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PubMed1992

Interesting problems in enteroviral inflammatory heart disease.

Enteroviral inflammatory heart disease is an established entity. Based upon the accumulated work from many laboratories, specific and definitive questions can be posed regarding the pathogenic nature of the viruses involved and how the host immune systems respond to the insult of enterovirus replication in the myocardium. The answers to these questions may well lead to efficient intervention therapies such as vaccination or effective anti-viral compounds, thus eradicating enterovirus-induced heart disease. Understanding the nature of the acute disease is the first requirement toward a complete understanding of the mechanisms at work in chronic inflammatory heart disease.

Animals↗
PubMed2001

The impact of emotions on coronary heart disease risk.

BACKGROUND: Coronary heart disease is now well recognized as a psychosomatic illness. Emotional disturbance increasingly appears to have an impact on both the development of coronary artery disease over time and the precipitation of acute coronary heart disease events. METHOD: This descriptive review is based on systematic literature reviews from 1980 to 2000 with an emphasis on predictive and prospective studies. RESULTS: The empirical evidence linking emotional disturbances such as anxiety, depression and anger to coronary heart disease is now robust. There is also increasing evidence for the underlying pathophysiology that may link emotions to coronary heart disease. CONCLUSIONS: Emotional disorders and coronary artery disease commonly coexist. Emotional disorders often follow events of coronary heart disease. Prospective studies, however, now show that emotional disturbance is also a significant risk factor for coronary artery disease and especially in those with pre-existing disease. It is important both to diagnose emotional disorders early in coronary heart disease patients and implement effective treatments with the likelihood of reducing subsequent morbidity and mortality.

Coronary Disease↗
PubMed2004

Treatment of Parkinson's disease with pergolide and relation to restrictive valvular heart disease.

BACKGROUND: Restrictive valvular heart disease has been reported in patients with Parkinson's disease treated with pergolide. However, few data are available on frequency, severity, dose dependency, and reversibility of pergolide-induced disease, nor on the pulmonary pressures of these patients. We aimed to clarify these characteristics in a large group of patients. METHODS: 78 patients with Parkinson's disease treated with pergolide and 18 never treated with an ergot-derived dopamine agonist (controls) were evaluated by echocardiography. A valvular scoring system was used, ranging from 1 (proven ergot-like restrictive valvular heart disease) to 4 (no disease). For the mitral valve, tenting areas and tenting distances were measured. Systolic pulmonary artery pressures were derived from the tricuspid regurgitant jet. FINDINGS: Restrictive valvular heart disease of any type was present in 26 (33%) patients in the pergolide group and none in controls (p=0.0025). Important disease (score 1 or 2) was present in 15 (19%) patients in the pergolide group and none in controls (p=0.066). Mean tenting distances and tenting areas of the mitral valve were 1.08 cm (range 0.55-2.66) and 2.39 cm2 (0.88-4.59) in the restrictive mitral valve group versus 0.63 cm (0.22-1.20) and 1.39 cm2 (0.39-3.23) in the non-restrictive group (p=0.003 and p<0.0001, respectively). Significant correlation was noted between cumulative doses of pergolide and tenting areas of the mitral valves (r=0.412, p=0.017). Mean systolic pulmonary artery pressures were 39.3 mm Hg (range 25-71) in the high-dose group versus 38.5 mm Hg (20-65) in the low-dose group (p=0.76) and 31 mm Hg (25-40) in controls (p=0.02 vs all patients given pergolide). In six patients, pergolide treatment was stopped because of restrictive valvular heart disease, in two of whom regression of disease was shown. INTERPRETATION: Restrictive valvular heart disease is not a rare finding in patients treated with pergolide. Clinicians should consider changing to a non-ergot drug if this disease is diagnosed.

Aged↗
PubMed1993

Inhaled nitric oxide in congenital heart disease.

BACKGROUND: Congenital heart lesions may be complicated by pulmonary arterial smooth muscle hyperplasia, hypertrophy, and hypertension. We assessed whether inhaling low levels of nitric oxide (NO), an endothelium-derived relaxing factor, would produce selective pulmonary vasodilation in pediatric patients with congenital heart disease and pulmonary hypertension. We also compared the pulmonary vasodilator potencies of inhaled NO and oxygen in these patients. METHODS AND RESULTS: In 10 sequentially presenting, spontaneously breathing patients, we determined whether inhaling 20-80 ppm by volume of NO at inspired oxygen concentrations (FIO2) of 0.21-0.3 and 0.9 would reduce the pulmonary vascular resistance index (Rp). We then compared breathing oxygen with inhaling NO. Inhaling 80 ppm NO at FIO2 0.21-0.3 reduced mean pulmonary artery pressure from 48 +/- 19 to 40 +/- 14 mm Hg and Rp from 658 +/- 421 to 491 +/- 417 dyne.sec.cm-5.m-2 (mean +/- SD, both p < 0.05). Increasing the FIO2 to 0.9 without adding NO did not reduce mean pulmonary artery pressure but reduced Rp and increased the ratio of pulmonary to systemic blood flow (Qp/Qs), primarily by increasing Qp (p < 0.05). Breathing 80 ppm NO at FIO2 0.9 reduced mean pulmonary artery pressure and Rp to the lowest levels and increased Qp and Qp/Qs (all p < 0.05). While breathing at FIO2 0.9, inhalation of 40 ppm NO reduced Rp (p < 0.05); the maximum reduction of Rp occurred while breathing 80 ppm NO. Inhaling 80 ppm NO at FIO2 0.21-0.9 did not alter mean aortic pressure or systemic vascular resistance. Methemoglobin levels were unchanged by breathing up to 80 ppm NO for 30 minutes. CONCLUSIONS: Inhaled NO is a potent and selective pulmonary vasodilator in pediatric patients with congenital heart disease complicated by pulmonary artery hypertension. Inhaling low levels of NO may provide an important and safe means for evaluating the pulmonary vasodilatory capacity of patients with congenital heart disease without producing systemic vasodilation.

Administration, Inhalation↗
PubMed1985

Prevalence of coronary artery disease in patients with valvular heart disease.

To evaluate the usefulness of preoperatie coronary angiography in patients undergoing preoperative investigation because of valvular heart disease, we performed coronary angiography in a consecutive series of 329 patients. The prevalence of significant coronary artery disease was 32%. Asymptomatic coronary artery disease was present in 13%. Angina pectoris proved to be a poor predictor of coronary artery disease in aortic valve disease. In mitral valve disease, however, the specificity was high. A cost-benefit calculation was carried out in order to assess what advantage routine coronary angiography might have. According to this, coronary angiography should be performed in all patients suffering from valvular heart disease with angina pectoris, whereas it can be omitted in younger patients without angina. A cut-off point of 60 years seems appropriate for aortic valve disease and 65 years for mitral valve disease.

Adult↗
PubMedDate not supplied

Relation of physical activity and cardiovascular fitness to coronary heart disease, Part I: A meta-analysis of the independent relation of physical activity and coronary heart disease.

BACKGROUND: This paper is the first of two reports that together review the scientific evidence regarding the inverse relation between physical activity and cardiovascular fitness and coronary heart disease (CHD). METHODS: In Part I, the evidence suggesting a causal link between physical activity and CHD protection independent of other CHD risk factors is reviewed, accounting for bias, confounding, and different study designs. RESULTS: A strong, consistent inverse relation is found. Using meta-analytic techniques, the relative risk of the independent relation of physical inactivity to CHD is 1.37, with a 95 percent confidence interval (1.27-1.48). CONCLUSIONS: A graded biologic response of CHD protection to physical activity is shown, but the intensity, duration, and frequency of activity necessary for CHD benefit remain unclear. Plausible biologic mechanisms for the inverse relation of physical activity to CHD are the risk factor modifications that accrue with physical activity.

Causality↗
PubMed2006

Treatment of depression in patients with coronary heart disease.

Depression and coronary heart disease are common conditions that often occur together. Evidence shows that the co-occurrence of these illnesses is not random but driven by depression as a risk factor for the occurrence and progression of coronary heart disease. This link is due, in part, to the impact that depression has on neuroendocrine pathways leading to increased platelet activation, cortisol and catecholamine excess, and altered autonomic nervous system function that influence the pathogenesis and progression of coronary atherosclerosis and subsequent heart disease. We know that treating depression in patients with coronary heart disease improves the symptoms and signs of depression. Evidence is less compelling that treating depression improves the morbidity and mortality of coronary heart disease. However, early findings suggest that some antidepressants may improve the course of coronary heart disease and improve patient compliance with various cardiac interventions. We outline a practical approach to the treatment of depression in patients with coronary heart disease. This approach includes education, counseling, antidepressant drugs, and referral when appropriate.

Antidepressive Agents↗
PubMed2003

Physicians' ability to predict the risk of coronary heart disease.

BACKGROUND: Coronary heart disease (CHD) is the leading cause of death in the United States. Previous research examining physicians ability to estimate cardiovascular risk has shown that physicians' generally overestimate the absolute risk of CHD events. This question has, however, only studied risk prediction for a limited number of patient care scenarios. The aim of this study is to measure the ability of physicians to estimate the risk of CHD events in patients with no previous history of coronary heart disease. METHODS: Twelve primary prevention scenarios with a 5-year risk of CHD events were developed. This questionnaire was surveyed at 3 university teaching hospitals where the participants were a convenience sample of internal medicine residents and fellows or attending physicians in general internal medicine or cardiology. For each scenario, physicians were asked to estimate the baseline 5-year risk of a coronary heart disease event and the revised risk if the patient were to receive lipid-lowering drug therapy. Estimates of the baseline 5-year risk were compared with values calculated from Framingham risk equations. Inaccurate responses were defined as those with a ratio of estimated to actual risk of more than 1.5 or less than 0.67. Physicians' estimates of the relative risk reduction with therapy were considered to be accurate if they were between 25% and 40%. RESULTS: 79 physicians (53 residents, 8 fellows, 18 attending physicians) completed the survey. Only 24% of physicians' risk estimates were accurate. In most cases, physicians overestimated the absolute risk of cardiovascular events without therapy (proportion overestimating ranged from 32-92% for the 12 individual scenarios). Physicians made larger errors in patient scenarios involving patients with high total or LDL cholesterol levels. Physicians' estimates of the relative risk reduction from treatment were more accurate: 43% of estimates were between 25 and 40%. Over 85% of physicians recommended treatment in 10 of 12 scenarios. CONCLUSIONS: Physicians overestimate the absolute risk of CHD events and the potential absolute benefit of drug therapy.

Age Factors↗
PubMed1988

Helsinki Heart Study. New perspectives in the prevention of coronary heart disease.

The Helsinki Heart Study tested the effect of modifying plasma low density lipoprotein (LDL)- and high density lipoprotein (HDL)-cholesterol on the primary prevention of coronary heart disease in middle-aged men with non-HDL-cholesterol greater than or equal to 5.2 mmol/L (200 mg/dl). One group (2046 men) received 600mg of gemfibrozil twice daily, and the other (2035 men) received placebo. Averaged over the 5-year trial period, gemfibrozil induced mean decreases of 11% in LDL-cholesterol and 35% in triglycerides and a mean increase of 11% in HDL-cholesterol compared with placebo. These changes were accompanied by a 34% reduction (number of end-points; 56 vs 84) in the incidence of coronary heart disease. The reduction was largest in subjects with type IIB hyperlipoproteinaemia and smallest in subjects with type IIA hyperlipoproteinaemia. The changes in serum HDL- and LDL-cholesterol during the trial were associated (p less than 0.02 and p less than 0.05, respectively) with the risk of coronary heart disease in the gemfibrozil group, but not in the placebo group.

Adult↗
PubMed1995

The hypothetical epidemic of coronary heart disease and atherosclerosis.

Accurate usage of the term 'epidemic' is important scientifically and it should ideally be used to mean only contagious diseases, not used loosely or emotively to mean non-infectious diseases, particularly coronary heart disease, which is a non-specific complication of many diseases. It should not be used as a surrogate term for atherosclerosis of indefinite severity. An epidemic of atherosclerosis is impossible, there being no variation in prevalence because the disease is ubiquitous. Moreover, vital statistics are too unreliable to determine the existence of an increase or decline in coronary heart disease. A coronary heart disease epidemic could be due to an increase in non-atherosclerotic coronary heart disease or increased severity of atherosclerosis. The former has not been studied and the latter would cause a shift to the left in age distribution and is inconsistent with the fall in 'all cause' and stroke mortality rates whilst coronary heart disease mortality allegedly increased alarmingly. A coronary heart disease epidemic, having no scientific basis, negates any reason for the sustained search for a speculative causative environmental factor.

Arteriosclerosis↗
PubMed2006

Physical performance is associated with markers of vascular inflammation in patients with coronary heart disease.

BACKGROUND: Coronary heart disease as well as major cardiovascular risk factors are associated with elevated levels of pro-inflammatory markers. There is, however, limited information about how changes in lifestyle improving the cardiovascular risk profile influence these levels. The aim of the study was to evaluate whether changes in lifestyle measures with special attention to physical activity, were associated with the levels of such markers. DESIGN: Coronary heart disease patients (n = 197) were randomized to either a comprehensive lifestyle intervention programme comprising regular physical activity, low fat diet and smoking cessation, or usual care with routine follow-up in the outpatient clinic for 6 months. An exercise test and fasting blood samples analysed for soluble cell adhesion molecules, C reactive protein and pro-inflammatory cytokines were evaluated before and at the end of the study. RESULTS: Improved diet, physical performance and reduction in smoking were obtained in the intervention programme when compared with usual care patients, but no significant group differences in levels of inflammatory markers were observed. In the total population, however, physical performance significantly and inversely predicted levels of soluble cell adhesion molecule 1, (P < 0.001), C-reactive protein (P < 0.001) and interleukin-6 (P = 0.01) at 6 months. Smokers had elevated levels of soluble cell adhesion molecule 1 when compared with non-smokers (P = 0.011). CONCLUSIONS: We demonstrated that physical performance is inversely correlated with levels of pro-inflammatory markers in coronary heart disease patients, possibly retarding the process of atherosclerosis. No effect on inflammatory markers was obtained with a 6-month lifestyle intervention programme when compared with patients who received usual care follow-up.

Biomarkers↗
PubMed1995

Self-reported physical activity predicts long-term coronary heart disease and all-cause mortalities. Twenty-one-year follow-up of the Israeli Ischemic Heart Disease Study.

OBJECTIVE: To determine whether self-reported physical activity predicts a decreased rate of coronary heart disease (CHD) and all-cause mortalities in middle-aged men when rates are adjusted for known confounders. DESIGN: Cohort Analytic Study of Israeli government employees in 1963. SUBJECTS: Eight thousand four hundred sixty-three Israeli male government employees, aged 40 years or older, representing six areas of birth, excluding those with known cardiovascular disease in either 1963 or 1965, from an original cohort of 10,059. MAIN OUTCOME MEASURE: Comparison of rates of death due to CHD and all causes, determined from death certificates in 21 years of follow-up, for subjects with different baseline levels of self-reported leisure-time and work-related physical activities measured in 1965. RESULTS: Self-reported leisure-time but not work-related physical activity was inversely related to both CHD (adjusted relative risk, 0.79; 95% confidence interval, 0.66 to 0.95) and all-cause mortalities (adjusted relative risk, 0.91; 95% confidence interval, 0.83 to 0.99). Most of the apparent benefit accrued was from light physical activity on less than a daily basis. These inverse relationships persisted after adjustment for age, systolic blood pressure, cigarette smoking, total and high-density lipoprotein cholesterol levels, body mass index, psychosocial factors, and other potential confounders. CONCLUSION: Baseline levels of self-reported leisure-time physical activity predicted a decreased rate of CHD and all-cause mortalities in employed middle-aged Israeli men followed up prospectively for 21 years.

Adult↗
PubMed2004

Potential errors resulting from sex and age difference in assessing family history of coronary heart disease.

BACKGROUND: Coronary heart disease occurs nearly exponentially with age and differently between men and women. Therefore, difference in sex and age of family members yields errors in assessing the family history as a risk factor. The influence of sex and age on the positivity of family history was assessed numerically. METHODS: Through questionnaires filled in by the parents of 2316 high school students, information was obtained on the past history of coronary heart disease among students' parents, grandparents, uncles, and aunts. The sex- and age-specific proportion of a positive history was calculated from the past history among the 24,071 family members. The influence of sex and age on a positive history was estimated as odds ratios by logistic regression analysis of the past history. RESULTS: The odds ratios obtained for sex and age difference were 1.61 (95% confidence interval: 1.42-1.83) and 1.07 (95% confidence interval: 1.06-1.07), respectively. This indicated that a positive history was 1.61 times higher among male members than among female members of the same age, and that a positive history increased by (1.07)y, where y was age difference by year. CONCLUSIONS: Potential errors resulting from disregarding the sex and age of family members can be substantial, judging from the above numerical figures. Some measures to control for the sex and age of family members are required in assessing family history of coronary heart disease.

Adult↗
PubMed2000

Repair of coronary arterioles after treatment with perindopril in hypertensive heart disease.

In hypertensive heart disease, no data are available on the repair of coronary resistance vessels in patients after long-term ACE inhibitor treatment. Fourteen patients with essential hypertension were studied with coronary flow reserve and with transvenous endomyocardial biopsy before and after 12 months of antihypertensive treatment with perindopril (4 to 8 mg/d, mean 5.9+/-2.3 mg/d). Left ventricular muscle mass index decreased by 11% (from 145+/-41 to 128+/-36 g/m(2), P=0.04). Maximal coronary blood flow was increased by 54% (from 170+/-46 to 263+/-142 mL. min(-1). 100 g(-1), P=0.001), and minimal coronary vascular resistance was diminished by 33% (from 0.67+/-0.21 to 0.45+/-0.19 mm Hg. min. 100 g. mL(-1), P=0.001); consequently, coronary reserve increased by 67% from 2.1+/-0.6 to 3. 5+/-1.9 (P=0.001). Structural analysis revealed regression of periarteriolar collagen area by 54% (from 558+/-270 to 260+/-173 microm(2), P=0.04) and of total interstitial collagen volume density by 22% (from 5.5+/-3.8 Vv% to 4.3+/-3.2 Vv%, P=0.04), whereas arteriolar wall area was slightly but not significantly reduced. Long-term therapy with the ACE inhibitor perindopril induces structural repair of coronary arterioles that is mainly characterized by the regression of periarteriolar fibrosis and associated with a marked improvement in coronary reserve. These findings indicate the beneficial reparative effects of ACE inhibition on coronary microcirculation in hypertensive heart disease.

Angiotensin-Converting Enzyme Inhibitors↗