CORONARY DISEASE AND DIABETES

Social class and coronary artery disease in India

See Article by Sajobi et al When I get diagnosed with obstructive coronary disease, and face a decision about whether to be treated medically, surgically, or percutaneously, I will want to know how I am likely to do—what my symptoms, function, and quality of life will be—with each treatment. I do not want to know the mean differences reported from clinical trials in which I would have likely been excluded, nor do I want to know what the guidelines say. What I want to know is how patients like me did, particularly with respect to their health status recovery, with each treatment. Only then will I have the information I need to make an informed decision as to whether the benefits of treatment warrant the risks. This vision, first articulated by Paul Ellwood 40 years ago in his 1988 Shattuck lecture,1 through the current era of funding by the Patient-Centered Outcomes Research Institute,2 has been at the forefront of my research interests. Early in the course of my career I worked to develop the means to quantify the health status of patients with coronary disease by developing the Seattle Angina Questionnaire.3 …

Objective To detect the level of visfatin in the peripheral blood ofpafients with coronary atherosclerotic heart disease (coronary heart disease),and investigate the conelation between the level of visfatin and the lesion degree of coronary heart disease.Methods Two hundred and twenty patients who were diagnosed as coronary heart disease by coronary artery angiography from January to June 2011 (coronary heart disease group) were enrolled in this study,including 74 cases with stable angina pectoris(stable angina pectoris group),60 cases with unstable angina pectoris (unstable angina pectoris group),and 86 cases with acute myocardial infarction (myocardial infarction group).And 20 healthy persons with normal coronary artery angiography were selected as control group.The biochemical parameters of triglyceride (TG),total cholesterol (TC),high density lipoprotein cholesterol (HDL-C) and low density lipoprotein cholesterol (LDL-C) were detected by biochemistry autoanalyzer.The level of serum visfatin was detected by ELISA analysis.The serum biochemical parameters and serum visfatin among all the groups were compared and the correlation between them was analyzed.ResuIts The level of serum visfatin of coronary heart disease group [(34.07 ±5.51) μg/L] was significantly higher than that of control group [(13.22 ±3.17) μg/L](P＜0.05).TC and LDL-C of different coronary heart disease groups had no significant differences compared with that of control group (P ＞ 0.05).TG,H DL-C and serum visfatin of stable angina pectoris group,unstable angina pectoris group and myocardial infarction group [(1.44 ±0.27) mmol/L,(1.16 ±0.12) mmol/L,(21.36 ± 3.35) μg/L; ( 1.84 ±0.32) mmol/L,(1.01 ± 0.08) mmol/L,(27.78 ±4.47) μg/L; (2.31 ±0.34)mmol/L,(0.93 ± 0.06) mmol/L,(33.14 ± 5.66) μ g/L] had statistical significance compared with those of control group [(0.93 ±0.25) mmol/L,(1.48 ± 0.24) mmol/L,(13.22 ±3.17) μg/L](P＜0.05 or ＜0.01).TG,C,ensini score and serum visfatin of unstable angina pectoris group were significantly higher than those of stable angina pectoris group and HDL-C was obviously lower than that of stable angina pectoris group (P ＜0.05).Gensini score and serum visfatin of myocardial infarction group were significantly higher than those of unstable angina pectoris group and HDL-C was obviously lower than that of unstable angina pectoris group (P ＜ 0.05).Spearman correlation analysis showed that the level of serum visfatin of coronary heart disease group was positively correlated with TG and Gensini score (P ＜0.05 or ＜0.01 ) and negatively correlatedwith HDL-C (P ＜ 0.01 ),and had no correlation with TC and LDL-C (P ＞ 0.05).Conclusions The highlevel expression of visfatin in the peripheral blood may be a risk factor of coronary heart disease.The changes of serum visfatin can reflect the lesion severity degree of coronary artery. Key words: Coronary disease; Visfatin; Severity of coronary artery disease

At least 25% of coronary patients have sudden death or nonfatal myocardial infarction without prior symptoms.1 Therefore, the search for coronary patients with subclinical disease who could potentially benefit from intensive primary prevention efforts is critically important. The American Heart Association’s (AHA) Prevention V Conference, “Beyond Secondary Prevention: Identifying the High Risk Patient for Primary Prevention,” addressed ways to identify more patients who are asymptomatic and clinically free of coronary heart disease (CHD) but at sufficiently high risk for a future coronary event to justify more intensive risk reduction efforts.2 In this report, we amplify on key findings and recommendations of the AHA Prevention V conference, highlight new research since the conference, and propose an approach to the use of office-based testing and additional noninvasive procedures in selected patients to better define their coronary event risk. The recommendations are concordant with the recently released approach to risk assessment and management from the third report of the Adult Treatment Panel of the National Cholesterol Education Program (ATP-III).3 Enthusiasm for primary prevention and risk assessment in asymptomatic people has been spurred by recent advances in prevention research. Lipid-lowering trials demonstrated that primary prevention of coronary events is feasible, evidenced by the West of Scotland Coronary Primary Prevention Study (WOSCOPS) trial4 of hypercholesterolemic men and by the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS) trial5 in average or typical risk men and women with only moderate lipid abnormalities. Aspirin6 or ACE inhibitors7 can also reduce risk in selected asymptomatic, high-risk people. Emerging coronary risk factors have been described including inflammatory, infectious, and thrombotic markers,8 and there has been a steady flow of reports that focus attention on potential new ways of predicting coronary risk.9 In addition, noninvasive tests for subclinical atherosclerotic disease are available …

The Complex Relationship Between Ischemic Heart Disease and COPD Exacerbations

To identify predictive factors for coronary artery disease in patients with stenosis of the aortic valve the clinical histories, haemodynamic measurements, biplane contrast left ventriculograms, and coronary angiograms of 83 consecutively catheterised patients with valvar aortic stenosis were examined retrospectively. The mean (SD) age was 66.4 (9.1) years and 78% were men. Fifty five patients had significant coronary artery disease (greater than or equal to 50% diameter narrowing). Forty five (82%) of 55 patients with and 23 (82%) of 28 patients without coronary disease had angina. Heart failure occurred in a third of the patients; these patients were on average older, were more likely to be female, and had lower ejection fractions and cardiac outputs than patients in whom failure did not occur. Calculated valve area, transvalvar gradient, and left ventricular end diastolic pressure did not discriminate between patients with and without coronary disease. Syncope was less common than angina and heart failure and was associated with significantly lower valve areas and higher gradients than those found in patients without syncope. Left ventricular regional wall motion abnormalities were equally common in the groups with and without angina and predicted coronary artery disease with 94% accuracy. The absence of regional wall motion abnormality was an insensitive marker of normal coronary arteries as 45% of such patients had coronary disease. Five of the 83 patients had significant coronary disease without angina or regional wall motion abnormality. In patients with aortic stenosis angina did not predict the presence of coronary artery disease; therefore, it is advisable to have the results of coronary angiography before aortic valve replacement in a population such as this. Two of the patients with heart failure and severe aortic stenosis had regional wall motion abnormality with normal coronary arteries. Thus in some patients left ventricular failure produced by increased afterload may itself be a cause of left ventricular regional wall motion abnormality.

Prognostic factors of coronary heart disease in asymptomatic diabetics for inclusion on the kidney transplant waiting list. Screening with coronary angiography.

Patients with coronary heart disease have recurrent cardiovascular events after systemic treatment is often one of the leading factors increasing the death and hospitalization rates, thereby adding to the economic burden of society. According to foreign and domestic reports, poor compliance of cardiac rehabilitation in patients with coronary heart disease is a common problem at present. Therefore, in the rehabilitation of patients with coronary heart disease, Improving cardiac rehabilitation compliance is important in regaining health and cost saving during coronary heart disease recovery treatment. This study summarized the status and influence factors of cardiac rehabilitation compliance among foreign and domestic coronary heart disease patients and the interventions recommended for improving cardiac rehabilitation compliance. Key words: Coronary disease; Cardiac rehabilitation; Affecting factors; Patient compliance; Nursing care; Review

Increased low-density lipoprotein (LDL) and decreased high-density lipoprotein cholesterol (HDL-C) predict premature coronary artery disease, as do elevated levels of apolipoprotein B or reduced levels of apolipoprotein AI. Probands were studied of families with common genetic forms of dyslipidaemia to determine if apo B or apo AI define genetic groups and if apo B or apo AI levels relate to premature coronary artery disease risk. Elevated apo B was characteristic of familial hypercholesterolaemia, familial combined hyperlipidaemia (FCHL), and was seen in individuals with elevated Lp(a). Normal apo B levels were seen in familial hypertriglyceridaemia and in 'coronary artery disease with low-HDL cholesterol'. Apo AI levels tended to be low in FCHL and were decreased in 'coronary disease with low-HDL cholesterol'. In familial hypertriglyceraemia, even though HDL-C levels were low, normal apo AI and apo B levels were seen in the absence of premature coronary artery disease. Therefore, in genetic dyslipidaemias elevated apo B levels and reduced apo AI levels (or increased apo B/AI ratio) differ and predict premature coronary artery disease.

Diastolic filling of hypertrophied left ventricles has frequently been observed by Doppler methods. We hypothesized that filling characteristics in hypertrophy vary with etiology and concurrent ischemia. For patients with hypertrophy, the left-ventricular ejection fraction was > 0.47 +/- 0.16, end-diastolic pressure was > 15 +/- 2 mm Hg, end-diastolic volume index was < 96 +/- 12 ml/m2 and left-ventricular mass index was 127 +/- 7 g/m2. Peak E (early) and peak A (late) diastolic velocities and E-wave deceleration time, respectively, were as follows (significant unless otherwise indicated): normal subjects (NS), 79 +/- 9 and 82 +/- 19 cm/s, and 151 +/- 7 ms; cardiomyopathic hypertrophy, 63 +/- 16, 83 +/- 15 (NS) and 193 +/- 63, aortic stenosis without coronary disease, 110 +/- 10, 128 +/- 12 and 158 +/- 22 (NS); aortic stenosis with coronary disease, 57 +/- 12, 86 +/- 26 (NS) and 187 +/- 39; hypertension without coronary disease, 107 +/- 9, 128 +/- 9 and 143 +/- 22 (NS); hypertension with coronary disease, 58 +/- 12, 84 +/- 26 (NS) and 189 +/- 29. Hypertrophied left ventricles filled with two diastolic Doppler patterns: a relaxation abnormality with low peak E and delayed deceleration in hypertrophic cardiomyopathy, and a compliance abnormality with tall peak E and normal deceleration in pressure overload hypertrophy. When coronary artery disease occurred with pressure overload hypertrophy, impaired relaxation was the dominant pattern. Therefore, in addition to the known physiologic influences on diastolic filling, the etiology and presence of coronary artery disease modulate the configuration of transmitral velocities into hypertrophied ventricles.

Plasma HDL cholesterol and risk of myocardial infarction

Analysis of spouse data from the Western Collaborative Group Study indicated that a number of the wives' behavioral characteristics and their social status were associated with the occurrence of coronary heart disease among their husbands. During 1970-1971, a total number of 130 case and control nuclear families were recruited on a voluntary basis to further investigate the familial component of the Type A/B behavior patterns and their behavioral and psycho-social correlates. When stratified by the behavior type of the husband, we found that Type A men married to women with 13 or more years of schooling had an increased odds ratio (OR) of 3.6 for coronary heart disease compared with 0.4 in Type B men with similarly educated wives. The wife's employment status outside the home did not show a significant association with coronary disease in the husband (OR = 1.3). A self-reported measure of perceived accomplishments of the wife showed an association with coronary disease of the husband that was independent of his Type A/B behavior type (OR = 2.7). Further analyses of the psychologic aspects of the marital partners, as assessed by the Thurstone Temperament Schedule, indicated that Type A husbands who had coronary disease were married to wives who were more active and dominant than wives of noncases. On the other hand, Type B men who had stable wives with 13 or more years of education seemed to be protected from coronary disease. The relationship between coronary disease and husbands' characteristics showed case husbands to be more dominant and reflective regardless of their Type A/B behavior.

There is epidemiologic evidence that the prognosis of patients with nonischemic heart failure is better than that for patients with ischemic heart failure. In addition, studies have revealed that patients with ischemic heart failure show a poorer response to medical therapy. However, the pathophysiologic difference between ischemic and nonischemic heart disease is unclear. To clarify this point, we measured atrial natriuretic peptide, brain natriuretic peptide, angiotensin II, endothelin (ET)-1. interleukin-1beta interleukin-6. tumor necrosis factor (TNF)-alpha soluble TNF receptor I, and soluble TNF receptor II concentrations in plasma and pericardial fluid in patients with ischemic or nonischemic heart disease undergoing cardiac surgery. The pericardial ET-1 concentration in patients with ischemic heart disease was statistically greater than that in patients with nonischemic heart disease (about 1.5-fold), although no difference was found in the plasma ET-1 concentration. These findings suggest that the production and secretion of ET-1 from the myocardium in patients with ischemic heart disease are augmented to a greater extent than in patients with nonischemic heart disease. This result may lead to a greater understanding of the pathophysiology of ischemic heart disease.

There are many elements that can expand your threat of getting coronary heart disease. Some of these elements are out of your control, however many of them can be prevented with the aid of deciding on to stay a wholesome lifestyle. Some of the danger elements you can't manage are: Gender, Age, Family History, Obesity, High Cholesterol, Smoking, High Blood Pressure, Diabetes, Other factors. Heart disorder is the main purpose of death. The motives and prevention of coronary heart disorder have been studied for years, and new facts are emerging. For the remaining a number of decades, saturated fats and ldl cholesterol have been concept to be primary contributors to coronary artery disease, and consequently human beings are usually suggested to strictly restrict these in their diet. However, latest research are indicating that it might also now not be sensible to strictly restriction the consumption of dietary saturated fatty acids or substitute them with polyunsaturated fatty acids when taking different fitness stipulations into consideration. Depending on a person’s genetics, eating regimen might also or may additionally no longer be an essential thing in stopping coronary heart disease. Exercise is additionally really helpful for everybody in stopping coronary heart disease. When thinking about human development, which includes the poor consequences of coronary heart disease, human beings nevertheless have a lot to study about the human physique and the interplay of diet, the environment, and genetics. CVDs, ailments of the coronary heart and blood vessels, are the range one purpose of dying ecumenically. CVDs encompass illnesses of the blood vessels imparting the coronary heart (coronary coronary heart disease), encephalon (cerebrovascular disease), and extremities (peripheral artery disease), in integration to illnesses immediately affecting the coronary heart (rheumatic coronary heart disease, congenital coronary heart disease), and ailments involving blood clots in the veins (thrombosis, embolism) World Health Organization. Ischemic coronary heart disorder (additionally referred to as coronary coronary heart disease) is ranked as the range one motive of ecumenical mortality and incapacitation). Albeit some folks with CVDs are recognized afore a culminating event, others end up vigilant of the ailment when affected via a coronary heart assault or stroke, prompted through limited blood go with the flow to the coronary heart (heart attack) or encephalon (stroke). Stroke is presently the second-leading motive of dying ecumenically). Environmental elements are kenned to have an effect on CVDs, exceptionally via their linkages with behavioral elements such as bodily activity, salubrious diet, and tobacco use, and publicity to tobacco smoke. As the variety one motive of dying and incapacitation ecumenically, CVDs demand interest and intervention, along with efforts to adjust environments to increment threat and embolden salubrious comportments. Most cardiovascular illnesses (CVDs) are age-cognate diseases. The incidence of cardiovascular chance elements will increase with age and cardiovascular ageing contributes to the improvement of CVDs. Mounting proof has established that dietary limit (DR), an alimental anti-aging intervention, confers cardiovascular aegis and may additionally reduce morbidity and mortality of CVDs. The mechanisms underlying the benign cardiovascular results of DR are multifaceted, however current investigations divulge that DR triggers an lively bulwark replication in opposition to stress. At the middle of this replication are cardiovascular defensive signals, which encompass the mammalian goal of rapamycin, AMP-activated kinase, endothelial nitric oxide synthase, and NAD+-dependent deacetylases known as sirtuins. Among them, sirtuins play two consequential roles: epigenomic legislation and post-translational modification. However, epigenomic legislation of the cardiovascular machine through DR has now not been plenarily demystified. In this chapter, we discuss the molecular mechanisms by means of which DR confers cardiovascular bulwark and the viable involution of sirtuins in epigenomic regulation. Cardiovascular disorder is viewed to be the main purpose of mortality ecumenical. Atherosclerosis is considered as the pathological system underlying cardiovascular ailment and clinically manifested as coronary disease, stroke or peripheral arterial disease. Epidemiological research published that persistent ingestion of inorganic arsenic has incremented the incidence of sundry cardiovascular diseases. Ischemic coronary heart disorder is extra prevalent. In arsenic-affected groundwater-contaminated areas in Asian countries, extra human beings are struggling from sundry cardiovascular diseases. One of the medical consequences of cardiovascular problems is peripheral arterial disease. It reasons astringent systemic arteriosclerosis as nicely as dry gangrene. In incredibly arsenic groundwater-contaminated areas of West Bengal, India, legs had to be amputated of these arsenicosis sufferers who had gangrene of feet. A special peripheral arterial disorder kenned as ‘Blackfoot disease’ was once mundane in West Bengal. Some arsenic-affected victims in signs and symptoms kindred to Blackfoot disease. It is now viewed that continual arsenic poisoning is an unbiased threat thing for cardiovascular disease. It is considered that arsenic-induced cardiovascular sickness to human may want to be resultant of interplay amongst genetic, alimental, and environmental factors. Albeit it is determined that human beings residing in exceptionally arsenic-contaminated areas and uncovered to excessive dose of arsenic are struggling extra from unfavourable cardiovascular effects, consequences of low dose is but to be established. It is withal regarded that cardiovascular results of long-term continual arsenic publicity should be irreversible. Involution of continual arsenic publicity with numerous subclinical problems in the circulatory machine has been documented. Chronic arsenic publicity thru imbibing dihydrogen monoxide in West Bengal withal pronounced the proof of dose–response relationship between arsenic in imbibing dihydrogen monoxide and incidence of carotid atherosclerosis. In a cohort and case manage research carried out in West Bengal, dose–response relationship was once determined consequential between degree of ingested arsenic and ischemic coronary heart disease. An incremented occurrence of hypertension in an epidemiological learn about in West Bengal in the endemic Blackfoot disorder location confirmed a dose–response relationship with ingested arsenic. A find out about of blood strain in arsenic-affected areas of Bangladesh used to be withal regular with the West Bengal report. Hypertension and vascular occlusions are regarded to be the jeopardy elements for dying from ischemic coronary heart ailment or different cardiovascular illness. The feasible mechanism for arsenic-cognate cardiovascular sickness is fortified by using organic mechanism. It is regarded that arsenic can engender reactive oxygen like hydrogen peroxide and hydroxyl radicals, and can set off changes of nitric oxide metabolism and endothelial function. Molecular imaging of cardiovascular ailments is of extraordinary scientific interest. A felicitous put into effect for this venture are radiopharmaceuticals labeled with the positronA¢Â€Âemitter 18F that provide the possibility to noninvasively look into the cardiovascular physiology and pathophysiology in vivo with the outstanding nuclear medicinal drug technological know-how positron emission tomography (PET).

Coronary artery bypass grafting (CABG) is one of the most studied operations in medical history, but many of the data forming the basis for clinical decisions in patients with coronary artery disease (CAD) were derived in the 1970s and 1980s, when the procedure and medical therapy were in their relative infancy. Advances in medical therapy (beta adrenergic blockers, thienopyridines, statins, and others), percutaneous coronary interventions (PCI), and surgical techniques have changed the decision making for patients with CAD. In addition, patient populations referred for surgery have changed since the original studies documenting advantages of CABG over other forms of therapy. Since percutaneous transluminal coronary angioplasty (PTCA) was introduced, significant advances have been made in the percutaneous treatment of CAD. When drug-eluting stents (DES) were introduced in the early 2000s, many predicted the demise of CABG surgery. Enthusiasm for percutaneous treatment of CAD has most recently led to promoting PCI for unprotected left main coronary artery (LMCA) disease, an anatomical state typically reserved for CABG [1-3]. Percutaneous options have indelibly changed the face of CABG surgery and raise questions concerning the “gold standard” of care in coronary revascularization. For instance, recent reports document that patients referred for redo coronary artery surgery have declined, presumably due to the increased enthusiasm, possibly among surgeons themselves, for PCI in this setting [4]. Despite this, few studies have actually compared PCI with CABG. Two notable studies are recently available, both demonstrating advantages for CABG over PCI for left main CAD and/or three-vessel CAD [5, 6]. Concurrently, details pertaining to short-term outcomes of CABG have been questioned. For example, historical saphenous vein graft (SVG) patencies were reported as approximately 50% at 10 years [7]. However, several studies published in the mid-2000s indicate that earlyterm patencies of aorto-coronary SVG conduits are not as good as the historical figures that are still often quoted [8-10]. While the long-term patency and performance of the left internal mammary artery (LIMA) has not been questioned, the recent poor performance of