摘要:

BackgroundLeft ventricular (LV) twist, the longitudinal gradient of circumferential rotation about the LV long axis, may play an important role in the storage of potential energy at end systole and its subsequent release as elastic recoil during early diastole; however, the effects of load and inotropic state on LV systolic twist and diastolic untwist in human subjects have not previously been characterized.Methods and ResultsSix cardiac transplant recipients with 12 implanted radiopaque midwall LV myocardial markers were studied 1 year after transplantation. Biplane cinefluoroscopic marker images and LV pressure were recorded during control conditions and after afterload augnentation (methoxamine, 5 to 10 μg· kg−1· min−1), inotropic stimulation (dobutamine, 5μg· kg−1min−1), and preload augmentation (volume loading with normal saline). Systolic twist dynamics were assessed by maximum twist (Tmax,[rad/cm]), peak negative twist rate (−dT/dtmin[rad. cm−1. s−1]), and the slope of the twist normalized-ejection fraction relation (T-nEFR, Msys)4rad/cm]) during systole. Diastolic untwist was assessed by the peak positive untwist rate (+dT/dtmax[rad. cm−1. s−1) and the slopes (rad/cm) of the T-nEFR during early diastole (Mear-dia) and mid diastole (Mmid-dia). Compared with control values, LV pressure and volume loading had no significant effect on Tmax, −dT/dtmin, or Msys,; however, inotropic stimulation significantly increased all parameters describing systolic twist (Tmax: −0.10±0.03 versus −0.06±0.02 rad/cm,P< .001; −dT/dtmin:−0.72±0.19 versus −0.44±0.22 rad. cm−1. s−1,P< .001; Msys: −0.10±0.03 versus −0.06±0.01 rad/cm,P< .001). Pressure loading had no effect on early diastolic untwisting; however, dobutamine significantly increased Maard.a (−0.24±0.06 versus −0.13±0.04 rad/cm,P< .0001) and +dT/dtma., (0.78±0.24 versus 0.45±0.16 rad. cm−1s−1,P< .001). Conversely, volume loading significantly decreased Mear-dia(−0.08±0.04 versus −0.13±0.04 rad/cm,P< .05). Mearéia correlated directly with LV contractile state (as assessed as maximum dP/dt,r= .60,P< .0001) and inversely with end-systolic volume (r= − .87,P< .0001) but was unrelated to stroke volume (r= .08,P= .30) or LV afterload (estimated as effective arterial elastance,r= .08,P= .29). Mmid-diadid not change during any intervention.ConclusionsIn conscious human transplant patients, (1) pressure and volume loading do not affect systolic LV twist; (2) dobutamine augments systolic twist and early diastolic untwisting, suggesting more end-systolic potential energy storage and early diastolic elastic recoil with enhanced inotropic state; (3) volume loading decreases early diastolic untwisting, possibly reflecting diminished recoil forces after preload augmentation associated with larger end-systolic volumes (ESV); and (4) Mear-diacorrelates strongly with ESV (in an inverse fashion), and less strongly, but directly, with LV dP/dtmax.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundIschemic cardiomyopathy is characterized by myocyte loss, reactive cellular hypertrophy, and ventricular scarring. However, the relative contribution of these tissue and cellular processes to late failure remains to be determined.Methods and ResultsTen hearts were obtained from individuals undergoing cardiac transplantation as a result of chronic coronary artery disease in its terminal stage. An identical number of control hearts were collected at autopsy from patients who died from causes other than cardiovascular disease, and morphometric methodologies were applied to the analysis of the left and right ventricular myocardium. Left ventricular hypertrophy evaluated as a change in organ weight, aggregate myocyte mass, and myocyte cell volume per nucleus showed increases of 85%, 47%, and 103%, respectively. Corresponding increases in the right ventricle were 75%, 74%, and 112%. Myocyte loss, which accounted for 28% and 30% in the left and right ventricles, was responsible for the difference in the assessment of myocyte hypertrophy at the ventricular, tissue, and cellular levels. Left ventricular muscle cell hyper-trophy was accomplished through a 16% and 51% increase in myocyte diameter and length, whereas right ventricular myocyte hypertrophy was the consequence of a 13% and 67% increase in these linear dimensions, respectively. Moreover, a 36% reduction in the number of myocytes included in the thickness of the left ventricular wall was found. Collagen accumulation in the form of segmental, replacement, and interstitial fibrosis comprised an average 28% and 13% of the left and right ventricular myocardia, respectively. The combination of cell loss and myocardial fibrosis, myocyte lengthening, and mural slippage of cells resulted in 4.6-fold expansion of left ventricular cavitary volume and a 56% reduction in the ventricular mass-to-chamber volume ratio.ConclusionsThese results are consistent with the contention that both myocyte and collagen compartments participate in the development of decompensated eccentric ventricular hypertrophy in the cardiomyopathic heart of ischemic origin.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundThe role of cholinergic pathways in modulating left ventricular contractile function in humans is not known. This study evaluated the effect of a cholinergic agonist (acetylcholine) and antagonist (atropine) on basal and β-adrenergically stimulated left ventricular contractile function in normal subjects and subjects with denervated hearts after cardiac transplantation.Methods and ResultsSix subjects with normal left ventricular function and seven subjects who were 1 to 3 years after cardiac transplantation were studied. Acetylcholine, atropine, and the β-adrenergic agonist dobutamine were infused via the left main coronary artery, and changes in left ventricular contractile function were assessed by measurement of peak +dP/dt. Intracoronary dobutamine increased +dP/dt by 70±15% and 66±20% in the normal subjects and transplant recipients, respectively. Intracoronary acetylcholine and atropine alone each had no effect on left ventricular +dP/dt in either normal subjects or transplant recipients. The concurrent infusion of acetylcholine with dobutamine reduced the response to dobutamine by 66±10% and 79±9% in normal subjects and transplant recipients, respectively. The concurrent infusion of atropine with dobutamine potentiated the response to dobutamine by 25±7% in normal subjects but had no effect in transplant recipients.ConclusionsStimulation and inhibition of cholinergic receptors in the human heart can modulate the positive inotropic response to β-adrenergic stimulation.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundDespite constant fluctuations in cardiac preload caused by the effects of respiration and changes in posture on venous return to the heart, arterial blood pressure remains remarkably constant. The effects of instantaneous lung volume (ILV) and variations of central venous pressure (CVP) on blood pressure (BP) were studied by use of frequency domain techniques to quantify the contribution of heart rate (HR) reflexes to attenuation of the effects of changes in right ventricular preload on arterial pressure.Methods and ResultsRandom independent variation of ILV, then CVP (obtained using lower-body negative pressure), was performed in eight humans in the supine position. HR, ILV, CVP, and systolic (SBP) and diastolic (DBP) BPs were recorded during control periods and after complete blockade obtained by use of 0.04 mg/kg atropine and 0.2 mg/kg propranolol. A frequency-domain analysis was performed on pairwise relations by the cross-spectral technique. During autonomic blockade, fluctuations in CVP were induced up to 0.14 Hz but caused corresponding changes in arterial pressure only up to 0.08 Hz (P< .02), indicating a mechanical damping effect of the heart and pulmonary vasculature. Fluctuations of BP were also delayed from CVP by 1.55 to 2.10 seconds. At frequencies <0.1 Hz, relations of CVP to all indices of BP increased with blockade (CVP-SBP, 0.9±0.5 versus 2.7±0.8 mm Hg/mm Hg,P< .01; CVP-DBP, 1.3±0.4 versus 4.3±1.4 mm Hg/mm Hg,P< .01; CVP-pulse pressure [PP], 1.0±0.3 versus 1.9±0.8 mm Hg/mm Hg,P< .05). Higher-frequency fluctuations of arterial BP were a relatively pure manifestation of respiratory activity. At frequencies from 0.15 to 0.35 Hz, the relation of ILV to SBP was unchanged with blockade, whereas relations of ILV to DBP and PP decreased (ILV-DBP, 6.1±3.5 versus 3.3±2.2 mm Hg/L,P< .02; ILV-PP, 7.0±4.3 versus 2.7±2.2 mm Hg/L,P< .01). An associated change in phase of these relations suggested that neurally mediated changes in HR may offset mechanical effects caused by respiration.ConclusionsBoth slow changes of BP (<0.08 Hz) induced by variations of CVP and more rapid changes induced by ILV are actively buffered by heart rate reflexes. During blockade, the mechanical properties of interposed cardiopulmonary structures limit CVP-induced fluctuations of BP. These findings have implications for BP regulation in pathological conditions associated with impairment of HR control.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundPressure-volume relations have been established as useful measures of left ventricular (LV) performance. Application of these methods to the intraoperative setting have been limited because of difficulties acquiring LV volume data. Transesophageal echocardiographic automated border detection can measure LV cross-sectional area as an index of volume, which can be coupled with pressure data to construct pressure-area loops on-line. The purpose of this study was to evaluate intraoperative LV performance in patients undergoing coronary bypass surgery before and immediately after cardiopulmonary bypass using on-line pressurearea relations.Methods and ResultsStudies were attempted in 13 consecutive patients. Simultaneous measures of LV cross-sectional area, LV pressure, and electromagnetic flow probe-derived aortic flow recorded on a computer work station interfaced with the ultrasound system. Pressure-area loops were compared with simultaneous pressure-volume loops constructed from pressure and flow data during inferior vena caval occlusions before and after bypass. Pressure-volume calculations (end-systolic elastance, maximal elastance, and preload- recruitable stroke work) were then applied to pressurearea loops with area substituted for volume data. Changes in stroke force from pressure-area loops were closely correlated with changes in estimates of stroke work from pressurevolume loops for individual patients before bypass (r= .99± .03, SEE=5±2%, n=10) and after bypass (r= .96±.05, SEE=5±2%, n=9). Pressure-area estimates of end-systolic elastance, maximal elastance, and preload-recruitable stroke force decreased significantly from before to after cardiopulmonary bypass in the 7 patients with paired data sets. Load-dependent measures of LV function (stroke volume, cardiac output, and fractional area change) were unchanged after surgery in these same patients.ConclusionsIntraoperative pressure-area loops may be acquired and displayed on-line using transesophageal echocardiographic automated border detection and readily analyzed in a manner similar to pressure-volume loops. LV performance was depressed immediately after cardiopulmonary bypass compared with before. On-line pressure-area relations may be clinically useful to assess LV performance in patients undergoing cardiac surgery in whom load and contractility may be expected to vary rapidly.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundNoninvasive predictors of important outcomes after valve replacement for mitral regurgitation have not been examined in a rheumatic population (in whom the results of valve repair are suboptimal) in the era of chordal preservation. Timing of valve replacement thus remains a difficult question in rheumatic mitral regurgitation.Methods and ResultsOf 278 patients followed after valve replacement, 66 had pure or predominant mitral regurgitation, and in 61 of these the etiology was rheumatic. The mean age was 24 years. After a mean follow-up of 24±10 months, the ability of preoperative clinical and echocardiographic data to predict outcome was assessed prospectively, and the possible impact of chordal preservation (n=35) on survival and postoperative left ventricular function was examined retrospectively. There were no perioperative deaths. There were six postoperative deaths, all the result of heart failure and all related to left ventricular dysfunction. The mean probability of survival was .90 at 16 months. In a stepwise Cox proportional hazards regression analysis, the only independent predictor of postoperative death was preoperative end-systolic diameter. According to a logistic model, the probabilities of death (n=6) and death or severe heart failure (n=7) increased abruptly at a preoperative end-systolic diameter of 51 mm (probabilities,.23 and .31, respectively), and the accuracy of this cut point for predicting outcomes was 97% and 98%, respectively. Multiple linear regression analysis identified a large preoperative endsystolic diameter and the need to use tricuspid annuloplasty as significant independent predictors of postoperative fractional shortening; the use of chordal preservation (n=35) was not a predictor of postoperative fractional shortening. A good outcome was predicted at a preoperative end-systolic diameter of 40 mm: probability of death or heart failure was .0001, and predicted mean postoperative fractional shortening was 0.27 after mitral valve replacement without tricuspid annuloplasty.ConclusionsWhen preoperative end-systolic diameter is more than 50 mm, a poor postoperative outcome is predicted despite chordal preservation in relatively young patients with rheumatic mitral regurgitation, and alternative strategies should therefore be considered. When preoperative end-systolic diameter is 40 mm or less, an excellent outcome is predicted, and close observation without surgery would appear to be reasonable in the absence of symptoms.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundThe age-associated decline in aerobic exercise capacity is partially reversible by endurance exercise training. Moderate-intensity endurance exercise training increases aerobic exercise capacity mediated, in part, by improvement of stroke volume and left ventricular performance in older men. The present study was designed to characterize the nature of cardiovascular adaptations to strenuous endurance exercise of long duration and to delineate the mechanisms underlying increased stroke volume and cardiac output in highly trained older endurance athletes.Methods and ResultsNine male master athletes (MA: 64±2 years old, mean±SEM) and 9 older sedentary healthy men (controls: 63±1 year) were studied. Left ventricular systolic function was evaluated with the use of cardiac blood pool imaging and echocardiography. Maximal 02uptake (Vo2max) was 50.4±1.7 mL. kg.−1min−1in the MA and 29.6±1.4 mL kg−1.min−1(P= .0001) in controls. Systolic and mean blood pressures at rest and during exercise were not different in the two groups. Left ventricular systolic function at peak exercise was higher in the MA than in sedentary controls as evidenced by (1) a higher left ventricular functional reserve (ΔEF: 12.4±2 versus 5.6±2.5,P= .05), (2) a large decrease in end-systolic volume during exercise (MA: 56±4 mL at rest and 42±5 mL at peak exercise,P= .007; controls: 43±2 mL at rest and 42±6 mL at peak exercise,P= .35) with no differences in systolic blood pressure, (3) a higher left ventricular fractional shortening at peak exercise (MA: 52±2.6%; controls: 45±1%,P= .046) at comparable values for end-systolic wall stress (MA: 56±12 g/cm2; controls: 53±7 g/cm2,P= .50), and (4) a greater decrease in end-systolic diameter at peak exercise in the MA than in controls (MA: −1.2±0.16 cm versus −0.57±0.13 cm,P= .014) despite no significant differences between the changes in end-systolic wall stress during exercise (MA: −15.5±7.5 g/cm2, controls: −11.0±9.0 g/cm2,P= .6). MA had a larger end-diastolic volume at rest (153±6 versus 132±4 mL,P= .009) with a normal wall thickness-to-radius ratio (0.34±0.02). Peak exercise stroke volume was higher (P= .023) in the MA (132±6 mL/min) than in the sedentary controls (111±6 mL/min). Changes in stroke volume correlated strongly with changes in ejection fraction in the MA (r= .80,P= .010) but not in sedentary controls (r= .59,P= .097). Further, changes in stroke volume from rest to exercise correlated strongly with changes in end-diastolic volume in both MA (r= .78,P= .013) and sedentary controls (r= .73,P= .026), suggestive of reliance of stroke volume on end-diastolic volume and preload. However, for a given increase in end-diastolic volume, the rise in stroke volume during exercise was significantly larger in the MA than in controls, which, in the absence of differences in mean blood pressures, indicates that enhanced left ventricular systolic function independent of preload plays an additional role in maintaining a higher stroke volume at peak exercise in the highly trained older men.ConclusionsCardiac adaptations in older endurance trained men are characterized by volume-overload left ventricular hypertrophy and enhancement of left ventricular systolic performance at peak exercise. These adaptive responses contribute to enhanced stroke volume at peak exercise in older endurance trained men.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundTorsade de pointes is characterized not only by its particular ECG pattern but by its context of congenital or acquired long QT syndrome and the long coupling interval of the initial premature beat.Methods and ResultsWe observed 14 patients aged 34.6±10 years (mean±SD) with no structural heart disease who presented with syncope related to a typical ECG aspect of torsade de pointes. However, there was no evidence of long QT syndrome, and the torsade had the unusual particularity of an extremely short coupling interval of the first beat or of the isolated premature beats (245±28 milliseconds). In 10 cases they deteriorated into ventricular fibrillation. Four patients had a familial history of sudden death. Only 2 patients had a tachyarrhythmia inducible by programmed stimulation. At Holter recordings the heart rate variability was globally and significantly depressed, the vagal limb of the autonomic nervous system being predominantly affected. During a mean follow-up of 7 years there were 5 deaths (4 sudden). Nine patients are alive, 3 with implanted defibrillators and 6 treated with verapamil alone. Unlike the other types of antiarrhythmic agents including 3-blockers and amiodarone, verapamil is in our experience the only drug apparently active on the arrhythmias; however, it does not prevent sudden death.ConclusionsThe short-coupled variant of torsade de pointes should be identified because of their ECG pattern and the risk of sudden death in young adults with no structural heart disease.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundTo establish the chronic stability of defibrillation thresholds (DFTs) in a transvenous cardioverter/defibrillator (TCD) system, we studied 37 consecutive patients with TCD systems implanted for >6 months.Methods and ResultsDFT was measured by a step-down method at implant and 2 and 6 months later. The mean ejection fraction was 34.5±14.3%. Coronary artery disease with previous myocardial infarction was present in 31 patients. The mean DFT rose from 13.3 ±4.3 J at implant to 16.5 ±4.7 J at 2 months (P< .001) and 17.6±5.4 J at 6 months (P< .0001). ANOVA revealed a statistically significant rise in DFT over time (P< .0005). At 2 months, 25 patients had a rise in DFT, and 14 had a rise ≥5 J. The observed rise at 2 months persisted in 19 patients. A chronic rise, defined as ≥5 J rise at 6 months, occurred in 17 patients. Univariate analysis of clinical as well as implant variables revealed no predictors of a rise in DFT in this group.ConclusionsWe conclude that there is a significant rise in DFT at 2 and 6 months in this TCD system. Although the chronic threshold remained well within the available energy range of the pulse generator, this observation has important implications for implantation guidelines, programming, and future pulse generator development for TCD patients.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundParoxysmal atrial fibrillation and paroxysmal supraventricular tachycardia are recognized clinically when patients seek treatment for symptoms due to recurrent arrhythmias; atrial fibrillation also increases the risk of stroke. The frequency with which asymptomatic arrhythmias occur in patients with these arrhythmias is unknown.Methods and ResultsTwenty-two patients with paroxysmal atrial fibrillation (n=8) or paroxysmal supraventricular tachycardia (n=14) were studied for 29 days with two different ambulatory ECG-monitoring techniques to measure the relative frequency of asymptomatic and symptomatic arrhythmias. All class I antiarrhythmic drugs, calcium channel blockers, β-blockers, and digitalis were withheld. Sustained asymptomatic arrhythmia events (defined as lasting at least 30 seconds) were documented using continuous ambulatory ECG monitoring once weekly for a total of 5 of the 29 study days; symptomatic arrhythmia events were documented using transtelephonic ECG monitoring for all 29 days of the study. In the group of patients with paroxysmal atrial fibrillation, asymp-tomatic arrhythmia events occurred significantly more frequently than symptomatic arrhythmia events; the mean rates, expressed as events/100 d/patient (95% confidence interval), were 62.5 (40.4, 87.3) and 5.2 (2.7, 9.0) (P< .01); the ratio of the mean rates was 12.1 (5.8, 26.4). In contrast, in the group of patients with paroxysmal supraventricular tachycardia, asymptomatic arrhythmia events were significantly less frequent than symptomatic arrhythmia events; the mean rates were 0.0 (0.0, 5.3) and 7.4 (5.0, 10.6) (P< = .02). The ratio of the mean rates was 0.0 (0.0, 0.8).ConclusionsIn a group of patients with paroxysmal atrial fibrillation, sustained asymptomatic atrial fibrillation occurs far more frequently than symptomatic atrial fibrillation. However, it is not known whether asymptomatic atrial fibrillation is a potential risk factor for stroke even when patients are not having symptomatic arrhythmias.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID