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PubMed2004

Update on clinical trials of tadalafil demonstrates no increased risk of cardiovascular adverse events.

INTRODUCTION: Cardiovascular disease and erectile dysfunction (ED) share similar risk factors and often occur concomitantly. Therefore, men with ED may be at increased risk for cardiovascular adverse events. AIM: The aim of this retrospective analysis was to evaluate the cardiovascular adverse events in clinical trials of tadalafil, an effective medication for the treatment of ED. METHODS: An integrated analysis of cardiovascular adverse events was performed on a database from 35 controlled clinical trials (placebo [N = 2,118] and tadalafil [N = 5,228]) and eight open-label trials of tadalafil (tadalafil [N = 6,939]). Some patients in controlled trials also received tadalafil in the open-label extension phase of four trials. Across all trials, the dose range of tadalafil was 2-25 mg, with the majority of patients receiving tadalafil 20 mg. This analysis represents an update of previous published results. RESULTS: In 35 controlled tadalafil clinical trials, the incidence of cardiovascular adverse events was low and comparable in tadalafil- and placebo-treated patients. The rate of myocardial infarction (MI) across all controlled and open-label studies was 0.33 per 100 patient-years in tadalafil-treated patients (N = 10,460, patient exposure = 5,088 patient-years). The MI rate in tadalafil-treated patients was comparable to that in placebo-treated patients (0.41 per 100 patient-years; N = 2,118; 489 patient-years), and to that in an age-standardized male population (0.6 per 100 patient-years). The cardiac mortality rate in tadalafil-treated patients across all studies (N = 10,460) was 0.12 per 100 patient-years which was not increased compared with the cardiac mortality rate of 0.26 per 100 patient-years reported in an age-standardized male population. CONCLUSIONS: In tadalafil clinical trials, the incidence of cardiovascular adverse events in patients receiving tadalafil was low and comparable to placebo. Tadalafil did not increase the rate of MI or cardiac mortality compared with reported rates from epidemiological studies. This favorable cardiovascular safety profile for tadalafil is important, because men with ED commonly have cardiovascular disease and may seek medical therapy for ED.

Adult↗

PubMed2005

Impact on cardiovascular events of increasing high density lipoprotein cholesterol with and without lipid lowering drugs.

OBJECTIVE: To estimate the impact on cardiovascular events of changes in high density lipoprotein (HDL) adjusted for changes in total cholesterol. DESIGN: Cohort study based on a record linkage database. SETTING: Community study in Tayside, Scotland, UK. PATIENTS: 18,815 patients were identified for the study between 1989 and 2001. MAIN OUTCOME MEASURES: Cardiovascular events. RESULTS: 5510 patients taking lipid lowering treatment who had not been hospitalised previously for cardiovascular disease had 314 cardiovascular events recorded (9407 person years of follow up). Patients whose HDL rose by > 20% were less likely to have an event (23.5/1000 person years, 95% confidence interval (CI) 17.3 to 29.6) compared with patients whose HDL did not rise (42.6/1000 person years, 95% CI 35.5 to 49.7, adjusted relative risk 0.60, 95% CI 0.44 to 0.83). HDL change and cardiovascular outcome were not significantly associated among patients who had been hospitalised previously for cardiovascular disease or among patients who were not taking lipid lowering drugs. CONCLUSION: In this study a rise in HDL independently predicted reduced cardiovascular risk in patients taking lipid lowering treatment who had not been hospitalised previously for cardiovascular disease.

Cardiovascular Diseases↗

PubMed1992

Childhood blood pressure, body build, and birthweight: geographical associations with cardiovascular mortality.

STUDY OBJECTIVE: The aim was to examine whether blood pressure, body build, and birthweight differ between areas of England and Wales with widely differing adult cardiovascular mortality rates. DESIGN: This was a cross sectional survey of children in five towns with exceptionally high and five towns with exceptionally low current adult cardiovascular mortality. SETTING: The study was a school based survey. SUBJECTS: 3842 children aged 5.0-7.5 years were selected by stratified random sampling of primary schools (response rate 76%). MEASUREMENTS AND MAIN RESULTS: Blood pressure, pulse rate, height, and weight were measured and birthweight was assessed by maternal recall. Children in towns with high cardiovascular mortality rates were significantly shorter than those in towns with low cardiovascular mortality rates (mean difference 0.9 cm, 95% confidence interval 0.4 to 1.4 cm) and had slightly higher body mass indices (mean difference 0.12 kg/m2, 95% CI -0.03 to 0.27 kg/m2). Mean birthweights were slightly lower in high mortality towns (mean difference 34 g, 95% CI -10 to 78 g), while the proportion of children with low birthweight (< 2500 g) (8.1%) was significantly higher than that in low mortality towns (5.5%) (p = 0.005). Mean differences in blood pressure between high and low mortality towns were small and non-significant, even after adjustment for height. The differences in height between high and low mortality towns were largely independent of social class. However, differences in mean birthweight were markedly reduced once social class was taken into account. CONCLUSIONS: No geographical relationship between childhood blood pressure and adult cardiovascular mortality was detected. Although it is possible that the differences in mean height and body mass index between towns with differing adult cardiovascular mortality may have implications for future patterns of health in these towns, the absence of marked differences in birthweight and blood pressure suggests that hypotheses proposing a direct relationship between intrauterine experience and adult cardiovascular mortality will have limited relevance to geographical variation in cardiovascular disease in this generation.

Adult↗

PubMed2000

Social distribution of cardiovascular disease risk factors: change among men in England 1984-1993.

OBJECTIVE: To investigate change in the social distribution of some of the main risk factors for cardiovascular disease in men in England during a period when inequality in cardiovascular disease mortality widened DESIGN: Age standardised comparison of the social distribution of seven known risk factors for cardiovascular disease (body mass index, waist to hip ratio, systolic and diastolic blood pressure, consumption of fresh green vegetables, leisure time exercise, cigarette smoking and levels of social support) in two large cross sectional representative samples of the English population. SUBJECTS: Men aged 20-64 years in the 1984 Health and Lifestyle Survey (excluding Scotland and Wales) first sweep and the 1993 Health Survey for England. MAIN OUTCOME MEASURES: Mean values of continuous variables; age adjusted proportions of categorical variables; change in the relative index of inequality for each risk factor. RESULTS: The overall prevalence of cardiovascular disease risk factors improved during the period in which cardiovascular disease mortality was falling. The social distribution of cardiovascular disease risk factors, in contrast, did not become more extreme. Increases in the relative index of inequality for angina from 1.75 to 1.86, for eating vegetables less than once a day from 1.76 in 1984 to 1.96 in 1993, and an apparently larger increase in inequality of social support, from 1.92 to 2.53 were not statistically significant. In most cases the degree of inequality in risk factors tended to narrow non-significantly: for example the relative index of inequality fell from 5.02 in 1984 to 3.07 in 1993 for systolic blood pressure, from 5.60 to 4.29 for current smoking and from 6.24 to 4.19 for eating other than wholemeal bread as the main form of bread in the diet. The two statistically significant changes in inequality were in the direction of narrowing inequality: from a relative index of inequality of 2.12 to 0.90 for diastolic blood pressure (p<0.01) and from 19.3 to 0.87 (p<0.01) for psychological distress as indicated by the General Health Questionnaire. CONCLUSIONS: Healthier lifestyle options have not been adopted at a significantly faster rate by middle class than working class people over this time period. At the population level the change in risk factors is consistent with falling cardiovascular mortality. The change in the social distribution of risk factors within the population, however, shows little or no relation to the pattern of widening inequality in cardiovascular mortality. This may be because the effect is lagged, or because the adoption of healthier behaviour confers greater benefits on those in higher socioeconomic status groups.

Adult↗

PubMed1999

Cardiovascular response to exercise.

This article is intended for instructors who teach cardiovascular physiology. In our physiology course exercise physiology is used as a tool to review and integrate cardiovascular and respiratory physiology. It is assumed that the students already have mastered the fundamentals of cardiovascular and respiratory physiology. Because this paper is part of a cardiovascular refresher course, I have deleted much of the respiratory physiology. The objectives of this presentation are for the student to 1) understand the relationship between maximal oxygen consumption and endurance during sustained exercise and be able to define "maximal oxygen consumption"; 2) understand the determinants of of maximal oxygen consumption; 3) understand the effects of dynamic exercise on the cardiovascular system and mechanisms for these effects; 4) understand the relationships between exercise intensity and major cardiorespiratory parameters, including heart rate, cardiac output, blood flow distribution, left ventricular stroke volume, arterial pressures, total peripheral resistance, and arterial and venous blood oxygen content; 5) be able to compare and contrast the cardiovascular effects of dynamic and isometric exercise in man and the mechanisms responsible for the major differences; and 6) be able to apply knowledge of the cardiovascular effects of exercise to understanding the causes of cardiovascular symptoms in disease and in diagnosis of disease states. This material contains many areas that stimulate discussion with students and allow exploration of concepts that are challenging for the student. This give and take between teachers and student is difficult to summarize in an article of this sort. Therefore, subjects that in my experience often stimulate questions and discussion with the students are indicated in the text.

Cardiovascular Physiological Phenomena↗

PubMed2005

Uric acid, microalbuminuria and cardiovascular events in high-risk patients.

BACKGROUND: Elevated levels of serum uric acid and albuminuria are associated with cardiovascular disease, but the relationships have not consistently been demonstrated to be independent of hypertension, other risk factors, or each other. The purpose of this study was to evaluate people at high risk for cardiovascular disease for the influence of uric acid and microalbuminuria on cardiovascular events. METHODS: Consecutive consenting patients undergoing elective angiography (n = 316) had coronary artery disease, risk factors, renal function and diuretic use assessed at baseline. Cardiovascular mortality and major clinical events (myocardial infarction, stroke, amputation, and kidney failure) were ascertained over 5 years. RESULTS: Cardiovascular events occurred in 10% of the patients. Significant correlates (p < 0.05) of cardiovascular events with baseline measures included uric acid > or =5.2 mg/dl, total cholesterol > or =200 mg/dl, severe angiographic coronary artery disease, loop diuretic therapy, and diagnosis of hypertension. A stepwise Cox modeling procedure identified uric acid (p = 0.040), the interaction of hypertension and uric acid (p = 0.029), the interaction of total cholesterol and severe coronary artery disease (p = 0.001) and loop diuretic therapy (p = 0.009) as significant independent predictors of events. Although microalbuminuria was not retained in the final multivariate model, it was associated with poorer cardiovascular disease outcomes. The mean event-free survival for albumin-to-creatinine >30 mg/g was 51 months and for albumin-to-creatinine <30 mg/g the mean was 57 months (p = 0.021). CONCLUSIONS: Uric acid > or =5.2 mg/dl independently imparted a 3.5-fold increased risk (OR 3.5, 95% CI 1.0-11.9) for cardiovascular death and major clinical events over a 5-year period. Uric acid may be a contributing factor to the progression of atherosclerosis and its complications.

Albuminuria↗

PubMed2006

Hyperhomocysteinaemia and vitamin B12 deficiency: the long-term effects in cardiovascular disease.

BACKGROUND: An elevated plasma homocysteine level is an established risk factor for cardiovascular disease. Vitamin B12 plays a key role in homocysteine metabolism and could be the main factor in causing cardiovascular disease as well. OBJECTIVES: The aim of this study was to assess whether vitamin B12 deficiency or hyperhomocysteinaemia is associated with recurrent cardiovascular events. METHODS: Overall, 211 patients discharged alive from our Coronary Care Unit were recruited from February till May 1998. Serum vitamin B12 and plasma homocysteine levels were measured in fasting blood samples. Patient characteristics, medical information and cardiovascular risk factors were assessed from medical files. Patients were followed for 5 years and the prevalence of cardiovascular mortality and morbidity was collected. RESULTS: In the follow-up period of 810 person-years, 48 (21%) of the patients experienced a nonfatal recurrent cardiovascular event and another 14 (7%) died of a cardiovascular cause. Among those with ischaemic heart disease at discharge, no difference in survival was found between the patients with a low (<250 pmol/l) or a high vitamin B12 level (p = 0.21). In patients with hyperhomocysteinaemia (>16 micromol/l), an increased risk of a recurrent cardio vascular event (p = 0.05) in comparison to those with normal plasma homocysteine levels was proven (adjusted hazard ratio of 2.22 (95% CI: 1.40-3.04). CONCLUSIONS: In conclusion, high plasma homocysteine concentration, but not a low serum vitamin B12 concentration, increases the risk of cardiovascular morbidity and mortality in patients with ischaemic heart disease.

Aged↗

PubMed2004

Incidence of obesity-associated cardiovascular disease is related to inflammation-sensitive plasma proteins: a population-based cohort study.

BACKGROUND: Although obesity is associated with increased inflammation, it is unclear whether this accounts for the increased cardiovascular risk in obesity. This population-based study explored whether inflammation-sensitive plasma proteins (ISPs) modify the cardiovascular risk in overweight or obese men. METHODS AND RESULTS: The ISPs (fibrinogen, orosomucoid, alpha1-antitrypsin, haptoglobin, ceruloplasmin) were measured in 6075 healthy men, aged 28 to 61 years. The incidences of cardiovascular events (myocardial infarction, stroke, cardiovascular deaths), cardiac events (fatal or nonfatal myocardial infarction), and stroke were followed-up over 18+/-4 years. High ISPs were associated with an increased cardiovascular risk in all categories of body mass index (BMI). The age-adjusted relative risks for cardiovascular events in obese men (BMI >30) were 2.1 (95% CI, 1.4 to 3.4), 2.4 (CI, 1.5 to 3.7), 3.7 (CI, 2.3 to 6.0), and 4.5 (CI, 3.0 to 6.6), respectively, for those with 0, 1, 2, and > or =3 ISPs in the top quartile (trend P=0.002) (reference: BMI <25 and no elevated ISP). This trend persisted after adjustments for several potential confounders (P=0.02). Incidence of cardiac events showed similar relations with the number of elevated ISPs in obese men. CONCLUSIONS: The cardiovascular risk varies widely between obese or overweight men with high and low ISPs. Relationships with ISPs contribute to, but cannot fully explain, the increased cardiovascular risk in obese men.

Adult↗

PubMed2004

Metabolic syndrome modifies the cardiovascular risk associated with angiographic coronary artery disease in women: a report from the Women's Ischemia Syndrome Evaluation.

BACKGROUND: The metabolic syndrome, which is characterized by a constellation of fasting hyperglycemia, hypertriglyceridemia, low HDL cholesterol, hypertension, and/or abdominal obesity, is a risk factor for the development of coronary artery disease (CAD) and cardiovascular events. The interrelationship between metabolic status and CAD on cardiovascular risk in women is not known. METHODS AND RESULTS: We evaluated interrelationships between angiographic CAD, the metabolic syndrome, and incident cardiovascular events among 755 women from the Women's Ischemia Syndrome Evaluation (WISE) study who were referred for coronary angiography to evaluate suspected myocardial ischemia; 25% of the cohort had the metabolic syndrome at study entry. Compared with women with normal metabolic status, women with the metabolic syndrome had a significantly lower 4-year survival rate (94.3% versus 97.8%, P=0.03) and event-free survival from major adverse cardiovascular events (death, nonfatal myocardial infarction, stroke, or congestive heart failure; 87.8% versus 93.5%, P=0.003). When the subjects were stratified by the presence or absence of angiographically significant CAD at study entry, in women with angiographically significant CAD, the metabolic syndrome resulted in significantly higher risk of cardiovascular events than in women with normal metabolic status (hazard ratio 4.93, 95% CI 1.02 to 23.76; P=0.05), whereas it did not result in increased 4-year cardiovascular risk in women without angiographically significant CAD (hazard ratio 1.41, 95% CI 0.32 to 6.32; P=0.65). CONCLUSIONS: These data suggest that in women with suspected myocardial ischemia, the metabolic syndrome modifies the cardiovascular risk associated with angiographic CAD. Specifically, the metabolic syndrome was found to be a predictor of 4-year cardiovascular risk only when associated with significant angiographic CAD.

Adult↗

PubMed1998

Calcium channel blockade and cardiovascular prognosis in the European trial on isolated systolic hypertension.

In the double-blind Systolic Hypertension in Europe (Syst-Eur) Trial, active treatment was initiated with nitrendipine (10 to 40 mg/d) with the possible addition of enalapril (5 to 20 mg/d) and/or hydrochlorothiazide (12.5 to 25 mg/d) titrated or combined to reduce sitting systolic blood pressure by at least 20 mm Hg to <150 mm Hg. In the control group, matching placebos were used similarly. In view of persistent concerns about the use of calcium channel blockers as first-line antihypertensive drugs, this report explored to what extent nitrendipine, administered alone, prevented cardiovascular complications. Age at randomization averaged 70.2 years and systolic/diastolic blood pressure 173.8/85.5 mm Hg. Of 2398 actively treated patients, 1327 took only nitrendipine (average dose, 23.4 mg/d), and 1042 progressed to other treatments including nitrendipine (n=757; 35.7 mg/d), enalapril (n=783; 13.4 mg/d), and/or hydrochlorothiazide (n=294; 21.0 mg/d). Compared with the whole placebo group (n=2297), patients receiving monotherapy with nitrendipine had 25% (P=0.05) fewer cardiovascular end points, and those progressing to other active treatments showed decreases (P</=0. 01) in total mortality (40%), stroke (59%), and all cardiovascular end points (39%). Among the control patients, 863 used only the first-line placebo. Compared with this subgroup, patients receiving monotherapy with nitrendipine showed a nearly 50% (P</=0.004) reduction of all types of end points, including total and cardiovascular mortality. The full relative benefit from nitrendipine was seen as early as 6 months after randomization. To ascertain that the benefit conferred by the dihydropyridine was not due to selection bias, the 1327 patients remaining on monotherapy with nitrendipine were matched by gender, age, previous cardiovascular complications, and systolic blood pressure at entry with an equal number of placebo patients. In this analysis, nitrendipine reduced (P</=0.05) cardiovascular mortality by 41%, all cardiovascular end points by 33%, and fatal and nonfatal cardiac end points by 33%. Despite the limitations inherent in post hoc analyses, the present findings suggest that the calcium channel blocker nitrendipine, given as a single antihypertensive medication, prevents cardiovascular complications in older patients with isolated systolic hypertension.

Aged↗

PubMed1999

Aortic pulse wave velocity as a marker of cardiovascular risk in hypertensive patients.

Large artery damage is a major contributory factor to cardiovascular morbidity and mortality of patients with hypertension. Pulse wave velocity (PWV), a classic evaluation of arterial distensibility, has never been ascertained as a cardiovascular risk marker. To determine the factors influencing aortic PWV and the potential predictor role of this measurement, we studied a cohort of 710 patients with essential hypertension. Atherosclerosis alterations (AA) were defined on the basis of clinical events. Calculation of cardiovascular risks, by use of Framingham equations, was performed in subjects without AA. PWV was higher in the presence of AA (14.9+/-4.0 versus 12.4+/-2.6 m/s, P<0.0001), even after adjustments on confounding factors and was the first determinant (P<0.0001) of the extent of atherosclerosis assessed as the sum of the atherosclerotic sites. In patients without AA, all cardiovascular risks increased constantly with PWV. Furthermore, at a given age, aortic PWV was the best predictor of cardiovascular mortality. The odds ratio of being in a high cardiovascular mortality risk group (>5% for 10 years) for patients in the upper quartile of PWV was 7.1 (95% confidence intervals 4.5 to 11.3). The presence of a PWV >13 m/s, taken alone, appeared as a strong predictor of cardiovascular mortality with high performance values. This study shows that aortic PWV is strongly associated with the presence and extent of atherosclerosis and constitutes a forceful marker and predictor of cardiovascular risk in hypertensive patients.

Age Factors↗

PubMed2006

Elevated matrix metalloproteinase-9 associated with stroke or cardiovascular death in patients with carotid stenosis.

BACKGROUND: Matrix metalloproteinase-9 could exhibit an important role in the destabilization of atherosclerotic carotid plaques. We hypothesized that in patients with carotid stenosis, elevated levels of plasma matrix metalloproteinase-9 are associated with ipsilateral stroke or cardiovascular death. METHODS AND RESULTS: We followed up 207 patients with > or = 50% carotid stenosis initially for a mean of 4.4 years, during which time 53 patients developed ipsilateral stroke or died of cardiovascular causes. The cumulative incidence of ipsilateral stroke or cardiovascular death was higher in those with matrix metalloproteinase-9 above versus below the median of 41.9 ng/mL (log-rank P=0.002). Matrix metalloproteinase-9 above versus below the median had a hazard ratio for ipsilateral stroke or cardiovascular death of 1.9 (95% confidence interval [CI], 1.1 to 3.5); during extended follow-up, this remained significant until 10 years. The absolute risk of ipsilateral stroke or cardiovascular death at 4.4 years was 34% and 17% in those with matrix metalloproteinase-9 above and below the median, respectively. Elevated matrix metalloproteinase-9 and an echolucent plaque on B-mode ultrasound versus a low matrix metalloproteinase-9 and an echorich plaque had a hazard ratio for ipsilateral stroke or cardiovascular death of 4.4 (95% CI, 1.8 to 11.1) and for ipsilateral stroke of 3.3 (95% CI, 1.1 to 9.7). CONCLUSIONS: Elevated levels of matrix metalloproteinase-9 in patients with > or = 50% carotid stenosis were associated with a 2-fold risk of ipsilateral stroke or cardiovascular death. Combining elevated matrix metalloproteinase-9 and plaque echolucency was associated with a 4-fold risk for ipsilateral stroke or cardiovascular death and a 3-fold risk for ipsilateral stroke.

Aged↗

PubMed2005

Biomarkers of endothelial dysfunction, cardiovascular risk factors and atherosclerosis in rheumatoid arthritis.

Cardiovascular event rates are markedly increased in rheumatoid arthritis (RA), and RA atherogenesis remains poorly understood. The relative contributions of traditional and nontraditional risk factors to cardiovascular disease in RA await elucidation. The present study comprises three components. First, we compared biomarkers of endothelial dysfunction (vascular cell adhesion molecule [VCAM]-1, intercellular adhesion molecule [ICAM]-1 and endothelial leucocyte adhesion molecule [ELAM]-1) in 74 RA patients and 80 healthy control individuals before and after controlling for traditional and nontraditional cardiovascular risk factors, including high-sensitivity C-reactive protein (hs-CRP), IL-1, IL-6 and tumor necrosis factor-alpha. Second, we investigated the potential role of an extensive range of patient characteristics in endothelial dysfunction in the 74 RA patients. Finally, we assessed associations between biomarkers of endothelial dysfunction and ultrasonographically determined common carotid artery intima-media thickness and plaque in RA. The three biomarkers of endothelial dysfunction, as well as hs-CRP, IL-1, IL-6 and tumor necrosis factor-alpha, were higher in patients than in control individuals (P < 0.0001). Patients were also older, exercised less and had a greater waist circumference, blood pressure and triglyceride levels (P <or= 0.04). Five patients had diabetes. Differences in endothelial function were no longer significant between patients and controls (P = 0.08) only after both traditional and nontraditional cardiovascular risk factors were controlled for. In the 74 RA patients, IL-6 predicted levels of all three biomarkers (P <or= 0.03), and rheumatoid factor titres and low glomerular filtration rate (GFR) both predicted levels of VCAM-1 and ICAM-1, independent of traditional cardiovascular risk factors (P <or= 0.02). VCAM-1 was associated with common carotid artery intima-media thickness (P = 0.02) and plaque (P = 0.04) in RA. Patients had impaired endothelial function, less favourable traditional cardiovascular risk factor profiles, and higher circulating concentrations of hs-CRP and cytokines compared with healthy control individuals. Both traditional and nontraditional cardiovascular risk factors contributed to the differences in endothelial function between RA patients and healthy control individuals. IL-6, rheumatoid factor titres and low GFR were independently predictive of endothelial dysfunction in RA. Disease-modifying agents that effectively suppress both cytokine and rheumatoid factor production, and interventions aimed at preserving renal function may attenuate cardiovascular risk in RA.

Adult↗

PubMed2003

New markers for cardiovascular disease risk in women: impact of endogenous estrogen status and exogenous postmenopausal hormone therapy.

The role of estrogen in altering cardiovascular disease risk in women is contentious. Menopause is associated with increased risk for ischemic heart disease and cerebrovascular disease, which collectively are the main causes of morbidity and mortality in women of developed nations. Observational studies suggest a protective role of estrogen, whereas recent randomized controlled trials report a negative role for oral estrogen in primary and secondary prevention of cardiovascular events. Inflammatory mechanisms underlie the process of arterial thrombus formation following atheromatous plaque rupture, and as such modulation of the inflammatory process may be a potential means of reducing cardiovascular risk. Sex steroids may influence inflammatory processes and hence modify cardiovascular risk. The objective of the study was to review the current understanding of the relationships between C-reactive protein (CRP), homocysteine, IL-6, and lipoprotein (a) [Lp(a)] and endogenous estrogen status, exogenous estrogen treatment, and cardiovascular disease risk. The design was a review of all relevant published, peer- reviewed studies. Raised levels of CRP, homocysteine, Lp(a), IL-6, and CRP are each independently associated with increased risk for cardiovascular events in women. Changes in these parameters across the menopausal transition cannot clearly be attributed to hormonal changes. With respect to the effects of exogenous postmenopausal therapy, oral estrogen use is consistently associated with elevations in CRP, no change or a reduction in homocysteine, varied effects on IL-6, and a consistent reduction in Lp(a). Transdermal estradiol overall has no significant effect on any of these parameters. Progestin use appears to attenuate the effect of oral estrogen on CRP and is associated with a reduction in Lp(a). Like oral estrogen, tibolone use is associated with a rise in CRP, with no change in homocysteine and consistent lowering of Lp(a). Selective estrogen receptor modulators modestly lower homocysteine and Lp(a), have varied effects on CRP, and have no reported effects on IL-6. Despite these varied effects of postmenopausal hormone treatment on inflammatory markers, homocysteine, and Lp(a), there is no evidence that change in these markers results in modification of cardiovascular risk. Further studies are required to specifically investigate whether treatments that increase or decrease these markers in fact modulate the risk of cardiovascular events in women.

Biomarkers↗

PubMed2001

Cardiovascular effects of air pollution: what to measure in ECG?

Epidemiologic evidence indicates that air pollution adversely affects the cardiovascular system, leading to increased cardiovascular morbidity and mortality. However, the mechanisms of such an association are unknown. Although potential mechanisms of deleterious effects of air pollution may involve response of the respiratory system, immunologic response, or coagulation abnormalities, the cardiovascular system seems to be the common end point of these pathways. Cardiovascular response to any stress (which may include air pollution) is a consequence of a complex interplay between the autonomic nervous system governing centrally mediated control of the cardiovascular system, a myocardial substrate (current state of the myocardium) altered in the course of disease processes, and myocardial vulnerability leading to arrhythmogenic or ischemic response. Through the use of standard electrocardiograms (ECGs), exercise ECG testing, and long-term ambulatory ECG monitoring, modern electrocardiology makes a valuable contribution to understanding the different mechanistic factors involved in the increase in adverse cardiovascular events due to air pollution. Heart rate variability analysis can provide quantitative insight into the autonomic response of the cardiovascular system to air pollution. Analysis of ventricular repolarization in an ECG (both duration and morphology) gives valuable information about the status and dynamic behavior of myocardium, reflecting myocardial substrate and vulnerability. ST-segment analysis of ECGs is used routinely to monitor the magnitude of ischemia and could be used to monitor subtle changes in the myocardium in subjects exposed to air pollution. Comprehensive analysis of ECG parameters describing the influence of the autonomic nervous system, the role of myocardial substrate, and the contribution of myocardial vulnerability could and should be employed in air pollution studies, especially as those mechanistic components have been proven to contribute to increased cardiovascular morbidity and mortality in general.

Air Pollutants↗

PubMed2002

Role of antibiotics for the prevention of cardiovascular disease.

OBJECTIVE: To evaluate the data regarding the use of antibiotic therapy for the prevention of cardiovascular events. DATA SOURCES: Pertinent literature was identified through a MEDLINE search (1966-September 2001) and through other secondary literature databases and/or bibliographies of pertinent articles. DATA SYNTHESIS: Cardiovascular disease is a common cause of morbidity and mortality among the general population, with well-defined risk factors (e.g., diabetes, hypertension, hyperlipidemia, cigarette smoking, genetic predisposition). Clinical data evaluating the association between the aforementioned risk factors and the development of atherosclerosis and subsequent cardiovascular disease are substantial; however, these risk factors may only partially explain the high prevalence of cardiovascular disease. The presence of Chlamydia pneumoniae within atherosclerotic lesions has been documented and may be an additional risk factor for the development and progression of cardiovascular disease. CONCLUSIONS: The results of primary and secondary prevention trials have shown conflicting evidence with regard to the beneficial effects of antibiotic therapy to reduce cardiovascular events. Currently, the lack of certainty in published data does not support the use of antibiotics for the prevention of cardiovascular disease. Clinicians should continue to emphasize interventions proven to reduce adverse cardiovascular events such as smoking cessation, reduction of hyperlipidemia, and control of hypertension.

Anti-Bacterial Agents↗

PubMed2005

Relationship between osteoporosis and cardiovascular disease in postmenopausal women.

UNLABELLED: In the placebo group of the MORE study, including 2576 postmenopausal women (mean age, 66.5 years), the authors describe a strong linear association between the severity grade of osteoporosis (from low BMD to presence of severe vertebral fractures) and the future risk of cardiovascular events. Accordingly, treatment of postmenopausal osteoporosis should include consideration of measures to prevent adverse cardiovascular outcomes. INTRODUCTION: Observations indicate an inverse association between BMD and the severity of peripheral atherosclerosis in postmenopausal women. The predictive value of osteoporosis and its different severity stages for the risk of acute cardiovascular events remains unknown. MATERIALS AND METHODS: Participants were 2576 women (mean age, 66.5 years) assigned to placebo and followed for 4 years in an osteoporosis treatment trial. Those with at least one vertebral fracture or total hip BMD T score < or = -2.5 at baseline were defined as having osteoporosis, whereas those without vertebral fracture and total hip BMD T score between -2.5 and -1 were defined as having low bone mass. The primary outcome for these posthoc analyses was the incidence of adjudicated fatal or nonfatal cardiovascular events. RESULTS: After adjustment for potential confounders, women with osteoporosis had a 3.9-fold (95% CI, 2.0-7.7; p < 0.001) increased risk for cardiovascular events compared with women with low bone mass. Under the same boundaries, a total hip BMD T score < or = -2.5 versus a T score between -2.5 and -1 was associated with a 2.1-fold (95% CI, 1.2-3.6; p < 0.01) increase in risk, whereas presence of at least one vertebral fracture versus no vertebral fracture at baseline was associated with a 3.0-fold (95% CI, 1.8-5.1; p < 0.001) increase in risk. The risk of cardiovascular events increased incrementally with the number and increasing severity of baseline vertebral fractures (both p < 0.001). CONCLUSIONS: Postmenopausal women with osteoporosis are at an increased risk for cardiovascular events that is proportional to the severity of osteoporosis at the time of the diagnosis. Treatment of postmenopausal osteoporosis should include consideration of measures to prevent cardiovascular outcomes.

Aged↗

PubMed2006

Cardiovascular function following surgical repair of pectus excavatum: a metaanalysis.

BACKGROUND: Despite numerous published reports, there is no consensus in the literature as to whether the surgical repair of the pectus excavatum improves cardiovascular function. As a result, it has been suggested that correction should be considered a cosmetic procedure, and therefore, many health insurance companies have questioned whether the repair of the pectus excavatum improves cardiovascular function and thus are reluctant to authorize the procedure. The purpose of this study was to apply metaanalysis methodology to generate a quantitative synthesis of the effects of surgical repair on cardiovascular function and to test the hypothesis that surgical repair of the pectus excavatum results in significant improvements in cardiovascular function. METHODS: Studies were retrieved via computerized literature searches, cross-referencing from original and review articles, and a review of the reference list by a recognized authority in the area of pectus excavatum repair. The inclusion criteria were as follows: (1) reporting quantitative measures of preoperative and postoperative cardiovascular function; (2) published in the English language; (3) indexed between January 1960 and May 2005; (4) reporting the duration between which preoperative and postoperative assessments were conducted; and (5) describing the cardiovascular assessment procedures. RESULTS: A comprehensive search of the literature identified eight studies that met all of the inclusion criteria. These studies, representing 169 pectus excavatum patients, were used for the metaanalysis. Random-effects modeling yielded a mean weighted effect size (ES) for cardiovascular function that was statistically significant (ES, 0.59; 95% confidence interval, 0.25 to 0.92; p = 0.0006). CONCLUSIONS: The findings of the present study indicated that surgical repair of the pectus excavatum significantly improves cardiovascular function and contradicts arguments that surgical repair is primarily cosmetic yielding minimal physiologic improvement.

Cardiovascular System↗