[Latent edema in heart disease; studies on certain hemodynamic data in heart diseases in phase of labile compensation or in function repression due to decompensation].
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Edema↗
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Family history of coronary heart disease is a stronger predictor of coronary heart disease morbidity and mortality than family history of non-insulin dependent diabetes mellitus.
The aim of this study was to compare the effect of family history of non-insulin dependent diabetes mellitus (NIDDM) and coronary heart disease (CHD) as risk factors for CHD morbidity and mortality. Altogether, 394 siblings of NIDDM probands and non-diabetic probands, with and without CHD, were followed for 8 years with respect to CHD events in a prospective population-based study. The baseline study was conducted from 1983 to 1985. Age- and sex-adjusted cumulative occurrence of CHD events was higher in the siblings of the probands with CHD and with NIDDM (13.1%; P = 0.037) and in the siblings of the probands with CHD and without NIDDM (15.4%; P = 0.054), compared with the siblings of the probands without NIDDM and without CHD (4.8%). The incidence of fatal CHD events tended to be higher in a group with a family history of NIDDM and CHD, but the trend was not statistically significant. In univariate logistic regression analyses, a family history of CHD was positively associated with cumulative occurrence of CHD events (odds ratio 2.53, P = 0.009), whereas a family history of NIDDM had no significant association (odds ratio 1.39, P = 0.312). After adjustment for age, sex, family history of NIDDM and major cardiovascular risk factors, the association between family history of CHD and cumulative occurrence of CHD events remained significant (odds ratio 2.25, P = 0.048). In conclusion, the present study indicates that a family history of CHD is a stronger predictor of future CHD events than a family history of NIDDM.
Aged↗
Congenital heart disease: the original heart failure syndrome.
Heart failure is characterised by a triad comprising cardiac abnormality, exercise limitation and neurohormonal activation. The 2% of the adult population who suffer with heart failure are known to derive both symptomatic and prognostic benefit from exercise and pharmacologic neurohormonal antagonism. The existence of heart failure has traditionally been considered in the context of ischaemic, hypertensive, valvular and myopathic disease but in this article we develop the argument that patients with congenital heart disease also manifest all the pathophysiological criteria that constitute the chronic heart failure syndrome. We discuss the inherent limitations to a purely anatomical approach to congenital heart disease, bring attention to the large and rapidly growing population of adults with this condition and conclude by calling for a therapeutic approach to congenital heart disease that is based on the heart failure paradigm.
Adult↗
A comparison between BMI and Conicity index on predicting coronary heart disease: the Framingham Heart Study.
PURPOSE: This study examined the relationship of mortality and morbidity of coronary heart disease with body mass index (BMI) and Conicity index (CI). METHODS: Among 5209 Framingham Heart Study participants, 1882 men and 2373 women had waist and weight measurement at the 4th examination period and height measured on the 5th visit. These were used for BMI and CI. RESULTS: During a 24-year follow-up, 597 men and 468 women developed CHD and 248 men and 150 women died from CHD associated causes. In men the relative risks (RR) (95% confidence interval) adjusted for age, hypertension, diabetes, smoking status, and total cholesterol for CHD incidence in 2nd, 3rd, and 4th quartiles of BMI were 1.28 (1.0, 1.65), 1.45 (1.13, 1.86), and 1.53 (1.19, 1.96). The RR for CHD incidence in the 4th quartile of BMI in women was 1.56 (1.16, 2.08). No CI quartiles were risk factors for CHD incidence. There was 86% higher risk of CHD related death in the 4th quartile of BMI than the 1st quartile of BMI in women. In men no significantly higher risks of death were found across the quartiles of BMI. No associations were found between CI quartiles and CHD mortality. CONCLUSIONS: Obesity as measured by BMI is an important risk factor for CHD incidence in men and women and for CHD mortality in women. CI was not associated with an increase in CHD incidence or mortality. Thus, BMI is a better marker than CI for predicting CHD incidence and mortality.
Adult↗
Surgical animal models of heart failure related to coronary heart disease.
Coronary heart disease is caused by atherosclerotic narrowing of coronary arteries. It accounts for about two-thirds of heart failure cases, which are frequently secondary to myocardial infarction. Despite considerable progress in the understanding and management of heart failure, its incidence, prevalence and economic burden are steadily increasing. Therefore, efficient preventive and therapeutic measures are urgently needed. In order to investigate the mechanisms involved in the pathogenesis of coronary heart disease-related heart failure and to develop therapies, appropriate animal models are indispensable. According to the aetiology of this disorder, surgical models are based on various methods allowing for the narrowing or occlusion of coronary arteries. Depending on the duration and extent of the impairment of coronary blood flow and its consequences for cardiac tissue, these are classified as models of myocardial infarction, cardiac ischemia/reperfusion injury, or chronic cardiac ischemia. In addition, factors such as species, strain, and gender of the laboratory animals also significantly contribute to the pathophysiology of the induced disorder and, therefore, have to be taken into consideration thoroughly when an animal model is to be established.
Animals↗
The relationship of left ventricular geometry and hypertrophy to left ventricular function in valvular heart disease.
Valvular heart disease imposes a hemodynamic load on the left or right ventricle. This load is compensated by the development of ventricular hypertrophy. The pattern of hypertrophy which develops is characteristic of each type of valvular lesion with concentric hypertrophy compensating the pressure overload of aortic stenosis, eccentric hypertrophy compensating the volume overload of mitral regurgitation and both concentric and eccentric hypertrophy compensating the combined pressure and volume overload of aortic regurgitation. While these patterns are characteristic, there is substantial variation in the geometric distribution of hypertrophy among individuals with the same valvular disease. This variability in turn produces variability in the amount of compensation from patient to patient. The geometric pattern of hypertrophy which develops primarily affects left ventricular function as it relates to the Laplace equation. An increase in the radius to thickness ratio increases wall stress while a decrease in this ratio decreases wall stress. Discussed below are the mechanisms by which the various geometries that develop in valvular heart disease affect loading to become adaptive or maladaptive or both.
Aortic Valve Insufficiency↗
[Discovery of susceptibility gene for coronary heart disease].
Coronary heart disease (CHD) is a leading cause of death for adults in many countries. It is multifactorial in origin with both genetic and environmental factors contributing to its development. But the molecular basis of CHD pathogenesis remains obscure, which represents a major obstacle to the identification of CHD susceptibility genes. Knowledge of genetic factors contributing to the pathogenesis of CHD will undoubtedly advance efforts to identify CHD susceptibility genes. The benefits promised are great, but progress to gene identification in CHD has been rather disappointing so far. This review aims to discuss the current and future approaches to gene discovery in CHD. And these approaches can be applied equally to other multifactorial traits in the cardiovascular arena--stroke, peripheral arterial occlusive disease, hypertension, heart failure and beyond.
Coronary Disease↗
Common cholesteryl ester transfer protein mutations, decreased HDL cholesterol, and possible decreased risk of ischemic heart disease: The Copenhagen City Heart Study.
BACKGROUND: Cholesteryl ester transfer protein (CETP) mediates the transfer of cholesteryl ester from HDL in exchange for triglycerides in apolipoprotein B-containing lipoproteins. METHODS AND RESULTS: We studied 2 common mutations in CETP, A373P and R451Q, in 8467 healthy women and men from the Danish general population and in 1636 Danish women and men with ischemic heart disease. The prevalence of 373P and 451Q was 0.10 and 0.07, respectively, for heterozygous carriers and 0.003 and 0.002, respectively, for homozygous carriers. All carriers of the 451Q allele also carried the 373P allele. HDL cholesterol in female noncarriers, heterozygotes, and homozygotes of 373P was 1.74+/-0.01 (mean+/-SE), 1.62+/-0.02, and 1.38+/-0.09 mmol/L, respectively (ANOVA, P:<0.001). In men, equivalent values were 1.40+/-0.01, 1.26+/-0.02, and 1.19+/-0.09 mmol/L, respectively (ANOVA, P:<0.001). HDL cholesterol decreased similarly as a function of 451Q genotypes and all 373P/451Q genotype combinations. Furthermore, apolipoprotein AI and the HDL cholesterol/apolipoprotein AI ratio was also lower in carriers of either of these mutations for both sexes. Finally, the CETP genotype was not associated with risk of ischemic heart disease unless we adjusted for HDL cholesterol: female heterozygous and homozygous carriers versus noncarriers had 36% lower risk of ischemic heart disease (95% CI 4% to 57%); in male carriers, we observed a similar trend. CONCLUSIONS: The A373P/R451Q polymorphism in CETP is associated with decreases in HDL cholesterol of 0.12 to 0.36 mmol/L in women and 0.14 to 0.21 mmol/L in men and possibly with a paradoxical 36% decrease in the risk of ischemic heart disease in women.
Alleles↗
Study of platelet diameter distribution in patients with valvular heart disease and with prosthetic heart valve replacement.
We have studied the platelet count and the megathrombocyte index (MI), or percentage of platelets that have a diameter greater than 2.9 micrometers, in 100 patients with valvular heart disease. The mean platelet count is significantly lower than in controls (p less than 0.0005) and the MI is significantly increased (p less than 0.01). No difference was observed in these two parameters according to the variety of the valvular heart disease. 45 of the same patients were studied after prosthetic heart valve replacement. Our results show a significant elevation of platelet count and a significant decrease of MI compared with the presurgical values in all groups except in the mitral one in which MI remains increased. This work demonstrates the presence of platelet abnormalities which reveal a compensated thrombocytolytic state in patients with valvular heart disease and its partial correction after aortic, but not mitral, valve replacement.
Adolescent↗
[Guidelines of the Spanish Society of Cardiology on valve heart disease].
Valvular heart diseases, which continue to be a major cause of morbidity and mortality world wide, have undergone radical changes since the first valve prostheses were implanted 40 years ago. These changes have been the result of both scientific progress and improved standard of living in developed countries. The availability of penicillin to treat streptococcal pharyngitis and less crowded living conditions have now made rheumatic fever uncommon in these countries. However, other forms of valve impairment have appeared over the past several years. The etiology of some of these valvular diseases remains obscure (e. g. myxomatous mitral valve); others, such as the senile type of calcific aortic valve stenosis, seem to be the price to be paid for the extension of life expectancy. With regard to diagnosis, echocardiography has constituted a formidable tool for visualizing anatomic valve changes, interpreting complex hemodynamic derangements, and evaluating repercussion on the left ventricle. In addition, the iteration of this non-invasive examination has allowed a much better understanding of the natural history of non-severe valvular disease and therefore of the precise timing for surgical intervention, without awaiting, in most cases, the appearance of advanced symptomatology. This has also been possible because of the great advances in cardiac surgery which can be summarised as: a) the improvement in extracorporeal circulation and myocardial preservation techniques; b) the greatly improved biologic and mechanic valve substitutes; c) the introduction of imaginative mitral valve repair procedures, and d) the use of intraoperative transesophageal echocardiography to assess the adequacy of valve repair. At the same time, percutaneous catheter balloon valvuloplasty has emerged as a valid alternative to mitral surgical commissurotomy for mitral stenosis. All these changes, and many more that can not be described in this brief summary, make a review of the management of patients with valve heart disease appropriate.
Cardiology↗
An analogue computer for pressure-time measurements in valvular heart disease.
Accurate measurement of pressure differences across a diseased heart valve involves either laborious planimetry or elaborate digital computing facilities. An analogue device is described, simple and inexpensive to construct, which derives from the recorder input of two pressure signals the time (seconds/minute) of valve opening and the mean pressure difference during this time. Measurements may be repeated over long periods. The importance of using pressure differences as compared with peak or end diastolic gradients is noted; serious errors in assessment of valvular disease may otherwise occur.
Blood Pressure↗
[Use of a psychoemotional stress test in ischemic heart disease, hypertension and heart rhythm disorders].
Forty male patients with coronary heart disease and essential hypertension, as well as 10 normal subjects, were examined, using a psychoemotional test with simultaneous monitoring of arterial blood pressure (BP), heart rate and ECG patterns. The test revealed disorders of cardiac rhythm in 28.6% of coronary patients and induced signs of myocardial ischemia and an anginal attack in 2. Signs of myocardial ischemia were more often provoked in coronary patients by physical stress tests as compared to those involving psychoemotional stress. In hypertensive patients, psychoemotional stress was associated with a more pronounced arterial BP rise, as compared to the results in normotensive individuals (normal subjects and coronary patients). Psychoemotional stress tests can be used alongside other kinds of tests in patients with coronary disease, essential hypertension and cardiac rhythm disorders.
Adult↗
[Late ventricular potentials and ventricular arrhythmia in patients with stable ischemic heart disease].
Ischaemic heart disease especially after previous myocardial infarction can predispose to the life-threatening ventricular arrhythmias. Late potentials (LP) are confirmed parameters predicting patients prone to sudden cardiac death in ventricular arrhythmias mechanism. Late potentials registered noninvasively from the body surface were analysed in 86 patients with stable ischaemic heart disease (67 males and 19 females aged 35-67, mean 53 years). Registration of signal average electrocardiograms (SA-ECG) were performed by Simson technic (X, Y, Z orthogonal leads) using identical analysing systems and quantitative SA-ECG criteria in all three participating centers. In all patients ventricular arrhythmias detected on 24-hour ecg Holter monitoring were assessed. The localisation of previous myocardial infarction and echocardiographic assessment of left ventricular function were also analysed in each case. The results of SA-ECG were correlated with these clinical findings. Late potentials were detected (according to two or three accepted criteria) in 16 pts (19%), in 53 pts (61%) SA-ECG were normal but in other 17 pts (20%) abnormal SA-ECG (according to only one criterium) were registered. Out of these 17 pts with abnormal SA-ECG, 14 pts had prolonged filtered QRS duration as the only incorrect SA-ECG parameter. Comparative analysis between studied groups shows higher incidence of previous Q-wave myocardial infarctions in patients with LP and with abnormal SA-ECG than in patients with normal SA-ECG (63% and 71% vs 43% respectively; p less than 0.01). Ventricular arrhythmias observed in studied patients occurred with similar frequency in all groups however in patients with LP and with abnormal SA-ECG complex ventricular arrhythmias were more common than in group with normal SA-ECG (56% and 53% vs 49% respectively: NS).(ABSTRACT TRUNCATED AT 250 WORDS)
Action Potentials↗
Periodontal disease and coronary heart disease: a reappraisal of the exposure.
BACKGROUND: Results from studies relating periodontal disease to cardiovascular disease have been mixed. Residual confounding by smoking and use of clinical measures of periodontal disease rather than measures of infection have been 2 major criticisms. The aims of this study were to investigate relationships between prevalent coronary heart disease (CHD) and 2 exposures, (1) clinical periodontal disease and (2) IgG antibodies to 17 oral organisms, and to evaluate the role of smoking in these relationships. METHODS AND RESULTS: Our study is based on a subset of participants in the Atherosclerosis Risk in Communities (ARIC) Study, who received a complete periodontal examination during visit 4 (1996-1998). The exposures were periodontal status and serum IgG antibody levels against 17 periodontal organisms, and the outcome was prevalent CHD at visit 4. Multivariable analyses indicate that periodontal status is not significantly associated with CHD in either ever smokers or never smokers. Similar analyses evaluating antibodies indicate that high antibodies (above the median) to Treponema denticola (odds ratio [OR]=1.7; 95% CI, 1.2 to 2.3), Prevotella intermedia (OR=1.5; 95% CI, 1.1 to 2.0), Capnocytophaga ochracea (OR=1.5; 95% CI, 1.1 to 2.1), and Veillonella parvula (OR=1.7; 95% CI, 1.2 to 2.3) are significantly associated with CHD among ever smokers, whereas Prevotella nigrescens (OR=1.7; 95% CI, 1.1 to 2.6), Actinobacillus actinomycetemcomitans (OR=1.7; 95% CI, 1.2 to 2.7), and Capnocytophaga ochracea (OR=2.0; 95% CI, 1.3 to 3.0) were associated with CHD among never smokers. CONCLUSIONS: Clinical signs of periodontal disease were not associated with CHD, whereas systemic antibody response was associated with CHD in ever smokers and never smokers. These findings indicate that the quality and quantity of the host response to oral bacteria may be an exposure more relevant to systemic atherothrombotic coronary events than clinical measures.
Antibodies, Bacterial↗
Changes in perceived heart disease risk and health during a community-based heart disease prevention program: the North Karelia project.
To test whether the cardiovascular disease declines in North Karelia were accompanied by subjective improvements in health, we analyzed responses to two questions about perceived risk of heart disease and health status on independent random population samples surveyed 10 years apart. Age stratified perceived risk of heart disease declined significantly more (p less than .01) and age stratified perceived health status improved significantly more in North Karelia than in the reference area (p less than .005).
Attitude to Health↗
Recreational activity and career choice recommendations for use by physicians counseling physical education directors, vocational counselors, parents and young patients with heart disease. Ad Hoc Committee on Habilitation of the Young Cardiac, Council on Rheumatic Fever and Congenital Heart Disease, American Heart Association.
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Adolescent↗
Myocardial blood flow distribution in patients with ischemic heart disease or dilated cardiomyopathy undergoing heart transplantation.
BACKGROUND: The present investigation was designed to obtain an absolute measurement of myocardial blood flow and of its transmural distribution in ischemic heart disease and idiopathic dilated cardiomyopathy and to provide a reference standard for cardiac imaging in nuclear cardiology. METHODS AND RESULTS: Regional myocardial blood flow and its transmural distribution were estimated by the reference microsphere method in eight patients with idiopathic dilated cardiomyopathy (n = 4) or ischemic heart disease (n = 4) during heart transplant procedure. Before aortic clamping, 99mTc-labeled human albumin microspheres were injected into the left atrium while arterial blood was sampled from the aorta at a constant rate. No complications were observed during or after the procedure. From the excised heart, myocardial slices for gamma camera imaging and well counting analysis were obtained. Myocardial blood flow was assessed by a well counter, correlated with the extent of fibrosis expressed as collagen per total tissue proteins obtained from 4-hydroxyproline and glycine as determined by high-performance liquid chromatography. Microsphere distribution, as seen by gamma camera images in a different slice, was correlated with the extent of fibrosis assessed by histological analysis of the same myocardial specimen. Mean transmural myocardial blood flow was 0.49 +/- 0.17 and 0.38 +/- 0.15 mL.min-1 x g-1 in idiopathic dilated cardiomyopathy and ischemic heart disease, respectively (P < .01). Endocardial-to-epicardial flow ratio was lower in ischemic heart disease than in idiopathic dilated cardiomyopathy patients (0.99 +/- 0.33 versus 1.16 +/- 0.30, P < .05). Mean myocardial fibrosis was 9 +/- 6% in idiopathic dilated cardiomyopathy and 25 +/- 28% in ischemic heart disease. In both groups, no correlation was found between myocardial blood flow values and the extent of fibrosis. In ischemic heart disease, regional myocardial blood flow was not significantly affected by the severity of coronary stenosis (< or = 70% or > 70%) either in the endocardium (0.44 +/- 0.24 versus 0.36 +/- 0.16 mL.min-1 x g-1, P = NS) or in the epicardium (0.50 +/- 0.33 versus 0.38 +/- 0.33 mL.min-1 x g-1, P = NS). By gamma camera imaging, transmural microsphere distribution appeared more homogeneous in idiopathic dilated cardiomyopathy than in ischemic heart disease (mean coefficient variation, 18% and 27%, respectively; P < .02); the severity of perfusion impairment did not correlate with the extent of fibrosis evaluated by histological criteria. CONCLUSIONS: Heart transplant surgery offers a valuable model to assess absolute myocardial perfusion in human heart failure. Myocardial blood flow is markedly depressed in failing hearts of both ischemic heart disease and idiopathic dilated cardiomyopathy patients; a different transmural myocardial blood flow distribution is observed in ischemic heart disease than in idiopathic dilated cardiomyopathy, with prevalent endocardial perfusion in the latter but not the former condition. In patients with end-stage heart failure, myocardial blood flow appears to be similarly impaired in fibrotic and viable regions. Mechanisms other than myocardial fibrosis and coronary lesions appear to operate in determining myocardial blood flow impairment in heart failure.
Adult↗
Dietary fat intake and risk of coronary heart disease: the Strong Heart Study.
BACKGROUND: The results of previous studies on the association between dietary fat intake and coronary heart disease (CHD) incidence are inconsistent. OBJECTIVE: The aim of this study was to examine the association between dietary fat intake and CHD incidence in American Indians in the Strong Heart Study. DESIGN: A total of 2938 participants aged 47-79 y and free of CHD at the second examination (1993-1995) were examined and followed for CHD, nonfatal CHD, and fatal CHD events to 31 December 2002. Dietary intake was assessed by using a 24-h diet recall and was calculated as percentages of energy. RESULTS: Participants were followed for a mean (+/-SD) of 7.2 +/- 2.3 y. During follow-up, 436 incident CHD cases (298 nonfatal CHD and 138 fatal CHD events) were ascertained. Participants aged 47-59 y in the highest quartile of intake of total fat, saturated fatty acids, or monounsaturated fatty acids had higher CHD mortality than did those in the lowest quartile [hazard ratio (95% CI): 3.57 (1.21, 10.49), 5.17 (1.64, 16.36), and 3.43 (1.17, 10.04), respectively] after confounders were controlled for. These associations were not observed for those aged 60-79 y. CONCLUSIONS: Total fat, saturated fatty acid, and monounsaturated fatty acid intake were strong predictors of CHD mortality in American Indians aged 47-59 y, independent of other established CHD risk factors. It may be prudent for American Indians to reduce their fat intake early in life to reduce the risk of dying from CHD.
Aged↗