ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Exercise conditioning involves adaptations in the heart, peripheral circulation, and trained skeletal muscle that result in improved exercise capacity. Since the specific influence of /β-adrenergic stimulation on these various adaptations has not been clear, we studied the effect of 3,1-selective and nonselective, β-adrenergic blockade on the exercise conditioning response of 24 healthy, sedentary men after an intensive 6 week aerobic training program. Subjects randomly assigned to receive placebo, 50 mg bid atenolol, or 40 mg bid nadolol were tested before and after training both on and off drugs. Comparable reductions in maximal exercise heart rate occurred with atenolol and nadolol, indicating equivalent /I-adrenergic blockade. Vascular 132-adrenergic selectivity was maintained with atenolol as determined by calf plethysmography during intravenous infusion of epinephrine. All subjects trained at greater than 85% of maximal heart rate and 80% of 'V02max determined on drug .02 max increased after training 16 ± 2% (p < .05) in the placebo group and 6 ± 2% (p < .05) in the atenolol group, while there was no change in the nadolol group. At maximal exercise, subjects receiving placebo increased their exercise duration and oxygen pulse significantly greater than those receiving atenolol or nadolol. During submaximal exercise there were reductions in heart rate and heart rate-blood pressure product in all three groups, but these reductions were greater with placebo than with either drug. Leg blood flow during submaximal exercise decreased 24 ± 2% (p < .01) in the placebo group but was unchanged in the atenolol and nadolol groups. Lactates in arterialized blood during submaximal exercise were reduced equivalently in all three groups after training. Capillary/fiber ratio in vastus lateralis muscle biopsy specimens increased 31 ± 6% in the placebo group and 21 ± 6% in the atenolol group (both p < .05) and tended to increase in the nadolol group. Succinic dehydrogenase and cytochrome oxidase activities in muscle biopsy specimens increased equivalently in all three groups after training. Thus, although exercise conditioning developed to some extent in both drug groups, especially during submaximal exercise, these changes were less marked than that with placebo. While /β-adrenergic blockade attenuated the exercise conditioning response, skeletal muscle adaptations including increases in oxidative enzymes, capillary supply, and decreases in exercise blood lactates were unaffected. Cardiac and peripheral vascular adaptations do appear to be affected by, β-adrenergic blockade during training. Cardioselectivity does not seem to be important in modifying these effects.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

An increase in left ventricular diastolic pressure has been repeatedly observed during angina in patients with coronary artery stenoses and regional demand ischemia, but the role of relaxation abnormalities versus left ventricular segmental dyssynchrony is controversial. In contrast, patients with angina due to aortic stenosis are likely to have diffuse rather than segmental ischemia and thus may provide an alternative model for examining the diastolic physiology of angina in man. Accordingly, we examined the hemodynamic manifestations of angina in eight patients with aortic stenosis without significant coronary artery disease. Angina was induced by pacing tachycardia, and hemodynamic and echocardiographic variables were measured in the control period and during angina in the beats immediately after cessation of pacing. Heart rate (control vs angina, 69 ± 12 vs 70 ± 11 beats/min, p = NS) and left ventricular peak systolic pressure (207 39 vs 222 22 mm Hg, p = NS) were similar in the control and postpacing angina periods. Left ventricular end-diastolic pressure, on the other hand, was significantly higher during postpacing angina (15 ± 7 vs 28 ± 8 mm Hg, p < .01). The time constant of left ventricular pressure decline during isovolumetric relaxation (TL), calculated as the slope of a linear fit of the natural log of pressure vs time, increased from 44 ± 5 to 51 ± 7 msec (p < .05); the time constant TD, derived from the slope of a linear fit of dP/dt vs pressure, also increased slightly, although the change was not statistically significant (69 ± 5 vs 75 ± 5 msec, p = .06). High-quality two-dimensional targeted M mode echocardiograms in the control and postpacing periods were available in four patients; left ventricular end-diastolic and end-systolic dimensions and percent fractional shortening were unchanged. The left ventricular diastolic pressure-volume relationship and pressure-wall thickness relationship were shifted upward during angina in these patients. We conclude that angina in patients with aortic stenosis is accompanied by a substantial and reversible increase in left ventricular end-diastolic pressure; this increase appears to be due in part to an impairment of diastolic distensibility of the left ventricle and left ventricular relaxation. These findings, which are similar to those observed during pacing-induced angina in patients with coronary stenoses, suggest that the increase in left ventricular end-diastolic pressure that occurs during angina is a manifestation of demand ischemia per se, and does not depend on the presence of dyssynergistic contraction of ischemic and nonischemic regions.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Angiographic results in patients with mitral regurgitation suggest that up to 50% of the regurgitant volume occurs during the preejection period. This contrasts markedly with the electromagnetic measurements of mitral regurgitant flow in anesthetized dogs, which suggest that only 5% of mitral regurgitant flow occurs during the preejection period. Therefore, we used two-dimensional and Doppler echocardiography to quantify mitral regurgitation during aortic ejection and in the preejection and postejection periods in eight patients with severe heart failure. Mitral regurgitant volume (RV) was calculated as the difference between total stroke volume (by two-dimensional echocardiography) and forward aortic flow (by pulsed Doppler). Regurgitant velocity (V) and time (RT) were measured by continuous-wave Doppler, and the mean regurgitant area (RAm) was calculated from the RT and mean regurgitant velocity (Vm): RAm - (RV/RT)/Vm. As a first approximation, the RA was assumed to be constant during systole, and the regurgitant volume during aortic ejection and during the preejection and postejection periods was calculated from: RVi = (Vmi) (RTi) (TAm), where Ti represents the duration of the appropriate period. Percentages of total regurgitant volume occurring during the preejection, ejection, and postejection periods were 13 ± 4%, 79 ± 5%, and 8 ± 5%. respectively. Thus, in contrast to previously reported angiographic studies, mitral regurgitation occurs predominantly during the aortic ejection period. These results were not substantially changed by assuming a 20% reduction in effective regurgitant orifice area between the preejection and ejection periods and are consistent with data from chronically instrumented dogs with mitral regurgitation. Furthermore, our findings are supported by a computer model of the central circulation that was modified to include an incompetent mitral valve. The model offers significant insight into the physiologic mechanisms governing phasic changes in mitral regurgitant volume.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Dilatation of infarcted segments (infarct expansion) may occur during recovery from myocardial infarction, but the fate of noninfarcted segments is uncertain. Accordingly, left ventricular geometric changes were assessed by left ventricular angiography and M mode echocardiography on admission and 2 weeks later in 30 patients with their first acute transmural myocardial infarction. All patients demonstrated chest pain, ST segment elevation with subsequent development of Q waves (15 anterior, 15 inferior), and elevation of cardiac enzymes. Sequential left ventricular angiographic and hemodynamic findings were available in these patients by virtue of their participation in a study of thrombolysis in acute myocardial infarction. By that study design, all patients treated successfully with thrombolytic therapy and demonstrating improvement of flow in an occluded coronary artery underwent repeat cardiac catheterization. At 2 weeks there was a significant decrease in left ventricular and pulmonary capillary wedge pressures (p < .0 1), whereas both left ventricular end-diastolic (LVEDV) and end-systolic (LVESV) volume indexes increased (p < .01). The increase in LVEDV correlated directly with the percentage of the ventriculographic silhouette that was akinetic or dyskinetic at the initial catheterization (r = .71, p < .001). To assess regional changes in both infarcted and noninfarcted segments, serial endocardial perimeter lengths of both the akinetic-dyskinetic segments (infarction zone) and of the remainder of the cardiac silhouette (noninfarction zone) were measured in all patients who demonstrated at least a 20% increase in their LVEDV at 2 weeks after myocardial infarction. Notably, there was a mean increase of 13% in the endocardial perimeter length of infarcted segments and a 19% increase in the endocardial perimeter length of noninfarcted segments. Serial M mode echocardiographic studies showed no significant change in the wall thickness of noninfarcted myocardial segments. Hemodynamic changes that occurred in this subgroup of patients included significant decreases in left ventricular end-diastolic and pulmonary capillary wedge pressures (p < .05) and significant increases in angiographic cardiac index (p < .01) and LVESV index (p < .01). We conclude that in patients who manifest cardiac dilatation in the early convalescent period after myocardial infarction, there is remodeling of the entire left ventricle including infarct expansion of akineticdyskinetic segments and volume-overload hypertrophy of noninfarcted segments. The magnitude of the remodeling process is directly proportional to infarct size as assessed by the extent of wall motion abnormality present during the acute phase of infarction. Moreover, the remodeling changes that occur are associated with hemodynamic improvement, including lower left ventricular filling pressures and increased cardiac output, but these hemodynamic changes appear to occur at the expense of a significant increase in left ventricular chamber volumes.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

We evaluated the relationship between baseline factors defined at 4.6 ± 2.1 hr after onset of acute myocardial infarction and 1 year survival in 245 patients entered in the Western Washington Intracoronary Streptokinase Trial. Univariate statistics identified a significant relationship between 10 of these factors and survival. Multivariate analysis identified three factors as being most closely related to survival: (1) left ventricular ejection fraction (LVEF) (p < .0001), (2) treatment with streptokinase (p = .03), and (3) location of infarction (p = .04). Mathematic models based on this analysis and applied to our patients identified high- and low-risk subgroups for 1 year mortality. Patients receiving standard, not interventional, therapy with anterior infarction and an LVEF of 50% or less and those with inferior infarction and an LVEF of 39% or less comprised the high-risk group. For patients receiving standard therapy, 1 year mortality was 41% in the high-risk group and 4% in the lowrisk group. The models illustrated the magnitude of benefit of streptokinase treatment and achievement of complete reperfusion for those at low and high risk. We conclude that LVEF determined in the first hours of acute myocardial infarction is the most important of all baseline factors for prediction of 1 year survival. Mathematic models based on left ventricular function measured as ejection fraction are useful for risk stratification in this setting.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

We examined, in age subsets, 2643 patients with acute myocardial infarction. Clinical features and 1 year morbidity and mortality were compared in 203 young patients (70 years). Ninety-two percent of young patients were men, and a family history of premature coronary artery disease was more common in young patients (41% compared with 28% of middle-aged and 12% of elderly patients). More young patients were currently smoking cigarettes (82% compared with 56% of middle-aged and 24% of elderly patients), and only 8% of young patients had never smoked. Previous myocardial infarction and history of angina pectoris or congestive heart failure were less common (p < .001) in the young patients than in middle-aged and elderly patients. In-hospital mortality was only 2.5% for young patients, compared with 9.0% in middle-aged and 21.4% in elderly patients (both p < .001). Postdischarge 1 year mortality was also strikingly low in young patients, at 2.6% compared with 10.3% in middle-aged and 24.4% in elderly patients. The incidence of reinfarction during the 1 year of follow-up was similar in all subsets. The statistical significance of 65 variables as predictors of 1 year mortality and reinfarction was tested and the following found to be significant (p < .05): hospital discharge on antiarrhythmic drugs, digoxin, or diuretics; history of previous myocardial infarction or congestive heart failure; chest x-ray findings of heart failure; low ejection fraction; and atrial fibrillation. Thus, young patients entering the hospital have an excellent 1 year prognosis, but those with prior infarction in whom there are selected abnormal findings at hospital discharge comprise a subgroup that may benefit from early aggressive management.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

We analyzed the resetting response (a noncompensatory pause after electrical stimulation) during 37 hemodynamically tolerated ventricular tachycardias (VTs) induced by programmed electrical stimulation in 32 patients with chronic coronary artery disease. The mean cycle length of VT was 369 ± 59 msec. Single extrastimuli were delivered at the right ventricular apex during all 37 VTs, and double extrastimuli were delivered at the same site during 23 VTs. The resetting response pattern was considered increasing, decreasing, or flat if the return cycle increased, decreased, or remained constant in response to progressively shorter coupling intervals of the extrastimuli. Ten VTs had an increasing pattern and nine a flat pattern. In 11 VTs the pattern was mixed (flat at longer coupling intervals and increasing at shorter ones), and in the remaining seven the pattern could not be defined. No VT had a decreasing pattern. The mean duration of the resetting interval (range of coupling intervals resulting in resetting) was 66 45 msec, or 17% of the cycle length of VT. VT with a mixed pattern had longer resetting intervals than VT with an increasing pattern (102 ± 34 vs 64 ± 40 msec; p < .035); however, cycle lengths of VT were similar (370 ± 58 vs 386 ± 86, p - NS). An excellent correlation was observed between the shortest return cycles in response to single and double extrastimuli (r = .99), with a mean difference of 5 msec. The cycle length of VT exceeded the return cycle (measured to the QRS onset) during 15 VTs (41 %). The findings of flat and mixed resetting response patterns and relatively long resetting intervals favor a reentrant circuit, which is at least in part anatomically defined, for the majority of these tachycardias.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The relative prognostic significance of ventricular tachycardia and ventricular fibrillation inducible at programmed stimulation within 1 month of acute myocardial infarction was compared in a prospective study of 403 clinically well survivors of transmural infarction who were 65 years old or younger. The prognostic significance of delayed potentials on the signal-averaged electrocardiogram was also examined in a subset of 306 patients without bundle branch block. Among the study patients, 20% had inducible ventricular tachycardia, 14% had inducible ventricular fibrillation, and 66% had no inducible arrhythmias. The 2 year probability of remaining free from cardiac death or nonfatal ventricular tachycardia or fibrillation was 0.73 for those with inducible ventricular tachycardia, 0.93 for those with inducible ventricular fibrillation, and 0.92 for those with no inducible arrhythmias. The cycle length of inducible ventricular tachycardia was 230 msec or more in 70% of the patients with inducible tachycardia who died. Of the patients studied by signal-averaged electrocardiography, 26% had delayed potentials. At 2 years, the probability of remaining free from cardiac death or nonfatal ventricular tachycardia or fibrillation was 0.73 for patients with delayed potentials and 0.95 for patients with no delayed potentials. There was a significant correlation (p < .001) between the presence of delayed potentials and the ability to induce ventricular tachycardia. In conclusion, in survivors of recent infarction who have not had spontaneous ventricular tachycardia or fibrillation, inducible tachycardia (but not inducible fibrillation) at programmed stimulation predicts a significant risk of death or spontaneous tachycardia or fibrillation. A similar risk is found for patients with delayed potentials on the signal-averaged electrocardiogram.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID