Postexercise changes in ejection fraction associated with coronary artery disease

Radionuclide measurement of left ventricular ejection fraction (LVEF) response to exercise has been proposed as a way to help identify patients with coronary artery disease (CAD). Previous studies were done using an exercise bicycle or a treadmill and showed that patients with CAD do not increase ejection fraction (EF) to the same extent as normal (control) subjects. The present studies were done using a coaxial Gamma Cor cardiac probe. Because radiocardiograms (RCG) obtained with the cardiac probe require 1/10 the dose required for a scintillation camera, serial measurements could be made before, during and following exercise. Although 3 of our 9 patients showed an unchanged and 3 showed a decreased EF at the time of maximal exercise, 3 others were able to increase their EF, and in 2 this increase occurred concomitantly with angina. Thus, not all the CAD patients could be identified by failure to increase EF in response to exercise. However, looking at the period just following exercise, one can see that most of our patients with CAD maintain or increase LVEF during the first 6 to 9 min after stopping exercise; normal (control) subjects rapidly return to the preexercise value. The normal pattern is an increase in EF during exercise followed by a prompt return toward normal after cessation of exercise. Changes of this normal pattern of EF increase and decrease occurred in all except 1 patient with CAD, and consequently provided a better indication of the presence of significant disease than the response during exercise alone.     

Food in chronic heart failure: improvement in central haemodynamics but deleterious effects on exercise tolerance.

Food has been known to have significant central haemodynamic effects for over half a century; it causes an increase in cardiac output and a fall in systemic vascular resistance. These changes are potentially desirable in patients with chronic heart failure but how they relate to exercise tolerance is unknown. This study was designed to examine the haemodynamic effects of food with changes in exercise capability in a group of patients with chronic heart failure. Fifteen patients with chronic heart failure and 10 normal control subjects were studied. They underwent treadmill exercise testing whilst fasting and after a standardized meal. Measurements were made of symptom-limited exercise tolerance, cardiac output, limb blood flow and respiratory gases. Superior mesenteric artery blood flow was measured fasting and postprandially only. Despite an increase in cardiac output, at rest and during exercise, which was not, however, as great as that in the control subjects, the symptom-limited exercise tolerance of the patients fell by 37 s postprandially (P < 0.05). Superior mesenteric artery blood flow increased postprandially by a mean of 133 ml.min-1 (P < 0.05) in the patients and 424 ml.min-1 (P < 0.01) in the control subjects. Calf blood flow increased in both groups during exercise, but there was no change in limb blood flow when comparisons were made between the fasting and postprandial states. The normal postprandial increase in oxygen consumption did not occur in the patients although their minute ventilation was higher than the control subjects (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Core and peripheral temperature response to exercise in patients with impaired left ventricular function.

OBJECTIVE--Exercise induced hypotension is a specific but insensitive indicator of severe coronary artery disease. Skin blood flow is subject to control by baroreceptor mediated reflexes as well as thermoregulatory reflexes. Monitoring skin temperature or the skin to central temperature gradient may be a more sensitive indicator of impaired cardiac output response to exercise than hypotension. DESIGN AND PARTICIPANTS--Central and skin temperature changes associated with exercise were studied in 10 normal volunteers and eight patients with impaired resting ventricular function due to ischaemic heart disease. Patients exercised according to a modified Bruce protocol. The two sample independent t test was applied to compare the central and peripheral temperatures in the two groups at three minute intervals during exercise and at two minute intervals after exercise. RESULTS--A significant decrease was found in mean (1 SEM) central temperature on exercise in our patient group (98.2(0.2) degrees F to 97.2(0.3) degrees F), compared with the normal increase in central temperature (97.7(0.2) degrees F to 98.3(0.3) degrees F). Mean (1 SEM) skin temperature changes reflected the expected skin blood flow changes with exercise in normal subjects. In the patient group skin temperature declined during exercise (89.7(2.1) degrees F to 86.6(1.7) degrees F) and was significantly lower than normal from six minutes onwards. CONCLUSIONS--The abnormal peripheral temperature changes of patients with impaired resting ventricular function is an early and sensitive indicator of an abnormal haemodynamic response to exercise. It is possible that skin temperature measurement during exercise could help detect exercise induced ventricular dysfunction due to ischaemia or impaired cardiac output due to valvar heart disease.     

Distribution of myocardial blood flow in the exercising dog with restricted coronary artery inflow.

The effect of a proximal coronary artery stenosis on transmural myocardial blood flow during exercise was studied in nine dogs with electromagnetic flowmeter probes and hydraulic occluders on the left circumflex coronary artery. Regional myocardial blood flow at rest and during treadmill exercise was estimated with radioactive microspheres 7-10 mum in diameter. Exercise studies were performed during unrestricted coronary artery inflow (control exercise) and during partial inflation of the occluder to a level which did not reduce flow at rest but which limited the increase in flow during exercise to 66 +/- 6% (mild restriction) or 44 +/- 3% (severe restriction) of the value during control exercise. Mean myocardial blood flow at rest was 0.94 +/- 0.06 ml/min per g of myocardium and increased to 2.45 +/- 0.15 ml/min per g during control exercise, with uniform distribution across the wall of the left ventricle. Flow to the subepicardial myocardium was significantly greater during exercise in the presence of a mild restriction than during control exercise, whereas flow to deeper layers of myocardium was progressively decreased below the control level. A similar pattern of redistribution of flow occurred during exercise in the presence of a severe restriction, but flow to all transmural layers was below that during mild restriction, resulting in more marked subendocardial underperfusion. Thus, exercise in the presence of stenosis resulted in transmural redistribution of myocardial blood flow with subendocardial underperfusion in proportion to the degree of restriction of coronary artery inflow.     

Noninvasive evaluation of cardiac function in patients with ischemic heart disease by the subclavian arterial blood flow response to exercise.

To evaluate cardiac function, the regional blood flow of the subclavian artery as a parameter of cardiac output was measured instead of measuring cardiac output itself in 12 normal subjects and 17 patients with ischemic heart disease. The measurement of the subclavian arterial blood flow was continuously and noninvasively made utilizing the Doppler ultrasonic flowmeter before, during and after exercise. The exercise was performed in the upright position on a bicycle ergometer for 3 minutes at the work load of 230 Kpm/min. Delta F Ratio, that is, the ratio of the increased blood flow during the exercise to the increased blood flow during the first 3 minutes after the termination of the exercise, was calculated in all subjects. Delta F Ratio as well as the response pattern of the blood flow to exercise was investigated. In patients with ischemic heart disease, the increase in the subclavian arterial blood flow during the exercise was slow, and the time required to return to the pre-exercise level was remarkably prolonged in comparison with normal subjects. The mean delta F Ratio of the younger normal group was 7.43, and that of the older normal group was 5.53. While in patients with ischemic heart disease, markedly lower values were observed. The mean delta F Ratio of the following subgroups of patients with ischemic heart disease, the myocardial infarction group, the angina pectoris group, and the group of ischemic heart disease without pain, were 1.25, 1.97, and 2.52 respectively. The difference in the mean delta F Ratio between the older normal group and each subgroup of ischemic heart disease was statistically significant. Low delta F Ratio in patients with ischemic heart disease is supposed to be the manifestation of diminished cardiac reserve due to decreased myocardial contractility. As a simple parameter of cardiac output, the continuous measurement of the subclavian arterial blood flow by the Doppler flowmeter is a useful method for the noninvasive evaluation of cardiac function. Especially, the calculation of delta F Ratio may provide the numerical presentation of cardiac function.     

Effect of respiration on variations of central venous blood temperature

We examined the course of right ventricular blood temperature before, during and after treadmill exercise in three patients with implanted cardiac pacemakers, and in two healthy volunteers. Temperature measurements were performed with a specially developed 5F electrode with an incorporated thermistor (measurement accuracy: 1/100 degrees C). After electronic amplification, the temperature signals were recorded on a three-channel strip chart recorder, together with ECG and respiration (measured by impedance plethysmography). In one of the volunteers, blood flow in the jugular and femoral veins was recorded by Doppler sonography, before and after exercise. We observed a decrease in central venous blood temperature with inspiration and an increase with expiration before, during and after exercise. The amplitudes of the variations became smaller during exercise, reached a maximum immediately after exercise and returned to their resting values within a few minutes after the end of exercise. We suppose different distributions of venous blood flow in different phases of the respiratory cycle to be the reason for the respiration-induced variations in central venous blood temperature. Under exercise conditions, the influence of respiration on the blood flow in the larger veins is small compared to the influence of an increased cardiac output; at rest, respiration has a more pronounced effect on venous blood flow. The analysis of our blood flow measurements in the femoral and jugular veins supported this assumption.     

Prevalence and significance of postexercise hypotension in apparently healthy subjects

Although a decrease in systolic blood pressure (BP) occurring during treadmill exercise is often a sign of severe left ventricular dysfunction, the prevalence and significance of postexertional hypotension is unclear. The postexercise systolic BP response to maximal treadmill exercise was analyzed in 781 asymptomatic volunteers, aged 21 to 96 years (mean 51 +/- 16) from the Baltimore Longitudinal Study on Aging. Fifteen subjects (1.9%) had a postexercise decrease in systolic BP of at least 20 mm Hg from preexercise sitting values, to a level of 90 mm Hg or less. The prevalence of postexercise hypotension was 3.1% (14 of 449) in subjects younger than 55 years, but only 0.3% (1 of 332) in those older than 55 (p less than 0.01). Before exercise these 15 subjects demonstrated a slight orthostatic decrease in systolic BP of -1.7 +/- 4.8 mm Hg compared with an increase of 5.3 +/- 5.1 mm Hg in age-matched control subjects (p less than 0.001). The lowest systolic BP averaged 78 +/- 9 mm Hg (range 62 to 90) and occurred between 4 and 9 minutes after exercise in 80% of cases. All but 3 episodes were symptomatic, with dizziness dominant. In only 2 subjects was the hypotension associated with vagal symptoms and bradycardia. Compared with control subjects, subjects with postexercise hypotension had higher maximal heart rates (184 +/- 15 vs 173 +/- 11 beats/min, p less than 0.05), but showed no difference in exercise tolerance or systolic BP at submaximal or maximal effort. Postexercise ST-segment abnormalities suggesting ischemia occurred in one-third of the hypotensive subjects but none of the control subjects (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Regulation of myocardial blood flow by oxygen consumption is maintained in the failing heart during exercise

The hemodynamic abnormalities and neurohumoral activation that accompany congestive heart failure (CHF) might be expected to impair the increase in coronary blood flow that occurs during exercise. This study was performed to determine the effects of CHF on myocardial oxygen consumption and coronary blood flow during exercise. Coronary blood flow was measured in chronically instrumented dogs at rest, during 2 stages of graded treadmill exercise under control conditions (n=10), and after the development of CHF produced by 3 weeks of rapid ventricular pacing (n=9). In the normal dogs, coronary blood flow increased during exercise in proportion to the increase in the heart rate x the left ventricular systolic blood pressure product (RPP). After the development of CHF, resting myocardial blood flow was 25% lower than normal (P<0.05). Myocardial blood flow increased during the first stage of exercise, but then failed to increase further during the second stage of exercise despite an additional increase in the RPP. Myocardial oxygen consumption during exercise was significantly lower in animals with CHF and paralleled coronary flow. Despite the lower values for coronary blood flow in animals with CHF, there was no evidence for myocardial ischemia. Thus, even during the second level of exercise when coronary flow failed to increase, myocardial lactate consumption continued and coronary venous pH did not fall. In addition, the failure of coronary flow to increase as the exercise level was increased from stage 1 to stage 2 was not associated with a further increase in myocardial oxygen extraction. Thus, cardiac failure was associated with decreased myocardial oxygen consumption and failure of oxygen consumption to increase with an increase in the level of exercise. This abnormality did not appear to result from inadequate oxygen availability, but more likely represented a reduction of myocardial oxygen usage with a secondary decrease in metabolic coronary vasodilation.     

Effects of physical stress on complete blood count and venous blood gas profile of individuals with sickle cell trait.

The association between sickle cell trait (SCT) and adverse effects of exercise has been controversial. While individuals with SCT are at higher risk of sudden death, the mechanism for this outcome remains to be elucidated. In order to shed light on this controversy, we have monitored venous blood count and blood gas parameter values in normal and SCT subjects during treadmill exercise. White and red blood cell counts and hemoglobin changed significantly over time in both the SCT and normal groups, with peak exercise values different from pre-exercise or post-exercise values. Red blood cell counts showed significant group-time interaction; increase in count during exercise was accentuated in SCT subjects. All blood gas parameters showed significant changes over time in both groups. O2 content was significantly higher in SCT than AA at all time intervals. O2 saturation, pO2 and CO binding to hemoglobin showed significant group-time interaction. Furthermore, O2 saturation for the combined groups was significantly greater at peak exercise and at rest than before exercise. It is possible that treadmill exercise causes microvascular shunting in SCT subjects, leading to a decrease in the peripheral utilization of oxygen.     

Changes in transthoracic electrical impedance during submaximal treadmill exercise in patients with ischemic heart disease--A preliminary report.

Twenty normal subjects and 32 patients with ischemic heart disease (IHD) were subjected to submaximal treadmill exercise. The mean transthoracic electrical impedance (TEI) was measured with a tetrapolar lead system and the changes were correlated to the extent of ST depression observed on an on-line digital computer. Six subjects of pre-excitation syndrome with "false" ST depression were also studied. The normal subjects did not show a significant change of TEI during exercise. The patients with IHD showed a steady and significant decrease in TEI, correlating with the extent of ST depression. Recovery was slow after the cessation of exercise. The subjects with false ST changes showed no decrease of TEI. The changes were more profound in subjects who developed anginal pain during the test. These findings are attributed to an increase in the thoracic blood volume and pulmonary extravascular water due to transient left ventricular dysfunction in angina.     

Attenuation of exercise-induced ST depression during combined isometric and dynamic exercise in coronary artery disease

ST-segment depression was measured during submaximal dynamic (treadmill) and combined isometric-dynamic (isodynamic) exercise at comparable rate-pressure products in 11 patients (mean age 63 years) with stable coronary artery disease who were participating in an exercise training program. Each patient completed 3 separate trials. Trial 1 (baseline) was a submaximal treadmill exercise test to determine the threshold heart rate-systolic blood pressure (rate-pressure product) for ST-segment depression (greater than or equal to 1.0 mm). During trials 2 and 3, patients performed (in random order) dynamic treadmill exercise and isodynamic exercise (treadmill walking 1.5 to 2.0 mph carrying 15 to 25 kg) until threshold rate-pressure product was achieved. During trial 1, each patient showed significant ST depression (mean 1.7 mm) at target rate-pressure product (mean 18,200). Subsequent dynamic exercise trials 2 and 3 showed similar mean ST depression (1.5 mm) and rate-pressure product (18,000). During isodynamic exercise trials 2 and 3, subjects showed only minimal ST depression (mean 0.4 mm) at a rate-pressure product similar to dynamic exercise (mean 18,590). Heart rates were significantly lower (-10/min) and systolic (+20 mm Hg) and diastolic (+25 mm Hg) pressure was higher during isodynamic exercise (p less than 0.05). The rate-pressure product is not a valid index of ST response during isodynamic exercise in stable exercise-trained cardiac patients. Attenuation of ST depression during isodynamic exercise may be attributed to a combination of increased diastolic perfusion pressure, decreased heart rate and possibly to reductions in venous return and ventricular diastolic wall tension due to increased intrathoracic and abdominal pressure.     

Exercise and antihypertensive therapy

The effects of exercise on central hemodynamic mechanisms and the changes induced by treatment have been studied invasively in approximately 500 men with essential hypertension. In patients with mild hypertension, the increase in blood pressure (BP) during dynamic exercise is similar to that seen in normal subjects, but in patients with severe hypertension it is steeper. During dynamic exercise total peripheral resistance is increased in all categories of hypertensive patients, including young subjects with apparently "normal" resistance at rest. The increase in stroke volume in transition from rest to exercise is subnormal, probably reflecting increased stiffness in the left ventricle. Static exercise causes dramatic increase in systolic as well as diastolic BP. Most antihypertensive agents control BP similarly during exercise and at rest. The hemodynamic mechanisms, however, differ greatly. The beta blockers induce a long-term reduction in cardiac output, muscle blood flow and, frequently, endurance capacity. In contrast, alpha-receptor blockers, calcium antagonists and angiotensin converting enzyme inhibitors all reduce total peripheral resistance and do not decrease blood flow. Increase in endurance time has been reported with long-term calcium antagonist treatment. It would seem logical to select an antihypertensive drug that does not reduce exercise capacity when treating physically active patients with mild and moderate hypertension.     

Decrease in systolic blood pressure during exercise testing: Reproducibility,response to coronary bypass surgery and prognostic significance

To investigate the reproduclbility and prognostic significance of an exercise-induced decrease in systolic blood pressure, 47 patients were Identified who manifested such a reduction below the pre-exercise standing level in a consecutive series of 436 patients who underwent treadmill exercise testing and cardiac catheterization during a 3 year period. The prevalence of this abnormal finding was 11 percent in the total group but 21 percent in the 124 patients with three vessel or left main coronary artery disease. Patients with an exercise-Induced reduction in systolic blood pressure were more likely to be male, have typical angina pectoris with class III or IV functional limitation and to have had a prior myocardial infarction than were patients without this finding (p < 0.05). Although no complications occurred during the exercise test of these 47 patients, the majority had severe ischemic responses, and 14 (30 percent) showed complex repetitive ventricular arrhythmias. Of the 47 patients, 24 (group 1a) received medical treatment and 23 (group 1b) underwent coronary bypass surgery. On repeat exercise testing In 42 patients, a decrease in systolic blood pressure during exercise was consistently present in group 1a (17 of 20) but entirely absent (0 of 22) in group 1b (p < 0.001). The mean treadmill time, peak heart rate and systolic blood pressure were not significantly different in the initial and on repeat exercise tests in patients in group 1a; however, in patients in group 1b, all of these variables were significantly higher in the repeat test (p < 0.001). At a mean follow-up time of 37 months, the total cardiac mortality rate was 8 percent (2 of 24) in group 1a and 4 percent (1 of 23) in group 1b. It is concluded that a decrease in systolic blood pressure during exercise testing is highly reproducible and appears to be reversed by coronary bypass surgery.     

Exercise-induced hypertension after repair of coarctation of the aorta: arm versus leg exercise

The etiology of exercise-induced upper limb hypertension after repair of coarctation of the aorta is unknown. We hypothesized that blood flow across the coarctation repair site is a major determinant of such exercise-induced hypertension. Because arm ergometry should produce a smaller increase in descending aortic blood flow than treadmill exercise, we compared the changes in upper limb pressure and the coarctation gradient produced by each type of exercise at equivalent levels of heart rate and peak oxygen consumption in 28 children with repaired coarctation of the aorta. The children were classified into three groups: Group I, resting gradient less than 15 mm Hg and treadmill gradient less than 20 mm Hg; Group II, resting gradient less than 15 mm Hg and treadmill gradient greater than 20 mm Hg; and Group III, resting gradient greater than or equal to 15 mm Hg. Twelve children with no heart disease served as control subjects. All children were exercised to exhaustion with 45 minutes' rest between the two exercise protocols. There were no differences in maximal heart rate and oxygen consumption between the two types of exercise. In all groups, treadmill exercise produced a larger increase in arm systolic blood pressure and arm-leg gradient than did arm exercise. With treadmill exercise coarctation Groups II and III developed a greater rise in both arm-leg gradient and arm systolic pressure than was observed in the control subjects (p less than 0.05). However, with arm exercise, Group III developed a significantly greater rise in both arm pressure and arm-leg gradient (p less than 0.05) than was observed in the control subjects.     

Effects of captopril on forearm oxygen consumption during dynamic handgrip exercise in patients with congestive heart failure

The maximal exercise capacity of patients with congestive heart failure (CHF) is frequently decreased because of decreased skeletal muscle oxygen utilization. In this study we examined whether forearm oxygen utilization is decreased during dynamic handgrip exercise in patients with CHF and whether captopril improves forearm oxygen utilization. They were divided into 3 groups according to the level of plasma renin activity (PRA) and New York Heart Association functional classification (NYHA): Group 1 consisted of 7 normal (control) subjects (PRA: 0.5 +/- 0.2 ng/ml/h, NYHA: 0); Group 2, 7 patients with severe CHF (PRA: 11.3 +/- 3.9 ng/ml/h, NYHA: 3.6 +/- 0.3); Group 3, 4 patients with mild CHF (PRA: 2.4 +/- 0.2 ng/ml/h, NYHA: 2 +/- 0). Forearm blood flow was measured by a strain gauge plethysmograph at rest and during dynamic handgrip exercise. Regional arterial venous oxygen content was measured and forearm oxygen consumption was calculated by the Fick principle. Forearm blood flow was less (p less than 0.05) at rest and during exercise in patients with severe CHF than in control subjects; this was compensated for by increased oxygen extraction, thus maintaining forearm oxygen consumption at a normal level at rest and during submaximal exercise. During maximal exercise, oxygen extraction was not different between normal control subjects and patients with severe CHF, thus forearm oxygen consumption was significantly less (p less than 0.01) in patients with severe CHF than in control subjects. In patients with mild CHF, forearm blood flow, oxygen extraction and oxygen consumption were not different from those in normal control subjects. Captopril (25 mg orally) did not alter forearm hemodynamics at rest and during exercise in control subjects and patients with mild CHF. In patients with severe CHF, captopril lowered systolic and mean blood pressure (p less than 0.05). Captopril increased forearm oxygen extraction (p less than 0.05) and tended to increase blood flow and thus increased oxygen consumption (p less than 0.01) during maximal exercise. Our data indicate that oxygen utilization was impaired in patients with severe CHF and that captopril improved forearm oxygen utilization during maximal handgrip exercise in patients with severe CHF.     

Resting and exercise renal blood flows in immature ovine aortic coarctation. Impact of gradient relief

The primary purpose of this study was to determine whether a neonatally induced thoracic aortic coarctation reduces renal blood flow during physiological stress (treadmill exercise), and whether relief of the gradient returned renal blood flow during exercise to normal. Two ancillary questions were also addressed: dose a coarctation after the responses of enteric and other visceral vascular beds to treadmill exercise? Eight newborn lambs that underwent sham thoracotomy with placement of left atrial lines served as controls; in seven lambs we also created a recently described form of dilatable juxtaductal coarctation. This preparation is unique in that, like human coarctation, the obstruction does not get worse as the animal grows. Rest and exercise vascular pressures and regional blood flows were determined 2-2 1/2 months after surgery. Coarctations were relieved with balloon dilation angioplasty catheters, inserted percutaneously. Postdilation rest and exercise hemodynamic studies were performed, at the same level of exercise, 24 hours after dilation. Renal blood flow did not change with exercise in the control animals. In lambs with coarctation, renal blood flow fell (-22%, P less than 0.01) during exercise. Unexpectedly, an exercise-induced fall in renal blood flow (-22%, P less than 0.001) persisted even after effective relief of the coarctation (descending aortic blood pressure fell 25% with exercise predilation, but remained unchanged with exercise postdilation). Blood flow to the terminal ileum and cecum followed a qualitatively similar pattern to that of renal blood flow in control, predilation, and postdilation lambs, and this pattern was distinct from that of other enteric and visceral organ flows. These results demonstrate an expected abnormality in the regulation of exercise renal blood flow in lambs with coarctation of the aorta; however, the persistence of this abnormality after effective gradient relief does not support the previously advanced theory that postcoarctation hypertension is largely nonrenal in origin. The apparent similarity between ileocecal and renal blood flow control under these circumstances may provide a clue to the known predilection of the terminal ileum to suffer ischemic injury.     

Changes in R wave amplitude during aerobic exercise stress testing in hypertensive adolescents

The change in R wave amplitude during progressive aerobic exercise was studied in hypertensive adolescent boys. A comparable control group consisted of normotensive adolescent boys matched for age, body size and race. Twenty-four normotensive and 22 hypertensive subjects exercised to exhaustion on a treadmill utilizing the Bruce protocol. Blood pressure and heart rate were monitored during exercise and recovery. The change in R wave amplitude in a lead V₅ electrocardiogram was determined at each level of exercise. The normotensive group demonstrated a progressive increase in systolic pressure, heart rate and rate-pressure product (heart rate × systolic pressure) during exercise and a progressive decrease in R wave amplitude with a significant correlation of R wave change versus the cardiac response variable (p < 0.001). Hypertensive subjects manifested a greater increase in systolic pressure, heart rate and rate-pressure product during exercise with no decrease in R wave amplitude until the exercise end point. The difference in R wave response to progressive exercise in the two groups was significant (p < 0.01). A variation in myocardial function in hypertensive adolescents as demonstrated by a difference in R wave response to exercise may reflect a level of peripheral vascular resistance greater than that of normotensive control subjects.     

Temperature-controlled Rate Responsive Pacing with the Aid of an Optimized Algorithm

On the basis of earlier studies of the behavior of the central venous blood temperature at rest and during exercise, we have developed an algorithm for the rate control of cardiac pacemakers. The central venous blood temperature serves as the control variable for the pacing rate. Control is effected via two different characteristic lines that relate pacing rate and temperature. A rest characteristic line relates absolute temperature values to heart rate and exercise lines relate relative changes in temperature to heart rate changes. The rest characteristic corresponds to conditions of slow temperature fluctations (e.g., fever and temperature changes due to circardian rhythm) and has a slope of 15 to 20 bpm per centigrade degree of temperature change. Starting at this rest characteristic, there are exercise characteristic lines that have a much greater slope and serve to regulate the pacing rate under exercise conditions. The two characteristics are distinguished via the temperature change per unit of time. In addition, a return characteristic connects the rest and exercise characteristics. This algorithm allows for optimized rate adaption of physiological cardiac pacemakers by central venous blood temperature. Clinical studies with the implanted device (Intermedics Nova MR) prove the correct function and beneficial effect of this algorithm in patients' everyday life.     

Role of adenosine in coronary vasodilation during exercise

This study examined the hypothesis that increases in myocardial blood flow during exercise are mediated by adenosine-induced coronary vasodilation. Active hyperemia associated with graded treadmill exercise and coronary reactive hyperemia were examined in chronically instrumented awake dogs during control conditions, after intracoronary infusion of adenosine deaminase (5 units/kg/min for 10 minutes), and after adenosine receptor blockade with 8-phenyltheophylline. Both adenosine deaminase and 8-phenyltheophylline caused a rightward shift of the dose-response curve to intracoronary adenosine; 8-phenyltheophylline was significantly more potent than adenosine deaminase. Adenosine deaminase caused a 33 +/- 7 to 39 +/- 3% decrease in reactive hyperemia blood flow following coronary occlusions of 5-20 seconds duration, respectively, while 8-phenyltheophylline produced a 40 +/- 6 to 62 +/- 8% decrease in reactive hyperemia. Increasing myocardial oxygen consumption during treadmill exercise was associated with progressive increase of coronary blood flow. Neither adenosine deaminase nor 8-phenyltheophylline attenuated the increase in coronary blood flow or the decrease of coronary vascular resistance during exercise. Neither agent altered the relation between myocardial oxygen consumption and coronary blood flow. Thus, although both adenosine deaminase and 8-phenyltheophylline antagonized coronary vasodilation in response to exogenous adenosine and blunted coronary reactive hyperemia, neither agent impaired coronary vasodilation associated with increased myocardial oxygen requirements produced by exercise. These findings fail to support a substantial role for adenosine in mediating coronary vasodilation during exercise.     

Regional blood flow in chronic heart failure: the reason for the lack of correlation between patients' exercise tolerance and cardiac output?

BACKGROUND--In patients with chronic heart failure there is no relation between cardiac output and symptom limited exercise tolerance measured on a bicycle or treadmill. Furthermore, the increase in cardiac output in response to treatment may not be matched by a similar increase in exercise tolerance. More important in determining exercise capability is blood flow to skeletal muscle. This implies that the reduction in skeletal muscle blood flow is not directly proportional to the reduction in cardiac output and that there are regional differences in blood flow in patients with heart failure. METHODS--Cardiac output and regional blood flow measured in 30 patients with chronic heart failure were compared with values obtained from 10 healthy controls. Measurements were made at rest and in response to treadmill exercise and were all made non-invasively. RESULTS--Cardiac output was lower in the patients at rest and during exercise. Blood flow in the superior mesenteric and renal arteries was also lower in the patients and represented a different proportion of cardiac output than in the controls. In response to exercise the increase in blood flow to the calf and therefore to skeletal muscle, was reduced in the patients. In the patients there was no correlation between resting cardiac output and blood flow in the superior mesenteric artery, renal artery, or calf. CONCLUSIONS--Because blood flow to skeletal muscle and to the kidneys is likely to be important in determining patients' symptoms this factor may explain why central haemodynamic variables do not correlate with the exercise tolerance in patients with chronic heart failure.