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PubMed2000

Calcification of the aortic arch: risk factors and association with coronary heart disease, stroke, and peripheral vascular disease.

CONTEXT: Calcium deposits in coronary and extracoronary arterial beds may indicate the extent of atherosclerosis. However, the incremental predictive value of vascular calcification, beyond traditional coronary risk factors, is not clearly established. OBJECTIVE: To evaluate risk factors for aortic arch calcification and its long-term association with cardiovascular diseases in a population-based sample. DESIGN AND SETTING: Cohort study conducted at a health maintenance organization in northern California. PARTICIPANTS: A total of 60,393 women and 55,916 men, aged 30 to 89 years at baseline who attended multiphasic health checkups between 1964 and 1973 and for whom incidence of hospitalizations and/or mortality data were ascertained using discharge diagnosis codes and death records through December 31, 1997 (median follow-up, 28 years). MAIN OUTCOME MEASURE: Hospitalization for or death due to coronary heart disease, ischemic stroke, hemorrhagic stroke, or peripheral vascular disease, as associated with aortic arch calcification found on chest radiograph at checkup from 1964-1973. RESULTS: Aortic arch calcification was present in 1.9% of men and 2.6% of women. It was independently associated with older age, no college education, current smoking, and hypertension in both sexes, but it was inversely related to body mass index and family history of myocardial infarction. In women, aortic arch calcification was also associated with black race and elevated serum cholesterol level. After adjustment for age, educational attainment, race/ethnicity, cigarette smoking, alcohol consumption, body mass index, serum cholesterol level, hypertension, diabetes, and family history of myocardial infarction, aortic arch calcification was associated with an increased risk of coronary heart disease (in men, relative risk [RR], 1.27; 95% confidence interval [CI], 1.11-1.45; in women, RR, 1. 22; 95% CI, 1.07-1.38). Among women, it was also independently associated with a 1.46-fold increased risk of ischemic stroke (95% CI, 1.28-1.67). CONCLUSION: In our population-based cohort, aortic arch calcification was independently related to coronary heart disease risk in both sexes as well as to ischemic stroke risk in women. JAMA. 2000;283:2810-2815

Adult↗
PubMed2002

Pulmonary arterial wall distensibility assessed by intravascular ultrasound in children with congenital heart disease: an indicator for pulmonary vascular disease?

BACKGROUND: Both pulmonary hypertension and pulmonary overflow are associated with functional and structural changes of the pulmonary arterial wall. Current techniques to evaluate the pulmonary vasculature neglect the pulsatile nature of pulmonary flow. STUDY OBJECTIVES: To determine whether the dynamic properties of the pulmonary arterial wall are altered in patients with abnormal pulmonary hemodynamics due to congenital heart defects, and whether these changes are associated with the progression of pulmonary vascular disease (PVD). PATIENTS AND METHODS: In 43 children with PVD due to congenital heart defects and 12 control subjects, pulmonary arterial pulsatility (the relative increase in vessel area during the cardiac cycle) and distensibility (the inverse of the stress/strain elastic modulus) were determined with intravascular ultrasound. Results were correlated with clinical and hemodynamic parameters. RESULTS: Pulsatility correlated with pulmonary pulse pressure (p < 0.001), pulmonary-to-systemic vascular resistance ratio (PVR/SVR) [p = 0.001], and hemoglobin concentration (p = 0.01). However, when corrected for these variables, pulsatility did not differ between patients and control subjects. In contrast, arterial wall distensibility decreased with the severity of PVD and correlated independently with pulmonary-to-systemic arterial pressure ratio (p < 0.001) and PVR/SVR (p = 0.03), and with hemoglobin concentration (p < 0.01). Adjusted for hemodynamic variables, distensibility was still decreased in patients with PVD compared to control subjects. CONCLUSIONS: These results demonstrate that pulmonary arterial wall distensibility is progressively decreased in PVD; moreover, this decreased distensibility is, in part, related to increased distending pressure as a result of pulmonary hypertension but also, in part, to stiffening of the arterial wall during the disease process. Arterial wall distensibility may be of additional value in the evaluation of pulmonary vasculature and ventricular workload.

Adolescent↗
PubMed1999

Increased expression of mast cell chymase in the lungs of patients with congenital heart disease associated with early pulmonary vascular disease.

The molecular mechanism involved in pulmonary vascular disease (PVD) associated with congenital heart disease (CHD) remains uncertain. Evidence suggesting that angiotensin converting enzyme plays an important role in pulmonary vascular pathology led us to hypothesize that mast cell chymase, another angiotensin I converting enzyme, also had the potential to contribute to the development of PVD in CHD. Twenty-three patients 3 mo to 45 yr of age with atrial or ventricular or both septal defects with increased pulmonary arterial blood flow and pressure, with pulmonary vascular resistance ranging from 1.3 to 8.1 units/m(2), were studied. Mast cells and mast cell chymase were immunohistochemically identified in the lung biopsy tissues obtained during corrective surgery. There was a significant difference in numbers of total mast cells between patients (n = 23) and control subjects (n = 10) with normal pulmonary circulation (p < 0.01). Moreover, chymase-containing mast cells in the lung tissues of patients with CHD showed striking differences from those of control subjects. In the patients, 72% of lung mast cells contained chymase, compared with only 15% in control subjects (p < 0.0001). Chymase-containing mast cells predominantly appeared in the media and adventitia of vessel walls. Importantly, angiotensin II was immunohistochemically detected in perivascular lesions where chymase was present, but not in the lesions where chymase was sparsely seen. Furthermore, the number of chymase-containing mast cells was correlated with pulmonary vascular resistance (r = 0.64). These findings suggest a possible role of mast cell chymase in the development of early-stage PVD in patients with CHD.

Adult↗
PubMed1999

Extra-virgin olive oil increases the resistance of LDL to oxidation more than refined olive oil in free-living men with peripheral vascular disease.

Patients with peripheral vascular disease (Fontaine stage II) are characterized by ischemia of the lower extremities, atherosclerosis and alteration of blood coagulation and fibrinolysis. A randomized, two-period, crossover design was used to compare the effects of extra-virgin (VO) and refined olive (RO) oils on plasma lipids and lipoprotein composition and LDL oxidation susceptibility in free-living men with peripheral vascular disease. The oils differed in their antioxidant profile (alpha-tocopherol: 300 vs. 200 mg/kg; phenolic compounds 800 vs. 60) and concentration but not in their fatty acid composition. Subjects were randomly assigned to two groups. The first group (n = 12) received VO with which to freely cook all meals for 3 mo, followed by a 3-mo wash-out period; they then received RO for the final 3 mo. The second group (n = 12) consumed the oils in the opposite order. Energy, fat, polyunsaturated fatty acids (PUFA) and alpha-tocopherol intakes were not different when patients consumed the two oils. Profiles of the major fatty acids in plasma and LDL were not different after consumption of VO and RO. The slope of the line for LDL oxidation vs. the line for copper concentration was significantly higher after the intake of RO than after the intake of VO. Total LDL taken up by macrophages was significantly greater when the men consumed RO rather than VO. We suggest that antioxidants present in VO may protect LDL against oxidation more than does RO in men with peripheral vascular disease.

Aged↗
PubMed2006

Mammography as a screening tool for peripheral vascular disease.

BACKGROUND: Peripheral vascular disease (PVD) is a progressive and debilitating disease often diagnosed only when patients become symptomatic. Currently there are no widespread screening tests available for the early detection of PVD. Patients with diabetes and coronary artery disease are known to have a higher incidence of PVD. Prior studies have indicated that benign vascular calcifications seen on routine screening mammogram are more prevalent in women with diabetes and coronary artery disease. The same association has not been shown for women with PVD. The purpose of this study was to identify an association between benign vascular calcifications identified on mammography and PVD. If such an association exists then screening mammography, already widely used as a screening tool for breast cancer, may identify women at high risk for PVD. METHODS: To determine the incidence of vascular calcifications in our general screening population we prospectively evaluated consecutive routine screening mammograms for the presence of benign vascular calcifications. We then identified a population of women with PVD by using a computerized database maintained by the Division of Vascular Surgery. The population of women identified with PVD was categorized further to identify those women who had received routine screening mammogram within our hospital system. These mammograms were reviewed retrospectively with particular attention to the presence of vascular calcifications. All mammograms were reviewed by our dedicated mammographers. Statistical analysis of the study group using the chi-square test was performed to determine the association of PVD and mammographic vascular calcifications. RESULTS: Prospective evaluation of 645 women undergoing consecutive routine screening mammography identified 123 (19%) with benign vascular calcifications. By using our PVD computerized database between the years 2002 and 2004 we identified 763 women with PVD. Of this group only 121 (15%) had undergone a routine screening mammogram in our hospital system. These mammograms were reviewed retrospectively by the same group evaluating the screening mammograms. On evaluation vascular calcifications were identified in 42% (51 of 121) of these women with PVD. Statistical analysis was performed using the chi-square test, odds ratio, and relative risk. A highly significant association was identified between PVD and the presence of mammographic vascular calcifications (P > .001). With a confidence interval of 95% the presence of benign vascular microcalcifications on routine screening mammogram identifies a significant risk for PVD with an odds ratio of 3.06. We showed through our analysis that women with calcifications are 2.19 times more likely to have PVD if microcalcifications are present. By using vascular calcifications identified on screening mammography as a means to identify women with PVD the sensitivity and specificity are 42% and 80%, respectively. The positive predictive value and the negative predictive value are 29% and 88%, respectively, with an accuracy of 75%. CONCLUSIONS: This initial study indicates that the presence of vascular calcifications identified on routine screening mammogram is significantly higher in women with PVD and the lack of vascular calcifications on screening mammography correlates well with a negative history of PVD. We have identified a significant association with PVD and vascular calcifications in our patient population. Further studies are indicated to determine if screening mammography may become a widespread inexpensive screening tool to identify women at risk for PVD. Additional studies are underway at our institution to evaluate the association of PVD, diabetes and coronary artery disease, and vascular calcifications identified on routine screening mammography.

Adult↗
PubMed2001

Gene transfer therapy in vascular diseases.

Somatic gene therapy of vascular diseases is a promising new field in modern medicine. Recent advancements in gene transfer technology have greatly evolved our understanding of the pathophysiologic role of candidate disease genes. With this knowledge, the expression of selective gene products provides the means to test the therapeutic use of gene therapy in a multitude of medical conditions. In addition, with the completion of genome sequencing programs, gene transfer can be used also to study the biologic function of novel genes in vivo. Novel genes are delivered to targeted tissue via several different vehicles. These vectors include adenoviruses, retroviruses, plasmids, plasmid/liposomes, and oligonucleotides. However, each one of these vectors has inherent limitations. Further investigations into developing delivery systems that not only allow for efficient, targeted gene transfer, but also are stable and nonimmunogenic, will optimize the clinical application of gene therapy in vascular diseases. This review further discusses the available mode of gene delivery and examines six major areas in vascular gene therapy, namely prevention of restenosis, thrombosis, hypertension, atherosclerosis, peripheral vascular disease in congestive heart failure, and ischemia. Although we highlight some of the recent advances in the use of gene therapy in treating vascular disease discovered primarily during the past two years, many excellent studies published during that period are not included in this review due to space limitations. The following is a selective review of practical uses of gene transfer therapy in vascular diseases. This review primarily covers work performed in the last 2 years. For earlier work, the reader may refer to several excellent review articles. For instance, Belalcazer et al. (6) reviewed general aspects of somatic gene therapy and the different vehicles used for the delivery of therapeutic genes. Gene therapy in restenosis and stimulation of angiogenesis in the cardiac muscle are discussed in reviews by several investigators (13,26,57,74,83). In another review, Meyerson et al. (43) discuss advances in gene therapy for vascular proliferative disorders and chronic peripheral and cardiac ischemia.

Animals↗
PubMed1995

Surgical therapy for coronary artery disease among patients with combined coronary artery and peripheral vascular disease.

BACKGROUND: Among patients with combined coronary artery and peripheral vascular disease, long-term benefits of surgical therapy compared with medical therapy for coronary artery disease are unknown. METHODS AND RESULTS: Using prospectively collected data from the Coronary Artery Surgery Study registry, we performed a retrospective cohort analysis of 1834 patients (mean age, 56 years; 20% women) with both coronary artery and peripheral vascular disease and evaluated their long-term outcomes. Of these patients, 986 received (nonrandomly) coronary artery bypass graft surgery, and 848 were treated medically. Perioperative mortality was 4.2% (2.9% in the absence of peripheral vascular disease; P = .02). In a mean follow-up period of 10.4 years, 1100 deaths occurred (80% due to cardiovascular causes). For the surgical group, 4-, 8-, 12-, and 16-year estimated probabilities of survival were 88%, 72%, 55%, and 41%, respectively, and 73%, 57%, 44%, and 34%, respectively, for the medical group (P < .0001). Multivariate analysis demonstrated that type of therapy was independently associated with survival (P = .0001; chi 2 = 15.34). Subgroup analysis suggested that benefits of surgical treatment on survival were limited to patients with three-vessel coronary artery disease and were inversely related to ejection fraction. Survival free of death or myocardial infarction was also significantly better among the surgical group. Type of therapy was significantly associated with occurrence of late events (P = .01; chi 2 = 6.55). Subgroup analysis again demonstrated that beneficial effects of surgery were limited to patients with three-vessel coronary artery disease and were inversely related to ejection fraction. CONCLUSIONS: Surgical treatment provides long-term benefit for certain subgroups of patients with combined coronary artery and peripheral arterial vascular disease.

Coronary Disease↗
PubMed2004

Depression and vascular disease: what is the relationship?

BACKGROUND: the 'vascular depression' hypothesis proposes that vascular disease predisposes to, precipitates or perpetuates depression, and this proposal has stimulated further research into the relationship of depression to vascular disease. METHODS: We investigated the nature of the relationship between depression and vascular diseases by reviewing epidemiological, clinical, neuroimaging and neuropathology studies which have reported on the relationship of depression to coronary artery disease, stroke disease, alterations in blood pressure, vascular dementia, diabetes mellitus and cholesterol levels and by reviewing potential mechanisms by which depression could be associated with vascular diseases. RESULTS: there is abundant and increasing evidence from these different lines of research that depression has a bidirectional association with vascular diseases and plausible mechanisms exist which explain how depression might increase these vascular diseases and vice versa. LIMITATIONS: this was not a systematic review and so not every report of relevance has been included. CONCLUSIONS: depression has a clear bidirectional relationship with vascular diseases. Further study is needed to clarify the mechanisms involved and to investigate the benefits of conventional and novel treatments for vascular diseases in depressive illness.

Blood Pressure↗
PubMed2004

Predictive power of cardiovascular risk factors for detecting peripheral vascular disease.

OBJECTIVES: Peripheral vascular disease (PVD) is underdiagnosed in primary care due to the absence of established criteria to warrant diagnostic testing. Our goal was to establish a risk factor hierarchy to enable earlier diagnosis of PVD. METHODS: Data sets of 142 patients with abnormal ankle brachial indices (ABI) were randomly selected from our patient database to determine the prevalence of specific cardiovascular risk factors and demographic data. An ABI score < 0.90 is diagnostic of PVD. Patients were stratified into mild (0.75-0.89), moderate (0.50-0.74), and severe disease (< 0.50). RESULTS: Mean age was 69 +/- 9.9, ABI 0.65 +/- 0.16. Risk factor prevalence: diabetes, 42%; hypertension, 87%; tobacco use, 34%; hyperlipidemia, 53%; obesity, 24%; cardiovascular disease (CVD), 69%; stroke, 15%. Total risk factors per patient v = 3.2 +/- 1.3. Disease severity stratifications: mild, n = 46 (age v = 68.6 +/- 10.4, ABI v = 0.82 +/- 0.05); moderate, n = 72 (age v = 69.9 +/- 9.4, ABI v = 0.62 +/- 0.07); severe, n = 24 (age v = 67.5 +/- 10.9, ABI v = 0.40 +/- 0.06). Independent variable mean differences: hypertension-CVD (P = 0.0002); CVD-hyperlipidemia (P = 0.002); hyperlipidemia-diabetes (P = 0.0008); diabetes-tobacco use (P = 0.001); tobacco use-obesity (P = 0.0003); obesity-stroke (P = 0.05). Independent variable mean differences were significant across disease severity (P < 0.00001). CONCLUSIONS: Our study establishes the following hierarchy of cardiovascular risk factors as predictors of PVD: hypertension, cardiovascular disease, hyperlipidemia, diabetes, tobacco use, obesity, stroke.

Aged↗
PubMed2006

Peripheral vascular disease: diagnosis and treatment.

Peripheral vascular disease is a manifestation of systemic atherosclerosis that leads to significant narrowing of arteries distal to the arch of the aorta. The most common symptom of peripheral vascular disease is intermittent claudication. At other times, peripheral vascular disease leads to acute or critical limb ischemia. Intermittent claudication manifests as pain in the muscles of the legs with exercise; it is experienced by 2 percent of persons older than 65 years. Physical findings include abnormal pedal pulses, femoral artery bruit, delayed venous filling time, cool skin, and abnormal skin color. Most patients present with subtle findings and lack classic symptoms, which makes the diagnosis difficult. The standard office-based test to determine the presence of peripheral vascular disease is calculation of the ankle-brachial index. Magnetic resonance arteriography, duplex scanning, and hemodynamic localization are noninvasive methods for lesion localization and may be helpful when symptoms or findings do not correlate with the ankle-brachial index. Contrast arteriography is used for definitive localization before intervention. Treatment is divided into lifestyle, medical, and surgical therapies. Lifestyle therapies focus on exercise, smoking cessation, and dietary modification. Medical therapy is directed at reducing platelet aggregation. In addition, patients with contributing disorders such as hypertension, diabetes, and hyperlipidemia need to have these conditions managed as aggressively as possible. Surgical therapies include stents, arterectomies, angioplasty, and bypass surgery.

Constriction, Pathologic↗
PubMed1989

Noninvasive and angiographic evaluation of coronary artery disease in patients with peripheral vascular disease.

The accuracy of exercise testing for detection of coronary artery disease in a population with a high incidence of claudication was evaluated in 58 consecutive patients with abdominal aortic aneurysms or lower extremity occlusive disease. Each patient was evaluated by history and physical examination, symptom-limited testing with exercise treadmill, arm ergometry and exercise radionuclide ventriculography. An algorithm was designed that retrospectively examined the results of each test in a stepwise fashion to simulate a clinical decision-making process. The results of the clinical examination, each of the exercise tests and the noninvasive diagnostic algorithm were compared with the results of coronary arteriography. The predictive accuracy of the clinical evaluation was 36%, treadmill stress testing 57%, treadmill stress plus arm ergometry 74%, exercise radionuclide ventriculography 57% and the noninvasive diagnostic algorithm 89%. When discriminant analysis was applied to all of the exercise variables, no individual test improved the accuracy of the noninvasive diagnostic algorithm. When the analysis considered only individual variables without the algorithm, the model correctly classified only 67% of the patients. Thus, accurate noninvasive evaluation of coronary artery disease is possible in patients with severe peripheral vascular disease when care is taken to design exercise protocols that allow adequate stress on the cardiovascular system.

Adult↗
PubMed2001

[Can blood homocysteine explain the family history of vascular diseases?].

INTRODUCTION AND AIMS: Family history of vascular disease is an important risk factor for vascular disease, independent of conventional risk factors. Homocysteinemia, a newly defined risk factor, is caused by genetics, such as cystathionine beta synthase deficiencies, and metabolic deficiencies. With the present work we intend to study the influence of family history of vascular disease in homocysteinemia. METHODS: We studied 204 normal persons (153 males), average age 38.7 +/- 10.9 years, in terms of family history of vascular disease (death due to myocardial infarction or a stroke), conventional risk factors, routine laboratory tests, fasting homocysteinemia and after oral methionine loading (0.1 g/Kg body weight). We compared laboratory results, conventional risk factors and homocysteinemia levels in persons with and without a family history of vascular disease. We performed covariance analysis to evaluate, in a multivariate model, factors that were related to basal or after methionine loading homocysteinemia. RESULTS: 35% of persons presented a family history of vascular disease (FHVD). Persons with FHVD presented higher age (45.6 +/- 8.9 versus 35.0 +/- 10.1, p < 0.001), and higher prevalence of hypertension (p = 0.002), dyslipidemia (p = 0.001), obesity (p = 0.03), and physical inactivity (p = 0.03). They presented a tendency, without statistical significance, to have a higher prevalence of diabetes and of hyperhomocysteinemia, and to present higher levels of basal and afterload homocysteinemia. Performing covariance analysis, basal homocysteinemia did not present any relation to FHVD. After methionine load homocysteinemia was strongly influenced by basal homocysteinemia (p = 0.0000), and significantly related to FHVD (p = 0.039). CONCLUSIONS: Homocysteinemia cannot explain most of the risk of family history of vascular disease, not explained by conventional risk factors. The only significant relationship between homocysteinemia and FHVD was observed with afterload homocysteinemia in the multivariate model. FHVD is clearly related to conventional risk factors.

Adult↗
PubMed1994

Renal artery stenosis: a common and important problem in patients with peripheral vascular disease.

OBJECTIVE: To study the prevalence, severity, vascular risk factors, and clinical implications of renal artery stenosis in patients with peripheral vascular disease. DESIGN: Cross-sectional study of consecutive patients who were electively referred from the department of vascular surgery for lower limb digital subtraction angiography. SETTING: St. George's Hospital, London, United Kingdom. SUBJECTS: One hundred twenty-seven patients presenting with intermittent claudication or lower limb ischemic ulceration. MAIN OUTCOME MEASURES: Prevalence and clinical importance of renal artery stenosis in patients with peripheral vascular disease adjusted for the confounding effects of age and hypertension. RESULTS: Of the 127 patients, 57 (44.9%) had renal artery disease, of whom 22 (17.3%) had mild disease, 20 (15.7%) had severe disease, and 15 (11.8%) had bilateral renal artery stenosis. There was a significant positive relationship between the presence of renal artery stenosis and the severity of peripheral vascular disease (p = 0.00015). The risk of having renal artery stenosis was nearly four times greater in those with three to four vessels affected and nearly seven times greater in those with five or more vessels affected as compared with those with a milder degree of peripheral vascular disease (one or two vessels affected). This association persisted when the confounding effect of age and hypertension was accounted for. Six patients (31.6%) with renal artery stenosis who underwent revascularization for peripheral vascular disease died during the early postoperative period of cardiac or renal complications. None of the patients with normal renal arteries who had similar surgery developed postoperative complications (p = 0.005). CONCLUSIONS: Renal artery stenosis is a common independent feature in patients with peripheral vascular disease, and its prevalence increases with the increasing severity of the peripheral vascular disease. The postoperative risk following revascularization for peripheral vascular disease appears to be greater in those patients with renal artery stenosis. All patients studied with digital subtraction angiography for peripheral vascular disease should have an aortic flush performed to image the renal arteries. This information may be used to identify those patients likely to develop postoperative complications during peripheral revascularization.

Aged↗
PubMed1997

Factors increasing the risk of allograft vascular disease in heart transplant recipients.

Allograft vascular disease is the major cause of late cardiac graft failure. A multifactorial etiopathogenesis is supposed. Our study investigated factors associated with allograft vascular disease occurrence. After stratifying our series on the basis of potential risk factors, we calculated allograft vascular disease incidence rate in 267 grafts from 258 patients who underwent transplant between November 1985 and August 1996. Chi-square test was used for the identification of univariate risk factors to be included in a multivariate model. Multivariate analysis was based on a Poisson model. Seventy of the 267 grafts (26.2%) were diagnosed with allograft vascular disease. Heart disease other than idiopathic dilated cardiomyopathy, donor's age, number of mismatches for HLA-B = 2, presence of systo-diastolic hypertension, number of acute rejection positive endomyocardial biopsies > or = 7 and the association of human Cytomegalovirus and hepatitis C virus infections proved to be univariate risk factors, and were included in the Poisson multivariate model. The association of Cytomegalovirus and hepatitis C infections multiplied allograft vascular disease incidence rate by 3.9, systo-diastolic hypertension by 2.2, occurrence of 2 HLA-B mismatches by 2, a high number (> or = 7) of acute rejection positive-endomyocardial biopsies by 1.8, and heart disease other than idiopathic dilated cardiomyopathy by 1.8. The association of human Cytomegalovirus and hepatitis C virus infections, of HLA-B mismatches, of acute rejection-positive endomyocardial biopsies, as well as post-transplantation hypertension and native heart disease other than idiopathic dilated cardiomyopathy, proved to be positively associated with an increased risk of allograft vascular disease. Given the concordance of our data with those of numerous prior series, we are going to adopt a special surveillance angiographic protocol for patients with these factors.

Adolescent↗
PubMed1980

Vasoconstriction and increased blood pressure in the development of accelerated vascular disease.

The pathogenesis of acute vascular lesions has been studied in two types of accelerated vascular disease. Firstly, vascular lesions were induced by a short-term (2 h) infusion of angiotensin II. Low doses of angiotensin II caused only a slight increase in blood pressure and non-destructive lesions. High doses caused a significant elevation of blood pressure and destructive vascular lesions. Secondly, in renovascular hypertension, renal vascular disease was induced by the removal of the stenosing clip from the renal artery. Incidence and severity of destructive vascular lesions were correlated with the calculated gradient between the pressure before and beyond the stenosis. Anaesthesia had a protective effect on the development of destructive vascular lesions in both models. Obviously, this effect is not related to a reduction of the systemic pressure, but rather to the suppression of abnormal vascular tone, characterized by focal constriction alternating with overdilation. Vasomotor changes, which cause a local overdilation, may be responsible for destructive vascular lesions even at normal to subnormal blood-pressure values. Destructive vascular lesions occur as a result of the exceeding of a critical wall tension. The necrosis of medial smooth-muscle cells in non-destructive lesions may be explained by an excessive contraction, which "surpasses" the metabolic capacity of the cells.

Anesthesia↗
PubMed1982

Influence of ischemic heart disease on early and late mortality after surgery for peripheral occlusive vascular disease.

The association of coronary artery disease and peripheral vascular disease was studied to determine the influence of coronary artery disease on early and late mortality rates after surgical reconstruction for peripheral occlusive vascular disease and abdominal aortic aneurysm. Between January 1976 and December 1978, 161 consecutive patients underwent surgery for peripheral occlusive vascular disease or abdominal aortic aneurysm. The patients were 35-86 years old (mean 63.3 years). Thirty patients (18.6%) had abdominal aortic aneurysmectomies, 59 (36.7%) had aortoiliac reconstruction with or without femoropopliteal bypass and 72 (44.7%) had procedures for femoropopliteal disease. The 30-day hospital mortality rate was 6.7% for abdominal aortic aneurysm (n = 2), 3.4% for aortoiliac reconstruction (n = 2) and 1.4% for femoropopliteal procedures (n = 1). Myocardial infarction was the cause of 40% (n = 2) of the early postoperative deaths. The early mortality rate of patients with a history of angina or myocardial infarction was 5.4% (two of 37), while the early mortality rate among patients without such a history was 2.4% (three of 124). The mortality rate from myocardial infarction during the late observation period was 65% (15 of 23). The freedom from myocardial infarction was 90% at 30 months and 75% at 60 months. The overall survival rate was 87% at 30 months and 71% at 60 months. The late mortality rate was assessed with respect to various risk factors: coronary artery disease (n = 31), previous vascular surgery (n = 19) and diabetes mellitus (n = 7). Among the 63 patients who had one or more of the risk factors, the late cardiac mortality rate was 20.6% (n = 13). The late cardiac mortality rate for for the 78 patients with no risk factors was 3.8% (n = 3). An additional 10 patients with previous coronary artery bypass (n = 9) or angiography (n = 1) experienced no early or late mortality. The freedom from late cardiac death at 60 months was 71% for the high-risk group (63% patients) and 96% for the low-risk group. The study shows that coronary artery disease is a major determinant of both early and late mortality after arterial reconstruction. The status of the myocardium should be assessed before peripheral vascular surgery, as selective myocardial revascularization may improve survival in these patients.

Adult↗