摘要:

We studied the control of forearm vascular resistance (FVR) by cardiopulmonary receptors in seven patients with hypertension and left ventricular hypertrophy (LVH) and in seven normotensive control subjects. Increasing levels of lower body negative pressure (LBNP) (−10 and −40 mm Hg) induced a progressive decrease in central venous pressure (CVP) and an increase in FVR. The changes in these two variables were correlated both in normal subjects and patients with hypertension (slope for normal subjects = −29.9, for patients with hypertension = −40.3, NS). After propranolol, there was a significant reduction in the increase in FVR induced by −40 mm Hg LBNP in normal subjects (+ 107 ± 5 vs + 129 ± 15 mm Hg/ml/sec, p < .05) but not in patients with hypertension. Consequently, the slope of the ACVP/AFVR regression was reduced in normal subjects (− 20.6, p < .01) but not in patients with hypertension. In another seven normal subjects and seven patients with hypertension and LVH we assessed the effects of − 10 and − 40 mm Hg LBNP on left ventricular filling pressure (LVFP). LBNP induced similar changes in CVP, LVFP, and total peripheral resistance both in normal subjects and in patients with hypertension. Propranolol failed to modify the effects of LBNP on CVP and LVFP in both groups and reduced the response of total peripheral resistance to − 40 mm Hg LBNP only in normal subjects. Propranolol did not reduce the response of FVR to the cold pressor test and sustained handgrip or the arterial baroreflex response to the injection of phenylephrine and increased neck tissue pressure. Thus, hypertension-induced LVH seems to be associated with a selective impairment of the left ventricular sensory receptors.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

We have developed a model for assessing the influence of the decaying contractile systolic tension on diastolic wall dynamics and the passive properties of left ventricular muscle. Total measured left ventricular diastolic pressure and stress (aT) are determined by two overlapping processes: (1) the decay of actively developed pressure and stress (5A) and (2) the buildup of passive filling pressure and stress (C*). The decaying contractile stress aA iS formulated in terms of a relaxation pressure with a time constant (T) assessed during the isovolumic relaxation interval. By subtracting the contribution of aA from aT we obtain 0*. With micromanometry, echocardiography, and cineangiography, total and passive stress-strain relations and strain rates were evaluated over the entire filling period in six normal control subjects and in seven patients with aortic stenosis. Elastic stiffness constants (k), the slopes of the linear passive stiffness vs 0* relations, did not differ in the two groups over a common lower stress range (6/6 normal, k = 9.37 + 1.23; 7/7 aortic stenosis, k = 9.34 + 1.08). Over a higher 0* range, transition into a much steeper linear region occurred, and k values were much larger (4/7 aortic stenosis, k = 28.76 + 2.02). When diastolic stress levels are elevated, passive stiffness-stress relations can be better described as bilinear, with a much greater wall stiffness constant in the higher than in the lower stress range. Dynamic effects of decaying systolic contractile wall stress components are important in the rapid filling phase in normal hearts as well as in those with aortic stenosis.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Forty adult patients underwent Doppler and two-dimensional echocardiographic examination of the pulmonary artery from multiple views to determine the variability in the magnitude of Doppler-determined flow velocity and pulmonary arterial diameter from various echocardiographic windows. Flows were recorded from two or more views in 32 patients (80%). Twelve of these patients (38%) had flow velocities recorded from two or more views that were within 6% of each other. Twenty of these patients (62%) had view-dependent differences in measured flow velocity ranging from 7% to 48%. The commonly used parasternal short-axis view yielded the highest pulmonary arterial flow velocity in only 35% of the patients studied. Determinations of pulmonary arterial blood flow can vary markedly when measured from different sites, and this is presumably due to varying ability to approximate a zero-degree Doppler angle from different views. Measurement of pulmonary arterial flow velocity should be attempted from multiple views, and the highest flow velocity should be selected as that obtained with the best zero-degree Doppler angle approximation.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

