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[Study on effects of acupuncture at the heart meridian on gene expression pattern of heart in rats with acute myocardial ischemia].

OBJECTIVE: To reveal the mechanism of acupuncture at the Heart meridian in treatment of myocardial ischemia from gene level. METHODS: A model of acute myocardial ischemia was made by ligation of left anterior descending branch of the coronary artery. Changes of gene expression pattern of the Lung meridian group, the Heart meridian group and the model group in the heart were compared. RESULTS: Differential expression genes and expression sequence tags (ESTs) were 14 with signal log ratio > or = 1 and 20 with signal log ratio < or = -1, mainly included immunological and inflammatory reaction relative genes, cell signal transduction and transferrin relative genes, and others, in the Lung meridian group vs the model group. Differential expression genes and ESTs were 20 with signal log ratio > or = 1 and 70 with signal log ratio < or = -1, mainly included ion channel and transport protein relative genes, cell apoptosis and stress reaction protein relative genes, metabolism relative genes, cell signal transduction and transferrin relative genes, DNA's binding, transcription and transcriptional factor relative genes, immunological and inflammatory reaction relative genes, and others, in the Heart meridian group vs the model group. CONCLUSION: In number and types of differential expression genes and ESTs with signal log ratio > or = 1 or < or = -1, the changes in the Heart meridian group vs the model group were obviously different from those in the Lung meridian group vs the model group, indicating that the Heart meridian has relative specificity in protecting against acute myocardial ischemia.

Acupuncture Therapy↗

Diastolic heart failure or heart failure with a normal ejection fraction.

Nearly half of patients with symptoms of heart failure are found to have an left ventricular (LV) ejection fraction which is within normal limits. These patients have variously been labeled as having diastolic heart failure, heart failure with preserved LV function or heart failure with normal ejection fraction (HFNEF). Since recent studies have shown that systolic function is not entirely normal in these patients, HFNEF is the better term. More common in elderly females it has a mortality similar to heart failure with a reduced ejection fraction (HFREF). The exact pathophysiology of the symtpoms is still not clear and, therefore, debated. As heart failure is often episodic, the underlying abnormal mechanisms may not be completely apparent at rest. It is likely there is a mixture of systolic and diastolic dysfunction which will be different to some degree in individual patients and isolated diastolic dysfunction or primary abnormalities of relaxation are probably extremely rare. The main difference between HFNEF and HFREF is the degree of ventricular remodeling with increased ventricular volumes in HFREF. The time course of remodeling depends to some extent on the aetiology being quicker post myocardial infarction--the commonest cause of HFREF, and slower with hypertension which is the most frequent aetiological factor in HFNEF. Ventricular volumes rather than ejection fraction or the concept of a pure diastolic abnormality can be used to classify patients in a more rational manner.

Aging↗

Adenine nucleotide content in cold preserved human donor hearts and subsequent cardiac performance after orthotopic heart transplantation.

Myocardial high-energy phosphate content has been used as a parameter to evaluate the adequacy of donor organ preservation. The purpose of this study was to assess current techniques of preservation by measuring high-energy phosphates in cold preserved (4 degrees C) human donor hearts. Endomyocardial biopsy samples of the donor heart right ventricular septum (n = 24) were compared with samples from patients with normal cardiac function evaluated before chemotherapy (n = 12). Left ventricular and right ventricular ejection fractions were measured by means of radionuclide angiography early (24 to 72 hours) and late (mean 42 days) postoperatively. Mean total cold ischemic time was 146 +/- 54 minutes (range, 89 to 340 minutes). ATP nmol/mg noncollagenous protein in donor hearts was 38.2 +/- 10.7 and 31.9 +/- 13.6 (p = NS) in normal hearts. Early postoperative left ventricular and right ventricular ejection fraction was 55% +/- 14% and 40% +/- 9%, respectively. Late postoperative left ventricular and right ventricular ejection fraction was 64% +/- 14% and 50% +/- 10%, respectively; both represent significant increases in right and left ventricular ejection fraction (p less than 0.05). No correlation was found between ischemic time and donor ATP, ischemic time and ejection fraction, or ejection fraction and ATP. Three patients with normal donor heart ATP content had severe, but reversible, early graft dysfunction. In summary, currently used human donor heart preservation techniques are associated with normal values of high-energy phosphates and usually excellent early and late postoperative graft function.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine Nucleotides↗

The effect of sulfhydryl reagents on the heart rate and coronary flow of the isolated perfused guinea-pig heart.

The action of a number of compounds able to react with thiols was tested on guinea-pig hearts perfused at constant pressure. The SH reagents used were NaNO2, oxidized glutathione, cystamine, diamide, 1,5-difluoro-2,4-dinitrobenzene, nitroglycerol, sodium nitroferricyanide and HgCl2. 6,6'-Dithiodinicotinic acid, an SH reagent that does not penetrate the cell, produced no effect. All the other SH reagents produced an increase in coronary flow. All except oxidized glutathione and nitroglycerol increased the heart rate. The increase in heart rate and oxygen consumption could be completely blocked by dichloroisoproterenol; the increase in coronary flow was not affected. Difluorodinitrobenzene, diamide, cystamine and NaNO2 significantly decreased the acid-soluble thiol content of the heart. For these compounds, there was a significant correlation between the decrease in coronary flow and the decrease in thiols. We conclude that in the isolated heart, most SH reagents, if used at the appropriate concentration, will increase the heart rate, probably by relaasing catecholamines. They will also decrease the coronary resistance, probably by a direct effect on the coronary vessels.

Animals↗

[Increase in weight and changes in the heart weight/body weight quotient of the embryonic heart in early pregnancy].

On the basis of measuring heart weight and body weight of 73 embryos it is shown that there is a close linear correlation between growth of the heart, increase of heart weight and body weight and age of pregnancy. The increase in heart weight, however, is not proportional to that of the increase in body weight during intrauterine development. There is a considerable shift in the heart weight/body weight ratio (i.e. a change in the cardio-fetal index: (formula; see text) In early pregnancy (5-7th weeks) the cardio-fetal index varies from 1.5 to 2.5 and in the course of pregnancy it decreases gradually. In the 12th-14th weeks it falls below 1, and following the 14th week it stays on a relatively constant level of 0.5-0.8. In early embryonic phase heart weight in relation to body weight is 2-5 times bigger than in the period following the 14th week. The significance of these findings is discussed.

Body Weight↗

Calcium channel blockers for heart rate control in atrial fibrillation complicated by congestive heart failure.

OBJECTIVES: To review the safety and efficacy of verapamil and diltiazem with respect to ventricular response in atrial fibrillation (AF) in the setting of left ventricular (LV) systolic dysfunction. DATA SOURCES: Pertinent articles were identified through a MEDLINE search of the English language literature from 1984 to 1993, followed by a manual search of the bibliographies of pertinent articles. STUDY SELECTION: Studies selected were case reports, controlled trials, review articles and editorials. DATA EXTRACTION: Effects of verapamil and diltiazem on hemodynamics, ventricular response in AF, clinical parameters and mortality were reviewed. DATA SYNTHESIS: There are limited data about the effects of verapamil and diltiazem on ventricular function in patients with congestive heart failure. In vitro diltiazem has fewer negative inotropic effects than verapamil. Clinically there are some reports of hemodynamic and clinical deterioration in patients with significant LV dysfunction given verapamil although most patients improve with verapamil. There are more data concerning diltiazem in the setting of AF complicated by congestive heart failure. The drug does not appear to exacerbate heart failure, although hypotension can result. In chronic AF complicated by heart failure, there is concern that diltiazem may increase mortality. Options for therapy are digoxin, beta-blockers and atrioventricular node ablation. CONCLUSIONS: Calcium channel blockers may have a role in the acute reduction of ventricular response in patients with AF complicated by congestive heart failure; however, their safety in chronic heart rate control remains to be proven.

Atrial Fibrillation↗

[The usefulness of portable 24-hour polygraphic monitoring--evaluation of autonomic nervous activity of the patients with ischemic heart disease by using heart rate variability during sleep].

Portable 24-hour polygraphic monitorings were performed on 109 cases with neurological or cardiovascular disorders, sleep disturbances and metabolic diseases to clarify its usefulness and limitations. Moreover, an evaluation of autonomic nervous activity was done in different stages of sleep in normal young (n = 9), normal middle-aged subjects (n = 8) and patients with ischemic heart disease (n = 7) using power spectral analysis of heart rate. The parameters recorded in this study were electroencepharogram(EEG), electrooculogram, electromyogram of chin muscles, electrocardiogram, respiratory curve, walking pulse and body position. Using polygraphic monitoring, the patients with cardiac arrhythmia showed abnormal EEG in 20% and those with neurological events in 86.7%. The improvement of sleep structure was found after pacemaker implantation in the patients with bradyarrhythmias (75%). Time spans of slow wave sleep and REM sleep of patients with ischemic heart disease decreased significantly from 120.9 +/- 40.6 min to 79.1 +/- 25.3 min, 112.8 +/- 16.5 min to 63.6 +/- 23.6 min, respectively (p < 0.05). RR50, that is number of R -R intervals greater than 50msec compared to the preceding R-R interval, decreased significantly in each stage of sleep in the patients with ischemic heart disease compared to normal subjects (stage 2: 18.3 +/- 6.1/min to 3.8 +/- 3.0/min, p < 0.01; SWS: 7.8 +/- 8.0/min to 3.2 +/- 2.5/min, p < 0.05; REM: 17.9 +/- 6.0/min to 4.4 +/- 4.3/min, p < 0.01). The HF power in all stages of sleep showed a trend of the decrease in the patients with ischemic heart disease. In REM sleep, the LF power in patients with ischemic disease was lower significantly compared to that in normal middle-aged subjects (6.1 +/- 3.2 to 12.1 +/- 4.1, p < 0.05). The L/H ratio also decreased significantly (1.08 +/- 0.30 vs. 2.35 +/- 1.03, p < 0.05). The slope of 1/fx above 0.15Hz in IHD patients was less in stage 2 (-0.404 +/- 0.280 vs. -0.849 +/- 0.183, p < 0.01) and in REM sleep (-0.294 +/- 0.368 vs. -0.665 +/- 0.291, p < 0.05). Above results suggest the involvement of a decrease of sympathetic activity in addition to decrease of parasympathetic activity especially in REM sleep in the patients with ischemic heart disease. In conclusion, polygraphic monitoring is useful for a detection of abnormality of EEG and an evaluation of autonomic activity in cardiovascular disorders.

Adult↗

Matching the heart donor and heart transplant recipient. Clues for successful expansion of the donor pool: a multivariable, multiinstitutional report. The Cardiac Transplant Research Database Group.

Little information is available regarding donor-specific parameters that predict success or failure after heart transplantation. Furthermore, with increasing numbers of patients awaiting heart transplantation, there is tremendous pressure to expand the donor pool by stretching the margins of donor acceptability. To gain insight into donor-related and donor-recipient interrelated predictors of death after transplantation, 1719 consecutive primary transplantations performed at 27 institutions between Jan. 1, 1990, and June 30, 1992, were analyzed. Mean follow-up of survivors was 13.9 months, and actuarial survival was 85% at 1 year. By multivariable analysis, risk factors for death included younger recipient age (p = 0.006), older recipient age (p = 0.0005), ventilator support at time of transplantation (p = 0.0006), higher pulmonary vascular resistance (p = 0.02), older donor age (p < 0.0001), smaller donor body surface area (female donor heart placed into larger male patient) (p = 0.003), greater donor inotropic support (p = 0.01), donor diabetes mellitus (p = 0.01), longer ischemic time (p = 0.0003), diffuse donor heart wall motion abnormalities by echocardiography (p = 0.06), and, for pediatric donors, death from causes other than closed head trauma (p = 0.02). The overall 30-day mortality rate was 7% but increased to 11% when donor age exceeded 50 years and was 12% when inotropic support exceeded 20 micrograms/kg/min dopamine plus dobutamine and 22% with diffuse echocardiographic wall motion abnormalities. The interaction of donor risk factors was such that the heart of a smaller female donor given high-dose inotropes placed into a larger male recipient produced a predicted 30-day mortality rate of 26% and the heart of a 25-year-old male donor given high-dose inotropes with diffuse echocardiographic wall motion abnormalities transplanted into a 50-year-old male recipient led to a predicted 30-day mortality rate of 17%. This analysis supports cautious extension of criteria for donor acceptance but with an anticipated greater risk in the presence of diffuse echocardiographic wall motion abnormalities and long anticipated ischemic time, particularly in older donors given inotropic support.

Actuarial Analysis↗

Expression of the Mf1 gene in developing mouse hearts: implication in the development of human congenital heart defects.

The transcription factor FKHL7 gene has recently been associated with the anterior segment dysgenesis disorder of the eye known as Axenfeld-Rieger anomaly (ARA). A growing body of evidence indicates that mutations in FKHL7 cause not only defects in the anterior segment of the eye but defects in the heart valves and septa as well. In order to evaluate its contribution to normal heart septation and valve formation, expression of the mouse homologue Mf1 in embryonic hearts was analyzed by in situ hybridization. A weak but significant level of Mf1 expression could be detected in the endocardium of mouse embryos as early as day 8.5 post-conception (p.c.). Mf1 expression was undetectable in the hearts of day 9.5 p.c. embryos, but by day 10.5-11 p.c., Mf1 transcripts could be found again in the endocardium of both the atrium and ventricle and a relatively strong signal was observed in the dorsal portion of the septum primum, in what appeared to be the spinal vestibule. At day 13 p.c. when aortic and pulmonary trunks are separated, relatively more Mf1 transcripts were detected in the leaflets of aortic, pulmonary, and venous valves, the ventral portion of the septum primum, as well as in the single layer of cells on the edges of the atrioventricular cushion tissues. Surprisingly, there was no signal detected in the developing interventricular septum. At day 15 p.c., overall Mf1 signals were greatly decreased. However, significant levels of expression could still be observed in the atrial septum, the tricuspid valve, the mitral valve, and in the venous valve but not in the interventricular septum. The temporal and spatial expression patterns of the Mf1 gene in developing mouse hearts suggest that Mf1 may play a critical role in the formation of valves and septa with the exception of the interventricular septum. This is further supported by our studies showing that mutations in the FKHL7 gene were associated with defects in the anterior segment of the eye as well as atrial septal defects or mitral valve defects. Dev Dyn 1999;216:16-27.

Animals↗

The heart rate response to exercise and circulating catecholamines in heart transplant recipients.

The plasma concentration of noradrenaline ([NA]) is higher than that of adrenaline ([A]) both in normal subjects and in heart transplant recipients (HTR). Since in both groups the myocardial density of beta1-adrenergenic receptors is much greater than that of beta2-adrenergenic receptors, the chronotropic response of a denervated heart to changes in plasma [NA] and [A] in the absence of reinnervation should be similar to that of agonist stimulation of beta1-receptors. To test this hypothesis, 17 HTR and 9 healthy subjects (CTL) performed incremental exercise on a cycle ergometer to voluntary exhaustion. Heart rate (HR) was recorded by electrocardiography. [NA] and [A] were measured by high-pressure liquid chromatography at rest and at increasing workloads (w). In both groups, HR and [NA+A] increased with w, and HR with [NA+A]. Normalized HR values, plotted against the logarithm of [NA+A], fitted significantly logistic curves. The affinity constants were different, i.e. 2599+/-350 and 487+/-37 ng.l(-1), for HTR and CTL, respectively. The chronotropic effect of changes in [NA+A] in HTR was similar to that of combined beta1- and beta2-adrenergic activation evoked by applying isoprenaline to isolated heart myocytes (Brodde OE, Pharmacol Ther 60:405-430, 1993). These findings suggest that over time sympathetic reinnervation and the modulation of beta-receptors may take place in HTR, ruling out the hypothesis of persistent heart denervation.

Adult↗

Validation of peak exercise oxygen consumption and the Heart Failure Survival Score for serial risk stratification in advanced heart failure.

The Heart Failure Survival Score (HFSS) and peak exercise oxygen consumption (VO2) accurately assess mortality in ambulatory patients who have advanced heart failure and are referred for initial cardiac transplant evaluation. We investigated the prognostic value of the HFSS and peak VO2 when applied serially to these patients. This study included 227 adults (mean age +/- SD 52 +/- 10 years old) who presented for reevaluation >60 days after initial evaluation (352 +/- 238 days). The HFSS was determined from mean arterial blood pressure, heart rate, left ventricular ejection fraction, serum sodium, peak VO2, heart failure etiology, and width of QRS complex. Survival without reevaluation, United Network of Organ Sharing 1 transplant, or left ventricular assist device was determined by the Kaplan-Meier method with censoring at United Network of Organ Sharing 2 transplant. Survival differed by HFSS stratum (p <0.001) and by peak VO2 stratum (p <0.001). Patients whose HFSS or peak VO2 deteriorated from low risk to medium or high risk had lower survival rates than did patients whose values remained at low risk (p <0.01 and p <0.001, respectively). Patients who started at medium or high risk and improved to low risk tended to have higher survival rates than those who remained medium or high risk (p = 0.06 and p <0.16, respectively). Patients who improved to low risk had a 1-year survival rate of 72% for HFSS and peak VO2. However, patients who improved to low risk and were treated with beta blockers had a 1-year survival rate (89% for HFSS and 83% for peak VO2) comparable to that after transplant (84%). Peak VO2 and the HFSS can be successfully used for serial evaluation of mortality risk in ambulatory patients who have advanced heart failure.

Adult↗

Incidence and risk distribution of heart failure in adolescents and adults with congenital heart disease after cardiac surgery.

Heart failure (HF) is a major problem in the long-term follow-up of adults with congenital heart disease (CHD) after cardiac surgery. The purpose of this study was to evaluate risk factors for HF in patients with CHD. N-terminal-pro-brain natriuretic peptide and maximal oxygen uptake (VO2max) were measured in 345 consecutive patients with CHD. HF was defined as an elevated N-terminal-pro-brain natriuretic peptide level (> or = 100 pg/ml) and reduced VO2max (< or = 25 ml/kg/min). The HF criteria were met by 89 patients. These patients were significantly older (mean +/- SEM 30.8 +/- 0.9 vs 24.8 +/- 0.5 years), had significantly lower maximal heart rates (149 +/- 3 vs 164 +/- 1 beats/min), and had larger end-diastolic right ventricular diameters (36 +/- 1 vs 27 +/- 1 mm) and right ventricular pressure estimated by Doppler flow velocities of tricuspid valve regurgitation (2.9 +/- 0.1 vs 2.3 +/- 0.03 m/s). Mean fractional shortening of the left ventricle was within the normal range. To estimate risk stratification, odds ratios for HF were determined for the most frequently occurring types of congenital heart defects and surgical procedures. In conclusion, HF in adults with CHD predominately depends on diagnosis, age, the frequency of reoperation, and right ventricular function and may be related to chronotropic incompetence indicated by lower maximal heart rates.

Adolescent↗

Report of the National Heart, Lung, and Blood Institute Working Group on research in adult congenital heart disease.

The Working Group on research in adult congenital heart disease (ACHD) was convened in September 2004 under the sponsorship of National Heart, Lung, and Blood Institute (NHLBI) and the Office of Rare Diseases, National Institutes of Health, Department of Health and Human Services, to make recommendations on research needs. The purpose of the Working Group was to advise the NHLBI on the current state of the science in ACHD and barriers to optimal clinical care, and to make specific recommendations for overcoming those barriers. The members of the Working Group were chosen to provide expert input on a broad range of research issues from both scientific and lay perspectives. The Working Group reviewed data on the epidemiology of ACHD, long-term outcomes of complex cardiovascular malformations, issues in assessing morphology and function with current imaging techniques, surgical and catheter-based interventions, management of related conditions including pregnancy and arrhythmias, quality of life, and informatics. After research and training barriers were discussed, the Working Group recommended outreach and educational programs for adults with congenital heart disease, a network of specialized adult congenital heart disease regional centers, technology development to support advances in imaging and modeling of abnormal structure and function, and a consensus on appropriate training for physicians to provide care for adults with congenital heart disease.

Adult↗

Long-term beta-blocker therapy improves autonomic nervous regulation in advanced congestive heart failure: a longitudinal heart rate variability study.

BACKGROUND: beta-Blocker therapy is believed to modulate the detrimental effect of overcompensating neurohormonal activation in chronic heart failure. However, clinical doubts remain, particularly the physiologic sympathovagal balance. METHODS: To respond to clinical concern about worsening autonomic nervous perturbation in beta-blocker therapy of advanced congestive heart failure, 15 consecutive patients were longitudinally studied to elucidate the evolution of cardiac function versus 24-hour heart rate variability (HRV) before and after 1, 3, and 6 to 9 months of atenolol-combined therapy. RESULTS: Two patients died prematurely within 1 month. All 13 surviving patients showed improvement in New York Heart Association functional class, with decrease in left ventricular end-systolic and end-diastolic dimensions and increase in fraction shortening and ejection fraction by echocardiography after at least 3 months of atenolol use. The retarded therapeutic effect was accompanied by a general rise of total, very low, low-, and high-frequency components (9.0 +/- 0.5, 8.8 +/- 0.5, 6.2 +/- 0.6, and 6.1 +/- 0.5 vs 10.9 +/- 0.3, 10.7 +/- 0.4, 8.6 +/- 0.3, and 7.8 +/- 0.3; all P <.02) of daily HRV. This implied recovery of parasympathetic and baroreceptor function. Return of sympathovagal interaction was further supported by the suppression of Cheyne-Stokes type HRV as detected by Wigner-Ville distribution. CONCLUSIONS: Long-term beta-blocker therapy for advanced congestive heart failure upwardly regulates the autonomic nervous interaction in synchrony with the evolution of cardiac function performance.

Adrenergic beta-Antagonists↗

Neurohumoral activations in congestive heart failure: correlations with cardiac function, heart rate variability, and baroreceptor sensitivity.

BACKGROUND: The clinical significance of the determination of heart rate variability and baroreceptor sensitivity relating to cardiac function and neurohumoral factors remains to be established. METHODS AND RESULTS: We investigated the relation between conventional clinical variables and frequency domain analysis of heart rate variability and baroreceptor sensitivity in 146 patients with heart failure. Cardiac function including left ventricular ejection fraction, left ventricular dimensions, and left atrial size was different by the plasma atrial natriuretic peptide level but not by the norepinephrine level. The total power and low-frequency power were correlated with plasma norepinephrine, whereas baroreceptor sensitivity was correlated with plasma atrial natriuretic peptide. None of the frequency domain variables and baroreceptor sensitivity was correlated with cardiac function. There was a positive correlation between the low-frequency power and baroreceptor sensitivity. CONCLUSIONS: Heart rate variability and baroreceptor sensitivity, which reflect autonomic regulation, may be an indicator independent from cardiac function in patients with heart failure.

Atrial Natriuretic Factor↗

Early autonomic and repolarization abnormalities contribute to lethal arrhythmias in chronic ischemic heart failure: characteristics of a novel heart failure model in dogs with postmyocardial infarction left ventricular dysfunction.

OBJECTIVES: Using a model of arrhythmias associated with ischemic left ventricular (LV) dysfunction, this study investigated autonomic and electrophysiologic mechanisms associated with sudden cardiac death (SCD) in chronic heart failure (HF). BACKGROUND: Left ventricular dysfunction from ischemic heart disease is associated with many instances of SCD. Electrophysiologic and autonomic derangements occur in HF, but their contribution to SCD risk is poorly understood. METHODS: Sudden death risk was assessed in 15 dogs with a healed anterior myocardial infarction (MI) during submaximal exercise and brief acute circumflex ischemia. Left ventricular dysfunction was then induced by repetitive circumflex microembolization until LV ejection fraction reached 35%. Before embolization, six dogs were susceptible to SCD, and nine were resistant. RESULTS: Baroreflex sensitivity was lower in susceptible dogs (10 ms/mm Hg +/- 4 ms/mm Hg vs. 20 ms/mm Hg +/- 11 ms/mm Hg, p = 0.04). QT intervals from susceptible dogs were longer after MI (246 ms +/- 26 ms susceptible vs. 231 ms +/- 20 ms resistant, p < 0.001) and prolonged within eight weeks after LV dysfunction was established (from 246 ms +/- 26 ms to 274 ms +/- 56 ms, +11%, p < 0.01). Heart rate in susceptible dogs increased during transient ischemia (+20%) and with progressive LV dysfunction (102 beats/min +/- 28 beats/min baseline to 154 beats/min +/- 7 beats/min LV dysfunction, p = 0.003). All susceptible dogs had spontaneous sustained ventricular tachycardia culminating in SCD. In contrast, QT intervals in resistant dogs prolonged after 24 +/- 6 weeks (from 231 ms +/- 20 ms to 238 ms +/- 15 ms, p < 0.05), and heart rates were unchanged. Only one resistant dog died suddenly with LV dysfunction. CONCLUSIONS: Depressed vagal and elevated sympathetic control of heart rate coupled with abnormal repolarization are associated with high SCD risk when post-MI LV dysfunction develops.

Animals↗

Heart transplantation an answer for end-stage heart failure.

Heart transplantation remains the best treatment option for end-stage heart failure. For patients who are not candidates for transplantation, better medical management and surgical options in heart failure can improve both the length and quality of a patient's life. Continuing research on xenotransplantation and the total artificial heart may decrease the need for human transplantation in years to come and may allow others with severe heart failure to have a chance at living longer.

Contraindications↗

Signs of vagal reinnervation 4 years after heart transplantation in spectra of heart rate variability.

Several investigators have shown signs of possible sympathetic but not parasympathetic reinnervation in heart transplanted patients. Spectral analysis of heart rate and blood pressure variability is a noninvasive tool appropriate to detect a functional autonomous reinnervation to the heart. In a follow-up study, 13 patients after heart transplantation (HTx) were investigated, mean age 50.6+/-8.5 years, 18 healthy volunteers were selected as control group. For each patient two recordings were performed which took part 14+/-5 months respectively 42+/-8 months after HTx. ECG and systolic blood pressure (SBP) have been recorded simultaneously for 5 min in supine position during controlled respiratory rate of 12 or 15 cycles/min. No graft rejection has been detected in the endomyocardial biopsy performed right after the recordings. Power spectral densities (PSD) were calculated for the beat-to-beat time series of RR-intervals (distance of two following QRS complexes) and SBPs. The area of PSD in the range of 0.05-0.17 Hz was defined as low frequency (LF) and that of 0.18-0.35 Hz as high frequency (HF). LF and HF are indicative of efferent sympathetic respectively parasympathetic activity at the sinus node. A significant increase of LF (226%) and HF (213%) during a mean period of 28 months could be found. No differences were to be shown for systolic blood pressure variability. Previous findings confirm that LF band increases 4 years after transplantation, suggesting a possible sympathetic reinnervation of the heart. On the other hand an increase of the HF band also suggests a parasympathetic reinnervation.

Adolescent↗