Occlusive Coronary Artery Disease Research Articles

Gene Polymorphisms of Homocysteine Metabolism-Related Enzymes in Chinese Patients with Occlusive Coronary Artery or Cerebral Vascular Diseases

The mutations in homocysteine (Hcy) metabolism-related enzyme genes including methylenetetrahydrofolate reductase (MTHFR) C677T, cystathionine β-synthase (CBS) 844ins68, and methionine synthase (MS) A2756G have been identified as genetic risk factors for thromboembolic events. It has been noticed that these gene mutations have heterogeneous distributions among different ethnic groups or geographic areas. The data on the prevalence of the gene mutations in Chinese population is not yet available. In the present study, we have investigated the frequency of the MTHFR C677T, CBS 844ins68, and MS A2756G mutations in 102 patients with ischemic stroke (IS), 73 patients with myocardial infarction (MI) and 100 healthy controls. The distributive frequencies of the gene variations are as follows: In the IS, MI and control groups, the mutant homozygote for MTHFR C677T is 15 (14.7%), 8 (11.7%) and 16 (16.0%), respectively, and the T allele frequency is 37.7%, 33.6% and 39.5%, respectively; the heterozygote for CBS 844ins68 is 1 (1.0%), 1 (1.4%) and 5 (5.0%), respectively; the heterozygote for MS A2756G is 18 (17.6%), 14 (19.2%) and 17 (17.0%), and the G allele frequency is 8.8%, 11.0% and 9.5%, respectively. The carrier of both MS A2756G and MTHFR C677T (combined mutations) is 14 (12.7%), 8(11.0%) and 12(12.0%), respectively. There is no statistically significant difference between the patient groups and the control group in the frequencies of these single mutation or combined mutations. The heterozygosity of CBS 844ins68 yields an odds ratio (OR) of 0.19 (95% confidence interval (CI) 0.02–1.43) for IS and 0.26 (95% CI 0.03–2.31) for MI. The T allele of MTHFR C677T yields an OR of 0.93 for IS (95% CI 0.62–1.39) and 0.77 for MI (95% CI 0.50–1.21). The G allele of MS A2756G yields an OR of 0.92(95% CI 0.47–1.81) for IS and 1.17 (95% CI 0.58–2.37) for MI. Our results suggest that neither single mutation nor combined mutations in MTHFR C677T, CBS 844ins68 and MS A2756G represent an independent risk factor for increasing IS and coronary artery disease risks in Chinese population. However, CBS 844ins68 may be a protective factor against vascular thromboembolic disease. The prevalence of CBS 844ins68 and MS A2756G in Chinese population is obviously lower than in Western Caucasian population.

Coronary artery disease in systemic lupus erythematosus: A review of the literature

Context: Coronary artery occlusive disease is a common though underappreciated complication of systemic lupus erythematosus (SLE), typically a disease of young women. A case of a premenopausal patient with SLE and an acute myocardial infarction is presented, and the etiology and management of coronary artery disease in SLE reviewed. Objectives: To review the incidence, risk factors, pathology and treatment of coronary artery disease in systemic lupus erythematosus. Data Sources: MEDLINE search of articles in English-language journals from 1980 to 2000. The index words “systemic lupus erythematosus” and the following co-indexing terms were used: “coronary artery disease,” “atherosclerosis,” “vasculitis,” “anticardiolipin antibodies,” “antiphospholipid syndrome.” Selection Synthesis and Abstraction: Papers identified were reviewed and abstracted by the authors with a presentation of a summary. Results: The prevalence of coronary artery disease among women with SLE between the ages of 35 and 44 years is at least 50-fold greater than among age-matched control subjects. Of these, coronary atherosclerosis accounts for the vast majority of cases; vasculitis of the coronary arteries and other causes generally believed to be more typical of SLE are comparatively rare. Conclusions: The evidence suggests that SLE is a significant risk factor for coronary atherosclerosis independent of the classic risk factors of hypertension, tobacco use, and hyperlipidemia. Semin Arthritis Rheum 30:436-443. Copyright © 2001 by W.B. Saunders Company

Anti-cholesterol antibodies (ACHA) in patients with different atherosclerotic vascular diseases and healthy individuals. Characterization of human ACHA

In animal experiments the protective role of anti-cholesterol antibodies (ACHA) in the development of atherosclerosis has been demonstrated. Despite the fact that ACHA are present in the serum of healthy humans, no data on the occurrence of these antibodies in human diseases are available. We determined serum concentrations of IgG type ACHA by an enzyme immunosorbent assay in 600 patients with atherosclerotic vascular diseases (86 patients with peripheral occlusive atherosclerosis, 146 patients with cerebrovascular diseases, 341 patients with severe coronary heart disease (CHD) who received aorto-coronary by-pass, 27 patients with myocardial infarction who did not undergo by-pass operation), in 57 patient controls (complaints of CHD, without coronarographic alterations) and in 218 healthy individuals. ACHA were present in the sera of all persons tested. No serum cofactor is needed for the binding of human ACHA to solid phase cholesterol, binding can be inhibited dose-dependently by LDL and even more strongly with LDL/VLDL preparations purified from human serum. ACHA levels were found to be considerably lower in patients with peripheral occlusive atherosclerosis and cerebrovascular diseases compared with the levels in healthy individuals. By contrast, the ACHA levels of patients with CHD were considerably higher. No differences in the IgG subclass distribution and binding efficiency of ACHA in the sera of CHD patients and controls were found. Thus, our present findings indicate that both low and high ACHA production may be associated with different atherosclerotic vascular diseases.

Coronary artery surgery for ischemic heart failure: Risks, benefits, and the importance of assessment of myocardial viability

Heart failure and left ventricular dysfunction are common and are most often caused by myocardial ischemia/infarction secondary to occlusive coronary artery disease. Although recent refinements in medical therapy have resulted in improved survival, morbidity and mortality remain high in patients with advanced heart failure. Heart transplantation remains an option for selected patients, and implantable left ventricular assist devices may soon provide another treatment strategy for such patients. However, patients with established postischemic heart failure, significant myocardial viability, and coronary artery anatomy amenable to surgical revascularization can derive significant functional and survival benefit after coronary artery surgery, albeit with an increased perioperative risk. We discuss the role of coronary artery surgery in ischemic heart failure and review the evidence for such an approach. Copyright © 2001 by W.B. Saunders Company

Copper-62-pyruvaldehyde bis(N4-methyl-thiosemicarbazone) PET imaging in the detection of coronary artery disease in humans

Background. Copper-62 (II)-pyruvaldehyde bis(N4-methyl-thiosemicarbazone) (PTSM) has been proposed for cardiac imaging with positron emission tomography (PET). This study evaluated the agreement between Cu-62-PTSM and coronary angiography in the detection of occlusive coronary artery disease. The normalcy rate for Cu-62-PTSM PET in a group of healthy volunteers was also assessed. Methods and Results. Forty-five subjects completed the study. Twenty-eight patients underwent stress technetium-99m sestamibi single photon emission computed tomography (SPECT) imaging and cardiac catheterization followed by Cu-62-PTSM rest/dipyridamole stress PET scans, and 17 volunteers underwent Cu-62-PTSM rest/dipyridamole stress PET scans. Cu-62-PTSM myocardial perfusion defects were identified in 100% of patients with 3-vessel disease (n = 8), 100% of patients with 2-vessel disease (n = 9), and 67% of patients with single-vessel disease (n = 6). When considering individual vessels, Cu-62-PTSM perfusion defects were seen in 72% of patients with occlusive disease in the left anterior descending artery territory, 67% in the left circumflex artery territory, and 60% in the right coronary artery territory, respectively. All 17 healthy volunteers had Cu-62-PTSM scans interpreted as normal, for a normalcy rate of 100%. Conclusions. Perfusion abnormalities are demonstrated by means of Cu-62-PTSM PET in 91% of patients with occlusive coronary artery disease seen at the time of cardiac catheterization, and it shows an excellent normalcy rate of 100%. (J Nucl Cardiol 2001;8:67-74.)

Estenosis preoclusiva de la arteria vertebral extracraneal. Tratamiento mediante angioplastia transluminal percutánea y colocación de endoprótesis

Atherosclerotic occlusive disease of the extracranial portion of the vertebral artery is relatively frequent and is usually related to vertebrobasilar ischemia. Due to the lack of a noninvasive diagnostic technique, at present it is often not diagnosed. Surgical treatment is difficult and risky. Percutaneous transluminal angioplasty (PTA) is only partly useful due to a high rate of restenosis. The recent development of stenting has led to an evident improvement of PTA results, reducing restenosis and offering an effective treatment with low morbidity and mortality. Sixty year old male patient, smoker and moderate drinker, who is hospitalized due to repeated ischemic strokes (cerebellar stroke in the left posterior and interior inferior cerebellar arteries, and cerebral stroke at occipito-parietal and ipsilateral capsulo-thalamic levels) in spite of antithrombotic treatment. Angiography showed: a) occlusion of the left vertebral artery; b) preocclusive stenosis of the right vertebral artery in the ostium; c) fetal origin of the right posterior cerebral artery, and d) left hypoplasic posterior communicating artery. PTA and stent placement at the right vertebral artery is performed with an excellent angiographic result, a partial recovery of neurological symptomatology and absence of new episodes of cerebral ischemia during a three-month follow-up. Percutaneous transluminal angioplasty and stent placement is an effective low morbidity-mortality treatment in occlusive atherosclerosis of the vertebral artery, although further randomized multicenter studies are required in order to validate this conclusion.

Aneurysmal and occlusive atherosclerosis of the human abdominal aorta

Purpose: The purpose of this study was to assess atherosclerotic plaque deposition and aortic wall responses in the abdominal aorta in relation to the development of aneurysmal and occlusive disease in the infrarenal aorta. Methods: Morphologic differences at five standardized locations in the infrarenal aorta in 67 pressure perfusion–fixed male cadaver aortas (aged, 41-98 years; mean, 66 years) were studied and compared with the supraceliac segment. Quantitative computer-assisted morphometry of histologic sections included measurement of plaque area, lumen area, lumen diameter, media thickness, number of medial elastic lamellae, and the area encompassed by the internal elastic lamina that best represents the artery size of each segment. The ratio of the supraceliac segment to the midabdominal segment (normally greater than 1.3) was used to define three groups: Group I (normal): ratio greater than or equal to 1.30 (n = 31); Group II (intermediate): ratio greater than or equal to 1.20 but less than 1.30 (n = 20); and Group III: ratio less than 1.20 (n = 16), which represented dilated midabdominal aortas. There was no significant difference in age among the groups. Results: Group I had minimal intimal plaque and little gross evidence of atherosclerosis. Group II had increased intimal plaque compared with Group I (P <.01) and gross evidence of atherosclerosis, which was maximally localized in the distal aorta; there was no aortic enlargement or thinning of the media underneath the plaque. Group III had more intimal plaque than Group I (P <.01) and Group II (P <.01) and was associated with localized aortic enlargement and media thinning compared with Group I (P <.05) and Group II (P <.01). Increasing intimal plaque in Group III correlated with an increase in lumen diameter (r = 0.61, P <.05), but this relationship was not significant in Group I and Group II. The aortic media in Group III had a reduced number of medial elastic lamellae, was reduced in thickness, and was more exposed to increased wall stress than the aortas in Groups I and II. Conclusion: These results suggest that there may be different local responses to atherosclerosis in the abdominal aorta in human beings. Plaque deposition associated with localized dilation, thinning of the media, and loss of medial elastic lamellae may predispose that segment of aorta to subsequent aneurysm formation. Plaque deposits without media thinning, without loss of elastic lamellae, and without artery wall dilation may predispose the aorta, in the event of continuing plaque accumulation, to the development of lumen stenosis. (J Vasc Surg 2001;33:91-6.)

Right Atrial Membrane Interfering with Insertion of Pulmonary Artery Catheter

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Plasma atherogenic markers in congestive heart failure and posttransplant (heart) patients

