Reproducibility of exercise tests in patients with symptomatic ischaemic heart disease.

This prospective study was conducted to determine the effect of Octreotide treatment on cardiovascular function in patients with active acromegaly. Ten acromegalic patients who failed to suppress growth hormone (GH) to < 5 mU/l during a 2 h oral glucose tolerance test were treated with 100 micrograms of Octreotide subcutaneously three times daily for 2 months, followed by 200 micrograms three times daily if the mean GH level was > 5 mU/l, for a total of 1 year. All patients had GH and insulin-like growth factor I (IGF-I) estimation, ejection fraction determined by Echocardiogram and multigated image acquisition scan, electrocardiogram (ECG), exercise ECG, 24-h ECG and chest x-ray. At 6 and 12 months, both GH and IGF-I were reduced but ECG, heart size and ejection fraction were unchanged. The patients improved symptomatically and had significant reduction in resting heart rate and increase in weight. Exercise time (mean +/- SD) increased from 637 +/- 137s at baseline to 787 +/- 101s at 1 year (p < 0.01) and work done increased from 9 +/- 3.3 to 11.9 +/- 2.7 metabolic equivalents (p < 0.001). We conclude that the decrease in GH and IGF-I following Octreotide treatment of acromegaly is accompanied by decreased heart rate and increased exercise capacity despite an unchanged ejection fraction.

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“…When repeated over long intervals, exercise tests show good reproducibility (26). A placebo effect cannot be discounted but seems unlikely.…”

Section: Discussionmentioning

confidence: 99%

Octreotide treatment increases exercise capacity in patients with acromegaly

Padayatty

Perrins²,

Belchetz³

1996

European Journal of Endocrinology

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“…The reduction in afterload is to some extent buffered by reflex tachycardia and peripheral vasoconstriction.22 Early exercise data suggested that nifedipine enhanced exercise capacity by a relative reduction in myocardial oxygen uptake (expressed by a lack of increase in the double product with increased performance) rather than by an increase (which would have been expressed by an increase in the double product). There has been some speculation about the possible mechanisms of the warm up effect.6 31 32 There is a near constant rate-pressure product at the threshold of angina'4 33 A recent study of patients with exertional angina who had isolated disease of the left anterior descending coronary artery showed that myocardial ischaemia was less during the second of two identical periods of pacing stress separated by [5][6][7][8][9][10][11][12][13][14][15] minutes.37 Peak coronary flow, however, was not significantly different during the second period but regional myocardial oxygen consumption was reduced; the authors attributed this result to an ischaemic faIl in contractility. Although this result does not support the suggestion that the warm up effect is due to coronary vasodilatation, it should be noted that their patients were not paced to a high rate-pressure product or to the same degree of ischaemia on the second occasion.…”

Section: Discussionmentioning

confidence: 99%

Observations on the warm up phenomenon in angina pectoris.

Joy¹,

Cairns²,

Sprigings³

1987

Heart

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SUMMARY Adaptation to exercise was investigated in 14 men aged 34-69 years (mean 51) with stable exertional angina caused by occlusive coronary artery disease. All underwent exercise electrocardiography to symptom limitation according to the Bruce protocol (first effort), and exercise to the onset of angina (warm up) followed by four minutes' rest, followed by exercise to symptom limitation (second effort). This protocol was repeated after sequential treatment for one month each with nifedipine 10mg three times a day and with timolol 10mg twice a day. Warm up significantly increased walking time to the onset of angina by 34-5% and to maximal exercise by 29-5%. The heart rate and rate-pressure product were significantly higher on second effort both at the onset of angina (by 7 0 % and 11 1% respectively) and at maximal exercise (by 10 5 % and 15A4% respectively). ST segment displacement was not significantly different after warm up. The effect of warm up on walking time to the onset of angina was markedly reduced after treatment with nifedipine but little influenced by timolol. Mean (SE) walking time after warm up on no treatment was 10 1 (0 7) min; after treatment with nifedipine it was 10 0 (0-6) min and after treatment with timolol it was 9-7 (0-4) min.These data demonstrate a substantial improvement in exercise performance after warm up and are consistent with the hypothesis that submaximal exercise in angina pectoris facilitates myocardial oxygen uptake by coronary vasodilatation.Heberden first described the loss of symptoms with continued exercise in a patient experiencing angina.2 It has been variously described; by Osler as "walking through"3 and by Wenckebach as the "second wind".4 Gallavardin recorded the "warming up" effect of previous exercise in angina pectoris5 and Price described the phenomenon as "first effort angina".6 Gallavardin claimed it was not an uncommon phenomenon' but others have been unable to demonstrate it.7 Wayne and Gaybriel described two patients whose exercise performance was enhanced when they re-exercised between five and 30 minutes after an attack of angina, the effect being lost when the interval was one hour.

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“…Similar results have been obtained when exercise tests are repeated at shorter intervals. For example, in a study designed to assess the reproducibility of exercise electrocardiography over intervals of 6 to 12 weeks in patients with stable ischaemic heart disease it was found that the reproducibility of arrhythmic events was poor (Fabian, Stolz, Janota & Ropac, 1975). In a more recent study using two identical tests separated by a period of 45 min it was shown that there was a significant reduction in the frequency of ventricular arrhythmias although there was no change in the grading of the arrhythmia (Sheps, Ernst, Briese, Lopez, Conde, Castellanos & Myerburg, 1977).…”

Section: The Exercise Electrocardiogrammentioning

confidence: 99%

The Electrocardiogram in the Assessment of the Effect of Drugs on Cardiac Arrhythmias

Reid¹

1980

Cardiovascular System

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upon Tyne NE7 7DNThe search for the ideal antiarrhythmic drug continues since none of the available agents offers optimum antiarrhythmic therapy. The continuing search coupled with the interest in the mechanisms of cardiac arrhythmias has led to the development of new techniques for the study of arrhythmias and antiarrhythmic drugs. In this article it is proposed to discuss the electrocardiographic methods used in the assessment of antiarrhythmic drugs. Firstly, to discuss the electrocardiogram in the assessment of the clinical electrophysiological properties of a drug and secondly, the electrocardiogram in the assessment of the value of the drug in the management of cardiac arrhythmias in man. Assessment of the electrophysiological effects of drugs Standard ECG intervalsThe standard electrocardiogram can give some information on the effects of a drug on automaticity and conduction velocity within the heart by analysis of the standard ECG intervals-P-P (or R-R), PR and QRS intervals (Table 1).The P-P interval reflects intrinsic sinus node function and the autonomic influences on the sinus node. Thus, any change in the P-P interval following drug administration can be a direct effect of that drug on sinus node function, or by its effect on the autonomic nervous system either directly or through reflex mechanisms. Thus, antiarrhythmic drugs such as quinidine and disopyramide can influence the P-P interval by their direct depressant effect on the sinus node, by their anticholinergic effects or by reflex autonomic changes as a result of a fall in systemic pressure.The P-R interval represents conduction through the atria, AV node and His purkinje tissue and changes in the PR interval following drug administration could reflect changes in any of these. However, because there is a difference in conduction velocity in the AV node and His purkinje system (it takes 100-120 ms for the impulse to cross the AV node and approximately 40 ms to traverse the His purkinje system), major changes in conduction in the His purkinje system have to occur before they are detected on the standard ECG run at conventional paper speeds of 25-50 mm/s. For example, a 10% change in AV nodal conduction may result in a change of 10-12 ms in PR interval, but a 10% change in His purkinje conduction will only be in the region of 4 ms. Thus, significant changes in His purkinje conduction can occur without being detected on the standard electrocardiogram.QRS duration reflects conduction through the ventricular myocardium and any change reflects changes in ventricular muscle conduction-e.g. procainamide prolongs QRS duration.Since the QT interval represents ventricular repolarization, analysis of the QT interval gives some information on the effect of the drug on ventricular repolarization time. Since repolarization time is dependent on heart rate it can be corrected for rate by formulas of Bazett (1920) or in children by that of Fraser, Froggatt & James (1964). Drugs that prolong ventricular repolarization such as amiodarone or quinidine will prolong...

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Reproducibility of exercise tests in patients with symptomatic ischaemic heart disease.

Cited by 34 publications

References 15 publications

Octreotide treatment increases exercise capacity in patients with acromegaly

Octreotide treatment increases exercise capacity in patients with acromegaly

Observations on the warm up phenomenon in angina pectoris.

The Electrocardiogram in the Assessment of the Effect of Drugs on Cardiac Arrhythmias

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