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At least 253 records · Page 14Linked to original sources
PubMed1998

Importance of heart failure as a cause of death. Changing contribution to overall mortality and coronary heart disease mortality in Scotland 1979-1992.

AIMS: As heart failure is a syndrome arising from another condition, such as coronary heart disease, it is rarely officially coded as the underlying cause of death regardless of the cause recorded by the physician at the time of certification. We sought to assess the true contribution of heart failure to overall mortality and coronary heart disease mortality and to examine how this contribution has changed over time. METHODS AND RESULTS: We carried out a retrospective analysis of all death certificates in Scotland between 1979 and 1992 for which heart failure was coded as the underlying or a contributory cause of death. From a total of 833622 deaths in Scotland between 1979 and 1992, heart failure was coded as the underlying cause in only 1.5% (13695), but as a contributory cause in a further 14.3% (126073). In 1979, 28.5% of male and 40.4% of female deaths attributed to coronary heart disease (coded as the underlying cause of death) also had a coding for heart failure. In 1992 these percentages had risen significantly to 34.1% and 44.8%, respectively (both P<0.001). Mortality rates for heart failure as the underlying or contributory cause of death, standardized by age and sex, fell significantly over the period studied in all ages and in both sexes: by 31% in men and 41% in women <65 years and 15.8% in men and 5.1% in women > or =65 years, respectively (P<0.01 for all changes). CONCLUSIONS: Death from heart failure is substantially underestimated by official statistics. Furthermore, one third or more of deaths currently attributed to coronary heart disease may be related to heart failure and this proportion appears to be increasing. While the absolute numbers of deaths caused by heart failure remains constant, this study is the first to show that standardized mortality rates are declining.

Age Distribution↗
PubMed1988

Asymptomatic episodes of ischaemia and their relation to heart rate changes in patients with chronic ischaemic heart disease.

The aim of our study was to evaluate the prevalence of asymptomatic episodes of ischaemia and their relation to heart rate in patients with effort angina pectoris undergoing continuous electrocardiographic monitoring for 24 h. We studied 91 patients with typical history of effort angina and positive stress testing (angina and rectilinear or downsloping ST segment depression more than 1 mm). During electrocardiographic monitoring 81 patients showed symptomatic or asymptomatic ischaemic episodes with ST segment depression, four patients a T wave inversion, while six patients did not show ischaemic episodes. The total number of ischaemic episodes registered was 284, of which 106 (37.32%) were symptomatic with significant heart rate increase, 130 (45.78%) asymptomatic with heart rate increase and 48 (16.9%) asymptomatic without heart rate changes. Twelve patients (13.18%) showed only symptomatic episodes of ischaemia with increase of heart rate, 26 patients (28.57%) symptomatic and asymptomatic episodes with heart rate enhancement, 12 patients (13.18%) only asymptomatic episodes with heart rate increase, eight patients (8.79%) symptomatic episodes of ischaemia with heart rate increase and asymptomatic ones with and without heart rate changes, and finally 23 patients (25.57%) showed symptomatic episodes with heart rate increase and asymptomatic ones without heart rate changes. In total, 31 (34.06%) of these patients showed during continuous electrocardiographic monitoring asymptomatic episodes of ischaemia without heart rate changes. These findings suggest a possible intervention of coronary tone modifications in determining asymptomatic ischaemic episodes without heart rate change in patients with effort angina.

Adult↗
PubMedDate not supplied

Heart rate adaptive optimization of spatial and temporal resolution for electrocardiogram-gated multislice spiral CT of the heart.

PURPOSE: We introduce a reconstruction method for electrocardiogram (ECG)-gated multislice spiral computed tomography (CT) examinations of the heart [adaptive cardio volume (ACV) reconstruction]. It is evaluated for a four-slice CT system (Siemens Somatom VolumeZoom). METHOD: State-of-the-art reconstruction techniques for ECG-gated multislice spiral CT use scan data from N consecutive heart cycles for image reconstruction. With increased N, the temporal resolution improves up to t rot /(2 N ) ( t rot is the 360 degrees rotation time of the scanner) but at the expense of insufficient volume coverage or loss of longitudinal resolution, especially at low heart rates. With the ACV technique, the number N of consecutive heart cycles used for image reconstruction is automatically adapted to the momentary heart rate of the patient, ranging from N = 1 at very low heart rates up to N = 3 at high heart rates, to maintain both high z resolution (reconstructed slice width close to the collimated slice width) and adequate temporal resolution. We evaluated slice sensitivity profiles and investigated 10 patients with different heart rates ranging from 55 to 110 beats/min for CT angiography (CTA) studies of the coronary arteries and compared the results with those from a reconstruction with fixed N ( N = 1 and N = 2). Axial images as well as multiplanar reformations were used for an evaluation of image quality. RESULTS: With the ACV approach, the complete heart may be scanned at 1 mm slice width within 25-35 s. A narrow slice sensitivity profile (full width at half-maximum of approximately 1.3 mm) is maintained for all heart rates. Diagnostic results can be obtained for heart rates up to about 95 beats/min by individual patient optimization of the ECG gating parameters. Improved temporal resolution at the expense of reduced longitudinal resolution may degrade the image quality of CTA studies at low heart rates by blurring plaques and stenoses. CONCLUSION: The results indicate the potential of the ACV reconstruction technique for high-resolution coronary CTA in a wide range of heart rates.

Algorithms↗
PubMed2006

Heart failure clinic in a community hospital improves outcome in heart failure patients.

PRINCIPLES: Heart failure is associated with a grim prognosis. Disease management programmes can improve prognosis in heart failure patients but the applicability to the general population remains limited. We aimed to compare the outcome, pharmacological therapy, and quality of life in unselected heart failure patients from a community hospital area who were managed either in the heart failure clinic or who received the usual care. METHODS AND RESULTS: We followed 115 patients receiving care in the heart failure clinic (n = 50) or the usual care (n = 65) for at least twelve months. During the follow-up of 561 (463, 701) days significantly less patients from the heart failure clinic were rehospitalized due to heart failure or died (42% vs 65%). Assignment to the heart failure clinic (Hazard ratio [HR] 0.39, 95% Confidence interval [CI] 0.20-0.75), New York Heart Association class (HR 2.32, 95% CI 1.22-4.41), and systolic blood pressure (HR 0.98, 95% CI 0.96-0.99) independently predicted occurrence of heart failure rehospitalisations or death. At the end of the follow-up patients from the heart failure clinic received more optimal pharmacological therapy and reported better quality of life. CONCLUSIONS: Patient management in the community hospital heart failure clinic reduced the incidence of heart failure rehospitalisation or death with further benefits in terms of pharmacological therapy and quality of life.

Aged↗
PubMed2003

Comparison of connexin expression patterns in the developing mouse heart and human foetal heart.

Heart muscle cells are electrically coupled by gap junctions, clusters of low-resistance transmembrane channels composed of connexins (Cx). The expression of the three major connexins (Cx43, Cx40 and Cx45) present in cardiac myocytes is known to be developmentally regulated but it is not clear how the patterns in the human heart compare with those found in the mouse. This issue is of importance given the wide use of transgenic mice to investigate gene function with the aim of extrapolating the results to human. In the present study we applied immunoconfocal microscopy to investigate the spatial distribution of the three connexins in the developing mouse heart and foetal human heart. Although Cx45 labelling was present at low levels throughout the developing mouse heart and human foetal (9-week) heart, it was most prominent in the conduction tissues. In the developing mouse heart, Cx40 was widely expressed at embryonic day 12.5 (E12.5) but at E17.5 expression was restricted to the conduction tissues and atria. In the 9-week human foetal heart, the Cx40 labelling pattern was similar to the E15 mouse heart, being far more abundant in conduction tissues (bundle branches to Purkinje fibres) and atria than in the ventricular muscle. Cx43 labelling became more apparent in the ventricular myocardium as development of the mouse heart progressed but was virtually undetectable in the central conduction system. In the human foetal heart Cx43 was virtually undetectable in the atria but was the predominant connexin in the ventricles. We conclude that, at least in some key aspects, the pattern of connexin expression in the developing mouse heart parallels that found in the human embryonic heart.

Animals↗
PubMedDate not supplied

Study of the relative incidences of psychosocial factors before and after heart transplantation and the influence of posttransplantation psychosocial factors on heart transplantation outcome.

Psychosocial factors substance abuse, noncompliance, psychiatric problems, and obesity in relation to the outcome of heart transplantation have been investigated. Data were gathered at the time of initial assessment, and patients (n = 53) were monitored during the follow-up after heart transplantation (mean 18 months). Noncompliance, psychiatric problems, or excessive weight before heart transplantation continued after heart transplantation. Significantly fewer substance abusers exhibited similar behavior after heart transplantation (p < 0.01), although in many cases this exposed other psychiatric or compliance problems. Patients with psychiatric problems after heart transplantation had a higher risk of infection (p < 0.01). Both these patients and those who were noncompliant had higher incidences of hospital readmission (p < 0.01) which were reflected in higher medical costs (p < 0.01) during the second year after heart transplantation in both subgroups. We conclude that (1) heart transplant recipients do not alter previous behavior after heart transplantation except with regard to substance abuse, (2) patients exhibiting substance abuse before heart transplantation and abstaining after heart transplantation have other psychosocial problems, (3) psychosocial problems after heart transplantation do not increase the risk for medical complications in the early posttransplantation period except with regard to infection, and (4) the presence of noncompliance and psychiatric problems after heart transplantation is related to increased readmissions and higher total medical costs.

Age Factors↗
PubMed1996

Heart failure and Starling's Law of the heart.

Coronary artery disease and ischemic myocardial damage form the most common cause of failure of the heart to pump enough blood for oxygenation of the body at a healthy blood pressure and at a low pressure in the veins. This paper gives an overview of the mechanisms involved in excitation-contraction coupling which are important to control of the force of the heartbeat. The inability of the heart in failure to eject a sufficient amount of blood in order to meet the needs of the body is thought to result from molecular changes in cardiac cells causing decreased active (systolic) force and impaired (diastolic) relaxation together with a greater stiffness of the remodelled ventricular wall. The failure to generate a forceful contraction is in part a consequence of derailment of the processes in the failing cardiac cells to manipulate calcium ions, despite the increased stimulus from nervous and hormone systems to enhance cardiac performance. By lack of adequate release and uptake of calcium ions, the amount of mechanical work that can be put out by the heart muscle is diminished and the heart may fail. Uptake of calcium ions by the intracellular store-the sarcoplasmic reticulum-is impaired in congestive heart failure probably as result of inadequate gene expression. In consequence, the amount of calcium that is released during each heartbeat is less than normal, thus force is reduced; in addition, the positive response of force to increased heart rate is lost. In normal heart muscle, the response of the contractile filaments to calcium ions depends strongly on sarcomere length thus explaining Starling's Law of the heart. Recent evidence suggests that this sensitivity is largely lost in congestive heart failure thereby reducing the effectiveness of stretch of cardiac cells on the mechanical output. The reduction of the maximal velocity of shortening of the cardiac sarcomere in heart failure is not well understood, but may in part be related to changes in the internal load as a result of changes in visco-elastic components of the myocardium Lastly, the effect of longstanding sympathetic drive to the heart during the development of heart failure induces a loss of sensitivity of the myocardium to catecholamines by loss of beta 1 receptors and partial uncoupling of the beta receptors from production of cyclic AMP; hence the effect of sympathetic activation is diminished and the heart has to rely more on Starling's Law. Increase of the filling pressure of the left ventricle may in part accommodate the ongoing demands of the body. However, in the case of a stenosed coronary arterial system, the increased end-diastolic pressure carries the substantial risk of aggravating pre-existent myocardial ischemia.

Calcium↗
PubMed2001

The loss of circadian heart rate variations in patients undergoing mitral valve replacement and Corridor procedure--comparison to heart transplant patients.

We have presently demonstrated that when added to mitral valve replacement (MVR) the corridor procedure is 75% efficient in restoring and maintaining sinus rhythm in patients with chronic atrial fibrillation (AF), caused by rheumatic mitral valve disease, (follow up 13.9months). In the same patient population, we observed that the typical day-night cycle heart rate (HR) variations were lost and our present study concentrates on this subject. Heart rate variability analysis based on 24-h Holter ECG recording (StrataScan 563 DelMar Avionics) or hospital discharge (12th-14th postoperative days) was performed in 3 patient groups: Group I: Patients with a Corridor procedure added to MVR (12pts, m/f 10/2, mean age 47.3+/-7.5yr); Group II (control): with patients MVR performed through the left atrial approach, without additional antiarrhythmic procedures (10pts, m/f 3/7 mean age 51.5+/-6.7yr), and Group III: heart transplant recipients (5pts, mean age 46.4+/-11.22yr). We analyzed the hourly heart rate over 24-h period divided into three 8-h segments (07-14h; 15-22h and 23-06h). Statistical comparison of mean hourly heart rate values was made between the three time periods of Holter monitoring. The Corridor procedure performed with mitral valve replacement resulted in conversion of sinus rhythm in 75% of patients (Group I), but postoperative heart rate variability analyses based on Holter monitoring disclosed that the mean heart rate was not statistically significantly difficult between the three 8-h segments of the day-night (P>0.05). The same results were found in the group of patients after heart transplant (P>0.05). The same results were found in the group of patients after heart transplant (P>0.05). In the second group (classical MVR), statistically significant differences in mean HR variation existed between the three 8-h intervals (P<0.05), and although atrial fibrillation occurred postoperatively physiologic circadian heart rate variations were preserved. With the Corridor procedure, both atria were surgically and electrically isolated and chronotropic function of the ventricles was restored by creating a small strip of atrial tissue with isolated sinus node and atrio-ventricular node, connected to the ventricles. This technique produced heart denervation nervous system influence, producing the loss of circadian HR variations, similar to the transplanted heart.

Cardiac Surgical Procedures↗
PubMed2002

Heart rate modulation by sympathetic nerves in dogs with heart failure.

To clarify heart rate modulation by the sympathetic nervous system, dogs with naturally acquired and experimentally induced heart failure were examined. Heart rate and plasma catecholamine concentrations were measured in clinically healthy dogs (control dogs) and dogs with mitral regurgitation (MR) during a resting period, a standing period, a period of standing in a medical examination room (to which the dogs were unaccustomed), a running period, and a period of recovery after running. The heart rate and plasma catecholamine concentration increased in control dogs during the standing period and the medical examination room period, relative to the resting period. However, dogs with MR did not exhibit any clear increase in heart rate or catecholamine concentration under these light stress conditions. Running stress increased plasma catecholamine levels in control dogs; however, dogs with MR did not exhibit any significant changes. Thirty-two dogs with naturally acquired heart disease were classified as grades I to III on the ISACHC scale. The degree of increase in heart rate and plasma catecholamine levels in dogs with naturally acquired heart failure depended on their degree of heart failure. In conclusion, an increased heart rate and an activated sympathetic nervous system were observed, even in mild heart failure. This chronically activated sympathetic activity is expected to increase myocardial oxygen consumption, myocardial hypertrophy, and fibrosis, and to portend a poorer prognosis in heart failure.

Animals↗
PubMedDate not supplied

Prognosis of alternative therapies in patients with heart failure not accepted for heart transplantation.

BACKGROUND AND METHODS: This article describes the outcome of alternative therapies in patients with end-stage heart failure, New York Heart Association class III-IV, referred for heart transplantation evaluation but not accepted for the procedure. From January 1988 through September 1992, 233 consecutive patients with severe heart failure were admitted to the thoracic transplantation center at Sahlgrenska University Hospital. At the time of admission all patients received standard medical treatment for heart failure. During the pretransplantation evaluation, an attempt to optimize the medical therapy was made in all patients. RESULTS: Eighteen patients (8%) died before a decision concerning transplantation was made, and 146 patients (63%) were accepted for heart transplantation. There were 69 patients (30%) who were denied heart transplantation for various reasons, and they were subgrouped: patients with contraindications (group 1, n = 23) or without indication (group 2, n = 10) for heart transplantation, patients with a positive response to intensified medical therapy (group 3, n = 25), and patients who underwent coronary artery bypass grafting and/or valvular heart surgery (group 4, n = 11). The 1-, 3-, and 5-year actuarial survival rates were as follows: group 1, 26%, 16%, and 8%; group 2, 100%, 77%, and 39%; group 3, 96%, 67%, and 53%; and group 4, 64%, 36%, and 27%, respectively. The corresponding figures for patients who had a heart transplantation were 85%, 79%, and 75%, respectively. During the first 2 to 3 years of follow-up the survival of group 2 and group 3 patients was similar to that of patients who underwent transplantation. However, late survival was worse compared with the heart transplant group. CONCLUSIONS: These results suggest that by close follow-up it may be possible to postpone heart transplantation in a selected group of patients.

Adult↗
PubMed1998

Cardiothoracic ratio and relative heart volume as predictors of coronary heart disease mortality. The Whitehall study 25 year follow-up.

AIM: To examine the association of radiographic measures of heart size with mortality from coronary heart disease. METHODS AND RESULTS: One thousand, one hundred and ninety-one male civil servants aged 40-69 years were followed-up for mortality over 25 years in relation to cardiothoracic ratio and relative heart volume. A high cardiothoracic ratio and relative heart volume predicted coronary (n = 196 deaths) and all-cause mortality, but not respiratory or malignant mortality. After adjustment for age, systolic and diastolic blood pressure, the highest (> or = 0.47) compared to the lowest quintile of the cardiothoracic ratio (< 0.40) was associated with a rate ratio of 1.84 (95% CI 1.14-2.97) for the effect on coronary heart disease mortality. Further adjustment for heart rate, smoking, cholesterol, angina and ECG ischaemia had little effect, reducing the rate ratio to 1.65 (95% CI 1.01-2.70). Similar rate ratios were observed for relative heart volume. CONCLUSIONS: Cardiothoracic ratio within the range considered 'normal' in clinical practice predicted coronary heart disease mortality independent of established coronary heart disease risk factors. The relative heart volume, which uses measurements from the lateral as well as the posteroanterior chest X-ray, did not predict coronary heart disease any better than the cardiothoracic ratio. The extent to which left ventricular mass and systolic dysfunction-- pathophysiological correlates of the cardiothoracic ratio and relative heart volume--are independent risk factors for coronary heart disease should be further investigated.

Adult↗
PubMed1990

Sex differences in time from self-reported heart trouble to heart disease death in the Alameda County Study. Significance of time dependence of risk variable effects.

In a previous analysis from the Alameda County Study, it was observed that although men had higher heart disease mortality rates than women, there was no male excess in the prevalence of self-reported heart disease morbidity at baseline or in new reports of morbidity 9 years past baseline. This apparent contradiction might occur because women report less severe heart disease than men. In the present study, this hypothesis was evaluated by examining whether self-reported heart trouble was more strongly associated with subsequent heart disease mortality for men than for women in a representative sample of the population of Alameda County, California, selected in 1965 and followed for mortality for 19 years (n = 3,742). In a time-dependent Cox model, self-reported heart trouble was a stronger predictor of heart disease mortality for men, but only during the early years of follow-up (p = 0.00). This effect was due to a shorter time to death for men who reported heart trouble. The relative hazard for men reporting heart trouble was 6.6 (95% confidence interval (CI) 3.7-11.6) at baseline, declining to 3.2 (95% CI 2.2-4.5) by 5 years past baseline and 1.5 (95% CI 0.9-2.5) by 10 years past baseline. Self-reported heart trouble was a consistent predictor of subsequent heart disease mortality for women over the 19-year follow-up period (relative hazard = 2.0, 95% CI 1.4-2.8). Sex differences in the prognosis of self-reported heart trouble were masked in non-time-dependent analyses. These results illustrate that consideration of time dependence may be required for meaningful analysis of long-term cohort studies. Possible explanations of the shorter time to death for men who reported heart trouble are discussed.

Adult↗
PubMed1996

Low magnesium enhances the pro-arrhythmic effect of low potassium in the hypertrophied rat heart but not in the normal rat heart.

OBJECTIVES: To investigate the influence of external magnesium on wall stress-induced arrhythmias and to establish whether early cardiac hypertrophy affects the sensitivity of the heart to these arrhythmias. METHODS: We used a modified isolated working heart model to compare hypertrophied hearts from the spontaneously hypertensive rat (SHR) with hearts from normotensive control rats from the Wistar and Wistar-Kyoto strains. Young rats (aged 137.9 +/- 2.04 days mean +/- SEM) were used to ensure left ventricular hypertrophy uncomplicated by fibrosis and cardiac failure. Arrhythmias were induced by 20 s increases in ventricular afterload during which the electrocardiogram was recorded. RESULTS: In control experiments SHR hearts showed a significantly greater arrhythmic response than did normotensive control rat hearts during perfusion with low-potassium (2.4 mmol/l) solutions. Concomitant low magnesium (0.4 mmol/l) perfusion significantly increased the arrhythmic response to 2.4 mmol/l potassium in SHR hearts but had no effect on arrhythmias in normotensive control rat hearts. With low magnesium, the number of ventricular premature beats was increased in SHR hearts compared with that in normotensive control rat hearts during perfusion with 4.2 and 2.4 mmol/l potassium. In addition, perfusion with low magnesium and 2.4 mmol/l potassium led to an increase in the complexity of arrhythmias, ventricular tachycardia occurring in nine of 10 SHR hearts but in only two of six normotensive control rat hearts. CONCLUSIONS: There is a synergistic effect of low magnesium and low potassium on wall-stress-induced arrhythmia in the SHR heart. An analogous effect might be important in patients with hypertension and left ventricular hypertrophy, in whom systolic blood pressure is frequently labile, leading to wide fluctuations in ventricular wall stress; combined potassium and magnesium depletion is a common complication of antihypertensive treatment.

Animals↗
PubMed1996

Control of the systemic heart and the portal heart of Myxine glutinosa

The effects of preload and afterload on the performance of the systemic heart of the hagfish Myxine glutinosa were investigated before and during sotalol treatment using an in situ perfusion technique. Elevation of input pressure (preload) increased flow by means of increased stroke volume and heart rate in accordance with Starling's law of the heart, while increased output pressure (afterload) decreased flow mainly because of decreased stroke volume. Treatment with the beta-adrenoceptor antagonist sotalol did not change the quality of the responses to increased preload or afterload, although power output decreased by 40 % and flow rate was reduced by 35 % mainly due to a decrease in heart rate. Isolated preparations of the systemic heart and the portal heart provided information on the chronotropic effects of different agonists and antagonists. Both the systemic heart and the portal heart were insensitive to adrenergic and cholinergic agonists, adrenocorticotropic hormone and the cholinoceptor antagonist atropine. Sotalol treatment lowered the rate of spontaneous contractions by 30 % in the systemic heart preparation and by 21 % in the portal heart preparation. This study has given further evidence for the existence of a tonic beta-adrenoceptor stimulation of the hagfish systemic heart and portal heart, and demonstrated the importance of that stimulation in maintaining systemic heart performance.

Journal Article↗
PubMed1988

Factors affecting the loss of mitochondrial function during zero-flow ischemia (autolysis) in slow and fast heart-rate hearts.

The (uninhibited) mitochondrial ATPase comprises approximately 90% of the total ATP hydrolyzing activity present in quiescent, ischemic canine heart muscle and its inhibition by its natural inhibitor protein plays a pivotal role in the slowing of tissue ATP depletion during ischemia. While dog heart mitochondria contain a full complement of mitochondrial ATPase inhibitor capable of fully down-regulating the enzyme activity present in this species, rat heart mitochondria contain a much lower level of inhibitor, sufficient to inhibit the enzyme activity present in this species by only approximately 20%. Moreover, this fractional complement of inhibitor remains largely inoperative in the ischemic rat heart. As shown in the present study, one apparent result of the lack of a functional complement of mitochondrial ATPase inhibitor in the rat heart is a more rapid rate of cell ATP depletion during zero-flow ischemia. This in turn results in a more rapidly developed and initially more severe cell acidosis in the ischemic rat heart because ATP hydrolysis produces protons. Finally, and consistent with earlier studies by us, the more rapid ATP depletion together with the more severe acidosis appears to result in a marked increase in the rate of loss of mitochondrial respiratory function in the ischemic rat heart compared to the ischemic dog heart. Our findings suggest that slow heart-rate hearts which contain in situ functional mitochondrial ATPase inhibitor, possess an effective mechanism for sparing cell ATP stores during early ischemia, whereas fast heart-rate hearts which lack in situ mitochondrial ATPase inhibitor function, possess a less effective ATP sparing mechanism.

Adenosine Triphosphatases↗
PubMed1990

Effect of chronic cocaine administration and cocaine withdrawal on coronary flow rate and heart rate responses to epinephrine and cocaine in isolated perfused rat hearts.

The acute dose-dependent effects of epinephrine and cocaine on heart rate and coronary flow rate (CFR) were examined in isolated, perfused (Langendorff) rat hearts from animals: i) pretreated with daily cocaine injections (20 mg/kg/day) for 8 weeks; ii) after 2-day withdrawal from 8-week cocaine pretreatment; iii) vehicle-treated controls. Chronic cocaine (CC) hearts were significantly less sensitive to the chronotropic effects of epinephrine than control (C) or withdrawal (CW) hearts. CW hearts exhibited significantly higher heart rates in response to epinephrine than C and CC hearts. Epinephrine alone (2.5 x 10(-7) M) decreased CFR 11% (C), 9%(CC), 14%(CW) from respective baseline levels. Cocaine alone had no significant effect on CFR in C hearts but produced slight dose-dependent decrements in CFR in CC and particularly CW hearts at higher doses. Cocaine plus epinephrine markedly decreased CFR in all groups, particularly in CW hearts. The results indicate that chronic daily cocaine administration produces a functional tolerance of the heart to the chronotropic actions of epinephrine but a 2-day withdrawal from chronic cocaine results in a rebound supersensitivity to adrenergic stimulation and cocaine's sympathomimetic effects. In addition, cocaine produces only minor decrements in coronary flow in the rat heart, while cocaine acts synergisticallly with epinephrine to produce a marked decrease in CFR.

Animals↗
PubMedDate not supplied

Measurements of heart scores and heart weights in horses of two different morphic body types.

Heart scores (the arithmetic mean of the QRS durations of the three bipolar limb leads for 10 cycles) and heart weights were determined from five draft type horses and five racing type horses, and evaluated for relationships between heart score and heart size within and between the two different types of horses. Horses were killed using a captive bolt gun, and actual heart weights were recorded using an electronic digital scale. The linear regression equation for heart weight versus heart score had a significant (P < 0.05) negative slope for racing types. The regression coefficients for heart weight versus heart score for draft types were not significantly (P > 0.05) different than zero. There was no significant (P > 0.05) difference found between draft and racing types. Significant (P < 0.01) differences were found between the heart ratios (heart weight as a percentage of live body weight) of racing and draft types. Heart scores were not found to be significantly (P > 0.05) different between racing and draft type horses.

Animals↗
PubMed1994

Vagally mediated heart rate recovery after exercise is accelerated in athletes but blunted in patients with chronic heart failure.

OBJECTIVES: Vagally mediated heart rate recovery after exercise was assessed in patients with chronic heart failure and in well trained athletes by analyzing the postexercise heart rate decay. BACKGROUND: Vagal reactivation is an important cardiac deceleration mechanism after exercise. However, alterations of this mechanism under pathologic conditions have not been characterized because of the lack of a specific index. METHODS: To find a vagally mediated component of heart rate recovery, the time constants of the beat-by-beat heart rate decay for the first 30 s (T30) and the first 120 s (T120) after exercise were obtained at six levels of exercise in eight normal volunteers: 1) at maximal exercise, 2) at anaerobic threshold, 3) at anaerobic threshold with propranolol administration, 4) at anaerobic threshold with atropine administration, 5) at anaerobic threshold with concomitant administration of both drugs, and 6) at 50% of anaerobic threshold. To investigate the effects of heart failure and endurance training on vagally mediated heart rate recovery, T30 and T120 at anaerobic threshold were obtained in 20 patients with chronic heart failure and in 9 cross-country skiers. RESULTS: In normal volunteers, T30 and T120 were markedly prolonged by atropine administration, indicating that both time constants are mediated by vagal reactivation. Moreover, T30 was almost independent of the exercise intensity and sympathetic blockade, whereas T120 was affected by sympathetic nerve activity and exercise work load. These results indicate that T30 is mediated primarily by vagal reactivation, independent of sympathetic withdrawal, and is significantly smaller in athletes (p < 0.01) and significantly larger in patients with chronic heart failure (p < 0.01) than that in respective age-matched normal control subjects. CONCLUSIONS: The T30 value could be a specific index for vagally mediated heart rate recovery. Vagally mediated heart rate recovery after exercise is accelerated in well trained athletes but blunted in patients with chronic heart failure.

Adult↗