Arterial stiffness and function in end-stage renal disease

Cardiovascular disease is a major cause of mortality in patients with end-stage renal disease, with damage to arteries as a major contributing factor. Arterial stiffness is a factor associated with high systolic and pulse pressure in these patients and is a strong independent factor associated with morbidity and mortality. Arterial stiffness is one of the principal factors opposing left ventricular ejection. The appropriate term to define the arterial factor(s) opposing left ventricular ejection is aortic input impedance. Aortic input impedance depends on TPR, arterial distensibility, and wave reflections. Distensibility defines the capacitive properties of arterial stiffness, whose role it is to dampen pressure and flow oscillations and to transform pulsatile flow and pressure in arteries into a steady flow and pressure in peripheral tissues. Stiffness is the reciprocal value of distensibility. These parameters are blood pressure dependent; arteries become stiffer at high pressure. While distensibility provides information about the elasticity of the artery as a hollow structure, the elastic incremental modulus characterizes the properties of the arterial wall biomaterials independent of vessel geometry. Alternatively, arterial distensibility can be evaluated by measuring pulse wave velocity, which increases with the stiffening of arteries. Arterial stiffening increases left ventricular afterload and alters the coronary perfusion. With increased pulse wave velocity, the wave reflections affects the aorta during systole, which increases systolic pressures and myocardial oxygen consumption and decreases diastolic blood pressure and coronary flow. The arterial stiffness is altered primarily in association with increased collagen content and alterations of extracellular matrix and calcification of the arterial wall. The arterial stiffening estimated by changes in aortic pulse wave velocity and intensity of wave reflections are independent predictors of survival in end-stage renal disease and in the general population. Improvement of arterial stiffening could be obtained by antihypertensive treatments as observed with calcium-channel blockers and angiotensin-converting enzyme inhibitors. Angiotensin-converting enzymes inhibitors increase AC and reduce wave reflections. It has been shown that reversibility of aortic stiffening and use of angiotensin-converting enzyme inhibitors had a favorable independent effect on survival in hypertensive patients with advanced renal disease.     

Studies on structural changes of the carotid arteries and the heart in asymptomatic renal transplant recipients.

BACKGROUND: The present study was designed to characterize early structural changes of large arteries in renal transplant recipients with no clinical evidence of cardiovascular disease and normal blood pressure values, and to analyse the relationship between arterial alterations and those of the heart. METHODS: Intima media thickness and atherosclerotic plaques of the carotid arteries as well as left ventricular geometry and function were examined in 35 asymtomatic renal transplant recipients and 29 age- and sex-matched healthy controls by high resolution B-mode ultrasound and by echocardiography. RESULTS: Intima-media thickness of the carotid arteries was significantly higher in renal transplant recipients (1.21+/-0.08 mm) than in healthy controls (0.74+/-0.04 mm) (P<0.001). Atherosclerotic plaques were found in the majority of renal transplant recipients (71% vs 14% in healthy controls, P<0.001). Left ventricular mass index was significantly increased in the group of renal transplant recipients (264+/-13 g, 146+/-7 g/m2) when compared with healthy controls (155+/-8 g, 83+/-4 g/m2) (P<0.001). Multiple regression analysis in renal transplant recipients showed that intima media thickness of the carotid arteries was significantly related to left ventricular mass index (P<0.02), but not to age, blood pressure, body mass index, serum creatinine, cholesterol and lipoprotein (a) levels. In the group of healthy controls, intima-media thickness of the carotid artery was related to age (P<0.002), but not to left ventricular mass index or the other independent variables. CONCLUSIONS: The present study documents pronounced intima-media thickening in asymptomatic renal transplant recipients. Atherosclerotic lesions are present in most renal transplant recipients with no clinical evidence of cardiovascular disease. We observed a parallelism between arterial wall thickening and left ventricular hypertrophy, although blood pressure levels were normal during haemodialysis therapy and after renal transplantation.     

Cold sensitivity of the hand in arterial occlusive disease.

Digital blood pressure was measured using photoplethysmography in patients with cold sensitivity of the hand. In 19 patients with Buerger's disease, or arteriosclerosis obliterans (arterial occlusion group), 90 of 91 fingers with cold sensitivity showed significantly low pressures. In 17 patients with typical Raynaud's phenomena due either to primary Raynaud's disease or secondary to collagen disease (Raynaud's group), decreased digital pressure was noted in only five of 123 fingers with cold sensitivity. Blood pressure measurements in the fingers after local cooling of the hand showed a more severe response to cold in the Raynaud group than in the arterial occlusion group. These results indicate that the pathophysiologic mechanism for cold sensitivity in arterial occlusive disease is different from that in Raynaud's disease. In the arterial occlusion group impaired circulation due to occlusions in the digital arteries or more proximal arteries is a necessary precondition for cold sensitivity, and an increased sympathetic response to cold is of less importance as an etiologic factor. Thus a patient with cold sensitivity of the hand and normal digital blood pressure should not be considered to have arterial occlusive disease as the underlying cause of cold sensitivity.     

Alterations of arterial function in end-stage renal disease

Cardiovascular disease is a major cause of morbidity and mortality in patients with end-stage renal disease (ESRD). Epidemiological and clinical studies have shown that this is most frequently related to damage of large conduit arteries. Macrovascular disease develops rapidly in uremic patients and is responsible for the high incidence of ischemic heart disease, sudden death, peripheral artery diseases, and congestive heart failure. The most frequent causes of these complications are occlusive lesions due to atherosclerosis. Nevertheless, atherosclerosis, a disease characterized by the presence of plaques, represents only one form of structural response to metabolic and hemodynamic alterations which interfere with the process of aging, i.e., arteriosclerosis, characterized by dilation/hypertrophy and stiffening of arteries. The vascular complications in ESRD are ascribed to two different but associated mechanisms, namely atherosclerosis and arteriosclerosis. Whereas the former principally affects the conduit function with ischemic lesions being the most characteristic consequence, the latter primarily disturbs the cushioning function of large arteries. Arteriosclerosis in ESRD patients is characterized by diffuse dilation and hypertrophy of large conduit arteries and stiffening of arterial walls and represents a clinical form of accelerated aging process. The main clinical characteristics of arterial stiffening concern changes in blood pressure with isolated increase in systolic pressure and normal or lower diastolic pressure. The consequences of these alterations are: (1) an increased left ventricular afterload with development of left ventricular hypertrophy and increased myocardial oxygen demand and (2) altered coronary perfusion and subendocardial blood flow distribution. Epidemiological studies have identified arterial remodeling and stiffening as independent predictors of overall and cardiac mortality in ESRD patients.     

Arterial stiffness in dialysis patients: where are we now?

Patients with end-stage renal disease treated by chronic dialysis have an impressive mortality, which more than half of this mortality is attributable to cardiovascular disease. Despite stratification for sex, race, and the presence of diabetes, cardiovascular disease mortality is 10–30 times higher in dialysis patients compared to general population. In dialysis patients, both atherosclerosis (mainly affecting the intima of the arteries) and arteriosclerosis (affecting predominantly the media of large- and middle-sized arteries diffusely) are highly prominent. Arteriosclerosis characterized by reduced arterial compliance (i.e., reduced elasticity of the arteries) is due to increased fibrosis, loss of elastic fibers, and extensive vessel wall calcification. Arteriosclerosis is closely related to arterial stiffness. A generally accepted mechanistic view is that an increase in arterial stiffness causes a premature return of reflected waves in late systole, increasing central pulse pressure, thus systolic. An increased arterial stiffness can increase the risk of stroke through several mechanisms, including an increase in central pulse pressure, influencing arterial remodeling both at the site of the extracranial and intracranial arteries, increasing carotid wall thickness, and the development of stenosis and plaques, and the likelihood of plaque rupture. Very importantly, it was also suggested that arterial stiffness itself independently plays a role in exacerbating chronic kidney disease progression. This review deals briefly with the definition of arterial stiffness, methods of measuring arterial stiffness and pathophysiology of arterial stiffness, and factors related with arterial stiffness.     

Creatinine clearance, pulse wave velocity, carotid compliance and essential hypertension

BACKGROUND: The vascular hallmark of subjects with end-stage renal disease is increased arterial stiffness independent of blood pressure, wall stress, and cardiovascular risk factors such as hypertension, plasma glucose and cholesterol, obesity, and tobacco consumption. Whether arterial stiffness and kidney function are statistically associated in subjects with plasma creatinine < or =130 micromol/L has not yet been determined. Material. In 1290 subjects with normal or elevated blood pressure values and plasma creatinine < or =130 micromol/L, subjects were divided into three tertiles according to the calculated creatinine clearance. Blood pressure, aortic pulse wave velocity (PWV), and standard cardiovascular risk factors were determined in parallel. In 112 of the hypertensive subjects, common carotid and radial artery structure and function (high-resolution echo-Doppler techniques) also were measured. RESULTS: From the 1290 subjects, only the low-tertile group presented a significant negative association between PWV and creatinine clearance independently of blood pressure and standard risk factors. This association was stronger in subjects < or =55 years of age. In the 112 hypertensive subjects, carotid compliance was positively correlated to creatinine clearance even after an adjustment for age, gender, and blood pressure. At less than 55 years of age, creatinine clearance represented 20% of the variance of carotid compliance. Such findings were not observed for radial artery compliance. CONCLUSION: Increased stiffness of central arteries is statistically associated with reduced creatinine clearance in subjects with mild-to-moderate renal insufficiency, indicating that kidney alterations may interact not only with small but also large arteries, and this is independent of age, blood pressure, and standard risk factors.     

Noninvasive penile arterial evaluation in 120 males with erectile dysfunction

One hundred twenty males referred to a hospital-based Medical Sexology Program for evaluation of erectile dysfunction had, as part of that workup, a noninvasive penile arterial assessment which included determination of (1) blood pressure in each of the six penile arteries, (2) patency of each cavernosal artery, and (3) brachial blood pressure. The systolic pressures in each of the six penile arteries were averaged and divided by the brachial systolic pressure to determine the penile brachial index (PBI). When a PBI of 0.75 or less was correlated with a history of myocardial infarction, coronary artery bypass, or cerebral vascular accident, a P value of 0.069 resulted, certainly suggesting that each is a manifestation of arterial disease.     

Arterial hypertension, chronic renal insufficiency and dialysis

The principal characteristic of hypertension in chronic kidney disease (CKD), especially at CKD stage 5. Is an increased systolic pressure, with normal or even low diastolic pressure. This isolated systolic hypertension is also characterized by ab abnormal increase in pulse pressure which is by itself an independent cardiovascular risk factor. The principal reason for these abnormalities is accelerated ageing of arterial system, principally the aorta and large central arteries. This ageing is characterized by stiffening of arteritis whose natural history is not clearly understood. One of the principal pathogenic factor associated with stiffening is extensive calcification of arterial walls, mainly the medial layer (media-calcinosis). Mineral metabolism disorders such as hyperphosphatemia, play a major role in pathophysiology of calcifications. Arterial stiffness is characterized by very steep volume-pressure relationship and for this reason is associated with hemodynamic instability. Small blood volume increase producing abnormally high pressure while small decrease in blood volume could be associated with deep hypotension.     

Regulator of G protein signaling 5 marks peripheral arterial smooth muscle cells and is downregulated in atherosclerotic plaque

OBJECTIVE: Regulator of G protein signaling 5 (RGS5), an inhibitor of Galpha(q) and Galpha(i) activation, was recently identified among genes highly expressed in smooth muscle cells (SMCs) of aorta but not vena cava. This finding prompted the hypothesis that RGS5 provides long-term G protein inhibition specific to normal arterial SMC populations and that loss of expression may in turn contribute to arterial disease. METHODS: To test this hypothesis we characterized RGS5 gene expression throughout the vasculature of nonhuman primates to determine whether RGS5 was restricted to arteries in other vascular beds and whether expression was altered in arterial disease. RESULTS: In situ hybridization localized RGS5 message to medial SMCs of peripheral arteries, including carotid, iliac, mammary, and renal arteries, but not accompanying veins. SMCs of many small arteries and arterioles also expressed RGS5, including glomerular afferent arterioles critical to blood pressure regulation. Differential expression persisted in culture, inasmuch as RGS5 message was significantly higher in SMCs derived from arteries than from veins at real-time polymerase chain reaction. It was remarkable that the only major arterial bed lacking RGS5 was the coronary circulation. In atherosclerotic peripheral arteries RGS5 was expressed in medial SMCs, but was sharply downregulated in plaque SMCs. CONCLUSION: These data identify RGS5 as a new member of a short list of genes uniquely expressed in peripheral arteries but not coronary arteries. Persistence of an arterial pattern of RGS5 expression in culture and lack of expression in coronary arteries support a unique SMC phenotype fixed by distinct lineage or differentiation pathways. The association between loss of expression and arterial wall disease has prompted the new hypothesis that prolonged inhibition by RGS5 of vasoactive or trophic G protein signaling is critical to normal peripheral artery function.     

Arterial stiffness after successful renal transplantation

Cardiovascular disease is a major barrier to the long-term survival of transplant recipients. The aim of this study was to determine whether successful renal transplantation improves the arterial stiffness resulting from chronic renal failure. This study involved a group of 9 recipients (23-56 years) who underwent successful renal transplantation at our clinic. The brachial-ankle pulse wave velocity and - intima-media thickness of the bilateral common carotid arteries were measured in each patient before and 1 year after successful renal transplantation. One year after renal transplantation, the 9 patients showed a mean serum creatinine level of 1.41 mg/dL. Assessment of arterial stiffness in this group revealed that the mean brachial-ankle pulse wave velocity was reduced after renal transplantation, but there was no reduction in the mean intima-media thickness of the bilateral common carotid arteries. There was a significant correlation between the variance ratios of pulse wave velocity and median blood pressure. The more effective blood pressure control provided by renal transplantation may functionally improve arterial stiffness. However, organic arterial stiffness remained unchanged 1 year after transplantation.     

正常血压IgA肾病患者动脉病变的意义

目的:传统观点认为动脉硬化与高血压有关。然而,部分IgA肾病患者,尽管血压正常,但仍有动脉硬化的改变。本研究的目的就是比较血压正常、伴有和不伴有动脉病变的IgA肾病患者的临床病理特点,探讨正常血压IgA肾病患者肾内动脉病变的影响因素及意义。方法:所有患者均经肾活检诊断为原发性IgA肾病,无高血压病史,肾活检前血压<140/90mmHg。动脉病变的定义为活检肾组织光镜下见动脉壁增厚和(或)动脉玻璃样变。符合标准的105例患者,根据动脉病变的有无分为两组,有动脉病变组52例、无动脉病变组53例,分别比较两组的临床病理特点。肾脏动脉病变的半定量分级标准:0:无损害;1:<25%;2:≥25%,<50%;3:≥50%。统计学方法:分别比较两组的临床病理特点,将差异有统计学意义的单因素指标作为多因素分析的入选指标,采用逐步回归方法分析动脉病变的影响因素,以P<0.05作为差异有统计学意义。结果:与无动脉病变组比较,动脉病变组肾活检时的年龄、血肌酐、血尿酸、尿蛋白定量、尿NAG酶、肾小球硬化、肾小管萎缩以及肾间质纤维化的程度显著增高,尿渗透压显著下降。多因素分析的结果表明,肾活检时的血肌酐、尿渗透压、肾小管萎缩及肾间质纤维化是正常血压IgA肾病动脉病变的独立影响因素。动脉病变的程度与血肌酐、肾小管萎缩及肾间质纤维化呈正相关;与尿渗透压呈负相关。结论:血压正常IgA肾病患者的肾内动脉病变,主要与年龄、血肌酐、血尿酸增高等因素有关,常伴有肾小管间质损害。     

Anesthesiology problems in Takayasu's syndrome]

Takayasu's disease is a rare form of nonspecific obliterative panarteritis of unknown origin, mainly located at supraaortic, renal, and pulmonary arteries and resulting in multiple stenoses and occlusion of major arteries. Predominantly young women in the first three decades of life are affected. Absence of arm pulses, vascular bruits, and retinopathy are classic symptoms. Another symptom is hypertension of the lower extremities and hypotension of the upper extremities, thus potentially impairing cerebral perfusion. A 25-year-old female patient with a 2-year history of Takayasu's disease presented for therapeutic abortion on the grounds of her medical condition. There were significant stenoses of the left common carotid artery and the internal carotid artery. The left subclavian artery was totally obliterated. The arterial blood supply to the left arm was accomplished by the left vertebral artery via a subclavian steal syndrome. Brachial and radial pulses were absent in both arms. General, spinal or epidural anesthesia can produce arterial hypotension. Blood pressure assessment at the lower extremities does not allow conclusions about perfusion of supraaortic arteries and cerebral perfusion pressure. Thus, a paracervical block was performed; sedation and analgesia were achieved with small doses of midazolam and alfentanil. We planned that if general anesthesia became necessary we would induce anesthesia with etomidate and alfentanil and maintain anesthesia by mask ventilation with nitrous oxide in oxygen and supplementary doses of alfentanil. Invasive monitoring such as arterial or Swan Ganz catheterization, was contraindicated because of the possibility that inflamed vessels would become irritated. Therefore, we only monitored ECG, blood pressure at the leg, ventilation parameters, and oxygen saturation at the ear lobe by pulse oximetry.(ABSTRACT TRUNCATED AT 250 WORDS)     

Preoperative balloon occlusion of arteriovenous malformations

Many materials have been utilized to embolize cerebral arteriovenous malformations (AVMs) preoperatively. Specific vascular anatomy with large feeding vessels deep to the nidus or aneurysms within feeding arteries favor the use of detachable balloons over other embolic agents. Detachable balloons allow test occlusion of a vascular pedicle before permanent occlusion and can obliterate aneurysms in feeding arteries. We describe 36 feeder arterial balloon occlusions performed in 31 patients. Twenty-nine patients subsequently had surgical resection. None of the patients developed normal perfusion pressure breakthrough or required blood transfusions. The preoperative balloon occlusion was judged by the neurosurgeon to decrease significantly the difficulty in surgical resection of the malformation. The remaining 2 patients underwent embolization before radiosurgery. One patient had aneurysms in the feeding artery, which was balloon-occluded to diminish the risk of hemorrhage. There were two neurological deficits and three asymptomatic arterial dissections related to the balloon procedure. Balloon occlusion of feeding arterial pedicles in selected cerebral AVMs may be a valuable surgical adjunct.     

Anaesthesia and isolated systolic hypertension--pathophysiology and anaesthesia risk

This review examines the pathophysiology of isolated systolic hypertension, changing medical perspectives on this condition as a cardiovascular risk factor in the community and evolving evidence of it being an independent risk factor for perioperative morbidity and mortality. Hypertension is regarded as an added risk in anaesthesia. Continuation of antihypertensive medication through the perioperative period is an established principle. Studies supporting this practice have demonstrated greater perioperative haemodynamic stability in association with general anaesthesia and surgery in patients with treated hypertension compared to untreated hypertension. Therapy has historically focused on control of diastolic blood pressure, rather than systolic blood pressure. Recent clinical trial data and data from large observational studies show a closer association of systolic hypertension with both coronary heart disease and stroke compared with diastolic hypertension. This has led to recommendations for aggressive treatment of isolated systolic hypertension, especially in patients over 65 years old. The association between decreased compliance of the central systemic arteries and isolated systolic hypertension is well understood. The fact that this same pathology, lack of compliance of central arteries, can cause a decrease in diastolic blood pressure is not so well recognised. This means that, in patients with isolated systolic hypertension, decreasing diastolic blood pressure can be associated with worsening arterial disease and that systolic minus diastolic blood pressure may give a better indication of the problem. Anaesthetic assessment and technique should be studied and potentially revised in the light of these changes in perspective on isolated systolic hypertension.     

Cerebral arterial responses to induced hypertension following subarachnoid hemorrhage in the monkey.

Regional cerebral blood flow (rCBF), angiographic cerebral arterial caliber, and cerebrospinal fluid (CSF) pressure were measured in rhesus monkeys to determine the effect of experimentally induced subarachnoid hemorrhage (SAH) on cerebral arterial responses to graded increases in blood pressure. These measurements were also performed in a control group of monkeys subjected to a mock SAH by injection of artificial CSF into the cerebral space. Before subarachnoid injection of blood or artificial CSF, graded increases in mean arterial blood pressure (MABP) to a level 40% to 50% above baseline values had no effect on rCBF. The major cerebral arteries constricted and CSF pressure remained unchanged. Similar responses were observed after injections of artificial CSF. When MABP was increased in animals that had been subjected to subarachnoid injection of blood, rCBF increased and was associated with dilatation of the major cerebral arteries and moderate increases in CSF pressure. These results demonstrate that cerebral arterial responses to increases in blood pressure may be abnormal in the presence of subarachnoid blood. The manner in which abnormal cerebral arterial reactivity, changes in blood pressure, and vasospasm combine to determine the level of cerebral perfusion following SAH is postulated.     

Radial to femoral arterial blood pressure differences during liver transplantation

This observational study compared femoral and radial arterial blood pressure in 72 patients undergoing liver transplant surgery. Simultaneous femoral and radial arterial blood pressures, cardiac index, core temperature and vasoconstrictor therapy were recorded at seven time points during the operation. No significant differences between radial and femoral pressures were found at the start of surgery. Femoral and radial systolic arterial blood pressures were statistically significantly different during liver reperfusion (mean (SD) arterial pressure = 92 (22) mmHg vs. 76 (22) mmHg, p < 0.01). Mean arterial blood pressures showed no statistically significant differences throughout the study. Vasoconstrictor drug administration was associated with a larger systolic pressure difference between femoral and radial arteries (28 (24) mmHg in patients being given vasoconstrictor drugs vs. 9 (19) mmHg in patients not needing vasoconstrictors during reperfusion, p < 0.001). In conclusion, differences in systolic arterial blood pressure occur between femoral and radial arterial monitoring sites during liver reperfusion, and in particular in patients being given vasoconstrictor therapy. Thus, if femoral arterial monitoring is not available, clinicians should rely on mean rather than systolic arterial pressure measurements from a radial artery catheter during liver transplantation.     

In pursuit of the best candidates and procedures for penile revascularization

Coronary bypass surgery to provide better blood flow to deficient areas of the heart is commonplace; the arteries of the heart in which blockage occurs are relatively large, and rerouting of blood is readily accomplished. In the penis, the internal pudendal system that provides arterial inflow can be easily bypassed when injury to a large vessel is the cause of erectile dysfunction. In the great majority of cases of penile arterial disruption, however, large-vessel disease cannot be demonstrated; the problem of low arterial flow originates within the corpora cavernosa, in the so-called helicine arteries. These arteries are very small, and are inaccessible unless the spongy erectile tissue of the corpora cavernosa is violated. In recent years, modest success has been reported in revascularizing the smaller arteries of the penis. The expert panelists in this symposium discuss the indications for such revascularization procedures, compare their techniques, and review the success rate in their work.     

Haemodialysis access-induced distal ischaemia (HAIDI) is caused by loco-regional hypotension but not by steal

ObjectivesSome haemodialysis patients with an arteriovenous fistula (AVF) suffer from chronic hand ischaemia (haemodialysis access-induced distal ischaemia, HAIDI). This overview discusses pathophysiological mechanisms of chronic HAIDI with emphasis on the role of steal and loco-regional hypotension.Materials and methodsThe literature obtained from Medline and Google using various terms including steal and hand ischaemia was studied for clues on pathophysiology of hand ischaemia in the presence of an AVF.ResultsConstructing an arteriovenous anastomosis as in a haemodialysis access leads to augmented blood flows in arm arteries. Due to increased shear stress, these arteries will remodel while hand perfusion pressures are maintained. However, arteries of some dialysis patients with diabetes mellitus and/or severe arteriosclerosis demonstrate insufficient remodelling leading to a gradual loss of perfusion pressures towards the periphery. A blood pressure drop associated with turbulent flow at the arteriovenous anastomosis intensifies the distal hypotension. By contrast, steal (reversal of blood flow) may reflect an upstream arterial stenosis and patent collaterals but its presence has no pathophysiological significance related to hand ischaemia.ConclusionHAIDI is caused by too low forearm and hand blood pressures. Therapy should focus on attenuating the loss of arterial pressure including optimalisation of inflow arteries and/or ligation of the AVF’s venous side branches. Surgery aimed at access flow reduction or distal revascularisation is only indicated if these measures fail.     

Natural history of atherosclerotic renal artery stenosis associated with aortic disease

The natural history of atherosclerotic renal artery stenosis has not been well defined, particularly when discovered in conjunction with aortic disease requiring correction. To better define the natural history of such lesions, 194 sequential aortograms in 48 patients were studied to define predictive criteria for stenoses at risk for progression. Sixty-six unsuspected atherosclerotic renal arterial stenoses were identified on the initial aortograms. Disease progressed in 42 arteries (53%), 14 bilateral and 28 unilateral. Seven arteries developed occlusion. All had stenoses averaging 80% (range 61% to 94%) noted on the most recent aortogram preceding occlusion. Risk factors including smoking, diabetes mellitus, elevated serum lipids, coronary artery disease, peripheral arterial disease, or change in blood pressure or creatinine, did not correlate with degree or rate of progression of the renal artery stenosis. A difference in kidney size, although varying inversely with degree of stenosis, was not a statistically significant marker of disease progression. This analysis suggests that identification of renal arterial stenoses that will progress is best determined by sequential aortography. Highly stenotic vessels are more prone to occlude than those less stenotic. Consequently, individuals with preocclusive lesions should benefit from prophylactic renal revascularization during aortic reconstruction.     

Combined carotid and coronary disease--a conservative strategy

The optimal approach to patients undergoing coronary bypass surgery for coronary artery disease with coexisting carotid disease is controversial. To determine the best approach to these patients, we screened carotid arteries in patients undergoing coronary artery bypass preoperatively with noninvasive ultrasonic duplex scanning. No correlation was noted between stroke and asymptomatic carotid disease in patients undergoing coronary revascularization. Prospective application of this finding in 2251 patients has yielded a very low incidence of perioperative stroke. We concluded that asymptomatic carotid arterial disease is not a significant risk to patients undergoing cardiopulmonary bypass and should be managed conservatively.