摘要:

BackgroundAs part of a population-based study of acute myocardial infarction, we examined changes over time in the incidence and in-hospital case-fatality rates of primary ventricular fibrillation complicating acute myocardial infarction.Methods and ResultsPatients with validated acute myocardial infarction hospitalized at 16 hospitals in the Worcester, Mass, metropolitan area between 1975 and 1990 comprised the study sample. During the 15-year study period, 5.1% of patients developed primary ventricular fibrillation in the setting of uncomplicated acute myocardial infarction, with this rate remaining relatively constant over time. Both age- and multivariable-adjusted analyses showed no significant trend in the incidence rates of primary ventricular fibrillation during the study period. The in-hospital case-fatality rate for patients with primary ventricular fibrillation was significantly elevated compared with the rate for those without primary ventricular fibrillation and uncomplicated acute myocardial infarction (48.3% versus 1.5%,P< .001). No significant change over time was noted in in-hospital case-fatality rates associated with primary ventricular fibrillation while controlling for a variety of short-term prognostic factors.ConclusionsThe results of this communitywide observational study suggest that neither the incidence nor the prognosis associated with primary ventricular fibrillation resulting from acute myocardial infarction has improved over time.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundOur study compares the effect of acute proximal stenosis of a coronary artery supplying a myocardial perfusion bed with that of stenosis of an adjacent artery resulting in collateral flow diversion supplied by the same perfusion bed. These alterations in coronary physiology were quantified by digital angiographic impulse response analysis of contrast material mean transit time for the coronary microcirculation, Tmicro, and by flowmeter and microsphere assessment of flow and regional flow distribution.Methods and ResultsIn 25 open-chest, anesthetized dogs, progressive circumflex artery stenosis led to a concordant decrease of circumflex artery resting and hyperemic flow, coronary flow reserve, and inverse angiographic mean transit time Tmicro−1(P< .01). Progressive left anterior descending artery stenosis led to no or only minor changes of circumflex artery resting or hyperemic flow or flow reserve; only occlusion induced a significant decrease of coronary flow reserve (from 4.0±0.7 to 3.2±0.5,P< .05), whereas resting flow was in-creased by +8.6±5.9%. In contrast, circumflex artery Tmicro−1diminished significantly with critical left anterior descending artery stenosis and occlusion (from 16.7±4.2 to 12.6±2.2[P< .05] and 12.0±3.0 min−1[P< .01], respectively). In 8 dogs, collateral flow induced by left anterior descending artery occlusion was quantified by microsphere injections. The decrease of circumflex artery Tmicro−1correlated with the magnitude of collateral flow (r= .76) and was associated with theangiographic extent of collateral filling.ConclusionsDigital angiographic impulse response analysis is a sensitive method to detect the influence of proximal artery stenosis on an artery's myocardial perfusion bed as well as the changes induced by an adjacent artery stenosis inducing collateral flow diversion from the supplying myocardial perfusion zone.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundExperimental studies have shown that fractional flow reserve (defined as the ratio of maximal achievable flow in a stenotic area to normal maximal achievable flow) can be calculated from coronary pressure measurements only. The objectives of this study were to alidate fractional flow reserve calculation in humans and to compare this information with that derived from quantitative coronary angiography.Methods and ResultsTwenty-two patients with an isolated, discrete proximal or mid left anterior descending coronary artery stenosis and normal left ventricular function were studied. Relative myocardial flow reserve, defined as the ratio of absolute myocardial perfusion during maximal vasodilation in the stenotic area to the absolute myocardial perfusion during maximal vasodilation (adenosine 140 jig. μkg−1· min−1intravenously during 4 minutes) in the contralateral normally perfused area, was assessed by15O-labeled water and positron emission tomography (PET). Myocardial and coronary fractional flow reserve were calculated from mean aortic, distal coronary, and right atrial pressures recorded during maximalvasodilation. Distal coronary pressures were measured by an ultrathin, pressure-monitoring guide wire with minimal influence on the transstenotic pressure gradient. Minimal obstruction area, percent area stenosis, and calculated stenosis flow reserve were assessed by quantitative coronary angiography.There was no difference in heart rate, mean aortic pressure, or rate-pressure product during maximal vasodilation during PET and during catheterization. Percent area stenosis rangedfrom 40% to 94% (mean, 77±13%), myocardial fractional flow reserve from 0.36 to 0.98 (mean, 0.61±0.17), and relative flow reserve from 0.27 to 1.23 (mean, 0.60±0.26). A close correlationwas found between relative flow reserve obtained by PET and both myocardial fractional flow reserve (r= .87) and coronary fractional flow reserve obtained by pressure recordings (r= .86). The correlations between relative flow reserve obtained by PET and stenosis easurements derived from quantitative coronary angiography were markedly weaker (minimal obstruction area,r= .66; percent area stenosis,r= − .70; and stenosis flow reserve,r= .68).ConclusionsFractional flow reserve derived from pressure measurements correlates more closely to relative flow reserve derived from PET than angiographic parameters. This validates in humans the use of fractional flow reserve as an index the physiological consequences of a given coronary artery stenosis.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundCross-sectional studies on human hypertension have suggested an association between sodium intake and left ventricular hypertrophy (LVH).Methods and ResultsThe effects on LVH of a nonpharmacological treatment program based mainly on sodium restriction were examined by serial echocardiography in a 12-month controlled, randomized study that included 76 previously untreated subjects with uncomplicated mild-to-moderate hypertension. The mean daily sodium excretion of 38 subjects randomized into the treatment group decreased from 195±95 to 94±73 mmol (P< .001) at 6 months and to 109±74 mmol (P< .001) at 12 months. This was accompanied by a weight decrease from 81.4±18.0 to 79.2±17.4 kg (P< .001) at 6 months and to 80.6 ± 17.5 kg (NS) at 12 months. The net blood pressure decrease (difference in change from baseline between the treatment and control groups) was 8.9 mm Hg (P< .001) in systolic blood pressure and 6.5 mm Hg (P< .001) in diastolic blood pressure during the first 6 months and 6.7 mm HgP< .01) in systolic blood pressure and 3.8 mm Hg (P< .01) in diastolic blood pressure during the last 6 months. After 12 months of sodium restriction, left ventricular mass (LVM) had decreased by 5.4% (from 238±63 to 225±51 g,P< .01), and LVM index (LVMI) had decreased by 4.7% (from 123±26 to 117±22 g/m2,P< .05), whereas no changes occurred in these parameters in the control group. In treated subjects with baseline LVMI of more than the median value of 133 g/m2in men and 107 g/m2in women, LVM decreased by 8.6% (from 272±62 to 249±51 g,P< .01), and LVMI decreased by 7.1% from 140±23 to 130±22 g/m2,P< .01). LVM and LVMI remained unchanged in treated subjects with LVMI values equal to or less than the median.ConclusionsOur data suggest that long-term nonpharmacological treatment with moderate sodium restriction decreases LVH.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundSkeletal muscle can be used for cardiac assistance after electrical stimulation over a period of several weeks. This will adapt it to do chronic work with no resulting fatigue. The result of this procedure, however, is a reduction of 80% in muscle power, >60% in muscle mass, and;≈ 85% in contractile speed. To minimize these disadvantages, the following study was done to develop and test a method to dynamically train skeletal muscle ventricles (SMVs).Methods and ResultsBarrel-shaped SMVs were tested in 15 Jersey calves. They were made from the latissimus dorsi muscle, which was wrapped around an elastic silicone training device. Six SMVs were used extrathoracically in a single layer and nine intrathoracically in a double layer. With dynamic training preserving contractile speed, the output increased to ≈5 L/min, the systolic pressure increased to >200 mm Hg, and power developed to ≈10 W after 3 months of dynamic training. The contractile speed of dynamically trained SMVs was between 250 and 700 mm/s. The diameter of the latissimus dorsi muscle increased to three times that of the corresponding contralateral muscle.ConclusionsThe combination of electrical conditioning with dynamic training of the SMVs resulted in a strong muscle pump that did not develop fatigue. Dynamic training for skeletal muscle represents a new and promising method for providing powerful autologous cardiac assist.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundEchocardiographically determined left ventricular (LV) mass predicts adverse cardiovascular events in the general population. We have assessed the correlates of LV mass in a population-based study focusing on lifestyle and salt intake.Methods and ResultsA random sample of 120 persons born in 1954 was invited; 93 (42 men) entered the study. The subjects' physical activity and alcohol, tobacco, and coffee consumption were quantified by 2-month diary follow-up, and sodium intake was quantified by 7-day food records. Blood pressure was averaged for casual cuff measurements made 2 months apart. LV mass was determined by M-mode echocardiography, and stroke volume was determined by Doppler. Hematocrit and serum insulin were measured. In multiple linear regression analysis, LV mass was related positively and independently (P< .05) to body weight, systolic blood pressure, stroke volume, sodium intake, hematocrit, and energy expenditure in leisure-time physical activity. Additional analyses showed that the relation of LV mass to daily sodium intake depended on blood pressure (P< .001 for the interaction); the multiple regression coefficient (±SE) was 0.41 ±0.11 g. mEq−1. d−1(P= .001) in subjects with systolic blood pressure above the population median but statistically nonsignificant (−0.15±0.10 g mEq−1d−1) in those with lower blood pressure. LV mass was clearly elevated only in persons with both blood pressure and sodium intake above the population medians.ConclusionsBody weight, blood pressure, stroke volume, sodium intake, physical activity, and hematocrit are independent predictors of LV mass among unselected persons aged 36 37 years. The synergistic interaction of dietary salt with blood pressure suggests that high sodium intake may sensitize the heart to the hypertrophic stimulus of pressure load. Prospective studies are needed to confirm these cross-sectional associations.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundAlthough early intravenous β-blocker therapy during acute myocardial infarction (AMI) reduces the incidence of fatal arrhythmias in patients not treated with thrombolytic agents, its antiarrhythmic effect in thrombolysed patients remains controversial. We investigated prospectively the arrhythmia incidence in 244 patients with AMI receiving alteplase and a double-blind randomized adjunctive therapy with intravenous atenolol, alinidine, or placebo. Moreover, the characteristics and prognostic significance of early arrhythmias and their relation with infarct size and coronary patency were evaluated.Methods and ResultsAll patients underwent 24-hour Holter monitoring on day 1 and were clinically followed in the hospital for 10 to 14 days. Coronary angiography was performed on day 10 to 14. Atenolol and alinidine significantly decreased the basic heart rate without causing more sinus arrest or higher-degree atrioventricular block. The prevalence atrial fibrillation in alinidine patients was lower than in the atenolol patients (P= .007) but not lower than in placebo patients (P= .11). There was no effect of either agent on the incidence and frequency distribution of ventricular or supraventricular premature beats or on the incidence and characteristics of nonsustained ventricular tachycardia, accelerated idioventricular rhythm, sustained ventricular tachycardia VT), or ventricular fibrillation (VF). On day 1, seven VF episodes were recorded in six patients (2.5%) and five VT episodes in five patients (2%). VF always started at <2.5 hours after start of thrombolytic treatment and VT always at >2.5 hours (average of 6 hours). Five of the seven VF and three of the five VT episodes started with an R-on-T. However, for all VT, the morphology of the first beat was the same as that of the following beats, suggesting that the sustained arrhythmia was not induced by an extrasystole. After day 1 and before hospital discharge, VF and VT developed in one and six patients, respectively. Three of the seven patients who developed VF during the first 2 weeks underwe nt coronary angiography; all three had an occluded infarct-related artery. In contrast, only one of nine patients with early or late VT had an occluded vessel. Patients with VT and VF on day 1 had asignificantly larger enzymatic infarct size than those without the arrhythmia (P= .02), and a similar trend was noted for VT or VF after day 1 (P= .19). However, none of the patients withVT or VF on day 1 developed a life- hreatening arrhythmia later during the hospital stay. Also, none of the seven patients with VT or VF after day 1 had experienced a major rhythm disturbance during the first 24 hours.Conclusions(1) Our data do not support the hypothesis that β-blockers or bradycardiac agents might reduce the incidence of major arrhythmias when used in conjunction with thrombolytic therapy. (2) The pathogeneses of VT and VF early during AMI are clearly distinct. (3) VT or VF during the first 2 weeks is a marker for a larger infarct. (4) We could not detect a relation between malignant arrhythmias on day 1 and recurrences within the following 2 weeks.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundThe differential diagnosis of supraventricular tachycardia with concentric atrial activation usually requires the inducibility of sustained tachycardia and needs a complex and time-consuming electrophysiological evaluation. To develop a simple test to establish if ventriculoatrial conduction uses a posteroseptal accessory pathway or the normal conduction system, we compared the ventriculoatrial intervals during right ventricular pacing from apical and posterobasal sites.Methods and ResultsContinuous pacing was performed from an apical and a posterobasal right ventricular site in 34 patients with retrograde conduction over the normal conduction system (group A) and in 22 patients with conduction over a posteroseptal accessory pathway (group B). During apical pacing, ventriculoatrial intervals in group A (176±40 milliseconds) were not significantly different than those in group B (197±47 milliseconds,P= NS). During posterobasal pacing, group B patients had significantly shorter ventriculoatrial intervals than group A patients (158±46 versus 197±39 milliseconds,P< .01). The difference between the ventriculoatrial interval obtained during apical pacing and that obtained during posterobasal pacing (ventriculoatrial index) discriminated between the two groups without overlapping: It was positive in all group B patients (39±19; range, +10 to +70 milliseconds) and negative in all except two group A patients (−21±13; range, −50 to +5 milliseconds;P< .001).ConclusionsThis ventriculoatrial index can identify accurately and in the absence of tachycardia whether concentric retrograde conduction is proceeding over a posteroseptal accessory pathway or over the normal conduction system.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundThe autonomic nervous system has been demonstrated to play a decisive role in the genesis of sudden cardiac death. The loss of protective vagal reflexes, in particular, appears to be associated with an increased incidence of malignant ventricular tachyarrhythmias. Two clinically applicable methods for assessment of cardiac autonomic control have been developed: determination of heart rate variability and evaluation of baroreflex sensitivity.Methods and ResultsTo compare the potential predictive value of both methods, two groups of patients were studied. Group 1 comprised 14 postinfarction patients who had experienced at least one episode of ventricular fibrillation or sustained ventricular tachycardia and who were studied after this event. Group 2 consisted of 14 postinfarction patients without tachyarrhythmic events after their infarct. Both groups were carefully matched with respect to age, sex, infarct location, extent of coronary artery disease, left ventricular ejection fraction, blood pressure, and heart rate at rest. Heart rate variability was assessed from 24-hour Holter recordings, and baroreflex sensitivity was determined by means of the phenylephrine method. Indices of heart rate variability were not significantly different between the two groups (SD of the mean RR interval, 84±30 milliseconds versus 103±20 milliseconds; proportion of adjacent RR intervals >50 milliseconds different, 2.8±3.2% versus 5.0±4.1% in group 1 versus 2). Baroreflex sensitivity, however, showed a striking difference: Group 1 patients had a mean value of 1.75±1.63 ms/mm Hg compared with 9.17±5.40 ms/mm Hg in group 2 (P= .0002). Eleven of 14 group 1 patients had a baroreflex sensitivity ≤3.0 ms/mm Hg. By contrast, only 1 of 14 group 2 patients had such a depressed value.ConclusionsThe results of this study indicate that postmyocardial infarction patients who develop life-threatening ventricular tachyarrhythmias, compared with carefully matched postinfarction patients without major arrhythmic episodes, differ strikingly in terms of baroreflex sensitivity but not in terms of heart rate variability. This finding may have implications for the risk stratification of postinfarction patients and may lead to a differential therapeutic strategy based on autonomic testing.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundRadio frequency catheter ablation is accepted therapy for patients with paroxysmal supraventricular tachycardia and has a low rate of complications. For patients with atrial arrhythmias, catheter ablation of the His bundle has been an option when drugs fail or produce untoward side effects. Although preventing rapid ventricular response, this procedure requires a permanent pacemaker and does not restore the atrium to normal rhythm. Therefore, we evaluated the safety and efficacy of radiofrequency ablation directed atthe atrial substrate.Methods and ResultsThirty-seven patients with 42 atrial arrhythmias (mean±SD age, 41±24 years) who had failed a median of three drugs were enrolled. Diagnoses were automatic atrial tachycardia in 12, atypical atrial flutter in 1, typical atrial flutter in 18, reentrant atrial tachycardia in 8, and sinus node reentry in 3 patients. Sites for atrial flutter ablation were based on anatomic barriers in the floor of the right atrium. For automatic atrial tachycardia, the site of earliest activation before the P wave was sought. All with reentrant atrial tachycardia had previous surgery for congenital heart disease and reentry around a surgical scar, anatomic defect, or atriotomy incision and our goal was to identify a site of early activation in a zone of slow conduction. At target sites, 20 to 50 W of radiofrequency energy was delivered during tachycardia between the 4- or 5-mm catheter tip and a skin patch, except in 4 patients with atrial flutter, in whom a catheter with a 10-mm thermistor-embedded tip was used. Procedure end point was inability to reinduce tachycardia. Acute success was achieved in 11 of 12 (92%) with automatic atrial tachycardia,17 of 18 (94%) with typical atrial flutter, 7 of 8 (88%) with reentrant atrial tachycardia, and 3 of 3 (100%) with sinus node reentry but not in the patient with atypical atrial flutter. For tachycardia involving reentry (reentrant atrial tachycardia and atrial flutter), successful ablation required severing an isthmus of slow conduction. For those with atrial flutter, this was between the tricuspid annulus and the coronary sinus os (10) or posterior (4) or posterolateral (3) between the inferior vena cava (2) or an atriotomy scar (1) and the tricuspid annulus. Deep venous thrombosis occurred in 1 patient. At mean follow-up of 290±40 days, the ablated arrhythmia recurred in 1 (9%) with automatic atrial tachycardia, 5 (29%) with atrial flutter, and 1 (14%) with reentrant atrial tachycardia, all of whom had successful repeat ablation. Previously undetected arrhythmias occurred in 2 patients who are either asymptomatic or controlled with medication.ConclusionsAblation of automatic and reentrant atrial tachycardia and atrial flutter had a high success rate and caused no complications from energy application. Repeat procedures may be required for long-term success, especially patients with atrial flutter. The mechanism by which ablation is successful is similar for atrial flutter and other forms of atrial reentry and involves severing a critical isthmus of slow conduction bounded by anatomic or structural obstacles. Automatic arrhythmias are abolished by directing lesions at the focus of abnormal impulse formation.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID