Do patients with suspected heart failure and preserved left ventricular systolic function suffer from "diastolic heart failure" or from misdiagnosis? A prospective descriptive study

OBJECTIVES: To characterise the clinical features of patients with suspected heart failure but preserved left ventricular systolic function to determine if they have other potential causes for their symptoms rather than being diagnosed with 'diastolic heart failure.' DESIGN: Prospective descriptive study. SETTING: Outpatient based direct access echocardiography service. PARTICIPANTS: 159 consecutive patients with suspected heart failure referred by general practitioners. MAIN OUTCOME MEASURES: Symptoms (including shortness of breath, ankle oedema, and paroxysmal nocturnal dyspnoea) and history of coronary heart disease and chronic pulmonary disease. Transthoracic echocardiography, body mass index, pulmonary function tests, and electrocardiography. RESULTS: 109 of 159 participants had suspected heart failure in the absence of left ventricular systolic dysfunction, valvular heart disease, or atrial fibrillation. Of these 109, 40 were either obese or very obese, 54 had a reduction in forced expiratory volume in 1 second to </=70%, and 97 had a peak expiratory flow rate </=70% of normal. Thirty one patients had a history of angina, 12 had had a myocardial infarction, and seven had undergone a coronary artery bypass graft. Only seven patients lacked a recognised explanation for their symptoms. CONCLUSIONS: For most patients with a diagnosis of heart failure but preserved left ventricular systolic function there is an alternative explanation for their symptoms-for example, obesity, lung disease, and myocardial ischaemia-and the diagnosis of diastolic heart failure is rarely needed. These alternative diagnoses should be rigorously sought and managed accordingly

Randomised controlled trial of specialist nurse intervention in heart failure

<p>Objectives. To determine whether specialist nurse intervention improves outcome in patients with chronic heart failure.</p> <p>Design. Randomised controlled trial.</p> <p>Setting. Acute medical admissions unit in a teaching hospital.</p> <p>Participants. 165 patients admitted with heart failure due to left ventricular systolic dysfunction. The intervention started before discharge and continued thereafter with home visits for up to 1 year.</p> <p>Main outcome measures. Time to first event analysis of death from all causes or readmission to hospital with worsening heart failure.</p> <p>Results. 31 patients (37%) in the intervention group died or were readmitted with heart failure compared with 45 (53%) in the usual care group (hazard ratio=0.61, 95% confidence interval 0.33 to 0.96).Compared with usual care, patients in the intervention group had fewer readmissions for any reason (86 v 114, P=0.018), fewer admissions for heart failure (19 v 45, P<0.001) and spent fewer days in hospital for heart failure (mean 3.43 v 7.46 days, P=0.0051).</p> <p>Conclusions. Specially trained nurses can improve the outcome of patients admitted to hospital with heart failure.</p&gt

Assessment of heart failure with plasma natriuretic peptides

SIR—Martin Cowie and colleagues1 are to be congratulated on assessing the usefulness of natriuretic peptides in clinical practice. Their report is, however, puzzling in several respects.<p></p> Too little information is given about the patients studied. Why did such a high proportion (11/35, 31%) of patients have an unknown cause for their heart failure? That Cowie and his co-workers chose to define heart failure, as opposed to left ventricular systolic dysfunction, is also puzzling, since it is the latter we generally wish to identify and know how to treat.2 and 3 At least ten of 35 patients would seem to have had causes other than left ventricular systolic dysfunction (for their heart failure) which would certainly be readily clinically apparent and merit further investigation in their own right (ie, atrial fibrillation, complete heart block, valvular disease). What they are really saying, it would seem, is that natriuretic peptides are useful in identifying that there is something wrong with the heart (hypertension, complete heart block, atrial fibrillation, &c). The more important question is, however, are natriuretic peptides useful or not in identifying left ventricular systolic dysfunction, in ordinary clinical practice? Can Cowie and colleagues provide an answer?<p></p&gt

Clinical epidemiology of heart failure: public and private health burden

Clinically overt heart failure is common, costly, disabling, and deadly; it remains so despite the tremendous benefit of angiotensin-converting enzyme inhibitors. Better treatments for and earlier detection of heart failure are needed if the situation to improve. However, even this may not be enough. The dramatic deterioration in quality of life and prognosis when a patient progresses from asymptomatic left ventricular dysfunction to overt heart failure suggests that only a programme of screening and prevention will effectively reduce the public health burden of heart failure. Moreover, the economic consequences of developing overt heart failure suggest that such an approach is likely to be cost-effective

Clinical epidemiology of heart failure: public and private health burden

Clinically overt heart failure is common, costly, disabling, and deadly; it remains so despite the tremendous benefit of angiotensin-converting enzyme inhibitors. Better treatments for and earlier detection of heart failure are needed if the situation to improve. However, even this may not be enough. The dramatic deterioration in quality of life and prognosis when a patient progresses from asymptomatic left ventricular dysfunction to overt heart failure suggests that only a programme of screening and prevention will effectively reduce the public health burden of heart failure. Moreover, the economic consequences of developing overt heart failure suggest that such an approach is likely to be cost-effective

Outcome from a rapid-assessment chest pain clinic

Chest pain accounts for much of the rising numbers of emergency admissions, but in-patient assessment is not necessarily the best way of dealing with these patients. We ran a 'rapid-assessment chest pain clinic' to provide an alternative route of assessment, and audited its outcome. General practitioners referred patients with recent-onset chest pain, increasing chest pain, chest pain at rest, or other chest pain of concern, on the understanding that they would be seen within 24 h. During 8 1/2 months, 334 patients were referred and 317 patients were seen, most of whom had exercise electrocardiography. A median of 6 months later, 278 patients were personally contacted to determine outcome. Of these, 18% had been admitted immediately with acute coronary syndromes, and 49% had been diagnosed as non-coronary chest pain (none of whom subsequently infarcted or died). Continuing symptoms were infrequent, and satisfaction was high, although 13% of patients had been revascularized. A significant number of patients required immediate admission and/or ultimate revascularization, but many more did not. The majority of these patients had non-coronary chest pain, and this diagnosis was substantiated by their excellent outcome and (in some cases) by further investigation

FBI-1 Can Stimulate HIV-1 Tat Activity and Is Targeted to a Novel Subnuclear Domain that Includes the Tat-P-TEFb—containing Nuclear Speckles

FBI-1 is a cellular POZ-domain–containing protein that binds to the HIV-1 LTR and associates with the HIV-1 transactivator protein Tat. Here we show that elevated levels of FBI-1 specifically stimulate Tat activity and that this effect is dependent on the same domain of FBI-1 that mediates Tat-FBI-1 association in vivo. FBI-1 also partially colocalizes with Tat and Tat's cellular cofactor, P-TEFb (Cdk9 and cyclin T1), at the splicing-factor–rich nuclear speckle domain. Further, a less-soluble population of FBI-1 distributes in a novel peripheral-speckle pattern of localization as well as in other nuclear regions. This distribution pattern is dependent on the FBI-1 DNA binding domain, on the presence of cellular DNA, and on active transcription. Taken together, these results suggest that FBI-1 is a cellular factor that preferentially associates with active chromatin and that can specifically stimulate Tat-activated HIV-1 transcription