Development Of Cardiovascular Morbidity Research Articles

A new metabolic syndrome prediction model for self-evaluation as a primary screening tool in an apparently MetS-free population

BackgroundMetabolic syndrome (MetS) is a growing global public health concern associated with increased morbidity and mortality. The study aimed to establish a simple self-evaluated prediction model to identify MetS. MethodsA cross-sectional study based on the American National Health and Nutrition Examination Survey database was performed. Participants aged ≥20 in the 2009–2018 surveys, with no current pregnancy or major morbidities, were included. The model was built with data from 2009 to 2016 and validated using 2017–2018 data. MetS was defined according to AHA/NHLBI guidelines. Multivariable logistic regression was applied to build a prediction model. The area under the receiver operating characteristic curve (AUC) was used to assess the discrimination ability and the maximal Youden's index was used to identify the optimal cut-off value. ResultsThe study included 4245 individuals (median age 37, IQR 28–49, 51.8% females) in the training group and 911 individuals (median age 37, IQR 28–52, 52.5% females) in the validation group. Older age, male gender, non-Black race, no postsecondary education, and higher BMI were significantly associated with increased risk of MetS. The final model included age, gender, race, education, and BMI, and showed good discrimination ability (AUC = 0.810, 95% CI 0.793–0.827, sensitivity 80.4%, specificity 66.2%, positive likelihood ratio 2.379, negative likelihood ratio 0.296, PPV 59.6% and NPV 84.5%). ConclusionA new model for self-evaluation may serve as a primary, easy-to-use screening tool to identify MetS in an apparently MetS-free population. A simple application may serve for primary and secondary prevention, thus enabling risk reduction in the development of cardiovascular morbidity and health expenditure.

Disturbances of Autonomic Regulation of Cardiovascular System at Different Working Regimes with Night Shifts

Aim To study temporal and spectral characteristics of heart rhythm variability (HRV) in night shift workers.Materials and methods Along with traditional risk factors, conditions of labor contribute to development of cardiovascular morbidity, including night shift work, which can be associated with disorders of the autonomic regulation detected by analysis of HRV. This study included 100 healthy men. 74 of them were engaged in shift work, including 53 men with rotating shift work, 21 men with fixed night shifts, and 26 men with day-time work. HRV was analyzed by data of 5-min electrocardiogram recording (background recording and orthostatic test).Results Night-shift workers had decreases in total power of regulation (ТР, SDNN) and in the parasympathetic branch (HF, pNN50). Rotating night-shift workers displayed significant decreases in SDNN and pNN50 and pronounced changes in the VLF / LF / HF ratio in the orthostatic test.Conclusion In work with night shifts, the type of autonomic regulation differs from the "standard" functioning of the autonomic nervous system (ANS). This study showed different effects of night work regimens on HRV indexes. With the rotating shift work, the ANS dysregulation was more profound and was evident by a significant decrease in the ANS total tone and parasympathetic activity (SDNN, pNN50) compared to night shifts with fixed working hours. The excessive weakening of the parasympathetic component in the passive orthostatic test can be considered as an early marker for ANS maladaptation.

P1225PREVALENCE AND PROGNOSTIC SIGNIFICANCE OF DIABETES IN PERITONEAL DIALYSIS: TECHNIQUE AND PATIENT SURVIVAL

Abstract Background and Aims Diabetes in recent years is climbing up as the number one cause of chronic kidney disease (CKD). Clinical statistics suggest that Diabetics on peritoneal dialysis (PD) tend to have a poorer prognosis than others. Thus, the aim of this study is to determine the clinical outcomes and to evaluate the survival rates as well as the predictors of mortality among this group. Method It‘s a retrospective study carried out in the nephrology Department of Fattouma Bourguiba Hospital (Monastir, Tunisia) from 1990 to 2017 including 304 PD patients. We compared two groups: diabetic and non diabetic patients in term of survival and factors in correlation. Results A total of 110 diabetic versus 194 non diabetic patients were reported. The mean age of diabetic group was 55.14 ± 15 years with a sex ratio 2.33 (men/women). In addition to diabetes, comorbid diseases included hypertension (47.3%) and cardiopathy (32.7%). The mean Charlson score of diabetic group was 5.22±1.5 versus 2.72±1.23 in the other group. A total of 62.7% (n=69) of the patients performed PD with the help of another person mostly a member of the family. The PD modality often used was CAPD (71%). Only six patients made a compulsory choice to begin PD due to vascular access while sixty diabetics chose PD to maintain autonomy (54.5%). During the follow-up period, transfers to hemodialysis (40.9%) and death (53.6%) were the most common cause of withdrawal from PD. In total, 45 patients were transferred to hemodialysis because of infectious complications (31%), Ultrafiltration failure (31%), catheter dysfunction (27%), and psychological intolerance (11%). The death was unrelated to PD in 83% of cases mostly due to considerable burden of cardiovascular events (23 patients). The median survival of the diabetic patients was 15.8 years versus 20.8 years in non diabetic ones with significant difference between the 2 groups (p=0.0001). Diabetes was associated with worse prognosis (OR:147, p=0.0001). The median survival adjusted to the diabetes group was 180 months. Kaplan–Meier analysis showed that diabetes was associated with a significant increase in mortality (p=0.006). Global median survival of the technique was estimated to 68 months (95%, IC [47 ,90]), and it was correlated to the presence or the absence of diabetes. In fact, the technique survival among diabetic patients was estimated to 80% after 12 years and 25% after 20 years whereas, in the other group it approaches 90% and 35% respectively. Conclusion This study confirms the pejorative impact of diabetes in the technique and patient survival in DP. So, it stresses the importance of organizing appropriate care upstream to prevent the development of cardiovascular morbidities and infectious complications in DP.

Association between ACE and AGT polymorphism and cardiovascular risk in acromegalic patients.

Whether the renin-angiotensin-aldosterone system plays a role or not in the development of cardiovascular morbidity in acromegaly patients is unknown. The aim of the study was to investigate the association between ACE (I/D) and AGT (M235T) gene polymorphisms and cardiovascular and metabolic disorders in the acromegaly. The study included one hundred and seventeen acromegalic patients (62F/55M, age: 50.2 ± 12.3 years) and 106 healthy controls (92F/14M, age: 41.4 ± 11.3 years). PCR method was used to evaluate the prevalence of ACE and AGT genotype. The genotypes of ACE polymorphism in acromegalic patients were distributed as follows; 41.0% (n: 48) for DD, 44.4% (n: 52) for ID and 14.5% (n: 17) for II genotype. The control group had significantly different distribution of the ACE polymorphism [48.1% (n: 51) for DD, 25.5% (n: 27) for ID and 26.4% (n: 28) for II genotype]compared to acromegalic group. Regarding AGT polymorphism, AGT-MT genotype was seen in 88.9% of the acromegalic patients while MM and TT genotype (9.4% and 1.7%, respectively) were present in the rest. The controls had similar distribution of the AGT genotype with the acromegaly group (80.2% MT genotype, 15.1% MM genotype and 4.7% TT genotype). Due to the small number of patients with TT allele (n: 2), T carriers for AGT genotype (AGT-MT+TT) were subgrouped and compared to those with AGT-MM group. ACE-DD, ID and II groups had similar anthropometric measures, blood pressure values and baseline GH and IGF-1 levels. Significantly higher baseline GH levels were found in AGT-MM group compared to T allele carriers [40 (16-60) vs. 12 (5-36)µg/L, p < 0.05]. The compared groups in both polymorphisms had similar fasting plasma glucose levels. Patients with ACE-II genotype had significantly higher HDL-C levels compared to those with ACE-DD and ACE-ID polymorphisms (p < 0.05) whereas there was no significant difference in lipid profile between AGT-MM group and AGT-T allele carriers. Moreover, the compared groups in both polymorphisms had similar distribution of hyperlipidemia, hypertension, impaired glucose metabolism (prediabetes or type 2 diabetes mellitus) and coronary artery disease. In terms of echocardiographic parameters, systolic and diastolic function was similar among the groups in ACE and AGT genotypes. Interestingly, AGT-MM group had higher mitral inflow Apeak values than T allele carriers (0.94 ± 0.46 vs. 0.73 ± 0.20; p = 0.051). No significant difference was observed in LV mass index values in acromegalic patients among the groups in both polymorphisms. Both ACE (I/D) and AGT (M235T) gene polymorphisms do not seem to have a significant effect on the development of clinical properties or cardiovascular comordities of acromegalic patients.

A Comparative Study of Serum Uric Acid Level in First Degree Relatives of Patients of Acute Coronary Syndrome and In Normal Subjects

1 Demonstrator, Department of Physiology, Assam Medical College, Dibrugarh-786002, Assam, India 2 Professor, Dept of Physiology, Fakhruddin Ali Ahmed Medical College, Barpeta-781301, Assam, India 3 Professor, Department of Cardiology, Assam Medical College, Dibrugarh-786002, Assam, India Corresponding Author Dr Subha Bhakta Department of Physiology, Assam Medical College, Dibrugarh, Assam-786002 Email: subha84b@gmail.com , Mobile no: 9435678993 ABSTRACT Background: Ischaemic heart disease (IHD) is a leading cause of worldwide morbidity and mortality. A number of risk factors have been described in the etiology of IHD. Uric acid is one of the modifiable risk factor plays a role in the development of cardiovascular morbidity in the general population. We can delay the development of IHD by better control of uric acid levels in first degree relatives (FDRs) of IHD patients. We conducted a study in which we were assess serum uric acid levels independent of other established risk factors in FDRs of IHD patients and in normal subjects. Method: Sixty first degree relatives of IHD patients were selected, who were the attendants of the patients coming to the cardiology OPD and patients admitted to Intensive Care Unit (ICU), Assam Medical College Dibrugarh. An equal number of subjects were selected as a control group who had no family history of IHD. After a detailed clinical history and physical examination, fasting blood samples were collected. Blood glucose, lipid profile and serum uric acid levels were estimated. Results: The serum uric acid levels were found to be significantly high in first degree relatives of acute coronary syndrome in comparison to healthy individuals. Conclusion: . We therefore conclude that high uric acid has a definite role in Cardiovascular disease in first degree relatives.

Association between Serum Uric Acid Levels and Hypertension: A Retrospective Study

Introduction: Elevated uric acid levels are frequently associated with lifestyle related diseases. Serum uric acid levels also have shown to play a very important role in the development of cardiovascular morbidity and renal disease progression in the patients with hypertension. We had undertaken this study to assess the relation between elevated uric acid levels with hypertension. Materials and Methods: 422 patient above the age of 18, with essential hypertension were included into this retrospective study. The medical records of these patients were reviewed for details such as medical history, age, sex, blood pressure at the time of diagnosis, the laboratory results for blood glucose levels, cholesterol and triglycerides, and the uric acid level. 50 healthy males and females with no hypertension and normal blood pressure and of similar age group were used as controls. Results: The number of males were 54.7% and females were 45.3%. Many of the patients who had hypertension had a family history of elevated blood pressure. There was no significant difference in the age groups and the BMI of the patients with the controls while, there was significant difference in the urea creatinine, triglycerides and cholesterol levels among the patients with elevated uric acid and hypertension, in both males and females than the respective controls. Higher uric acid levels were observed in 64% of the males and 59% females. Conclusion: We have observed a high prevalence of elevated serum uric acid levels among the patients with hypertension, irrespective of their age and gender with a positive correlation between the SUA and systolic and diastolic blood pressure. Keywords: Serum Uric Acid, Hypertension, association

Effect of moderate exercise on VO2 max and blood pressure in individuals with different body mass index

Background: Cardiorespiratory fitness is important for a person to efficiently perform his day to day life activities. Obesity influences this fitness leading to the development of cardiovascular morbidity and mortality. Fitness can be improved through physical exercise which could be categorized into moderate or severe based on the maximum heart rate. Maximum oxygen uptake (VO2 max) is yet another equivalent parameter in use to assess the severity of the exercise. This study aims to study if there is any influence of moderate exercise on the VO2 max in individuals with greater BMI. Materials and Methods: Institutional Ethics Committee approval was obtained and a written informed consent was obtained from all the study participants. Sixty four young adults of mean age (19.66 + 0.2years) underwent a 30 minutes normal walking in order to perform a moderate exercise using a pedometer counting 3000 steps. Pre and post exercise variables like blood pressure and heart rate was recorded using a semiautomatic digital sphygmomanometer(OMRON HEM 401,India).Maximum oxygen uptake (VO2 max) was calculated and the difference between the pre and post exercise condition was derived. Paired ‘t’ test was done using SPSS 17.0 and the statistical significance value was set at p

A Comparative Study of Serum Uric Acid levels and Lipid Ratios in Coronary Artery Disease Patients

Introduction:Coronary Artery Disease (CAD) appears to be common in the Indian population of different geographical origins, religions and languages. Measurement of lipid fractions and ratios are widely recommended for risk assessment. A few studies have shown that serum uric acid plays a role in the development of cardiovascular morbidity. Very few reports are cited linking serum uric acid with the lipid fraction in CAD. Objectives:To find the significance of non-HDL cholesterol, LDL-c/HDL-c ratio, TC/HDL ratio and serum uric acid level in CAD patients. Subjects and Methodology:In this study, we included fifty CAD patients as subjects and an equal number of controls. Both subjects and controls were assessed for anthropometric, physiological and biochemical parameters. Results:The present study showed significant increased levels of total cholesterol (p=0.002), TAGs (p&lt;0.001), HDL (p=0.005), LDL (p&lt;0.006) and non-HDL cholesterol (p&lt;0.001). LDL-c/HDL-c ratio (p&lt;0.001) and TC/HDL ratio (p&lt;0.001) in CAD patients (subjects) were also significant when compared to controls. Uric acid level in CAD patients was increased (p&lt;0.001). Conclusion:Serum Uric Acid, TC/HDL and LDL/HDL ratios could be regarded as objective markers, in association with existing atherogenic dyslipidemia in patients with CAD.

Analysis of risk factors in obese patients with coronary artery disease, with and without diabetes mellitus type two

Diabetes mellitus type 2 is one of the leading chronic diseases in the world and in our country, which is an important risk factor for development of cardiovascular morbidity and mortality. Objective. The aim of this research was making the estimation of risk factors in the etiology of coronary heart disease in obese patients with diabetes mellitus type 2. The study included 82 obese patients, of which 52 with diabetes mellitus and 30 without diabetes mellitus, in all of them coronary artery disease proven by coronary angiography. All were examined by clinical examination, laboratory tests and echocardiography. Based on the test results we found that the distribution of risk factors such as hypertension, family burden coronary artery disease, smoking, alcohol intake was the same in the obese patients with diabetes mellitus, and of those without diabetes mellitus. Echocardiography showed significantly larger left ventricle, lower ejection fraction, larger left atrium and significant mitral regurgitation. Also, in a group of patients with diabetes mellitus, there was significantly higher number of patients with multiple vessel coronary disease. Despite the small sample, we can conclude that the present of diabetes mellitus in obese patients is crucial for severe forms of coronary artery disease. Severity is expressed through significant structural and functional changes in the left ventricle and the number of diseased coronary arteries.

Association between osteoprotegerin, fetuin-A, carotid intima media thickness, and urinary albumin excretion in Type 2 diabetes

Vascular calcification and atherosclerosis play a vital role in the development of cardiovascular morbidity and mortality in diabetic patients, especially when complications of diabetic nephropathy occur. Osteoprotegerin (OPG) and fetuin-A are two markers of vascular calcification. We evaluated the association between these vascular markers and urinary albumin excretion in diabetic patients. Three groups were arranged containing 40 patients: normoalbuminuric (Group 1), microalbuminuric (Group 2), and macroalbuminuric (Group 3). In addition to the obtained data, levels of hs-CRP (high sensitivity-CRP) and homocysteine were examined. OPG levels of patients in Group 2 were higher than in Group 1 (p = 0.058). OPG levels in Group 3 were lower than in Groups 1 or 2 (p = 0.014 and 0.000, respectively). Levels of fetuin-A in Group 2 were determined to be lower than in Groups 1 and 3 (p = 0.001 and 0.000, respectively). Carotid intima media thickness (CIMT) in Group 3 was higher than in Group 1 (p = 0.002). CIMT in Group 2 was also higher than in Group 1 (p = 0.039). A positive correlation between fetuin-A and OPG was found (p = 0.012, r = 0.393). Additionally, a positive correlation between hs-CRP and fetuin-A in Group 2 (p = 0.020, r = 0.367) and a negative correlation between hs-CRP and OPG in Group 3 (p = 0.036, r = -0.333) were observed. The differences found between albuminuria and OPG or fetuin-A may be due to the different doses and variety of medications the patients received, in addition to genetic and racial factors. So far, in our country, polymorphisms related to OPG and fetuin-A have not been defined. Further detailed studies about polymorphisms will have additional value.

Tissue‐specific expression of angiotensin‐converting enzyme 2 (ACE2) from two promoter regions is unaffected by elevated levels of renin and angiotensinogen

Angiotensin‐Converting Enzyme type 2 (ACE2) counteracts Renin‐Angiotensin System (RAS) over‐activity and has been proposed to protect against the development of cardiovascular morbidity. ACE2 is transcribed from a proximal and distal promoter. ACE2 gene regulation is furthermore dependent on tissue type. Hypothesis: tissue‐specific regulation of the ACE2 gene in response to RAS over‐activity is due to tissue‐specific promoter usage. We developed real‐time qRT‐PCR assays for a proximal promoter transcript (PPT) and a distal promoter transcript (DPT). We analyzed brain, kidney, lung, and heart RNA from wild‐type mice and hypertensive transgenic mice with overactive RAS due to expression of human renin and angiotensinogen. Surprisingly, the genotype did not affect the ACE2 transcript levels. However, the tissues differed in promoter usage: the PPT is significantly (p &lt; 0.001) more abundant than the DPT in the kidney, brain, and heart (&gt;20‐fold), whereas the DPT is significantly more abundant than the PPT in the lung (49‐fold). Among tissues, the kidney had the highest concentration of the PPT whereas the lung had the highest concentration of the DPT. Our work illustrates that tissue‐specific promoter usage should be taken into account when developing new therapies based on modulating ACE2 expression. Support: NIH/NHLBI HL093148, NCRR P20RR016456, and Louisiana Board of Regents Support Fund.

Changes in adiponectin and the risk of sudden death, stroke, myocardial infarction, and mortality in hemodialysis patients

Adiponectin is an adipocyte-specific cytokine that has a protective role in the development of cardiovascular morbidities. As chronic kidney disease progresses, adiponectin levels increase and cardiovascular risk profiles change. Here we determined the association of baseline and longitudinal changes in adiponectin with different cardiovascular outcomes in 1255 type 2 diabetic hemodialysis patients in the German Diabetes and Dialysis Study. Within 4 years of follow-up, the hazard ratios to reach pre-specified, adjudicated end points were determined. The increased risk of cardiovascular events observed with high adiponectin levels at baseline was associated with high risks of sudden death and stroke but not of myocardial infarction. Adiponectin was negatively correlated with C-reactive protein and positively correlated with NT-pro-BNP, the latter significantly attenuating the associations with adverse outcome. Increased longitudinal levels of adiponectin during follow-up were associated with higher risks of adverse cardiovascular outcomes and death; associations weakened by a confounding effect of increased NT-pro-BNP. Our study suggests that high basal and increasing adiponectin levels in the dialysis population largely reflect a consequence of disease circumstances. Most likely, this rise is a counter-regulatory response to worsening health in keeping with adiponectin's potential to counteract inflammation.

Oxidative Stress—A Unifying Paradigm in Obstructive Sleep Apnea and Comorbidities

Obstructive sleep apnea (OSA), a highly prevalent breathing disorder in sleep, characterized by intermittent and recurrent pauses in respiration, has emerged as an independent risk factor for cardiovascular morbidity and mortality. Accumulated evidence implicates the apnea-related multiple cycles of hypoxia/reoxygenation in promoting the formation of reactive oxygen species and inducing oxidative stress. The ramifications of oxidative stress are pivotal; they can cause damage to biomolecules, and alter cellular functions, but they also function as signaling molecules in physiologic and pathophysiologic conditions. Oxidative stress alters signaling pathways and activates inflammatory/immune responses via increased interactions of blood cells with endothelial cells, facilitating endothelial cell injury and dysfunction. Such events can promote atherosclerosis and the development of cardiovascular morbidities in OSA. Oxidative stress is also a crucial component of obesity and metabolic disorders such as dyslipidemia and type 2 diabetes mellitus/insulin resistance, which cluster with OSA and involve inflammatory pathways as well. These converging lines of evidence point at oxidative stress as the unifying paradigm underlying the cardiovascular morbidity in OSA and very likely also in promoting the metabolic disorders associated. If left untreated, this cascade of events may eventually lead to overt cardiovascular morbidity.

Eculizumab Reduces Pulmonary Hypertension through Inhibition of Hemolysis-Associated Nitric Oxide Consumption in Patients with Paroxysmal Nocturnal Hemoglobinuria

The depletion of nitric oxide (NO) by cell-free plasma hemoglobin and arginase during intravascular hemolysis has been implicated in the dysregulation of vasomotor tone and the enhancement of procoagulant and prothrombotic activities. Pulmonary hypertension (PHT), an emerging common complication of hereditary hemolytic anemias, has been mechanistically and epidemiologically linked to intravascular hemolysis and NO depletion. Paroxysmal nocturnal hemoglobinuria (PNH) is a disease characterized by chronic and brisk hemolysis, as well as elevated cell-free plasma hemoglobin. We have previously reported that approximately 50% of PNH patients have PHT as measured by doppler echocardiograpy. Further, the level of N-terminal pro-B-type natriuretic peptide (NT-proBNP) has been generally demonstrated to be a sensitive and specific measure of right-sided cardiac stress due to PHT and has more recently been shown to be a strong predictor of pulmonary hypertension (PHT) and mortality in patients with hemolytic anemias (defined as NT-proBNP ≥ 160 pg/ml). Eculizumab, a terminal complement inhibitor, has been demonstrated to significantly and rapidly reduce hemolysis, thereby providing beneficial effects on regulation of smooth muscle tone and thrombosis in patients with PNH. To evaluate the efficacy of eculizumab in the regulation of cell-free plasma hemoglobin levels, nitric oxide depletion, and subsequent cardiovascular morbidities in patients with PNH. Levels of hemoglobinemia, arginase and nitric oxide depletion were assessed in 73 evaluable eculizumab- and placebo-treated PNH in the phase III randomized, placebo-controlled trial (TRIUMPH). In addition, levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP) were assessed as a measure of PHT, and systolic and diastolic systemic arterial pressures were examined in eculizumab- and placebo-treated patients. At baseline, levels of lactate dehydrogenase (LDH), cell-free plasma hemoglobin, arginase 1 and arginase 1 enzyme activity were highly elevated compared to normal values. Levels of hemolysis and NO consumption were shown to be much greater in PNH (more than 6- and 10-fold, respectively) than in patients with other hemolytic diseases. There were substantial correlations between cell-free plasma hemoglobin levels and both LDH (R = 0.5094) and plasma consumption of nitric oxide (NO) (R = 0.9529). Strong correlations between arginase 1 and both cell-free plasma hemoglobin (R = 0.9367) and arginase 1 enzyme activity (R = 0.9081) were also demonstrated. Following eculizumab therapy, measures of hemolysis were significantly reduced from baseline, including LDH (2200 ± 158 to 327 ± 68 U/L) and cell-free plasma hemoglobin (98.8 ± 23.24 to 15.2 ± 5.05 mg/dL), while levels in placebo-treated patients remained unchanged; a concomitant reduction in NO consumption was also observed (see Figure). In addition, at baseline, 46.6% (34/73) of PNH patients in the TRIUMPH study had levels of NT-proBNP ≥ 160 pg/ml, indicating PHT in these patients. Eculizumab-treated patients showed a 50% reduction in the incidence of PHT over the course of the 26-week treatment period from 52.5% to 26.3%, while PHT did not change with placebo (39.4% to 43.8%; P<0.001). Additionally, eculizumab significantly improved dyspnea (EORTC-QLQ-C30) compared to placebo (Effect size 0.69; P=0.0002). Similarly, eculizumab treatment was associated with a concomitant decrease in systemic arterial blood pressure as compared to patients receiving placebo. To summarize, in patients with hemolytic anemia, the depletion of NO is associated with the development of cardiovascular morbidities, including PHT. The current data demonstrate that intravascular hemolysis in untreated patients with PNH is associated with high levels of plasma ferrous oxyhemoglobin, which stoichiometrically catabolizes NO, and high levels of plasma arginase 1, which catabolizes arginine – all leading to significant depletion of NO. We show a high prevalence of PHT in untreated patients with PNH as indicated by levels of NT-proBNP. Further, the data demonstrate that in a placebo-controlled study, the anti-hemolytic effect of chronic eculizumab treatment significantly increases nitric oxide bioavailability and reduces pulmonary hypertension. [Display omitted]

Remaining teeth, cardiovascular morbidity and death among adult Danes

Objective To examine if number of remaining teeth was associated with development of cardiovascular morbidity and mortality over 5–12 years. Methods Prospective observational study among 1474 men and 1458 women born 1922, 1932, 1942 or 1952 from The Danish MONICA follow up study (MONItoring trends in and determinants of CArdiovascular disease) in 1987–88 and 1993–94. Subjects were followed in Danish registers for fatal and non-fatal cardiovascular disease, coronary heart disease or stroke. Results Tooth loss was strongly associated with incidence of stroke, and to a lesser extent, incidence of cardiovascular disease and coronary heart disease, during averagely 7.5 years of follow-up. Compared to those with most teeth remaining, the edentulous suffered > 3-fold increased Hazard (HR) of developing stroke (HR = 3.25; 95% CI: 1.48–7.14), whereas the risk of developing any cardiovascular disease was increased by 50% (HR = 1.50; 95% CI: 1.02–2.19). Risk for coronary heart disease was increased by 31%, but was not significant, after the adjustment for education, age, smoking, diabetes, alcohol intake, systolic blood pressure and body mass index (HR = 1.31; 95% CI: 0.74–2.31). Associations were similar for men and women. Conclusion These findings may have implications for future prevention of cardiovascular disease in general, and of stroke in particular, because tooth loss may serve as a simple, and early means to identify high-risk individuals.

Vascular Calcifications in Uremia: Old Concepts and New Insights

The annual mortality rate in uremic patients, corrected for age, sex, and race, is significantly higher than in the general population. This is primarily due to cardiovascular events. Vascular calcifications play a vital role in the development of cardiovascular morbidity and subsequent increased mortality. Vascular calcification affects both vascular intima and media layers and its mechanism remains poorly understood. Over the last few years it has been shown that, in addition to traditional cardiovascular risk factors, disturbances in mineral metabolism in the uremic milieu, calcium-containing phosphate binders, and vitamin D treatment of secondary hyperparathyroidism may contribute to the pathogenesis of vascular calcifications. Other uremia-related risk factors (e.g.increased oxidized low-density lipoprotein cholesterol, uremic toxins, increased oxidative stress, dialysis and dialysate-related factors, hemodynamic overload, hyperhomocysteinemia) may also play a role. In uremic patients, apart from these facilitating factors, decreased levels of endogenous calcification inhibitors such as fetuin-Amatrix Gla protein, osteoprotegerin, and osteopontin have also been associated with increased calcium-phosphate precipitation in extraskeletal tissues. Finally, vascular calcification is the outcome of the active and dynamic balance of procalcifying and anticalcifying influences. For the prevention and treatment of vascular calcifications, it is essential to avoid treatment modalities that lead to calcium overload, achieve good metabolic control, and optimize dialysis.

Acute beta blocker overdose: factors associated with the development of cardiovascular morbidity.

To identify factors in exposures to beta blockers (beta-adrenergic receptor antagonists) that are associated with the development of cardiovascular morbidity and contribute to disposition decisions from the emergency department. Prospective cohort of 280 beta blocker exposures reported to 2 regional poison centers. Multiple logistic regression was used to determine association of various clinical factors and outcome. In this series of beta blocker exposures, 41 (15%) developed cardiovascular morbidity and 4 (1.4%) died. A history of cardioactive coingestant was the only factor significantly associated with the development of cardiovascular morbidity (p < .05). When cases reporting cardioactive coingestants were excluded, a history of ingesting a beta blocker with membrane stabilizing activity was significantly associated with the development of cardiovascular morbidity (p < .05). All those in whom the timing of symptoms could be determined, developed symptoms within 6 hours of ingestion. The single most important factor associated with the development of cardiovascular morbidity in beta blocker ingestion is a history of a cardioactive coingestant, primarily calcium channel blockers, cyclic antidepressants, and neuroleptics. In the absence of such coingestion, exposure to a beta blocker with membrane stabilizing activity is associated with an increased risk of cardiovascular morbidity. Beta blocker ingestion is unlikely to result in symptoms if the patient remains asymptomatic for 6 hours after the time of ingestion.

Blood Pressure and Organ Damage

Casual blood pressure measurements can predict the development of cardiovascular morbidity and mortality, but especially in mild hypertension the correlation indices between casual measurements of blood pressure and the subsequent occurrence of complications are low. Casual and office blood pressure measurements, however, provide a very limited and biased assessment of blood pressure as a risk factor since blood pressure is known to change from moment to moment and to be influenced by its very measurement. Considerable advances in our understanding of the factors influencing blood pressure during daily life and in assessing blood pressure variability have been made possible by use of portable equipment for continuous intraarterial recording of blood pressure. Equipment for noninvasive ambulatory blood pressure monitoring is also available; this equipment is more practical than intraarterial equipment, but is associated with some degree of error and several limitations. Data are reported from a recent study conducted by our group in which target organ damage in 108 hypertensive patients was correlated with blood pressure values as measured by a cuff sphygmomanometer and with various indices derived from 24-h intraarterial blood pressure monitoring. The findings indicate that the incidence and severity of organ damage are more closely related to 24-h blood pressure means than to cuff values. They also provide the first unequivocal evidence that target organ damage also relates to blood pressure variability.