ISSN:0009-7322    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

BackgroundThe importance of the contribution of atrial systole to ventricular filling in mitral stenosis is controversial. The cause of reduced cardiac output following the onset of atrial fibrillation may be due to an increased heart rate, a loss of booster pump function, or both.Methods and ResultsWe studied the atrial contribution to filling under a variety of conditions by combining noninvasive studies of patients with computer modeling. Thirty patients in sinus rhythm with mild-to-severe stenosis were studied with two-dimensional and Doppler echocardiography for measurement of mitral flow velocity and mitral valve area (MVA). The mean ± SD atrial contribution to left ventricular filling volume was 18 ± 10% and varied inversely with mitral resistance. Patients with mild mitral stenosis (MVA, 1.8 ± 0.7 cm2) and severe mitral stenosis (MVA, 0.9 ± 0.2 cm2) had atrial contributions of 29 ± 4% and 9 ± 5%, respectively. The pathophysiological mechanisms responsible for these trends were further investigated by the computer model. In modeled severe mitral stenosis, increasing heart rate from 75 to 150 beats/min caused an increase of 5.2 mm Hg in mean left atrial pressure, whereas loss of atrial contraction at a heart rate of 150 beats/min caused only a 1.3 mm Hg increase.ConclusionsThe atrial booster pump contributes less to ventricular filling in mitral stenosis than in the normal heart, and the loss of atrial pump function is less important than the effect increasing heart rate as the cause of decompensation during atrial fibrillation.

ISSN:0009-7322    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

BackgroundImaging of the flow convergence region (FCR) proximal to a regurgitant orifice has been shown to provide a method for quantifying the regurgitant flow rate. According to the continuity principle, the FCR is constituted by concentric hemispheric isovelocity surfaces centered at the orifice. The flow rate is constant across all isovelocity surfaces and equals the flow rate through the orifice. For any isovelocity surface the flow rate (Q) is given by:Q= 2n−r2 Vr, where 2wrr2 is the area of the hemisphere and Vr is the velocity at the radial distance (r) from the orifice.Methods and ResultsWe studied 52 consecutive patients with mitral regurgitation (mean age, 49 years; age range, 21–66 years) verified by left ventricular angiography using color flow mapping. The FCR r was measured as the distance between the first aliasing limit-at a Nyquist limit obtained by zero-shifting the velocity cutoff to 38 cm/sec and the regurgitant orifice. Seven patients without evidence of an FCR had only grade 1 + mitral regurgitation angiographically. There was a significant relation between the Doppler-derived maximal instantaneous regurgitant flow rate and the angiographic degree of mitral regurgitation in the other patients (rs= 0.91,p< 00.001). The regurgitant flow rate by Doppler also correlated with the angiographic regurgitant volume (r= 0.93, SEE = 123 ml/sec) in the 15 patients in normal sinus rhythm and without other regurgitant lesions in whom it could be measured. The correlation between regurgitant jet area within the left atrium and the angiographic grade was only fair (rs= 0.75,p< 0.001).ConclusionsColor flow Doppler provides new velocity information about the proximal FCR in patients with mitral regurgitation. According to the continuity principle, the maximal instantaneous regurgitant flow rate, obtained with the FCR method, may provide a quantitative estimate of the severity of mitral regurgitation, which is relatively independent of technical factors.

ISSN:0009-7322    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

BackgroundThis study was designed to evaluate the effect of severe peripheral arterial insufficiency on carnitine concentrations and carnitine acetyltransferase and palmitoyltransferase activities in the ischemic skeletal muscles of patients with severe peripheral vascular disease.Methds and ResultsNine biopsy specimens of ischemic muscles were obtained from five patients undergoing reconstructive vascular surgery. Biopsies from 35 normal subjects served as controls. Ischemic muscles showed a significant reduction in total carnitine from the control value of 20.9 ± 52 to 11.6 + 6.2 nmol/mg noncollagen protein (p< 0.01). A significantly lower fee carnitine and acylcarnitine content contributed to this reduction. Similarly, carnitine acetyltransferase activity was reduced in the ischemic muscles from the control value of 102.1 ± 412 to 52.9 ± 22.1 nmol/min/mg noncollagen protein (p< 0.01). On the contrary, carnitine palmitoyltransferase activity did not show any change (029 ± 0.05 nmol/min/mg noncollagen protein in the ischemic muscles and 0.28 ± 0.07 nmoUVmin/mg noncollagen protein in controls). Carnitine, acylcarnitines, and enzyme activities were also measured in the ischemic muscles in four additional patients 2 days after intravenous administration of L-propionylcarnitine (1.5 g as a single bolus followed by an infusion of 1 mg/kg/min for 30 minutes). Treatment restored normal levels of carnitine and its esters in the ischemic muscles but did not affect enzyme activities.ConclusionsDemonstration of carnitine deficiency in severe peripheral vascular disease substantiates previous findings showing the efficacy of carnitine supplementation to ischemic muscles. Furthermore, the feasibility of restoring carnitine homeostasis with L-propionylcarnitine provides the basis for clinical trials aimed at assessing the efficacy of this carnitine ester in the treatment of peripheral vascular disease.

ISSN:0009-7322    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

BackgroundRegional nonuniformity has been suggested to be closely related to left ventricular (LV) relaxation in diseased heart. The purpose of the present study was to assess LV global and regional relaxation in patients with nonobstructive hypertrophic cardiomyopathy (HCM).Methods and ResultsLeft ventriculography was conducted simultaneously with pressure micromanometry in 10 normal control subjects and 11 patients with nonobstructive HCM. LV silhouettes in the right anterior oblique projection were divided into eight regions, and regional wall stress during isovolumic relaxation was computed for six regions from the midventricle to the apex. In HCM patients, isovolumic relaxation time (IRT) and the time constant of LV pressure decrease (Tp) were greater than in control subjects (IRT, 84 ± 13 versus 66 ± 6 msec; Tp, 51 ± 8 versus 36 ± 5 msec, respectively,p< 0.01). In HCM patients, the (−)dP/dt upstroke pattem was convexdownward, and dP/dt(20/60), the ratio ofdP/dt values 20 and 60 msec after peak (−)dP/dt, was less than in control subjects (1.46 ± 0.16 versus 2.15 + 0.14,p< 0.01). These findings suggest that there is impaired LV relaxation in HCM patients. End-systolic regional wall stress was lower, and the time constant ofregional stress decrease (Tst) was prolonged for each region in HCM patients compared with control subjects. In the HCM group, Tst tended to be more prolonged in regions with increased wail thickness than in regions with normal wall thickness (60 ± 15 versus 50 ± 11 msec,p< 0.01). The coefficient of variation for Tst values in six areas of the left ventricle was calculated in each subject and was greater in HCM patients than in control subjects (13 ± 7% versus 7 + 3%,p< 0.05), indicating regional nonuniformity in Tst during isovolumic relaxation in HCM patients.CondusionsSignificant correlations existed between the coefficients of variation for Tst and Tp (r= 0.80,p< 0.01), IRT (r= 0.79,p< 0.01), and dP/dt(20/60) (r= −0.67,p< 0.05) in the HCM group. Thus, regional nonunifonnity is closely related to the impairment of LV relaxation in HCM.

ISSN:0009-7322    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

BackgroundQRST isointegral maps (I-maps) have been useful in detecting repolarization abnormalities. We investigated the body surface distribution of abnormally low QkST areas in patients with left ventricular hypertrophy (LVH) and the relation of the abnormalities in I-map to the severity of LVH as assessed by echocardiography.Methods and ResultsQRST area departure maps were constructed from electrocardiographic (ECG) data recorded in patients with LVH and precordial negative T waves resulting from aortic stenosis (AS) (10 patients), aortic regurgitation (AR) (12 patients), or hypertrophic cardiomyopathy (HCM) with asymmetric septal hypertrophy (22 patients). Fifty normal subjects served as controls. The I-map was constructed from 87 body surface electrocardiograms recorded simultaneously at a sampling interval of 1 msec. The area where the QRST area was smaller than normal limits (mean-2 SD) was designated the “-2 SD area.” The echocardiographic left ventricular (LV) mass was calculated by Devereux,s method. Patients with large LV masses due to AS or AR had 2 SD areas located over the left anterior chest or the midanterior chest, respectively. The 2 SD area was located over the left shoulder and left anterior chest and had a lingual shape ih patients with HCM. The sum of QRST area values less than the normal range (IQRST) was significantly correlated with LV mass in patients with AS or AR (r= 0.83 andr= 0.69,p< 0.01 andp< 0.05). However, there was no significant correlation between IQRST and the severity of LVH in patients with HCM. EQRST divided by the number of electrodes in the 2 SD area was significantly greater in patients with HCM than in those with AS or AR.ConclusionsThese findings suggest that abnormalities in patients with HCM are manifest even in mild LVH and that there is a greater disparity of repolarization in hypertrophied left ventricles due to HCM than in LVH due to aortic valve disease. QRST isointegral departure maps may provide ECG evidence of LV mass of patients with AS or AR and of susceptibility to malignant arrhythmias in patients with HCM.

ISSN:0009-7322    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

BackgroundIn myocardial infarction patients, heart rate-adjusted QT interval (QT), an electrocardiographic indicator of sympathetic balance, is prognostic for survival.Methods and ResultsIn a 28-year follow-up, the association between QT, and all-cause, cardiovascular, and ischemic heart disease mortality was studied in a population of 3,091 apparently healthy Dutch civil servants and their spouses, aged 40–65 years, who participated in a medical examination during 1953–1954. Moderate (QTc, 420–440 msec) and extensive (QTc, more than 440 msec) QTc prolongations significantly predict all-cause mortality during the first 15 years among men (adjusted respective relative risks [RRs], 1.5 and 1.7) and among women (RRs, 1.7 and 1.6). In men, cardiovascular (RRs, 1.6 and 1.8) and ischemic heart disease mortality (RRs, 1.8 and 2.1) mainly account for this association. In women, the association cannot be attributed specifically to cardiovascular and ischemic heart disease mortality. RRs for a subpopulation without any sign of heart disease at baseline are similar. The same is observed for QT, prolongation after light exercise, although in this situation most associations are not statistically significant, probably because of smaller numbers in the QTc prolongation categories.ConclusionsOur results suggest that QT, contributes independently to cardiovascular risk. If autonomic imbalance is an important mechanism, it might be speculated that changes in life-style (e.g., with regard to physical exercise and smoking) may have a preventive impact.

ISSN:0009-7322    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

Backgroundinternational long QT syndrome (LQTS) study, 30 patients with corrected QT interval (QTj) of more than 0.44 second,Z were identified who had permanent pacemakers implanted for management of recurrent syncope or aborted cardiac arrest.Methods and ResultsPacemakers were implanted on average 7 years after the onset of the first syncopal episode. Most of the patients were female (87%), the average age at implantation was 19 + 13 years, the mean QT, was 0.55 ± 0.08 second, and 57% were receiving antiadrenergic treatment for LQTS when the pacemaker was placed. Using birth as the time origin, the mediacardiac event rate was significantly (p< 0.001) reduced by pacing from 0.5 to 0 events per patient per year, with 21 patients experiencing no cardiac events during an average pacemaker follow-up of 49 months per patient. In 10 patients in whom the demand atrial pacing rate was faster than the intrinsic sinus rate, the average heart rate was increased 23 beats/min (from 58 to 81 beats/min) with pacing with reduction in the QT interval from 0.59 seconds to 0.46 seconds.ConclusionsThe beneficial effects of pacing in high-risk LQTS patients probably relate to the prevention of bradycardia, pauses, and the shortening of long QT intervals-factors that are known to be arrhythmogenic in this syndrome. Permanent cardiac pacing reduces the rate of recurrent syncopal events in high-risk LQTS patients, but it does not provide complete protection.

