ISSN:0009-7322    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

ABSTRACTWe used multiple linear regression to study predictors of systolic blood pressure response (SBPR), i.e., the increase in pressure above baseline after 3, 6, and 9 min of treadmill exercise, in 4262 men and women. Predictors considered were usual SBP, the difference (&Dgr; SBP) between resting SBP and SBP immediately before exercise, age, education, obesity index, alcohol consumption, cigarette smoking, preexercise heart rate and, in women, gonadal hormone use. In men, age, obesity index, and cigarette smoking were positively associated with SBPR and in women 20 to 49 years old, age, obesity index, and alcohol consumption were positively associated with SBPR. In women 50 years old or older, usual SBP was negatively associated with SBPR. In both men and women a larger &Dgr; SBP was associated with a smaller SBPR. These results help explain the considerable variation in SBPR, and the &Dgr; SBP results suggest that potential SBPR may, to certain extent, have a specific, finite range. The similarity of predictor variables for SBPR to predictor variables for hypertension is concordant with the previous observation that a high SBPR may foreshadow subsequent hypertension.Circulation 68, No. 2, 225‐233, 1983.

ISSN:0009-7322    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

ABSTRACTArterial baroreflex sensitivity, plasma norepinephrine (NE) and epinephrine (E), and pressor and depressor responses were assessed in 25 patients with essential hypertension and 29 normotensive control subjects. Sensitivity of the cardiac limb of the baroreflex was determined by blood pressure and interbeat interval responses associated with the Valsalva maneuver, externally applied neck suction and pressure, and injection of phenylephrine and nitroglycerin. By all these techniques, patients with essential hypertension had significantly decreased baroreflex sensitivity, even after adjustment for age mismatching between the hypertensive and normotensive groups. Hypertensive patients also had significantly higher mean levels of plasma NE and E in both brachial arterial and antecubital venous blood (246 vs 154 pg/ml arterial NE, 286 vs 184 pg/ml venous NE, 99 vs 55 pg/ml arterial E, and 65 vs 35 pg/ml venous E) and significantly larger pressor responses to injected phenylephrine (30.9 mm Hg/100 &mgr;g vs 16.7 mm Hg/100 &mgr;g). When baroreflex‐cardiac sensitivity values measured by the various techniques were averaged, there was a significant inverse relationship between sensitivity and venous NE and between sensitivity and pressor responsiveness. The results indicate that decreased baroreflex‐cardiac sensitivity, increased sympathetic outflow, and pressor hyperresponsiveness tend to occur together in some patients with essential hypertension. Decreased arterial distensibility and altered central neural integration can account for these findings.Circulation 68, No. 2, 234‐240, 1983.

ISSN:0009-7322    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

ABSTRACTHeart failure is associated with a reduction in tissue norepinephrine concentration, catecholamine fluorescence, and tyrosine hydroxylase activity. We hypothesized that this attrition of sympathetic nerve function might also be associated with a reduction in the ability of the neuronal membrane to sequester catecholamines. Since the heart does not release epinephrine, the cardiac extraction of epinephrine should be an index of the membrane uptake system. In 12 patients with documented left ventricular failure (pulmonary edema) secondary to mechanical overload and in 10 patients with no history of heart failure, we measured simultaneous plasma catecholamine concentrations in the aorta, coronary sinus, and femoral vein. The aortocoronary sinus extraction of epinephrine was 43 ± 17% in the group with no evidence of heart failure but 0 ± 14% in the group with failure. Net norepinephrine outflow (release minus extraction) was significantly higher in the group with failure, possibly because of reduced extraction. There was neither a reduction in the ability of the lower limb to extract epinephrine nor an increased norepinephrine outflow from the limb. These findings suggest that the sympathetic neuronal membrane uptake system is also depressed in the failing heart and that if the mechanism of catecholamine sequestration in the heart is related to that in the lower limb, the ablation of sympathetic nerve function is specific to the heart and is not a result of a generalized depression of the peripheral sympathetic nervous system.Circulation 68, No. 2, 241‐244, 1983.

ISSN:0009-7322    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

ABSTRACTOf 12 healthy men with a mean age 50 ± 4 years who had been at bed rest for 10 days, six were randomly assigned to perform individually prescribed physical exercise daily for 60 days after bed rest (exercise group) and six simply resumed their customary activities (control group). Exercise group subjects were significantly more active than control subjects during this interval (p < .05). Two classic training effects observed in the 60 days after bed rest were significantly larger among exercise than among control group subjects; compared with values immediately after bed rest, heart rate at a constant submaximal workload declined by 36 ± 11 beats/min in the exercise group vs 16 ± 8 beats/min in the control group and peak oxygen consumption increased by 4.8 ± 4.2 vs 2.2 ± 5.0 ml/kg/min (both p < .05). Despite these differences in the cardiovascular response to exercise, peak oxygen consumption in both groups returned to before‐bed rest levels by 30 days after bed rest, and this was accompanied by significant (p < .05) and similar increases in resting left ventricular end‐diastolic and stroke volumes in both groups. Simple resumption of usual physical activities after bed rest was as effective as formal exercise conditioning in restoring functional capacity to before‐bed rest levels.Circulation 68, No. 2, 245‐250, 1983.

ISSN:0009-7322    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

ABSTRACTArrhythmogenic right ventricular dysplasia (ARVD) is a recently described entity characterized by right ventricular myopathic changes and right ventricular tachycardia. The presence or extent of left ventricular dysfunction in ARVD is not known. We assessed right ventricular and left ventricular function and size in six patients with ARVD by echocardiography and radionuclide angiocardiography done in patients at rest and during exercise. All patients had recurrent ventricular tachycardia of left bundle branch block morphology, and right ventricular origin of the ventricular tachycardia was confirmed by endocardial mapping in four patients. The results were compared with those of 10 normal subjects and five patients with Wolff‐Parkinson‐White syndrome taking amiodarone. The latter group was a control group, since we did not withhold amiodarone therapy in four patients with ARVD. Mean (± SD) right ventricular ejection fraction (EF) in patients with ARVD was 25 ± 11% at rest and 26 ± 12% during exercise. In normal subjects right ventricular EF was 51 ± 4% at rest and 59 ± 6% during exercise (p < .001). The right ventricular/left ventricular end‐diastolic diameter ratio was 0.60 ± 0.24 in patients with ARVD and 0.37 ± 0.10 in normal subjects (p < .05). Right ventricular/left ventricular end‐diastolic volume ratio was 2.41 ± 1.05 in patients with ARVD and 1.16 ± 0.21 in normal subjects (p < .001). Measured in patients at rest, a subnormal left ventricular EF was present in two patients with ARVD but an abnormal left ventricular EF was present in all six patients during exercise. Mean left ventricular EF in patients with ARVD was 57 ± 8% at rest and 55 ± 10% during exercise (p > .05). In normal subjects, left ventricular EF was 61 ± 4% at rest and 72 ± 5% during exercise (p < .001). New left ventricular wall motion abnormalities were seen during exercise in all but one patient with ARVD. At rest and exercise, left ventricular and right ventricular EF in patients with Wolff‐Parkinson‐White syndrome were similar (p > .05) to those of normal subjects. We conclude that right ventricular dysfunction predominates in patients with ARVD but latent left ventricular dysfunction is present more often than is commonly recognized. These findings may have important diagnostic and therapeutic implications.Circulation 68, No. 2, 251‐257, 1983.

ISSN:0009-7322    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

ABSTRACTTo determine the prognosis of variant angina and the factors influencing it, 169 consecutive patients hospitalized in our coronary unit were followed for a mean of 15.3 months (range 1 to 68). Survival at 1, 2, and 3 years was 95%, 90%, and 87%, respectively; survival without myocardial infarction was 80%, 78%, and 75%. Twenty of the 22 myocardial infarctions and eight of the 14 deaths occurred within the first 3 months. Mantel‐Haenszel log‐rank analysis demonstrated that coronary disease, ventricular function, and the degree of disease activity were significant interdependent variables that influenced both survival and survival without infarction. At 1, 2, and 3 years, survival for patients with multivessel disease was 81%, 76%, and 66%; for patients with one‐vessel disease, 97%, 92%, and 92%; and for patients without stenoses ≥ 70%, 98% at each year (p = .0003). Survival without infarction at 1 year was 88% in patients with no stenoses ≥ 70% and 82% in patients with single‐vessel disease; it did not change thereafter in either group, but was 62%, 58%, and 50% at 1, 2, and 3 years in patients with multivessel disease (p = .001). Treatment did not influence survival in any subgroup (only 14 patients died overall) or survival without infarction in patients with multivessel disease. However, in patients without multivessel disease, treatment with nifedipine, diltiazem, and verapamil improved survival without infarction compared to treatment with perhexiline maleate or long‐acting nitrates alone (92% vs 67% at 1, 2, and 3 years; p < .005). Thus in addition to preventing angina, nifedipine, diltiazem, and verapamil appear to reduce complications in patients with variant angina without multivessel disease.Circulation 68, No. 2, 258‐265, 1983.

ISSN:0009-7322    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

ABSTRACTIn 13 patients on respiratory support we combined two‐dimensional echocardiography with hemodynamic monitoring to determine the mechanism of cyclic changes in arterial pulse, defined as an inspiratory rise in radial artery pulse pressure. Beat‐to‐beat evaluation of cardiac performance was obtained during the following three distinct consecutive phases of the controlled respiratory cycle: exhalation (phase I), preinspiratory pause (phase II), and lung inflation (phase III). Airway pressure, left ventricular filling pressure (i.e., pulmonary capillary wedge minus esophageal pressure), and pulmonary artery and radial artery pressures were simultaneously recorded during mechanical ventilation along with beat‐to‐beat two‐dimensional echocardiographic left ventricular end‐systolic and end‐diastolic dimensions. From a reference value for pulmonary artery and radial artery pulse contour obtained during a brief period of imposed apnea, beat‐to‐beat measurements of left and right ventricular stroke output were also performed during the controlled respiratory cycle with the pulse contour method. Cyclic changes in arterial pulse appeared to result directly from a transitory increase in left ventricular stroke output during lung inflation (41.4 ± 14.6 ml/m2), whereas right ventricular stroke output exhibited a steep fall (31.7 ± 12.4 ml/m2) at this time. An opposite variation was also observed during exhalation, during which a fall in left ventricular stroke output (31.9 ± 11.2 ml/m2) was accompanied by a rise in right ventricular stroke output (38.6 ± 11.9 ml/m2). Both stroke outputs reached an identical level during preinspiratory pause (37.4 ± 14.1 ml/m2for left ventricle and 39.1 ± 13.8 ml/m2for right ventricle). Such an inspiratory increase in left ventricular stroke output during lung inflation was no doubt largely due to a transient improvement in left ventricular preload and this is supported by our finding of a concomitant increase in left ventricular filling pressure and end‐diastolic dimensions during the inspiratory phase.Circulation 68, No. 2, 266‐274, 1983.

ISSN:0009-7322    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

ABSTRACTLate potentials can be recorded noninvasively with the averaging technique in about one‐third of patients with coronary heart disease in whom ventricular tachyarrhythmias have not been previously documented. The prognostic significance of these findings has not yet been established. Therefore, the presence or absence of late potentials was correlated to the results of programmed ventricular stimulation (single and double premature stimuli during sinus rhythm and a paced ventricular rhythm, cycle lengths 500, 430, 370, and 330 msec) in 110 male patients (age 52 ± 5.9 years, mean ± SD). The end of the stimulation protocol was reached as soon as 4 or more ventricular echo beats (defined as an abnormal response) were induced. Late potentials were recorded in 40 patients (36.4%). The duration of late potentials was less than 20 msec in 12 patients, between 20 and 39 msec in 16 patients, and 40 msec or more in another 12 patients. In those patients with late potentials, four or more consecutive ventricular echo beats (repetitive ventricular response) were recorded more frequently (63%) than in those without (33%). The incidence of abnormal responses increased from 42% in those with late potentials of less than 20 msec to 56% in those with late potentials of between 20 to 39 msec and to 92% in those with late potentials of 40 msec or more. There was a significant correlation between left ventricular function and presence and duration of late potentials (&khgr;2= 12.96; p < .0115) and between left ventricular function and the results of programmed ventricular stimulation (&khgr;2= 16.24; p < .0003). In contrast, late potentials and the results of programmed ventricular stimulation were less closely associated (&khgr;2= 5.49; p < .0643). In conclusion, late potentials proved to be a noninvasive indicator of abnormal left ventricular function, indicating an increase in ventricular vulnerability in patients that were free of symptomatic ventricular tachyarrhythmias. The predictive value of both late potentials and repetitive ventricular responses alone or in combination with regard to the occurrence of ventricular tachycardia or sudden death is still to be established.Circulation 68, No. 2, 275‐281, 1983.

ISSN:0009-7322    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

ABSTRACTDynamic obstruction to left ventricular outflow in patients with hypertrophic cardio‐myopathy usually occurs when the anterior mitral leaflet moves forward in systole and approaches or contacts the ventricular septum. However, we have recently identified, by M mode and two‐dimensional echocardiography, 21 patients with hypertrophic cardiomyopathy who had a unique pattern of mitral valve motion characterized by abnormal mitral valve coaptation and systolic anterior motion of the posterior mitral leaflet. This abnormality of mitral valve motion was most reliably identified with two‐dimensional echocardiography in views of the left ventricle obtained from the apex. At end‐diastole the anterior and posterior mitral leaflets did not appear to coapt at their distal free margins. Rather, at mitral valve closure, the anterior mitral leaflet contacted the basal portion of posterior mitral leaflet. Subsequently, during systole the “residual” distal portion of posterior mitral leaflet approached or contacted the ventricular septum. Morphologic observations in nine other patients with hypertrophic cardiomyopathy suggested that systolic anterior motion of the posterior mitral leaflet is due to elongation of the middle scallop of the posterior leaflet, which probably comes into apposition with the ventricular septum during systole by passing through the space created by the normal pattern of chordal attachments onto the anterior mitral leaflet. Of the 16 patients who underwent cardiac catheterization, nine had basal subaortic gradients of 20 to 85 mm Hg, which were apparently due to moderate or marked systolic anterior motion of the posterior mitral leaflet. Ventricular septal myotomy‐myectomies were performed in two patients and resulted in markedly diminished systolic anterior motion of the posterior mitral leaflet in each and abolition of subaortic gradient in the one patient who underwent postoperative cardiac catheterization. Hence, in patients with hypertrophic cardiomyopathy, systolic anterior motion of the posterior mitral leaflet (1) is not uncommon (identifiable in about 10% of a consecutively studied series of patients), (2) constitutes a previously undescribed mechanism for dynamic subaortic obstruction, and (3) is due to a malformation of the posterior mitral leaflet.Circulation 68, No. 2, 282‐293, 1983.

ISSN:0009-7322    

出版商:OVID    

年代:1983

数据来源: OVID