摘要:

ABSTRACT Isoarea maps during the PQRST sequence were computed in 22 healthy subjects and 48 patients with Wolff-Parkinson-White (WPW) syndrome. Thirty-eight patients with WPW were on no medication and 10 were treated with class I, II, or III antiarrhythmic drugs. Seventeen isoarea maps were recorded before and 17 were recorded after accessory pathway ablation. One patient had intermittent preexcitation. Body surface maps from all healthy subjects were similar, although the magnitudes of the maxima and minima showed significant variability. In all patients with WPW who were on no medication and in those on class I and II agents, PQRST maps were normal. Two patients taking amiodarone had abnormal PQRST maps, as did patients early after surgery. In the patient with intermittent preexcitation, PQRST maps were very similar during normal and preexcited beats. In conclusion, our results support the theory that the PQRST time integral reflects intrinsic recovery properties of the heart and is independent of the activation sequence.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

ABSTRACT The large cohort of white men (317, 871) 35 to 57 years old at initial screening for possible enrollment into the Multiple Risk Factor Intervention Trial (MRFIT) was examined with regard to initial blood pressure levels and subsequent coronary heart disease (CHD), stroke, and all-cause mortality. The overall prevalence of isolated systolic hypertension (ISH), defined as systolic blood pressure (SBP) greater than or equal to 160 mm Hg and diastolic blood pressure (DBP) less than 90 mm Hg, was 0.67% among white men screened for MRFIT and increased with age (0.31% among 35- to 39-year-olds to 1.7% among 55- to 57-year-olds). The 6 year CHD and all-cause mortality rates in men over 50 were highest in those with ISH compared with both subjects with diastolic hypertension and those with normal pressure. The relative risk of death from stroke in those with ISH, compared with that in those with SBP less than 160 mm Hg and those with DBP less than 90 mm Hg, was 3.0 (95% confidence interval 1.3 to 6.8). In addition, at any level of DBP, the level of SBP appeared to be the major determinant of all-cause and CHD mortality. The determinants of ISH in individuals under 60 years of age as well as the possible efficacy of its treatment should be evaluated further.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

ABSTRACT Left ventricular cineangiography and micromanometry were performed simultaneously in 27 patients with chronic severe mitral regurgitation (MR group) and in 23 normal subjects (NL group). Stress (σ) and volume (V) were computed frame by frame. Measurements were repeated after pharmacologic load manipulation in subsets of MR (n = 10) and NL (n = 11) groups. An inverse relationship (r = −.90) between EFc(ejection fraction determined from a common preload) and σes(afterload) was observed for the NL group. For the MR group, 10 of 14 with EFs less than 0.60 and four of 13 with EFs greater than 0.60 had muscle dysfunction, falling below the 95% prediction band of the normal EFc-σesrelationship. Maximum myocardial stiffness (maxEN) determined from the end-systolic stress-strain relationship of Mirsky, σes= maxEN‘γ’;loge(Ves/V0), was 1398 ± 716 in the MR (n = 10) vs 1165 ± 394 in the NL group (n = 11, NS). EF was 0.62 ± 0.13 in the MR and 0.65 ± 0.08 in the NL group. Mitral valve surgery was performed on 19 of the patients with MR. All survived and all but one were symptomatically improved; that patient required reoperation in the early postoperative period because of transverse midventricular disruption. Thus, contractile function as assessed by stress-strain and EFc-afterload relationships is frequently normal in individuals with MR when EF is normal. When EF is depressed, contractile function as assessed by EFc-afterload relationships is frequently depressed, but this does not preclude a satisfactory surgical result.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

ABSTRACT Intracoronary thrombus is regarded as a potentially important factor in the etiology of unstable angina, but the incidence of intracoronary thrombus in unstable angina has not been clearly defined. To determine the occurrence of intracoronary thrombus during ongoing angina pectoris, coronary angiography was performed during spontaneous ischemic attacks in 37 patients with prolonged rest angina. All patients exhibited significant (>50%) stenoses of at least one major coronary artery. Of the 37 patients, 21 (57%) had intracoronary thrombus in major coronary arteries, whereas 14 (38%) had fixed narrowings without evidence of intracoronary thrombus and two exhibited coronary spasm. ST segment elevation was observed in 16 of 21 patients with thrombus and in all of the patients with coronary spasm, but all the patients with organic stable obstruction showed ST segment depression. Twenty of the 21 patients with thrombus improved after thrombolytic therapy with intracoronary injection of urokinase; obstructed arteries were reopened, or narrowings were attenuated, with relief of ischemic symptoms. In patients with fixed obstructions, the rate-pressure product during active symptoms was significantly higher than during an asymptomatic period, indicating that a transient increase in myocardial oxygen demand may contribute to the ischemic attack in these patients. A high incidence (71%) of recurrent symptoms was observed in patients with intracoronary thrombus even after successful thrombolysis, in contrast to a much lower incidence (36%) in those without intracoronary thrombus. Myocardial infarction within 4 weeks after catheterization was observed more frequently in patients with intracoronary thrombus (24%) than in those without thrombus (7%). Thus our results indicate that the incidence of intracoronary thrombus is quite high during ongoing attacks of unstable angina, although a transient increase of myocardial oxygen demand also plays an important etiologic role. It is also suggested that patients with thrombus fare less well than those with organic stable obstruction.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

ABSTRACT Multivessel coronary spasm has been described but its incidence in patients with variant angina still remains unclear. Thirty-three patients with variant angina were studied during coronary angiographic examination with selective intracoronary injection of acetylcholine (ACh). In all but three patients, the location of ischemia during attack was determined by the electrocardiographic findings, by exercise201Tl myocardial scintigraphy, and by two-dimensional echocardiography during a hyper-ventilation test, and the coronary artery (or arteries) responsible for the attack was predicted before the study. ACh induced spasm of at least one coronary artery in all but one patient. ACh induced spasm of both the left and right coronary arteries (i.e., multivessel coronary spasm) in 24 patients: in two of the four patients who were predicted to have spasm of the left coronary artery, in six of the 11 predicted to have spasm of the right coronary artery, in 13 of the 15 predicted to have spasm of both the left and right coronary arteries, and in three of the three in whom coronary artery responsible for attack had not been predicted. This ACh-induced spasm of the left and right coronary arteries occurred separately and no patients showed hemodynamic instability during attack. In one patient in whom multivessel coronary spasm had been predicted and ACh failed to induice coronary spasm, ergonovine maleate (0.2 mg) induced spasm of both the left and right coronary arteries simultaneously, resulting in severe prolonged hypotension. Nineteen of the 25 patients in whom multivessel coronary spasm was documented showed angiographically normal or nearly normal coronary arteries after administration of nitroglycerin. In conclusion, multivessel coronary spasm is not a rare phenomenon but can occur or be induced in many patients with variant angina, especially those with normal or almost normal coronary arteries in a Japanese population. Intracoronary injection of ACh is a useful, safe, and reliable method to document multivessel coronary spasm in patients with variant angina.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

ABSTRACT To determine the mechanisms by which blood flow increases across the mitral and aortic valves during exercise, 18 normal men were studied during graded supine and upright bicycle exercise at matched workloads. Mitral valve orifice and ascending aortic blood velocities were recorded by Doppler echocardiography during steady states at each stage of exercise. Parasternal two-dimensional echocardiographic imaging of the ascending aorta adjacent to the aortic valve orifice and the mitral valve orifice at the tips of the valve leaflets was used to calculate changes in cross-sectional area during exercise. Heart rate increased from rest to exercise from 67 to 150 beats/min (124%) during supine exercise and from 72 to 147 beats/min (104%) during upright exercise. Stroke volume increased 20% during supine and 46% during upright exercise; the increase in stroke volume was statistically significant when rest and exercise were compared and when the magnitude of change was compared vs position (p < .05). The increase in stroke volume measured at the ascending aorta was accomplished by an increase in the velocity-time integral (+15% supine and + 48% upright, p < .05), with little change in aortic cross-sectional area (5% supine and 0% upright, p = NS). By contrast, the increase in flow rate measured at the mitral valve was predominantly due to an increase in mean diastolic cross-sectional area (+ 29% supine and 34% upright, p < .05); the velocity-time integral did not increase significantly (−10% supine and 4% upright; p = NS). The data contrast the mechanisms by which aortic and mitral valve flow increase with exercise, and demonstrate an increase in cross-sectional area at the mitral valve orifice and the importance of an increase in velocity-time integral at the aortic valve. These observations support the use of changes in the heart rate times velocity-time integral as an indicator of changes in cardiac output at the aortic valve, but stress the importance of serial cross-sectional area measurements at the mitral valve orifice in the assessments of changes in cardiac output.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

ABSTRACT This study was designed to determine the pathophysiologic basis of increased exercise ventilation in the presence of chronic heart failure. Sixty-four ambulatory patients with chronic heart failure and 38 age-matched normal control subjects performed exercise according to identical staged, symptom-limited bicycle exercise protocols with measurement of hemodynamic, ventilatory, and metabolic responses. Compared with normal subjects, ventilation and the ratio of ventilation to CO2production (Ve/VCO2), and pulmonary capillary wedge pressure were elevated in patients at rest and during exercise. The ratio of pulmonary dead space to tidal volume (Vd/Vt) also was elevated in the heart failure group at rest and during exercise and was closely related to Ve/VCO2(all r > .72, p < .001). Rest and exercise arterial Pco2regulation was normal in patients. Peak exercise Ve/VCO2did not correlate with pulmonary vascular pressures, but was inversely related to cardiac output (r = −.49, p < .001). Thus, neurohumoral ventilatory control mechanisms are intact in patients with chronic heart failure and act to maintain normal Paco2levels in the face of increased pulmonary dead space. Activation of abnormal reflexes due to hemodynamic derangements during exercise are not important in determining ventilation in the presence of chronic heart failure. The demonstration of a correlation between decreased cardiac output and increased ventilation in the patient group suggests that attenuated pulmonary perfusion may play a role in causing exercise hyperpnea in the presence of chronic heart failure by producing ventilation perfusion abnormalities and thereby increasing physiologic pulmonary dead space.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

ABSTRACT Electrophysiologic studies were performed in 16 patients 11 to 45 years old (mean 33 years) with idiopathic sustained (lasting more than 5 min) ventricular tachycardia (VT) originating from the left ventricle. Endocardial mapping during VT showed that the earliest site of activation was at the apical inferior portion of the left ventricle in 14 patients whose QRS morphology during VT showed a right bundle branch block pattern and left-axis deviation, but at the apical anterosuperior portion of the left ventricle in two patients whose QRS morphology during VT showed a right bundle branch block and right-axis deviation. Single programmed ventricular stimulation induced VT in 13 patients, and rapid ventricular pacing induced VT in the remaining three patients. Rapid ventricular pacing terminated VT in all patients. The relationship between the coupling interval and the echo interval was inverse in all eight patients with a wide VT inducible zone. Entrainment was recognized in three of six patients. The initiation of VT by constant pacing depended on the number of pacing beats but not the duration of pacing in all four patients tested. Intravenous verapamil terminated the VT in 13 of 14 patients. Long-term oral verapamil was also effective in all five patients who required long-term oral therapy for their symptoms associated with VT. In conclusion (1) idiopathic left ventricular tachycardia has unique electrocardiographic, electrophysiologic, and electropharmacological properties, (2) the electrophysiologic characteristics suggest that the mechanism is reentry, and (3) verapamil is effective in both the short- and long-term treatment of VT.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

ABSTRACT Transient entrainment was demonstrated during 59 pacing events in 18 episodes of sustained uniform ventricular tachycardia (VT) while recording electrograms from the site of origin of tachycardia (LE-SOO). During entrainment, the morphology of the initial component of the LE-SOO was identical to the morphology observed during the tachycardia in 13 VTs (group I), but in five VTs (group II), the initial component changed at a “critical” paced cycle length. The presence of the proposed surface electrocardiographic criteria for entrainment — fixed fusion and a first postpacing complex without fusion but occurring at the paced cycle length — were integrally dependent on the morphologic changes in the local presystolic electrogram. Fixed fusion of the surface electrocardiogram at one or more paced cycle lengths was detected during entrainment at 35 of 59 paced cycle lengths in 12 of 18 tachycardias, 10 of which were group I and two of which were group II VTs. Fixed fusion demonstrated by analysis of the LE-SOO was observed at one or more pacing cycle lengths in 17 of 18 VTs. In five tachycardias in which surface electrocardiographic fusion was not observed, fixed fusion was evident on analysis of the left ventricular LE-SOO during right ventricular pacing. The first postpacing interval, as measured at the surface electrocardiogram, was consistently equal to the paced cycle length in only one of 18 tachycardias and was greater than the VT cycle length in eight of 17 tachycardias. A pathway with a long conduction time was demonstrated during entrainment. However, in those 12 VTs in patients in whom pacing was performed at more than one cycle length and there was preservation of the LE-SOO morphology, the conduction time between the stimulus and presystolic electrogram remained constant. Thus, no evidence for “atrioventricular nodal-like” decremental conduction was observed over a wide range of pacing cycle lengths. We conclude that: (1) two of the previously proposed criteria for diagnosis of entrainment (fixed fusion on the surface electrocardiogram and a first postpacing interval equal to the paced cycle length) are overly restrictive criteria for definition of “entrainment” of VT, (2) analysis of endocardial recordings from the site of origin of tachycardia during attempted entrainment of VT is useful for documenting the presence of entrainment, and (3) such analysis provides a basis for the understanding of surface electrocardiographic phenomenon associated with entrainment.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID