ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Cigarette smoking is associated with increased mortality from cardiovascular disease that declines after cessation. This study extends the evidence regarding the effects of chronic smoking on platelets and the vessel wall in vivo. Excretion of a major urinary thromboxane metabolite, 2,3- dinor-thromboxane B2, is significantly (p < .01) elevated in apparently healthy chronic smokers (20 cigarettes daily) compared with that in nonsmoking control subjects. This difference in excretion of 2,3-dinor-thromboxane B2 was abolished by the administration of 20 mg aspirin twice daily, a dose shown to selectively inhibit platelet cyclooxygenase. After aspirin, the return of the excretion of 2,3- dinor-thromboxane B2 to pretreatment levels paralleled the recovery of platelet cyclooxygenase. These findings indicate that excessive thromboxane A2 generation in chronic smokers predominantly derives from platelets. The urinary excretion of the prostacyclin metabolite 2,3-dinor-6-keto-prostaglandin F1αalso is increased during chronic cigarette smoking, as is the case with other diseases associated with accelerated interaction of platelets with the vessel wall. We have found evidence of platelet and vascular dysfunction in vivo in chronic cigarette smokers before the manifestation of overt cardiovascular disease. The results would also be consistent with the hypothesis that in chronic smokers, the platelet defect is largely reflective of smoking-induced vascular injury.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

We investigated several rheologic variables in 17 patients (11 men, six women, mean age = 52. 1 ± 9.8 years) with chronic stable angina. None took any medication except for sublingual nitroglycerin for 2 weeks before the study, and all had angiographically proven coronary artery disease with no history of myocardial infarction. Rheologic measurements included hematocrit, whole blood and plasma viscosity (750 and 1500 sec−1), degree of red cell aggregation via the zeta sedimentation ratio, and the extent and rate of red cell aggregation after stasis (Myrenne aggregometer). Compared with normal control donors, salient observations in the patients as a group included: (1) a small (6%) but significant increase in hematocrit, (2) a significant elevation in plasma viscosity (9%), (3) significant increases in whole blood viscosity at both shear rates (14% and 16%), (4) significant increases in the degree (12%), the extent (41 %), and the rate (28% faster time constant) of red cell aggregation, (5) an elevated a2 level (15% increase) and a significantly increased fibrinogen concentration (25% increase), both of which correlated with the enhanced red cell aggregation. Rheologic abnormalities were evident when patients with disease in either one vessel or two to three vessels were compared with controls, but differences between these subgroups of patients were not significant. We conclude that patients with angina have rheologic abnormalities that are compatible with disturbed blood flow and an enhanced tendency for coronary arterial thrombosis.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Long RP′ supraventricular tachycardias (SVT) often demonstrate both slow and decremental conduction properties in the retrograde pathway of the reentrant circuit. The electrophysiologic properties of these pathways are poorly understood. We studied 10 patients with long RP′ SVT (RP′/RR, 0.52 to 0.71); five had the unusual form of atrioventricular nodal reentry (fast-slow) and five patients had accessory AV pathways with slow, decremental retrograde conduction properties. During SVT, the effects of intravenous adenosine (37.5 to 150 μg/kg), which increases potassium current (QK) in supraventricular tissue and hyperpolarizes membrane potential toward Ek (−90 mV), and the response to slow-inward channel blockade with verapamil (0.10 to 0.20 mg/kg iv) were evaluated. Adenosine and verapamil has similar effects in the presence of fast-slow AV nodal reentry since both agents terminated SVT by producing block in the retrograde slow AV nodal pathway. In contrast, adenosine and verapamil had differential effects on retrograde conduction in decremental accessory pathways. Adenosine terminated all episodes of SVT in the retrograde decremental pathway, whereas verapamil had a direct effect on this tissue in only two of five patients. Decremental retrograde accessory pathways can therefore demonstrate at least two types of electrophysiologic responses. Pathways that respond only to adenosine-induced hyperpolarizing K′ current likely comprise depressed fast-Na± channel tissue, i.e., partially depolarized (> −60 to −70 mV) atrial tissue. In contrast, decremental accessory pathways that respond to both modulation of the slow-inward calcium current and K′ conductance have pharmacologic properties similar to those of the AV node and may represent more completely depolarized atrial fibers with resting membrane potentials of − 60 mV or less.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

This investigation was designed to calculate left ventricular maximum time-varying elastance (Emax), to define the relationship between Emax and pressure-volume (P-V) relations at other, more easily defined measured of end-systole, and to determine whether these measures of left ventricular contractile function can be normalized in man. Accordingly, we studied 10 subjects with simultaneous high-fidelity micromanometer left ventricular and ascending aortic pressure recordings and biplane contrast cineangiograms at control conditions and during infusion of methoxamine and nitroprusside. Emax was defined as the maximum slope of the linear relation of isochronal, instantaneous P-V data points obtained from each of the three loading conditions. Left ventricular end-systole was also defined for each loading condition as: the time of the maximum P-V ratio (maxPV), minimum ventricular volume (minPV), (−) dP/dt. [(i−) dP/dtPV], and zero systolic flow approximated by the central aortic dicrotic notch (AodiPV). The mean heart rates and LV (±) dP/dtmax were insignificantly altered during the three loading conditions. Isochronal Emax ranged from 3.38 to 6.73 mm Hg/ml (mean 5.48 ± 1.23 [SD] mm Hg/ml) and the volume-axis intercepts at zero pressure ranged from −2 to 51 ml (mean 18 ± 16 ml). The isochronal slope calculations were reproducible (r = .97 to .99). The endsystolic P-V slope values for the maxPV, minPV, (−) dP/dtPV, and AodiPV relations correlated with isochronal Emax (r = .90, .88, .69, and .74, respectively). The average slope values for these endsystolic P-V relations, however, underestimated the mean Emax (p < .01 to p < .001). The mean extrapolated volume-axis intercepts for these end-systolic P-V relations also underestimated that for Emax. Finally, the isochronal Emax and other end-systolic P-V relation slope values demonstrated inverse linear relationships with left ventricular mass (r = − .68 to − .91, p < .05 to p < .001). Only the Emax volume-axis intercepts showed a linear relationship with left ventricular end-diastolic volume (r = .75). Thus we conclude that the time-varying elastic properties of the left ventricle can be calculated in man, that commonly used end-systolic P-V relations significantly underestimate isochronal Emax, and that normalization of isochronal Ema, and other end-systolic P-V relation slope values might be performed in man with left ventricular mass; no obvious relationship between volume-axis intercepts and measures of left ventricular or body size was apparent.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Impairment of left ventricular function is the major predictor of mortality after acute myocardial infarction, but it is not known whether this is best described by ejection fraction or by endsystolic or end-diastolic volume. We measured volumes, ejection fractions, and severity of coronary arterial occlusions and stenoses in 605 male patients under 60 years of age at 1 to 2 months after a first (n = 443) or recurrent (n = 162) myocardial infarction and followed these patients for a mean of 78 months for survivors (range 15 to 165 months). There were 101 cardiac deaths, 71 (70%) of which were sudden (instantaneous or found dead). Multivariate analysis with log rank testing and the Cox proportional hazards model showed that end-systolic volume (X2 = 82.9) had greater predictive value for survival than end-diastolic volume (X2 = 59.0) or ejection fraction (X2 = 46.6), whereas stepwise analysis showed that once the relationship between survival and end-systolic volume had been fitted, there was no additional significant predictive information in either end-diastolic volume or ejection fraction. Severity of coronary occlusions and stenoses showed additional prediction of only borderline significance (p = .04 in one analysis), but continued cigarette smoking did remain an independent risk factor after stepwise analysis. For a subset of patients (n = 200) who had taken part in a randomized trial of coronary artery surgery after recovery from infarction, surgical "intention to treat" showed no predictive value. We conclude that for prediction, end-systolic volume is the primary predictor of survival after myocardial infarction, being superior to ejection fraction when ejection fraction is low (<50%) or when end-systolic volume is high (< 100 ml). Treatment of infarction should be aimed at limitation of infarct size and prevention of ventricular dilation.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The effect of heart rate on cardiac output in the fetal heart is controversial. We used Doppler echocardiography to investigate the effects of increasing heart rate on stroke volume and ventricular output in the normal human fetal heart. Heart rate was increased in 25 human fetuses (mean age 36 weeks) by auditory stimulation with a sound emitter placed on the mother's abdomen. Aortic or pulmonary diameters were measured at valve level from two-dimensional echocardiographic images and cross-sectional areas were calculated. Blood flow velocity spectra from the pulmonary artery or aorta were digitized to obtain flow velocity integrals before and after auditory stimulation. Stroke volume was calculated as the product of the flow velocity integral and the area of the great vessel. Prestimulation mean heart rate was 132 ± 8 beats/min and increased after auditory stimulation to 158 ± 9 beats/min (p < .001). Stroke volume decreased with the increase in heart rate from 3.7 ± 1.4 ml before stimulation to 3.0 ± 1. 1 ml after stimulation (p < .001), but ventricular output calculated as the product of stroke volume and heart rate remained unchanged (0.48 0.18 liter/min before vs 0.48 ± 0.17 liter/min after stimulation). The decrease in stroke volume was accompanied by a decrease in ventricular end-diastolic area, although there was no change either in end-systolic area or fractional change in area. This study demonstrates that increases in heart rate within the physiologic range in the normal human fetus result in a decrease in ventricular size and stroke volume but no change in ventricular output or ventricular shortening.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Simultaneous left ventricular micromanometry and biplane cineangiography were performed in nine control subjects (group 1), 14 patients with chronic mitral regurgitation and an ejection fraction of 57% or greater (group 2), and 13 patients with mitral regurgitation and an ejection fraction of less than 57% (group 3). End-diastolic volume index was increased in both groups with mitral regurgitation (p < .001) compared with the control group. Left ventricular end-diastolic wall thickness did not differ among the three groups, but the left ventricular muscle mass index was greater in both groups with mitral regurgitation than in controls (p < .001). End-diastolic pressure was elevated in both groups 2 and 3 compared with group 1 (p < .05), but peak systolic, mean systolic, and incisural pressure were not different among the three groups. End-diastolic stress was larger in groups 2 and 3 than in group 1 (p < .05). Muscle fiber stretch was greater in group 2 than in the control group (p < .05) but was not different between the controls and group 3. End-systolic stress, determined as the circumferential stress at aortic valve closure, at the maximal pressure/volume ratio, or using a nonsimultaneous method, was larger in group 3 than in groups 1 and 2. Mean systolic stress was evaluated from aortic valve opening to aortic valve closure in all patients; mean stress from end-diastole to aortic valve closure and from end-diastole to minimum volume was assessed in mitral regurgitation alone. For all three intervals, mean stress determinations were larger in group 3 than the mean stress from aortic valve opening to closure in the controls (p < .05), whereas only the mean stress determined from aortic valve opening to closure was greater in group 2 than in the control group (p < .01). For each of the intervals, the calculated mean stress was larger in group 3 than in group 2 (p < .05). Evaluation of the endsystolic stress- and mean ejection stress-ejection fraction relationships revealed an overlap of control with group 2 data, group 3 values were downwardly displaced. The absence of an upward shift of group 2 values in the setting of an augmented preload suggests that these patients maintained only a normal level of ventricular performance with the use of preload reserve and were operating at a somewhat reduced contractile state. The downward displacement of group 3 data points in the presence of only moderately higher levels of afterload than in groups 1 and 2 implies impaired myocardial contractility. Recognition of chronic mitral regurgitation as a stress overload state may provide insight into the mechanism of myocardial injury that occurs in both volume and pressure overload.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

In this study we reevaluated whether the sole cause of mitral valve prolapse (MVP) and aortic valve prolapse (AVP) is myxomatous degeneration. Forty-two surgical cases of prolapsed valves with mitral and/or aortic regurgitation were reviewed (AVP in nine, MVP in 27, and combined AVP and MVP [CVP] in six). On microscopic examination, myxomatous degeneration was observed in 20 patients, including six with AVP, 13 with MVP, and one with CVP. In the other 22 patients, including three with AVP, 14 with MVP, and five with CVP, microscopic examination revealed fibrosis with vascularization and scattered infiltration of inflammatory round cells caused by postinflammatory changes with or without chronic inflammation. We coined the term "postinflammatory valve prolapse" (PIVP) to describe these valves. Both postinflammatory and myxomatous degeneration were observed in seven patients with floppy mitral valves attributable to PIVP. Rupture of chordae tendineae was present in six patients with myxomatous mitral valve and three with PIVP. Seven patients with PIVP had a history of rheumatic fever. The results suggest that valvular prolapse is produced not only by myxomatous degeneration but also by postinflammatory changes, including those caused by rheumatic fever.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

We prospectively studied 16 patients with isolated aortic stenosis and eight with isolated aortic regurgitation undergoing aortic valve replacement, using two-dimensional echocardiography preoperatively, intraoperatively, and 41 ± 7 days postoperatively to (1) calculate the intraoperative change in afterload, (2) quantify the postoperative changes in left ventricular chamber size, architecture, load and function, (3) determine whether the postoperative left ventricular remodeling correlated with the intraoperative change in afterload in aortic stenosis and aortic regurgitation, and (4) assess whether preoperative afterload excess precluded postoperative improvement in left ventricular function. Preoperative left ventricular mass, end-systolic meridional and circumferential wall stresses, ejection fraction, and stress-shortening relations in patients with aortic stenosis and aortic regurgitation were similar. However, our patients with aortic regurgitation had severe systolic dysfunction, with ejection fraction less than 55% in all but one patient, compared with only 10 of 16 patients with aortic stenosis. Left ventricular end-diastolic volume, mass/volume ratio, and chamber shape were significantly different in patients with aortic stenosis and aortic regurgitation (174 ± 64 vs 294 ± 140 ml, p < .01; 1.81 ± 0.63 vs 1.14 ± 0.18, p < .01;and0.59 ± 0.09vs0.69 ± 0.09, p <.05, respectively). Intraoperative end-systolic meridional and circumferential stresses fell significantly in patients with aortic stenosis but remained unchanged in those with aortic regurgitation. The changes in left ventricular volume and ejection fraction during early postoperative remodeling (6 weeks) correlated with the intraoperative change in afterload in patients with aortic stenosis. In contrast, there was no intraoperative change in afterload in patients with aortic regurgitation and no significant changes in left ventricular volume, architecture, or function at 6 weeks or at 6 months. The differences in left ventricular remodeling and changes in function between patients with aortic stenosis and aortic regurgitation in the early postoperative period most probably relates to the major difference in intraoperative reduction in afterload, although a contributory role may have been played by the preoperative left ventricular dysfunction in those with aortic regurgitation that was underestimated by measurement of ejection fraction.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID