Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HEART”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 541 records · Page 30Linked to original sources
PubMedDate not supplied

Receptor systems affecting force of contraction in the human heart and their alterations in chronic heart failure.

Catecholamines acting through beta 1- and beta 2-adrenergic receptors cause positive inotropic and chronotropic effects in the human heart. However, recent evidence suggests that in the human heart other receptor systems can also affect heart rate and contractility. Positive inotropic effects can be mediated by receptor systems acting through accumulation of intracellular cyclic adenosine monophosphate (cAMP; Gs-protein-coupled receptors such as 5-hydroxytryptamine(5-HT)4-like, histamine H2, and vasoactive intestinal peptide) or by receptor systems acting independently of cAMP, possibly through the phospholipase C/diacylglycerol/inositol-1,4,5-trisphophate pathway (such as alpha 1-adrenergic, angiotensin II, and endothelin). In the nonfailing human heart, activation of all these receptor systems induces only submaximal positive inotropic effects compared with those caused by beta-adrenergic receptor stimulation, indicating that in humans the cardiac beta-adrenergic receptor/Gs-protein/adenylate cyclase pathway is the most powerful mechanism to increase heart rate and contractility. However, the human heart contains only a few spare receptors for beta-adrenergic receptor-mediated positive inotropic effects and nearly all beta-adrenergic receptors are needed to cause maximal inotropic effects. Thus any decrease in the number of beta-adrenergic receptors will automatically lead to a reduction in functional responsiveness of beta-adrenergic receptors. In chronic heart failure the number and responsiveness of cardiac beta-adrenergic receptors are reduced, presumably because of the enhanced sympathetic drive to the heart and hence endogenous down-regulation by an elevated release of (cardiac-derived) norepinephrine, and this loss in cardiac beta-adrenergic receptor function is strongly related to the severity of the disease. However, beta 1- and beta 2-adrenergic receptors are differentially changed in different forms of heart failure. In dilated cardiomyopathy and possibly in aortic valve disease the number of cardiac beta 1-adrenergic receptors is selectively reduced without alteration in the number of beta 2-adrenergic receptors (although beta 2-adrenergic receptors become somewhat uncoupled). In ischemic cardiomyopathy, mitral valve disease, and possibly tetralogy of Fallot, the number of both beta 1- and beta 2-adrenergic receptors is concomitantly decreased. Because of the lack of a substantial receptor reserve, such a decrease in the number of beta-adrenergic receptors is accompanied by reduced inotropic and chronotropic responses to beta-adrenergic receptor stimulation in vitro and in vivo.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenylyl Cyclases↗
PubMedDate not supplied

Health status of heart transplant recipients versus patients awaiting heart transplantation: a preliminary evaluation of the SF-36 questionnaire.

Measures of the effects of health care on patients' lives are being requested to evaluate heart transplantation programs. A relatively short, 36-item, questionnaire (SF-36) designed to measure health status is being evaluated as an outcome measure for a variety of conditions. The SF-36 was sent to all adults awaiting heart transplantation (n = 48) and heart transplant recipients (n = 177) at the University of Minnesota as a pilot study of the SF-36 applied to heart transplantation. Response rates were 88% and 81%, respectively. Heart transplant recipients had significantly (p < 0.0001) better scores for general health perceptions (70 +/- 21 versus 33 +/- 21), vitality (62 +/- 19 versus 39 +/- 2), physical function (71 +/- 22 versus 36 +/- 24), ability to perform roles without physical limitations (62 +/- 41 versus 27 +/- 35), and social function (85 +/- 18 versus 63 +/- 31) compared with patients awaiting heart transplantation. Mental function and ability to perform roles without emotional problems were good in both groups and not significantly different. Mean SF-36 scores for the heart transplant recipients were uniformly not as high as scores for a historical group with only minor medical problems. These preliminary data suggest that the SF-36 is sensitive to the effects of heart transplantation. Additional studies of the SF-36 as an outcome measure for heart transplantation are warranted and should include methods to control for extraneous variability and to provide unbiased data collection.

Female↗
PubMed1993

Isolated congenital heart block: fetal and infant outcome and familial incidence of heart block.

OBJECTIVE: To determine the 1-year outcome of infants with isolated congenital heart block, the risk of fetal loss in mothers of affected infants, and the risk of recurrence of congenital heart block. METHODS: The outcomes of 34 infants with isolated congenital heart block and of the 109 pregnancies in the 32 mothers of these infants were analyzed retrospectively. A control group consisted of 170 pregnancies in 64 women individually matched for age, parity, and socioeconomic status. RESULTS: Five (15%) of the 34 infants with isolated congenital heart block died before 1 year of age. The relative risk for fetal loss in mothers of affected children, after the exclusion of a mother with 16 spontaneous abortions, was 1.9 (95% confidence interval 0.9-3.8; P = .094). The prevalence of congenital heart block in all siblings of children with congenital heart block was 4% (two of 45). The risk of having a child with congenital heart block after a previous birth of an affected child was 8% (two of 26). CONCLUSIONS: Infant mortality in isolated congenital heart block is considerable, and mothers of affected children tend to have an increased risk of fetal loss. However, the risk of recurrence of congenital heart block is low.

Abortion, Spontaneous↗
PubMed1977

[Heart size and left ventricular function in coronary artery disease: I. Heart size, exercise tolerance, cardiac output and filling pressures (author's transl)].

The possible relationship between the cardiac volume, as determined radiologically in the supine position in 119 patients with angiographically proven coronary artery disease, and the results of ergometry and balloon catheterization was investigated. There was no relationship between the heart size on the one side and the maximum exercise tolerance and the maximum cardiac output on the other, except for the fact, that these parameters tended to decrease with increasing heart size. This was especially true in patients with angina. The maximum cardiac output of patients with angina was always below the value of patients without angina but comparable heart size. Reduced cardiac output under exercise (exertional cardiac insufficiency) was present in 50% of patients with enlarged hearts but already in 22% of patients with heart volumes in the lower range of normal. The diastolic pulmonary artery pressure, determined under exercise, was the only parameter with a significant relationship to the heart size: The larger the heart size, the higher the diastolic pulmonary artery pressure. On the other hand: the diastolic pulmonary artery pressure at rest was abnormal with significant frequency only, when the heart was enlarged. Our data suggest, that the hemodynamics are determined by 2 factors: Myocardial scarring secondary to infarction and coronary insufficiency (ischemia). Of these two factors only the former influences cardiac size. Therefore, determination of the heart volume helps evaluating the respective role of these two factors in individual cases.

Adult↗
PubMed1998

Transplantation with older donor hearts for presumed "stable" recipients: an analysis of the Joint International Society for Heart and Lung Transplantation/United Network for Organ Sharing Thoracic Registry.

BACKGROUND: We have previously demonstrated that the use of older donor hearts (>45 years) increases the odds of death nearly twofold in the early posttransplantation period when compared with the use of hearts from younger donors. Before excluding this segment of the donor pool, however, the mortality risk for remaining on the waiting list compared with that of receiving an older donor heart should also be considered. METHODS: We examined all adult status 2 patients added to the United Network for Organ Sharing heart transplant waiting list for primary transplantation between 1992 and 1995 (n = 4681). To account for the transient increased risk after transplantation, we used a time-dependent nonproportional hazards model with an exponential decay component for the analysis. For patients with an equal time since listing, the resulting risk ratios represent the ratio of mortality risk for a patient who receives an older donor heart to the mortality risk for a patient who remains on the waiting list. RESULTS: After 30 days posttransplantation, the risk of death for recipients of 45- to 49-year-old donor hearts was lower than if they had remained on the waiting list, and by 6 months the relative risk was 0.37 (95% confidence interval: 0.22, 0.62). For recipients of hearts from donors 50 years or older, the risk after transplantation was lower after 64 days, and by 6 months the relative risk was 0.48 (95% confidence interval: 0.31, 0.75). CONCLUSION: These results suggest that in spite of a high initial risk resulting from the transplant procedure, there was a clear long-term survival benefit for status 2 recipients of older donor hearts. Thus overall, in spite of the increased risk of death associated with receiving older donor hearts, the risk of death without a transplant was even greater. On the basis of this analysis we cannot support the exclusion of older donors from the donor pool.

Adolescent↗
PubMed1998

Heart failure clinical guideline. South African Medical Association Heart Failure Working Group.

OBJECTIVE: This Guideline targets chronic heart failure (CHF) due to left ventricular systolic dysfunction. The approach to both diagnosis and management of the CHF syndrome is included in this document. Although the aetiology of the heart failure may differ among the different racial groups (hypertension, end-stage rheumatic heart disease and idiopathic cardiomyopathy in black patients, and ischaemic heart disease in white, coloured and Indian patients), the end result is a dysfunctional left ventricle. The therapy applied is therefore applicable to a wide spectrum of CHF patients. This allows for the compilation of a CHF Guideline that is relevant to a large group of patients. All health care workers are targeted in this Guideline, although the general practitioner and specialist physician would probably gain the most from it. The clinical recognition of heart failure as well as its management is a difficult clinical problem and a primary care guideline will have to be a separate document, although the summary of this Guideline can be appreciated at a primary level of care. The motivation for the development of this guideline includes: Congestive heart failure is probably the most important cardiovascular condition that is still increasing in incidence and prevalence. A major problem is the clinical recognition of the heart failure syndrome, and this Guideline concentrates on outlining a practical approach to obtaining a history and doing a relevant examination. Unless the condition is correctly diagnosed, any recommendations on therapy lose their relevance. Numerous large, randomised, international, double-blind randomised trials are a feature of this condition and a Guideline giving clear recommendations for therapy based on these trials is crucial. The ordinary busy practitioner cannot be expected to read all these published studies and assimilate them into a coherent protocol of management. South Africa has not published a guideline on CHF that sets the standard of care that is considered acceptable. With the emergence of essential drug lists, managed health care groups and a more litigious society in South Africa, this Guideline will serve as the standard for the optimal management of CHF. OUTCOMES: Improvement in the quality of life, reduced CHF hospitalisations and mortality were the major considerations in the development of this Guideline. No economic analysis was made to assess cost-effective therapy, as this was not the brief of this document. The Directorate Medical Schemes, Supplies and Pharmaceutical Services (EDL) was a member of the working group. EVIDENCE: All the data were gathered from the published literature. Preference was given to the evidence provided by the numerous, large randomised CHF trials, the respective heart failure guidelines published by the European Society of Cardiology and the ACC/AHA Task Force and the clinical practice guidelines published by the US Department of Health and Human Services. An expert panel was then assembled and changes were made to the draft guideline both at a convened meeting and later on the basis of written comments following the distribution of a second draft. Where the evidence available was inconclusive or non-existent, a consensus of expert opinion was obtained. The most recent publications considered were published in 1997, but the literature was scanned on an ongoing basis for new data that may have changed the recommendations. METHODOLOGY/SPONSORSHIP: See Annexure B, p. 1155. RECOMMENDATIONS: A clear history should be obtained identifying the symptoms of the heart failure syndrome together with an attempt at identifying an aetiology and precipitating factor(s) underlying the syndrome. Clinical examination is emphasised, including identifying the three tenets of the clinical diagnosis of CHF (syndrome, aetiology, precipitating factor(s)). The CXR, ECG (resting, effort), selected blood tests are recommended as a routine in the diagnosis of CHF. Echocardiograph

Algorithms↗
PubMed1997

Increased ventricular sialylation in patients with heart failure secondary to ischemic heart disease.

BACKGROUND: Elevated serum sialic acids are associated with increased cardiovascular mortality, but sialic acid levels have not been studied in cardiac tissue. METHODS: Myocardial samples were obtained at the time of transplantation from 23 patients (age 54 +/- 12 years) with heart failure secondary to ischemic heart disease and 16 patients (age 51 +/- 7 years) with idiopathic dilated cardiomyopathy (DCM). A control group comprised postmortem samples obtained from 14 patients (age 70 +/- 5 years) who died of non-cardiovascular causes. Ventricular sialylation was quantitated using the sialic acid-specific lectins Maackia amurensis agglutinin (MAA) and Sambucus nigra agglutinin (SNA) using a chemiluminescence assay. Results are expressed as the percentage (+/-standard error of the mean) of the binding of lectin to a standardized control sample of human myocardium. RESULTS: Ventricular sialylation recognized by MAA was 55 +/- 7% in patients with heart failure secondary to ischemic heart disease compared with 26 +/- 7% for DCM (p = 0.006) and 32 +/- 8% for controls (p = 0.04), and that recognized by SNA was 69 +/- 7% in patients with heart failure secondary to ischemic heart disease compared with 42 +/- 6% for DCM (p = 0.006) and 38 +/- 7% for controls (p = 0.006). No significant difference in ventricular sialylation was observed between patients with DCM and controls. CONCLUSION: Myocardial levels of sialic acids are significantly increased in patients with heart failure secondary to ischemic heart disease compared with patients with idiopathic dilated cardiomyopathy and controls. Our findings are important in view of recent reports of an association between serum sialic acid concentration and cardiovascular mortality and require further investigation.

Aged↗
PubMed2001

Autoantibodies against neonatal heart M1 muscarinic acetylcholine receptor in children with congenital heart block.

Isolated congenital heart block may be associated with autoimmune disorder such as Sjögren Syndrome and systemic lupus erythematosus. In this work we demonstrate circulating autoantibodies against neonatal heart M1 muscarinic acetylcholine receptor (mAChR) in the sera of children with congenital heart block. This antibody were able to react with the second extracellular loop of the human M1 mAChR as demonstrated using a synthetic peptide in enzyme immune assay and binding assay. Affinity purified anti-peptide IgG as well as total IgG from children with congenital heart block, interfered with the specific radioligand occupancy from neonatal heart M1 mAChR, interacting irreversibly. The antipeptide antibodies also displayed an 'agonist-like' activity, i.e. decreased contractility, activated nitric oxide synthase activity and increased production of cyclic GMP. All of these effects were selectively blunted by pirenzepine and neutralized by the synthetic M1 peptide. Both binding and biological effects were obtained using neonatal rat heart instead adult heart and were independent of Ro/SS-A and La/SS-B antibodies and were also absent in the sera of normal children. A clinical relevance of these findings is demonstrated by a strong association between the existence of circulating M1 mAChR antipeptide antibodies and the presence of isolated congenital heart block, making these antibodies a proper marker of this disease.

Amino Acid Sequence↗
PubMed1997

Heart rate changes in cardiac transplant patients and in the denervated cat heart after edrophonium.

PURPOSE: The effect of edrophonium on heart rate in cardiac transplant patients and in an animal model of acute cardiac denervation were studied, to evaluate the functional state of the peripheral parasympathetic pathway following cardiac denervation. METHODS: Edrophonium was studied in patients with normally innervated hearts (controls) and in cardiac transplants. Edrophonium was also studied in vagotomized, beta-blocked cats. In Group I animals, the vagus nerve was not stimulated. In Groups 2 & 3 the right vagus nerve was electrically stimulated to produce approximately 20% and 40% reductions in baseline heart rate, respectively. RESULTS: Maximum heart rate reduction in transplants (7.3 +/- 0.8 beats.min-1 with 0.6 +/- 0.08 mg.kg-1) was less than in controls (13.3 +/- 1.6 beats.min-1 with 0.4 + 0.05 mg.kg-1, P < 0.01). In Group I animals heart rate decreased maximally by 20.9 +/- 2.5 beats.min-1 with 9.0 +/- 1.9 mg.kg-1. In Groups 2 and 3, with doses < 1.5 mg.kg-1, reductions in heart rate were greater than in Group I and maximum reductions were obtained with lower doses (Group 2: maximum reduction by 20.3 +/- 2.8 beats.min-1 with 1.3 +/- 0.1 mg.kg-1; Group 3:22.6 +/- 4.0 beats.min-1 with 0.8 +/- 0.2 mg.kg-1, P < 0.001). Doses > 1.5 mg.kg-1 in Groups 2 and 3 produced increases in heart rate. CONCLUSION: Edrophonium produced bradycardia in cardiac transplants suggesting spontaneous release of acetylcholine from parasympathetic postganglionic neurons in the transplanted heart. The magnitude of the bradycardia was less in transplant than in control patients. Findings from animal studies suggest that the reduction in transplants can be attributed to diminution or absence of tonic cardiac parasympathetic drive. At high doses, edrophonium may interfere with parasympathetic neuron activation.

Acetylcholine↗
PubMed2004

Towards defining heart failure in adults with congenital heart disease.

Injury to the myocardium disrupts geometric integrity and results in changes to intracardiac pressure, wall stress and tension, and the pattern of blood flow through the heart. Significant disruption to pump function results in heart failure which is defined in terms of symptoms: breathlessness and fatigue, signs of salt and water retention, and neurohormonal activation. This syndrome most commonly occurs in the context of injury due to ischaemic heart disease and dilated cardiomyopathy but because patients with congenital heart disease (CHD) are born with sometimes gross distortions of cardiac anatomy they too are subject to the forces that drive heart failure. This paper explores the available data relating to the clinical and neurohormonal manifestations of heart failure in patients with congenital heart disease and describes how, by additionally exploring events at a cellular level, we may be able to arrive at a definition of heart failure relevant to this population.

Heart↗
PubMed2005

Hypoplastic left heart syndrome: Rheumatic heart disease of the fetus?

Hypoplastic left heart syndrome (HLHS) accounts for nearly 25% of deaths among neonates with congenital heart disease. The essential feature of HLHS is a small left ventricle (LV) incapable of supporting the circulation. The etiology of HLHS is unknown. A hypothesis is proposed implicating an immune mechanism involving maternal antibodies produced in response to pharyngitis caused by group A beta-hemolytic streptococci (GABHS) ("strep throat"). After crossing the placenta, the antibodies injure the developing fetal heart, leading to HLHS either because of direct injury to the LV or secondary to reduced blood flow through affected aortic and mitral valves. Analogy is drawn to rheumatic heart disease (RHD), a known sequela of strep throat. In RHD a misdirected immune response originally intended for GABHS leads to cardiac injury through "molecular mimicry"; the normal heart antigens supposedly mimic the GABHS antigens. A similar pathogenesis is proposed for HLHS and related heart defects. HLHS may represent an extreme form of injury, while a milder insult may present as only mild aortic stenosis or a bicuspid aortic valve, conditions with wide prevalence among the general population. The injury may indeed superimpose on many other congenital heart defects, leading to a variable presentation of these other diseases. Beside remarkable likenesses between HLHS and RHD, the hypothesis is also supported by increasing evidence for the role of deleterious transplacental antibodies in the pathogenesis of other fetal diseases. Implications for other congenital heart diseases and the broader picture of global public health are discussed.

Female↗
PubMed2003

Late recovery of atrioventricular conduction after pacemaker implantation for complete heart block associated with surgery for congenital heart disease.

OBJECTIVES: Pacemaker implantation is a standard recommendation for patients with persistent complete heart block following surgery for congenital heart disease. This study was performed to determine the incidence and clinical significance of late recovery of atrioventricular conduction following pacemaker implantation. METHODS: Between 1990 and 2001, 5662 open cardiac procedures for congenital heart defects were performed at our institution. The postoperative course of all patients with complete heart block in whom a permanent pacemaker was implanted was followed on a monthly basis, by either clinical or transtelephonic follow-up. RESULTS: A total of 72 patients with persistent postoperative complete heart block underwent pacemaker implantation. After insertion of the pacemaker, recovery of atrioventricular conduction was recognized in 7 of 72 patients (9.6%) at a median of 41 days (18-113 days) after the initial cardiac operation. These included 3 patients with ventricular septal defect, 2 with ventricular inversion or single ventricle, and 1 each with left ventricular outflow tract obstruction and atrioventricular septal defect. During a mean follow-up of 4.4 +/- 2.6 years, there was no late recurrence of heart block. Three patients had residual right bundle branch block and 1 had first-degree atrioventricular block. CONCLUSIONS: Atrioventricular conduction may return in a small but significant percentage of patients following pacemaker implantation for complete heart block associated with congenital heart surgery. When recovery of atrioventricular conduction occurs within the first months after surgery it appears reliable, which suggests that lifelong cardiac pacing may not be necessary in these individuals.

Atrioventricular Node↗
PubMed2001

Effect of beta-blockade on heart rate variability in decompensated heart failure.

BACKGROUND: One of the putative mechanisms for the salutary effects of beta-blockers in patients with congestive heart failure is their ability to improve autonomic dysfunction. However, patients with profound neurohumoral abnormalities derive little survival benefit from beta-blockers. The purpose of the current study was to evaluate the effect of beta-blockers on heart rate variability in decompensated heart failure. METHODS: Time and frequency domain heart rate variability indices were obtained from 24-h Holter recordings and compared to assess the role of beta-blockade in 199 patients (mean age 60+/-14 years [range 21 to 87]) with decompensated heart failure (New York Heart Association functional class III [66%] and IV [34%]). RESULTS: All heart rate variability indices were markedly suppressed but were substantially higher in patients who were on beta-blockers. Time domain measures of parasympathetic cardiac activity, the percentage of RR intervals with >50 ms variation (4.9+/-0.6 vs. 7.7+/-1.2%, P=0.006) and the square root of mean squared differences of successive RR intervals (22.7+/-2.0 vs. 31.6+/-4.1 ms, P=0.004), were higher in the beta-blocker group. Spectral analysis revealed that the total power and the ultra low frequency power were significantly higher in patients on beta-blockers (82% and 59%, respectively). The high frequency power, a spectral index of parasympathetic modulation, was 41% higher in the beta-blocker group (121+/-25 vs. 171+/-27 ms(2), P=0.02). Multiple linear regression, adjusted for clinical parameters and drug therapies, revealed a strong positive relationship between beta-blockade and higher values of time and frequency domain measures. The mean number of ventricular tachycardia episodes were significantly lower in patients on beta-blocker therapy (3.6+/-1.5 vs. 19.0+/-5.3, P=0.04). CONCLUSIONS: beta-blockers improve the impaired cardiac autonomic regulation during high sympathetic stress of decompensated heart failure.

Adrenergic beta-Antagonists↗
PubMed1999

Arterial baroreflex modulation of heart rate in patients early after heart transplantation: lack of parasympathetic reinnervation.

BACKGROUND: Orthotopic heart transplantation results in cardiac denervation. The presence of cardiac parasympathetic reinnervation in humans has been widely debated based on the application of differing indirect measures of autonomic control. However no attempt has been made to analyse the reflex heart rate response to baroreceptor stimulation whose occurrence is generally considered a reliable marker of the ability to activate cardiac vagal reflexes. This study tested the hypothesis that the presence of donor heart RR interval lengthening following phenylephrine induced blood pressure increase would be an index of parasympathetic reinnervation. METHODS: Baroreflex sensitivity (BRS) was assessed in 30 patients (mean age 51+/-12 years) 1-24 months after heart transplantation carried out by the standard Lower-Shumway technique. In 6 patients the recipient atrium rate response (P-P interval) to baroreceptor stimulation by phenylephrine was also simultaneously determined by transesophageal recording. RESULTS: None of the 30 patients showed prolongation of RR intervals in the donor heart. The average BRS value was -0.28+/-0.54 ms/mmHg (range -1.3-0.7 ms/mm Hg). In the 6 patients in whom BRS was obtained at both the recipient atrium (P-P) and donor heart (R-R) the changes were 7.6+/-5.7 ms/mm Hg and -0.38+/-0.58 ms/mm Hg respectively (p = 0.02), thus confirming that the absent RR interval lengthening in the donor heart is the consequence of efferent vagal fiber interruption. CONCLUSIONS: The absence of any RR interval prolongation following phenylephrine induced baroreceptor stimulation demonstrates that vagal efferent reinnervation of the donor heart does not occur up to 24 months in patients operated via the standard Lower-Shumway procedure. It is also suggested that analysis of baroreceptor reflexes is a more specific method in the examination of cardiac parasympathetic reinnervation.

Arteries↗
PubMed2001

Heart function challenged with beta-receptor agonism or antagonism in a heart failure model.

We have shown that chronic treatment with carteolol, a non-selective beta-adrenergic receptor antagonist, improved left ventricular (LV) function and survival in an avian model of dilated cardiomyopathy (DCM). The aim of the present study was to compare ex vivo heart function with and without beta-agonist and antagonist challenge. We investigated whether intracoronary infusion of a beta-blocker, carteolol or beta-agonist, isoproterenol decreased contractility. In the DCM group, isoproterenol resulted in a significantly greater increase in heart rate (71% vs. 28% compared to control hearts). To investigate the mechanism for the increase in heart rate, we exposed spontaneously beating neonatal cardiomyocytes to serum immunoglobulin (IgG) isolated from DCM animals. Serum IgG resulted in a significant increase in spontaneous beating rate in neonatal rat cardiomyocytes that was blocked by pre-treatment with a beta-blocker. Carteolol challenge did not significantly change heart rate but did significantly increase LV peak pressure in DCM hearts (62%) while coronary artery flow remained unchanged (2.7+/-0.1 vs 2.7+/-0.5 ml/min/g). These results show that 1) beta-receptor stimulation results in a greater tachycardic response in DCM animals, and 2) carteolol challenge improves myocardial contractility in hearts from DCM animals independent of heart rate or changes in coronary artery flow.

Adrenergic beta-Agonists↗
PubMed2003

Beta-blocker efficacy according to heart rate and rhythm in patients with heart failure. Commentary on the Cardiac Insufficiency Bisoprolol Study II analysis.

Large randomized trials have demonstrated that beta-blocker treatment reduces morbidity and mortality in patients in chronic heart failure. Questions remain about the influence of individual characteristics on the magnitude of the benefit of beta-blockers in patients with heart failure including the influence of heart rate and cardiac rhythm. In the Cardiac Insufficiency Bisoprolol Study II, baseline heart rate and heart rate change over time had prognostic value but treatment with bisoprolol was associated with a benefit at all levels of baseline heart rate and additional benefit related to heart rate slowing was observed. In the subgroup of patients with atrial fibrillation, morbidity and mortality rates were similar in placebo and bisoprolol treated patients. It is possible that patients with atrial fibrillation had a higher level of sympathetic stimulation that would have required higher doses of bisoprolol to achieve a similar level of beta-blockade. Alternatively, the failure to observe improved outcome in the subgroup with atrial fibrillation may have been due to chance. However, because this finding was not observed in other large trials, and because there was no clear explanation, it should not be concluded that patients with chronic heart failure and atrial fibrillation do not benefit from beta-blockade.

Adrenergic beta-Antagonists↗
PubMed1996

Clinical relevance of heart rate variability changes after heart transplantation.

Heart rate variability (HRV) of the healthy innervated heart is controlled and regulated by the autonomous nervous system and is influenced by respiratory frequency. Physiologically, there are slow and fast variations of heart rate which are of sympathetic or parasympathetic origin respectively. Spectral analysis of heart rate variability permits a selective quantification of these periodic influences of autonomous neural control. In the absence of neural influence on the pacemaker of the donor heart, we do not expect a high periodic heart rate variability (HRV). Due to the almost rigid heart rhythm we only anticipate a slight deviation of the R-R intervals from their mean value. Interventions such as valsalva maneuvers, controlled respiration and tilt table result in a very small but significant change of heart rate variability. These changes are most likely due to local influences at the donor sinus node. Neural influences from reinnervation may also play an important role in patients long after transplantation.

Acute Disease↗
PubMed1989

Cardiopulmonary response to dynamic exercise after heart and combined heart-lung transplantation.

The exercise capacity and cardiopulmonary response to progressive dynamic exercise of eight healthy recipients of heart-lung transplants were compared with those of matched recipients of orthotopic cardiac transplants and normal controls. In both transplant groups the maximum workloads were lower than that in the normal group. The transplant recipients had higher pre-exercise heart rates and lower maximum heart rates than the normal controls. Ventilation during submaximal exercise was similar in the heart transplant group and the controls. The heart-lung group had an increased ventilatory response associated with lower end tidal carbon dioxide concentrations. Exercise capacity after combined heart-lung transplantation is similar to that after cardiac transplantation. Transplant recipients have an abnormal heart rate response during exercise related to cardiac denervation. The altered ventilatory response in heart-lung recipients may be the result of pulmonary denervation.

Adolescent↗