In this study, we tested the hypothesis that myocardial ischemia induced by exercise in patients is associated with diminished metabolism and/or delayed clearance of an intravenously injected fatty acid, iodine 123-labeled phenylpentadecanoic acid (IPPA). Fifteen normal volunteers and 18 patients with significant coronary heart disease (CHD) received IPPA during exercise. In the patients with CHD, radionuclide ventriculograms were also obtained during exercise. The normal volunteers had relatively uniform initial left ventricular segmental IPPA activity after exercise and uniform IPPA clearance in the interval from 4 to 20 min immediately after exercise. In contrast, the patients with CHD had increased initial left ventricular segmental IPPA activity (63%, p < .001) and delayed IPPA clearance (44%, p < .01) in segments supplied by significantly narrowed coronary arteries. Based on analysis with the mean values + 1 SD for initial IPPA activity, clearance, or both in normal volunteers, the sensitivity and specificity of exercise IPPA scintigraphy for detecting CHD were 89% and 67%, respectively; when + 2 SD differences from the mean values in the normal volunteers were considered, the sensitivity and specificity were 72% and 100%, respectively. Among the total of 27 noninfarcted left ventricular segments supplied by significantly narrowed coronary arteries in the study patients, 26 (96%) had an abnormality (mean + 1 SD) of either initial IPPA activity or clearance compared with corresponding segments in the normal volunteers and/or with other left ventricular segments in the same image that were not supplied by significantly narrowed coronary arteries. Thus, these data suggest that IPPA scintigraphy may be used in the identification of myocardial ischemia in patients with CHD by demonstrating abnormal initial left ventricular segmental IPPA activity and/or delayed clearance after exercise.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Signal processing of the electrocardiogram (ECG) was performed during supraventricular tachycardia (SVT) in 24 patients in an attempt to locate the P wave and to characterize its morphology in three orthogonal planes. In patients with atrioventricular reciprocating tachycardia, a discrete atrial signal could be identified within the ST segment and/or T wave with inferior-to-superior orientation. Atrial activation was identified in patients with primary atrial tachycardia as long as there was a constant relationship between each QRS complex and the preceding atrial signal. Patients with atrioventricular nodal reentrant tachycardia were deduced to have simultaneous atrial and ventricular activation when no atrial signal could be seen elsewhere in the cycle. Mean maximum P wave amplitude was 25.4 + 6.3, V during SVT, with a mean noise level below 1.0, uV. Signal processing of the ECG during SVT enhances the detection of the P wave and the appreciation of P wave morphology, both of which are important factors in the noninvasive determination of the electrophysiologic mechanisms of SVT.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

In a group of 39 patients who received fibrinolytic therapy for acute myocardial infarction, serum crosslinked fibrin degradation products (XLDP) were quantitated by an enzymelinked immunosorbent assay (ELISA) using an antibody reactive with a site near the yy crosslink of fibrin, and characterized by a gel electrophoretic method to distinguish fibrinogen degradation products (FDP) from XLDP. After coronary artery reperfusion, 63 of 81 (69%) serum samples showed XLDP by gel analysis, whereas the incidence of positive samples before reperfusion, 53 of 144 (37%), was significantly less (p < .0001). The first appearance of serum XLDP by gel analysis was most often in the 15 min interval immediately before or after angiographic documentation of reperfusion, and the elapsed treatment time required to produce a positive test was shorter with more intensive treatment regimens. However, the appearance of serum XLDP was not a specific indicator of reperfusion in individual patients, since one or more serum samples was positive in five of eight patients who did not show reperfusion as well as in 27 of 29 patients who did show reperfusion. Furthermore, the concentration of serum XLDP as measured by ELISA showed no significant difference in samples from patients who did or did not have reperfusion or between samples taken before or after reperfusion. There was a close temporal correlation between the first appearance of serum XLDP (gel analysis) and the initial decrease in plasma fibrinogen (systemic lytic state), and the degree of elevation of serum XLDP (ELISA) was also correlated with the intensity of the systemic lytic state. In addition, electrophoretic analysis of pretreatment plasma samples demonstrated crosslinked fibrin polymers that disappeared during fibrinolytic therapy coincident with the appearance of serum XLDP and in parallel with fibrinogen conversion to degradation products (fragments X, Y, and D). Two patients without a lytic state showed no change in plasma fibrin polymers during therapy, and XLDP were not present in serum despite coronary reperfusion in one patient. Thus the results indicate that XLDP appearing in the blood during fibrinolytic therapy for acute myocardial infarction are not predictive of successful fibrinolytic therapy, but rather may reflect degradation of circulating fibrin polymers associated with the fibrinogenolysis of the systemic lytic state.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Induction of rapid ventricular tachycardia or fibrillation during therapy with amiodarone is associated with an increased risk of sudden death. To determine whether the addition of a type IA antiarrhythmic agent to therapy would improve outcome, 37 patients in whom ventricular tachyarrhythmia of a cycle length less than 350 msec was induced after 14 + 2 days of amiodarone were randomly assigned to therapy with amiodarone alone (group 1, 20 patients) or amiodarone plus type IA agent (group 2, 17 patients). Type IA therapy consisted of procainamide in 13 patients and quinidine in four procainamide-intolerant patients. To assess the short-term effects of a type IA agent on inducibility of ventricular tachyarrhythmia, cycle length, and hemodynamic tolerance, 16 of 20 patients in group 1 and all patients in group 2 underwent repeat programmed stimulation after the intravenous administration of procainamide during amiodarone therapy (mean procainamide serum concentration 7.2 + 2.0 1ag/ml). Procainamide prevented induction of sustained arrhythmia in only two of 33 patients. Procainamide increased the cycle length of induced ventricular tachycardia from 283 30 to 352 46 msec (p < .001). After the addition of procainamide, 16 of 31 patients vs 10 of 37 patients on amiodarone alone had an induced arrhythmia that was tolerated hemodynamically (p < .05). There were no differences between groups 1 and 2 with respect to patient or arrhythmia characteristics, response to short-term procainamide, or duration of follow-up. The mean follow-up for all patients was 14 + 10 months. By life table analysis, outcome did not differ between group 1 and group 2 patients with respect to either development of sudden death or syncope (four patients in group 1 vs five patients in group 2) or the development of any arrhythmia event or side effect that required withdrawal of antiarrhythmic therapy (nine patients in group 1 patients vs 12 patients in group 2). Forty percent of group 2 patients developed adverse effects necessitating withdrawal of drug. We conclude in patients in whom rapid ventricular tachycardia is induced on amiodarone (1) type IA agents increase the cycle length and result in improved hemodynamic tolerance but rarely prevent induction of ventricular tachycardia, and (2) outcome is not improved by the addition of a type IA agent to therapy.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Five patients with chronic or recurrent ectopic supraventricular tachycardias unresponsive to drugs underwent programmed stimulation, endocardial mapping, and attempted catheter ablation of the arrhythmia focus. For attempted ablation, an intracardiac electrode catheter was positioned near the exit point of the tachycardia and served as the cathode while a chest wall patch served as the anode. In two patients with tachycardia originating near the coronary sinus, discharges of 200 or 400 J each were delivered to two electrodes at the earliest area of endocardial activation. These two patients with incessant tachycardia remain free of tachycardia for 17 and 11 months, respectively. In one patient with tachycardia originating from the right atrial appendage, both catheter and surgical ablation proved unsuccessful in that a new focus of atrial tachycardia supervened. This patient subsequently underwent successful catheter ablation of the atrioventricular junction. Two patients with junctional tachycardia underwent catheter ablation of the atrioventricular junction. Complete atrioventricular block followed atrioventricular junctional ablation and these patients required pernanent cardiac pacing. The junctional tachycardia was replaced by sinus rhythm with episodes of unsustained atrial tachycardia. However, after 13 + 5 months follow-up, neither of the patients require antiarrhythmic drugs. Catheter ablation can be effective for atrial foci near the coronary sinus os, and can be performed with preservation of atrioventricular conduction. Arrhythmia ablation is possible in those with atrioventricular junctional tachycardia but requires the sacrifice of atrioventricular conduction. After ablation, other automatic atrial foci may become operative and complicate use of dual-chamber pacemakers. BSTRACT Induction of rapid ventricular tachycardia or fibrillation during therapy with amiodarone is associated with an increased risk of sudden death. To determine whether the addition of a type IA antiarrhythmic agent to therapy would improve outcome, 37 patients in whom ventricular tachyarrhythmia of a cycle length less than 350 msec was induced after 14 + 2 days of amiodarone were randomly assigned to therapy with amiodarone alone (group 1, 20 patients) or amiodarone plus type IA agent (group 2, 17 patients). Type IA therapy consisted of procainamide in 13 patients and quinidine in four procainamide-intolerant patients. To assess the short-term effects of a type IA agent on inducibility of ventricular tachyarrhythmia, cycle length, and hemodynamic tolerance, 16 of 20 patients in group 1 and all patients in group 2 underwent repeat programmed stimulation after the intravenous administration of procainamide during amiodarone therapy (mean procainamide serum concentration 7.2 + 2.0 1ag/ml). Procainamide prevented induction of sustained arrhythmia in only two of 33 patients. Procainamide increased the cycle length of induced ventricular tachycardia from 283 30 to 352 46 msec (p < .001). After the addition of procainamide, 16 of 31 patients vs 10 of 37 patients on amiodarone alone had an induced arrhythmia that was tolerated hemodynamically (p < .05). There were no differences between groups 1 and 2 with respect to patient or arrhythmia characteristics, response to short-term procainamide, or duration of follow-up. The mean follow-up for all patients was 14 + 10 months. By life table analysis, outcome did not differ between group 1 and group 2 patients with respect to either development of sudden death or syncope (four patients in group 1 vs five patients in group 2) or the development of any arrhythmia event or side effect that required withdrawal of antiarrhythmic therapy (nine patients in group 1 patients vs 12 patients in group 2). Forty percent of group 2 patients developed adverse effects necessitating withdrawal of drug. We conclude in patients in whom rapid ventricular tachycardia is induced on amiodarone (1) type IA agents increase the cycle length and result in improved hemodynamic tolerance but rarely prevent induction of ventricular tachycardia, and (2) outcome is not improved by the addition of a type IA agent to therapy.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

We recently reported a retrospective experience with serial Holter monitoring as a guide to therapy in patients with sustained ventricular tachycardia treated with amiodarone. To confirm and substantiate these findings, a prospective study was designed that included baseline 24 hr Holter monitoring and serial Holter monitoring after 1 week of therapy with amiodarone. Fifty-two patients with documented sustained ventricular tachycardia who manifest nonsustained ventricular tachycardia on baseline Holter monitoring were treated with amiodarone. Thirty-four patients (group I) had nonsustained ventricular tachycardia completely suppressed and 18 patients (group II) had continued nonsustained ventricular tachycardia on serial Holter monitoring performed on days 8, 9, and 10 of therapy. At 11.6 + 1.0 (mean ± SE) months follow-up, three (9%) group I patients and 12 (67%) group II patients had recurrent sustained ventricular tachycardia or sudden cardiac death (p < .01). The sensitivity, specificity, positive and negative predictive value, and predictive accuracy of ventricular tachycardia on 24, 48, and 72 hr Holter monitoring over days 8, 9, and 10 for predicting recurrent sustained ventricular tachycardia or sudden cardiac death were analyzed. The positive and negative predictive values were 89% and 84%, 69% and 89%, and 67% and 91Y% for 24, 48, and 72 hr Holter monitoring, respectively. Overall predictive accuracy was 85%, 83%, and 83%, respectively. We conclude that early Holter monitoring is useful in assessing the clinical efficacy of amiodarone in patients with sustained ventricular tachycardia who manifest nonsustained ventricular tachycardia on baseline Holter monitoring.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Nine normal volunteers underwent assessment of renal, forearm, and hormonal responses to orthostasis (quiet standing) in the presence and absence of 1 week of oral propranolol (160 mg/day). This was done to test the hypothesis that physiologic decrements in renal function (glomerular filtration rate, effective renal plasma flow, and absolute urinary sodium excretion) are attenuated by propranolol during quiet standing. The present studies, however, demonstrate that propranolol exaggerates the physiologic decrement in glomerular filtration rate, effective renal plasma flow, and absolute urinary sodium excretion during orthostasis. Forearm and renal vascular resistances were also accentuated in the presence of propranolol during quiet standing. These responses were associated with significant increases in plasma norepinephrine. We conclude that long-term administration of propranolol accentuates the physiologic decrement in renal hemodynamic and excretory function as well as in the forearm hemodynamic response to orthostasis in normal subjects.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID