Influence of the force--frequency relationship on haemodynamics and left ventricular function in patients with non-failing hearts and in patients with dilated cardiomyopathy

In isolated human myocardium it was shown that a positive force-frequencyrelationship occurs in non-failing myocardium; however, theforce-frequency relationship was found to be inverse in myocardiumfrom failing human hearts. In order to investigate the clinicalrelevance of these experimental findings, the influence of heartrate changes on haemodynamics and left ventricular functionwas studied in eight patients without heart failure and in ninewith failing dilated cardiomyopathy (NYHA II–III). Rightventricular pacing was performed at a rate slightly above sinusrate and at 100, 120 and 140 beats. min^–1 Haemodynamicparameters were obtained by right heart catheterization andby high-fidelity left ventricular pressure measurements. Leftventricular angiography was performed at basal pacing rate andat 100 and 140 beats. min^–1 With increasing heart rate,cardiac index increased in patients with normal left ventricularfunction from 2·9 ± 0·2 to 3·5 ±0·21. min^–1. m^–2 (P<0·01) and decreasedcontinuously in patients with dilated cardiornyopathy from 2·6± 0·1 to 2·2 ± 0·11. min^–1. m^–2 (P<0·05). With increasing heart rate,the maximum rate of left ventricular pressure rise increasedin non-failing hearts from 1388 ± 86 to 1671 ±88 mmHg. s^–1 (P<0·01) and did not change infailing hearts. Ejection fraction decreased from 27 ± 3% to 19 ±2% in patients with dilated cardiomyopathy (P<0·05)when the pacing rate was changed from 84 ± 2 beats. min^–1to 140 beats. min^–1, which was associated with a significantlyincrease in end-systolic volume without significantly changesin end-diastolic volume. In patients with normal left ventricularfunction, when the pacing rate was changed from 85 ±3 beats. min^–1 to 140 beats. min^–1, end-diastolicvolume decreased significantly by 13%, whereas left ventricularend-systolic volume and ejection fraction did not significantlychange. Left ventricular systolic and end-diastolic pressuresdid not significantly change with pacing tachycardia in eithergroup. The frequency-related changes in left ventricular volumesand pressures indicate that the differrent haemodynamic effectsof pacing tachycardia in both groups of patients result predominantlyfrom frequency effects on myocardial function and not from frequencyeffects on preload or afterload. These data indicate that recentexperimental findings of positive force-frequency effects innon-failing and negative force-frequency effects in failinghuman myocardium are relevant for the intact heart.     

Myocardial beta adrenoceptor density in primary and secondary left ventricular hypertrophy

OBJECTIVES: Myocardial ß-adrenoceptor density has been found tobe reduced in hypertrophic cardiomyopathy, even when systolicfunction is preserved. Our purpose in the current study wasto investigate whether ß-adrenoceptor down-regulationwas unique to hypertrophic cardiomyopathy, or is also presentin secondary myocardial hypertrophy. METHODS: Myocardial ß-adrenoceptor density was measured in11 patients with hypertrophic cardiomyopathy, eight patientswith left ventricular hypertrophy secondary to arterial hypertensionor aortic valve disease and 18 normal control subjects, usingpositron emission tomography with ¹¹C-CGP-12177 as the myocardialß-adrenoceptor ligand. RESULTS: Reflecting the natural incidence of the conditions, the ageof the hypertrophic cardiomyopathy patients was 37 (10) [mean(SD), range 20–51] years and that of the secondary hypertrophypatients 64 (18), [range 26–80] years; P<0.01. Thecontrols' ages were 50 (13), [range 21–65] years; however,since ß-adrenoceptor density is known to be influencedby age, the controls' data was split into groups matched tothe hypertrophic cardiomyopathy and secondary hypertrophy patientsets. For the hypertrophic cardiomyopathy patients, mean leftventricular ß-adrenoceptor was 7.70 (186) pmol . g^–1compared to 10.17 (244) pmol . g^–1 for a matched set of15 controls; P<0.01. In secondary left ventricular hypertrophy,ß-adrenoceptor was 6.35 (1.70) pmol . g^–1 comparedto 9.16 (2.00)pmol . g^–1 for a matched set of 10 controls;P<0.01. Plasma noradrenaline was 5.5 (2.2)nmol . 1^–1in hypertrophic cardiomyopathy and 2.5 (1.0)nmol. 1^–1for the matched controls; P<0.01. The results for adrenalinewere 2.2 (1.1) vs 0.4 (0.3) nmol . 1^–1 respectively; P<0.001.For the secondary hypertrophy patients, the corresponding figureswere 2.5 (1.2) vs 2.5 (1.0) nmol . 1^–1 for noradrenalinefor patients and controls respectively (P=ns); and for adrenaline0.2 (0.1) and 0.3 (0.2) nmol . 1^–1 respectively, P=ns.On multiple regression analysis, no relationships could be demonstratedamongst plasma catecholamines, ß-adrenoceptor, myocardialblood flow and echocardiographic E/A ratio and fractional shortening. CONCLUSION: Myocardial ß-adrenoceptor density appears to be comparablydecreased in both primary and secondary left ventricular hypertrophyin the presence of preserved left ventricular systolic function.     

Prevalence of myocarditis and cardiotropic virus infection in Africans with HIV-associated cardiomyopathy,idiopathic dilated cardiomyopathy and heart transplant recipients: a pilot study

Background:

The prevalence of myocarditis and cardiotropic viral infection in human immunodeficiency virus (HIV)-associated cardiomyopathy is unknown in Africa.

Methods

Between April 2002 and December 2007, we compared the prevalence of myocarditis and cardiotropic viral genomes in HIV-associated cardiomyopathy cases with HIV-negative idiopathic dilated cardiomyopathy patients (i.e. negative controls for immunodeficiency) and heart transplant recipients (i.e. positive controls for immunodeficiency) who were seen at Groote Schuur Hospital, Cape Town, South Africa. Myocarditis was sought on endomyocardial biopsy using the imunohistological criteria of the World Heart Federation in 33 patients, 14 of whom had HIV-associated cardiomyopathy, eight with idiopathic dilated cardiomyopathy and 11 heart transplant recipients.

Results

Myocarditis was present in 44% of HIV-associated cardiomyopathy cases, 36% of heart transplant recipients, and 25% of participants with idiopathic dilated cardiomyopathy. While myocarditis was acute in 50% of HIV- and heart transplant-associated myocarditis, it was chronic in all those with idiopathic dilated cardiomyopathy. Cardiotropic viral infection was present in all HIV-associated cardiomyopathy and idiopathic dilated cardiomyopathy cases, and in 90% of heart transplant recipients. Multiple viruses were identified in the majority of cases, with HIV-associated cardiomyopathy, heart transplant recipients and idiopathic dilated cardiomyopathy patients having an average of 2.5, 2.2 and 1.1 viruses per individual, respectively.

Conclusions

Acute myocarditis was present in 21% of cases of HIV-associated cardiomyopathy, compared to none of those with idiopathic dilated cardiomyopathy. Infection with multiple cardiotropic viruses may be ubiquitous in Africans, with a greater burden of infection in acquired immunodeficiency states.     

Coronary vasodilator reserve in primary and secondary left ventricular hypertrophy: A study with positron emission tomography