OBJECTIVESWe hypothesized that plasma factors important for the development of atherosclerosis play a major role in the occurrence of cardiac allograft vasculopathy (CAV).BACKGROUNDCardiac allograft vasculopathy is a major cause of death among heart transplant recipients, has a poorly understood pathogenesis and has similarities to atherosclerotic coronary disease.METHODSThe study population consisted of 93 postcardiac transplant recipients. Thirty-one patients with congestive heart failure (CHF) and 18 healthy individuals served as control subjects. Posttransplant coronary anatomy was evaluated by angiography and intravascular ultrasound. Laboratory analyses of lipids, homocysteine, vitamin B12 and folate, fibrinogen, vonWillebrand factor antigen (vWFAg) and renin were obtained on all participants.RESULTSPosttransplant patients were found to have elevated serum triglycerides, total cholesterol/high-density lipoprotein cholesterol ratio, lipoprotein (a), homocysteine, vWFAg, fibrinogen and renin and lower high-density lipoprotein cholesterol. Most of these laboratory atherogenic factors were also elevated to a similar degree in the CHF control population. Although most atherogenic markers were elevated, there was little correlation with CAV severity. Cardiac allograft vasculopathy severity varied with time after transplantation, 3-hydroxy-methyl-glutaryl-coenzyme A reductase inhibitor use and prior cytomegalovirus infection. Even within the normal range, lower RBC folate levels were associated with increased severity of CAV.CONCLUSIONSThe posttransplant course is associated with increased clinical and laboratory atherogenic factors, some of which likely contribute to the severity of coronary vasculopathy. Compared with normal control subjects, many of these markers are already increased in pretransplant CHF patients with or without occlusive coronary artery disease.

Surgical Management of Concomitant Carotid and Coronary Artery Occlusive Disease

The management of concomitant coronary and carotid disease is controversial. We report our experience of simultaneous coronary artery bypass surgery and carotid artery endarterectomy on 70 consecutive patients (34 males and 36 females) with a mean age of 68 years. The oldest patient was 91 years old. The average percent of carotid artery stenosis was 86% (range 60%–99%). The average number of grafts per patient was 3.35 (range 1–6). Two patients experienced postoperative strokes (2.86%), 1 had a perioperative infarct (1.42%), and 4 died in the hospital (5.7%). The simultaneous approach offers the advantage of shorter hospital stays, decreased anesthesia exposure, and significant cost savings. The causes of death include stroke, renal failure, and bowel infarction. This review indicates the simultaneous approach has a higher incidence of adverse outcomes compared with elective carotid endarterectomy or elective coronary artery bypass surgery. These patients, however, are at significantly higher risk due to their poor medical conditions, extensive atheromatous disease, and often emergent medical condition.

Surgical management of concomitant carotid and coronary artery occlusive disease

Surgical management of concomitant carotid and coronary artery occlusive disease

Mechanical behavior of calcified plaques: a summary of compression and stress-relaxation experiments.

This paper summarizes the results from mechanical testing of atherosclerotic plaques performed in the Cardiovascular Mechanics Laboratory and the Laboratory for Implantable Materials at UMBC. The motivation for our work is that balloon angioplasty, stenting, and roto-ablation are mechanical processes that are designed to permanently alter the shape of an occluded arterial lumen. The mechanisms of permanent plaque deformation are not known. Therefore, to study the mechanical behavior of plaques, we performed mechanical tests on atherosclerotic lesions with different compositions and investigated differences in the materials' mechanical responses. Atherosclerotic plaque specimens were subjected to two main types of loading: multiple cyclic compression and stress-relaxation. The multiple-cycle test protocol was two fifteen-cycle loading phases that were separated by a 10-15 minute unloaded "rest" period. The compressive stress-relaxation test protocol was a series of three consecutive loadings (called phases I, II, and III). Each phase consisted of a 25% compression that was achieved in less than 1 second, a 10 minute relaxation period, and a 10 minute unloaded "rest" period between loadings. In the multiple cycle compressive loading, plaques exhibited three distinct types of behavior, which corresponded to the plaque compositions. Calcified plaques showed behaviors distinct from other plaque types and healthy vessels. In contrast to the cyclic compression results, plaque types could not be distinguished solely on the basis of stress relaxation behavior. Calcified and fibrous plaques had similar behavior, and therefore histology was used for definite identification. Calcified plaques have unique mechanical properties, and therefore interventions like angioplasty, roto-ablation, and stenting may require protocols specific for calcified lesions. The optimum protocols for calcified plaques may be quite different from plaques with other compositions. It is essential to learn more about the mechanical behavior of all plaque types to increase the success rate of occlusive atherosclerosis treatments.

Serological evidence of Chlamydia pneumoniae lipopolysaccharide antibodies in atherosclerosis of various vascular regions.

The role of Chlamydia pneumoniae in the pathogenesis of atherosclerosis has so far mainly been investigated in patients suffering from coronary heart disease; the other vascular regions have virtually been ignored. The aim of this study was to carry out a statistical survey of serological markers of a C. pneumoniae infection in patients with different patterns of atherosclerosis manifestation. 340 patients were examined for the atherosclerotic alteration of peripheral arteries of the lower limbs, carotid arteries and coronary arteries by ultrasound scan and/or angiography. Immunoglobulin(Ig)G and IgA-rELISA were used to measure chlamydial lipopolysaccharide antibodies. Species determination was performed using the IgG micro-immunofluorescence test. 24.0% of atherosclerotic cases (A) and 52.3% of controls (C) were negative for C. pneumoniae lipopolysaccharide antibodies (p = 0.00002). By contrast, 45.1% of atherosclerotic cases and 16.9% of controls were positive for both IgG and IgA (p = 0.00002). The mean antibody titers of the atherosclerosis group were higher than in the control group (IgG positive xAIgG = 344, xCIgG = 272; IgG and IgA positive xAIgG = 576, xCIgG = 486 and xAIgA = 120, xCIgA = 91). Concerning atherosclerosis manifestation in various vascular regions, no significant differences were found between IgG and IgA antibody titers and prevalence. The results show that a persistent C, pneumoniae infection with evidence of lipopolysaccharide immunoglobulin G and A is equally associated with the atherosclerotic alteration of coronary arteries, carotid arteries and peripheral arterial occlusive disease, irrespective of the severity of atherosclerosis and with no predisposition to any particular vascular region.

Transcription factors and age-related decline in apolipoprotein A-I expression

Apolipoprotein (apo)A-I alone or as a component of high density lipoprotein particles has antiatherogenic properties. The age-dependent decline in abundance of this protein may underlie the higher risk for developing occlusive coronary artery disease (CAD) in older individuals. Similar to humans, expression of rat apoA-I also declines with age. Results in rats showed that levels of serum apoA-I protein, hepatic mRNA, and transcription of the gene were decreased to 39%, 18%, and 38%, respectively, in 180-day-old animals compared to those of newborn rats. These findings suggest that a nuclear mechanism(s) may account for the decline in apoA-I expression. Accordingly, we examined hepatic nuclear binding activity to four specific cis-acting elements of the rat apoA-I promoter. There were age-dependent changes of binding activity to two proximal sites, B and C, but not to the more distal elements, IRCE and A. Decreased B-site binding activity correlated with lower mRNA levels encoding the activator, HNF-3β. The age-dependent change in the pattern of binding to site C was due to a switch from the activator, HNF-4, to the repressor, ARP-1.▪In summary, the age-related decline in apoA-I expression may arise from a reduction in the activity of both cis-acting elements, B and C.—Nakamura, T., A. Fox-Robichaud, R. Kikkawa, A. Kashiwagi, H. Kojima, M. Fujimiya, and N. C. W. Wong. Transcription factors and age-related decline in apolipoprotein A-I expression. J. Lipid Res. 1999. 40: 1709–1718.

Early results of percutaneous intervention for severe coexisting carotid and coronary artery disease

Fifty-one patients with severe coexisting carotid and symptomatic coronary artery occlusive disease successfully underwent staged or simultaneous coronary angioplasty and carotid stenting. One pericardial effusion and 2 minor strokes with full recovery occurred in the hospital, but no major neurologic events, myocardial infarction, or death were observed and no repeat revascularization was required within the 30-day follow-up.

Discussion

Attempts to extract clot from an infarct-related coronary artery have underestimated the frequency and pathophysiologic significance of thrombus in acute coronary syndromes. The overwhelming body of evidence garnered over the last 20 years, especially the achievement of reperfusion (Thrombolysis In Myocardial Infarction trial grade 2 and 3 flow) with most of the newer thrombolytic agents in >80% of cases, incontrovertibly establishes a critical role for thrombus in acute occlusive coronary artery disease.

Genetic causes of mild hyperhomocysteinemia in patients with premature occlusive coronary artery diseases

Elevated plasma homocysteine is increasingly being recognized as a risk factor for coronary artery disease (CAD). Although there is general agreement on the importance of micronutrients and genetic predisposition to elevated plasma homocysteine, the exact influence of the known prevalent mutations in genes which regulate homocysteine metabolism is not clear. We studied 376 cases of individuals with premature CAD with respect to their fasting and post-methionine load (PML) total homocysteine (tHcy) concentrations. We also determined the presence or absence of the T 833C and G 919A mutations of the cystathionine- β-synthase (CBS) gene, the C 677T mutation of the methylene tetrahydrofolate reductase (MTHFR) gene, and the A 2756G transition of the B 12 dependent methionine synthase (MS) gene. Our objectives were therefore both to confirm the relationship of plasma homocysteine with premature CAD and to examine the importance of genetic influence on both fasting and PML homocysteine. Approximately 32% of the CAD patients had fasting hyperhomocysteinemia and 16% had PML hyperhomocysteinemia. Of these, 8.5% had both forms of hyperhomocysteinemia (combined hyperhomocysteinemia). The T 833C mutation in the CBS gene and the thermolabile C 677T mutation in the MTHFR gene seem to play an important role in the subset of individuals with combined hyperhomocysteinemia. The A 2756G transition in the MS gene is not associated with elevated plasma tHcy. Many cases (47%) of hyperhomocysteinemia are not associated with micronutrient deficiencies, impaired renal function, and/or currently known genetic mutations. Further work is needed to study whether unknown mutations, particularly those residing in the intronic sequences of the genes involved in homocysteine metabolism, other environmental factors, or interaction of gene, nutrient, and environmental factors may be the cause of currently unexplained cases of mild hyperhomocysteinemia.

Homocyst(E)Ine and Heart Disease: Pathophysiology of Extracellular Matrix

Occlusive coronary artery disease is an important factor of cardiovascular morbidity and mortality. The rupture of the thin fibrous cap of the atheroma may be one of the causes of acute coronary syndrome, however, the mechanism of formation of fibrous plaque are poorly understood. Elevation of plasma homocysteine, hyperhomocystinemia, H(e), has emerged as an independent risk factor for hypertension and fibrotic heart disease. The extracellular matrix (ECM) components, particularly fibrillar collagen, are elevated in the atherosclerotic lesions and are the essential integral element in holding the oxidized low density lipoproteins (LDL), homocystine, macrophage and foam cells in milieu, constituting the primary atherosclerotic and secondary restenotic lesions. In vivo and in vitro physiological, morphological, cellular, biochemical and molecular experiments have suggested the role of tissue homocystine in cardiovascular fibrosis and adverse ECM remodeling following H(e). The tissue homocystine induces cardiovascular fibrosis and may lead to heart failure via the redox-receptor pathway. The underlying cause and mechanism of cardiovascular fibrosis associated with arteriosclerosis, atherosclerosis, hypertension and coronary heart disease, involve changes in the levels of tissue redox state.

A methylenetetrahydrofolate reductase gene polymorphism in ischaemic stroke and in carotid artery stenosis.

A biallelic polymorphism of the methylenetretrahydrofolate reductase (MTHFR) gene, reported to influence the plasma level of homocysteine (Hcy), was investigated for a possible role in influencing the risk of ischaemic cerebrovascular disease (ICVD) and occlusive atherosclerosis in 126 patients with ischaemic stroke and 70 patients with internal carotid artery (ICA) stenosis. Only minor differences were observed between different groups of patients and control subjects. Although 47% of ICA stenosis patients had increased plasma Hcy, the MTHFR genotype did not correlate with levels of either Hcy, folic acid or vitamin B12. In addition, the MTHFR genotype did not affect Hcy levels, even in the presence of low blood folate. We conclude that this common MTHFR gene polymorphism does not exert a significant influence on the risk of developing ICVD or ICA stenosis, and does not cause the increased level of Hcy observed in ICA stenosis.

Angina por robo subclavio-coronario en pacientes revascularizados con arteria mamaria interna

After coronary bypass surgery in the left internal mammary artery, occlusive atherosclerosis in the proximal subclavian artery can produce reverse flow in the mammary artery and myocardial ischemia (coronary-subclavian steal syndrome). This is a rare cause of recurrent myocardial ischemia. We present two patients with postoperative complete obstruction in the proximal subclavian artery and inverse flow in the mammary artery producing severe ischemia in the left anterior descending artery territory. Both patients were treated with subclavian-subclavian bypass, which in one patient was ineffective in producing an adequate anterograde flow in the left internal mammary artery. We review clinical management, diagnostic methods and therapeutic options used in the coronary-subclavian steal syndrome.