Raised concentrations of plasma atrial natriuretic peptides in cardiac transplant recipients.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to L B Tan.
Explore the source record for details and available documents.
Every cardiac pump has its own maximum performance, which denotes its pumping capability. The difference between the performance in the resting state and that at maximum is called pumping reserve. Cardiac pumping performance is therefore best quantified by its hydraulic power output. Cardiac pumping capability is predictive of the ultimate prognosis of patients in severe heart failure whereas pumping reserve is a major determinant of exercise capacity. The therapeutic efficacy of cardiotonic drugs used in the treatment of ambulant heart failure patients should be evaluated with reference to the way they alter the relation between cardiac pumping reserve and exercise capacity.
A recently proposed analytical technique to determine whether an inotropic agent improves cardiac pumping performance via its vasodilatory or its positive inotropic effects was adopted to evaluate the pharmacological properties of a positive inotropic agent, dobutamine, and a vasodilatory calcium antagonist, felodipine, in patients with severe heart failure. This technique used a new principle of pump-load interaction, which states that for a given change in vascular input impedance unaccompanied by any direct alteration in the pumping characteristics all possible values of pump power output due to the change in impedance per se are confined within two calculated limits. When dobutamine was infused at 10 micrograms.kg-1.min-1 seven out of 10 patients had power output values above the defined limits, implying that the technique can identify correctly in vivo the direct positive inotropic effects of dobutamine in the presence of its vasodilating activity. In contrast, when 5-10 mg of felodipine was given to 10 patients the consequent power outputs were all within the defined limits, implying that the effects can be explained by vasodilatation alone. In conclusion, this study showed that the analytical technique can be applied clinically to detect the presence of drug induced positive inotropic effects in the midst of vasodilatation and therefore may be useful in determining whether inotropic agents actually improve cardiac function via their positive inotropic effects.
Dopexamine is a novel compound that has DA1-dopaminergic and beta 2-adrenergic agonist properties capable of producing beneficial systemic and renal vasodilation. The acute haemodynamic effects in 10 patients with low-output-state ischaemic cardiac failure (NYHA IV) were recorded before (control) and during graded incremental doses of dopexamine infusion from 0.5 to 6.0 micrograms/kg/min. Dopexamine produced a marked increase in cardiac index from 1.6 +/- 0.2 (control) to a maximum of 2.8 +/- 0.4 L/min/m2 (p less than 0.001) primarily by inducing vasodilation, with reduction in systemic vascular resistance from 1,720 +/- 136 (control) to 1,116 +/- 136 dynes.s.cm-5 (p less than 0.05). Using a more sophisticated analytical technique which enables us to separate direct inotropic from vasodilatory effects, we were able to identify, in eight of the patients, a direct dopexamine-induced positive inotropism. These beneficial central haemodynamic effects of dopexamine, when coupled with its known DA1-dopaminergic agonist property, indicate that dopexamine may have a place in the management of patients in severe heart failure.
An attempt was made to stratify risk of subsequent cardiac events in post-infarct patients according to a combination of the results of clinical assessment, routine diagnostic investigations, and pre-discharge exercise testing in 350 consecutive patients who were followed up for one year. Patients were classified prospectively on the basis of the extent of myocardial damage as assessed by peak enzyme release, reciprocal change on the electrocardiogram at the time of myocardial infarction, Norris prognostic index, ability to perform a pre-discharge exercise test (and test result), and ability to tolerate beta adrenergic blockade on discharge. Of the 50 patients with contraindications to pre-discharge exercise testing, 26% died or had reinfarctions compared with 9% of the 300 exercised patients; the 24 non-exercised patients with evidence of extensive myocardial damage or reciprocal changes on the electrocardiogram were particularly at risk. Similarly, among the 300 exercised patients, extensive myocardial damage, reciprocal change on the electrocardiogram, and ST depression on exercise testing were the major risk markers in that each identified at least 75% of the patients who had subsequent cardiac events. The 63 exercised patients who had all three of these major risk markers constituted a high risk group: 18 (29%) died or had reinfarction. Of the remaining 237 patients, only 9 (4%) had cardiac events. The 35 high risk patients with exercise induced angina pectoris or clinical contraindications to beta blockade were particularly at risk; 15 (43%) died or had reinfarction. This approach to risk stratification identified a small cohort of high risk patients in a large population of myocardial infarction survivors; it also identified a large group with a very low risk of subsequent cardiac events.
Previous open studies have suggested that felodipine, a selective calcium antagonist and vasodilator, may be useful in the treatment of heart failure. A double blind placebo controlled crossover trial was therefore conducted to investigate the clinical and haemodynamic effects of felodipine in 15 patients with chronic ischaemic heart failure in New York Heart Association symptom class III. Felodipine significantly increased resting and exercise (25W bicycle ergometry) cardiac output without producing concomitant changes in resting or exercise heart rate or right and left ventricular filling pressures. Felodipine did not significantly improve symptom scores or exercise capacity in the group as a whole. It also resulted in significant fluid retention as shown by a rise in ankle circumference, body weight, and a fall in haematocrit. Further research is required to elucidate the mechanism that is responsible for the discrepancy between the haemodynamic and clinical effects of felodipine in patients with moderately severe heart failure.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In 63 patients with severe acute or chronic heart failure maximum cardiac performance was determined by calculation of the maximum hydraulic power output achieved by the heart during dobutamine challenge. After one year, all but 3 of the 23 patients with maximum cardiac power output (Wmax) less than the normal resting value of 1 W had died of progressive heart failure. Of the 40 with Wmax more than 1 W, all but 4 (who died suddenly) survived longer than one year. Hydraulic power output is a clinically important measure of cardiac pumping performance and a maximum power output value below the normal resting value indicates that long-term survival is unlikely.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A 76 year old man developed a left pneumothorax after implantation of a permanent endocardial pacemaker via the left subclavian vein. The resulting surgical emphysema caused temporary failure of the pacing system.
Explore the source record for details and available documents.
The management of toxic shock syndrome poses a challenge to clinicians because the syndrome has only been recently recognized and new complications are still being described. This report describes the major complications which arose in our case and highlights a severe bleeding disorder which was the cause of the patient's death. The bleeding disorder was characterized by normal in vitro coagulation screens, normal platelet aggregation tests, but prolonged skin bleeding time. It was not improved by haemodialysis, platelet transfusion or steroid therapy. We conclude that in cases with severe toxaemia, despite early recognition and appropriate treatment, there is still no effective method of preventing complications. Current avenues for investigation include plasmapheresis, the administration of fresh frozen plasma, and the development of a specific anti-toxin.
Explore the source record for details and available documents.
Explore the source record for details and available documents.