Objectives Coronary vasodilator reserve is reduced in hypertrophiccardiomyopathy and secondary left ventricular hypertrophy despiteangiographically normal coronaries. The aim of the present studywas to assess whether quantitative differences exist betweenthese conditions. Methods Using positron emission tomography with H₂¹⁵O, myocardialblood flow was measured at baseline and following intravenousdipyridamole (0·56 mg. kg ^–1) in 12 hypertrophiccardiomyopathy patients (age 34 (11) years, mean (SD), all male),16 secondary left ventricular hypertrophy patients (age 58 (20)years, P<0·01 vs hypertrophic cardiomyopathy; 10 female)and 40 normal controls (age 54 (20), 13 female). In view ofthe known decline of post-dipyridamole myocardial blood flowwith age, myocardial blood flow was compared between the patientgroups and appropriately matched subsets of the total controlgroup. Results Baseline myocardial blood flow in the hypertrophic cardiomyopathypatients was 0·82 (0·23) ml. min^–1 . g^–1vs 0·94 (0·14) ml. min^–1 . g^–1 inits matched control group, P=ns. For the secondary left ventricularhypertrophy patient group, baseline myocardial blood flow was1·17 (0·40) ml . min^–1 . g^–1 vs 1·06(0·28) ml . min^–1 . g^–1 for the secondaryleft ventricular hypertrophy matched control group, P=ns. Followingdipyridamole, myocardial blood flow was 1·64 (0·44)ml . min^–1 . g^–1 in hypertrophic cardiomyopathypatients vs 3·50 (0·95) ml . min^–1 . g^–1forthe hypertrophic cardiomyopathy matched control group, P=0·0001.For the left ventricular hypertrophy patients, post-dipyridamolemyocardial blood flow was 2·27 (0·60)ml . min^–1. g^–1 vs 2·94(1·29) ml . min^–1 . g^–1for the left ventricular hypertrophy controls, P 0·06.Coronary vasodilator reserve (dipyridamole-myocardial bloodflow/baseline-myocardial blood flow) was 2·05 (0·61)for hypertrophic cardiomyopathy patients vs 3·81 (0·98)for the hypertrophic cardiomyopathy controls (P=0 0001, patientsvs controls) and 2·06 (0·62) for left ventricularhypertrophy patients vs 2·90 (1·38) for the leftventricular hypertrophy controls, P<0·03 patientsvs controls. After correction of baseline myocardial blood flowfor baseline heart rate x systolic pressure product, coronaryvasodilator reserve for the hypertrophic cardiomyopathy patientswas 2·06 (1·06) vs 4·34 (1·54) forthe hypertrophic cardiomyopathy controls, P=0·0002 andin the secondary left ventricular hypertrophy patients, thevalues were 2·13 (0·64) vs 2·89 (1·42)in the secondary left ventricular hypertrophy controls, P<0·05. Conclusions In both hypertrophic cardiomyopathy and secondaryleft ventricular hypertrophy, the computed coronary vasodilatorreserve is impaired, even after correction for baseline cardiacwork. However, the extent of the reduction is greater in thehypertrophic cardiomyopathy patients. In the blunting of vasodilatorreserve of secondary left ventricular hypertrophy, the patients'greater hyperaemic response is partly offset by the higher baselinemyocardial blood flow.     

Clinical, adrenergic and heart endocrine measures in chronic atrial fibrillation as predictors of conversion and maintenance of sinus rhythm after direct current cardioversion

The aim of this study was to evaluate clinical, adrenergic andendocrine factors that could predict sinus rhythm maintenanceafter direct current cardioversion in chronic atrial fibrillation. Nineteen patients with chronic non-rheumatic atrial fibrillation(mean duration 6±5 months) were studied. They were exercised24 h before cardioversion at maximum effort with the Naughtonprotocol. Heart rate and blood pressure at rest and exercisewere recorded and blood samples were taken for the assessmentof adrenergic activity, by measuring cyclic adenosine monophosphate,heart endocrine function, atrial natriuretic peptide and itssecond messenger, cyclic guanosine monophosphate. Fifteen ofthe 19 patients were initially converted to sinus rhythm (eightpatients with external and seven patients with internal DC shocks).After 3 months eight patients remained in sinus rhythm and 11had relapsed, most of them within the first month. On exercisethe chronotropic response was lower in the group who remainedin sinus rhythm than in the group in atrial fibrillation (peakheart rate 147±11 beats.min^–1 vs 165±24beats.min^–1 p=0·02). During exercise, the systolicblood pressure in the sinus group reached higher values thanin the group who relapsed (192±17 mmHg vs 176±18mmHg, p=0·03). Cyclic adenosine monophosphate increasedsignificantly from rest to peak exercise in the sinus rhythmgroup (from 23±9 pmol.ml^–1 to 31±15 mol.ml^–1,p=0·02) while it remained unchanged in the atrial fibrillationgroup (25±10 pmol.ml^–1 to 24±8 pmol.ml^–1,p=0·02). For all 19 patients the differ ence in cyclicadenosine monophosphate between rest and exercise was negativelycorrelated with maximum heart rate (r=0·58, p=0·009).Atrial natriuretic peptide increased from rest to peak exercisein the sinus rhythm group (from l29±58 fmol.ml^–1to 140±66fmol.ml^–1 while it remained unchangedin the group in which atrial fibrillation persisted or recurred(from 112±58 fmol.ml^–1 to 111±53 fmol.ml^–1p=0· A significant correlation between atrial natriureticpeptide and cyclic guanosine monophosphate levels at exercisebefore cardioversion was found for the sinus rhythm group only(r=0·76, p=0·02). In patients with non-rheumatic chronic atrial fibrillation evaluationof clinical parameters such as heart rate and blood pressurechanges during maximal exercise can be useful in the choiceof suitable therapy. An inadequate increase in plasma cyclic-adenosinemonophosphate and atrial natriuretic peptide on exercise couldpredict patients with more severe underlying disease, wherecardioversion should not be recommended.     

Arrhythmogenic right ventricular cardiomyopathy: a 'final common pathway' that defines clinical phenotype.

Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C)is a primary heart muscle disease with distinct characteristics.ARVD/C predominantly affects the right ventricle (RV), withRV dilation and thinning due to fibrofatty infiltration of theventricular myocardium, and ultimately depressed systolic functionleading to right heart failure or biventricular failure.¹ Earlyin its clinical course, ARVD/C typically presents with ventriculararrhythmias (usually with a left bundle branch pattern), syncope,or sudden cardiac death.² Tragically, this clinical scenariocommonly occurs in young, healthy, athletic individuals. A setof clinical criteria, known as the ‘Task Force Criteria’,first described by McKenna et al.³ in 1994 and later modifiedfor inclusion of family members,⁴ utilizes     

Dilated cardiomyopathy and coronary flow reserve.

We read with interest the article by Rigo et al.¹ aboutthe prognostic impact of coronary flow reserve (CFR) by Dopplerechocardiography in dilated cardiomyopathy. The authors concludethat in patients with idiopathic dilated cardiomyopathy, theprognostic role of impaired microvascular CFR has been shownto be unfavourable. In our opinion, some points of     

Improvement of left ventricular diastolic function after alcohol septal ablation for obstructive hypertrophic cardiomyopathy? Yes, of course, but...

Recently, I have read with a great interest a very importantpaper by Jassal et al.¹ The authors reported their resultsof non-invasive evaluation of left ventricular (LV) diastolicfunction in 30 selected patients with a highly symptomatic obstructivehypertrophic cardiomyopathy (HCM) treated by alcohol septalablation (ASA). The authors concluded that positive changesin Doppler variables are likely     

The link between acute haemodynamic adrenergic beta-blockade and long-term effects in patients with heart failure: A study on diastolic function, heart rate and myocardial metabolism following intravenous metoprolol

The present study was performed to find possible mechanismslinking the early effects of beta-blockade with the observedlong-term effects in patients with heart failure. In 57 patients with heart failure, 13±3.1 mg of metoprololwas given intravenously. The patients were investigated by invasivehaemodynamics (n = 34), including collection of myocardial metabolicdata during atrial pacing stress (n = 16), by radionuclide angiographyduring physiological atrial pacing (n = 13), and by a bedsideevaluation (n = 10). Diastolic function, measured by early peak filling rate, followedchanges in heart rate, but was similar when heart rate was heldconstant by atrial pacing before and after beta-blockade. Followingbeta-blockade and slower heart rates, diastolic filling volumeswere redistributed to late diastole. Metoprolol induced a paralleldecrease in coronary sinus flow and myocardial oxygen consumption.Myocardial oxygen consumption following beta-blockade decreasedboth during spontaneous rhythm (25±15 to 16±8.8ml. min^–1; P = 0.006), and during atrial pacing stress(30±13 to 23±11 ml.min^–1; P = 0.004). Cardiacindex decreased owing to reduction of heart rate (2.3±1.0to 1.9±0.64 l.min^–1.m²; P = 0.0003), while leftventricular filling pressure was unchanged. Ejection fractionand ventricular volumes were unaltered following atrial pacingor beta-blockade. There was a reflex increase in noradenalineconcentration after beta-blockade injection (0.96±0.66to 1.20±0.91 nmol.l^–1; P = 0.002), whereas myocardialnoradrenaline overflow was unchanged. There was a trend towardsan increase in myocardial lactate consumption after beta-blockadeadministration during atrial pacing stress. It is suggested that the surprisingly good tolerability seenafter acute administration of beta-blockers to patients withsevere heart failure may be explained by prolongation of thediastolic filling phase, which outweighs the negative ino tropiceffects. The reduced myocardial metabolic demand may allow thefailing myocardium to recover and explain the excellent long-termeffect on heart function following beta-blockade treatment.     

