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Biomedical subjects

A L Mark

Publications and source records attributed to A L Mark.

At least 73 records · Page 4Linked to original sources
PubMed1991

Mental stress increases sympathetic nerve activity during sustained baroreceptor stimulation in humans.

Muscle sympathetic nerve activity (MSNA) in humans is regulated in part by arterial baroreceptors. However, although mental stress increases blood pressure, it also increases MSNA. This suggests that baroreceptor control of MSNA is altered during mental stress. In nine healthy men (age range, 20-26 years), we recorded heart rate, blood pressure, and efferent MSNA (peroneal nerve, microneurography) during a 4-minute mental arithmetic task performed both before and during infusion of phenylephrine sufficient to markedly suppress resting MSNA. Before phenylephrine, mental stress significantly increased mean blood pressure (p less than 0.01), heart rate (p less than 0.01), and MSNA (from 18.5 +/- 3.2 to 24.8 +/- 3.5 bursts/min, p less than 0.001). Phenylephrine infusion increased resting mean blood pressure (from 84.0 +/- 2.6 to 90.0 +/- 2.7 mm Hg, p less than 0.01) and decreased resting heart rate (from 65.6 +/- 1.7 to 55.6 +/- 2.0 beats/min, p less than 0.01). Resting MSNA decreased dramatically during phenylephrine (from 18.5 +/- 3.2 to 3.3 +/- 1.3 bursts/min, p less than 0.01). During phenylephrine, mental stress again significantly (p less than 0.01) increased mean blood pressure, heart rate, and MSNA (from 3.1 +/- 1.4 to 10.9 +/- 1.8 bursts/min). The magnitude of stress-induced increases in MSNA and heart rate were comparable before and during phenylephrine infusion despite the greater elevation in diastolic pressure during stress plus phenylephrine. The present study demonstrates that mental stress produces sympathoexcitatory and pressor responses even during sustained stimulation of arterial baroreceptors.

Adult↗
PubMed1991

Central command increases sympathetic nerve activity during spontaneous locomotion in cats.

A controversial issue in exercise physiology is the relative contribution of central command versus afferent input from contracting muscles and baroreceptors in the regulation of sympathetic nerve activity (SNA) during exercise. Recent studies of exercising humans have suggested that central command increases cutaneous sympathetic sudomotor nerve activity but have challenged the concept that central command contributes importantly to increases in sympathetic vasoconstrictor nerve activity to skin and skeletal muscle. The purpose of this study was to examine the influence of central command on renal SNA and lumbar SNA during spontaneous locomotion in decorticate cats. Unanesthetized decorticate cats that developed locomotion spontaneously or during electrical stimulation of the subthalamic locomotor region were studied in the presence and absence of input from skeletal muscle and baroreceptor afferents. Spontaneous rhythmic locomotion in the unparalyzed state was associated with significant increases in mean arterial pressure (MAP) from 106 +/- 10 to 133 +/- 11 mm Hg (p less than 0.05) and increases in renal SNA of 301 +/- 100% (p less than 0.05). During spontaneous fictive rhythmic locomotion in paralyzed cats, there were also significant (p less than 0.05) increases in MAP (43 +/- 6%), renal SNA (183 +/- 32%), and lumbar SNA (223 +/- 83%). Baroreceptor denervation did not attenuate increases in MAP, renal SNA, and lumbar SNA during locomotion. During electrical stimulation of the subthalamic locomotor region in paralyzed cats, MAP increased by 43 +/- 17% (p less than 0.05), and renal SNA increased by 175 +/- 47% (p less than 0.05). These findings indicate that central command is capable of increasing sympathetic neural drive in unanesthetized decorticate cats. This increase in sympathetic drive occurs even in the absence of feedback from contracting muscles or from arterial and cardiopulmonary baroreceptors.

Animals↗
PubMed1991

Interaction of baroreceptor and chemoreceptor reflex control of sympathetic nerve activity in normal humans.

Animal studies have demonstrated that activation of the baroreflex by increases in arterial pressure inhibits cardiovascular and ventilatory responses to activation of peripheral chemoreceptors (PC) with hypoxia. In this study, we examined the influences of baroreflex activation on the sympathetic response to stimulation of PC and central chemoreceptors in humans. PC were stimulated by hypoxia (10% O2/90% N2) (n = 6) and central chemoreceptors by hypercapnia (7% CO2/93% O2) (n = 6). Responses to a cold pressor stimulus were also obtained as an internal reflex control to determine the selectivity of the interactive influence of baroreflex activation. Baroreflex activation was achieved by raising mean blood pressure by greater than 10 mmHg with intravenous infusion of phenylephrine (PE). Sympathetic nerve activity (SNA) to muscle was recorded from a peroneal nerve (microneurography). During hypoxia alone, SNA increased from 255 +/- 92 to 354 +/- 107 U/min (P less than 0.05). During PE alone, mean blood pressure increased and SNA decreased to 87 +/- 45 U/min (P less than 0.05). With hypoxia during baroreflex activation with PE, SNA did not increase (50 +/- 23 U/min). During hypercapnia alone, SNA increased from 116 +/- 39 to 234 +/- 72 U/min (P less than 0.01). Hypercapnia during baroreflex activation with PE increased SNA from 32 +/- 25 U/min during PE alone to 61 +/- 26 U/min during hypercapnia and PE (P less than 0.05). Like hypercapnia (but unlike hypoxia) the cold pressor test also increased SNA during PE. We conclude that baroreflex activation selectively abolishes the SNA response to hypoxia but not to hypercapnia or the cold pressor test. The inhibitory interaction of the baroreflex and the peripheral chemoreflex may be explained by convergence of baroreceptor and peripheral chemoreceptor afferents on neurons in the medulla.

Adult↗
PubMed1991

Hyperinsulinemia produces both sympathetic neural activation and vasodilation in normal humans.

Hyperinsulinemia may contribute to hypertension by increasing sympathetic activity and vascular resistance. We sought to determine if insulin increases central sympathetic neural outflow and vascular resistance in humans. We recorded muscle sympathetic nerve activity (MSNA; microneurography, peroneal nerve), forearm blood flow (plethysmography), heart rate, and blood pressure in 14 normotensive males during 1-h infusions of low (38 mU/m2/min) and high (76 mU/m2/min) doses of insulin while holding blood glucose constant. Plasma insulin rose from 8 +/- 1 microU/ml during control, to 72 +/- 8 and 144 +/- 13 microU/ml during the low and high insulin doses, respectively, and fell to 15 +/- 6 microU/ml 1 h after insulin infusion was stopped. MSNA, which averaged 21.5 +/- 1.5 bursts/min in control, increased significantly (P less than 0.001) during both the low and high doses of insulin (+/- 5.4 and +/- 9.3 bursts/min, respectively) and further increased during 1-h recovery (+15.2 bursts/min). Plasma norepinephrine levels (119 +/- 19 pg/ml during control) rose during both low (258 +/- 25; P less than 0.02) and high (285 +/- 95; P less than 0.01) doses of insulin and recovery (316 +/- 23; P less than 0.01). Plasma epinephrine levels did not change during insulin infusion. Despite the increased MSNA and plasma norepinephrine, there were significant (P less than 0.001) increases in forearm blood flow and decreases in forearm vascular resistance during both doses of insulin. Systolic pressure did not change significantly during infusion of insulin and diastolic pressure fell approximately 4-5 mmHg (P less than 0.01). This study suggests that acute increases in plasma insulin within the physiological range elevate sympathetic neural outflow but produce forearm vasodilation and do not elevate arterial pressure in normal humans.

Adult↗
PubMed1991

Atrial pacing with two-dimensional echocardiography for evaluation of chest pain: comparison with thallium 201 scintigraphy.

Atrial pacing was performed with two-dimensional (2-D) echocardiography and thallium 201 scintigraphy in 40 men with stable chest pain. Coronary angiography showed significant (one or more lesions greater than or equal to 50%) coronary artery disease (CAD) in 36 patients and no or insignificant CAD in 4. Two dimensional echocardiography showed a left ventricular wall motion abnormality (WMA) either at rest or with pacing in 28 (78%) patients with CAD, with 17 (47%) showing a new or worsened WMA with pacing. A thallium scan showing abnormality (reversible or fixed perfusion defect) was seen in 26 (72%) patients with CAD; 18 (50%) had a reversible defect. In all, 34 of the 36 patients with CAD (94%) had a WMA, a perfusion defect, or both (specificity 50%). Occurrence of both a WMA and a perfusion defect in individual segments ranged from 10 of 25 patients with septal abnormalities to 0 of 12 with abnormalities of the lateral segment. Sensitivity of 2-D echocardiography for identifying CAD in specific vessels was 81% for the left anterior descending (LAD) artery, 30% for the right coronary artery, and 20% for the circumflex artery (both p less than .001 compared with the LAD artery). Corresponding sensitivities for thallium 201 imaging were 54% (p less than .05 compared with 2-D echocardiography), 27%, and 8% (both p less than .05 compared with the LAD artery). When combined with atrial pacing, 2-D echocardiography and thallium 201 perfusion imaging are of similar value for diagnosing the presence of CAD in patients with stable chest pain. Two-dimensional echocardiography is superior to thallium 201 imaging for identifying the presence of significant CAD in the LAD artery, but both tests are limited in their ability to detect lesions of the right coronary or circumflex arteries.

Aged↗
PubMed1991

Sympathetic nerve responses to sustained stimulation of somatic afferents in Dahl rats.

We tested the hypothesis that the hypotensive and sympathoinhibitory responses which occur after somatic afferent stimulation would be augmented in prehypertensive rats genetically predisposed to hypertension (Dahl salt-sensitive, DS) compared with rats resistant to the development of hypertension (Dahl salt-resistant, DR). For this purpose, we recorded mean arterial pressure (MAP), heart rate and renal sympathetic nerve activity (RSNA) during and following 30-min sciatic nerve stimulation in DS and DR rats fed a 0.4% NaCl diet. Baseline MAP did not differ significantly in the DS and DR rats. Somatic afferent stimulation in DS rats increased (P less than 0.05) MAP and heart rate and tended to increase RSNA whereas, in DR rats, stimulation increased (P less than 0.05) heart rate and tended to increase RSNA and MAP. Following somatic afferent stimulation, there were significant reductions (P less than 0.05) in both MAP (-20 +/- 6 mmHg) and RSNA (-36 +/- 8%) in DS rats. In contrast, DR rats did not exhibit significant poststimulation changes in MAP, and RSNA remained elevated from control following somatic afferent stimulation. These results suggest that the poststimulation inhibition of RSNA in DS rats may be related to the genetic predisposition of these rats to develop hypertension.

Afferent Pathways↗
PubMed1990

Thallium-201 perfusion imaging with atrial pacing or dipyridamole stress testing for evaluation of cardiac risk prior to nonvascular surgery.

Preoperative assessment of cardiac risk using thallium-201 scintigraphy and atrial pacing (n = 42) or dipyridamole stress testing (n = 35) was performed in 77 patients (mean age 65 +/- 7 years), who subsequently underwent elective nonvascular surgery. All patients were at low cardiac risk by clinical criteria; none could perform exercise stress testing due to physical limitations. ST depression consistent with ischemia occurred in 11 patients during atrial pacing and in 1 patient during dipyridamole stress testing (p less than 0.01). Nine patients had reversible perfusion defects with atrial pacing, and 10 patients with dipyridamole stress testing; fixed defects were present in 15 and 8 patients, respectively. Only one patient (fixed perfusion defect with atrial pacing, left main disease on coronary angiography) underwent preoperative coronary revascularization. Two patients subsequently had postoperative cardiac events. One patient (reversible perfusion defect with dipyridamole stress testing) experienced sudden death after a nonvascular procedure, while a second patient (normal thallium images with dipyridamole testing) had a nonfatal myocardial infarction. In patients having atrial pacing or dipyridamole stress testing, thallium-201 scans that are normal or show only a fixed perfusion defect confirm a low risk of cardiac complications following nonvascular surgery. The presence of a reversible perfusion defect does not preclude a postoperative course free of cardiac complications in patients at low cardiac risk by clinical criteria.

Aged↗
PubMed1990

Pathophysiologic levels of atrial natriuretic factor do not alter reflex sympathetic control: direct evidence from microneurographic studies in humans.

To determine if circulating levels of atrial natriuretic factor comparable with those seen in pathophysiologic states alter autonomic control of the circulation, direct recordings of hemodynamic variables and efferent sympathetic nerve activity to muscle (microneurography) were obtained during two separate protocols in a total of 21 normal men (age 25 +/- 1 years). In protocol 1, the responses of 10 men were compared during incremental mechanical unloading of cardiopulmonary baroreceptors with lower body negative pressure versus responses to comparable unloading during infusion of alpha-human atrial natriuretic factor. Lower body negative pressure decreased pulmonary artery diastolic and right atrial pressures, did not alter arterial pressure or heart rate and increased muscle sympathetic nerve activity from 205.2 +/- 36.3 to 438.7 +/- 100.2 units/min (p less than 0.01). Intravenous infusion of atrial natriuretic factor (25 ng/kg per min) increased plasma levels of the hormone from 24 +/- 4 to 322 +/- 34 pg/ml (p less than 0.01, n = 6), produced similar decreases in pulmonary artery diastolic and right atrial pressures, did not alter arterial pressure, increased heart rate and increased sympathetic nerve activity from 233.1 +/- 35.6 to 387.2 +/- 64.9 units/min (p less than 0.05). Thus, during similar hemodynamic perturbations produced by lower body negative pressure or infusion of atrial natriuretic factor at the dose used in this study, these subjects exhibited comparable sympathoexcitatory responses, with a 109 +/- 23% increase in sympathetic activity during lower body negative pressure and a 76 +/- 19% increase during atrial natriuretic factor infusion (p = NS). In protocol 2, the responses of 11 additional men were examined during lower body negative pressure performed before and again during infusion of atrial natriuretic factor (12.5 ng/kg per min). During baseline (prehormone) trials, lower body negative pressure (-14.5 +/- 1.6 mm Hg) decreased central venous pressure, did not change arterial pressure or heart rate and increased sympathetic nerve activity from 215 +/- 47.7 to 372.3 +/- 64.3 units/min (p less than 0.001). Infusion of atrial natriuretic factor increased plasma levels of the hormone from 39 +/- 8 to 313 +/- 18 pg/ml (p less than 0.01, n = 7); central venous pressure was held constant during hormone infusion by intravenous infusion of saline solution.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1990

Adrenaline facilitates neurogenic vasoconstriction in borderline hypertensive subjects.

Adrenaline facilitates the neural release of endogenous noradrenaline by stimulating prejunctional beta-receptors on adrenergic nerve endings. Recently, we demonstrated the functional significance of this action in the control of vascular resistance in young subjects with normal blood pressure. In the present study, we tested the hypothesis that the effects of adrenaline on neurogenic vasoconstriction are exaggerated in humans with borderline hypertension. Forearm blood flow was measured simultaneously in the experimental and contralateral arms of seven young men with borderline hypertension. We compared forearm vasoconstrictor responses to a reflex stimulus to noradrenaline release (lower-body negative pressure, LBNP) and to intra-arterial infusion of noradrenaline before and 30 min after brachial artery infusion of adrenaline (50 ng/min). These doses had no systemic effects. In the experimental arm, the vasoconstrictor response to LBNP was 65% greater 30 min after the adrenaline infusion (P = 0.075), whereas the response to intra-arterial noradrenaline decreased by 36% (P greater than 0.1). Forearm vascular responses to LBNP in the contralateral control arm that did not receive adrenaline were similar before and after the adrenaline infusion. The ratio of forearm vasoconstrictor responses (i.e. the increase in forearm vascular resistance) with LBNP to the forearm vasoconstrictor response to noradrenaline in the experimental arm was used as an index of neural release of the neurotransmitter noradrenaline. This ratio increased from 0.8 to 2.1 (P less than 0.05) after the adrenaline infusion. These facilitatory neural after-effects of adrenaline were similar in magnitude to our previous observation in young normotensive subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Inhibition of renal sympathetic activity and heart rate by vasopressin in hemorrhaged diabetes insipidus rats.

Hypotensive hemorrhage paradoxically decreases renal sympathetic nerve activity (SNA) and heart rate (HR) in normal rats. Interruption of vagal reflexes by cervical vagotomy prevents these inhibitory responses but does not unmask expected increases in either renal SNA or HR. Arginine vasopressin (AVP), which increases markedly during hemorrhage, may also exert an inhibitory action on responses of renal SNA and HR to hemorrhage. We tested the hypothesis that inhibition of renal SNA and HR by hemorrhage is absent in AVP-deficient diabetes insipidus (DI) rats and is restored by intravenous AVP replacement (1 mU.kg-1.min-1 before hemorrhage and 10 mU.kg-1.min-1 during hemorrhage). We also determined whether vagotomy unmasks significant increases in renal SNA and HR during hemorrhage in DI rats and whether AVP replacement prevents these increases. Under chloralose anesthesia, hemorrhage to 50 mmHg mean arterial pressure for 8 min did not decrease renal SNA or HR in AVP-deficient DI rats but decreased (P less than 0.05) renal SNA and HR in normal Long-Evans rats and in DI rats receiving AVP replacement. After vagotomy, hemorrhage increased (P less than 0.05) renal SNA and HR in AVP-deficient DI rats but did not alter renal SNA or HR in Long-Evans rats and AVP-treated DI rats. Thus renal SNA and HR during hemorrhage were consistently higher (P less than 0.05) in AVP-deficient DI rats compared with Long-Evans or AVP-treated DI rats both before and after vagotomy. In addition, vagotomy attenuated the inhibitory action of AVP on the response of HR but not the response of renal SNA to hemorrhage in DI rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Prolonged renal sympathoinhibition following sustained elevation in arterial pressure.

We tested the hypothesis that sustained elevations in mean arterial pressure (MAP) would produce an abbreviated suppression of renal sympathetic nerve activity (RSNA) in spontaneously hypertensive (SH) compared with Wistar-Kyoto (WKY) normotensive rats. For this purpose, we recorded RSNA during and after a 30-min elevation in MAP. Elevations in MAP (35-40 mmHg) induced by phenylephrine resulted in a suppression of RSNA in SH and WKY rats that persisted after MAP had returned to control levels. The prolonged suppression of RSNA was eliminated following sinoaortic denervation, indicating that this response was dependent on afferent baroreceptor mechanisms. The simultaneous recording of RSNA and aortic depressor nerve (ADN) activity provided additional evidence that baroreceptor afferents contribute to this prolonged suppression of RSNA in SH rats. Despite the return of MAP to control levels following the sustained pressure elevation in SH rats, there was a paradoxical increase in ADN activity (39 +/- 14%) compared with control values. In contrast, both ADN activity and MAP returned to control levels in WKY rats following the sustained pressure elevation. The sustained increase of ADN activity in SH rats did not account for the entire magnitude of the prolonged recovery of RSNA. In summary, both SH and WKY rats exhibit prolonged suppression of RSNA, whereas ADN activity is paradoxically elevated in only SH rats following a sustained elevation in MAP.

Animals↗
PubMed1990

Effects of interstrain renal transplantation on NaCl-induced hypertension in Dahl rats.

Previous studies using renal transplantation suggested that the genotype of a homograft kidney plays the primary role in determining chronic arterial pressure levels in Dahl salt-sensitive (DS) and salt-resistant (DR) rats, but this conclusion derived largely from observations during low NaCl diet. Recent studies indicate that extrarenal factors, including the sympathetic nervous system, play a critical role in the development of NaCl-induced hypertension in DS rats. To assess the contribution of extrarenal and renal factors in the development of NaCl-induced hypertension in Dahl rats, we performed renal transplantation in DS and DR rats. Both kidneys of the recipient were removed at the time of transplantation. Four groups of rats (n = 18-23 in each group) were fed a high NaCl (8.0%) diet for 2 weeks after renal transplantation. These included DRR, DRS, DSR, and DSS, where DR or DS indicates the recipient strain and the subscript indicates the homograft strain. Mean arterial pressure was measured from the femoral artery in conscious rats. On a high NaCl diet, mean arterial pressure was significantly lower (p less than 0.05) in DRR (103 +/- 2 mm Hg; mean +/- SEM) compared with DRS (145 +/- 5 mm Hg), DSR (151 +/- 7 mm Hg), and DSS (160 +/- 5 mm Hg). The finding that DR rats with a DS kidney (DRS) developed hypertension during high NaCl diet confirms the concept that the kidney plays an important hypertensinogenic role in the Dahl strain. The fact that DS rats with a DR kidney (DSR) also developed hypertension indicates that extrarenal factors also contribute significantly to NaCl-induced hypertension in DS rats.

Animals↗
PubMed1990

Regulation of sympathetic nerve activity in mild human hypertension.

There is substantial evidence for increased sympathetic nerve activity in young, mildly hypertensive humans. This evidence has been derived mainly from measurements of plasma catecholamines and from responses to adrenergic antagonists and agonists in normotensive and mildly hypertensive subjects. In addition, in recent studies direct measurements of sympathetic nerve activity to the muscle circulation have been obtained by microneurography. These data also indicate that sympathetic nerve activity is increased in young, mildly hypertensive humans. The present paper reviews this work with microneurographic measurements and highlights several concepts. (1) The increases in sympathetic nerve activity to the muscle in mild hypertension are not a result of impairment in the inhibitory influence of arterial baroreceptors; presumably, they reflect a heightened central nervous system sympathetic drive. (2) In the supine position the inhibitory influence of cardiopulmonary baroreceptors on sympathetic nerve activity is increased in mild hypertension. This increase in cardiopulmonary baroreflex control buffers the heightened sympathetic neural drive in mildly hypertensive subjects in the supine position, but withdrawal of this increase during orthostatic stress produces exaggerated reflex sympathetic vasoconstrictor responses to orthostasis in mildly hypertensive subjects. (3) Arterial chemoreceptor reflexes are increased in mildly hypertensive subjects and lead to exaggerated increases in sympathetic nerve activity during hypoxia. (4) There is increasing evidence that two humoral agents, epinephrine and insulin, exert excitatory effects on sympathetic neural outflow, which may contribute to the increased sympathetic activity and arterial pressure in human hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Chemoreceptor Cells↗
PubMed1989

Prognostic value of atrial pacing and thallium-201 scintigraphy in patients with stable chest pain.

The value of atrial pacing and thallium-201 scintigraphy for assessing risk of subsequent cardiac events was examined in 210 patients with stable chest pain. Follow-up information was complete in 195 patients (mean age 61 years). Over an average follow-up of 19 months, cardiac events occurred in 38 patients--unstable angina in 20, nonfatal acute myocardial infarction in 6 and death from cardiac causes in 12. A history of previous myocardial infarction, diabetes mellitus, systemic hypertension or peripheral vascular disease at the time of pacing was not associated with an increased frequency of subsequent cardiac events. Six of 38 patients with later cardiac events had a history of congestive heart failure, compared with 8 of 157 without cardiac events (p less than 0.05). Neither pacing-induced angina, ST depression, nor the presence of a fixed perfusion defect was significantly more frequent in patients with cardiac events as a whole compared with patients without such events. Reversible defects and abnormal scans (reversible or fixed defects) were present, respectively, in 19 and 31 of 38 patients with cardiac events, compared with 42 and 79 patients, respectively, of the 157 patients without cardiac events (both p less than 0.01). In patients who developed unstable angina, a reversible defect was seen in 13 and an abnormal scan in 16 (both p less than 0.01 compared with patients without cardiac events). In 12 patients who died from a primary cardiac event, fixed defects were present in 8 and an abnormal scan in 11 (p less than 0.05 and p less than 0.01, respectively, compared with patients without cardiac events).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Atrial pacing and thallium-201 scintigraphy in patients with chest pain: correlation with coronary anatomy.

Atrial pacing and thallium-201 scintigraphy were performed in 72 patients referred for evaluation of chest pain. Coronary artery disease (CAD) was present in 63 patients, as documented by cardiac catheterization performed at the same time or within 2 months of atrial pacing. Nine patients had no or insignificant (less than 50% stenosis) CAD. The sensitivity of pacing-induced angina for CAD was 51%, and was 49% for ST depression. Specificities were 89% and 78%, respectively. A reversible perfusion defect was seen in 54% of patients with CAD (specificity 89%), and a fixed defect in 29% (specificity 100%). The sensitivity of an abnormal thallium-201 scan (one or more reversible or fixed defects) was 79% (p less than 0.05 compared to angina or ST depression). Combined sensitivity of ST depression and/or an abnormal thallium-201 scan was 87%. There were no significant changes in any of these sensitivities as the number of vessels with CAD increased. Thallium-201 scintigraphy correctly identified 11 of 19 (58%) patients with single-vessel disease as having CAD in only one vessel, but underestimated the extent of disease in all but a few patients with multivessel disease. The sensitivity of perfusion imaging to identify lesions in specific vessels ranged from 27% (circumflex) to 57% (right coronary artery). Specificities were 100% for circumflex, 78% for anterior descending, and 83% for right coronary artery lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Diagnostic value of atrial pacing and thallium-201 scintigraphy for the assessment of patients with chest pain.

Atrial pacing was performed either alone (n = 23) or in combination with thallium-201 scintigraphy (n = 113) in 136 patients referred for evaluation of chest pain. The presence of coronary artery disease (CAD) was excluded by cardiac catheterization in 12 patients and confirmed in 124. Both pacing-induced ST depression and angina had sensitivities of 48% for CAD; specificities were 75% and 83%, respectively. An abnormal thallium-201 scan (one or more reversible and/or fixed perfusion defects) was seen in 72% of patients with CAD (specificity 83%). Reversible perfusion defects were present in 47% of patients with CAD (specificity 83%), and fixed defects in 36% (specificity 100%). Pacing was associated with either ST depression or an abnormal perfusion scan in 81% of patients (specificity 67%). There were no significant differences in the results of atria pacing or thallium-201 scintigraphy in patients with or without a history of myocardial infarction, or in those with or without previous coronary artery bypass surgery. Pacing-induced ST depression, or both ST depression and a reversible perfusion defect occurred significantly less frequently in patients with peripheral vascular disease than in those without this diagnosis (p less than .05). With only one exception, there were no significant differences in the sensitivities of any indicators of ischemia (ST depression, angina, or perfusion scans), either individually or in combination, as the peak pacing rate or double product achieved increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Preoperative evaluation of cardiac risk by means of atrial pacing and thallium 201 scintigraphy.

Atrial pacing and thallium 201 scintigraphy were done in 61 patients with known or suspected coronary artery disease referred for evaluation of cardiac risk before elective vascular surgery. All patients had noncardiac limitations precluding performance of an adequate exercise stress test. Before atrial pacing all were considered to be at low risk of a postoperative cardiac event based on assessment of clinical parameters. Vascular surgery was subsequently performed in 47 patients. In these patients, pacing-induced ST segment depression greater than or equal to 1 mm occurred in 18, a fixed perfusion defect occurred in 11, and a reversible defect occurred in six. Two of the six patients with reversible perfusion defects had preoperative coronary angiography; both had significant coronary artery disease (one or more lesions greater than or equal to 50%). Two patients (one of whom had a reversible perfusion defect) underwent preoperative coronary revascularization and tolerated subsequent vascular surgery well. All other patients received only medical therapy. None of the 47 patients undergoing vascular surgery had a postoperative cardiac event (unstable angina, congestive heart failure, myocardial infarction, or cardiac death). Of the 14 patients in whom vascular surgery was deferred or canceled, surgery was canceled for noncardiac reasons in seven. Six of these seven patients had a normal perfusion scan; none had a reversible perfusion defect or marked (greater than or equal to 2 mm) ST segment depression. No cardiac event occurred during a 3-month period after atrial pacing in any of these patients. Six of the remaining seven patients had reversible perfusion defects.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