Effect of repetitive episodes of exercise induced myocardial ischaemia on left ventricular function in patients with chronic stable angina: evidence for cumulative stunning or ischaemic preconditioning?

BACKGROUND: Myocardial stunning is known to occur following a single episode of effort angina in patients with coronary artery disease. The effect on left ventricular (LV) function of repeated episodes of ischaemia is unknown. OBJECTIVES: To investigate the effects of repeated episodes of exercise induced ischaemia on LV function in patients with chronic stable angina. METHODS: Patients with significant coronary artery disease and normal LV function underwent two episodes of symptom limited treadmill exercise separated by three different time intervals: either 30 minutes (group A, n = 14); 60 minutes (group B, n = 14); or 240 minutes (group C, n = 14). Quantitative stress echocardiography was performed at repeated intervals between the two exercises and for 240 minutes following the second test. RESULTS: For all groups there was no difference between the degree of ischaemia judged by maximal ST depression during the two tests. All episodes of exercise induced ischaemia produced prolonged abnormalities of LV systolic and diastolic function despite rapid normalisation of haemodynamic and ECG changes. In group A (30 minutes) these abnormalities were less pronounced after the second test than after the first, while in group B (60 minutes) they were more severe and long lasting. In group C (240 minutes) the two tests produced similar abnormalities of LV function. CONCLUSIONS: Prolonged abnormalities of LV function occurred following exercise induced ischaemia with a time course consistent with myocardial stunning. The severity and degree of LV dysfunction caused by a further episode of ischaemia appear to be dependent on the time interval between ischaemic episodes.     

Increase of plasma levels of beta-endorphin during maximum bicycle ergometry effort in sedentary and trained subjects

Plasmatic levels of beta-endorphin during maximal graded bicycle stress test were measured by RIA on extracted plasma in 10 well-trained (A group) and in 8 untrained subjects (C group). Blood samples were obtained at rest, at peak work load and at the third, 10th and 90th min of recovery. For every stress test the following were evaluated: exercise time, maximum work load, total work load, maximum double product and mean K (an index of velocity of heart rate recovery during the first three minutes after the exercise). Both groups A and C showed a significant rise in beta-endorphin activity at the third minute of recovery; the increase was significantly greater in trained rather than in sedentary subjects (p less than 0.01). Beta-endorphin release was closely related to mean K; no relationship was found between exercise time, maximum work load, total work load, maximum double product and beta-endorphin rise. Our data shows that a release of beta-endorphin occurs during the initial phase of recovery after a maximal stress test; beta-endorphin rise is greater in trained subjects and correlates with the speed of heart rate recovery, but has no relationship with the duration and the grade of the effort. Whether beta-endorphin increase plays a role in the rapid decrease of adrenergic tone which occurs after exercise or represents a secondary phenomenon remains to be determined.     

Adaptation to effort myocardial ischemia]

BACKGROUND. During PTCA it has been observed that in two sequential coronary occlusions, the second is characterized by less subjective anginal discomfort, less ST segment depression, less myocardial lactate production and lower mean pulmonary pressure than that recorded during the first inflation. The phenomenon is known as "cardiac adaptation to ischemia". PTCA, as a model for controlled, reversible myocardial ischemia must be viewed in a substantially different context from other models concerning different types of ischemia. The purpose of our investigation was to examine the hypothesis that phenomena similar to those observed during PTCA can occur during effort ischemia. METHODS. Six patients with stable effort ischemia, fixed ischemic threshold (bpm x mmHg variability less than 3200) and fixed recovery period (variability of time at ST on isoelectric line less than 1 min and variability of rate-pressure product at ST on isoelectric line less than 2000 bpm x mmHg) were studied. Our aim was to study the ischemic threshold (IT) and the recovery period in an exercise test performed a short time after an initial one. The programme consisted of: 1) exercise test at a fixed load (the load was predetermined by the level of ischemia reached in a previous multistage exercise test); 2) exercise test ending at ST decreases 1 mm; 3) recovery period; 4) 2nd exercise test similar to the first one and ending at ST decreases 1 mm, to be performed 3 minutes after the end of recovery period (that is, 3 minutes after ST on isoelectric line). In both exercise tests we registered rate-pressure product at ischemia (RPPI), time to ischemia (TI), rate-pressure product at ST on isoelectric line (rate-pressure product at normalization: RPPN) and time at ST on isoelectric line (time of normalization: TN). RESULTS. [table: see text] In all pts RPPI in the second exercise test was similar to RPPI registered in the first one, while RPPN in the second exercise test was higher than in the first. In the second exercise test, time to ST on isoelectric line was also shorter. CONCLUSIONS. We think that the shorter recovery period from myocardial ischemia in the second exercise test may be an expression of a "cardiac adaptation to ischemia", a phenomenon which has been previously observed during PTCA.     

Electrophysiological study of young patients with exercise related paroxysms of palpitation: role of atropine and isoprenaline for initiation of supraventricular tachycardia.

Electrophysiological studies were performed in eight patients (four men and four women, mean (SD) age 24 (5) years with paroxysmal attacks of palpitation during or immediately after exercise. Five patients were competitive athletes at college. In two patients spontaneous supraventricular tachycardia during exercise was recorded by ambulatory electrocardiographic monitoring and in another it was induced by treadmill exercise testing. Two had dual atrioventricular nodal pathways, three had manifest atrioventricular accessory pathways, and three had concealed atrioventricular pathways. Programmed stimulation induced sustained supraventricular tachycardia in six patients--in two after intravenous injection of atropine sulphate (1 mg) and in four during infusion of isoprenaline (0.01 microgram/kg/min). In one patient, non-sustained atrioventricular nodal reentrant tachycardia was induced during isoprenaline infusion. In the remaining patient, who had dual atrioventricular nodal pathways, tachycardia was not inducible. AH block prevented maintenance of reentry in five patients. In five patients shortening of the effective refractory period of the atrioventricular node with atropine (one patient) and isoprenaline (four patients) caused sustained supraventricular tachycardia. The present study indicates that treatment with atropine and isoprenaline may be an important factor in the initiation of supraventricular tachycardia in patients with exercise related paroxysms of palpitation.     

Electrophysiological study of young patients with exercise related paroxysms of palpitation: role of atropine and isoprenaline for initiation of supraventricular tachycardia

Electrophysiological studies were performed in eight patients (four men and four women, mean (SD) age 24 (5) years with paroxysmal attacks of palpitation during or immediately after exercise. Five patients were competitive athletes at college. In two patients spontaneous supraventricular tachycardia during exercise was recorded by ambulatory electrocardiographic monitoring and in another it was induced by treadmill exercise testing. Two had dual atrioventricular nodal pathways, three had manifest atrioventricular accessory pathways, and three had concealed atrioventricular pathways. Programmed stimulation induced sustained supraventricular tachycardia in six patients--in two after intravenous injection of atropine sulphate (1 mg) and in four during infusion of isoprenaline (0.01 microgram/kg/min). In one patient, non-sustained atrioventricular nodal reentrant tachycardia was induced during isoprenaline infusion. In the remaining patient, who had dual atrioventricular nodal pathways, tachycardia was not inducible. AH block prevented maintenance of reentry in five patients. In five patients shortening of the effective refractory period of the atrioventricular node with atropine (one patient) and isoprenaline (four patients) caused sustained supraventricular tachycardia. The present study indicates that treatment with atropine and isoprenaline may be an important factor in the initiation of supraventricular tachycardia in patients with exercise related paroxysms of palpitation.     

平板运动试验诱发心律失常的特点分析

目的:分析平板运动试验诱发心律失常的特点。方法:选择1654例患者应用标准Bruce方案进行次极量或极量平板运动试验,同步监测12导联心电图和血压,记录运动前、运动中及恢复期的心电图和血压。结果:运动试验阳性304例,阴性1350例;运动诱发心律失常共234例,诱发率14.1%;阳性者心律失常60例(60/304,19.7%),明显高于阴性者174例(174/1350,12.9%,P0.01)。运动诱发偶发室早146例(8.8%),明显多于偶发房早52例(3.1%,P0.05)。运动诱发的心律失常185例(79.1%)在运动中和/或恢复期前期(前3min)出现,多于恢复后期(后3min)出现的49例(20.9%,P0.05)。运动诱发的心律失常在恢复期前期(前3min)/或恢复期后期(后3min)消失的(80.3%,188/234)明显多于超过6min消失的(19.7%,46/234,P0.05)。其中1例持续性室性心动过速者通过用药才能消失。结论:运动试验阳性者易诱发心律失常,以室性心律失常最为常见。运动诱发的心律失常多在运动中和/或恢复期前期出现,且大多可在恢复期消失,但有些严重的心律失常较难消失。     

Adaptation to the stress of tachycardia in patients with coronary artery disease: insight into the mechanism of the warm-up phenomenon

Adaptation to exercise or the "warm up phenomenon" has been observed in some patients with angina pectoris. To investigate adaptation, eleven patients with exertional angina pectoris and angiographic evidence of coronary artery disease underwent two identical bouts of sequential tachycardia stress separated by a brief recovery period. Manifestations of ischemia were less during the second stress, as evidenced by a reduction in the severity of angina pectoris, less ST segment depression, and improved lactate extraction. Peak coronary blood flow during the second stress (81 +/- 20 ml/min) was not significantly different from that during the first (95 +/- 32 ml/min). Regional myocardial oxygen consumption, however, was significantly (p = .03) lower during the second stress (8.8 +/- 2.4 ml O2/min) when compared with the first (11.4 +/- 3.0 ml O2/min). Thus, patients with coronary artery disease can develop anginal tolerance to the stress of tachycardia similar to that observed after repeated bouts of exercise. A relative reduction in myocardial oxygen consumption, rather than an increase in coronary blood flow, appears to account for this phenomenon.     

Prolonged left ventricular dysfunction occurs in patients with coronary artery disease after both dobutamine and exercise induced myocardial ischaemia

OBJECTIVE: To determine whether pharmacological stress leads to prolonged but reversible left ventricular dysfunction in patients with coronary artery disease, similar to that seen after exercise. DESIGN: A randomised crossover study of recovery time of systolic and diastolic left ventricular function after exercise and dobutamine induced ischaemia. SUBJECTS: 10 patients with stable angina, angiographically proven coronary artery disease, and normal left ventricular function. INTERVENTIONS: Treadmill exercise and dobutamine stress were performed on different days. Quantitative assessment of systolic and diastolic left ventricular function was performed using transthoracic echocardiography at baseline and at regular intervals after each test. RESULTS: Both forms of stress led to prolonged but reversible systolic and diastolic dysfunction. There was no difference in the maximum double product (p = 0.53) or ST depression (p = 0.63) with either form of stress. After exercise, ejection fraction was reduced at 15 and 30 minutes compared with baseline (mean (SEM), -5.6 (1.5)%, p < 0.05; and -6.1 (2.2)%, p < 0. 01), and at 30 and 45 minutes after dobutamine (-10.8 (1.8)% and -5. 5 (1.8)%, both p < 0.01). Regional analysis showed a reduction in the worst affected segment 15 and 30 minutes after exercise (-27.9 (7.2)% and -28.6 (5.7)%, both p < 0.01), and at 30 minutes after dobutamine (-32 (5.3)%, p < 0.01). The isovolumic relaxation period was prolonged 45 minutes after each form of stress (p < 0.05). CONCLUSIONS: In patients with coronary artery disease, dobutamine induced ischaemia results in prolonged reversible left ventricular dysfunction, presumed to be myocardial stunning, similar to that seen after exercise. Dobutamine induced ischaemia could therefore be used to study the pathophysiology of this phenomenon further in patients with coronary artery disease.     

Effect of quinapril on the attenuated heart rate recovery of type 2 diabetic subjects without known coronary artery disease

BACKGROUND: Heart rate (HR) recovery at 1 min is a measure of the vagal reactivation that occurs after cessation of exercise. Despite ample evidence about the association of attenuated HR recovery with increased mortality, pharmacologic modification of this predictor has not been shown. On the other hand, angiotensin-converting enzyme (ACE) inhibitors are known to have vagomimetic activity. HYPOTHESIS: We hypothesized that ACE inhibition would increase HR recovery in a group of subjects known to have reduced HR recovery, namely diabetics. METHODS: Maximal treadmill exercise stress test was performed in 31 type 2 diabetic and 31 nondiabetic male subjects with similar age, body mass index, and hypertensive status. None of the subjects had known heart disease or evidence of myocardial ischemia during the test. The diabetic subjects, after 2 weeks of treatment with quinapril, underwent a second exercise test. A third test was performed 2 to 3 weeks after cessation of quinapril treatment. RESULTS: At baseline, despite similar exercise capacity, the diabetics had a lower HR recovery at 1 min than nondiabetics (25 +/- 8 vs. 31 +/- 8 beats/min, p < 0.01). Quinapril significantly increased HR recovery at 1 min in diabetics (25 +/- 8 beats/min at baseline vs. 28 +/- 8 beats/min with quinapril vs. 25 +/- 7 beats/min off-therapy, p < 0.01 by analysis of variance). CONCLUSIONS: The attenuated HR recovery of type 2 diabetics can be improved by quinapril. Whether the improvement in HR recovery with ACE inhibition can lead to decreased mortality is currently unknown.     

Value of the isoprenaline test in arrhythmogenic heart diseases

The sympathetic nervous system seems to play a major role in the genesis of ventricular arrhythmias. The authors studied this adrenergic factor prospectively by exercise stress testing and intravenous isoprenaline in 107 patients referred for evaluation of arrhythmias or symptoms thought to be due to arrhythmias: 30 patients had morphologically normal hearts (15 ventricular extrasystoles, 15 bursts of ventricular tachycardia); 55 patients had dilated cardiomyopathy and 22 had probable or proven arrhythmogenic right ventricular dysplasia. Exercise testing was carried out with 30 watt increments every 3 minutes. Ventricular tachycardia was induced in 6 patients with apparently normal hearts (17%), 13 patients with dilated cardiomyopathy (31%) and 7 patients with arrhythmogenic right ventricular dysplasia (40%). Isoprenaline was infused for 3 minutes at a dose of 8-12 g/min: ventricular tachycardia was induced in 7 patients with apparently normal hearts (24%) and 23 patients with dilated cardiomyopathy. In some patients presenting with syncope, an arrhythmogenic response to isoprenaline was the only abnormality detected by the study protocol. An arrhythmia was induced by isoprenaline in 17 of the 18 patients with confirmed right ventricular dysplasia (94%), 12 of whom had sustained mono or polymorphic ventricular tachycardia. Two of these patients did not have significant right ventricular wall motion abnormalities. Four asymptomatic subjects related to patients with right ventricular dysplasia underwent the isoprenaline test; bursts of ventricular tachycardia were recorded in 3 of them. Polymorphic ventricular tachycardia was specifically associated with cardiac disease. The maximum heart rate attained by exercise testing (148 +/- 19/min) was higher than that attained with isoprenaline (148 +/- 22/min).(ABSTRACT TRUNCATED AT 250 WORDS)     

Antidromic reciprocating rhythm in Wolff-Parkinson-White syndrome precipitated by a ventricular extrasystole arising at the emergence of the preexcitation pathway

A 9 year old child was investigated for attacks of wide QRS complex tachycardia occurring exclusively during the daytime and favoured by exercise or stress, with ventricular extrasystoles of the same form occurring between attacks. Endocavitary investigation showed a concealed atrioventricular accessory pathway during sinus rhythm with anterograde 1/1 conduction up to 270/min; retrograde conduction was not so good with block occurring at 175/min. The spontaneous tachycardia was reproduced by catecholamine infusion: it was an antidromic reciprocating rhythm triggered by a ventricular extrasystole of identical form to that of a pure preexcitation complex and to that of the tachycardia complexes. Spontaneous termination of attacks always occurred when conduction from the ventricle to the atria stopped. The attacks could be induced by ventricular extrastimuli when they caused an increment in retrograde conduction time resulting from retrograde conduction up the nodohisian pathway and not the Kent bundle. The tachycardia could also be initiated by atrial extrastimuli providing pure pre-excitation could be obtained. In both cases, retrograde conduction of the nodohisian pathway had to be improved by catecholamines. When the patient was given betablocker therapy the attacks of tachycardia completely disappeared. The association of ventricular extrasystoles and antidromic reciprocating rhythm and their morphological identity suggest that these extrasystoles were in fact automatic activity of the Kent bundle. Escape phenomena as signs of passive automatism have been described in this conditions but, to our knowledge, extrasystoles suggesting an active automatic process have not been previously reported.     

Idiopathic orthostatic tachycardia. Etiology, diagnosis and treatment

For nearly a century, physicians have been aware of a syndrome consisting of a relatively stereotyped presentation, usually in young patients, who complain of fatigue, malaise and effort intolerance, sometimes of trembling and weakness of the lower limbs. This is associated with an excessive tachycardia in the orthostatic position. This syndrome has recently been called idiopathic orthostatic tachycardia. The tilt test has enabled "quantification" of normal responses. Patients complaining of the symptoms described above and which, during the first minutes of orthostatism, increase their heart rates by more than 30 beats per minute or attain a rate of at least 110/min, are considered to be suffering from this syndrome. The physiopathology is not clear but, globally, there seems to be two sub-groups, the first considered to be a partial dysautonomic disorder and the second, the result of hypersensitivity of the beta-receptors. Besides the tilt test, the diagnosis can also be presumed after an excessive tachycardia response to an intravenous infusion of 1 microgram/min of isoprenaline. The treatment of these patients is uncertain as there is no single approach which is always effective. In addition to "simple" but essential advice, a number of drugs may be used although there is no means of predicting the efficacy of the result in a given patient. A major principle should be emphasised: ablation of the sinus node for inappropriate tachycardia may eliminate the only compensatory mechanism of autonomic dystonia and make the patients even more symptomatic than they were.     

Diastolic time during recovery from upright exercise in persons without heart disease

To assess the relation between heart rate and diastolic time (cardiac cycle minus electromechanical systole) during the recovery period from upright exercise, 12 normal volunteers were studied immediately after and 2 and 5 minutes after exercise in the upright position. Although heart rate was significantly lower at 5 minutes compared with 2 minutes after exercise (106 vs 116 beats/min), there was significant shortening of diastolic time (from 251 to 230 ms) and total diastole per minute (from 28,634 to 24,220 ms/min). The explanation of this phenomenon appears to be disproportionate lengthening of diastolic time at 2 minutes after exercise, which must represent physiologic response due to increased left ventricular filling as well as continuing adrenergic effects, which would be diminished at 5 minutes. This lengthening of diastolic time also would maintain decreased subendocardial blood flow caused by increased end-diastolic volume.     

Diagnostic value of the isoproterenol test in effort tachycardia

An isoproterenol test was performed in 69 patients during electrophysiological investigation to assess its diagnostic value in adrenergic supraventricular or ventricular tachycardia. Sixteen control subjects had no symptoms on exercise and routine exercise stress testing did not trigger any hyperexcitability. Sixteen patients had reproducible documented supraventricular tachycardia induced by exercise (13 paroxysmal junctional tachycardias, 3 focal atrial tachycardias). Eight patients had ventricular hyperexcitability related to effort. Twenty-nine patients had supraventricular and/or ventricular hyperexcitability only at rest. Electrophysiological investigations included paired atrial stimulation during sinus rhythm and paced rhythm followed by programmed ventricular stimulation using one and then two extrastimuli delivered during sinus rhythm and paced ventricular rhythm. These stimulation studies were carried out under basal conditions and then during low dose isoproterenol infusion (10 to 40 micrograms) which accelerated the heart rate to 130/mn. Electrophysiological and conduction parameters and the mode of induction of the tachycardia (defined as at least 5 successive echos with a configuration similar to the clinical tachycardia) were studied. We observed an acceleration of anterograde and retrograde conduction and a shortening of the effective atrial and ventricular refractory periods but these changes were found equally in the different groups of patients and were not related to the induction of tachycardias. The induction of paroxysmal junctional tachycardia by isoproterenol was a very sensitive (92%) and specific (100%) diagnostic method. Its diagnostic value was much greater than Holter monitoring (25%) and exercise stress testing (12.5%). Induction of ventricular tachycardia by isoproterenol was also very sensitive (75%) and specific (95%). The diagnostic value was higher than exercise stress testing (71%) and Holter monitoring (62%). Isoproterenol did not affect the induction of spontaneous tachyarrythmias unrelated to effort and even suppressed the triggering of some episodes. In conclusion, the induction by atrial or ventricular pacing or spontaneous supraventricular or ventricular tachycardia during isoproterenol infusion was very specific and correlated with the concept of tachycardia induced by exercise and therefore of adrenergic nature. The sensitivity of this test was excellent in patients with supraventricular tachycardia (95%) and very good in ventricular tachycardia (75%). On the other hand, the changes in the electrophysiological parameters were not specific for a group of patients.     

The reproducibility of heart rate recovery after treadmill exercise test

Background: Although predictive value of heart rate recovery (HRR) has been tested in large populations, the reproducibility of HRR in treadmill exercise test has not been assessed prospectively. This prospective study examined whether HRR index has test–retest stability in the short term. Methods: A total of 52 healthy volunteers without cardiovascular risk factors (mean age, 30 ± 10 years, 30 females) underwent standardized graded treadmill exercise test, and the test was repeated on the 7th and the 30th days. The subjects’ maximal heart rates and the decrease of heart rate from the peak exercise level to the level of 1, 2, 3, 4, and 5 minutes after the termination of the exercise were examined on each test, and heart rates for each minute from the first, second, and third tests were compared for each individual. Results: The maximal heart rates on the 1st, 7th, and the 30th days were 179 ± 11, 177 ± 10, 178 ± 10 beats/min, respectively [P = 0.07, intraclass correlation coefficient (ICC) = 0.92], and the 1st minute HRR indices after peak exercise were 33 ± 10, 33 ± 10, 33 ± 11, respectively (P = 0.66, ICC = 0.88). There was no statistical difference in the 2nd, 3rd, 4th, and 5th minute heart rates of the recovery phase among the 1st, 7th, and 30th day treadmill exercise tests, either. Conclusion: Maximal heart rates and the decline of heart rate to the 5th minute on recovery phase after treadmill exercise test have short‐term reproducibility. Ann Noninvasive Electrocardiol 2011;16(4):365–372     

Usefulness of transesophageal electrophysiological study during the ergometric test in the evaluation of supraventricular paroxysmal tachycardia occurring during exertion

Transesophageal electrophysiologic study has recently been proposed for the evaluation of supraventricular arrhythmias. In this report we present 13 cases, with palpitations occurring only during effort, due to a suspected supraventricular tachycardia, in which the usefulness of the transesophageal electrophysiologic study performed during stress test was evaluated. Of these 13 patients, nine were male and four were female, mean age was 29 yrs. Twelve cases had no heart disease, one had a moderate mitral valve insufficiency. Nine cases had a normal ECG, four had a WPW pattern. In 9/13 cases no significant arrhythmia was ever documented, in 1/13 ventricular premature beats were present in the basal ECG, in 1/13 a atrial fibrillation and in 2/13 a supraventricular reciprocating tachycardia was recorded. In all cases a maximal exercise test and a 24-hour Holter monitoring were performed. In all pts a transesophageal electrophysiologic study was performed both at rest and during extra-stimuli and incremental atrial pacing. The end point of transesophageal study was the induction of a sustained (greater than 30") supraventricular tachycardia. RESULTS. Maximal exercise test was negative in 11/13 cases; it showed ventricular premature beats in one case and initiated a supraventricular tachycardia in one. The 24 hour Holter monitoring was negative in 12/13 cases while it showed frequent ventricular premature beats in one. Resting transesophageal electrophysiologic study revealed dual A-V nodal pathways in six pts: in one of them a junctional re-entry was induced; in two a single echo beat was observed, while in three no reentry was observed. In three cases a supraventricular tachycardia was induced which was sustained in one and unsustained (7" and 24") in two cases. In 4 cases transesophageal electrophysiologic study gave no information. Transesophageal stimulation during exercise induced a greater than 30" reciprocating tachycardia in all patients, at work loads of 30-180 watts. Six pts had an intranodal tachycardia (V-A less than 70 msec) a further six pts had a atrioventricular tachycardia involving a Kent bundle (V-A greater than or equal to 70 msec), which was concealed in two, and one had a atrial tachycardia. In four cases (3 with intranodal and 1 with atrioventricular tachycardia), exercise transesophageal study was repeated after chronic therapy with betablockers (sotalol 240 mg/die or metoprolol 200 mg/die). In all cases, after therapy, the induced tachycardia had a longer cycle and in two cases it was induced at a higher work load. In a further two cases flecainide (200 mg/die) was tested. In one case (with atrial tachycardia), the arrhythmia was no longer inducible after therapy, in another case (with intranodal tachycardia) the drug had no effect. CONCLUSIONS. In patients with paroxysmal supraventricular tachyarrhythmias occurring during effort the basal ECG is normal or shows a WPW pattern. The maximal exercise test and 24 hour Holter monitoring give no information in over 90% of cases.(ABSTRACT TRUNCATED AT 400 WORDS)     

Reproducibility of the Dobutamine-Atropine Echocardiography Stress Test

To assess the reproducibility of dobutamine-atropine echocardiography testing, two studies (1 to 20 days apart [mean 3.3 days]) were performed in 23 patients with stable effort angina pectoris or chest pain. During the study, 20 (87%) patients were receiving beta blockers alone or combined with nitrates or calcium antagonists. Dobutamine was infused at doses of 10 μg/kg per minute every 3 minutes up to a maximum of 40 μg/kg per minute and this maximal dose was continued for 6 minutes. In patients not achieving 85% predicted maximal heart rate or myocardial ischemia, atropine (0.25–1 mg) was added and dobutamine continued for another 3 minutes, until either an adequate heart rate was achieved or the test was considered positive. During dobutamine infusion, electrocardiographic, echocardiographic, and blood pressure monitoring were obtained in each patient. Side effects including tremor, nausea, palpitation, dizziness, headache, and nonsustained ventricular tachycardia occurred in three patients. The same symptoms, but no ventricular tachycardia, developed during the same stage of the second test. Angina pectoris (eight patients), electrocardiographic changes (six patients), and ischemic wall-motion abnormalities (six patients) were observed at the same stage of the two tests. The mean values of heart rate, blood pressure, and rate-pressure product were comparable for each stage in duplicate tests. Our data show that pharmacological stress echocardiography using dobutamine-atropine has good reproducibility and provides a useful tool for assessing disease progression and the effects of therapeutic interventions in patients with coronary artery disease.     

Effects of Myocardial Perfusion on QT Dispersion in Patients with Hypertrophic Cardiomyopathy

