ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Coronary angiography demonstrates only collateral arteries that are already in use (spontaneously visible collaterals). Percutaneous transluminal coronary angioplasty (PTCA) provides an opportunity to uncover collaterals ready to become functional in case of occlusion of the recipient artery (recruitable collaterals). The incidence of recruitable collaterals and their relation to the distal pressure in the occluded artery (coronary wedge pressure) during a 30 sec or longer balloon occlusion was assesed in 57 coronary arteries of 49 patients undergoing PTCA for a proximal coronary stenosis or occlusion. Collaterals to 75% of the arteries were present. Spontaneously visible collaterals were four times as frequent as recruitable collaterals. Coronary wedge pressure was significantly higher in arteries with spontaneously visible and recruitable collaterals (41 ± 12 and 36 ± 12 mm Hg, respectively) than in arteries without collaterals (18 ± 4 mm Hg). A coronary wedge pressure of 30 mm Hg or higher was found exclusively in the presence of collaterals. Electrocardiographic changes during balloon occlusion were found more frequently with arteries without collaterals than with arteries with spontaneously visible or recruitable collaterals. Chest pain was more frequent in patients without collaterals or with recruitable collaterals than in those with spontaneously visible collaterals. Major inhospital events occurred in three patients with collaterals, with a salutary influence of the collaterals in two. The coronary wedge pressure allows prediction of recruitable collaterals. Their clinical impact remains to be investigated in long-term studies on large patient populations.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

There is ample evidence for efferent cardiac denervation in patients after cardiac transplantation. However, little is known regarding the effects of the cardiac deafferentation that also results. We examined responses to graded lower-body negative pressure and thus cardiopulmonary baroreceptor unloading in 23 patients 3 to 12 months after cardiac transplantation and compared their responses with those of nine normal subjects. Responses of mean arterial pressure, forearm vascular resistance, and plasma norepinephrine were assessed during lower-body negative pressure and the cold pressor test. Reflex increases in forearm vascular resistance (1.5 ± 1, 5.0 1.4, and 6.4 ± 2.1 vs 14.5 ± 4.5, 20.3 ± 6.5, and 34 ± 1 1 units) and plasma norepinephrine (42 12, 58 ± 15, and 62 ± 13 vs 49 ± 14, 94 ± 25, and 173 4- 36 pg/ml) during lower-body negative pressure (at − 10, − 20, and − 40 mm Hg) were strikingly smaller in cardiac transplant patients than in normal subjects. The impaired responses of the cardiac transplant patients were not the result of a nonspecific depression of cardiovascular reflexes, since increases in mean arterial pressure (12 3 vs 10 ± 2 mm Hg), forearm vascular resistance (19.5 ± 3.4 vs 18 ± 5.8 units), and plasma norepinephrine (56 8 vs 42 1 1 pg/ml) during cold pressor test were not significantly different in the two groups. Furthermore, the impaired responses were not caused by the immunosuppressive agents used to treat the cardiac transplant patients, since patients with renal transplants on similar regimens had augmented forearm vasoconstrictor responses. The technique of orthotopic transplantation we used results mainly in ventricular deafferentation. Thus our data suggest that cardiopulmonary baroreflex control of forearm vascular resistance is impaired after cardiac transplantation and that this is due mainly to ventricular deafferentation.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

To define the effects of circulating norepinephrine and epinephrine on cardiac function and to determine whether left ventricular function is influenced by parasympathetic mechanisms during catecholamine stimulation, hemodynamic changes were investigated in healthy young human subjects who were supine and awake during infusion of (1) intravenous norepinephrine alone (125 ng/kg/min) (n = 6), (2) norepinephrine (125 ng/kg/min) plus epinephrine (50 ng/kg/min) (n = 6), and (3) norepinephrine plus epinephrine plus parasympathetic blockade induced by atropine (2 mg intravenously) (n 5). Ejection fraction and changes in cardiac volumes were measured by radionuclide ventriculography. During the infusion of norepinephrine plus epinephrine, plasma norepinephrine increased from 358 ± 35 to 1782 ± 123 pg/ml (mean ± SE) and plasma epinephrine increased from 31 ± S to 355 ± 90 pg/ml (both p < .01 vs baseline). These increases in plasma catecholamines were associated with increases in the heart rate (58 ± 3 to 67 2 beats/min, p = NS), systolic blood pressure (113 ± 3 to 140 ± 6 mm Hg, p < .01), ejection fraction (0.64 ± 0.02 to 0.72 0.02 ejection fraction units, p < .01), stroke volume (± 41 5%, p < .01), and cardiac output (± 54 8%, p < .01), and a decrease in systemic vascular resistance (−31 3%, p < .01). Administration of atropine during the concurrent infusion of catecholamines led to additional increases in heart rate (127 ± 5 beats/min), systolic pressure (179 ± 10 mm Hg), ejection fraction (0.83 ± 0.05), stroke volume (±58 ± 5%), and cardiac output (+ 262 ± 18%), and a decrease in systemic vascular resistance (−63 ± 1%) (all p < .05 compared with baseline and with norepinephrine plus epinephrine alone). These findings define in part the range of hemodynamic changes controlled by sympathetic and parasympathetic mechanisms in normal subjects. The augmentation of ejection fraction and stroke volume by the infusion of atropine supports the concept that parasympathetic inhibition of ventricular performance occurs in man.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Electrophysiologic studies were performed in 28 patients with documented atrioventricular (AV) nodal reentrant supraventricular tachycardia (SVT) to investigate the presence of AV nodal tissue situated between the tachycardia circuit and both the atrium (upper common pathway, UCP) and the His bundle (lower common pathway, LCP). All patients demonstrated a 1:1 AV relationship during SVT. The study protocol consisted of atrial then ventricular pacing at the SVT cycle length. UCPs were manifested in eight of 28 (29%) patients by either antegrade AV Wenckebach (six patients) or a paced atrium-His (AH) interval exceeding the AH in SVT (two patients, differences 5 and 9 msec). LCPs were manifested in 21 of 28 (75%) patients by either retrograde Wenckebach periodicity (two patients) or a paced HA interval exceeding the HA in SVT (19 patients, mean difference 25 ± 20 msec). By these criteria, eight patients (29%) had evidence for both UCPs and LCPs. UCPs were more likely than LCPs to be manifested by Wenckebach criteria (p < .05). Thus (1) the AV nodal reentrant SVT circuit appears to be intranodal and is frequently surrounded by AV nodal tissue (UCP and LCP), (2) antegrade and retrograde conduction properties of these common pathways are discordant in some cases, and (3) conduction properties of UCP tissue differ from those of LCP tissue. These findings may have relevance in that the UCP or LCP may limit the ability of premature extrastimuli to penetrate the circuit to initiate or terminate AV nodal SVT.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

In clinical cardiac tamponade, open-catheter intrapericardial pressure (IPP) may be used to estimate left ventricular transmural filling pressure (TMFP). However, it has been suggested recently that right atrial pressure (RAP) is superior to IPP in assessing true extracardiac pressure during pericardial drainage. In 10 patients with subacute cardiac tamponade, pulmonary wedge pressure (PWP), RAP, and IPP were measured along with indexes of systolic function. To test the relative merits of IPP and RAP in assessing true pericardial pressure, three TMFP estimates were analyzed: TMFP1 = (PWP − IPP); TMFP2 = (PWP − 1/3 RAP − 2/3 IPP); and TMFP3 = (PWP − RAP). An accurate TMFP presumably should increase during pericardiocentesis and correlate with left ventricular stroke work. In addition, to test the role of preload variation in pulsus paradoxus, respiratory variation in TMFP was analyzed. In the initial tamponade state, RAP and IPP were essentially equal, so all three TMFP estimates gave equivalent results. For instance, TMFP1 averaged 4 ± 2 mm Hg but fell to 0.2 ± 1.3 mm Hg during inspiration (p < .001 vs expiration) and showed beat-by-beat correlation with pulse arterial pressure. After intermediate pericardiocentesis (280 ± 160 ml), the IPP of 6 ± 3 mm Hg fell significantly below the RAP of 10 ± 3 mm Hg (p < .001), but with a 570 ± 320 ml residual effusion suggesting continued IPP measurement accuracy. By complete pericardiocentesis (810 ± 430 ml) there was a significant increase in TMFP1 to 8 ± 4 mm Hg (p < .05 vs tamponade) but not in the TMFP3 of 1 ± 3 mm Hg. Encompassing tamponade and pericardiocentesis data, left ventricular stroke work index showed positive correlation with TMFP1 (r = .59) and TMFP2 (r = .52) but not with TMFP3. Thus cardiac tamponade often may be diagnosed with a TMFP averaging well above zero, and diastolic equalization of PWP, RAP, and IPP may be a predominantly inspiratory finding ("inspiratory tracking"). This supports the role of preload variation in the genesis of pulsus paradoxus. On the other hand, true pericardial pressure may fall substantially below RAP in the course of pericardial drainage. This may be reconciled with the concept that normal pericardial pressure nearly equals RAP by hypothesizing an increased pericardial capacity in subacute tamponade so that pericardiocentesis produces a state analogous to removal of normal pericardial constraint.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

ABSTRACT Patients who develop pregnancy-induced hypertension exhibit a lesser increment in prostacyclin biosynthesis than healthy pregnant subjects. Whether this precedes the development of clinical disease and therefore may be important in the pathogenesis of pregnancy-induced hypertension or is a secondary event is unknown. We prospectively determined prostacyclin biosynthesis in pregnant subjects at risk of developing pregnancy-induced hypertension by use of noninvasive approach, measurement of the urinary metabolite 2,3-dinor-6-keto-prostaglandin F1α. Patients were recruited at less than 20 weeks gestation. After delivery, patients were retrospectively allocated by use of preset criteria, to one of four groups: (1) pregnancy-induced hypertension (n 12), (2) hypertension in labor (n = 22), (3) chronic hypertension (n = 9), and (4) normotension (n = 24). There was a significant increase in prostacyclin biosynthesis in all study groups during gestation. However, patients who developed pregnancy-induced hypertension exhibited a lesser increment and this difference persisted throughout gestation. These results are consistent with a pathophysiologic role for altered prostacyclin biosynthesis in women with pregnancy-induced hypertension. In addition, decreased prostacyclin formation identifies a population at risk of developing pregnancy-induced hypertension. Such information would assist the design of clinical trials of drugs, such as aspirin, that might prevent the development of this disease.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The new concept of systolic myocardial stiffness was applied to the study of ejection mechanics in aortic valve disease. Frame-by-frame analysis of stress (σ) and volume (V) was performed for two differently loaded beats in 26 patients who underwent simultaneous cineangiography and micromanometry: nine normal subjects, eight with isolated aortic regurgitation (AR), and nine with aortic stenosis (AS). Maximum myocardial stiffness (maxEav) was defined as the slope of the endsystolic (es) stress-strain relationship. End-systole was defined as the frame where stiffness was maximal, and strain was defined as E = loge (Dm/Dom), where Dmis left ventricular midwall diameter and Do. is the theoretical Dm at zero stress. Expressed in terms of cavity volume, ε = γ · log, (V/V0), where γ is the geometric factor relating Dm to V during systole. V. was obtained by extrapolating to Ces 0 the function, σes, which was fit to the end-systolic data. VO always had a value greater than zero. Max Eav was preserved in the AR group (1575 ± 565) and increased in the AS group (1877 ± 544; p = .02) compared with normal (1320 ± 268), suggesting maintenance of contractile force per unit of myocardium in these two lesions. However, theoretical "unloaded" shortening fraction (SFO) was depressed in the AS group (0.30 ± 0.06; p = .01) compared with normal (0.37 ± 0.04), preserved in the AR group (0.34 ± 0.07; p = .24), and inversely related to max Eav (r − .66, p .01), suggesting a disparity between shortening potential and force potential. Systolic σ-V profiles had a characteristic pattern in the presence of AS when ejection fraction was normal, with stiffness approaching maximum earlier in ejection than in normal subjects or in the AR group. This difference in early systolic myocardial stiffness might be caused by ventricular resistance arising from different velocity profiles or from different aortic outflow resistance.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Congenital aortic stenosis in children is characterized by low left ventricular systolic wall stress allowing for supernormal ejection performance. In contrast, adults with acquired aortic stenosis have normal or excessive systolic wall stress resulting in either normal or subnormal ejection performance. In this study young children with congenital aortic stenosis, older children and dults with congenital aortic stenosis, and adults with acquired aortic stenosis were evaluated to test the hypothesis that the childhood pattern of low wall stress would convert to the adult pattern with advancing age. Left ventricular end systolic wall stress was lower in both congenital aortic stenosis groups when compared with that in age-matched normal subjects or adults with acquired aortic stenosis. Ejection fraction was higher in both groups of patients with congenital aortic stenosis than in age-matched controls. There was no tendency in the 16 patients with congenital aortic stenosis, some of whom were followed to the age of 33, for the congenital pattern of wall stress and ventricular performance to convert to the adult pattern. These results suggest that there is a fundamental difference in the hypertrophic response to a pressure overload present at birth compared with the response to one acquired later in life.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID