The heart rate performance curve and left ventricular function during exercise in patients after myocardial infarction

PURPOSE: The aim of the study was to investigate the heart rate turn point (HRTP) in the time course of the heart rate performance curve (HRPC) in patients after myocardial infarction, and the relationship between the HRTP, the left ventricular function, and the second lactate turn point (LTP2). METHODS: We studied the degree and the direction of the HRPC and the left ventricular ejection fraction (LVEF) in 49 male patients 57 +/- 8 d after their first posterior wall infarction (MI). An incremental cycle ergometer test was performed and three phases of energy supply were defined (I: aerobic; II: aerobic-anaerobic transition; III: anaerobic) via blood lactate LA concentration. HRTP and LVEF-turn points (LVEFTP) were assessed by linear turn point analysis. The degree and direction of the deflection of HRPC were described as factor k (k > 0.1: downward deflection; -0.1 < k < 0.1: linear time curse; k < -0.1: upward deflection). The LVEF was determined by RNA. The difference between Pmax and LTP2 was calculated for LVEF (delta LVEF). RESULTS: An HRTP could be found in 44 and a LVEFTP in 47 cases. The HRTP occurred at 85 +/- 17 Watt (W), which correlated (r = 0.95; P < 0.001) with the LTP2 (84 +/- 17 W) and the LVEFTP (84 +/- 17 W, r = 0.93; P < 0.001). From LTP2 to Pmax a significant decrease in LVEF was found. There was a correlation between the percentage of HRmax at the HRTP and k (r = 0.70), as well as delta LVEF (r = 0.56). CONCLUSIONS: To prevent myocardial overloading, it seems to be useful to determine the HRTP, which indicate the workload where LVEF decreases.     

Prognostic significance of silent myocardial ischaemia during maximal exercise testing after a first acute myocardial infarction

Clinical, exercise, and angiographic variables, and long-term follow-up were compared in patients, who, during maximal Bruce exercise testing after a first acute myocardial infarction (AMI), had positive responses to exercise testing (n = 116, 38% of 303) with (n = 23, group I) or without (n = 93, group II) angina. Group I patients more often (52 vs 19%, P < 0.001) had a history of pre-infarction angina. Group II had a greater proportion (75 vs 52%, P < 0.05) of inferior wall AMI, whereas group I had a greater proportion (30 vs 19%, P < 0.01) of non-Q wave AMI. Total exercise duration was significantly (P < 0.01) longer in group II (7.6 +/- 3.2 vs 5.5 +/- 3.1 min). Maximal exercise heart rate (144 +/- 22 vs 133 +/- 21, beats.min-1 P < 0.05) was also higher in group II. A greater proportion of group II patients (37 vs 9%, P < 0.05) had single-vessel disease, whereas multivessel disease was more common (91 vs 63%, P < 0.03) in group I. Left ventricular function was similar in both groups. During follow-up (48 +/- 22 months) the incidence of cardiac death (group I, 3.3%, group II, 4.8%), of recurrent infarction (group I, 4.8%, group II 3.3%), and of revascularization procedures (group I, 28.5%, group II, 19.8%) were similar in both groups. Although asymptomatic exercise-induced ischaemia was associated with better exercise performance and less extensive coronary disease than symptomatic ischaemia, it had the same long-term prognostic implications.     

Hemodynamic effects of thiothixene and chlorpromazine in schizophrenic patients at rest and during exercise

The hemodynamic effects and plasma levels of noradrenaline were studied in schizophrenic patients at rest and during exercise after long-term treatment with chlorpromazine (150-600 mg daily) and thiothixene (60-80 mg daily). The results are compared with those from previous studies in untreated patients and patients receiving very large doses of chlorpromazine. The effects of thiothixene on the different hemodynamic variables were very moderate, and the observed differences between this group and the control group may be due to the different patient materials. In the two groups of patients receiving chlorpromazine, the heart rate at rest and durng exercise tended to be higher than in the control group. There was also a tendency towards a lower stroke volume after this drug and thiothixene during exercise. The noradrenaline levels in plasma were highest after the high dose of chlorpromazine both at rest and during exercise, while they were lower after the moderate chlorpromazine dose. After thiothixene, the values were between those of the group on the low chlorpromazine dose and those of the control group.     

Occurrence of sustained increase in QT dispersion following exercise in patients with residual myocardial ischemia after healing of anterior wall myocardial infarction

Our objective was to evaluate the effect of exercise on QT dispersion over the next 3 hours, as seen on a standard 12-lead electrocardiogram in patients with healed myocardial infarction with or without residual ischemia. We measured QT and QTc dispersion before, immediately after, and 1 and 2 hours after symptom-limited, dynamic treadmill exercise tests in 28 patients with healed anterior wall myocardial infarction with (group I, n = 18) and without (group II, n = 10) residual ischemia. The same protocol was followed in 5 group I patients after successful performance of coronary angioplasty. QT and QTc dispersion did not change immediately after exercise in group II. These parameters increased in group I (QT dispersion at rest [mean +/- SD] 57 +/- 22 ms, and after exercise 87 +/- 27 ms; QTc dispersion at rest 62 +/- 25 ms, and after exercise 114 +/- 36 ms). The increases in QT and QTc dispersion were sustained for at least 2 hours. After a successful coronary angioplasty in 5 patients, these parameters no longer increased with exercise. Thus, QT dispersion increased for at least 2 hours after exercise in patients who had residual ischemia after healing of myocardial infarction. Data obtained in 5 of these patients after coronary angioplasty support the idea that residual ischemia plays a key role in the sustained increase in QT dispersion after exercise.     

Cardiorespiratory effects of breathing and relaxation instruction in myocardial infarction patients

The effect of individual instruction in relaxation and breathing, additional to an exercise training program, was investigated in 76 post-myocardial infarction patients after rehabilitation and at 3 months follow-up. Respiration rate (RR), heart rate (HR) and respiratory sinus arrhythmia (RSA) were the outcome variables used to compare experimental (exercise plus relaxation) and control (exercise without relaxation) groups. HR and RR decreased slightly during 20-min sessions of supine measurement. This response did not vary between sessions (pre-rehabilitation, post-rehabilitation and after 3-month follow-up). RSA tended to decrease during the sessions. The within-session reduction in RSA became more apparent in the control group after treatment and less so in the experimental group. RR decreased in the experimental group after rehabilitation, but not in the control group. HR decreased for all patients, but the decrease was larger in the experimental group. This effect was associated with the lower RR. RSA did not change in the control group but increased in the experimental group, during both normal and deep breathing. This effect was also associated with a slower RR and became marginally significant when RR was statistically controlled for. We conclude that the relaxation intervention induced a slower breathing pattern which was associated with beneficial effects on resting HR and RSA. Further study is warranted to clarify the degree to which reduced respiration rate is an indicator of lower sympathetic arousal or merely a concomitant of the learned breathing technique.     

Predicting severe ischemic events after uncomplicated myocardial infarction by exercise testing and rest and exercise radionuclide ventriculography

BACKGROUND: In 183 patients with uncomplicated myocardial infarction, exercise-induced angina, ST segment depression, decrease in ejection fraction, or inadequate increase in systolic blood pressure and low exercise tolerance were significantly associated with 4-year incidence of hard ischemic events. METHODS AND RESULTS: Only the onset of both ST segment depression and a decrease in left ventricular ejection fraction with exercise was an independent predictor. ST segment depression and decrease in left ventricular ejection fraction had low sensitivity (61% and 70%) and specificity (56% and 51%) for hard ischemic events, but specificity increased to 78% when both were present. During medical therapy, 22 of 53 patients with both ST segment depression and a decrease in left ventricular ejection fraction with exercise had an ischemic event (i.e., 48.1% 4-year probability on Kaplan-Meier analysis vs 19.2% in the remaining 130 patients [p < 0.0005]). CONCLUSIONS: Even if no single variable, derived from exercise testing, is a highly sensitive and specific predictor, specificity increases to a clinically relevant level by combining ST segment depression and a decrease in left ventricular ejection fraction with exercise, and in this way patients with recent infarction may be selected for coronary arteriography.     

Dipyridamole stress echocardiography and exercise testing for risk stratification after uncomplicated myocardial infarction

BACKGROUND: Risk stratification for subsequent cardiac events after an acute infarction can be obtained by exercise testing or dipyridamole stress echocardiography. It remains to be determined whether these modalities are equivalent and provide incremental information on top of clinical evaluation. The aim of our study was to compare the prognostic information obtained early after an acute uncomplicated myocardial infarction of high dose dipyridamole coupled with echocardiography (stress echo) or maximal symptom-limited exercise testing. METHODS AND RESULTS: Ninety patients underwent dipyridamole stress echo and exercise testing at a mean +/- SD of 9 +/- 4 days after admission for acute uncomplicated first myocardial infarction. All patients were prospectively followed for 22 +/- 16 months. There were 9 hard events (3 cardiac deaths and 6 acute myocardial infarctions) and 12 soft events due to post MI angina (6 angioplasty and 6 bypass surgery procedures). Univariate predictor of hard events was rest-stress wall motion score index variation (p = 0.009); univariate predictors of all events (hard + soft) were: positive exercise testing (p = 0.001), positive stress echo (p = 0.001), rest-stress wall motion score index variation (p = 0.002), extent of ischemia at echo (p = 0.008). Multivariate analysis by Cox selected a non-Q wave infarction and rest-stress wall motion score index variation as predictors of death or reinfarction (overall chi-square for the model 12.2, p = 0.0022). CONCLUSIONS: Stress echo is superior to ergometric variables for predicting events after uncomplicated myocardial infarction.     

Clinical applications of signal-averaged electrocardiography in patients after myocardial infarction

In conclusion, signal-averaged electrocardiography is a useful, noninvasive technique to identify patients after myocardial infarction at risk for future arrhythmic events, especially in conjunction to existing tools, such as 24 hour ambulatory monitoring, echocardiography, nucleotide angiography and coronary angiography. It has a limited positive predictive value, but has an excellent negative predictive value. The optimum time to do signal-averaged electrocardiograms after myocardial infarction is unclear, 6 to 14 days after myocardial infarction has the highest sensitivity. Time domain analysis remains the most common method used to record late potentials. The definition of late potential and the scoring of a high resolution electrocardiogram as normal and abnormal have not yet been resolved. The criteria proposed by the Task Force Committee of the European Society of Cardiology, the American Heart Association and the American College of Cardiology (see introduction) should be observed at present. Many studies on signal-averaging were done in the prethrombolytic era. In patients who have received thrombolytic therapy, the positive predictive value of signal-averaged electrocardiograms has decreased. There are other limitations in applying signal averaging technique. The faster the ventricular tachycardia is induced in electrophysiological studies, the shorter is the late potential. Thus, a faster tachycardia which causes sudden cardiac death may not be detected by late potentials. The management strategies for patients who have abnormal signal-averaged electrocardiograms after myocardial infarction have not be defined. One should note that any management strategy has to prove that it improves prognosis. More prospective, randomized clinical trials are required to address these issues.     

Two-level spinal stenosis in minipigs. Hemodynamic effects of exercise

STUDY DESIGN: Twenty-two G?ttingen minipigs were trained to run on a treadmill. Two-level lumbar spinal stenosis was created in 12 pigs, 10 were unoperated control subjects. Blood flow of the spinal cord and nerve roots was determined with microspheres at rest, during exercise, and after exercise. OBJECTIVES: To study the effect of lumbar spinal stenosis and exercise on blood flow of spinal neural tissue. SUMMARY OF BACKGROUND DATA: Neurogenic claudication, the key symptom of lumbar spinal stenosis, may be caused by vascular impairment or mechanical distress of neural tissue during exercise. Experimental compression of the cauda equina causes reversible nerve root edema, stasis, blood flow decrease, and compromised neural function. The vascular pathophysiology of spinal stenosis during exercise has not been studied previously. METHODS: Pigs were trained daily for 3 months. Two-level 25% lumbar spinal stenosis was introduced by placement of stenosing bands around the dural sac. Neurologic function was monitored before surgery by evoked potentials and after surgery by the Tarlov score. Regional blood flow in lumbosacral neural tissue was measured 3 days after chronic catheterization using microspheres at rest, during exercise at 3 km/h for 15 minutes, and at rest 30 minutes after exercise. RESULTS: Blood flow of grey and white matter increased during exercise in both groups, with no differences between groups. slight hyperemia prevailed after exercise in white matter of the stenotic area but not in grey matter. Nerve root blood flow was largely unchanged in control subjects during exercise but was reduced in spinal stenosis at rest, further depressed during exercise, and normalized after exercise. Dural blood flow was elevated throughout. CONCLUSION: The study suggests that exercise-induced impairment of spinal nerve root blood flow plays a role in the pathophysiology of neurogenic claudication.     

Changes in smoking behavior after a myocardial infarction.

Among 383 myocardial infarction (MI) patients, 230 (mean age 54.2 yrs) smoked at the time of the MI. 40.6% had resumed smoking 6 mo after the MI, whereas 49.4% smoked at a 3–5 yr follow-up. Resumption of smoking within 6 mo was associated with increased anxiety and depression during the 1st weeks after discharge, less cardiac health knowledge, and less severe MI. In Ss who relapsed later, resumption was associated with decline in general cardiac health knowledge and in correct understanding of smoking as a risk factor. Long-term changes in smoking status were related to previous heart disease, premorbid work instability, age, and severity of MI. Antismoking counseling of MI patients should not be limited to health risks associated with smoking, and training in coping with negative affect without smoking may be valuable in promoting smoking cessation. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effect of percutaneous transluminal coronary angioplasty on exercise in patients with and without previous myocardial infarction

Improvement in exercise capacity is an important clinical effect of percutaneous transluminal coronary angioplasty (PTCA), and was assessed in patients with and without previous myocardial infarction (MI) undergoing PTCA. We prospectively followed patients with exercise testing before and 2 weeks after angioplasty in 415 patients, 170 (41%) of whom had a previous MI. A third exercise test was performed 20 +/- 2 weeks after PTCA in 403 patients. From left ventricular angiography obtained before PTCA, regional dyskinesia was classified into anterior or posterior locations. Both patients with and without previous MI had a significant increase in exercise capacity from before to 2 and 20 weeks after PTCA (previous MI: 31.9% and 29.3%; no MI: 50.7% and 38.2%; p <0.0001 [analysis of variance]). In patients with MI and anterior dyskinesia, in whom lesions on the left anterior descending artery were dilated or posterior dyskinesia in whom lesions on the right coronary artery were dilated, exercise capacity increased significantly from before to 2 and 20 weeks after PTCA (left anterior descending artery: 53.1% and 39.7%, p <0.0001; right coronary artery: 16.9% and 27.6%, p = 0.01 [analysis of variance]). Multivariate regression analysis revealed that male sex, no previous MI, and dilation of left anterior descending artery were significantly associated with increased exercise capacity after angioplasty adjusted for age and smoking habits, whereas left ventricular ejection fraction and end-diastolic pressure were not associated with increased exercise capacity.     

Long-term prognosis of young patients after myocardial infarction in the thrombolytic era

