S.G. Williams

Left ventricular volume reduction without ventriculectomy

Partial left ventriculectomy (the Batista procedure) to achieve left ventricular volume reduction (LVVR) has been advocated as an alternative to cardiac transplantation in patients with end-stage dilated left ventricles. Here, we describe a new technique of LVVR that uses realignment of the papillary muscles, thus avoiding ventriculectomy, and report preliminary results. Eight patients (all male, mean age 49.3 [range 38 to 70] years) underwent LVVR between October 1998 and March 2000 as an adjunct to surgical coronary revascularization. Five were assessed with echocardiography and cardiopulmonary exercise testing before and after (mean follow-up time 267 [range 94 to 416] days) the operation. LVVR significantly improved left ventricular end-diastolic volume (254 +/- 32 to 218 +/- 36 mL, p = 0.03), left ventricular ejection fraction (20.14% +/- 1.36% to 31.28% +/- 2.32%, p = 0.007), and exercise duration (from 394 +/- 88 to 611 +/- 79 seconds, p = 0.03). A nonsignificant improvement in maximal oxygen consumption was also observed. This technique of LVVR is relatively simple to perform and is accomplished through a small apical cardiotomy. Preliminary results show an encouraging functional improvement following surgery. Future controlled studies are required to assess this novel technique further.

Is plasma N-BNP a good indicator of the functional reserve of failing hearts? the FRESH-BNP study

Whether plasma N‐terminal brain natriuretic peptide (N‐BNP) is useful in the diagnosis of heart failure (HF) depends traditionally on whether it is as good as the putative ‘gold‐standard’, left ventricular ejection fraction (LVEF), in indicating cardiac dysfunction. However, since HF is primarily an impairment of function of the cardiac pump, we explored the relationship between N‐BNP and direct and indirect indicators of cardiac pump dysfunction.

Rationale and study design of the REM-HF study: remote management of heart failure using implanted devices and formalized follow-up procedures

We wish to assess the clinical and cost‐effectiveness of remote monitoring of heart failure patients with cardiac implanted electronic devices.

Is early, low level, short term exercise cardiac rehabilitation following coronary bypass surgery beneficial? A randomised controlled trial

Through the relief of myocardial ischaemia, the goal of coronary artery bypass grafting (CABG) is to preserve and if possible to restore cardiac function towards normality. Evaluation of cardiovascular haemodynamics has enhanced our understanding of functional disability in cardiac patients, and provided prognostic classification.1 It is therefore important to investigate whether exercise rehabilitation following CABG is able to confer further improvements in cardiac performance as well as increasing functional capacity. Exercise rehabilitation has been reported to improve the prognosis,2 exercise capacity, and cardiac performance of patients with coronary artery disease. The levels of cardiac rehabilitation service provision within the UK are very varied.3 We have therefore investigated whether a representative hospital based supervised cardiac rehabilitation programme providing early, low level, and short term exercise training can improve the cardiac and physical functional status of patients post-CABG. We interviewed 100 patients who were on the waiting list for CABG and found that only 22 of them expressed no preference either for or against exercise rehabilitation following their surgery. They performed a familiarising cardiopulmonary exercise test. Six weeks postoperatively the patients were randomised either to attend the hospital based exercise rehabilitation programme or supervise their own recovery. Those in the rehabilitation group attended once a week for six …

Does balloon mitral valvuloplasty improve cardiac function? A mechanistic investigation into impact on exercise capacity

Procedural technical success of balloon mitral valvuloplasty (BMV) is indicated by an increase in valve area and a reduction in transvalvar gradient, but there are conflicting results regarding whether these indicators correlate with subsequent improvements in exercise capacity. We conducted a study to explore the effects of valvuloplasty on cardiac function to gain insight into the mechanisms responsible for the impact on exercise ability. Sixteen patients with mitral stenosis participated in the study and the five who did not proceed to valvuloplasty served as the control group. All patients performed maximal cardiopulmonary exercise tests before and 6 weeks after valvuloplasty (without valvuloplasty in controls). Central haemodynamics including cardiac output were measured non-invasively at rest and peak exercise. At baseline, the cardiopulmonary exercise test results were similar in the two groups. Following valvuloplasty, cardiac output did not alter at rest, but increased significantly at peak exercise (8.7+/-1.7 to 10.5+/-2.1 l min(-1), P<0.01), as did peak cardiac power output (1.88+/-0.55 to 2.28+/-0.74, P<0.05) and cardiac reserve (1.07+/-0.33 to 1.45+/-0.55 watts, P<0.05). Aerobic exercise capacity improved (13.9+/-4.2 to 16.4+/-4.3 ml kg(-1) min(-1), P<0.01) as did exercise duration (354+/-270 to 500+/-266 s, P<0.01). There were no significant changes in the controls. There was a significant correlation between the changes in peak VO(2) and changes in cardiac reserve (r=0.62, P<0.01) but not with changes in resting haemodynamics. These changes did not correlate with changes in peri-procedural mitral valve haemodynamics, despite increases in mitral valve area from 1.05+/-0.16 to 1.74+/-0.4 cm(2) (P<0.0001), accompanied by falls in the transvalvar gradient and pulmonary artery pressure (12.4+/-4.7 to 4.5+/-3 mmHg, and 26.8+/-8.4 to 17.4+/-5.2 mmHg, respectively, all P<0.0001). In conclusion, we found that successful mitral valvuloplasty in our patient cohort led to improved cardiac and physical functional capacity but not resting haemodynamics. Neither indicators of technical success nor resting haemodynamics were very reliable in predicting functional improvement.

Safe use of brain natriuretic protein to rule out the diagnosis of heart failure depends on the selection of cut off value.

The recently published National Institute for Clinical Excellence (NICE) chronic heart failure (CHF) guideline1 has recommended the use of brain natriuretic peptide (BNP) to help rule out the diagnosis of CHF, and quoted a sensitivity of 90–97%. Moreover, for purposes of medical audit, patients previously labelled as having CHF, but without a confirmation of the diagnosis, may need to be reassessed by measuring their plasma BNP concentrations. Recent papers highlighted that even BNP concentrations below accepted cut off values may actually be associated with elevated cardiovascular risk.2 When clinicians consider whether to adopt a BNP assay in the diagnostic work up of CHF, one important concern is whether the false negatives could include severe CHF cases and thereby jeopardise their subsequent care through misdiagnosis. We explored this possibility by measuring N-terminal pro-BNP (N-BNP) in a cohort of subjects including those with a confirmed diagnosis of CHF and a wide range of New York Heart Association (NYHA) functional classes and healthy volunteers. Functional cardiac status was quantitatively graded according to aerobic exercise capacity, measured by peak oxygen consumption (V˙o2).3 Although receiver operating characteristic curves and sensitivity/specificity methods are conventionally used to evaluate diagnostic techniques, for clinicians dealing with individual patients, the simpler method of plotting individual values relative to cut off values is more direct and more easily understood and is therefore employed in this study. Ninety six subjects participated in this study, including 86 consecutive stable CHF patients (diagnosed by practising heart failure specialists according to standard international and national heart failure guidelines: 64% had an underlying ischaemic aetiology, while the remainder had dilated cardiomyopathy (30%) and valve diseases) undergoing cardiopulmonary exercise testing (mean (SD) age 55.7 (12.0) years; 72 male; …

Cardiogenic Shock: Physiological and Biochemical Concepts

Because cardiogenic shock is the culmination of cumulative abnormalities in the heart and because it is associated with the most dire of prognoses, any attempt at its diagnosis and appropriate management demands a clear understanding of the pathophysiological processes involved in the individual patient. For example, treating cardiogenic shock with aggressive diuresis to reduce the central venous pressure when the shock is predominantly secondary to extensive right ventricular infarction may significantly reduce filling of the left ventricle, thereby further exacerbating the cardiogenic shock. Similarly, a misplaced attempt at alleviating the distress of severe dyspnea secondary to acute pulmonary edema by using large doses of morphine or diamorphine may result in marked respiratory depression and precipitate respiratory arrest or alternatively may reduce the arterial pressure so as to compromise the coronary perfusion further, worsening the cardiogenic shock. Erroneous concepts lead to erroneous treatment. Above all else, it is worth remembering that during cardiogenic shock, the cardiac pump is performing in an unstable state. As a mechanical pump, the heart is unusual in that its performance is somewhat dependent on its own output. When the aortic pressure that it generates falls below the critical pressure for coronary perfusion (usually a mean pressure of about 60 mm Hg), left ventricular myocardium is at risk for