The gap between policy and practice: a systematic review of patient-centred care interventions in chronic heart failure.

Patient-centred care (PCC) is recommended in policy documents for chronic heart failure (CHF) service provision, yet it lacks an agreed definition. A systematic review was conducted to identify PCC interventions in CHF and to describe the PCC domains and outcomes. Medline, Embase, CINAHL, PsycINFO, ASSIA, the Cochrane database, clinicaltrials.gov, key journals and citations were searched for original studies on patients with CHF staged II-IV using the New York Heart Association (NYHA) classification. Included interventions actively supported patients to play informed, active roles in decision-making about their goals of care. Search terms included 'patient-centred care', 'quality of life' and 'shared decision making'. Of 13,944 screened citations, 15 articles regarding 10 studies were included involving 2540 CHF patients. Three studies were randomised controlled trials, and seven were non-randomised studies. PCC interventions focused on collaborative goal setting between patients and healthcare professionals regarding immediate clinical choices and future care. Core domains included healthcare professional-patient collaboration, identification of patient preferences, patient-identified goals and patient motivation. While the strength of evidence is poor, PCC has been shown to reduce symptom burden, improve health-related quality of life, reduce readmission rates and enhance patient engagement for patients with CHF. There is a small but growing body of evidence, which demonstrates the benefits of a PCC approach to care for CHF patients. Research is needed to identify the key components of effective PCC interventions before being able to deliver on policy recommendations.

A multicentre analysis of troponin use in clinical practice.

BACKGROUND: The role of troponin quantification in evaluation of patients with suspected acute coronary syndrome is established, but with cost implications. Emerging high-sensitivity troponin and novel multi-marker assays herald further resource implications. AIMS: The objective of this study was to quantify recent trends in troponin usage and costs in a cross-section of hospitals. METHODS: A cross-sectional survey seeking data on troponin usage and costs from six tertiary referral, public access teaching hospitals for consecutive years between 2003 and 2009 was carried out. RESULTS: A median annual increase in the volume of troponin assays requested was identified in all six hospitals, with an average median annual increase of 6.9 % across hospitals (interquartile range 3.4, 10.1 %). This annual increase was not accompanied by a corresponding increase in volume of patients presenting to the Emergency Department (ED) with chest pain. The majority (44-67 %) of troponin requests originated in the ED of hospitals. The median annual spend on troponins per hospital was 115,612 (interquartile range 80,452, 140,918). An analysis of results of assays performed in one centre found that the majority (91 %) of troponin assays performed were in the normal range. CONCLUSIONS: An annual increase in troponin requests without a corresponding increase in patient activity raises the possibility of increasingly indiscriminate troponin testing. The cumulative direct and indirect costs of inappropriate testing are significant. Corrective strategies are necessary to improve patient selection and testing protocols, particularly in the advent of the high-sensitivity troponin assays and novel multi-marker strategies.

Clinical implications of anti-cardiac immunity in dilated cardiomyopathy.

Criteria of organ-specific autoimmunity are fulfilled in a subset of patients with myocarditis/dilated cardiomyopathy (DCM). In particular, circulating heart-reactive autoantibodies are found in such patients and symptom-free relatives. These autoantibodies are directed against multiple antigens, some of which are expressed in the heart (organ-specific), others in heart and some skeletal muscle fibres (partially heart-specific) or in heart and skeletal muscle (muscle-specific). Distinct autoantibodies have different frequency in disease and normal controls. Different techniques detect one or more antibodies, thus they cannot be used interchangeably for screening. It is unknown whether the same patients produce more antibodies or different patient groups develop autoimmunity to distinct antigens. IgG antibodies, shown to be cardiac- and disease-specific for myocarditis/DCM, can be used as autoimmune markers for relatives at risk as well as for identifying patients in whom immunosuppression may be beneficial. Some autoantibodies may also have a functional role, but further work is needed.

Comparison between biventricular pacing and single site pacing in patients with poor ventricular function: a hemodynamic study.

Biventricular pacing has been suggested as offering greater hemodynamic benefit than single site pacing in patients with advanced heart failure and left bundle branch block. This was tested using acute multisite pacing. Eighteen such patients were atrialsensed, ventricular multisite paced in random order for 5 minutes. The best achieved measure of cardiac output (CO), pulmonary capillary wedge pressure (PCWP) and left ventricular (LV) + dP/dtmax at RV, LV, and biventricular pacing sites compared. Baseline PCWP, CO, and LV + dP/dtmax were 20 +/- 10 mmHg 4.8 +/- 1.3 L/min and 680 +/- 173 mmHg/s respectively. In all 18 patients CO and in 17 of 18 patients LV + dP/dtmax and PCWP improved with pacing. In the group as a whole, no significant hemodynamic difference between pacing sites was observed in PCWP (pacing site RV 19 +/- 10 mmHg, LV 17 +/- 10, biventricular 18 +/- 11) or CO (RV 5.2 +/- 1.5 L/min, LV 5.1 +/- 1.5, biventricular 5.3 +/- 1.7). Increased stroke volume/PCWP with LV (5.6 +/- 3.7 mLs/mmHg) and biventricular pacing (5.4 +/- 4.0) were not significantly greater compared to RV pacing (4.7 +/- 3.0, ANOVA P = 0.20). Increase in LV + dP/dtmax with pacing at LV (814 +/- 190 mmHg/s) and biventricular (839 +/- 290) sites was not significantly greater than the increase with RV pacing (769 +/- 203 mmHg/s, ANOVA P = 0.30). Pacing in patients with heart failure and conduction delay can produce a hemodynamic benefit. There is individual variation in the pacing site that leads to the greatest improvement. In the group as a whole, biventricular and LV pacing produced only modest improvements compared to RV pacing.

Isolated chylopericardium.

A 25-year-old male was discovered to have an asymptomatic pericardial effusion during routine pre-employment medical evaluation. During pericardiocentesis 1200 ml of milky-white fluid was obtained; subsequent biochemical evaluation confirmed the chylous nature of this fluid. Following thorough evaluation a diagnosis of isolated chylopericardium was made. Following several recurrences he underwent thoracotomy with ligation of the thoracic duct and creation of a pericardial window. There are relatively few published reports of true isolated chylopericardium and the aetiology and pathogenesis remain unknown. A primary abnormality of the thoracic lymphatic valve system is postulated. The most effective treatment is surgical with ligation of the thoracic duct above the diaphragm and creation of a pericardial window

Effect of multisite pacing on ventricular coordination.

OBJECTIVE: To determine the effect of multisite pacing on left ventricular function. DESIGN: Prospective observational study. PATIENTS: 18 patients with heart failure with a dilated poorly functioning left ventricle (LV) and left bundle branch block. INTERVENTIONS: Pacing for 5 minutes in random order at the right ventricle (RV) apex, RV outflow tract, mid posterolateral LV, RV apex and LV simultaneously, and RV outflow tract and LV simultaneously. The best achieved measurements with RV, LV, and biventricular pacing were compared. MAIN OUTCOME MEASURES: LV dimension, filling characteristics, and long axis indices were measured on echocardiography simultaneously with LV pressure. Cycle efficiency (%)--that is, the ratio of the area of the acquired pressure dimension loop to that of the ideal loop for that segment--quantified coordination. RESULTS: The pacing site that gave the best achieved cycle efficiency differed between patients (biventricular in five, LV in two, RV in seven, and no site in four). In patients with baseline incoordination (cycle efficiency < or = 72%, n = 12) cycle efficiency improved significantly with RV pacing (cycle efficiency 76%, p = 0.01) but not with LV (65%) or biventricular (67%) pacing. LV based pacing induced premature short axis contraction in a subset of patients (n = 4), which was associated with a prolonged time from the Q wave on the ECG to the onset of inward movement of the long axis (from apex to mitral ring): biventricular 145 ms, LV 105 ms, RV 85 ms (biventricular v RV, p < 0.05). Excluding patients with baseline incoordination in whom premature activation occurred, pacing at all sites led to a similar increase in cycle efficiency (RV 78%, LV 72%, biventricular 73%). CONCLUSIONS: Ventricular coordination can be improved with pacing in patients with baseline incoordination. Short and long axis fibres may be asynchronised in a subset of patients with LV or biventricular pacing, which may worsen coordination. The clinical significance of these findings remains to be defined.

Genetic polymorphisms in the renin-angiotensin-aldosterone system associated with expression of left ventricular hypertrophy in hypertrophic cardiomyopathy: a study of five polymorphic genes in a family with a disease causing mutation in the myosin binding protein C gene.

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is an inherited disease of the sarcomere characterised clinically by myocardial hypertrophy and its consequences. Phenotypic expression is heterogeneous even within families with the same aetiological mutation and may be influenced by additional genetic factors. OBJECTIVE: To determine the influence of genetic polymorphisms of the renin-angiotensin-aldosterone system (RAAS) on ECG and two dimensional echocardiographic left ventricular hypertrophy (LVH) in genetically identical patients with HCM. PATIENTS AND METHODS: Polymorphisms of five RAAS components were determined in 26 gene carriers from a single family with HCM caused by a previously identified myosin binding protein C mutation. Genotypes associated with a higher activation status of the RAAS were labelled "pro-LVH genotypes". RESULTS: There was a non-biased distribution of pro-LVH genotypes in the gene carriers. Those without pro-LVH genotypes did not manifest cardiac hypertrophy whereas gene carriers with pro-LVH genotypes did (mean (SD) left ventricular muscle mass 190 (48) v 320 (113), p = 0.002; interventricular septal thickness 11.5 (2.0) v 16.4 (6.7), p = 0.01; pathological ECG 0% (0 of 10) v 63% (10 of 16), respectively). Multivariate analysis controlling for age, sex, and hypertension confirmed an independent association between the presence of pro-LVH polymorphisms and left ventricular mass. When each polymorphism was assessed individually, carriers of each pro-LVH genotype had a significantly greater left ventricular mass than those with no pro-LVH mutation; these associations, with the exception of cardiac chymase A AA polymorphism (p = 0.06), remained significant in multivariate analysis. CONCLUSION: Genetic polymorphisms of the RAAS influence penetrance and degree of LVH in 26 gene carriers from one family with HCM caused by a myosin binding protein C mutation.

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.

Relation between severity of left-ventricular hypertrophy and prognosis in patients with hypertrophic cardiomyopathy.

BACKGROUND: A previous study suggested that severe left-ventricular hypertrophy (maximum wall thickness > or = 30 mm) in patients with hypertrophic cardiomyopathy is associated with a risk of sudden cardiac death sufficient to warrant consideration for implantation of a cardioverter defibrillator (ICD). However, the prognostic significance of left-ventricular hypertrophy in relation to other clinical risk factors is poorly characterised. METHODS: We studied 630 patients consecutively referred to one hospital in London, UK (mean age 37 years [SD 16]; 382 male; mean follow-up 59 months). Patients underwent two-dimensional and doppler echocardiography, upright exercise testing, and Holter monitoring. FINDINGS: 39 patients died suddenly or had an appropriate ICD discharge; nine died from progressive heart failure; 11 from other cardiovascular causes and 23 from non-cardiac causes. There was a trend towards higher probability of sudden death or ICD discharge with increasing wall thickness (p=0.029, relative risk per 5 mm increment 1.31 [95% CI 1.03-1.66]). Of the 39 patients who died suddenly or had an ICD discharge, ten had a wall thickness of 30 mm or more. Patients with wall thickness of 30 mm or more had higher probability of sudden death or ICD discharge than patients with wall thickness less than 30 mm (p=0.049, 2.07 [1.00-4.25]. When considered together, the number of additional risk factors (one to three) was a better predictor of risk of sudden death or ICD discharge than wall thickness (p=0.0001, relative risk per additional factor 2.00 [1.43-2.79] vs p=0.058, 1.26 per 5 mm increment [0.99-1.60]). There was no relation between the pattern of hypertrophy and survival. INTERPRETATION: The risk of sudden death associated with a wall thickness of 30 mm or more in patients without other risk factors is insufficient to justify aggressive prophylactic therapy. Most sudden deaths occurred in patients with wall thickness less than 30 mm, so the presence of mild hypertrophy cannot be used to reassure patients that they are at low risk.

Sudden death in hypertrophic cardiomyopathy: identification of high risk patients.

OBJECTIVES: We sought to identify patients with hypertrophic cardiomyopathy (HCM) at high risk of sudden death (SD). BACKGROUND: Relatively low mortality rates in HCM make conventional analysis of multiple clinical risk markers for SD problematic. This study used a referral center registry to investigate a smaller number of generally accepted noninvasive risk markers. METHODS: We studied 368 patients (14 to 65 years old, 239 males) with HCM. There were five variables: nonsustained ventricular tachycardia (NSVT), syncope, exercise blood pressure response (BPR), family history of sudden death (FHSD) and left ventricular wall thickness (LVWT). RESULTS: During follow-up (3.6+/-2.5 years [range 2 days to 9.6 years]), 36 patients (9.8%) died, 22 of them suddenly. Two patients received heart transplants. The six-year SD-free survival rate was 91% (95% confidence interval [CI] 87% to 95%). In the Cox model, there was a significant pairwise interaction between FHSD and syncope (p = 0.01), and these were subsequently considered together. The multivariate SD risk ratios (with 95% CIs) were 1.8 for BPR (0.7 to 4.4) (p = 0.22); 5.3 for FHSD and syncope (1.9 to 14.9) (p = 0.002); 1.9 for NSVT (0.7 to 5.0) (p = 0.18) and 2.9 for LVWT (1.1 to 7.1) (p = 0.03). Patients with no risk factors (n = 203) had an estimated six-year SD-free survival rate of 95% (95% CI 91% to 99%). The corresponding six-year estimates (with 95% CIs) for one (n = 122), two (n = 36) and three (n = 7) risk factors were 93% (87% to 99%), 82% (67% to 96%) and 36% (0% to 75%), respectively. Patients with two or more risk factors had a lower six-year SD survival rate (95% CI) compared with patients with one or no risk factors (72% [56% to 88%] vs. 94% [91% to 98%]) (p = 0.0001). CONCLUSIONS: This study demonstrates that patients with multiple risk factors have a substantially increased risk of SD sufficient to warrant consideration for prophylactic therapy.

Haemochromatosis gene mutations in idiopathic dilated cardiomyopathy.

BACKGROUND: Two common mutations of the haemochromatosis associated gene (HFE) (cys282tyr (C282Y) and his63asp (H63D)) have been implicated in haemochromatosis and as modulators in cardiovascular disease. OBJECTIVE: To investigate the role of these mutations in the pathogenesis of idiopathic dilated cardiomyopathy. DESIGN AND SETTING: Case-control and prospective cohort study of patients attending a cardiomyopathy unit in a tertiary referral cardiac centre. METHODS: 207 unrelated white patients with dilated cardiomyopathy, followed up for 259 patient years, and 200 controls were tested for HFE C282Y and H63D mutations by polymerase chain reaction and restriction digestion. RESULTS: 31/207 patients (15%) v 24/200 controls (12%) carried C282Y (adjusted odds ratio (OR) 1.2 (95% confidence interval 0.7 to 2.2)), 74/207 (36%) v 53/200 (27%) carried H63D (OR 1.6 (1.1 to 2.5)), and 10/207 (4.8%) v 4/200 (2%) were compound heterozygotes (OR 2.6 (0.8 to 8.5)). Four patients and six controls were H63D homozygous and one was C282Y homozygous. There was a progressive increase in mean serum iron ([Fe]) and transferrin saturations from patients with no mutation ([Fe] = 16.3 micromol/l, transferrin saturation = 23.7%) through H63D heterozygotes (17.5 micromol/l, 25.8%), C282Y heterozygotes (17.1 micromol/l, 26.6%), H63D homozygotes (20.0 micromol/l, 33.5%), compound heterozygotes (26.8 micromol/l, 41.7%), and C282Y homozygotes (34 micromol/l, 71%). At follow up (median 90 months) the rate of death or cardiac transplantation was 52/207 (25%). C282Y heterozygotes had less ventricular dilatation (mean (SD): 59.9 (1.7) mm v 64.9 (0.9) mm, p < 0.05), better fractional shortening (24 (1. 7)% v 18.8 (1.4)%, p < 0.01), and a trend towards improved survival without transplantation. [Fe] and transferrin saturation did not correlate with disease severity and were not associated with reduced survival. CONCLUSIONS: The frequency of the H63D mutation is significantly increased in patients with idiopathic dilated cardiomyopathy. As H63D has a relatively minor effect on iron status, the mechanism of this association may be unrelated to iron metabolism.

Predictive value of wavelet decomposition of the signal-averaged electrocardiogram in idiopathic dilated cardiomyopathy.

BACKGROUND: Wavelet decomposition of the signal-averaged electrocardiogram has been proposed as a method of detecting small and transient irregularities hidden within the QRS complex and of overcoming some of the limitations of time domain analysis of the signal-averaged electrocardiogram. AIM: This study evaluated the potential utility of wavelet decomposition analysis in the risk stratification of patients with idiopathic dilated cardiomyopathy. METHODS AND RESULTS: Both wavelet decomposition and time domain analysis were applied to the signal-averaged electrocardiogram recordings of 82 patients with idiopathic dilated cardiomyopathy (mean age 43 +/- 14 years, 60 men) and 72 normal controls (mean age 44 +/- 15 years, 48 men). Three conventional time domain indices and four wavelet decomposition analysis parameters (QRS length, maximum count, surface area, and relative length) were derived from each recording using a Del Mar CEWS system and an in-house software package, respectively. The results showed that (1) more patients with idiopathic dilated cardiomyopathy than without had late potentials, and that the filtered QRS duration was significantly longer in patients than in controls (P<0.001). Similarly, abnormal wavelet decomposition analysis was more common in patients and wavelet decomposition measurements were significantly different between patients and controls (P<0.01); (2) conventional time domain analysis did not distinguish between clinically stable patients and patients who developed progressive heart failure, or between patients with and without arrhythmic events; (3) wavelet decomposition analysis identified patients who went on to develop progressive heart failure but failed to distinguish patients with arrhythmic events from those without; (4) survival analyses of a mean follow-up of 23 months showed that patients with late potentials tended to develop progressive heart failure more frequently than others (P=0.06). Patients with an abnormal wavelet decomposition result more frequently developed progressive heart failure than those with a normal wavelet decomposition result (P=0.027); (5) in a univariate analysis (Cox model), wavelet decomposition measurements but not time domain indices significantly correlated with the development of progressive heart failure (P=0.01). Multivariate analysis showed that only left ventricular end-diastolic dimension and peak oxygen consumption during exercise remained significant predictors of progressive heart failure. CONCLUSION: Wavelet decomposition analysis of the signal-averaged electrocardiogram is superior to conventional time domain analysis for identifying patients with idiopathic dilated cardiomyopathy at increased risk of clinical deterioration. Wavelet decomposition analysis, however, is unlikely to prospectively distinguish patients at a high risk of arrhythmic events in idiopathic dilated cardiomyopathy in its present form.

Health related quality of life and psychological wellbeing in patients with dilated cardiomyopathy.

OBJECTIVE: To assess the health related quality of life and psychological wellbeing of patients with dilated cardiomyopathy, and relate these to clinical variables and psychological adjustment. DESIGN: Postal questionnaire survey of 99 adult patients with dilated cardiomyopathy, selected at random from a larger database (60.6% response rate). Assessments included the short form 36 (SF-36) health survey, the hospital anxiety and depression scales, the sleep problems index, and a measure of psychological adjustment to cardiomyopathy. RESULTS: Patients with dilated cardiomyopathy reported significant impairments in physical functioning, role limitations owing to physical and emotional problems, social functioning, mental health, perceptions of general health, sleep, and vitality. Anxiety and depression levels were higher than in population samples. Impairment in several domains of quality of life was associated with low shortening fraction, high left ventricular end diastolic diameter, and the presence of heart failure and mitral regurgitation. Patients with familial cardiomyopathy had less impairment in quality of life than those with non-familial disease. Psychological adjustment scores were associated with several aspects of quality of life and emotional wellbeing. In multivariate analysis, demographic and clinical variables accounted for 0.1-40.7% of the variance in different domains of quality of life, and psychological adjustment scores accounted for an additional 0.5-22.4% of variance. CONCLUSIONS: Patients with dilated cardiomyopathy experience pronounced restrictions in quality of life and psychological wellbeing. These limitations are only partly accounted for by symptoms and the severity of underlying disease. Patients may benefit from efforts to improve psychological adjustment to the condition.

Gender differences in the management and outcome of acute myocardial infarction in unselected patients in the thrombolytic era.

This study compares the clinical features, management, and outcome in men and women from a consecutive, unselected series of patients with acute myocardial infarction (AMI) who were admitted to a university cardiac center over a 3-year period. It is a retrospective observational study of 1,059 admissions with AMI identified through the Hospital In-Patient Enquiry (HIPE) registry, validated according to Minnesota Manual criteria, and followed for a period of up to 5 years (median 36 months). Women comprised 40% of all admissions, had a higher hospital mortality (24% vs. 16%, p<0.001), and were less likely to receive thrombolysis (23% vs. 33%, p<0.01), admission to coronary care (65% vs. 77%, p<0.001), or subsequent invasive or noninvasive investigations (55% vs. 63%, p<0.01). However, women with AMI were older than men with AMI (71 vs. 65 years, p<0.001). After adjusting for age, differences that remained significant were prevalence of hypertension (odds ratio [OR] 2.12, 95% confidence intervals [CI] 1.56 to 2.88) and cigarette smoking (OR 0.47, 95% CI 0.35 to 0.65), management in coronary care (OR 0.66, 95% CI 0.49 to 0.88), and hospital mortality (OR 1.48, 95% CI 1.07 to 2.04). Excess mortality occurred predominantly in women <65 years old (18% vs. 8%, OR [multivariate] 2.35, 95% CI 1.19 to 4.56), among whom multivariate analysis demonstrated a significantly lower thrombolysis rate (OR 0.48, 95% CI 0.27 to 0.86). In this group, lack of thrombolysis independently predicted hospital mortality (OR 5.37, 95% CI 1.45 to 19.82). Female gender was not an independent predictor of mortality following AMI (OR 1.42, 95% CI 0.90 to 2.26). Thus, among unselected patients, female gender is associated with, but not an independent predictor of, reduced survival after AMI. Gender differences in mortality are greatest in younger patients, who are less likely to receive thrombolysis and in whom lack of thrombolysis is independently associated with mortality after AMI.

Abnormal cardiopulmonary exercise variables in asymptomatic relatives of patients with dilated cardiomyopathy who have left ventricular enlargement.

