ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

ABSTRACTTotal left ventricular external power and aortic input impedance spectra were calculated from recordings of pulsatile pressure and flow in the ascending aorta of 22 human subjects undergoing cardiac catheterization. Eleven subjects had increased aortic pressure (systolic 153 ± 3.8[SEM] mm Hg, p < .001; diastolic 91 ± 2.4 mm Hg, p < .03; mean 118 ± 2.4 mm Hg, p < .001) and constituted the group with mild hypertension (average age 50 ± 1.9 years). The other 11 (age-matched) subjects had normal arterial pressures and constituted the control group. Cardiac output in the hypertensive group was abnormally high (6.9 ± 0.3 liters/min, p < .04) compared with that in control subjects (6.1 + 0.2 liters/min), so that peripheral resistance was similar. Characteristic aortic impedance (index of aortic elastance) was increased in the hypertensive group (142 + 19 vs 72 ± 4.5 dyne-sec-cm-5, p < .002), as was the fluctuation of impedance moduli and phase. These elevated pulsatile components of arterial load were associated with a significant (p < .002) increase in pulsatile left ventricular external power (89%), and the increased cardiac output was associated with a significant (p < .001) increase in steady flow power (31%). The ratio of pulsatile to total power was also increased (38%) in the hypertensive group (p < .001). Increased characteristic aortic impedance in the hypertensive group suggests that the human aorta is stiffer, and fluctuations in the impedance spectra suggest increased or less dispersed wave reflections. These alterations in the systemic arterial tree suggest that factors other than blood pressure and peripheral resistance impose an additional, functionally important hydraulic load on the left ventricle of subjects with mild or borderline hypertension.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

ABSTRACTRight ventricular loading leads to diastolic septal flattening in man without necessarily requiring right ventricular pressure to exceed left ventricular pressure. This observation suggested that the unstressed septal configuration is flat and that its normal concave shape is due to the left-to-right transseptal pressure gradient. To examine this hypothesis, we studied septal configuration by twodimensional echocardiography in nine patients with normal global and regional left ventricular function during surgery for coronary artery disease. The transseptal pressure gradient was obtained from pulmonary capillary wedge pressure minus right atrial pressure. Measurements were obtained at control (open chest, intact pericardium [C]), with the pericardium open (OP), on cardiopulmonary bypass (CPB), and after cardiac arrest (CA). There were no changes in any measurements between C and OP or between CPB and CA. Left ventricular end-diastolic cavity area decreased from 16.5 ± 2.1 cm2 at C to 11.1 ± 4.5 cm2 after CPB, and further decreased to 8.9 ± 3.5 cm2 after CA (p < .001), yet the septum flattened, as shown by an increase in its radius of curvature from 1.7 0.5 cm during C to 2.5 0.7 cm after CPB, and to 2.9 ± 1.0 cm after CA (p < .001), or from 0.4 0.1 to 0.8 0.4 to 1.1 0.5 U (p < .001) when normalized for cavity area. Diastolic transseptal pressure gradient was reduced from 4.1 ± 2.3 mm Hg during C to 1. 1 ± 1.8 mm Hg after CPB, and to 0.5 ± 1.4 mm Hg after CA (p < .01). Thus, in the unloaded human heart, the interventricular septum is more flat and occupies a neutral position between the left and right ventricle. Septal flattening due to a reduced but not reversed transseptal left-to-right gradient results from assumption of this unstressed shape as the right ventricular end-diastolic pressure approaches the left ventricular end-diastolic pressure. Circulation 74, No. 3, 463–468, 1986.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

ABSTRACTWe have shown improvement in collateral filling immediately after sudden controlled coronary occlusion in human subjects undergoing elective coronary angioplasty. It has been suggested but not proved that collateral circulation can limit myocardial ischemia. We prospectively studied 23 patients with isolated left anterior descending (n = 14) or right coronary (n = 9) disease and normal left ventriculograms during elective coronary angioplasty. A second arterial catheter was used for injection of the contralateral artery to assess collateral filling before balloon placement and during coronary occlusion by balloon inflation. Left ventriculography was performed during another inflation. Grading of collateral filling was as follows: 0 = none, 1 = filling of side branches only, 2 = partial filling of the epicardial segment, 3 = complete filling of the epicardial segment. Indexes of myocardial ischemia included percent of the left ventricular perimeter showing new hypocontractility and the sum of ST segment elevation measured on a simultaneous 12-lead electrocardiogram recorded during each inflation. Collateral filling during balloon occlusion and indexes of ischemia were assessed at 30 to 40 sec into inflation. Aortic pressure and heart rate did not correlate with the percent hypocontractile perimeter nor the sum of ST segment elevation. There was a significant correlation between the grade of collateral filling during inflation and both percent hypocontractile perimeter (r = − .85) and the sum of ST segment elevation (r = − .87). Anginal pain occurred in all patients with grade 0 or 1 collateral filling but in only 36% of patients with grade 2 or 3 collaterals. In conclusion, collateral circulation limits myocardial ischemia as assessed by the extent of new ventricular asynergy and electrocardiographic changes during coronary occlusion in patients. Circulation 74, No. 3, 469-476, 1986.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

ABSTRACTUsing nondenaturing polyacrylamide gel electrophoresis, we have identified two distinct myosin isoenzymes in human atrial tissue that correspond to the V1 and V3 isomyosins found in rat ventricular tissue. Normal left and right atrial appendages have approximately 50% V3. When the left atrium was exposed to hemodynamic overload secondary to mitral stenosis, the percent V3 increased to 77 + 10% (n = 10); exposure to hemodynamic overload secondary to mitral regurgitation caused an increase to 70 14% (n = 6). Changes in the isoenzyme pattern were seen in the right atria of patients with mitral stenosis and markedly elevated pulmonary arterial pressures compared with control subjects and patients with mitral stenosis without severe pulmonary hypertension. Several clinical variables were examined to determine which factors might influence isoenzyme expression. Age, sex, the presence of atrial fibrillation, and pulmonary capillary wedge pressure did not predict the isoenzyme pattern. However, patients with mitral valvular disease and only slightly enlarged left atria tended to have a higher percent V3 than those with massively enlarged atria. These data confirm that human atrial tissue, like rat ventricular tissue, can alter its isomyosin composition in response to a hemodynamic load. The data further suggest that the isoenzyme shift is an early adaptation to the imposed load.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

ABSTRACTContinuous-wave Doppler echocardiography was used to estimate pulmonary artery pressures by measuring pulmonary regurgitant flow velocity in 21 patients with pulmonary hypertension (mean pulmonary artery pressure - 20 mm Hg) and 24 patients without pulmonary hypertension. The pulmonary regurgitant flow velocity patterns, characterized by a rapid rise in flow velocity immediately after closure of the pulmonary valve and a gradual deceleration until the next pulmonary valve opening, were successfully obtained in 18 of the 21 patients with pulmonary hypertension and in 13 of the 24 patients without pulmonary hypertension. As pulmonary artery pressure increased, pulmonary regurgitant flow velocity became higher; the pulmonary artery-to-right ventricular pressure gradient in diastole (PG) was estimated from the pulmonary regurgitant flow velocity (V) by means of the simplified Bernoulli equation (PG = 4V2). The Doppler-determined pressure gradient at enddiastole correlated well with the catheter measurement of the pressure gradient at end-diastole (r = .94, SEE = 3 mm Hg) and with pulmonary artery end-diastolic pressure (r = .92, SEE = 4 mm Hg). The peak of Doppler-determined pressure gradient during diastole correlated well with mean pulmonary artery pressure (r = .92, SEE = 5 mm Hg). Thus continuous-wave Doppler echocardiography was useful for noninvasive estimation of pulmonary artery pressures.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

ABSTRACTIn this study we sought to determine whether characteristics of ventricular-induced atrial preexcitation during reciprocating tachycardia could help differentiate atrioventricular (AV) nodal reentry from orthodromic AV reentry using an accessory pathway and to identify the site of accessory pathways in patients with Wolff-Parkinson-White syndrome. Fifty-five patients with orthodromic AV reciprocating tachycardia and 22 patients with AV nodal reentrant tachycardia were studied with standard electrophysiologic techniques. There were 24 left free wall, 23 posterior septal, seven anterior septal, and one right free wall accessory pathways. Progressively premature right ventricular complexes (V2) were introduced during reciprocating tachycardia (V1V1). The VIV, interval during tachycardia minus the longest VIV2 at which atrial preexcitation occurred defined a preexcitation index (PI). Atrial preexcitation occurred in 49 of 55 (89%) patients with AV reentry compared with only three of 22 (14%) patients with AV nodal reentry (p < .001). In the three patients with AV nodal reentry who demonstrated atrial preexcitation, the PI was distinct from that of the septal pathways and was in the upper range of values for left free wall pathways. The percentage of tachycardias demonstrating atrial preexcitation was not different between the free wall and septal pathways, but His bundle activation was visible at the time of atrial preexcitation in only six of 17 (35%) left free wall compared with 13 of 16 (81%) posterior septal and seven of seven (100%) anterior septal pathways (p < .05 free wall vs posterior or anterior septal). Mean PI was 88, 38, and 17 msec for left free wall, posterior septal, and anterior septal pathways, respectively; all values were significantly different from each other. PI differentiated septal from left free wall pathways in 37 of 48 (77%) patients; a PI of 75 msec or greater occurred only with left free wall pathways and a PI under 45 msec only with septal pathways. Thus characteristics of ventricular-induced atrial preexcitation during reciprocating tachycardia help differentiate between AV nodal reentry and AV reentry and between left free wall and septal accessory pathways. Circulation 74, No. 493–500, 1986.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

ABSTRACTThe Fab fragments of antimyosin antibodies, labeled with 9mTc, were used in the scintigraphic examination of 30 patients with myocardial infarction. The ability to detect necrosis and determine its extent from the antimyosin scan were compared with the results of quantitative regional wall motion analysis by contrast ventriculography at 10 to 14 days and 99mTc-pyrophosphate imaging. Antimyosin images recorded by planar and single photon-emission computed tomography (SPECT) delineated areas of myocardial necrosis in 27 of 30 patients (90%) compared with a 91% sensitivity of pyrophosphate in 21 of 23 patients. Infarct size was determined by both antimyosin and pyrophosphate SPECT images. Results by both techniques showed a significant correlation with computer-derived hypokinetic segment length (r = .79 for both, p = .002) and peak creatine kinase (r = .9 for both, p < .01). Although sensitivity for and correlations with markers of necrosis were similar with both techniques, infarct size by pyrophosphate SPECT was 1.7 times larger than infarct size by antimyosin SPECT (p < .01). Certain zones in the infarct area were differentially labeled; the nature and irreversibility of injury within these zones remains to be clarified. Circulation 74, No. 3, 501–508, 1986.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID