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PubMed1976

Community surveillance for coronary heart disease: the Framingham Cardiovascular Disease survey. Comparisons with the Framingham Heart Study and previous short-term studies.

It appears likely that intervention trials on a community scale against one or more coronary heart disease risk factors will begin in the near future. Prerequisite to the evaluation of the effectiveness of these trials is the accurate determination of coronary heart disease incidence rates. The Framingham Cardiovascular Disease Survey was undertaken to test the hypothesis that a short-term surveillance study of a defined population can generate accurate incidence rates for at least some categories of cardiovascular disease and that these rates are comparable with those obtained by longitudinal survey of the same population. In conjunction with the 1970 U.S. census, a 1 year survey was made of all new coronary heart disease events occurring in the town of Framingham, Mass. Surveillance was performed by several methods that were intentionally overlapping. During the study period, 244 coronary heart disease events occurred. Despite the relatively small size of the population, many of the well established epidemiologic characteristics of this disease were evident. The rates obtained by the cardiovascular disease survey were comparable with those obtained by the Framingham Heart Study, for the harder end points of myocardial infarction and death from coronary heart disease, but much smaller for the softer end point of angina pectoris, especially in women. These data and those from similar studies indicate that periodic short-term surveillance studies of target populations of major intervention programs can provide an economic method of generating incidence data for the evaluation of the impact of such programs on myocardial infarction and death from coronary heart disease.

Age Factors↗
PubMed1986

Lipids and lipoproteins as predictors of coronary heart disease, stroke, and cancer in the Honolulu Heart Program.

A group of 2,122 healthy men in the Honolulu Heart Program who participated in the Cooperative Lipoprotein Phenotyping Study, 1970 to 1972, were followed for 10 years by repeated examinations and surveillance of hospital discharge and mortality records in order to diagnose new cases of coronary heart disease, stroke, cancer, and other deaths. Total cholesterol and low-density lipoprotein cholesterol were significantly associated with all clinical types of coronary heart disease in multivariate analyses, whereas high-density lipoprotein cholesterol was inversely associated with nonfatal myocardial infarction and total coronary heart disease, but not with fatal coronary heart disease nor angina. Triglyceride and very-low-density lipoprotein cholesterol were associated with total coronary heart disease by univariate but not multivariate analysis. None of the other specific chronic diseases were significantly associated with any lipid or lipoprotein, although there were trends of inverse associations of all noncardiovascular disease with total cholesterol and low-density lipoprotein cholesterol. Thus, for total disease (coronary heart disease, stroke, cancer, and other deaths), the optimal range for lowest disease incidence was about 200 to 220 mg/dl for total cholesterol and 120 to 140 mg/dl for low-density lipoprotein cholesterol. A strong inverse pattern of total disease with high-density lipoprotein cholesterol indicated that the highest levels were the optimal levels.

Age Factors↗
PubMed1989

Comparison of lipoprotein lipase activity in heart myocytes and perfused hearts.

This study was initiated to compare lipoprotein lipase activity in isolated heart myocytes and the heparin residual compartment of perfused hearts from adult rats. Heart lipoprotein lipase activity was divided into two fractions by 1 min of heparin perfusion. Heparin-residual and myocyte lipoprotein lipase activity were lower in hearts obtained from fasted compared to fed rats. In each case, the myocyte enzyme activity was 55 to 60% of heparin-residual levels. The difference between myocyte and heparin-residual activity may be a consequence of the time and treatment required to isolate cells in that long-term in vitro exposure of heart tissue to heparin also reduces residual activity. In vivo treatment with endotoxin decreased both heparin-residual and myocyte lipoprotein lipase activities; whereas, colchicine administration increased both activities compared to saline injected rats. In this latter experiment heart heparin-residual and myocyte lipoprotein lipase activities were positively correlated (r = 0.90). The results indicate that in the mature heart intracellular lipoprotein lipase activity is primarily associated with myocytes.

Animals↗
PubMed2004

The Warfarin/Aspirin Study in Heart failure (WASH): a randomized trial comparing antithrombotic strategies for patients with heart failure.

BACKGROUND: Heart failure is commonly associated with vascular disease and a high rate of athero-thrombotic events, but the risks and benefits of antithrombotic therapy are unknown. METHODS: The current study was an open-label, randomized, controlled trial comparing no antithrombotic therapy, aspirin (300 mg/day), and warfarin (target international normalized ratio 2.5) in patients with heart failure and left ventricular systolic dysfunction requiring diuretic therapy. The primary objective was to demonstrate the feasibility and inform the design of a larger outcome study. The primary clinical outcome was death, nonfatal myocardial infarction, or nonfatal stroke. RESULTS: Two hundred seventy-nine patients were randomized and 627 patient-years exposure were accumulated over a mean follow-up time of 27 +/- 1 months. Twenty-six (26%), 29 (32%), and 23 (26%) patients randomized to no antithrombotic treatment, aspirin, and warfarin, respectively, reached the primary outcome (ns). There were trends to a worse outcome among those randomized to aspirin for a number of secondary outcomes. Significantly (P =.044) more patients randomized to aspirin were hospitalized for cardiovascular reasons, especially worsening heart failure. CONCLUSIONS: The Warfarin/Aspirin Study in Heart failure (WASH) provides no evidence that aspirin is effective or safe in patients with heart failure. The benefits of warfarin for patients with heart failure in sinus rhythm have not been established. Antithrombotic therapy in patients with heart failure is not evidence based but commonly contributes to polypharmacy.

Aged↗
PubMed1998

Heart microvessels and aortic endothelial cells express the 15 kDa heart-type fatty acid-binding proteins.

Due to their hydrophobic nature, free fatty acids require carriers for transport across and within the cells. The endothelial layer is the first barrier to be traversed by the fatty acids, from the plasma to the underlying cells and tissues. We tried to find out whether cytosolic fatty acid-binding proteins (FABPs) are present in the endothelium of large vessels (aortic endothelial cells) and small vessels (myocardial capillaries) using the following experimental approaches: (i) loading the delipidated aortic endothelial cell (EC) homogenate and the heart cytosolic proteins and membrane proteins with [14C]palmitate or [14C]oleate, respectively, followed by autoradiographic detection of electrophoretically separated bands; (ii) detection by immunoprecipitation of heart-type FABP (H-FABP) using an affinity-purified antibody raised against bovine H-FABP (anti-H-FABP), and (iii) localization of FABP by indirect immunofluorescence and gold-immunocytochemistry applied to cultured EC and to thick and thin frozen sections of mouse heart. The results showed that: (i) within the EC homogenate proteins that express affinity for [14C]palmitate have an apparent Mr of 15000, and 40000-45000, that correspond as molecular mass to cytosolic and membrane FABPs, respectively. Similar affinity was found by incubation with [14C]oleate, that binds to a protein of Mr 15000 in the heart cytosol, and to a 40-45 kDa protein in the membrane fraction; (ii) anti-H-FABP immunoprecipitated specifically a cytosolic 15 kDa peptide (H-FABP); (iii) by indirect immunofluorescence, cytosolic H-FABP was localized on heart microvessels and myocytes and also in cultured aortic EC where intense spotted fluorescence characteristic for cytosolic antigens was present; (iv) by immunocytochemistry, H-FABP was detected in the EC cytoplasm, and in close proximity to the cytoplasmic aspect of plasmalemma and vesicle membranes. Together the data attest the presence of the 15 kDa, heart-type FABP in the endothelium of aorta and heart microvessels.

Animals↗
PubMed1985

Diet and 20-year mortality from coronary heart disease. The Ireland-Boston Diet-Heart Study.

In a prospective epidemiologic study of 1001 middle-aged men, we examined the relation between dietary information collected approximately 20 years ago and subsequent mortality from coronary heart disease. The men were initially enrolled in three cohorts: one of men born and living in Ireland, another of those born in Ireland who had emigrated to Boston, and the third of those born in the Boston area of Irish immigrants. There were no differences in mortality from coronary heart disease among the three cohorts. In within-population analyses, those who died of coronary heart disease had higher Keys (P = 0.06) and modified Hegsted (P = 0.02) dietary scores than did those who did not (a high score indicates a high intake of saturated fatty acids and cholesterol and a relatively low intake of polyunsaturated fatty acids). These associations were significant (P = 0.03 for the Keys and P = 0.04 for the modified Hegsted scores) after adjustment for other risk factors for coronary heart disease. Fiber intake (P = 0.04) and a vegetable-foods score, which rose with increased intake of fiber, vegetable protein, and starch (P = 0.02), were lower among those who died from coronary heart disease, though not significantly so after adjustment for other risk factors. A higher Keys score carried an increased risk of coronary heart disease (relative risk, 1.60), and a higher fiber intake carried a decreased risk (relative risk, 0.57). Overall, these results tend to support the hypothesis that diet is related, albeit weakly, to the development of coronary heart disease.

Adult↗
PubMed1983

Spouse behavior and coronary heart disease in men: prospective results from the Framingham heart study. II. Modification of risk in type A husbands according to the social and psychological status of their wives.

Analyses of spouse data from the Framingham Heart Study indicated that the risk of developing coronary heart disease among Type A men, compared with Type B men, was modified by the behavior or social status of their wives. Between 1965 and 1967, 269 spouse pairs, in which the husbands were 45-64 years of age, were administered an extensive psychosocial questionnaire. These pairs were followed over a 10-year period for the development of heart disease. When Type A and Type B men were stratified by the social and personality characteristics of their wives, it was found that the differential rate of heart disease between Type A and Type B men was present only in situations where the wives' characteristics might be deemed stressful. Type A husbands were 2.5 times as likely to develop coronary heart disease as Type B husbands if married to women with 13 or more years of education, and had 3.5 times the coronary risk of Type B husbands if married to a woman employed outside the home. When spouses were stratified by behavior type, employed outside the home. When spouses were stratified by behavior type, the highest rates of coronary heart disease were among Type A men married to Type B wives (25%). This rate was over three times the rate among Type B men married to Type B wives (7.8%). When tests for interaction between the behavior type of husbands and characteristics of wives were calculated, significant effects were found among blue-collar men on all variables except wives' educational level. This indicates that Type A men in white-collar occupations are at higher risk of heart disease regardless of wives' characteristics; whereas, the effect of behavior type among men in blue-collar occupations was interrelated with and modified by wives' characteristics. These results were apparent regardless of the husbands' standard coronary risk factors.

Behavior↗
PubMed1991

Heart-specific autoantibodies can be eluted from the hearts of Coxsackievirus B3-infected mice.

This study was undertaken to determine if immunoglobulin G (IgG) antibodies could be eluted from the hearts of mice with Coxsackievirus B3-induced autoimmune myocarditis and to characterize the immunoreactivity of any elutable autoantibodies. Susceptible (A/J) and resistant (B10.A) mice were administered the virus or the control treatment and killed at various times after treatment. Acid eluates from pooled heart tissue from each treatment group and each time were tested for IgG reactivity with normal heart tissue by immunohistochemistry and with normal heart extracts by Western immunostaining. Eluates from infected A/J mice reacted strongly with syngeneic heart and modestly with syngeneic skeletal muscle tissue. Eluates from infected B10.A or control mice of either strain exhibited little reactivity with either tissue. Tissue reactivity was similar when allogeneic tissue was used as the substrate. Eluates from infected A/J mice recognized the heavy chain of cardiac myosin and several other cardiac antigens by Western immunostaining while eluates from the other treatment groups exhibited little or no reactivity with any normal heart constituents. These results indicate that in vivo IgG deposition occurs in the hearts of mice with post-infectious autoimmune myocarditis and that the specificity of these antibodies is similar to that reported for serum from animals with this disease. The mechanism(s) leading to myocardial IgG deposition and its possible role in pathogenesis remain to be elucidated.

Animals↗
PubMed2002

"Diastolic heart failure" or heart failure caused by subtle left ventricular systolic dysfunction?

OBJECTIVES: To determine whether patients with suspected heart failure but preserved systolic function, as determined by conventional echocardiographic measures (often said to have "diastolic heart failure), might have subtle left ventricular systolic dysfunction detectable by a new measure of left ventricular systolic function-left ventricular systolic atrioventricular plane displacement. DESIGN: Observational study. SETTING: Direct access echocardiography. PATIENTS: 147 patients with suspected heart failure referred by general practitioners. MEASUREMENTS: Echocardiographic assessment of conventional measures of left ventricular systolic function (fractional shortening, ejection fraction (by Simpson's biplane method) and "eyeball" assessment) and measurement of left ventricular systolic atrioventricular plane displacement. RESULTS: Between 21% and 33% of patients with "normal" left ventricular systolic function by conventional methods were found to have abnormal left ventricular systolic atrioventricular plane displacement. CONCLUSIONS: Approximately one quarter of patients with suspected heart failure but preserved systolic function by conventional methods have abnormal atrioventricular plane displacement. These patients with suspected heart failure but preserved systolic function by conventional echocardiographic measures may have heart failure caused by subtle systolic dysfunction rather than isolated "diastolic heart failure".

Aged↗
PubMed2001

Differential activation of signal transduction pathways in human hearts with hypertrophy versus advanced heart failure.

BACKGROUND: Left ventricular failure is commonly preceded by a period of hypertrophy. Intriguingly, many of the signaling pathways that have been implicated in the regulation of hypertrophy, including the 3 mitogen-activated protein kinases (MAPKs: extracellular signal-regulated kinase, stress-activated protein kinase, and p38), protein phosphatase, calcineurin, and the protein kinase Akt and its target glycogen synthase kinase-3 (GSK-3), also regulate the apoptotic response. METHODS AND RESULTS: To understand the mechanisms that might regulate the progression of heart failure, we analyzed the activity of these signaling pathways in the hearts of patients with advanced heart failure, patients with compensated cardiac hypertrophy, and normal subjects. In patients with hypertrophy, neither the MAPK nor the Akt/GSK-3 pathways were activated, and the dominant signaling pathway was calcineurin. In failing hearts, calcineurin activity was increased but less so than in the hypertrophied hearts, and all 3 MAPKs and Akt were activated (and, accordingly, GSK-3ss was inhibited), irrespective of whether the underlying diagnosis was ischemic or idiopathic cardiomyopathy. CONCLUSIONS: In the failing heart, there is a clear prohypertrophic activity profile, likely occurring in response to increased systolic wall stress and neurohormonal mediators. However, with the activation of these hypertrophic pathways, potent proapoptotic and antiapoptotic signals may also be generated. Therapies directed at altering the balance of activity of these signaling pathways could potentially alter the progression of heart failure.

Calcineurin↗
PubMed1992

Chronic Chlamydia pneumoniae infection as a risk factor for coronary heart disease in the Helsinki Heart Study.

OBJECTIVE: To investigate in the prospective Helsinki Heart Study, whether chronic Chlamydia pneumoniae infection, indicated by elevated antibody titers against the pathogen, chlamydial lipopolysaccharide-containing immune complexes, or both, is a risk factor for coronary heart disease. DESIGN AND SETTING: The Helsinki Heart Study was a randomized, double-blind, 5-year clinical trial to test the efficacy of gemfibrozil in reducing the risk for coronary heart disease. Participants were randomized to receive either gemfibrozil (2046 patients) or placebo (2035 patients). Fatal and nonfatal myocardial infarction and sudden cardiac death were the main study end points. Serum samples were collected at 3-month intervals from all patients. PATIENTS: One hundred forty cardiac events occurred during the follow-up period. Serum samples from 103 case patients obtained 3 to 6 months before a cardiac end point were matched with those from controls for time point, locality, and treatment. Samples were tested for markers of chronic chlamydial infection. MEASUREMENTS: Immunoglobulin A (IgA) and G (IgG) antibodies to C. pneumoniae were measured using the microimmunofluorescence method. Lipopolysaccharide-containing immune complexes were measured using two antigen-specific enzyme immunoassays, the lipopolysaccharide-capture and immunoglobulin M (IgM)-capture methods. MAIN RESULTS: Using a conditional logistic regression model, odds ratios for the development of coronary heart disease were 2.7 (95% CI, 1.1 to 6.5) for elevated IgA titers, 2.1 (CI, 1.1 to 3.9) for the presence of immune complexes, and 2.9 (CI, 1.5 to 5.4) for the presence of both factors. If we adjusted for other coronary heart disease risk factors such as age, hypertension, and smoking, the corresponding values would be 2.3 (CI, 0.9 to 6.2), 1.8 (CI, 0.9 to 3.6), and 2.6 (CI, 1.3 to 5.2), respectively. CONCLUSION: The results suggest that chronic C. pneumoniae infection may be a significant risk factor for the development of coronary heart disease.

Adult↗
PubMed1985

Heterotopic heart transplantation in three patients at the Texas Heart Institute.

Seventy-three orthotopic and three heterotopic transplantations have been done in our institution, and in this report, we describe the procedure and outcome of those who underwent heterotopic transplantation. Three patients were in critical condition while awaiting donors for heart transplantation, and in each case, a suitable donor could not be found. Smaller donor hearts became available, and knowing that these patients would die without some kind of immediate action, we performed heterotopic heart transplantations. Patient Number 1 was a 53-year-old diabetic man who was in the last stages of heart disease when a small donor heart became available. Because of his rapidly deteriorating condition, we did a heterotopic transplantation. The patient is presently well and functioning normally. Patient Number 2 was a 26-year-old woman who received the heart of a 13-year-old donor after it became obvious that she could not wait for a suitable donor. We performed a heterotopic transplantation, after which the patient continues to function well. Patient Number 3 was a 53-year-old man who weighed 260 lbs. When a suitable donor could not be found, the heart of a 170-lb man became available and was used in a heterotopic transplantation. This patient also continues to be active and well. After considering the various advantages and disadvantages of heterotopic transplantation, we are convinced that there is a definite place for this procedure in some patients with end-stage cardiac failure, although we still believe that orthotopic transplantation should be offered to most recipients.

Journal Article↗
PubMed2002

Subcellular redistribution of la/SSB autoantigen during physiologic apoptosis in the fetal mouse heart and conduction system: a clue to the pathogenesis of congenital heart block.

OBJECTIVE: In isolated congenital heart block, the mechanism by which maternal autoantibodies target the intracellular components of the Ro/La RNP complex is unclear. Previous studies have demonstrated that cultured fetal cardiac myocytes rendered apoptotic bind antibodies to 48-kd La/SSB. This study further investigated the subcellular distribution of the La antigen during apoptosis in the fetal mouse heart and conduction system. METHODS: The atrioventricular (AV) node, AV bundle, and sinoatrial (SA) node were identified in serial sections prepared from paraffin blocks of normal mouse fetuses on days 15, 17, and 19 of gestation. Apoptosis was detected by TUNEL assay. Under confocal microscopy, fluorescent labeling of fragmented DNA in apoptotic cells was assessed by TUNEL, and La protein localization was visualized simultaneously using a murine monoclonal antibody or affinity-purified human polyclonal anti-La antibodies. RESULTS: Apoptotic cells were detected in and at the periphery of the AV and SA nodes as well as in the fetal heart valve insertions and working myocardium. In contrast, no apoptosis was detected in the adult heart AV node or surrounding myocardium. As expected, the La antigen was predominantly immunolocalized to the nucleus in nonapoptotic cells. However, apoptotic cells showed a marked reduction of nuclear La and redistribution of La to the cytoplasm. High-resolution confocal microscopy revealed that in cells that had undergone apoptosis, La antigen asymmetrically clustered near the surface of TUNEL-positive nuclei and apoptotic bodies. CONCLUSION: These data provide the first in vivo demonstration of the subcellular translocation of La autoantigen during apoptosis in the fetal heart and the conduction system under physiologic conditions. This observation supports the hypothesis that subcellular redistribution of La in the normally developing heart facilitates the binding of cognate maternal antibodies and subsequent tissue damage.

Animals↗
PubMed2006

22q11 microdeletion studies in the heart tissue of an abortus involving a familial form of congenital heart disease.

Microdeletion of chromosome 22 is responsible for DiGeorge syndrome, Velo Cardio Facial syndrome, and conotruncal defects. Here, we report on a case of microdeletion 22q11.2 in the heart tissue of a miscarried fetus in a family whose two children had died due to complex congenital heart disease. Fluorescence in situ hybridization (FISH) analysis in the couple revealed that the mother was mosaic for microdeletion of chromosome 22q11.2 in 10% of her peripheral lymphocytes. Prenatal diagnosis was offered to her in her third pregnancy. On routine ultrasonography at 10 weeks, the overall view of the heart was normal. However, before any further tests could be performed, she miscarried at 16 weeks. FISH studies on the heart tissue of the abortus revealed 22q11.2 microdeletion with two different cell lines. This suggests the importance of performing FISH studies when there is a history of congenital heart disease, even though ultrasonography shows a normal view of the heart.

Aborted Fetus↗
PubMed1978

Relationships between mean velocity of circumferential fiber shortening (VCF) and heart rate - the diagnostic value of a normalization of VCF to heart rate.

Previous studies relating mean velocity of circumferential fiber shortening (VCF) to heart rate suggested a linear correlation. Since there is considerable variability in the heart rate of normal subjects and in patients with myocardial disease, a normalization of VCF to heart rate could possibly increase the reliability of this echocardiographic parameter of myocardial function. In 106 normal subjects, a linear correlation between VCF and heart rate was confirmed (r=0.87). Values normalized to an arbitrary heart rate of 60/min by the calculated regression were called "relative velocity of contraction" (RVC). Because of the independence of RVC from heart rate, the RVC shows an obviously smaller physiological variation than VCF. Two hundred seventy-six patients were grouped and classified according to hemodynamic and angiographic parameters. These parameters correlated closer to RVC than to VCF. In addition, RVC gave definitely superior diagnostic information in separating patients with cardiac abnormality from normal individuals than did VCF.

Echocardiography↗
PubMed1990

Comparative study of mouse heart and heart-lung transplantations.

Heart transplantation in mice using a double anastomosis technique has become the standard method regardless of its technical difficulty. Heart-lung transplantation performed by single anastomosis in rats was also applied to mice, showing the identical operative result in addition to the advantage of easy applicability. We compared the heart transplant made by double anastomosis with the heart-lung transplantation using single aortic anastomosis in terms of graft survival and histologic features. The results were as follows: 1) During the follow-up period of 100 days after the transplantation in mice that survived 7 days after the operation, there were no deaths among the hosts and no evidence of nonfunction of the grafts in the six mice in each group. 2) In terms of monocyte infiltration perivascularily or interstitially, myocyte necrosis, interstitial hemorrhage, neutrophilic infiltration, and endocardial changes, histologic changes in the grafts were less in single anastomosis of heart-lung transplants than in double anastomosis. As a result, we can deduce that heart-lung transplantation using the single anastomosis technique is a good experimental model for the study of transplant reaction.

Anastomosis, Surgical↗
PubMed2001

Lipid metabolism in the heart--contribution of BMIPP to the diseased heart.

Lipid contributes greatly in cardiac metabolism to produce high energy ATPs, and is suggested to be related to the progression and deterioration of heart disease. It is fortunate that the I-123-betamethyliodophenylpentadecanoic acid (BMIPP) imaging technique is now available in determining heart condition, but we must be cautious about the interpretation of images obtained with this new tracer. From the uptake of BMIPP into the cell to breakdown and catabolism of it, there exist so many critical enzymatical pathways relating to the modification of BMIPP imaging. In clinical evaluation, the image will be translated as the integral effects of these pathways. In other words, we must be aware of these critical pathways regulating lipid metabolism and modifying factors in order to correctly understand BMIPP imaging. Lipid transport is affected by the albumin/FFA ratio in the blood, and extraction with membrane transporter proteins. Fatty acid binding protein (FABP) in the cytosole will play an important role in regulating lipid flux and following metabolism. Lipid will be utilized either for oxidation, triglyceride or phospholipid formation. For oxidation, carnitine palmitoil transferase is the key enzyme for the entrance of lipid into mitochondria, and oxidative enzymes such as acyl CoA dehydrogenase (MCAD, LCAD, HAD) will determine lipid use for the TCA cycle. ATPs produced in the mitochondria again limit the TG store. It is well known that BMIPP imaging completely changes in the ischemic condition, and is also shown that lipid metabolical regulation completely differs from normal in the very early phase of cardiac hypertrophy. In the process of deteriorating heart failure, metabolical switching of lipid with glucose will take place. In such a different heart disease conditions, it is clear that lipid metabolical regulation, including many lipid enzymes, works differently from in the healthy condition. These lipid enzymes are regulated by nuclear factor peroxisome proliferator-activated receptors (PPAR) just like a conductor of an orchestra. Most of the regulating mechanisms of the PPAR are still unknown, but reduction of this nuclear factor is shown in the process of decompensated heart failure. This review is based by mostly on our fundamental and Japanese clinical data. BMIPP has been used clinically in abundant cases in Japan. In such situations, further correct information on lipid metabolism, including BMIPP, will contribute to the understanding of deteriorating heart disease and its prognosis.

Animals↗
PubMed1989

Decreased spontaneous heart rate variability in congestive heart failure.

Heart rate (HR) variability is a noninvasive index of the neural activity of the heart. Although also dependent on the sympathetic activity of the heart, HR variability is mainly determined by the vagal outflow of the heart. Several HR abnormalities have been described in patients with congestive heart failure (CHF); however, there are no data on HR variability in CHF patients. In the present study HR variability was assessed in 20 CHF patients and 20 control subjects from 24-hour Holter tapes. HR variability was evaluated by calculating the mean hourly HR standard deviation and by analyzing the 24-hour RR histogram. Mean hourly HR standard deviation was markedly and significantly reduced in CHF patients both over the 24-hour period (97.5 +/- 41 vs 233.2 +/- 26 ms, p less than 0.001) as well as during most of the individual hours examined. The 24-hour RR histogram of CHF patients had a different shape and had a decreased variation compared to control subjects (total variability 356 +/- 102 vs 757 +/- 156 ms, p less than 0.001). Thus, CHF patients with depressed ejection fraction (less than 30%) have a low HR variability compared to normal individuals. This result can be interpreted as adjunctive evidence for decreased parasympathetic activity to the heart during CHF.

Adult↗