Remote monitoring of cardiovascular disease: great promise, but do not forget the patient!

After more than 20 years, the conflict of interest (COI) movement has failed to substantiate its central claim that interactions between physicians, researchers and the medical products industry cause physicians to make clinical decisions that are adverse to the best interests of their patients. The COI movement's instigators have produced no solid evidence of harm commensurate with their extravagant allegations. At the same time, they have diverted resources away from more worthwhile pursuits, such as basic and applied medical research, clinical care and medical education towards onerous compliance exercises and obtrusive laws. Perhaps worst of all, they have made it respectable to ignore the epistemological foundations of medical science, diverting attention away from the scientific merit of the information presented and focusing it instead on the identity and motives of those who present the information.

Heart rate deceleration after exercise predicts patients most likely to respond to cardiac resynchronisation therapy.

OBJECTIVE: This study examines the relationship between heart rate recovery following exercise and subsequent response to cardiac resynchronisation therapy (CRT). BACKGROUND: Blunted heart rate recovery is an adverse prognostic marker in heart failure and has been shown to correlate with disease severity. METHODS: 37 patients receiving biventricular pacemakers for conventional indications underwent functional assessments; cardiopulmonary exercise test, 6-min walk test and quality-of-life assessment, together with echo analyses, before and at 3 months following implant. Heart rate deceleration (HRD) gradients were calculated at 30-, 60-, 90- and 120-s intervals following cessation of the baseline exercise test and compared with subsequent markers of response to CRT. Functional response was defined as > or =20% improvement in any two of the three functional assessments, and echo response defined as > or =5% increase in ejection fraction. RESULTS: Functional responders demonstrated steeper HRD gradients than non-responders at 30, 60 and 90 s. Echo responders also demonstrated steeper HRD at 30 and 60 s from the cessation of exercise. Receiver-operating curve analysis demonstrates area under the curve of 0.87 and 0.82, respectively, for HRD30 to predict functional and echo response to CRT. A cut-off value of 3 for HRD30, equating to a 5% reduction in HR between peak exercise and 30 s into recovery, demonstrates the optimal sensitivity/specificity profile to perform this function. CONCLUSIONS: HRD following exercise correlates with functional and echocardiographic response to CRT. Application of this parameter in addition to standard criteria may provide valuable supplementary information in the evaluation of prospective CRT candidates.

Late opening of the infarct related artery: an open or shut case?

Is there a place for the late opening of infarct related arteries, beyond the time window for myocardial salvage?

Warfarin for non-rheumatic atrial fibrillation: five year experience in a district general hospital.

OBJECTIVES: To assess the long term efficacy of and risks associated with computer aided oral anticoagulation for non-rheumatic atrial fibrillation (NRAF) in a district hospital setting. DESIGN: Retrospective, age stratified, event driven clinical database analysis. SETTING: District general hospital. PARTICIPANTS: 739 patients receiving warfarin for NRAF between 1996 and 2001. Patients were selected from an anticoagulation database through appropriate filter settings. MAIN OUTCOME MEASURES: Anticoagulation control (international normalised ratio (INR)) and hospitalisations for bleeding complications, thromboembolic events, and stroke. RESULTS: Over 1484 patient-years, computer assisted anticoagulation was uncontrolled in 38.3% of patients (INR < 2.0 or > 3.0). No significant differences in INR control were observed with respect to patient age (< 65, 65-75, and > 75 years), although to achieve adequate control of anticoagulation, the frequency of testing increased significantly with age. Annual risks of bleeding complications, thromboembolism, and stroke were 0.76%, 0.35%, and 0.84%, respectively. No significant differences in these events were observed between the three age groups studied. Patients who had thromboembolic events and haemorrhagic complications were significantly more likely to have been under-anticoagulated (INR < 2.0) and over-anticoagulated (INR > 3.0), respectively, at the time of their clinical event. CONCLUSIONS: Computerised long term oral anticoagulation for NRAF in a community setting of elderly and diverse patients is safe and effective. Anticoagulation control, bleeding events, thromboembolic episodes, and stroke rates are directly comparable with those reported in major clinical trials. The authors therefore support the strategy of rate control with long term oral anticoagulation for NRAF in general clinical practice.

Troponin I, laboratory issues, and clinical outcomes in a district general hospital: crossover study with "traditional" markers of myocardial infarction in a total of 1990 patients.

AIMS: Review of the clinical outcomes and practical issues of replacing traditional cardiac enzymes with troponin I (cTnI) in a district general hospital. METHODS: Crossover study of three sequential three month stages during which serial cardiac enzymes were replaced with a single cTnI measurement available at three set times within 24 hours for the duration of the second three month stage. The study was carried out in a 630 bed district general hospital with 1990 admissions of suspected cardiac ischaemia over the study period as a whole. Account was taken of seasonal factors. RESULTS: The introduction of troponin was associated with 8.5% more patients with non-ischaemic heart disease (IHD) being discharged on the day after admission, saving approximately 107 bed days each year. Approximately 50% more patients were diagnosed with myocardial infarction during the cTnI stage. There was no increase in readmission within one month or early death with cTnI. Approximately 3% false positive and 1.5% false negative cTnI results were recorded. All false positive cTnI results were coding errors or attributable to known assay interference effects. All false negatives were potentially explained by sample timing factors. The lack of standardisation in troponin assay services impacts clinically. CONCLUSION: Younger patients without IHD were discharged earlier during the cTnI stage in apparent safety. Blood sample timing needs to be verified when cTnI is used as an adjunct to early discharge. There were no unexplained false positives or negatives. Standardisation related issues arose.

Postinfarction left ventricular remodeling: a pathophysiological and therapeutic review.

Over the last 50 years, studies investigating the pathogenesis of left ventricular dysfunction have resulted in many potential therapeutic targets being identified and novel classes of drugs designed to treat this condition. Despite this, the long-term prognosis of patients with clinical heart failure remains poor with mortality rates equivalent to many terminal malignancies. This article reviews our present understanding of the pathophysiology of post-infarction left ventricular dysfunction and provides a rationale for current drug usage, drugs undergoing clinical trials and compounds still under pre-clinical development. In addition, the complexities involved in deciphering intra-cellular signalling pathways mediating ventricular hypertrophy which may form the basis of future treatments are also discussed.

The open artery hypothesis: potential mechanisms of action.

The postinfarction period is one of intense dynamic activity because the cardiovascular system undergoes a number of adaptive responses attempting to maintain cardiac output. These homeostatic responses contribute to the processes involved in postinfarction ventricular remodeling and involve acute, chronic, systemic, and local reactions. Almost immediately, neurohormones are activated that alter hemodynamic load, and, later, stimulate myocyte hypertrophy, while locally, inflammatory processes clear necrotic debris, reorganize the extracellular matrix, and orchestrate scar formation. Where the initial cardiac insult is sufficiently large (eg, necrosis of more than 40% of left ventricular mass), remodeling responses are exaggerated and may become maladaptive, contributing to the poor long-term prognosis associated with myocardial infarction. Although several studies have shown clear benefits after neurohormonal modulation and/or manipulation of ventricular loading forces in the postinfarction setting, relatively few studies have investigated the potential merits of a patent infarct-related artery during postinfarction ventricular remodeling. In particular, the salutary effects of late revascularization of previously occluded vessels remains controversial. Thus, though this issue remains speculative, our present practice must be governed by circumstantial evidence and hypothetical arguments. This article discusses the potential mechanisms whereby late reperfusion of an infarcted myocardial region may benefit long-term prognosis.