity to heat shock proteins has been implicated in the development of autoimmune disease and tissue expression of heat shock proteins and increased levels of anti-Hsp antibodies have also been reported in vascular disease. This study compared circulating levels of Hsp60 and Hsp70 and antihuman Hsp60, antihuman Hsp70, and antimycobacterial Hsp65 antibodies in peripheral (PVD) and renal (RVD) vascular disease with those in age- and sex-matched controls. Levels of Hsp70 were higher in both PVD (median 580 vs 40; P < 0.01) and RVD (median 160 vs 0; P < 0.03), whereas there were no differences in Hsp60 levels. Anti-Hsp60 antibody levels were elevated in PVD (146 vs 81 arbitrary units/ml; P < 0.04), but not RVD. This is the first study to demonstrate increased levels of circulating Hsp70 in pathological disease states; however, its physiological role remains to be determined.

Aged↗
PubMed1995

Expression of vascular endothelial growth factor in renal vascular disease and renal allografts.

Vascular endothelial growth factor (VEGF) is a dimeric glycoprotein that exerts a proliferative effect specifically on endothelial cells. VEGF can increase vascular permeability and collagenase activity, is chemotactic for monocytes, and may dilate blood vessels. It can be induced by phorbol ester and cAMP in both mesenchymal and epithelial cells. In vitro cell culture experiments suggest that VEGF is upregulated by oxygen deprivation. In this study we tested whether in vivo acute and/or chronic reduction of renal blood flow by vascular obstruction would result in increased expression of VEGF mRNA and protein. Three normal kidneys, five human kidneys with narrowing of preglomerular vessels by vascular rejection or by vasculitis, and eight kidneys with nephrosclerosis and/or diabetic nephropathy were examined. In situ hybridization with 35S-labelled riboprobes showed a pronounced expression of VEGF mRNA in acutely hypoxic proximal and distal tubules of both the cortex and medulla; VEGF protein was demonstrated in the epithelia of these tubules by immunohistochemistry. In kidneys with chronically reduced blood flow, the majority of atrophic tubules were negative for VEGF mRNA and protein, although interstitial cells expressed VEGF mRNA. In arcuate arteries showing intimal and adventitial fibrosis, some medial smooth muscle cells were positive for VEGF mRNA. In glomeruli with segmental sclerosis, viable podocytes showed a prominent signal for VEGF mRNA. Mesangial cells did not express VEGF in the cases studied. It is possible that hypoxia itself led to the upregulation of VEGF in tubular epithelia and vascular smooth muscle cells. The vasodilatory and permeability-promoting effects of the endothelial growth factor produced by damaged tubular epithelia may constitute a mechanism to alleviate a decrease in blood flow and substrate availability and to re-establish vascular integrity.

Acute Disease↗