BACKGROUND: Myocardial infarction (MI) in young adults is a rare event. In the Framingham study, the 10-year incidence rate of MI per 1,000 was 12.9 in men 30-34 years old. Overall, 4-8% of patients with acute MI are < or = 40 years old. HYPOTHESIS: It was the purpose of this study to assess the in-hospital and long-term morbidity and mortality in patients < or = 40 years old with acute myocardial infarction compared with older patients in the thrombolytic era. METHODS: A consecutive series of 75 patients aged < or = 40 years (mean 35.0 +/- 4.8) with acute myocardial infarction was compared with an equally sized group of patients aged > 40 years (mean 65.1 +/- 9.8). RESULTS: Thrombolysis or direct percutaneous transluminal coronary angioplasty was performed in 52 versus 24% (p = 0.0004) and 5.3 versus 2.7% (p = NS) in younger and older patients, respectively. Significantly fewer young patients had multivessel disease (28 vs. 64%, p < 0.004). No in-hospital mortality was observed in patients with reperfusion therapy irrespective of age. After a mean followup time of 47 +/- 35 months, cardiac mortality was 0 and 11% (p < 0.03), respectively, in young and older patients with, and 3 versus 24% (p < 0.02) without reperfusion therapy, respectively. In addition, significantly fewer patients in the younger age group developed recurrent angina pectoris (12 vs. 39%, p = 0.0004) or congestive heart failure (9 vs. 34%, p = 0.0005) irrespective of reperfusion therapy. CONCLUSION: Our observations demonstrate that long-term prognosis after myocardial infarction in young patients is excellent in the thrombolytic era.     

Alpha-adrenergic blockade improves recovery of myocardial perfusion and function after coronary stenting in patients with acute myocardial infarction

BACKGROUND: AMI reperfusion by thrombolysis does not improve TIMI flow and LV function. The role of infarct-related artery (IRA) stenosis and superimposed changes in coronary vasomotor tone in maintaining LV dysfunction must be elucidated. METHODS AND RESULTS: Forty patients underwent diagnostic angiography 24 hours after thrombolysis. Seventy-two hours after thrombolysis, the culprit lesion was dilated with coronary stenting. During angioplasty, LV function was monitored by transesophageal echocardiography. Percent regional systolic thickening was quantitatively assessed before PTCA, soon after stenting, 15 minutes after stenting, and after phentolamine 12 microg/kg IC (n=10), the alpha1-blocker urapidil 600 microg/kg IV (n=10), or saline (n=10). Ten patients pretreated with beta-blockers received urapidil 10 mg IC. Coronary stenting significantly improved thickening in IRA-dependent and in non-IRA-dependent myocardium (from 27+/-15% to 38+/-16% and from 40+/-15% to 45+/-15%, respectively). Simultaneously, TIMI frame count decreased from 39+/-11 and 40+/-11 in the IRA and non-IRA, respectively, to 23+/-10 and 25+/-7 (P<0.05). Fifteen minutes after stenting, thickening worsened in both IRA- and non-IRA-dependent myocardium (to 19+/-14% and 28+/-14%, P<0.05), and TIMI frame count returned, in both the IRA and non-IRA, to the values obtained before stenting. Phentolamine and urapidil increased thickening to 36+/-17% and 41+/-14% in IRA and to 48+/-11% and 49+/-17% in non-IRA myocardium respectively, and TIMI frame count decreased to 16+/-6 and to 17+/-5, respectively. Changes were attenuated with beta-blocker pretreatment. CONCLUSIONS: Our finding that alpha-adrenergic blockade attenuates vasoconstriction and postischemic LV dysfunction supports the hypothesis of an important role of neural mechanisms in this phenomenon.     

Hemodynamic effects of dobutamine after cardiopulmonary bypass in children

The synthetic inotropic agent, dobutamine, has reportedly increased cardiac output in adults after cardiopulmonary bypass with minimal side effects. Its use in children, after surgical correction of congenital heart disease, was tested by infusing the drug at 1, 4, 7, and 10 micrograms/kg x min in 11 children. While significant increases in cardiac index above control (23, 23, and 16% at 4, 7, and 10 micrograms/kg x min, respectively) were observed, this was achieved at the expense of significant increases in heart rate (15, 24, and 10%). This increase in heart rate (47% in one child) necessitated discontinuing the infusion in 4 subjects. There were also significant increases in systolic and mean blood pressure with no change in stroke volume or peripheral vascular resistance. The authors conclude that in children, dobutamine is an effective inotropic agent acting principally by stimulating beta 1-receptors in the myocardium producing a predominantly chronotropic effect without significant changes in peripheral vascular resistance. Given the intrinsically higher heart rate of children, the levels of tachycardia produced by the drug in some instances reach unacceptable levels and as such, may make dopabutamine unsuitable for use in children after cardiopulmonary bypass.