Background: In patients with hypertrophic cardiomyopathy (HCM), myocardial ischemia and myocardial fibrosis as well as ventricular tachyarrhythmia are frequently observed. An increase of heterogeneity of repolarization provided the development of ventricular tachyarrhythmia. The aims of the present study are to evaluate the influence of exercise‐induced myocardial perfusion abnormalities on QT dispersion and to assess whether QT dispersion was involved in ventricular tachycardia (VT) in patients with HCM. Methods: Thirty‐eight patients with HCM and 20 control subjects underwent an exercise stress test, and QT intervals were measured pre‐exercise and at 3 minutes after peak exercise. All subjects underwent thallium (TI)‐201 stress myocardial imaging, and their TI‐201 defect score and exerciseinduced myocardial ischemia were evaluated. Results: Twelve patients (31%) revealed sustained or nonsustained VT. The pre‐exercise QTc dispersion (QTcD) was significantly correlated with the Tl‐201 defect score (r = 0.61, P < 0.0001). The QTcD at 3 minutes after peak exercise was significantly greater in patients with exerciseinduced myocardial ischemia than without exercise‐induced myocardial ischemia (96 ± 36, 72 ± 24 ms^1/2, P < 0.03). The QTcD at 3 minutes after peak exercise was significantly greater in patients with VT than without VT (111 ± 23, 64 ± 17 ms^1/2, P < 0.0001). Conclusion: It is suggested that the degree of myocardial fibrosis influences the pre‐exercise QTcD, and exercise‐induced myocardial ischemia precipitates the increase in the QTcD at 3 minutes after peak exercise in patients with HCM. The increased QTcD at 3 minutes after peak exercise may play a role in identifying patients at a potentially higher risk. A.N.E. 2000;5(1):60–67     

Post-prandial worsening of angina: all due to changes in cardiac output?

BACKGROUND--The precise mechanism leading to the post-prandial worsening of angina has yet to be adequately defined. It has been attributed to an increase in double product but is perhaps more likely to be related to an increase in cardiac output after food. This study was designed to evaluate the effects of food on patients' exercise tolerance and compare these with changes in haemodynamic variables. METHODS--23 patients with chronic stable angina who had post-prandial worsening of their angina were studied. The patients were evaluated on two occasions and at each visit they underwent two symptom limited treadmill exercise tests. They remained fasting on the first visit and were given a 1400 kcal meal 60 minutes before the second exercise test on the second visit. Time to onset of 1 mm ST segment depression, heart rate, systemic arterial blood pressure, and cardiac output were measured at rest and during exercise. RESULTS--There were no differences in any of the variables during the two exercise tests on the day the patients remained fasting. After the meal exercise tolerance fell significantly by 136 seconds and the stage at which 1 mm ST segment depression was first seen was also significantly reduced. Resting cardiac output increased significantly by 0.86 1/min with the patients sitting and by 0.89 1/min standing. The exercise times after food were significantly related to cardiac output even when fasting times were taken into account. Resting heart rate increased significantly by 8.3 beats per minute sitting and 10.4 beats per minute standing. There was little change in blood pressure and no evidence that the double product predicted the post-prandial exercise time. CONCLUSIONS--Worsening of angina was related to the increase in cardiac output after a meal and successful treatment will depend upon the prevention of this increase.     

Post-prandial worsening of angina: all due to changes in cardiac output?

BACKGROUND--The precise mechanism leading to the post-prandial worsening of angina has yet to be adequately defined. It has been attributed to an increase in double product but is perhaps more likely to be related to an increase in cardiac output after food. This study was designed to evaluate the effects of food on patients' exercise tolerance and compare these with changes in haemodynamic variables. METHODS--23 patients with chronic stable angina who had post-prandial worsening of their angina were studied. The patients were evaluated on two occasions and at each visit they underwent two symptom limited treadmill exercise tests. They remained fasting on the first visit and were given a 1400 kcal meal 60 minutes before the second exercise test on the second visit. Time to onset of 1 mm ST segment depression, heart rate, systemic arterial blood pressure, and cardiac output were measured at rest and during exercise. RESULTS--There were no differences in any of the variables during the two exercise tests on the day the patients remained fasting. After the meal exercise tolerance fell significantly by 136 seconds and the stage at which 1 mm ST segment depression was first seen was also significantly reduced. Resting cardiac output increased significantly by 0.86 1/min with the patients sitting and by 0.89 1/min standing. The exercise times after food were significantly related to cardiac output even when fasting times were taken into account. Resting heart rate increased significantly by 8.3 beats per minute sitting and 10.4 beats per minute standing. There was little change in blood pressure and no evidence that the double product predicted the post-prandial exercise time. CONCLUSIONS--Worsening of angina was related to the increase in cardiac output after a meal and successful treatment will depend upon the prevention of this increase.