ISSN:0009-7322    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

BackgroundThe idiopathic long QT syndrome (LQTS) is characterized by electrocardiographic abnormalities and by a high incidence of lethal arrhythmias. The present case/control study demonstrates the frequent occurrence of unusual and specific ventricular wall motion abnormalities in LQTS and their association with history of syncope or cardiac arrest. These anomalies were present in 23 of 42 LQTS patients (55%) and in two of 42 healthy controls (5%,p< 0.0001) matched for age, sex, height, and weight.Methods and ResultsTwo new measurements were developed to assess quantitatively the abnormalities observed. The first, Thl/2, is an index of the rapidity of the early contraction phase; the second, TSTh, is an index of the presence of a slow movement in the late thickening phase. Thl/2 was smaller in LQTS patients (15.0 + 4.1 versus 19.9 + 3.9% of the cardiac cycle,p< 0.001), indicating that they reach half-maximal systolic contraction more rapidly than controls. TSTh was greater in LQTS patients (9.37 ± 6.82 versus 2.88 ± 4.46%,p< 0.001), indicating that they spend more time at a very low thickening rate. A peculiar double peak pattern of late thickening was present in 11 patients and in no controls. These abnormalities were more frequent in symptomatic than in asymptomatic patients (20 of 26, 77%, versus three of 16, 19%,p< 0.005; relative risk, 2.75). They were not affected by α-blockade or by left cardiac sympathetic denervation. The same echocardiographic abnormalities were produced by right stellectomy in nine of nine anesthetized dogs, were not dependent on cycle length, and were not modified by subsequent left stellectomy.ConclusionsThis study demonstrates a previously unsuspected abnormality in the ventricular contraction pattern of LQTS patients and, for the first time, provides evidence that a noninvasively detected cardiac abnormality is associated with a higher risk for syncope/cardiac arrest. The experimental reproduction of this echocardiographic abnormality by right stellectomy indicates that this newly found clinical characteristic of LQTS does not contradict the “sympathetic imbalance” hypothesis.

ISSN:0009-7322    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

BackgroundDuring a 2.9-year period, 11 patients developed polymorphous ventricular tachycardia 1–13 days after acute anterior (seven patients) or inferior (four patients) myocardial infarction. None of the 11 patients had sinus bradycardia (mean heart rate, 90 ± 23 beats/min), but three had a sinus pause immediately before the onset of polymorphous ventricular tachycardia. In all 11 patients, the QT interval and corrected QT interval (QTj) were normal or minimally prolonged (QT, 385 + 34 msec; QT, 442 ± 40 msec). None had significant hypokalemia (mean serum potassium concentration, 43 ± 0.5 meq/l) or a grossly abnormal serum magnesium or calcium concentration (2.1 ± 0.4 and 8.9 ± 0.7 mg/dl, respectively).Methods and ResultsImmediately before the onset of polymorphous ventricular tachycardia, symptoms and/or electrocardiographic changes consistent with recurrent myocardial ischemia occurred in nine of 11 patients. One patient died before drug therapy could be initiated. Lidocaine was used in 10 patients and proved to be effective in only one. Intravenous procainamide was used in six patients: one improved, and five had recurrence of polymorphous ventricular tachycardia. Bretylium was used in five patients and was ineffective in all cases. Overdrive pacing was used in four patients and failed to suppress recurrent arrhythmias in all cases. Four patients with persistent polymorphous ventricular tachycardia unresponsive to lidocaine, procainamide, or bretylium responded to intravenous amiodarone. One patient with polymorphous ventricular tachycardia that was consistently preceded by ST segment elevation responded to intravenous nitroglycerin. Two patients with persistent polymorphous ventricular tachycardia and obvious recurrent ischemia unresponsive to pharmacological intervention responded to emergency coronary revascularization. A third patient who experienced recurrent angina and polymorphous tachycardia was initially stabilized with pharmacological therapy but subsequently underwent elective revascularization and has remained stable without antiarrhythmic therapy.ConclusionsPost-myocardial infarction polymorphous ventricular tachycardia is not consistently related to an abnormally long QT interval, sinus bradycardia, preceding sinus pauses, or electrolyte abnormalities. This arrhythmia has a variable response to class I antiarrhythmics but may be suppressed by intravenous amiodarone therapy. It is often associated with signs or symptoms of recurrent myocardial ischemia. Furthermore, coronary revascularization appears to be effective in preventing the recurrence of polymorphous ventricular tachycardia when associated with recurrent postinfarction angina.

ISSN:0009-7322    

出版商:OVID    

年代:1991

数据来源: OVID