Search

We have employed a percutaneous cardiopulmonary bypass (PCPB) system during high risk interventional procedures in the cardiac catheterization laboratory. Eight patients (group 1) were elective and six (group 2) were emergencies. Group 1 (ages 39 - 80 years, mean 56 years) includes seven patients who were high risk percutaneous transluminal coronary angioplasty (PTCA) and one patient who underwent balloon aortic valvuloplasty. Group 2 (ages 54 - 80 years, mean 66 years) were in cardiogenic shock, five of whom had arrested.

SummaryThe clinical syndrome of heart failure has been investigated so extensively that it may now almost be regarded as a metabolic disorder. Although an initial insult reduces cardiac pump efficacy, the resultant physiological response culminates in complex neurohormonal dysfunction. This has created confusion and prevented the acceptance of a universal definition of cardiac failure. With much current research concentrating on the pharmacological modification of neuro-endocrine imbalance, it is easy to lose sight of the fundamental principles behind heart failure management, namely, to improve cardiac function. In attempting to achieve this, the issues of morbidity and mortality must be addressed jointly; they are not mutually exclusive entities. Discrepant results between mortality studies and changes in exercise capacity have undermined the value of exercise testing. Because a treatment enhances longevity we should not ignore its effect on symptomatic status, and likewise we should not discard a therapy, which improves function because adverse events result in occasional premature deaths. Informed patient choice must exist.Historically, exercise testing has been quintessential in our understanding and evaluation of heart failure. Peak oxygen consumption remains the best overall indicator of symptomatic status, exercise capacity, prognosis and hospitalisation. Unfortunately, muddling of surrogate and true end-points has confused many of these issues. Improved comprehension may be gained by applying the concept of cardiac reserve which has been described in a variety of heart conditions and used in cardiac failure patients to provide an indication of prognosis and functional capacity.

This study evaluated the efficacy of computer-controlled closed-loop delivery of a new synthetic catecholamine, arbutamine, when given to induce myocardial ischemia detected by electrocardiography and echocardiography with a high (10 beats/min/min) and low (6 beats/min/min) rate of increase in heart rate (heart rate slope) in 70 patients with coronary artery disease. The electrocardiographic sensitivity for the detection of myocardial ischemia was 52% for the low slope and 51% for the high slope. The corresponding figures for echocardiographic sensitivity were 83% and 79% for the low and high slopes, respectively. There were no significant differences in changes from baseline to maximum in pharmacodynamic variables, although the mean times to reach maximum heart rate and systolic blood pressure were 1.4 minutes shorter (p=0.001) and 3.7 minutes shorter (p<0.05), respectively, for the high-slope regimen. The duration of the infusion was shorter (p<0.001) for the high slope. In this study, closed-loop arbutamine administration was effective and safe in the detection of coronary artery disease for both heart rate slope regimens.

Objective To investigate whether physiological cardiac reserve can be measured in man without invasive procedures and whether it is a major determinant of exercise capacity. Design Development of method of measurement and an observational study. Setting A regional cardiothoracic centre. Subjects 70 subjects with a wide range of cardiac function, from heart failure patients to athletes. Methods Subjects underwent treadmill, symptom limited cardiopulmonary exercise tests to measure aerobic exercise capacity (represented by |$$|APVo ₂max) and cardiac reserve. Cardiac output was measured non-invasively using the CO ₂ rebreathing technique. Results Cardiac power output (CPO _max) at peak exercise was found to be significantly related to aerobic capacity: CPO _max (W) = 0.35 + 1.5|$$|APVo ₂max (l/min), r = 0.87, p &lt; 0.001. It also correlated well with exercise duration (r = 0.62, p &lt; 0.001), suggesting that cardiac reserve is a major determinant of exercise capacity. In the study, cardiac reserve ranged from 0.27 to 5.65 W, indicating a 20-fold difference between the most impaired cardiac function and that of the fittest subject. Conclusions A non-invasive method of estimating physiological cardiac reserve was developed. The reserve was found to be a major determinant of exercise capacity in a population of normal subjects and patients with heart disease. This method may thus be used to provide a clearer definition of the extent of cardiac impairment in patients with heart failure.

The haemodynamic effects of intravenous cyclizine, an antiemetic that is widely given with opioids in left ventricular failure and myocardial infarction, were studied in 11 patients with severe heart failure. Cyclizine significantly increased systemic and pulmonary arterial pressures, and right and left ventricular filling pressures, and negated the venodilatory effects of diamorphine. The use of cyclizine in patients with heart failure should, therefore, be avoided.