Background: Altered metabolism is thought to play an important role in the pathogenesis of heart failure.Study of the metabolism may provide insights into the pathology of heart failure and may provide new diagnostic tools.Proton magnetic resonance spectroscopy (MRS) allows us to quantify total creatine, which plays an essential role in the transport of energy from the mitochondria to the myofibrils.Experimental autoimmune myocarditis (EAM) in rodents is an accepted model of myocarditis and dilated cardiomyopathy.As of yet, proton MRS has not been used to study the changes occurring in this model of heart failure.We aimed to study the metabolic changes occurring in an animal model of EAM, and compare these to the findings in healthy animals.Methods: Myocardial tissue of 10 male young Lewis rats with EAM (35 days after immunization with 0.25 mg porcine myocardial myosine) was analysed using 1H-MAS-MRS (Bruker 600 MHz).The metabolic profile was compared to fresh (n ¼ 7) and frozen (n ¼ 8) healthy controls and to the results from histology and immunohistochemistry (CD68).For fresh control samples the spectra were taken less than 10 min after death.Frozen control samples and myocarditis samples were shock-frozen in liquid nitrogen and stored for 4-6 months at -808C before measurements.Myocardial tissue from a basalcavity slice of the the left ventricle (30-40 mg) excluding epicardial tissue was placed in a 4 mm zirconium rotor, packed homogeneously using a spacer and spun at 4 kHz at 293 K.A water suppression pulse sequence was applied to obtain the proton spectrum (ns ¼ 128, t ¼ 7 min).Spectra were phased and baseline correction using polynomial fit to the region of interest was applied before integration of the peaks.Results: The metabolic ratio of taurine to creatine obtained by spectral analysis proved to be a significant biomarker for diagnosis of myocarditis compared to healthy controls (taurine/creatine ratio in myocarditis: 4.47(+0.83),fresh control: 2.59(+0.09),frozen control: 2.59(+0.28);P , 0.001).Myocarditis was confirmed histologically with an inflammatory cellular infiltrate and CD68 positive staining.Conclusions: Myocardial taurine/creatine ratio as detected by proton MRS is able to differentiate between healthy myocardium and myocardium from rats with EAM.This variation may occur due to creatine depletion as described in heart failure and/or an increase in taurine due to its antioxidant activity in inflammatory reactions.1237

Introduction Patients presenting with chest pain, raised troponin but non-obstructive coronary arteries pose a clinical challenge in diagnosis, prognosis and management. We hypothesised that early cardiovascular magnetic resonance (CMR) imaging can provide a diagnosis and comprehensive characterisation for acute myocardial injury of indeterminate aetiology. Methods and results 120 patients presenting with chest pain, positive troponin (TnI>0.04 µg/l) and non-obstructive coronary arteries prospectively underwent early CMR (median 3 days, range 0–14 days) at 1.5 T, including cine imaging for function, T2-weighted imaging for oedema and late gadolinium enhancement (LGE) imaging for myocardial necrosis/scarring. The mean age=50±17 years (50% female); median TnI=3.99 ug/l (0.07–60 µg/l); mean left ventricular ejection fraction=64±12%. There was a high CMR diagnostic yield of 95%. Significant oedema was detected in 79% and LGE in 61%. The commonest diagnosis was myocarditis (37.5%), followed by Takotsubo cardiomyopathy (22.5%), myocardial infarction (17.5%), acute regional stunning (9.2%; wall motion abnormality with oedema but no LGE), dilated cardiomyopathy (4.2%), hypertrophic cardiomyopathy (3.3%), and missed pulmonary embolism (0.8%). Eleven of the 21 patients with MI (52%) had a patent foramen ovale (PFO) demonstrated on transthoracic echocardiography with agitated saline contrast and presumably suffered a paradoxical embolism to a coronary artery. The remaining 5.0% of patients had no clear diagnosis identified. Conclusions CMR has a high diagnostic yield (95%) in patients presenting with troponin-positive chest pain but non-obstructive coronary arteries when performed early (median 3 days). This study highlights the importance and usefulness of early access to CMR in this group of patients. When no apparent cause is identified, early conventional CMR was able to exclude myocardial infarction, wall motion abnormality, significant oedema or scarring.

Background-Changes in the myocardium in acute ischemia are dynamic and complex, and the characteristics of myocardial tissue on cardiovascular magnetic resonance in the acute setting are not fully defined. We investigated changes in edema and late gadolinium enhancement (LGE) with serial imaging early after acute myocardial infarction, relating these to global and segmental myocardial function at 6 months.Methods and Results-Cardiovascular magnetic resonance scans were performed on 30 patients with ST-elevation-myocardial infarction treated by primary percutaneous coronary intervention at each of 4 time points: 12 to 48 hours; 5 to 7 days; 14 to 17 days; and 6 months. All patients showed edema at 24 hours. The mean volume of edema (% left ventricle) was 37 +/- 16 at 24 hours and 39 +/- 17 at 1 week, with a reduction to 24 +/- 13 (P<0.01) by 2 weeks. Myocardial segments with edema also had increased signal on LGE at 24 hours (kappa=0.77; P<0.001). The volume of LGE decreased significantly between 24 hours and 6 months (27 +/- 15% versus 22 +/- 12%; P=0.002). Of segments showing LGE at 24 hours, 50% showed resolution by 6 months. In segments with such a reduction in LGE, 65% also showed improved wall motion (P<0.0001). The area of LGE measured at 6 months correlated more strongly with troponin at 48 hours (r=0.9; P<0.01) than LGE at 24 hours (r=0.7). The difference in LGE between 24 hours and 6 months had profound effects on the calculation of salvage index (26 +/- 21% at 24 hours versus 42 +/- 23% at 6 months; P=0.02).Conclusions-Myocardial edema is maximal and constant over the first week after myocardial infarction, providing a stable window for the retrospective evaluation of area at risk. By contrast, myocardial areas with high signal intensity in LGE images recede over time with corresponding recovery of function, indicating that acutely detected LGE does not necessarily equate with irreversible injury and may severely underestimate salvaged myocardium. (Circ Cardiovasc Imaging. 2011;4:228-236.)

Introduction Repeat revascularisation after coronary angioplasty and stenting is well recognised, a feature of most prospective trials of percutaneous intervention (PCI) and is a major difference reported in trials comparing surgical to percutaneous revascularisation strategies. We investigated outcomes and repeat procedures in some 25 000 consecutive patients over 9 years from a UK teaching hospital. Methods Between January 2001 and August 2009, 24 521 patients presented to the John Radcliffe Hospital Oxford for coronary angiography. Revascularisation procedures in the follow-up period were analysed using the procedural database, stored angiographic images and from casenote review. Results 10 697 (43.6%) underwent PCI with stenting, 832 (3.4%) PCI alone, 4589 (18.7%) coronary artery bypass surgery (CABG) and 8133 (33.2%) medical treatment. Two thousand four hundred and seventy-seven of the 10 697 stented patients (23.2%) returned for a second angiogram and 1314 (12.3%) underwent further stenting and 211 (2.0%) CABG over a median follow-up of 4.25 years (IQR 2.13–6.13 years). Three hundred and eighty-four patients (29.2%) of those requiring a second stenting procedure underwent a third angiogram during the follow-up period and 161 (12.3%) underwent further stenting and 33 (2.5%) CABG. Rates of stenting for the fourth, fifth and sixth procedures were respectively 21%, 24% and 38% representing 0.3%, 0.1% and 0.02% of the initial stented cohort (Abstract 130 Figure 1). 59.9% of repeat PCI stenting procedures were elective, 38.1% urgent and 1.5% primary. Clinical indications for repeat stenting are shown in Abstract 130 Figure 2. A minority of patients (15.7%) required restenting for in-stent restenosis with most patients returning either with disease progression in an unstented area (45.2%) or for staged PCI (25.2%). Stent thrombosis as an indication for repeat stenting was rare (3.3%). Of those requiring restenting, 37.2% patients received drug eluting stents (DES) in their first stenting procedure and 62.8% received bare metal stents (BMS) alone. 5.4% of patients had both DES and BMS in the same procedure. This did not differ significantly from the ratio of DES/BMS in those patients undergoing stenting who did not require further revascularisation in the follow-up period (39% DES, 61% BMS, 14.8% both DES and BMS). 19.3% people requiring a second stenting procedure had multi vessel stenting at first PCI. Abstract 130 Figure 1 Patient undergoing multiple restenting procedures. Abstract 130 Figure 2 Most common indications for restenting procedures. Conclusion and Implications This study shows that in a large unselected ‘real world’ cohort of patients undergoing stenting, a substantial minority of patients undergoing a first stenting procedure will require repeat assessment (23%) and/or repeat stenting (12%). However the driving force behind repeat stenting procedures is progression of disease distant from the site of the first stent (45%) and staged PCI (25%) rather than isolated stent-related restenosis which accounts for under 16% of second stenting procedures and thus a minority of restenting cases.

Background: Craniofacial abnormalities and increased pharyngeal collapsibility due to abnormal connective tissue suggest the possibility of an increased prevalence of obstructive sleep apnoea (OSA) in patients with Marfan's syndrome but the actual prevalence is uncertain. Aortic dilatation and dissection are life threatening manifestations of Marfan's syndrome and case reports have suggested a possible association with OSA but data from cohort studies are not available.Methods: A sleep study was performed in 61 patients with Ghent criteria positive Marfan's syndrome (mean age 38.3 (SD 12.9) years; 37 females) and in 26 control subjects matched for age, gender, height and weight. OSA was defined using two conventional levels of apnoea-hypopnoea index (AHI), >5 and >15/h. In patients with Marfan's syndrome, aortic root diameter was measured by echocardiography.Results: More patients with Marfan's syndrome than controls had OSA (AHI >5, 32.8% compared with 11.5%, mean difference + 21.3%, 95% CI 4.2% to 38.3%, p = 0.04; AHI >15, 18.0% compared with 0%, mean difference + 18.0%, 95% CI 8.4% to 27.7%, p = 0.02). AHI was correlated with aortic root diameter (r = 0.50, 95% CI 0.26 to 0.69, p = 0.0003), and mean aortic root diameter was significantly greater in patients with OSA (4.5 (SD 0.6) cm) compared with those without OSA (3.7 (0.6) cm) (mean difference 0.8 cm, 95% CI 0.4 to 1.2 cm, p < 0.0001).Conclusions: In patients with Marfan's syndrome, the prevalence of OSA is considerably higher than in matched control subjects. OSA may be a risk factor for aortic root dilatation in Marfan's syndrome.

A 63-year-old man presented with unstable angina with dynamic lateral ST depression. Fifteen years previously he underwent coronary bypass surgery. Coronary angiography demonstrated subtotal occlusion of the ostium of the saphenous vein graft (SVG) to the circumflex marginal branch. Passage of a coronary wire and subsequent low pressure dilatation …

Kawasaki disease (mucocutaneous lymph node syndrome) is a syndrome of generalised vasculitis and is the leading cause of acquired heart disease in children. Coronary arterial abnormalties occur in 20% of cases, with coronary artery aneurysms being the most predominant vascular abnormality in this condition. Although death may occur secondary to thrombotic coronary artery occlusion usually within the first year of the illness, myocardial infarction may occur several years after the onset of the disease. Here, we report a case of a young man presenting with ischaemic chest pain, an ECG suggestive of an anteroseptal infarction and a childhood illness consistent with Kawasaki disease.

The safety and predictability of percutaneous coronary intervention (PCI) has improved dramatically in the last decade. The increased numbers of patients suitable for the procedures have placed pressure on existing health care systems. Treating patients with chronic stable angina on a day case basis without an overnight stay has several attractions,1 but there are some concerns over the safety of this approach. Troponin I is released rapidly following myocardial necrosis, it is highly sensitive, and may be more specific than other enzymatic markers of cardiac damage. Elevation of cardiac markers, mainly creatine kinase-MB, after both elective percutaneous and surgical revascularisation reflects myocardial necrosis and is associated with increased risk of in-hospital and long term adverse events.2 Glycoprotein (Gp) IIb/IIIa inhibitors appear to be particularly beneficial in reducing this complication,3 but day case intervention precludes overnight administration of Gp IIb/IIIa inhibitors. This audit determined the incidence of serum troponin I elevation after 6–8 hours in patients discharged the same day according to pre-specified clinical, angiographic, and procedural criteria. Two hundred and twenty nine consecutive patients were admitted for elective day case PCI from January to July 2002. This represents 30% of the total PCIs in our institution during this period (n = 762). Predetermined clinical and angiographic inclusion and exclusion criteria were …

An 80-year-old woman was referred with non-sustained palpitations, intermittent presyncope, and atypical chest pain. Examination revealed a loud “plopping” first heart sound and presystolic thrill at the lower left sternal edge. Echocardiography showed a large cystic lesion attached to the septal leaflet of the tricuspid valve, dilatation of the right heart chambers, and moderate tricuspid regurgitation (Figure 1). Three-dimensional contrast echocardiography confirmed the mobile cyst and revealed small lesions within it (Figure 2a); during systole, the cyst became deformable within the ventricle, resulting in a “heart” shape (Figure 2b). The following day, her clinical findings had changed, with loss of the “plopping” first heart sound, a new systolic murmur at the left sternal edge, and loss of the presystolic thrill. Echocardiography confirmed cyst migration into the right ventricular outflow tract with partial obstruction (Figure 3). Emergency resection on cardiopulmonary bypass revealed a blood-filled cyst with small interior cysts that was attached to the tricuspid valve. Histological examination confirmed a simple blood-filled cyst. The patient had an uncomplicated recovery. Blood -filled cysts are typically small and asymptomatic and are most commonly found in infants. In most cases, they regress spontaneously and are rare in adults, but they occasionally obstruct, as in this case.

Cardiac abnormalities, cardiomyopathy and skeletal muscle weakness have been described in female carriers of the Xp21 (Duchenne and Becker) muscular dystrophies (J Neurol 1975;209(4):279–285; Br Med J 1969;2:418–420; J AmMed Assoc 1996;275(17):1335–1338; Neurology 1980;30(5):497–501; Neuromusc Disord 1999;9:347–351; Arch Neurol 1989;46:673–675). We have screened volunteers from our Xp21 genetics register and found the prevalence of previously unrecognized, clinically relevant, abnormalities in this group to be less than previously reported. We studied 91 women (56 carriers and 35 controls), aged between 18 and 69 years, from our local population known to the Oxford Regional Genetics Register. Our study included controls, with the investigators being blind to the subject's genetic status. The prevalence of previously unrecognised cardiac abnormalities on echocardiogram and ECG was 18% (10/56). Seven percent (4/56) of carriers had cardiomyopathy, defined by significant LV dilatation and decreased shortening fraction. In most cases, subjects with abnormal cardiac findings were asymptomatic. Echocardiography was more frequently abnormal than electrocardiography, but in many subjects the measurements of left ventricular dimensions were only just outside the normal ranges. The prevalence of skeletal muscle weakness was 12% (7/56). It was usually recognized by the individual, although not previously volunteered, but was mild and did not substantially affect activities of daily living.

A number of therapies have been proposed for intractable ventricular fibrillation, though none has a high chance of success. Many out-of-hospital cardiac arrests relate to new ischaemia [ [1] Spaulding C.M. Joly L.M. Rosenberg A. et al. Immediate coronary angiography in survivors of out-of-hospital cardiac arrest. N. Engl. J. Med. 1997; 336: 1629-1633 Google Scholar ]. Therefore, if VF is intractable, measures that relieve ischaemia may restore sinus rhythm. Recently, we treated a young 28-year-old man in intractable ventricular fibrillation successfully with ‘blind’ coronary surgery. He had been sent by his general practitioner to the ECG department with atypical chest pain. A 12-lead ECG was performed (Fig. 1) after which he collapsed in cardiac arrest with coarse ventricular fibrillation. Despite intubation, full oxygenation, effective and immediate CPR and DC cardioversion (with intermittent adrenaline) he remained in ventricular fibrillation. After 55 minutes of resuscitation, with intractable cardiac arrest, having had more than 20 shocks, a cardiac surgeon was called, who, on the basis that his EGG suggested LAD territory ischaemia, agreed to emergency CABG. At operation the LAD territory was noted to be dusky, consistent with infarction. A single reverse saphenous vein aorto-coronary graft was anastamosed to the left anterior descending coronary artery. Bypass was discontinued with ease, with the patient in sinus rhythm. Post operative course was uncomplicated, with no evidence of cerebral injury, and no further ventricular arrhythmias. His ECG subsequently showed anterior Q waves. Subsequent coronary angiography showed substantial hypokinesia in the LAD territory and a critical stenosis in the proximal portion of the LAD, with no lesions elsewhere. The patient was subsequently treated with ACE inhibitor and B-blocker therapy and he remains alive and well 8 years later. The final diagnosis was refractory VF related to an acute anterior wall myocardial infarction, terminated by coronary surgery.

We present a case of spontaneous rupture of a right coronary bypass vein graft in a 57-year-old woman 10 years after coronary by-pass surgery. Although rare, this diagnosis should be considered in such patients presenting with appropriate symptoms.

Background The role of percutaneous transluminal coronary angioplasty (PTCA) in the management of patients with angina remains controversial, particularly in patients whose symptoms are adequately controlled by medical treatment.Methods RITA-2 is a randomised trial comparing the long-term effects of PTCA and conservative (medical) care in patients with coronary artery disease considered suitable for either treatment option. 1018 patients were recruited from 20 cardiology centres in UK and Ireland. The 504 randomised to PTCA were intended to have dilatation within 3 months. The 514 assigned to medical treatment received antianginal drugs; those whose symptoms were not controlled by optimum medical therapy could cross-over to myocardial revascularisation. The primary endpoint was the combined frequency of death from all causes and definite non-fatal myocardial infarction.Findings This report covers a median 2.7 years' follow-up. At randomisation 53% of patients had grade 2 or worse angina, and 40% had two or more diseased coronary arteries. 93% of patients randomised to PTCA had this procedure carried out, within a median of 5 weeks. Death or definite myocardial infarction occurred in 32 patients (6.3%) treated with PTCA and in 17 patients (3.3%) with medical care (absolute difference 3.0% [95% CI 0.4-5.7%], p=0.02). This difference was mainly due to one death and seven non-fatal myocardial infarctions related to the randomised procedures. There were 18 deaths (11 PTCA, seven medical) of which ten were not due to heart disease. Of the patients in the PTCA group, 40 (7.9%) required coronary artery bypass grafting (CABG), including nine instead of PTCA and seven emergencies following unsuccessful PTCA. 56 other PTCA patients (11.1%) required further non-randomised PTCA. In the medical group 118 patients (23.0%) underwent a revascularisation procedure during follow-up, mostly because of worsening symptoms. Angina improved in both groups, but more so in the PTCA group. There was a 165% absolute excess of grade 2 or worse angina in the medical group 3 months after randomisation (p<0.001), which attenuated to 7.6% after 2 years. Total exercise time (Bruce protocol) also improved in both groups, again with a treatment difference in favour of PTCA: mean advantage of 35 s at 3 months (p<0.001). These benefits of PTCA were greater in patients with more severe angina at baseline, judged by high initial grade of angina and short initial exercise-time.Interpretation In patients with coronary artery disease considered suitable for either PTCA or medical care, early intervention with PTCA was associated with greater symptomatic improvement, especially in patients with more severe angina. When managing individuals with angina, clinicians must balance these benefits against the small excess hazard associated with PTCA due to procedure-related complications.

BACKGROUND:The majority of patients presenting to cardiac clinics with chest pain who are reassured they do not have heart disease or other serious physical disorder continue to experience symptoms, worry about heart disease and restrict their activities. This randomized trial investigated the effectiveness of psychological treatment within routine cardiac care.METHODS:Consecutive patients presenting with chest pain and reassured by a cardiologist they do not have heart disease were reassessed 6 weeks later. Those with persistent limiting symptoms were offered the opportunity to participate in a trial of cognitive behavioural therapy.RESULTS:Thirty-seven subjects agreed to take part. A number of subjects were unenthusiastic about psychological intervention or, following explanation of the study, regarded further treatment as not being necessary. At 3 months there were significant differences between the treatment group and the control group on key outcome measures of symptoms, mood and activity. At 6 months there were fewer differences but significant advantages of treatment in terms of limitation of activities and worry about physical symptoms.CONCLUSION:We conclude that there is a need for 'stepped' further care following reassurance in the cardiac clinic and that cognitive behavioural treatment is effective with those with persistent disabling symptoms.

OBJECTIVE:To study the effect of transdermal scopolamine on heart rate variability, baroreflex sensitivity, and exercise performance in patients with heart failure and age matched healthy volunteers.DESIGN:Double blind, randomised, placebo controlled, crossover study.PATIENTS:16 patients with chronic, stable heart failure due to ischaemic cardiomyopathy (mean (SEM) age 58 (2) years; mean (SEM) radionuclide left ventricular ejection fraction 28 (2)%; New York Heart Association class II-III) and eight age matched healthy controls.INTERVENTION:Transdermal scopolamine (500 micrograms delivered over 72 h) or a placebo patch was administered for 48 h.MAIN OUTCOME MEASURES:Indices of tonic and reflex cardiac vagal activity and exercise performance.RESULTS:In both groups scopolamine produced a reduction in the 24 h average heart rate and an increase in the time domain measures of heart rate variability. Both the incidence and severity of ventricular arrhythmias remained unchanged. Baroreflex sensitivity, evaluated by the phenylephrine technique, increased significantly (P < 0.001) with scopolamine in patients with heart failure (6.22 (2.81) ms/mm Hg) and in healthy volunteers (5.97 (2.20) ms/mm Hg) as did the amplitude of respiratory sinus arrhythmia, computed by autoregressive spectral analysis of 10 min electrocardiographic recordings (319.9 (123.5) and 657.3 (126.6) ms2 respectively, P < 0.001). While exercise performance did not change, heart rate at submaximal exercise was significantly reduced by scopolamine in each group.CONCLUSIONS:In patients with mild to moderate heart failure low doses of scopolamine increased tonic and reflex cardiac vagal activity. This was achieved without affecting exercise tolerance or the incidence and severity of ventricular arrhythmias.

OBJECTIVES--To assess the characteristics of consecutive patients referred from general practice with the presenting disorder of chest pain or palpitations, and to determine the outcome at six months and three years. SETTING--A single consultant teaching hospital cardiac clinic receiving new referrals from a health district. DESIGN--94 consecutive referrals by general practitioners to a cardiac clinic with the presenting disorder of chest pain or palpitations were assessed at first attendance (research interview, cardiologists' ratings, systematic medical case note information), home interview six months later, and by a postal questionnaire at three years. OUTCOME MEASURES--Physical and psychological symptoms, limitation of activities, satisfaction with care, and use of health care resources. RESULTS--39 patients were given a cardiac diagnosis and 51 patients were not given a cardiac or other major physical diagnosis. The non-cardiac group was more likely to be young women, and to report other physical symptoms and previous psychiatric problems. The cardiac and non-cardiac groups reported progressive improvement in presenting symptoms and disability at the six months and three year follow up, but little change in mental state. Even so, three quarters of the non-cardiac subjects described continuing limitation of activities, concern about the cause of their symptoms, and dissatisfaction with medical care. CONCLUSIONS--A substantial proportion of the consecutive referrals continued to describe symptoms and disability throughout the three years after clinic attendance. Outcome was poor for those who had negative investigations and were reassured that they had no cardiac disorder or other serious physical finding. These results have implications for defining the role of psychological assessment and for the formulation of cost effective clinical measures to (a) minimise disability associated with cardiac disorder; and (b) prevent and treat handicaps in those without major physical diagnoses.

OBJECTIVE--To study QT dispersion in left ventricular hypertrophy and chronic heart failure and to determine the relation to ventricular arrhythmias. SETTING--Investigational laboratory of a tertiary referral centre. STUDY DESIGN--Patients with left ventricular hypertrophy and normal systolic function (n = 14) and patients with chronic heart failure (n = 18) were matched with controls (n = 17). The QT dispersion was examined in relation to abnormalities in resting mechanical and autonomic function and to the findings of 24 hour Holter monitoring. MAIN OUTCOME MEASURES--QT dispersion is the difference between the maximum and the minimum QT values from the 12 lead electrocardiogram. Mean(SD) QT dispersion from the 10 lead electrocardiogram was also examined once the 12 lead minimum and maximum values had been removed. The QT distribution is the curve describing the distance from the mean for all QT intervals (ms). RESULTS--All measures of QT dispersion were increased significantly in left ventricular hypertrophy and tended to increase in those with heart failure. The QT distribution was abnormal in both heart failure and left ventricular hypertrophy. There was no relation between the degree of change in QT dispersion and the incidence of ventricular arrhythmia on 24 hour Holter monitoring. Also there was no relation between QT dispersion and autonomic or mechanical abnormalities. The QT dispersion was related to QRS duration. CONCLUSION--Though QT dispersion and distribution are abnormal in left ventricular hypertrophy these findings do not support the hypothesis that QT dispersion reflects arrhythmic risk in either hypertrophy or heart failure.

Twenty-five patients (aged 62 +/- 2 years) with stable, moderate to severe ischemic congestive heart failure (CHF) (New York Heart Association class II/III: 15/10; ejection fraction 21.6 +/- 2%; and peak oxygen uptake 13.6 +/- 0.7 ml/kg/min) were studied to evaluate the ability of different methods to characterize autonomic tone in chronic CHF. Sympathovagal balance was assessed by: (1) heart rate variability in the time domain, assessed by the SD of RR intervals; (2) heart rate variability in the frequency domain, assessed by low- (0.03 to 0.14 Hz) and high- (0.18 to 0.40 Hz) frequency components of heart rate variability by autoregressive power spectral analysis; (3) 24-hour, daytime and nighttime heart rate; (4) submaximal heart rate during upright bicycle exercise, with respiratory gas analysis to obtain peak oxygen uptake; and (5) radiolabeled norepinephrine spillover. These methods did not correlate, with the exception of day and nighttime heart rate (r = 0.74; p<0.001) and the expected inverse correlation between low and high frequency (r = -0.92; p<0.001). No method correlated significantly with peak oxygen uptake, exercise tolerance or ejection fraction.After 8 weeks of physical training at home, all methods showed improvement in autonomic balance: increases in SD of RR intervals (+21%; p<0.02) and high frequency (+41%; p<0.007), and decreases in low frequency (-19%; p<0.002), low-/high-frequency ratio (-48%; p<0.03), norepinephrine spillover (-28.9%; p<0.03), 24-hour heart rate (-2.7%; p<0.005) and submaximal heart rate (-10.8%; p<0.01). However, neither the absolute values nor percent changes of the individual measures of autonomic function after training showed a significant correlation between each other. In patients with CHF, the individual parameters of autonomic control reflect different aspects of circulatory control. A comprehensive description of autonomic tone probably needs multiple methods.