Relevant bibliographies by topics / Coronary heart disease – Pathogenesis

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Academic literature on the topic 'Coronary heart disease – Pathogenesis'

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Published: 4 June 2021
Last updated: 3 February 2022

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Journal articles on the topic "Coronary heart disease – Pathogenesis"

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Nurmamadovna, Ishankulova Nasiba. "Coronary Heart Disease." American Journal of Medical Sciences and Pharmaceutical Research 03, no. 02 (February 28, 2021): 31–36. http://dx.doi.org/10.37547/tajmspr/volume03issue02-04.

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The article covers the etiology, pathogenesis, classification, diagnosis, clinical picture and treatment of coronary heart disease, provides a literature review. Cardiovascular disease (CVD) represents the leading cause of death among women as well as men. The number of deaths due to CVD in women are greater than in men. There are significant gender-related differences concerning CVD.
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Renaud, Serge, and Dominique Lanzmann-Petithory. "Coronary heart disease: dietary links and pathogenesis." Public Health Nutrition 4, no. 2b (April 2001): 459–74. http://dx.doi.org/10.1079/phn2001134.

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AbstractFor decades it has been postulated that the main environmental factor for coronary heart disease (CHD) was the intake of saturated fatty acids (SFA). Nevertheless, confirmation of the role of SFA in CHD through intervention trials has been disappointing. It was only when the diet was enriched in n-3 fatty acids that CHD was significantly prevented, especially cardiac death.In addition to n-3 fatty acids, many other foodstuffs or nutrients such as fibers, antioxidants, folic acid, calcium and even alcohol contribute to prevent CHD. Thus the relationship between diet and CHD morbidity and mortality appears to be much more complex than formerly suspected considering as key factors only SFA, linoleic acid, cholesterol and atherosclerosis. Some of the mechanisms are briefly described, but many additional nutrients (or non nutrients) may also play an important role in the pathogenesis of CHD.Finally, as a result of the most recent epidemiologic studies the ideal diet may comprise: 8% energy from SFA, 5% from polyunsaturated fatty acids with a ratio 5/1 of linoleic/alpha-linolenic acid+longer chains n-3, oleic acid as desired, large intake of cereals, vegetables, legumes and fruits, fish twice a week, cheese and yogurt as dairy products, rapeseed and olive oils as edible fat. Without side effects, such a diet can be highly palatable, easily enjoyed by many populations and may prevent effectively and rapidly (within a few weeks or months) CHD.
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Renaud, Serge, and Dominique Lanzmann-Petithory. "Dietary fats and coronary heart disease pathogenesis." Current Atherosclerosis Reports 4, no. 6 (November 2002): 419–24. http://dx.doi.org/10.1007/s11883-002-0045-z.

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OLIVEIRA, José Alberto Mello de. "HEART ANEURYSM IN CHAGAS' DISEASE." Revista do Instituto de Medicina Tropical de São Paulo 40, no. 5 (September 1998): 301–7. http://dx.doi.org/10.1590/s0036-46651998000500007.

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This prospective study on 41 autopsy collected human hearts concerns the "apical" lesion in Chagas' disease. Previous report did not show a correlation between lesion frequency and heart weight then discarding a vascular factor in its pathogenesis. The present paper involves other variables besides the heart weight to evaluate the relative coronary insufficiency. Distinct colored gel (green and red) injected through the capillary beds of both coronary arteries defined the extent of both vessels before separating the atria and removing the sub-epicardium fat. The Right Ventricle (RV) and Left Ventricle (LV) free walls furnished the RV/LV mass ratio. The myocardium mass colored green (right coronary artery - RC) and the whole Ventricular Weight (VW) determined the RC/VW mass ratio. The heart weight plus these mass ratios, graded and added, composed a score inversely proportional to the myocardium irrigation condition. It intended to be a more sensitive morphologic evaluation of the relative ischaemia to correlate to the apical lesion. This study showed a right deviation for the relative accumulated frequency of lesions plotted as a score function and a significant difference for higher scores in hearts with aneurysm. It suggests a ischaemic factor intervening in the apical lesion pathogenesis in Chagas' cardiopathy.
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OLIVER, M. "New horizons in the pathogenesis of coronary heart disease." European Journal of Clinical Investigation 22, no. 12 (December 1992): 761–63. http://dx.doi.org/10.1111/j.1365-2362.1992.tb01442.x.

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Kirichenko, A. A. "Coronary heart disease and inflammation." Clinical Medicine (Russian Journal) 96, no. 8 (December 20, 2018): 688–95. http://dx.doi.org/10.18821/0023-2149-2018-96-8-688-695.

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The increased content of inflammation markers in the blood is a significant prognostic sign of coronary events in persons with stable or asymptomatic course of coronary heart disease (CHD) and suggests that the inflammation underlying the destabilization of CHD has an independent character and is largely independent of the severity of stenotic lesions of coronary vessels. Activation of the local inflammatory process in the atherosclerotic plaque leads to the destruction of the fibrous capsule in combination with an increase in the activity of cellular and plasma factors of the coagulation system and inhibition of the fibrinolytic system. Cytomegalovirus, Chlamydia pneumoniae, pathogens of periodontal disease are nominated for the role of inducers of inflammatory reactions. The synergistic effect of several pathogens is reflected in the concept of burden of infection (“infectious burden”). Immuno-inflammatory rheumatic diseases are characterized by a high risk of cardiovascular complications. An important place in their prevention is an effective anti-inflammatory therapy: methotrexate, suppressing the formation of interleukin 1ft and tumor necrosis factor a, allows not only to modify the course of the disease, but also to reduce the risk of cardiovascular accidents. Chronic inflammation, as a key element of atherosclerosis pathogenesis, can be caused not only by infectious and immune factors, but also by metabolic factors. The activation of inflammasomes induced by cholesterol crystals in macrophages is an important link between cholesterol metabolism and inflammation in atherosclerotic plaques. Confirmation of the important pathogenetic role of inflammation is to reduce the risk of cardiovascular complications (CVD) on the background of anti-inflammatory therapy. In statin therapy, the decrease in The level of C-reactive protein (CRP) was significantly correlated with the suppression of atherosclerosis progression and a decrease in the risk of SSR, regardless of the degree of lowering the low-density lipoprotein cholesterol level. Taking colchicine in a low dose in patients with stable coronary artery disease, who received standard therapy, reduced the risk of acute coronary syndrome and sudden cardiac death. Secondary prevention of cardiovascular complications by human monoclonal antibodies to interleukin 1ft (kanakinumab) led to a decrease in the risk of SSR regardless of sex, Smoking, and lipid levels.
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Tennant, Christopher C., and Pauline M. Langeluddecke. "Psychological correlates of coronary heart disease." Psychological Medicine 15, no. 3 (August 1985): 581–88. http://dx.doi.org/10.1017/s0033291700031433.

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SynopsisThe Type A behaviour pattern and other measures of psychological traits and symptom states were assessed in 92 subjects (predominantly male) presenting for coronary angiography. These measures were correlated with three angiographic indices of coronary heart disease (CHD) severity and two clinical indices (angina and the duration of CHD). The only psychological measures associated with atherosclerosis (assessed by angiography) were indices of personality: Type A (the Jenkins Activity Survey), trait tension, trait anxiety and suppression of anger. It was concluded that these traits may have some role in the pathogenesis of coronary atherosclerosis. None of the measures of psychological symptoms showed a significant association with angiography indices. However, depressive symptoms and expressed hostility were associated with the severity of angina and duration of heart disease. It was concluded that these affects are the consequences of the physical disability of CHD.
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Sönmez, Hüseyin, Selma Süer, Turgut Ulutin, Emine Kökoglu, and Nergiz Uçişik. "The Relationship of Various Factors in the Pathogenesis of Atherosclerosis." Clinical and Applied Thrombosis/Hemostasis 4, no. 2 (April 1998): 105–10. http://dx.doi.org/10.1177/107602969800400205.

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In this study we investigated the levels of lipid parameters, fibronectin, tissue-type plasminogen activator and plasminogen activator inhibitor (t-PA-PAI-1) complex and si alidase in patients with coronary heart disease and a control group. Total cholesterol, triglyceride, low-density lipoprotein (LDL), and very-low-density lipoprotein (VLDL) cholesterol and lipoprotein Lp(a), levels in patients with coronary heart disease were found to be significantly higher than in the control group (p < .001). High-density lipoprotein (HDL) cholesterol levels in patient group were significantly lower than control group (p < .001). Plasma fibronectin and t-PA-PAI-1 complex levels in patients with coronary heart disease were found to be significantly higher than control group (p < .05 and p < .001, respectively). In addition, we found that serum sialidase levels in patients with coronary heart disease were significantly higher than in the control group (p < .001). The electrophoretic mobility of lipoproteins from patients with coronary heart dis ease was found to be greater than those from the control group. As a result Lp(a) may play an important role in the pathogen esis of atherosclerosis by causing foam cell formation because of interacting with LDL or fibronectin and by interfering with the fibrinolytic system because of binding to plasminogen re ceptors. In addition, modifications of Lp(a) (including desi alylation) may effect these events. Key words: Coronary heart disease—tPA-PAI-1 complex-Fibronectin-sialidase-Lipid parameters.
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Chazova, T. E., and G. A. Melnichenko. "Diabetes mellitus and coronary heart disease." Problems of Endocrinology 44, no. 1 (February 1, 1998): 54. http://dx.doi.org/10.14341/probl199844154-54.

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Atherosclerosis and related disorders of carbohydrate metabolism go beyond narrow cardiological problems and, in one way or another, are the subject of close attention of doctors of various specialties, including endocrinologists. In everyday practice, most endocrinologists leave the solution of issues related to hyperlipidemia “for later”, because, first, for many decades, full compensation for diabetes and hypothyroidism - conditions in which secondary hyperlipidemia is most common - was difficult ; secondly, there were no effective and safe means for treating hyperlipidemia, which made generations of doctors skeptical about the possibility of real correction of lipid metabolism disorders. Improving the methods for compensating for diabetes mellitus and the possibilities for treating hypothyroidism have brought clinicians to the problem of the need for additional therapy with lipid-lowering drugs, so the pathogenesis and treatment of hyperlipidemia are of great interest to them.
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Marin-Neto, José Antonio, Marcus V. Simões, Elias M. Ayres-Neto, J. Luiz Attab-Santos, L. Gallo Jr., Dalmo Souza Amorim, and Benedito Carlos Maciel. "Studies of the coronary circulation in Chagas' heart disease." Sao Paulo Medical Journal 113, no. 2 (April 1995): 826–34. http://dx.doi.org/10.1590/s1516-31801995000200014.

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Pathogenesis of chronic Chagas' heart disease may include various disturbances in the coronary circulation, that could be responsible for the myocardial lesions seen in human hearts and in experimental models of the disease. In this paper we critically reviewed the anatomical and functional abnormalities described in chronic chagasic patients, pertaining to the so-called vascular pathogenetic theory of Chagas' disease. The epicardial coronary arteries are usually free of significant obstructive disease in nonselected groups of chagasic patients examined at autopsy or by coronary angiography. However, chagasic patients who were studied after an episode of acute myocardial infarction, show the same patterns of atherosclerotic coronary artery disease seen in the general nonchagasic population. Studies of chagasic patients with angiographically normal coronary arteries, by several scintigraphy methods, revealed myocardial perfusion abnormalities which may be caused by the microcirculatory derangements described in animals experimentally infected with the T. cruzi. Since hypoperfusion has been detected in regions with normal or mildly impaired wall motion, it is likely that the microvascular disturbances precede and may be a causative mechanism for the subsequent myocardial damage. We speculate that hibernating ventricular areas may occur in chagasic patients, on the basis of the evidence gathered from these studies. Recent investigations of chronic patients with Chagas' disease and chest pain showed attenuation of the vasomotor responses to physiological and pharmacological stimuli, in the epicardial coronary arteries.
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Dissertations / Theses on the topic "Coronary heart disease – Pathogenesis"

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Cao, Fei. "Chlamydia pneumoniae, toll-like receptors and pathogenesis of atherosclerotic heart disease." View the abstract Download the full-text PDF version (on campus access only), 2007. http://etd.utmem.edu/ABSTRACTS/2007-022-Cao-index.html.

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Thesis (Ph.D. )--University of Tennessee Health Science Center, 2007.
Title from title page screen (viewed on May 16, 2008 ). Research advisor: Gerald I. Byrne, Ph.D. Document formatted into pages (xi, 114 p. : ill.). Vita. Abstract. Includes bibliographical references (p. 65-107).
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Dane-Stewart, Cheryl Ann. "Postprandial lipoprotein metabolism in patients at high risk of coronary artery disease : effects of statin therapy." University of Western Australia. School of Medicine and Pharmacology, 2003. http://theses.library.uwa.edu.au/adt-WU2004.0061.

