Die Sitzung wurde von Prof. Dr. Freek W. A. Verheught (Nijmegen, Niederlande) eröffnet, welcher über kardiovasku- läre Auswirkungen der Hormontherapie bei Frauen referierte. Er zeigte Daten für die orale Kontrazeption, unter welcher das Risiko der Entstehung einer tiefen Beinvenenthrombose um den Faktor 2,5 erhöht ist. Unter der in Europa zu heterozygot 5 % und homozygot 0,5 % verbreiteten Faktor-V-Leiden- Mutation und der dadurch verursachten Resistenz gegenüber aktiviertem Protein C (APC-Resistenz) steigt dieses Risiko auf bis zu 35-fach an. Darüber hinaus illustrierte Prof. Verheught anhand der Women’s Health Initiative (WHI) sehr anschau- lich den Zusammenhang zwischen der Hormonersatztherapie und dem erhöhten Auftreten von thromboembolischen zereb- ralen Insulten (relative risk [RR] 1,20; 95 %-CI: 1,01–1,40) sowie ganz allgemein venös thromboembolischen Ereignis- sen (RR 2,14; 95 %-CI: 1,64–2,81), wobei das höchste Risiko dafür im ersten Jahr besteht. Des Weiteren erhöht sich die Inzidenz für Brustkrebs-, Endometrium- und Ovarial-Karzi- nome sowie für Cholelithiasis und Cholezystitis bei post- menopausalen Frauen unter Hormonersatztherapie. Die bis- lang geäußerte Vermutung einer Erniedrigung von kardiovas- kulären Ereignissen durch den Hormonersatz konnte mittler- weile widerlegt werden, so berichtet die WHI sogar über ein häufigeres Auftreten von akuten koronarvaskulären Ereignis- sen („hazard ratio“ [HR] 1,29; 95 %-CI: 1,02–1,63) sowie eine damit verbundene erhöhte Mortalität. Vorteile der Hor- monersatztherapie sind neben der Verringerung der klimakte- rischen Beschwerden sowie einer damit einhergehenden Stei- gerung der Lebensqualität zweifelsohne eine geringe Inzidenz der Osteoporose sowie ein aus Metaanalysen von 18 Studien
A correlation has been observed between Lp(a) and cholesterol concentration. 12 In this study a significant difference between the prevalence of high levels of Lp(a) and the severity and extent of CAD was not identified. On the other hand, some studies did not show an association between Lp (a) serum levels and CAD 14 . others reported a valid predictive value to the sub- population of Lp(a) with high fibrin affinity. 15 Moliterno et al showed no corelation between plasma Lp(a) concentration and the precence or absence of CAD in Africa-Americans. 16 Determination of definite cut-off point for Lp(a) is difficult. Frolkis, 17 Willeit et al (18), Buldassarre et al (19) and Jurgens et al (20) regarede 32 mg/dL, 30 mg/dL , >24 mg/dL and >20 mg/dL as cut-off points for high Lp(a) concentration respectively. Since the relationship between Lp (a) serum concentration andcoronary atherosclerosis was determined significant at levels over 30 mg/dL in our study, we considered Lp (a) ≥30 mg/dL as cut-off point for our population study. Veeranna et al, 21 showed between traditional cardiac risk factor only diabetes mellitus emerged as an independent predictor of obstructive coronaryarterydisease burden, that was similar to our results, that diabetes was more frequent in case than control groups (29.1% vs 5.7%) and had a significant relationship with the severity of coronarydisease (P=0.001). The limitation of our study was the very small sample size, so we propose larger study in the future.
We included patients aged over 30 years, of both sexes, with indication for MRS and CAD confirmed by coronary angiography. Patients who had undergone MRS combined with other surgeries including valve surgeries, carotid endarterectomy, vascular surgeries were excluded. Systemic hypertension, diabetes mellitus, dyslipidemia, current or past smoking, sedentary lifestyle, chronic renal failure and obesity were considered riskfactors for CAD. Hospitalization costs related to medications, laboratory tests, imaging tests, materials, and healthcare professionals, provided by the cost center, were collected from patients’ medical records. We used the micro-costing method, in which each intervention performed was individually counted for the total hospitalization costs. The values used as basis of cost estimation were obtained from the Table of Procedures and Medications of SUS Managing System (SIGTAP).
tery disease may have the same behavior in regard to morbi- dity, because data on mortality in the entire country are simi- lar. Our findings about the prevalence of riskfactors in the state of Rio Grande do Sul (tab. I) suggest the relevance that the morbidity of coronaryarterydisease may have in our environment. With health programs for the population ex- plaining and fighting the riskfactors, we will be able to de- crease their prevalence and reach effective and favorable results in the struggle against morbidity due to coronary ar- tery disease.
Cardiovascular disease is the most important cause of mortality and morbidity in developed countries worldwide. Secondary prevention is important to combat the further progression of atherosclerotic diseaseand to reduce mortality from coronaryarterydisease. Although there is an established association between regular physical activity and cardiac riskfactors in the secondary prevention of coronaryarterydisease (2), the authors did not mention the relationships between physical activity and reductions in blood pressure, fasting glucose levels, and BMI. We think that the results of the study would be stronger if the authors addressed the issue of physical activity in their patient cohort.
Coronary heart disease in diabetes mellitus: riskfactorsand epidemiology Cardiovascular complications in diabetic patients, especially type 2, can be classified as microvascular (renal, ophthalmologic and neurologic) and macrovascular (coronary, cerebrovascular and peripheral vascular). Type 1 and 2 diabetic patients have increased cardiovascular risk, especially for coronaryarterydisease. This has been well established through high-quality studies, as have inter- ventions to ameliorate the major riskfactors. The main riskfactors for increased incidence of coronaryarterydisease in diabetic patients include hyperlipidemia, hypertension, smoking, microalbuminuria and
The hypothesis of myocardial ischemia should also be considered, because the patient had riskfactors for coronaryarterydisease, had previous acute ischemic syndrome, and his electrocardiogram showed new abnormalities (atrial fibrillation and right bundle branch block). The fact that this acute relapse had not occurred during angina is what makes this diagnosis less probable. In addition to an atherosclerotic ischemic event, an embolic ischemic event may not be ruled out, although it is an uncommon complication also reported in patients with advanced dilated cardiomyopathy 10 .
Myocardial Infarction (MI) happened after atherosclerosis phenomena in the coronary heart artery. It is one of the most common diseases with high mortality and morbidity in human beings. There are many known riskfactors in CoronaryArteryDisease (CAD) like; old age, male gender, cigarette smoking, hypertension, diabetes mellitus and hyperlipidemia [1-4] .
Objective: To correlate non-invasively detectable indicators of coronary atherosclerosis, or CoronaryArteryDisease (i.e., classical riskfactors, hs-CRP test results, carotid intima-media thickness, endothelial function, ankle-brachial index and calcium score by computed tomography) with the extent of coronarydisease assessed by the Friesinger index from conventional coronary angiography. METHODS: We conducted a prospective study of 100 consecutive patients, mean age 55.1 ± 10.7 years, 55% men and 45% women. Patients with acute coronary syndrome, renal dialytic insufficiency, collagen diseaseand cancer were not included. All patients were subjected to clinical evaluation and laboratory tests. Endothelial function of the brachial arteryand carotid artery were evaluated by high-resolution ultrasound; ankle-brachial index and computed tomography for coronary determination of calcium score were also performed, and non-HDL cholesterol and TG/HDL-c ratio were calculated. All patients were subjected to coronary angiography at the request of the assistant physician. We considered patients without an obstructive lesion (< 29% stenosis) demonstrated by coronary angiography to be normal.
Diabetes mellitus is one of the major riskfactors for coronaryarterydisease. The disease progresses faster in diabetic patients and is associated w ith a w orse prognosis. Although bypass sur- gery or percutaneous interventions w ith stent implantation pro- vide quick symptomatic relief for patients w ith stable coronary ar- tery disease, it has no substantial prognostic benefit. A multifactorial intervention including dietary measures, blood-glucose control, anti- hypertensive treatment, and regular physical exercise does have a positive influence on the modifiable riskfactors, and improves among others cardiovascular fitness and angina-free exercise tol- erance.
Dyslipidemia is a well-established risk factor for CAD in different populations, with and without diabetes mel- litus . In our high risk group, approximately 80% of patients had dyslipidemia. Low levels of HDL choles- terol, often associated with elevated triglyceride levels, are the most prevalent pattern of dyslipidemia in per- sons with T2DM . Both alterations were more preva- lent in T2DM with CAD in our group. This lipid modification is commonly associated with insulin resist- ance [27,28]. However, we found no differences between HOMA-IR between the groups. It is noteworthy that the HOMA-IR in patients with T2DM was much higher when compared to normoglycemic individuals, in agree- ment with the role of insulin resistance in T2DM (Table 1). If elevated LDL-cholesterol is a well defined causal risk factor for CAD, uncertainty exists about whether elevated triglyceride levels represents an add- itional independent CVD risk factor . Of course, data from these epidemiological studies do not necessarily
The prevalence of classic riskfactorsand plasma aminothiol profile were evaluated in healthy subjects from Ponta Delgada (PDL) and Lisbon cities, aiming to find precocious biomarker(s) of the disease. The concentrations of aminothiols in both plasma and erythrocyte, as well as several redox parameters were also determined in 174 angiographically documented CAD and non-CAD azorean subjects under medication, searching for biochemical predictors of CAD and its severity.
visible in females. The association of ACE I/D DD geno- type with CAD in men but not in women, has been reported previously in several studies [27,28]. While our patient subpopulation was in Hardy-Weinberg equilib- rium for I/D polymorphism of ACE gene, the control sub- population was not, due to an excess of heterozygotes ID. Similar results were previously reported [5,29] and may be interpreted as a case of heterosis, or even confirm the higher risk homozygotes DD have to develop CAD. The deletion polymorphism of the ACE gene has been shown to be associated with both CAD and MI [5,30,31]. The mechanism by which the ACE I/D or ACE11860 gen- otypes may predispose an individual to the development of MI remains unclear. ACE is responsible for the conver- sion of angiotensin I to the peptide precursor angiotensin II, which has been implicated in the pathogenesis of atherosclerosis [32,33]. In contrast, other studies con- cluded that ACE polymorphisms did not influence the development of MI or other manifestations of CAD [34,35]. There are several possible reasons for these dis- crepancies: besides the different genetic backgrounds of the study populations, some of the studies cited have only minor statistical power or the associations between ACE gene polymorphisms and CAD or MI have been restricted to relatively small subgroups. Even more, in some studies, the presence or absence of CAD was not determined by angiography and might even have used false-negative con- trol populations. These findings also stress the necessity of considering ethnic factors in the assessment of genetic risk identifiers.
Additionally, in 1997, Grau et al. clinically assessed a group of 166 patients with acute ischemic stroke and 166 control subjects. They used the total dental index (TDI) to determine the status of caries, periapical lesions, periodontitis, and other dental lesions. Considering the low social status of participants and the riskfactors for cerebrovascular ischemia (e.g., diabetes and tobacco smoking), poor dental status, as defined by TDI, was associated with an increased risk of cerebrovascular ischemic events. However, the authors noted that this relationship was less evident after taking other CVD riskfactors into account (13).
Genetic component – The participation of the genetic component in the population with coronaryarterydisease is unknown. In clinical practice, investigation of the probable hereditary component influencing the development of atherosclerosis is basically performed through the verification of the presence of precocious coronaryarterydisease in parents, i. e., diagnosis of coronaryarterydisease in the father before the age of 55 years and in the mother before the age of 65 years, or in the siblings. This analysis, even though signi- ficant, has little sensitivity and does not consider the existence, isolated or in association, of other potential riskfactors in these patients, which may significantly influence the develop- ment of an ischemic coronary process or even a peripheral thromboembolic episode. One of the classic examples is the adverse effect of tobacco potentiated by the use of contra- ceptives. This predisposition to thromboembolic events is as- sociated with disorders in the coagulation system, such as elevated serum levels of fibrinogen (due to tobacco) or reduced serum levels of vitamin C (genetically transmitted). In the same way, the influence of the polymorphism of the genes responsi- ble for the coagulation factors in this interaction is discussed. Therefore, investigators have begun to analyze the association of genetic polymorphisms with coronaryarterydisease.
limited to 12 months, whereas most DTS and SPECT studies lasted more than 3 years. An atherosclerotic plaque, even a vulnerable one, does not always lead to a clinical event within a 12-month period, and it may become unstable even later on, depending on the control of riskfactors. Stress testing methods, however, could detect early changes, for instance, perfusion defi cit could be detected by SPECT. Patients with two or more riskfactors for coronaryarterydisease were purposely chosen for this study, since this population is more susceptible to events and probably has a greater number of coronaries involved. It is known that exercise stress testing has greater sensitivity in multiartery disease patients, what may have increased DTS sensitivity. The same is true, however, for SPECT and with any other stress testing
From November 29, 2009, to february 3, 2010, 255 participants were included. Table 1 shows the results according to the presence of CAD, clinical history and different STAXI subscales. The patients with CAD most frequently had previous cardiac procedures (CABG and PCIp) and a lower mean level of anger control than patients without CAD, who most often were married as compared to the former. Other riskfactors, previous medical history and anger subscales showed no significant differences. The multiple logistic regression analysis (Table 2) identified a relationship between CAD and low anger control, previous CABG or PCI, and marital status.
inson et al., 1995; Hofmann et al., 2001; Andreassi et al., 2003). Hcy, an amino acid derived from protein catabolism, is present in the plasma in several forms, with the greatest proportion (70%) bound to albumin (Doevendans et al., 2001). High levels of Hcy (hyperhomocysteinemia) have been identified as a risk factor for atherosclerosis (Bova et al., 1999; Hankey and Eikelboom, 1999; Lobo et al., 1999; Doevendans et al., 2001; Andreassi et al., 2003). The mechanism for the vascular lesions induced by hyperhomocysteinemia remains unclear. Experimental evi- dence suggests that Hcy facilitates the vascular oxidative process, thereby altering the coagulation system, and re- duces the vasomotor regulation of the endothelium (Welch et al., 1997; Tyagi, 1998; Hankey and Eikelboom, 1999; Hofmann et al., 2001). The aim of this study was to assess the relationship between MTHFR gene polymorphism and plasma homocysteine level with the traditional riskfactors of coronaryarterydisease in a north Indian population.
suggest subclinical atherosclerotic illness was proposed, called emerging factors, including peripheral vascular disease, thickening of the intima-media wall of the carotid arteryand calcium contents in coronary arteries, which contribute to an increase in cardiovascular risk levels, as they are markers of endothelial injury. In addition, the consideration of other factors was suggested for the sake of cardiovascular risk assessment: C-reactive protein, presence of the metabolic syndrome and traditional riskfactors like a family history of premature coronaryarterydisease (4) . Similarly to this proposal, other riskfactors were also added to the traditional Framingham score, called aggravating factors, such as left ventricular hypertrophy (LVH) via electrocardiography, microalbuminuria (30 to 300 mg/24h) and chronic kidney disease (plasma creatinine levels higher than 1.5 mg/dL or creatinine iltration below 60 mL/min) (13) . According
fractions for multiple riskfactors for incident myocardial infarction in several regions of the world. It was revealed that abnormal lipids, smoking, hypertension, diabetes, abdominal obesity, psychosocial stress, decreased consumption of fruits and vegetables, moderate consumption of alcohol, and physical activity accounted for most of the risk of myocardial infarction worldwide. Collectively, these nine riskfactors accounted for 90 per cent of the population attributable risk (PAR) in men and 94 per cent in women. The risk of heart attacks imposed by these riskfactors was similar in both sexes, for all the population\groups studied at all ages in all regions emphasizing the role of environmental origin of cardiovascular riskfactors for all the ethnicities of the world. The effect of the riskfactors is particularly striking in young men (PAR about 93%) and women (about 96%), indicating that most premature myocardial infarction is preventable. Worldwide, the two most important riskfactors are smoking and abnormal lipids. Together they account for about two-thirds of the PAR of an acute myocardial infarction. Psychosocial factors, abdominal obesity, diabetes, and hypertension were the next most important riskfactors in men and women, but their relative effect varied in different regions of the world. The usual measure of obesity (body-mass index) showed a modest relation with acute myocardial infarction but was not significant when abdominal obesity was included in the analysis. The South Asian component of this study confirmed that deaths due to acute myocardial infarction in south Asians occur at 5-10 years earlier than western population. This higher risk for premature coronaryarterydisease is largely determined by the higher levels of riskfactorsand the nine conventional riskfactors (abnormal lipids, smoking, hypertension, diabetes, abdominal obesity, psychosocial factors, consumption of fruits & vegetables, alcohol and regular physical activity) collectively explain 86 per cent of the AMI risk in south Asians. In South Asians too, abnormal Apo-B/ApoA-1 ratio and smoking are the most important riskfactors. Low education level is associated with increased risk of AMI worldwide. Protective lifestyle factors such as leisure time physical activity and regular intake of fruits and vegetables are markedly lower among south Asians than western population, while harmful riskfactors