BACKGROUND: Left ventricular enlargement with normal systolic function is common in asymptomatic relatives of patients with familial dilated cardiomyopathy, many of whom progress to overt dilated cardiomyopathy at follow up. OBJECTIVE: To examine maximal and submaximal gas exchange variables of cardiopulmonary exercise testing in asymptomatic relatives with left ventricular enlargement. DESIGN AND SETTING: Controlled evaluation of metabolic exercise performance of patients with dilated cardiomyopathy and asymptomatic relatives with left ventricular enlargement identified through prospective family screening in a cardiomyopathy outpatient clinic. METHODS: 23 relatives with left ventricular enlargement, 33 normal controls, 29 patients with dilated cardiomyopathy, and 10 elite athletes with echocardiographic criteria of left ventricular enlargement ("physiological" enlargement) underwent symptom limited upright cycle ergometry using a ramp protocol. RESULTS: Peak oxygen consumption (pVO(2); mean (SD)) was significantly reduced in relatives with left ventricular enlargement (78 (16.3)%) v normal controls (96%, p < 0.01) and athletes (152%, p < 0.001), but was higher than in patients with dilated cardiomyopathy (69%, p < 0.01). pVO(2) was less than 80% of predicted in 75% of patients, 58% of relatives, 22% of controls, and none of the athletes. Oxygen pulse (pVO(2)/heart rate) was less than 80% of predicted in 69% of patients, 35% of relatives, 6% of controls, and none of the athletes. The slope of minute ventilation v CO(2) production (DeltaVE/DeltaVCO(2)) was > 30 in 68% of patients, 50% of relatives, and in none of the controls or athletes. Anaerobic threshold, occurring in relatives at 37 (14)% of the predicted VO(2), was higher than in the patients (32%, p < 0.01) and lower than in the controls (45%, p < 0.05) or in the athletes (55%, p < 0.001). CONCLUSIONS: Maximal and submaximal cardiopulmonary exercise test variables are abnormal in asymptomatic relatives with left ventricular enlargement, in spite of normal systolic function. This provides further evidence that left ventricular enlargement represents subclinical disease in relatives of patients with dilated cardiomyopathy. Metabolic exercise testing can complement echocardiography in identifying relatives at risk for the development of dilated cardiomyopathy.

Characteristics and outcomes in patients with acute myocardial infarction with ST-segment depression on initial electrocardiogram.

BACKGROUND: Acute myocardial infarction (AMI) with nonreciprocal ST-segment depression is said to have a poor prognosis, and early diagnosis and treatment are problematic. The aim of this study was to determine the proportion of unselected consecutive patients admitted to a university center with AMI with nonreciprocal ST-segment depression and to characterize these patients in terms of clinical features, treatment, and short- and long-term prognoses. METHODS AND RESULTS: Admission electrocardiographic data on 852 consecutive admissions with AMI were analyzed. Nonreciprocal ST-depression was an admitting feature in 95 (11%) patients, the majority of whom had ST depression >3 mm. These were older (70.3 vs 66.8 years, P <.05), more likely to have had myocardial infarction (40% vs 25%, P <.01), and to have left ventricular failure (56% vs 42%, P <.5), cardiogenic shock (15% vs 9% P =.06), and atrial fibrillation (34% vs 19%, P <.01). Hospital mortality rate was significantly higher (31% vs 17%, P <.01). Patients were less likely to undergo thrombolysis (17% vs 31%, P <.01), angiography (22% vs 35%, P <.05), or percutaneous revascularization (5% vs 9%, P <.01). Patients with ST depression undergoing coronary angiography were more likely to have 3-vessel disease (71% vs 47%, P <.05). Mortality rate at follow-up (median 36 months) was significantly higher in patients with ST depression (56% vs 32%, P <.001). Analysis by individual electrocardiography demonstrated ST-segment depression to be the third most frequent presentation after ST elevation (n = 327) and T-wave changes (n = 258), in whom hospital mortality rates were 24% and 9%, respectively. In multivariate analysis, previous myocardial infarction was an independent predictor of nonreciprocal ST depression at initial examination (odds ratio 2.04 [1.25 to 3.34], P <.005). No electrocardiographic presentation was an independent predictor of death in the hospital after AMI. CONCLUSIONS: In unselected cases of AMI, patients with ST-segment depression make up a significant minority (11%), who are likely to be older with a high prevalence of previous myocardial infarction and multivessel disease, and who have a poor prognosis.