Platelet function, thrombin and fibrinolytic activity in patients with heart failure

Assays which detect the release of platelet proteins and ofpep tides during thrombogenesis and are considered markers ofactivation of platelets and the coagulation system have recentlybeen developed. This study was designed to utilize these haemostasis-relatedmarkers to lest the hypothesis that a prethrombotic state isrelated to the presence, aetiology and severity of heart failure.Seventy patients with heart failure were evaluated and datawere compared with 36 normal volunteers and 41 patients withcoronary artery disease without heart failure (CAD). Thrombogenesiswas documented using assays which measure platelet function,thrombin activity and fibrinolysis. Platelet function was measuredby determining plasma concentrations of platelet factor 4 (PF4)and beta-thromboglobulin (BTG). Thrombin antithrombin III complexes(TAT) and fibrinopeptide A (FPA) were determined to evaluatethrombin activity. Fibrinolyric activity was assessed by measuringD-Dimer levels. Patients with heart failure, when compared tonormals, had increased plasma levels of BTG (89±62 IU.ml^–1 vs 50±59 IU. ml^–1, P<0.01), TAT (4.6±4.3µg. l^–1 vs 2.3±0.64 µg. l^–1,P<0.005 and D-Dimer levels (506±444 IU. ml^–1vs 191±144 IU. ml^–1, P < 0.0001). Patients withheart failure, when compared to the CAD group, had increasedplasma levels of D-Dimer (506±444 ng. ml^–1 vs 191±144ng. ml^–1, P <0.05). Aetiology of heart failure didnot affect these measurements. Patients with severe heart failure,as determined by high plasma norepinephrine concentration orlow ejection fraction, were more likely to have activation ofplatelets and the coagulation system. Our study indicates thatpatients with heart failure have evidence of increased plateletand thrombin activation and fibrinolytic activity. These abnormalitiesare most pronounced in patients with severe heart failure.     

Respiratory muscle weakness and normal ventilatory drive in dilative cardiomyopathy

BACKGROUND: In dilative cardiomyopathy several factors influence dyspnoea.Patients with chronic heart failure may demonstrate impairmentof breathing pattern, ventilatory drive and respiratory musclestrength, as well as reduction of ventilatory efficiency. Thepurpose of this study was to evaluate whether dilative cardiomyopathyis accompanied by changes in breathing pattern, respiratorymuscle weakness and ventilatory neural drive. METHODS: We investigated 47 patients (36 men, mean age=47·8±11·2years) with chronic heart failure due to dilative cardiomyopathy,and 30 healthy subjects (10 men, mean age=35·4±11·7years) served as controls. Patients and controls underwent evaluationof left ventricular ejection fraction by 2D echocardiography,spirometry, body plethysmography, mouth occlusion pressure andrespiratory muscle strength, as well as by submaximal treadmillexercise testing with gas exchange measurements. The patients'results were compared to controls and predicted standard normalvalues, and evaluated for differences according to the degreeof severity of functional impairment. RESULTS: Patients with dilative cardiomyopathy demonstrated a slightreduction in lung volumes (15% of the patients with obstructiveand 15% with restrictive lung function pattern) and diffusioncapacity (20·4±6·8 vs 15·4±6·7ml. min^–1 . kPa^–1; P<0·01). In neuraldrive, as assessed by mouth occlusion pressure, there was nosignificant difference between patients and controls. Therewas a slight but significant reduction in respiratory musclestrength, as assessed by measuring maximal inspiratory pressurein patients with dilative cardiomyopathy (6·7±2·4kPavs 8·6±3·5kPa; P<0·01). The observedchanges were more pronounced in the severe chronic heart failurepatients (with a reduction in ventilatory efficiency) whereasno relationship among indices of cardiac or respiratory functionwas found. CONCLUSION: Patients with chronic heart failure due to dilative cardiomyopathydevelop respiratory muscle weakness without changes in neuralventilatory drive, and slight changes in breathing pattern relatedto the severity of the disease.     

Linkage between elevated PDGF-C expression and myocardial fibrogenesis in coxsackievirus B3-induced chronic myocarditis.

Coxsackievirus B3 (CVB3) is the most common causative agentof myocarditis.¹ Acute myocarditis caused by CVB3 infectioneither recovers completely without any functional and morphologicaldefects or progresses to chronic myocarditis, which is characterizedby chronic inflammation and interstitial hyperplasia that maybe related to progressive intrinsic dysfunction, degeneration,and loss of cardiomyocyte viability.² In later stages of thisdisease, CVB3 persists in the myocardium and results in chronicactivation of fibroblasts and progressive fibrosis of the myocardium,reflected by the accumulation of connective tissue and extracellularmatrix, which is characteristic of dilated cardiomyopathy (DCM).^3,4However, the molecular mechanisms by which acute myocarditisprogresses to chronic myocarditis and DCM still     

Pattern of left ventricular filling in hypertrophic cardiomyopathy: Assessment by Doppler echocardiography and radionuclide angiography

Aims The left ventricle in hypertrophic cardiomyopathy is anatomicallyand functionally non-uniform. This study was undertaken to verifywhether a heterogeneity in the pattern of diastolic fillingcan be detected along the left ventricular inflow tract in hypertrophiccardiomyopathy. Methods and results Early (E) and late (A) diastolic velocitieswere recorded by Doppler echocardiography at mitral and at mid-ventricularlevel in 16 normal volunteers and 30 patients with hypertrophiccardiomyopathy. Patients with hypertrophic cardiomyopathy alsounderwent radionuclide angiography to assess left ventricularfunction. E wave decreased significantly in normal volunteers(80±15 to 60±14cm.s^–1;P<0·001),but it increased in hypertrophic cardiomyopathy (76±22to 87±28cm.s^–1;P=0·04), whereas the A wavedecreased similarly in both. By multivariate analysis, systolicasynchrony and the ejection fraction of left ventricular lateralwall were directly related to the pattern of early filling progression(r=0·656; F=9·467;P<0·002). Moreover,systolic asynchrony showed a univariate direct correlation withchanges in E velocity (r=0·42;P=0·02). Conclusion Many patients with hypertrophic cardio-myopathy havean acceleration of filling within the left ventricular inflowtract; this phenomenon is directly related to systolic asynchronyand ejection fraction of the left ventricular lateral wall,suggesting increased suction.     

Pathophysiology of 'Tako-Tsubo' cardiomyopathy: collecting pieces of a puzzle.

It was with great interest that we read the paper of Yoshidaet al.¹ published in the November issue of this Journal. Theauthors who investigated patients with Tako-Tsubo cardiomyopathy(TTC) using     

Absence of viral nucleic acids in early and late dilated cardiomyopathy

OBJECTIVE—To investigate whether viral infection acts as a trigger factor for the development of dilated cardiomyopathy in genetically predisposed individuals with a family history of disease.
SETTING—Patients attending the cardiomyopathy unit in a cardiac tertiary referral centre.
DESIGN—Nested polymerase chain reaction (nPCR) was used to determine whether enteroviral, adenoviral, or cytomegaloviral nucleic acids were detectable in the myocardium of 19 asymptomatic relatives of patients with dilated cardiomyopathy; all these relatives had echocardiographic abnormalities thought to represent early disease. Explanted hearts from patients with end stage dilated cardiomyopathy were also studied and were compared with 25 controls (ischaemic heart disease (21), valvar heart disease (2), hypertrophic cardiomyopathy (1), restrictive cardiomyopathy (1)). Myocardial tissue from two fatal cases of culture positive coxsackie myocarditis was used as a positive control.
RESULTS—No viral nucleic acid was detected in any group other than in those with myocarditis. Spiking of random wells with purified recombinant viral nucleic acids confirmed the sensitivity and reproducibility of the assays.
CONCLUSIONS—Myocardial viral infection is not detectable in relatives of patients with dilated cardiomyopathy who are suspected of having early disease. There is no evidence that viruses act as a trigger factor for initiating the dilated cardiomyopathy in these patients.


