To study the prevalence and medium term outcome of subclinical rheumatic heart disease (RHD) in India.
Cross sectional echocardiographic screening study.
School children aged 5-15 years living in ...rural areas of north India.
A cross sectional echocardiographic screening study was carried out among 6270 randomly selected school children aged 5-15 years (10.8 ± 2.6 years; 52.7% male). Of all the abnormal cases, 100 children (78%) were restudied at a mean follow-up of 15.4 ± 6.6 months.
Echocardiographic screening.
Echocardiography-Doppler criteria based prevalence of RHD.
Clinical examination detected mitral regurgitation in five patients and the estimated prevalence of clinical RHD was 0.8/1000 school children. Echocardiography-Doppler diagnosed RHD in 128 cases, giving a prevalence of 20.4/1000 school children (95% CI 16.9 to 23.9/1000 children). On multivariate analysis, older age (OR 1.93, 95% CI 1.29 to 2.88; p = 0.001), female sex (OR 1.84, 95% CI 1.25 to 2.72; p = 0.002) and government funded school student, which is a surrogate measure of lower socioeconomic status (OR 1.55, 95% CI 1.02 to 2.34; p = 0.039) were found to be independent predictors of RHD. On follow up, the severity of subclinical RHD was non-progressive in 68 children (68%) while it worsened in four (4%) and regressed in 28 children (28%).
The prevalence of RHD is several fold higher using echocardiographic screening compared with clinical examination. The prevalence is higher among girls and children of lower socioeconomic status. In the majority of cases, subclinical RHD appears to be non-progressive on medium term follow up. Routine echocardiographic screening may be indicated in populations at high risk of RHD.
Heart failure is commonly associated with vascular disease and a high rate of athero-thrombotic events, but the risks and benefits of antithrombotic therapy are unknown.
The current study was an ...open-label, randomized, controlled trial comparing no antithrombotic therapy, aspirin (300 mg/day), and warfarin (target international normalized ratio 2.5) in patients with heart failure and left ventricular systolic dysfunction requiring diuretic therapy. The primary objective was to demonstrate the feasibility and inform the design of a larger outcome study. The primary clinical outcome was death, nonfatal myocardial infarction, or nonfatal stroke.
Two hundred seventy-nine patients were randomized and 627 patient-years exposure were accumulated over a mean follow-up time of 27 ± 1 months. Twenty-six (26%), 29 (32%), and 23 (26%) patients randomized to no antithrombotic treatment, aspirin, and warfarin, respectively, reached the primary outcome (ns). There were trends to a worse outcome among those randomized to aspirin for a number of secondary outcomes. Significantly (
P = .044) more patients randomized to aspirin were hospitalized for cardiovascular reasons, especially worsening heart failure.
The Warfarin/Aspirin Study in Heart failure (WASH) provides no evidence that aspirin is effective or safe in patients with heart failure. The benefits of warfarin for patients with heart failure in sinus rhythm have not been established. Antithrombotic therapy in patients with heart failure is not evidence based but commonly contributes to polypharmacy.
Current guidelines suggest that, for patients at moderate risk of death from unstable coronary-artery disease, either an interventional strategy (angiography followed by revascularisation) or a ...conservative strategy (ischaemia-driven or symptom-driven angiography) is appropriate. We aimed to test the hypothesis that an interventional strategy is better than a conservative strategy in such patients.
We did a randomised multicentre trial of 1810 patients with non-ST-elevation acute coronary syndromes (mean age 62 years, 38% women). Patients were assigned an early intervention or conservative strategy. The antithrombin agent in both groups was enoxaparin. The coprimary endpoints were a combined rate of death, non-fatal myocardial infarction, or refractory angina at 4 months; and a combined rate of death or non-fatal myocardial infarction at 1 year. Analysis was by intention to treat.
At 4 months, 86 (9·6%) of 895 patients in the intervention group had died or had a myocardial infarction or refractory angina, compared with 133 (14·5%) of 915 patients in the conservative group (risk ratio 0·66, 95% CI 0·51–0·85, p=0·001). This difference was mainly due to a halving of refractory angina in the intervention group. Death or myocardial infarction was similar in both treatment groups at 1 year (68 7·6% vs 76 8·3%, respectively; risk ratio 0·91, 95% CI 0·67–1·25, p=0·58). Symptoms of angina were improved and use of antianginal medications significantly reduced with the interventional strategy (p<0·0001).
In patients presenting with unstable coronaryartery disease, an interventional strategy is preferable to a conservative strategy, mainly because of the halving of refractory or severe angina, and with no increased risk of death or myocardial infarction.
Published online September 1, 2002. http://image.thelancet.com/extras/02art8090web.pdf
The ELITE study showed an association between the angiotensin II antagonist losartan and an unexpected survival benefit in elderly heart-failure patients, compared with captopril, an ...angiotensin-converting-enzyme (ACE) inhibitor. We did the ELITE II Losartan Heart Failure Survival Study to confirm whether losartan is superior to captopril in improving survival and is better tolerated.
We undertook a double-blind, randomised, controlled trial of 3152 patients aged 60 years or older with New York Heart Association class II–IV heart failure and ejection fraction of 40% or less. Patients, stratified for β-blocker use, were randomly assigned losartan (n=1578) titrated to 50 mg once daily or captopril (n=1574) titrated to 50 mg three times daily. The primary and secondary endpoints were all-cause mortality, and sudden death or resuscitated arrest. We assessed safety and tolerability. Analysis was by intention to treat.
Median follow-up was 555 days. There were no significant differences in all-cause mortality (11·7 vs 10·4% average annual mortality rate) or sudden death or resuscitated arrests (9·0 vs 7·3%) between the two treatment groups (hazard ratios 1·13 95·7% Cl 0·95–1·35, p=0·16 and 1·25 95% Cl 0·98–1·60, p=0·08). Significantly fewer patients in the losartan group (excluding those who died) discontinued study treatment because of adverse effects (9·7 vs 14·7%, p < 0·001), including cough (0·3 vs 2·7%).
Losartan was not superior to captopril in improving survival in elderly heart-failure patients, but was significantly better tolerated. We believe that ACE inhibitors should be the initial treatment for heart failure, although angiotensin II receptor antagonists may be useful to block the renin angiotensin aldosterone system when ACE inhibitors are not tolerated.
β blockers reduce mortality in patients who have chronic heart failure, systolic dysfunction, and are on background treatment with diuretics and angiotensin-converting enzyme inhibitors. We aimed to ...compare the effects of carvedilol and metoprolol on clinical outcome.
In a multicentre, double-blind, and randomised parallel group trial, we assigned 1511 patients with chronic heart failure to treatment with carvedilol (target dose 25 mg twice daily) and 1518 to metoprolol (metoprolol tartrate, target dose 50 mg twice daily). Patients were required to have chronic heart failure (NYHA II–IV), previous admission for a cardiovascular reason, an ejection fraction of less than 0·35, and to have been treated optimally with diuretics and angiotensin-converting enzyme inhibitors unless not tolerated. The primary endpoints were all-cause mortality and the composite endpoint of all-cause mortality or all-cause admission. Analysis was done by intention to treat.
The mean study duration was 58 months (SD 6). The mean ejection fraction was 0·26 (0·07) and the mean age 62 years (11). The all-cause mortality was 34% (512 of 1511) for carvedilol and 40% (600 of 1518) for metoprolol (hazard ratio 0·83 95% CI 0·74–0–93, p=0–0017). The reduction of all-cause mortality was consistent across predefined subgroups. The composite endpoint of mortality or all-cause admission occurred in 1116 (74%) of 1511 on carvedilol and in 1160 (76%) of 1518 on metoprolol (0·94 0·86–1–02, p=0·122). Incidence of side-effects and drug withdrawals did not differ by much between the two study groups.
Our results suggest that carvedilol extends survival compared with metoprolol.
Aims
Heart failure (HF) in the elderly carries a poor prognosis. We used the SENIORS dataset of elderly HF patients aged ≥70 years in order to develop a risk model for this population.
Methods and ...results
The SENIORS trial evaluated the effects of nebivolol and enrolled 2128 patients ≥70 years with HF (ejection fraction ≤35%, or recent HF admission). We randomly selected 1400 patients from the full dataset to produce a derivation cohort and the remaining 728 patients were used as a validation cohort. Baseline variables were entered into a bootstrap model with 200 iterations to determine their association with two outcomes, the composite of all‐cause mortality or cardiovascular hospitalization, or all‐cause mortality alone. Variables retaining a significant association with these outcomes in a multivariate model were used to develop a risk prediction score tested in the validation cohort. Five factors were associated with increased risk of both outcomes in the multivariate model: higher New York Heart Association class, higher uric acid level, lower body mass index, prior myocardial infarction, and larger left atrial (LA) dimension. For the composite outcome, peripheral arterial disease, years with heart failure, right bundle branch block, diabetes mellitus, and orthopnoea were also retained. For all‐cause mortality, creatinine, 6 min walk test distance, coronary artery disease, and age were retained.
Conclusion
In addition to conventional prognostic markers, uric acid and LA dimension appear to be important novel risk prediction markers in elderly patients with heart failure, and could be useful in guiding management.
Immune activation in patients with chronic heart failure may be secondary to endotoxin (lipopolysaccharide) action. We investigated the hypothesis that altered gut permeability with bacterial ...translocation and endotoxaemia would be increased in patients with oedema secondary to congestive heart failure.
We compared 20 patients who had chronic heart failure with recent-onset peripheral oedema (mean age 64 years SD 10, New York Heart Association NYHA class 3·3 0·7), 20 stable non-oedematous patients with chronic heart failure (mean age 63 years 19, NYHA class 2·6 0·7), and 14 healthy volunteers (mean age 55 years 16). Biochemical markers of endotoxaemia, inflammation, and immune activation were measured. Ten patients were studied within 1 week of complete resolution of oedema. Five patients survived longer than 6 months and were restudied again after remaining free of oedema for more than 3 months.
Mean endotoxin concentrations were higher in oedematous patients with chronic heart failure than in stable patients with chronic heart failure (0·74 SD 0·45
vs 0·37 EU/mL 0·23, p=0·0009) and controls (0·46 EU/mL 0·21, p=0·02). Oedematous patients had the highest concentrations of several cytokines. After short-term diuretic treatment, endotoxin concentrations decreased from 0·84 EU/mL 0·49 to 0·45 EU/mL 0·21, p<0·05) but cytokines remained raised. After freedom of oedema for more than 3 months after oedema resolved, endotoxin concentrations remained unchanged from the previous visit (0·49 EU/mL 0·06, p=0·45).
Raised concentrations of endotoxin and cytokines are found in patients with chronic heart failure during acute oedematous exacerbation. Intensified diuretic treatment can normalise endotoxin concentrations. Our preliminary findings suggest that endotoxin may trigger immune activation in patients with chronic heart failure during oedematous episodes.
OBJECTIVE To describe the survival of a population based cohort of patients with incident (new) heart failure and the clinical features associated with mortality. DESIGN A population based ...observational study. SETTING Population of 151 000 served by 82 general practitioners in west London. PATIENTS New cases of heart failure were identified by daily surveillance of acute hospital admissions to the local district general hospital, and by general practitioner referral of all suspected new cases of heart failure to a rapid access clinic. INTERVENTIONS All patients with suspected heart failure underwent clinical assessment, and chest radiography, ECG, and echocardiogram were performed. A panel of three cardiologists reviewed all the data and determined whether the definition of heart failure had been met. Patients were subsequently managed by the general practitioner in consultation with the local cardiologist or admitting physician. MAIN OUTCOME MEASURES Death, overall and from cardiovascular causes. RESULTS There were 90 deaths (83 cardiovascular deaths) in the cohort of 220 patients with incident heart failure over a median follow up of 16 months. Survival was 81% at one month, 75% at three months, 70% at six months, 62% at 12 months, and 57% at 18 months. Lower systolic blood pressure, higher serum creatinine concentration, and greater extent of crackles on auscultation of the lungs were independently predictive of cardiovascular mortality (all p < 0.001). CONCLUSIONS In patients with new heart failure, mortality is high in the first few weeks after diagnosis. Simple clinical features can identify a group of patients at especially high risk of death.
Background:
Sleep disordered breathing (SDB) is common in severe chronic heart failure (CHF) and is associated with increased morbidity and mortality. The prevalence of SDB in mild symptomatic CHF is ...unknown.
Aim:
The aim of this study was to determine the prevalence and characteristics of SDB in male patients with NYHA class II symptoms of CHF.
Methods and results:
55 male patients with mild symptomatic CHF underwent assessment of quality of life, echocardiography, cardiopulmonary exercise, chemoreflex testing and polysomnography. 53% of the patients had SDB. 38% had central sleep apnoea (CSA) and 15% had obstructive sleep apnoea. SDB patients had steeper VE/VCO2 slope median (inter-quartile range) 31.1 (28-37) vs. 28.1 (27-30) respectively; p=0.04, enhanced chemoreflexes to carbon dioxide during wakefulness mean±sd: 2.4±1.6 vs. 1.5±0.7%VE Max/mmHg CO2 respectively; p=0.03, and significantly higher levels of brain natriuretic peptide and endothelin-1 compared to patients without SDB. No differences in left ventricular ejection fraction, percent predicted peak oxygen uptake, or symptoms of SDB were observed.
Conclusions:
A high prevalence of SDB was found in men with mild symptomatic CHF. Patients with SDB could not be differentiated by symptoms or by routine cardiac assessment making clinical diagnosis of SDB in CHF difficult.
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