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[Formulae and special characters can only be approximated here. Please see the pdf version of the abstract for an accurate reproduction.] Atherosclerosis is a common degenerative disease in which the clinical manifestations are often through stroke or myocardial infarction. Some of the established risk factors for atherosclerosis include elevated plasma low-density lipoprotein (LDL)-cholesterol levels, obesity, diabetes mellitus (DM) and cigarette smoking. Of the risk factors, an elevation in plasma LDL is one of the most established and the most researched. This is partly a consequence of the deposition of cholesterol within arterial intima being a crucial step in the progression of atherosclerosis, combined with the finding that LDL particles are a major transporter of cholesterol in circulation. Recently there is increasing evidence showing a role of the other major transporter of cholesterol in circulation, chylomicron remnants, in the progression of atherosclerosis. The notion of atherosclerosis as a postprandial phenomenon has been further substantiated by the emergence of evidence showing a direct role of chylomicron remnants in arterial cholesterol deposition. Based on evidence that chylomicron remnants are proatherogenic, the suggestion arises that accumulation of postprandial lipoproteins in plasma may add another dimension of risk to the development of coronary artery disease (CAD). This thesis tests the general hypothesis that individuals with or at high risk of CAD have postprandial dyslipidaemia and that this metabolic abnormality is correctable with a class of lipid-lowering drugs called statins. To test the hypothesis, clinical studies were conducted in normolipidaemic CAD patients, heterozygous familial hypercholesterolaemia (FH) and postmenopausal women with type 2 DM. Determination of postprandial dyslipidaemia by comparison with control populations were conducted initially in each patient group (Studies 1, 3 and 5), followed by intervention studies investigating possible modulation of the dyslipidaemia with a statin (Studies 2, 4 and 6). Six observation statements based on case-control comparisons of postprandial lipaemia in patients with or at risk of CAD and the effects of statins on postprandial dyslipidaemia in the patient groups were derived from the general hypothesis. The observation statements were examined in the individual studies described below. Postprandial lipoprotein metabolism was assessed using a number of methods. For comparison of postprandial lipaemia in Studies 1 and 2, a classic oral fat challenge was utilised. As markers of chylomicrons and chylomicron remnants, retinyl palmitate and triglyceride were measured postprandially as well as apolipoprotein (apo) B48 concentrations, a specific marker of intestinal lipoproteins. ApoB48 was also measured in the fasting state and found to predict the postprandial responses of retinyl palmitate, triglyceride and apoB48. This suggested that fasting measurement of apoB48 could be used as a simple indicator of postprandial dyslipidaemia. Consequently for Studies 3 - 6, fasting apoB48 measurements were used as primary markers of postprandial dyslipidaemia. Other markers for chylomicrons and their remnants utilised were fasting plasma concentrations of remnant-like particle-cholesterol (RLP-C) and apoC-III. As well as these static markers, chylomicron remnant catabolism was measured using a stable isotope breath test. The breath test involves the intravenous injection of a chylomicron remnant-like emulsion labelled with ¹³C-oleate and measurement of enriched ¹³CO2 in expired breath by isotope ratio mass spectrometry. The fractional catabolic rate (FCR) of the injected emulsion was subsequently calculated using multi-compartmental modeling (SAAM II). The studies are presented in this thesis as published and unpublished works. In Study 1, postprandial lipoprotein metabolism was compared between 18 normolipidaemic CAD patients (cholesterol 4.54 ± 0.12 mmol/L, triglyceride 1.09 ± 0.16) with 13 asymptomatic healthy controls using an oral fat challenge. Normolipidaemic CAD patients had higher postprandial area-under-curve (AUC) for triglyceride (+34%, p=0.019), retinyl palmitate (+74%, p=0.032) and apoB48 (+36%, p<0.001). Fasting apoB48 was also higher (+41%, p=0.001) and found to correlate significantly with AUC of triglyceride (p=0.017), retinyl palmitate (p=0.001) and apoB48 (p<0.001). The data suggest that normolipidaemic CAD patients have increased concentrations of intestinal lipoproteins in the fasting and postprandial state. In addition to these findings, significant correlations of fasting apoB48 with postprandial markers (p<0.02) suggests the fasting marker to be a simpler surrogate marker for the degree of total postprandial lipaemia. Study 2 investigated the effect of atorvastatin treatment on postprandial dyslipidaemia found in the 18 near-normolipidaemic CAD patients from Study 1. The trial was conducted in a randomised, placebo-controlled design, using oral fat challenges before and after 12-weeks atorvastatin/placebo treatment. Compared with the placebo group, atorvastatin decreased the total postprandial AUC for iii triglyceride (-22%, p=0.05) and apoB48 (-34%, p=0.013). Fasting markers of apoB48 (-35%, p=0.019) and RLP-C (-36%, p=0.032) also decreased significantly. Atorvastatin was also found to increase LDL-receptor activity by +218% (p<0.001) as reflected in binding studies. The data suggest atorvastatin reduces the fasting levels of intestinal lipoproteins as well as total postprandial lipaemia, but without acute dynamic changes in postprandial lipaemia. The reduction in fasting and total postprandial lipoprotein levels could be partly attributed to an increase in LDL-receptor mediated removal from circulation. In Study 3, postprandial lipaemia was compared in 15 heterozygous FH patients with 15 healthy controls. FH patients had higher fasting concentrations of apoB48 (+56%, p<0.001) and RLP-C (+48%, p=0.003). The elevation in these fasting markers of chylomicrons and their remnants suggests FH patients have postprandial dyslipidaemia due to an accumulation of these particles in plasma. Study 4 examined the effects of long- (> 6 months) and short-term (4 weeks) simvastatin treatment on modulating postprandial dyslipidaemia found in the 15 FH patients from Study 3. Short- and long-term simvastatin treatment decreased the fasting concentrations of apoB48 (-29% and 15% respectively, p<0.05) and RLP-C (both -38%, p<0.001), but did not significantly alter the FCR of the injected chylomicron remnant-like emulsion. The data suggest that in heterozygous FH both long- and short-term simvastatin treatments decrease the fasting markers of postprandial lipoproteins by mechanisms that may not be mediated via processes differentiated by the 13CO2 breath test. This implies that the effect on postprandial lipaemia may be from a decrease in production and/or a possible increase in catabolism of triglyceride-rich lipoproteins (TRLs). In Study 5, postprandial lipaemia was compared in 24 postmenopausal women age and body mass index matched with 14 postmenopausal women with type 2 DM. Postmenopausal diabetic women were found to have higher fasting concentrations of apoB48 (+21%, p=0.021) and apoC-III (+16%, p=0.042) as well as lower FCR of the chylomicron remnant-like emulsion (-50%, p<0.001). The data suggest that postmenopausal diabetic women have postprandial dyslipidaemia, and that this is due to delayed catabolism of chylomicron remnants. Study 6 was an hypothesis-generating exercise examining the effects of 4-weeks pravastatin treatment on postprandial dyslipidaemia found in 7 postmenopausal women with type 2 DM from Study 5. Although plasma LDL-cholesterol was reduced (-19%, p=0.028), there were no significant effects found on fasting apoB48 concentrations (-12%, p=0.116) or the FCR of the chylomicron remnant-like emulsion (+38%, p=0.345). A larger sample size of patients and/or treatment with a more potent statin at a dosage known to affect chylomicron remnant metabolism would be required to demonstrate a significant reduction in postprandial dyslipidaemia in postmenopausal women with type 2 DM. The results of the above mentioned studies combined support the general hypothesis that postprandial dyslipidaemia is a feature of patients with or at risk of CAD. This defect may be demonstrated using fasting apoB48 as an indicator of the degree of postprandial lipaemia. Postprandial dyslipidaemia may reflect a reduction in catabolism, as suggested with the breath test in type 2 DM, and/or an over overproduction of chylomicrons. Both these mechanisms would also increase competition for lipolysis and clearance pathways between hepatically and intestinally-derived lipoproteins. The exact mechanisms by which postprandial dyslipidaemia occurs are yet to be determined. Statins appear to improve defective postprandial lipaemia in patients with or at risk of CAD, which is in agreement with the general hypothesis. The effectiveness of a statin is dependant on their potency in inhibiting cholesterol biosynthesis and increasing receptor mediated clearance of LDL and chylomicron remnants. The studies conducted in this thesis show that postprandial dyslipidaemia can be reduced by statins but not to the extent demonstrated in controls. However, the demonstrated reduction in fasting and total postprandial lipaemia translates to a lowering in overall arterial exposure to circulating proatherogenic particles. The elevation in fasting and postprandial levels of proatherogenic chylomicron remnants found in the patient groups described in this thesis indicates another dimension to their risk of coronary disease. The reductions in the overall levels of proatherogenic particles in patients with or at high CAD risk, infers a possible reduction in the risk of coronary disease in these patients.
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Brouilette, Scott Wayne. "Telomeres and coronary heart disease." Thesis, University of Leicester, 2004. http://hdl.handle.net/2381/29899.

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Using mean telomere length as a marker of biological age, I show that: 1. Subjects with premature myocardial infarction (MI) have significantly shorter telomeres than age-sex matched, healthy, controls. The mean telomere length in MI subjects was similar to controls almost 11 years older. 2. Healthy young adult children of families with a strong history of premature MI have shorter telomeres than age matched children of families without such a history. 3. Shorter telomere lengths are associated with increase risk of subsequent CHD events in a prospective study. This analysis was carried out on samples collected in the West of Scotland Coronary Prevention Study (WOSCOPS). This randomised blinded trial was designated to examine the benefits of statin treatment on preventing CHD and showed a 30% reduction of events in those treated with pravastatin. Interestingly, my analysis showed that this benefit of statin is only seen in those subjects at higher risk of CHD based on their telomere length.;As the final part of the thesis I carried out a quantitative linkage trait (QTL) analysis in sib-pairs in an attempt to identify genetic loci regulating telomere length. I report the mapping of a major QTL on chromosome 12 that determines almost 50% of the inter-individual variation in mean telomere length.;These findings support a novel "telomere" hypothesis of CHD. They indicate that telomere biology is intimately linked to the genetic aetiology and pathogenesis of CHD. Specifically, the findings suggest that (i) those individuals born with shorter telomeres may be at increased risk of CHD (ii) rather than individual genes, a more global structural property of the genetic material may explain the familial basis of CHD (iii) variation in telomere length may explain, in part, the variable age of onset of CHD. The findings provide several new avenues for future research.
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Lee, Chi-hang. "Microvascular obstruction following percutaneous coronary intervention for coronary artery disease." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43278723.

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Danesh, John. "Chronic infection and coronary heart disease." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326020.

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Kounali, Daphne. "Early growth and coronary heart disease." Thesis, University of Southampton, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.436926.

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Heiser, Claire Anne. "Personality predictors of coronary heart disease." Thesis, Virginia Polytechnic Institute and State University, 1985. http://hdl.handle.net/10919/50027.

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Fifty percent of the diagnosed cases of coronary heart disease in the United States are of unknown etiology. This study proposed that five personality traits— achievement, dominance, aggression, succorance and Critical Parent—differentiate individuals with coronary heart disease manifestations. The ultimate goal of this research was to formulate a predictive profile of at-risk individuals of developing coronary heart disease. Cardiac rehabilitation units' participants from across the United States were recruited as subjects. Randomly selected cardiac rehabilitation units were sent an initial letter inquiring whether their staff would be willing to participate in the study by administering the instruments to their participants. Eight units from each of the 50 states were contacted. A total of fourteen units agreed to participate. One hundred sixty-nine subjects completed the Demographic Data Questionnaire and the Adjective Check List. Five scale scores, representing the five personality differentials, were analyzed. Comparison of the male subject population (n=135) and the male normative population (n=198) revealed no significant differences in terms of the five traits. Comparison of diagnostic subgroups of the subject population also revealed no significant differences. It was concluded that the subject population did not differ significantly from the normative population in terms of the five traits assess by the instrument used. The goal of a predictive profile was not realized due to this lack of findings.
Master of Science
incomplete_metadata
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Lee, Chi-hang, and 李志恆. "Microvascular obstruction following percutaneous coronary interventionfor coronary artery disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43278723.

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Zapanta, Laurence (Laurence F. ). "Heart rate variability in mice with coronary heart disease." Thesis, Massachusetts Institute of Technology, 2005. http://hdl.handle.net/1721.1/34118.

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Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2005.
Includes bibliographical references (leaves 69-71).
Heart rate variability (HRV), the beat-to-beat fluctuation of the heart rate, is a non-invasive test that measures the autonomic regulation of the heart. Assessment of HRV has been shown to predict the risk of mortality in patients after an acute myocardial infarction. Recently, the Krieger lab at MIT developed genetically engineered double knockout (dKO) mice that develop coronary artery disease accompanied by spontaneous myocardial infarctions and die at a very young age. This thesis investigated whether HRV could function as a prognostic indicator in the dKO mouse. A novel method for estimating physiological state of the mouse from the electrocardiogram using an innovative activity index was developed in order to compare HRV variables at different times while controlling for physiologic state. Traditional time and frequency domain variables were used to assess the prognostic power of HRV. Results have shown that none of the HRV variables were helpful in predicting mortality in the dKO mice. Mean heart rate showed some prognostic power, but it was not consistent in all the dKO mice. Finally, the activity index developed in this thesis provided a reliable metric for activity in mice as validated by a camera with motion detection.
by Laurence Zapanta.
S.M.
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Rose, Edward Leslie. "Coronary heart disease in patients with peripheral vascular disease." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305544.

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Books on the topic "Coronary heart disease – Pathogenesis"

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Demurov, E. A. Metabolicheskie i neĭrogumoralʹnye mekhanizmy ishemicheskikh povrezhdeniĭ miokarda. Moskva: VINITI, 1985.

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Meerson, F. Z. Adaptive protection of the heart: Protecting against stress and ischemic damage. Boca Raton: CRC Press, 1991.

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Grimes, David Stuart. The effect of sunshine on blood cholestrol, its relationship to vitamin D metabolism andimplications for the pathogenesis of coronary heart disease. Manchester: University of Manchester, 1993.

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Graft arteriosclerosis in heart transplantation. Austin: R.G. Landes, 1993.

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National Dairy Council. Nutrition Service. Coronary heart disease. London: National Dairy Council, 1993.

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National Board for Nursing, Midwifery and Health Visiting for Scotland. Coronary heart disease. Edinburgh: The Board, 1998.

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Coronary heart disease. New Hyde Park, N.Y: Medical Examination Pub. Co., 1985.

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Sandler, Gerald, ed. Coronary Heart Disease. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-010-9218-0.

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Vlodaver, Zeev, Robert F. Wilson, and Daniel J. Garry, eds. Coronary Heart Disease. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-1475-9.

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Royal Colleges of Physicians of the United Kingdom. Committee on Health Promotion. Coronary heart disease. London: Faculty of Community Medicine of the Royal Colleges of Physicians of the United Kingdom, 1988.

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Book chapters on the topic "Coronary heart disease – Pathogenesis"

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Antman, Elliott M., and John D. Rutherford. "Pathogenesis and Pathology of Ischemic Heart Disease Syndromes." In Coronary Care Medicine, 1–18. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2303-7_1.

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Vega, Gloria Lena, and Scott M. Grundy. "Pathogenesis of Hypertriglyceridemia: Implications for Coronary Heart Disease and Therapy." In Advances in Experimental Medicine and Biology, 311–26. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-0733-4_39.

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Jiang, Joseph P., Charles L. Feldman, and Peter H. Stone. "Models of the intracoronary pathogenesis of acute coronary heart disease." In Developments in Cardiovascular Medicine, 237–57. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-1577-0_15.

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Yamaji, Kyohei, and Takeshi Kimura. "Gender Differences in Outcome After Coronary Revascularization." In Gender Differences in the Pathogenesis and Management of Heart Disease, 239–45. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-71135-5_13.

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Lee, Suegene K., Jay Khambhati, and Puja K. Mehta. "Angina and Ischemia in Women with No Obstructive Coronary Artery Disease." In Gender Differences in the Pathogenesis and Management of Heart Disease, 101–33. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-71135-5_8.

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Bergersen, Lisa, Susan Foerster, Audrey C. Marshall, and Jeffery Meadows. "Coronary Angiography." In Congenital Heart Disease, 143–50. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-77292-9_23.

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Abdelhafiz, Ahmed H. "Coronary heart disease." In Diabetes in Old Age, 67–83. Chichester, UK: John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781118954621.ch7.

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Schenck-Gustafsson, Karin. "Coronary Heart Disease." In Handbook of Clinical Gender Medicine, 190–205. Basel: KARGER, 2012. http://dx.doi.org/10.1159/000336385.

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Kalmar, Jayne M., Brigid M. Lynch, Christine M. Friedenreich, Lee W. Jones, A. N. Bosch, Alessandro Blandino, Elisabetta Toso, et al. "Coronary Heart Disease." In Encyclopedia of Exercise Medicine in Health and Disease, 213–16. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_51.

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Tsuboi, Hirohito, Katsunori Kondo, Hiroshi Kaneko, and Hiroko Yamamoto. "Coronary Heart Disease." In Social Determinants of Health in Non-communicable Diseases, 41–52. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-1831-7_5.

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Conference papers on the topic "Coronary heart disease – Pathogenesis"

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Mahmoud, Ahmed M., Daniel H. Cortes, S. Jamal Mustafa, and Osama M. Mukdadi. "High Frequency Precise Ultrasound Imaging System to Assess Mouse Hearts and Blood Vessels." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192836.

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Genetically modified mice provide a powerful tool for understanding the molecular mechanisms and pathogenesis of human cardiovascular diseases like human atherosclerosis [1]. Numerous mouse strains are available today with phenotypes relevant to human cardiovascular diseases [1,2]. These mouse strains have prompted the development of techniques for assessing the cardiovascular function and morphology of living mice. Recently, several imaging techniques have been emerged as promising non-invasive imaging modalities, such as electron-beam computed tomography, magnetic resonance imaging, positron emission tomography, optical coherent tomography, and ultrasound biomicroscopy (UBM) [3,4]. Although these systems are capable of detecting anatomic and functional information, they may not be suitable to image mouse heart vasculatures. The small size and rapid movement of mouse hearts require systems acquiring images using temporal resolution of less than 10 ms with spatial resolution of 100 μm or less [4]. However, in mice, which have extremely small coronary arteries and high heart rates, the coronary circulation constitutes a great challenge for these available imaging techniques.
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Meade, T. W. "THE EPIDEMIOLOGY OF HAEMOSTATIC AND OTHER VARIABLES IN CORONARY ARTERY DISEASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643833.

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The increase in the clinical manifestations of coronary artery disease (CAD) since the 1920s cannot be explained solely in terms of atheroma. Another major process such as thrombogenesis must also be involved. Pathological studies show that thrombosis contributes not only to myocardial infarction but to nearly all cases of sudden coronary death as well. Epidemiologically, it is the coagulation system rather than platelet function that has so far been more rewarding in attempting to identify characteristics of the haemostatic system that are associated with the subsequent risk of CAD. In particular, two clotting factors - factor VII coagulant activity, VIIc, and fibrinogen - may be involved. Factor VII has several characteristics that are required for a system to secure rapid haemostasis after injury. The question is whether an exaggeration of the physiological state of readiness implied by these features may predispose to thrombosis. There are at least four pathways through which high fibrinogen levels, however they are determined, may operate to increase the risk of CAD - involvement in atherogenesis, determination of blood and plasma viscosity, effects on platelet aggregability and an influence on the amount of fibrin formed. The prospective Northwick Park Heart Study (NPHS) has shown an association between high VIIc levels and an increased risk of CAD. NPHS and three other prospective studies have also demonstrated a clear association between high levels of plasma fibrinogen and an increased risk of CAD, this association generally being stronger than for more familiar markers of risk such as the blood cholesterol level. There may well be an interaction between fibrinogen and blood pressure, the occurrence of high levels of both increasing CAD or stroke risk to a greater extent than would be expected from the sum of their separate effects. Several pathological and clinical observations support a “hypercoagulable state” not simply as a concept but as a demonstrable abnormality in which characteristics of the circulating blood influence the course of events. These include the effects of anti-thrombotic agents (particularly oral anticoagulants) on re—infarction rates and the likelihood that high VIIc levels lead to increased levels of thrombin production. The general epidemiology of VIIc and fibrinogen is consistent with the view that high levels of each are of pathogenetic significance. Thus, increasing age, obesity, oral contraceptive usage, the occurrence of the menopause and diabetes are all associated with high levels of VIIc and fibrinogen and with an increased risk of CAD. Psychosocial influences may increase the risk of CAD through effects on the plasma fibrinogen level. There is strong evidence that dietary habit, particularly the consumption of fat, is a leading determinant of the VIIc level. A substantial proportion of the relationship between cigarette smoking and CAD is probably mediated through the plasma fibrinogen level. The most radical implication of a “hypercoagulable state” is for the pharmacological prophylaxis of CAD which, it may turn out, is better approached by anti—thrombotic measures than by the use of lipid-lowering agents.
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Vengrenyuk, Yuliya, Theodore J. Kaplan, Luis Cardoso, Gwendalyn J. Randolph, and Sheldon Weinbaum. "Biomechanical Modeling of Atherosclerotic Lesions in ApoE Deficient Mice." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206571.

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Cardiovascular disease remains the principal killer in the western world despite major advances in treatment of its patients [1]. It is generally accepted that sudden rupture of vulnerable plaque followed by thrombus formation underlies most cases of myocardial infarction and is responsible for more than a half of 500,000 coronary heart disease deaths every year. Although histopathological analysis of postmortem specimens have provided important data on histological features of ruptured human plaques, there is an urgent need for good representative animal models of plaque rupture. Over the last decade and a half, genetically engineered mice have been widely used to study the pathogenesis and potential treatment of atherosclerotic lesions, as well as genetic, hormonal and environmental influences on development of atherosclerosis. Though many of the features of plaque development and progression that occur in human plaques are similarly observed in murine plaques, these mouse models have long been regarded as poor models to study plaque rupture because the aortic sinus lesions seldom show any signs of fibrous cap disruption. Several recent studies reported potentially unstable atherosclerotic lesions in older apoE-deficient mice in another anatomic site, the proximal part of the brachiocephalic artery (BCA) [2, 3]. The unusual stability of aortic lesions compared to the BCA lesions in ApoE knockout mice is an unexplained paradox in developing a mouse model of plaque rupture. In this paper, we use histology based finite element analysis to evaluate peak circumferential stresses in aortic and BCA lesions from high fat fed ApoE KO mice.
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Terres, W., C. Hamm, W. Kupper, and W. Bleifeld. "PLATELET AGGREGABLLITY AND METABOLISM IN PATIENTS WITH UNSTABLE ANGINA PECTORIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643777.

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Several platelet products indicating platelet activation have been detected in blood and urine of patients (PTS) with angina pectoris (AP) at rest. Platelet activation mainly depends on local changes in the morphology or biochemical behaviour of the vessels. Whether platelet hyperaggregability is of additional importance in the pathogenesis of unstable AP is up to now unclear. In a prospective trial we therefore evaluated 32 patients (PTS) with coronary heart disease, 16 with AP at rest during the last 8 hours before blood collection and 16 age and sex matched controls with stable exertional AP. Platelet aggregation was measured upon stimulation with ADP (0.5, 1 and 10 μmol/l) and collagen (1and 5μg/ml), and c-AMP was determined in platelet rich plasma before, and, as an estimate of platelet adenylate cyclase activity, after stimulation of this enzyme with PGE 1 (10 μmol/l for 30 s). For all concentrations of both ADP and collagen no significant differences in the rates and extents of aggregation could be found between the groups. Correspondingly, the mean (±. 2 SEM) concentrations of c-AMP were similar, basally (4.1 ±.1.4 pmol/ml for PTS withunstable AP and 5.3 t 1.3 pmol/ml for PTS with stable AP)and after stimulation of platelet adenylate cyclase with PGE 1 (14.8 ± 4.1 vs. 17.2 ± 2.8 pmol/ml).Conclusion: No generalized platelet hyperaggregability could be detected in our PTS with unstable AP when compared to controls with stable exertional AP.
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Falk, E. A. "UNSTABLE ANGINA PECTORIS: PATHOLOGIC ASPECTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643711.

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Unstable angina pectoris represents a common and important manifestation of acute ischemic heart disease encompassing the broad spectrum of clinical syndromes between stable effort angina and acute myocardial infarction. This group of patientsisfar from uniform concerning underlying pathogenetic mechanisms and prognosis, but generally the risk of infarction or deathis increased during the unstable period. Most patients are presenting with new or worsening effort angina or angina at rest,and especially patients with rest anginaassociated with transient ECG changes seem to constitute a high risk subgroup. Transient reductions in coronary blood flow,rather than increases in myocardial oxygen demand, seem to play the major role in rest angina, indicating an underlying 'dynamic' coronary stenosis.Furthermore, unstable angina seems to beagood clinicalmarker for actively progressing coronary-artery disease.Pathologically, a rapidly evolving coronary-artery lesion represented by a disrupted atherosclerotic plaque with variable degree of plaque hemorrhage and luminalthrombosis usually is present in patientscoming to autopsy after a period of rest angina. The thrombus at the rupture site may be mural and limited (just sealing therupture) or occlusive depending on the degree of preexisting atherosclerotic stenosis. An occlusive thrombus is seldom seen over ruptured plaques causing less tha15% stenosis (histologic area stenosis), but is found with increasing frequency when stenosis severety increases beyond 15%.Most occlusive thrombi have a layered structure with thrombus material of differing age indicating an episodic growth by repeated mural deposits. Aggregated platelets usually can be identified in the mostrecent part of the thrombus, while older parts are more homogeneous due to fibrin infiltration/stabilization. Additionally,microemboli and microinfarcts are frequently found in the myocardium downstream tocoronary thrombi. So, the period of unstable angina preceding a fatal heart attackseems to be characterized by an ongoing thrombotic process in a major coronary artery where recurrent mural thrombus formation alternates with intermittent thrombus fragmentation and peripheral embolization. Such a dynamic thrombosis (with or without a concomitant focal vasospastic phenomenon) at the site of an unstable (ruptured) atherosclerotic lesion obviously may lead to the other clearly thrombus-related acute ischemic events: myocardial infarction or sudden death.Clinical studies using coronary angiography and coronary angioscopy during the acute phase of unstable angina have revealed a high frequency of ulcerated (unstable) atherothrombotic lesion in arteries responsible for the acute ischemia. Furthermore, episodic platelet activation (usually associated with chest pain) has recently been demonstrated in patients with unstable angina.The mechanism underlying pain/ischemia(predominantly spasm?) and the rapid plaque progression (plaque hemorr.hage/luminal thrombosis?) during unstable angina maydiffer. Accordingly, therapy directed against a possible spasm (nitrates, calcium antagonists) usually relieves pain effectively without having any documented effect on infarction/survival, while antithr-ombotic therapy (aspirin, heparin) clearlyimproves the prognosis without apparent antianginal effect. Therefore, with the objective not only of relieving pain but also of improving the prognosis, more attention should be paid to the potentially fatal thrombotic process that apparently isgoing on in a major coronary artery of many patients with unstable angina.
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Lin, Shisong, Xiaodong Zhuang, Shiyun Huang, Yahui Liu, Linlin Shen, and Xinxue Liao. "Face Analysis for Coronary Heart Disease Diagnosis." In 2019 12th International Congress on Image and Signal Processing, BioMedical Engineering and Informatics (CISP-BMEI). IEEE, 2019. http://dx.doi.org/10.1109/cisp-bmei48845.2019.8966020.

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Pareek, Vishakha, and R. K. Sharma. "Coronary heart disease detection from voice analysis." In 2016 IEEE Students' Conference on Electrical, Electronics and Computer Science (SCEECS). IEEE, 2016. http://dx.doi.org/10.1109/sceecs.2016.7509344.

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Mangathayaru, Nimmala, B. Padmaja Rani, V. Janaki, Lakshmi Sowmya Kotturi, Manasa Vallabhapurapu, and G. Vikas. "Heart Rate Variability for Predicting Coronary Heart Disease using Photoplethysmography." In 2020 Fourth International Conference on I-SMAC (IoT in Social, Mobile, Analytics and Cloud) (I-SMAC). IEEE, 2020. http://dx.doi.org/10.1109/i-smac49090.2020.9243316.

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Runjing, Zhou, and Li Keyang. "Fisher classifier in diagnosis of coronary heart disease." In 2011 4th International Congress on Image and Signal Processing (CISP). IEEE, 2011. http://dx.doi.org/10.1109/cisp.2011.6100787.

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Gonsalves, Amanda H., Fadi Thabtah, Rami Mustafa A. Mohammad, and Gurpreet Singh. "Prediction of Coronary Heart Disease using Machine Learning." In the 2019 3rd International Conference. New York, New York, USA: ACM Press, 2019. http://dx.doi.org/10.1145/3342999.3343015.

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Reports on the topic "Coronary heart disease – Pathogenesis"

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Dong, Guoqi, Mengye Lu, Xiaoliang Wu, Hao Chen, Hongru Zhang, and Yihuang Gu. Network meta-analysis of Traditional Chinese medicines for depression in coronary heart disease patients. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2020. http://dx.doi.org/10.37766/inplasy2020.5.0036.

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Wienke, Andreas, Anne M. Herskind, Kaare Christensen, Axel Skytthe, and Anatoli I. Yashin. The influence of smoking and BMI on heritability in susceptibility to coronary heart disease. Rostock: Max Planck Institute for Demographic Research, January 2002. http://dx.doi.org/10.4054/mpidr-wp-2002-003.

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Cai, Ruping, Yuli Xu, and Qiang Su. Meta-analysis of blood lipid reduction for patients with coronary heart disease by combination of pitavastatin and ezetimibe. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2021. http://dx.doi.org/10.37766/inplasy2021.5.0072.

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Ghambaryan, Anna. Heart Rate Variability, Catecholamine and Hemodynamic Responses During Rest and Stress in Coronary Artery Disease Patients: The PIMI Study. Fort Belvoir, VA: Defense Technical Information Center, January 2007. http://dx.doi.org/10.21236/ad1013978.

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Pan, JianLue, Pangning Huang, Yuanwen Zhang, RongFa Huang, QiuCen Chen, and HuiBing Chen. Commonly Traditional Chinese Medicine in treatment of Coronary Atherosclerotic Heart Disease with Anxiety and Depression: a network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2021. http://dx.doi.org/10.37766/inplasy2021.4.0124.

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Liu, Chao, Jing Bai, Lanchun Liu, Jialiang Gao, and Jie Wang. Effectiveness and safety of Yufengningxin for treating coronary heart disease angina: A protocol for a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2020. http://dx.doi.org/10.37766/inplasy2020.11.0040.

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Wang, Lina, Yangli Sun, Jie Zhan, Zhiyuan Wu, Peiming Zhang, Xiaopeng Wen, Shuqi Ge, Xu Han, and Liming Lu. Effects of exercise therapy on anxiety and depression in patients with coronary heart disease: a meta-analysis of a randomized controlled study. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2021. http://dx.doi.org/10.37766/inplasy2021.6.0017.

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Fan, Maoxia, Ying Tian, and Dong Guo. Efficacy and safety of Xinkeshu in the treatment of angina pectoris of coronary heart disease: A systematic review and meta-analysis protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2021. http://dx.doi.org/10.37766/inplasy2021.9.0026.

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Li, Xing-xing, Zong-jing Fan, Jie Cui, Rui Zhuang, Rong-peng Liu, Quan Lin, and Yang Wu. Cardiac rehabilitation of Baduanjin exercise in coronary heart disease after PCI: a protocol for systematic review and meta-analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2021. http://dx.doi.org/10.37766/inplasy2021.3.0065.

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Xu, Xiangmei, Wenna Yang, Xuan Chen, Yixuan Kong, Jie Wang, and Jinghui Zheng. Traditional Chinese Medicine Injection Combined with Conventional Western Medicine in Treating Coronary Heart Disease after PCI:A Protocol systematic review and meta analysis of overview. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2020. http://dx.doi.org/10.37766/inplasy2020.7.0087.

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