Keywords: viral infection; dilated cardiomyopathy     

Self-estimated physical functioning poorly predicts actual exercise capacity in adolescents and adults with congenital heart disease

Aims: The aim of this study is to compare self-reported health-relatedquality-of-life (HRQoL) with the objective of exercise performancein patients with congenital heart disease (CHD) according todiagnosis. Methods and results: 564 patients (255 females, 14–73 years) with various CHD(62 shunt, 66 left heart obstruction, 33 PS/PR, 47 Ebstein,96 Fallot, 98 TGA after atrial switch, 38 other TGA, 31 Fontan,32 palliated/native cyanotic, 61 others) and a group of 53 healthycontrols (18 females, 14–57 years) completed a QoL questionnaire(SF-36) and performed a symptom-limited cardiopulmonary exercisetest. Despite several limitations at exercise (P = 1.30 x 10^–33),patients only reported reductions in HRQoL concerning physicalfunctioning (P = 4.41 x 10^–15) and general health (P =6.17 x 10^–5) and not psychosocial aspects. This couldbe confirmed in all diagnostic subgroups. Correlation to peakoxygen uptake was found in physical functioning (r = 0.435,P = 1.72 x 10^–27) and general health (r = 0.275, P = 3.79x 10^–11). However, there was severe overestimation ofphysical functioning in most patients when compared with actualexercise test results. Conclusion: Patients with CHD rate their HRQoL impaired only in physicalfunctioning and general health and not in any psychosocial aspect.Self-estimated physical functioning poorly predicts actual exercisecapacity.     

C-reactive protein in ischaemic cardiomyopathy: assessing vascular risk in heart failure.

The paper ‘High-sensitivity C-reactive protein: potentialadjunct for risk stratification in patients with stable congestiveheart failure’ by Lamblin et al.¹ clearly demonstratesthe prognostic value of this measurement in patients with well-compensatedheart failure due to ischaemic cardiomyopathy. Importantly,C-reactive protein did not provide significant prognostic informationin the population with dilated cardiomyopathy without evidenceof coronary artery disease. The study included 545 patients referred for evaluation of symptomaticheart failure. During a median follow-up of 972 days, a C-reactiveprotein >3 mg/L was found to be highly predictive ofcardiovascular mortality in patients with ischaemic etiology(113 events, 80% 3-year survival) with a hazard ratio of 2.17(     

When renal and cardiac insufficiencies intersect: is there a role for natriuretic peptide testing in the 'cardio-renal syndrome'?

This editorial refers to ‘Renal dysfunction, as measuredby the modification of diet in renal disease equations, andoutcome in patients with advanced heart failure’ by R.S.Gardner et al., on page 3027 Gardner et al.,¹ report that NT-proBNP maintains strongprognosis in heart failure (HF) patients with renal impairment.This is an interesting contribution to the debate about theutility of NT-proBNP in renal impairment; chronic kidney diseaseis an important complication in patients suffering from HF,while there is often heated discussion about the usefulnessof BNP and NT-proBNP measurement in patients with renal insufficiency. Because of considerable overlap of risk factors and a myriadof pathophysiologic mechanisms, insufficiencies of the renaland cardiac system are tightly related.² Furthermore, when     

Comparison of two methods of determining renal perfusion with and without captopril pretreatment in groups of patients with left ventricular dysfunction

Methods of effective renal plasma flow measurement by ¹²⁵I-orthoiodohippurateelimination and para-aminohippurate clearance were comparedwith and without captopril pretreatment in 10 chronic heartfailure patients and in 20 patients after transmural myocardialinfarction. In the chronic heart failure group measurements of effectiverenal plasma flow by the two techniques were strongly correlated(r=0·92, P<0·00001), as was the captopril-mediatedchange in effective renal plasma flow by the two methods (r=0·85,P=0·002). However, in absolute terms para-aminohippurateclearance significantly exceeded ¹²⁵I-orthoiodohippurate clearanceby a mean (± SD) of 24·8 ± 43·7ml. min^–1 (P<0·05) so that only using the formertechnique was a signifincant in renal perfusion observed inresponse to converting enzyme inhibition. In the post-myocardial infarction group, correlations betweenthe two methods were variable and much poorer than in the chronicheart failure group (r=0·54, P=0·01 and r=0·74,P=0·002 on consecutive days). Furthermore, captoprilmediatedincrements in effective renal plasma flow by the two techniqueswere unrelated (r= – 0·19, P=0·59). In thisgroup ¹²⁵I-orthoiodohippurate elimination significantly exceededpara-aminohippurate clearance (P<0·05). This reversedassociation and the weaker relationships between methods inpost-infarction as compared to chronic heart failure patientsmay be related to interference by thrombolytic or aspirin treatments.