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Biomedical subjects

D W Ferguson

Publications and source records attributed to D W Ferguson.

At least 37 records · Page 2Linked to original sources
PubMed1991

Aortic valve replacement with pulmonary or aortic allografts.

Limited availability of aortic valve allografts suggests consideration of pulmonary valve allografts for aortic valve replacement (AVR). From 1987 through 1990, 20 patients underwent AVR with cryopreserved aortic allografts (group 1). Five patients underwent AVR with pulmonary allografts (group 2) because no aortic allografts of the appropriate size were available. Indications for AVR in group 1 were endocarditis in five patients, aortic insufficiency in six, and aortic stenosis in nine. Indications for AVR in group 2 were endocarditis in two patients and aortic insufficiency in three. In group 1 there was one operative death and two late deaths resulting from noncardiac causes. There were no operative or late deaths in group 2. Follow-up was complete (group 1: 1-32 months [mean, 14 months]; group 2: 1-24 months [mean, 13 months]). All surviving patients remain in New York Heart Association (NYHA) class I or II. Postoperative catheterization was performed in 21 of 24 surviving patients. All patients have been followed since hospitalization with serial studies that included computerized cine tomography of the chest and echocardiograms. No false aneurysms, stenoses, or clinically significant regurgitation have occurred, although one patient in group 2 showed 2+ insufficiency at catheterization. One group 1 patient required repeat AVR for recurrent endocarditis. There were no reoperations in group 2. Although longer-term follow-up with larger numbers of patients is necessary, it seems that operative and early postoperative results for AVR have been similar with aortic and pulmonary valve allografts. In selected patients AVR with pulmonary allografts may be appropriate to consider when properly sized aortic allografts are unavailable.

Adult↗
PubMed1990

Clinical and hemodynamic correlates of sympathetic nerve activity in normal humans and patients with heart failure: evidence from direct microneurographic recordings.

To characterize the neural excitatory state of heart failure, simultaneous measurements of efferent sympathetic nerve activity to muscle (by microneurography) and rest hemodynamics were obtained in 10 normal subjects (age 25 +/- 2 years, mean +/- SEM) and 29 patients with heart failure (age 49 +/- 2 years; New York Heart Association functional class II to IV; left ventricular ejection fraction 21 +/- 1%; cardiac index = 2.16 +/- 0.13 liters/min per m2; pulmonary capillary wedge pressure 23 +/- 2 mm Hg). Sympathetic nerve activity was significantly higher in the patients with heart failure (54.7 +/- 4.5 bursts/min) than in normal subjects (16.7 +/- 2.2 bursts/min, p less than 0.001). Multiple linear regression analyses indicated that sympathetic activity in these human subjects was most strongly and inversely correlated with left ventricular stroke work index (r = -0.86, p less than 0.0001) and stroke volume index (r = -0.85, p less than 0.0001). There was a strong positive correlation between sympathetic nerve activity and pulmonary artery diastolic (r = 0.82, p less than 0.0001) and mean (r = 0.81, p less than 0.0001) pressures. Similar correlations were seen when patients with heart failure were analyzed separately. There was no significant correlation between sympathetic nerve activity and mean arterial pressure, left ventricular ejection fraction (by radionuclide ventriculography), cardiac chamber size (by echocardiography) or arterial oxygen tension in the patients with heart failure. Direct measurements of sympathetic nerve activity correlated closely with plasma norepinephrine (r = 0.72, p less than 0.0001) in patients with heart failure. Thus, sympathetic nerve activity at rest parallels impairment of cardiac performance in patients with heart failure.

Adult↗
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↗
PubMed1989

Survival after myocardial infarction caused by acute left main coronary artery occlusion: case report and review of the literature.

We report a 44-year-old white male presenting with an acute anterior myocardial infarction. Cardiac catheterization at 2 weeks postinfarction revealed total occlusion of the left main coronary artery. There was a normal dominant right coronary artery supplying moderate collaterals to the left coronary system. The patient was managed with conservative therapy and was N.Y.H.A. functional class II on followup 2 years later. A review of the literature relative to myocardial infarction caused by acute left main coronary artery occlusion is presented, and unique features of these cases are described.

Adult↗
PubMed1989

Surgical implications of atrial septal defect complicating aortic balloon valvuloplasty.

An 80-year-old man underwent percutaneous transluminal balloon valvuloplasty for critical aortic stenosis. The procedure was performed by the antegrade atrial transseptal approach and was complicated by a persistent atrial septal defect. Symptoms recurred 6 months later, restenosis of the aortic valve was confirmed, and the atrial septal defect yielded a substantially greater left-to-right shunt. This complication of percutaneous transluminal balloon valvuloplasty poses important problems in hemodynamic assessment and operative management of patients who undergo subsequent aortic valve replacement.

Aged↗
PubMed1989

Diastolic pressure determines autonomic responses to pressure perturbation in humans.

Arterial baroreceptors reflexly regulate sympathetic and heart rate responses to alteration of blood pressure. The primary mechanical determinant of arterial baroreceptor activity in humans remains unclear. We examined the influence of systolic, diastolic, pulse, and mean arterial pressures on efferent muscle sympathetic nerve activity (MSNA, microneurography) and heart rate responses during perturbation of arterial pressure in 10 normal human subjects [age 25 +/- 2 (SE) yr]. We directly measured arterial pressure, heart rate, and MSNA during intravenous vasodilator infusion (nitroprusside, 6 +/- 1 micrograms.kg-1.min-1, n = 6; or hydralazine, 16 +/- 2 mg, n = 4) while central venous pressure was held constant by simultaneous volume expansion. Changes in arterial pressures were compared with changes in heart rate and MSNA over 3-min periods of vasodilator infusion during which we observed increases in systolic and pulse pressures with simultaneous decreases in mean and diastolic pressures. During vasodilator infusion, there were increases in systolic (124.2 +/- 2.1 to 131.7 +/- 2.9 Torr, P less than 0.001) and pulse pressures (57.0 +/- 2.2 to 72.7 +/- 2.7 Torr, P less than 0.001) although mean arterial pressure fell (88.0 +/- 2.6 to 80.4 +/- 2.7 Torr, P less than 0.001) because of decreases in diastolic pressure (67.2 +/- 3.0 to 59.0 +/- 2.7 Torr, P less than 0.001). The changes in arterial pressures were accompanied by simultaneous increases in heart rate (66.4 +/- 3.0 to 92.6 +/- 4.8 beats/min, P less than 0.001) and MSNA (327 +/- 59 to 936 +/- 171 U, P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Importance of aortic baroreflex in regulation of sympathetic responses during hypotension. Evidence from direct sympathetic nerve recordings in humans.

Arterial baroreceptors in the carotid sinus and aortic arch regions reflexly regulate heart rate and peripheral vascular responses during changes in arterial pressure. The relative influence of these two arterial baroreflex pathways on the control of these autonomic responses is debatable. Recent studies in our laboratory demonstrate that the aortic baroreflex produces substantial and sustained inhibition of efferent sympathetic nerve activity to muscle (MSNA) during increases in arterial pressure. The regulation of MSNA by these two baroreflexes in humans during hypotension, and particularly the role of the aortic baroreflex, remains undefined. We therefore performed a new series of studies to assess the relative influence of the aortic and carotid baroreflexes on MSNA responses during sustained decreases in arterial pressure. In eight normal male subjects, aged 23 +/- 1 years (mean +/- SEM), we directly measured mean arterial pressure, heart rate, central venous pressure, and MSNA (microneurography) during hypotension (combined aortic and carotid baroreceptor deactivation) produced by intravenous infusion of sodium nitroprusside and during nitroprusside infusion with superimposed application of external neck suction. Neck suction was applied at levels sufficient to maintain transmural carotid sinus pressure above control levels (carotid baroreceptor activation) while the aortic baroreflexes remained deactivated. Central venous pressure was maintained constant with volume infusion. We also studied responses of these same subjects to direct carotid baroreceptor deactivation with the application of external neck pressure. During neck pressure alone, there was a reflex increase in mean arterial pressure; thus, during this portion of the protocol, we achieved carotid baroreceptor deactivation with some aortic baroreceptor activation. Nitroprusside infusion (combined aortic and carotid deactivation) decreased mean arterial pressure from 90.8 +/- 3.1 to 77.8 +/- 1.1 mm Hg (p less than 0.01) with concomitant increases in heart rate from 62.6 +/- 3.0 to 89.7 +/- 6.1 beats/min (p less than 0.001) and in MSNA from 273.8 +/- 43.0 to 950.6 +/- 133.5 units (p less than 0.001). During continued nitroprusside infusion with superimposed neck suction (aortic baroreceptor deactivation and carotid baroreceptor activation), mean arterial pressure decreased to 70.3 +/- 1.9 mm Hg (p less than 0.001 vs. control), heart rate decreased to 82.5 +/- 6.5 beats/min (p less than 0.01 vs. control or vs. nitroprusside alone), but MSNA remained markedly increased at 889.7 +/- 105.1 units (p less than 0.001 vs. control; p = NS vs. nitroprusside alone).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1989

Evidence for cholinergically mediated vasodilation at the beginning of isometric exercise in humans.

Vasodilation occurs in the nonexercising forearm at the beginning of isometric handgrip despite activation of sympathetic vasoconstrictor reflexes. The mechanism of this response remains unclear. In 33 normal humans, age 24 +/- 1 years (mean +/- SEM), we measured mean arterial pressure, heart rate, and forearm blood flow (plethysmography) in the nonexercising arm during sustained contralateral isometric handgrip at 30% maximal voluntary contraction. Sympathetic nerve activity to calf muscles (microneurography) was also measured in 15 subjects. Handgrip resulted in increases in arterial pressure from 86 +/- 2 to 97 +/- 3 mm Hg (p less than 0.05). Despite increases in nerve activity to calf muscles from 229 +/- 43 to 337 +/- 66 units (p less than 0.005), which would be expected to produce forearm vasoconstriction, forearm vascular resistance in the contralateral resting arm decreased from 20 +/- 3 to 18 +/- 2 units (p less than 0.05). To determine the mechanism of this vasodilatory influence, additional studies were performed with regional autonomic blockade with intra-arterial administration of atropine (0.8 mg, 10 subjects) or propranolol (2.0 mg, eight subjects) into the nonexercising forearm before contraction. Propranolol and vehicle had no effect on forearm vascular responses in the resting arm during SHG in the other arm. In contrast, atropine blocked the vasodilatory response in the resting arm during contraction (delta forearm vascular resistance during contraction, control = -2.1 +/- 0.6 units; postatropine = +0.2 +/- 0.9 units, p less than 0.05). Atropine did not attenuate the vasodilator response to isoproterenol or the vasoconstrictor response to norepinephrine. We conclude 1) a dissociation exists between sympathetic neural and forearm vascular responses to isometric exercise; 2) the vasodilatory response in the nonexercising forearm is not due to sympathetic withdrawal or beta 2-adrenergic-mediated vasodilation; and 3) this response is mediated primarily by cholinergic mechanisms. These studies provide the first direct evidence for active, cholinergically mediated vasodilation during exercise in humans.

Adult↗
PubMed1989

Sympathoinhibitory responses to digitalis glycosides in heart failure patients. Direct evidence from sympathetic neural recordings.

Digitalis glycosides exert both excitatory and inhibitory autonomic actions in animals and produce vasoconstriction in normal humans but produce vasodilation in heart failure patients. To determine whether or not these contrasting vascular responses are due to differing autonomic actions of the drug, we compared the responses to intravenous administration of Cedilanid-D (0.02 mg/kg) in eight normal subjects (mean age, 23 +/- 1 years) and eight patients with moderate-to-severe heart failure (mean age, 52 +/- 5 years, NYHA Class III-IV). Hemodynamics and efferent sympathetic nerve activity to muscle (MSNA) were measured during 5-minute periods before (control) and 20 minutes after drug administration. In the heart failure patients, Cedilanid-D significantly increased systolic and pulse pressures, whereas mean arterial pressure was unchanged. There was a decrease in right atrial pressure and a tendency for a decrease in pulmonary artery diastolic pressure with a slowing of heart rate. Cardiac index increased by 24 +/- 7%. Short-term administration of digitalis in these heart failure patients produced a fall in forearm vascular resistance (from 37.6 +/- 8.2 to 31.8 +/- 8.1 units, p less than 0.05) and an early, profound, and sustained decrease in MSNA (from 831.0 +/- 118.4 to 474.4 +/- 103.6 units/100 heart beats, p less than 0.01). Digitalis glycosides produced different vascular and MSNA responses in the normal subjects. In the normal volunteers, the drug significantly increased systolic, mean, and pulse pressures and decreased central venous pressure and heart rate. Despite the significant increase in arterial pressure, there was no change in forearm vascular resistance (from 11.7 +/- 1.0 to 12.7 +/- 1.0 units, p = NS) or MSNA (from 494.8 +/- 88.5 to 369.1 +/- 60.5 units/100 heart beats, p = NS), suggesting a sympathoexcitatory response in normal subjects. To determine whether or not the digitalis-induced sympathoinhibition in the heart failure patients was simply due to an inotropic effect (stimulation of inhibitory cardiac mechanoreceptors), we studied the responses of seven additional patients with heart failure before and during administration of dobutamine (3.4 +/- 0.4 micrograms/kg/min). Dobutamine produced a 34 +/- 3% increase in cardiac index, no significant change in systemic arterial pressures, a decrease in pulmonary artery diastolic and right atrial pressures, and no change in heart rate or forearm vascular resistance (from 30.2 +/- 4.3 to 26.5 +/- 4.7 units, p = NS).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1989

Nifedipine potentiates cardiopulmonary baroreflex control of sympathetic nerve activity in healthy humans. Direct evidence from microneurographic studies.

Nifedipine augments baroreflex mechanisms in in vivo animal models. Previous studies in our laboratory demonstrate that nifedipine potentiates baroreflex control of heart rate and vascular resistance in normal human subjects. To further define the neuroeffector mechanism of the autonomic effects of nifedipine, we directly measured postganglionic sympathetic nerve activity to muscle (MSNA, microneurography), before and after drug administration, during selective unloading of cardiopulmonary baroreceptors with lower body negative pressure (-10 mm Hg, LBNP-10), and during the cold pressor test. Twenty-three normal subjects (age, 23 +/- 1 years; mean +/- SEM) were studied in the control state and 20 minutes after administration of either nifedipine (10 mg s.l., 10 subjects), during nitroprusside infusion (0.37 +/- 0.03 microgram/kg/min i.v., eight subjects), or 20 minutes after sublingual administration of placebo (five subjects). We measured systemic arterial pressure, central venous pressure, heart rate, and MSNA. Nifedipine and nitroprusside produced similar increases in resting heart rate and MSNA and similar decreases in central venous pressure, whereas placebo had no effect on resting hemodynamics. During LBNP-10, hemodynamic changes were not significantly different among the three treatment groups. However, the percentage increase in MSNA during LBNP-10 was significantly augmented from a 24 +/- 9% increase before nifedipine to a 56 +/- 7% increase after nifedipine (p less than 0.05). Decreases in central venous pressure with LBNP-10 were nearly identical before compared with after nifedipine. Thus, nifedipine increased the cardiopulmonary baroreflex sympathetic sensitivity (change in total MSNA per mm Hg decrease in central venous pressure during LBNP-10) from 26.5 +/- 10.7 units/mm Hg to 74.9 +/- 19.0 units/mm Hg (p less than 0.01). In contrast, administration of hemodynamically similar doses of nitroprusside resulted in an attenuation of MSNA responses to LBNP-10. During LBNP-10, MSNA increased 57 +/- 12% before nitroprusside but only 14 +/- 4% during nitroprusside (p less than 0.01). The cardiopulmonary baroreflex sympathetic sensitivity was not significantly altered by nitroprusside (45.1 +/- 12.4 units/mm Hg before compared with 33.1 +/- 20.8 units/mm Hg during nitroprusside, p = NS). Placebo had no effect on the responses to LBNP-10. Nifedipine did not augment MSNA responses to the cold pressor test. To evaluate the linearity of sympathetic responses to cardiopulmonary baroreceptor unloading, graded LBNP (0, -5, -10, and -15 mm Hg) was applied in three additional subjects before and after nifedipine (10 mg s.l.).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1988

Factors affecting transthoracic impedance during electrical cardioversion.

Successful cardioversion is dependent on the delivery of sufficient current. Current is determined by energy and transthoracic impedance (TTI). Our purpose was to assess factors affecting TTI in humans. Twenty-eight patients undergoing elective cardioversion were monitored up to 48 hours after shock delivery. We also studied 10 normal subjects, who did not receive shocks, for comparison. TTI declined 8% in the first hour in patients who received shocks, but also 6% in the normal subjects who wore the same pads for 1 hour but received no shocks. Twenty-four hours later, TTI returned to baseline in the nonshocked subjects but remained reduced (93% of control, p less than 0.05) in the shocked patients. There was a correlation between the total energy delivered and the decline in TTI (r = 0.69). TTI was 9% lower at end-expiration than at end-inspiration (55 +/- 3 vs 50 +/- 3 ohms, mean +/- standard error of the mean, p less than 0.01, paired t test). In the normal subjects, when a nonsalt-containing coupling agent (ultrasound coupling gel) was compared with a salt-containing gel (Redux paste), TTI was 20% higher (65 +/- 5 vs 54 +/- 4 ohms, p less than 0.01) with the nonsalt-containing gel. When no coupling agent was used, TTI was markedly higher, 160 +/- 18 ohms (p less than 0.01 vs control). After 1 hour, TTI decreased 6% in the normal subjects when salt-containing gel was used, but did not change when a nonsalt gel was used.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1988

Cardiopulmonary baroreflexes fail to modulate sympathetic responses during isometric exercise in humans: direct evidence from microneurographic studies.

To further evaluate the reported interaction in animals and humans between cardiopulmonary baroreflexes and the somatic pressor reflex, studies were performed in 16 normal men using direct measurements of efferent sympathetic nerve activity to muscle (microneurography) during sustained isometric handgrip (30% maximal voluntary contraction). Forearm vasoconstrictor (plethysmography) and muscle sympathetic nerve activity responses to sustained handgrip were measured during cardiopulmonary baroreceptor deactivation (lower body negative pressure, n = 8) and activation (volume expansion, n = 8). In addition, responses to posthandgrip muscle ischemia were studied during these perturbations of cardiopulmonary baroreflexes. No evidence of an interaction between these two reflex pathways was found. When handgrip was performed during lower body negative pressure, the percent increase in muscle sympathetic nerve activity (+115 +/- 17%) was not different from the sum of the individual sympathetic responses to handgrip and lower body negative pressure performed separately (+106 +/- 19%, p = NS). Likewise, the change in forearm vascular resistance (+3.9 +/- 0.8 U) for sustained handgrip performed during lower body negative pressure was not different from the algebraic sum of the responses to handgrip and lower body negative pressure when these were performed separately (+4.7 +/- 2.7 U, p = NS). No difference was noted in forearm vasoconstrictor and sympathetic nerve activity responses to posthandgrip muscle ischemia and lower body negative pressure when these were performed alone or in combination. Volume expansion also failed to uncover an inhibitory interaction. Handgrip performed before volume expansion resulted in forearm vascular resistance responses (-1.2 +/- 0.9 U) that were not different from the responses when such handgrip was performed after volume infusion (+0.9 +/- 0.9 U, p = NS). Rather than producing the predicted inhibition of muscle sympathetic nerve activity responses to sustained handgrip, volume infusion actually increased these responses. During prevolume sustained handgrip, the increase in sympathetic nerve activity (+64.5 +/- 15.7%) was significantly less than the increase when handgrip was performed after volume infusion (+105.6 +/- 20.1%, p less than 0.01). A similar lack of inhibitory modulation was seen during posthandgrip muscle ischemia performed before and after volume expansion. These data indicate that the efferent sympathetic responses to the somatic pressor reflex are not modulated by the cardiopulmonary baroreflexes in normal humans.

Adult↗
PubMed1988

Arterial baroreflex control of sympathetic nerve activity during elevation of blood pressure in normal man: dominance of aortic baroreflexes.

Arterial baroreceptors in the carotid sinus (CBR) and aortic arch (ABR) regions exert important control over heart rate and peripheral vascular responses to changes in arterial pressure. The relative roles of these two baroreflex pathways on control of sympathetic nerve activity during sustained elevation of arterial pressure in man is unknown. We therefore studied the relative contributions of the carotid versus the aortic baroreflexes on the control of muscle sympathetic nerve activity (MSNA) during elevation of arterial pressure in normal human subjects. In eight normal men (group I), we measured MSNA (microneurography) during sustained elevation of arterial pressure produced by intravenous infusion of phenylephrine (PE) alone (combined ABR and CBR activation) versus during PE infusion with superimposed application of sustained external neck pressure (NP). NP was applied during sustained PE infusion to eliminate the increase in transmural carotid sinus pressure and thus remove CBR activation, thereby causing ABR stimulation alone. Mean arterial pressure was measured directly, central venous pressure was held constant during PE infusion, and MSNA was measured as total activity (burst frequency X amplitude) and expressed as units. Infusion of PE (ABR and CBR activation) increased mean arterial pressure from 87.2 +/- 2.8 to 94.9 +/- 2.9 mm Hg (+/- SE, p less than .001). This was accompanied by a decrease in heart rate from 65.8 +/- 3.4 to 56.1 +/- 3.3 beats/min (p less than .001) and a decrease in MSNA from 236.2 +/- 47.5 to 84.5 +/- 19.3 units (p less than .001). During infusion of PE with superimposed NP (ABR activation alone), mean arterial pressure increased further to 101.2 +/- 2.9 mm Hg (p less than .001 versus control or PE alone), and heart rate returned to control levels of 62.9 +/- 2.0 beats/min (p = NS vs control; p less than .01 PE vs PE plus NP), but MSNA remained reduced at 48.6 +/- 9.2 units (p less than .01 vs control; p = NS vs PE alone). Thus, combined activation of ABR and CBR resulted in a 65 +/- 5% attenution of MSNA, while activation of ABR alone resulted in a 73 +/- 7% attenuation of MSNA. In a separate series of experiments in seven subjects (group II) we used sustained external neck suction alone to activate the CBR (leaving the ABR either unchanged or minimally deactivated) and studied the MSNA responses to this CBR activation.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1988

Coronary artery vasospasm complicating acute myocarditis. A rare association.

A 17-year-old boy had a 2-day prodrome of fever and mild sore throat followed by 2 episodes of severe anginal chest discomfort and substantial transient ST-segment elevations in the anterior leads of the electrocardiogram. A subsequent evaluation showed the 2 episodes were most likely coronary vasospasm complicating acute viral myocarditis.

Acute Disease↗
PubMed1987

Influence of nifedipine on arterial baroreflex modulation of heart rate control during dynamic increases in arterial pressure: studies in normal man.

Studies in animals have demonstrated that calcium channel blocking agents exert important influences on autonomic mechanisms in addition to their direct vascular effects. Previous studies in our laboratory showed that clinical doses of nifedipine sensitized baroreceptor-mediated control of peripheral vascular resistance in normal human subjects. However, baroreflex control of vascular tone does not necessarily imply parallel control of heart rate. A series of experiments was therefore performed to test the hypothesis that therapeutic doses of nifedipine would potentiate arterial baroreflex modulation of heart rate during ramp increases of arterial pressure in normal volunteers. Arterial baroreflex control was assessed by measuring heart interval (HI) responses to dynamic ramp elevation of systolic arterial pressure (SAP) with bolus administration of phenylephrine (PE) before and after nifedipine or placebo in 19 normal subjects. Arterial baroreflex control was calculated from the slope of the regression of SAP on succeeding HI during the first 18 cardiac cycles following onset of rise of SAP after PE bolus. In 13 subjects, bolus PE produced an increase in SAP from 125 +/- 3 mm Hg to 152 +/- 5 mm Hg (p less than 0.01), with a resultant increase in HI from 1110 +/- 57 msec to 1541 +/- 87 msec (p less than 0.01). The baroreflex response was linear (r greater than 0.80, p less than 0.025) and = 17.8 +/- 3.3 msec/mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

Acute rupture of myxomatous mitral valve presenting as refractory cardiopulmonary arrest.

A 59 year old white woman had an out of hospital sudden cardiac arrest. Resuscitation at the scene restored spontaneous pulse, blood pressure and respiration but cardiovascular collapse recurred within 30 minutes of hospital arrival. Medically refractory cardiogenic shock of unclear origin prompted the placement of an intraaortic balloon pump, and hemodynamic stabilization was achieved over several hours. Acute rupture of the chordae tendineae of myxomatous mitral valve was diagnosed as the cause of the cardiac arrest. Mitral valve replacement was performed and the patient made an uneventful recovery. This report describes the first known case of rupture of a myxomatous mitral valve presenting as sudden cardiac death. The differential diagnosis of sudden death in this disorder is reviewed, the role of mechanical circulatory assistance in refractory cardiac arrest is discussed and several interesting hemodynamic aspects of the case are considered.

Female↗
PubMed1986

Effect of high-dose cyclophosphamide and total-body irradiation on left ventricular function in adult patients with leukemia undergoing allogeneic bone marrow transplantation.

Protocols used to prepare patients with leukemia for bone marrow transplantation have the potential for cardiac toxicity due to high-dose cyclophosphamide and total-body irradiation. We have reported one regimen, combining cytarabine (5 mg/kg), cyclophosphamide (90 mg/kg), and total-body irradiation (900 cGy), which is relatively effective in the treatment of leukemia. To assess cardiac effects of this treatment regimen, we performed serial echocardiography and radionuclide ventriculography in 28 patients with leukemia (age range, 18-48 years; mean, 31; 21 males) undergoing allogeneic bone marrow transplantation. No significant change in left ventricular fractional minor axis shortening or increase in left ventricular diastolic dimension was seen with weekly echocardiography. At an average of 77 days (range, 28-358) after transplant, repeat radionuclide ventriculography in 17 patients revealed no significant change in resting left ventricular ejection fraction compared to that on admission to the hospital (58% +/- 6.8% vs 56% +/- 8.0% SD; P = not significant). In seven of these 17 patients (41%), resting ejection fraction fell between baseline and discharge (from mean of 60% to 50%). Resting ejection fraction in four of these patients (23% of the entire group) fell into the abnormal range (from mean of 56% to 44%; lowest, 41%). Ten patients also had exercise radionuclide ventriculography and all had normal responses (greater than 5% increase with exercise) pre- and post-transplant. We conclude that this effective bone marrow transplantation regimen has little apparent short-term cardiac toxicity in the majority of patients; since a few patients do exhibit a deterioration in left ventricular function, continued cardiac surveillance is probably indicated in posttransplant patients.

Adolescent↗