ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundWe studied the effects of recombinant growth hormone (rhGH) on exercise capacity and cardiac function in patients with ischemic cardiomyopathy.Methods and Results-Seven patients (aged 55 +/- 9 years) with mild to moderate congestive heart failure (ejection fraction 31 +/- 4%) who were on standard therapy were included. The patients were studied at baseline, after 3 months of rhGH treatment, and 3 months after rhGH discontinuation. Cardiac function was assessed by exercise capacity, right heart catheterization at rest and after submaximal exercise, MRI, echocardiography, and Holter monitoring. When administered at a dose of 2 IU/d, rhGH doubled the serum concentration of insulin-like growth factor-I. rhGH improved clinical symptoms and exercise capacity significantly (New York Heart Association class 2.4 +/- 0.5 initially versus 1.4 +/- 0.5 at 3 months [mean +/- SD], P<0.05; VO2max 13.6 +/- 3.8 versus 17.4 +/- 5.4 mL [middle dot] kg-1[middle dot] min-1, P<0.05). Additionally, pulmonary capillary wedge pressures at rest and after submaximal exercise were reduced significantly. Cardiac output increased, particularly at rest (5.0 +/- 1.1 versus 5.8 +/- 1.3 L/min; P<0.05). Posterior wall thickness was increased (1.08 +/- 0.1 versus 1.24 +/- 0.3 cm; P<0.05), and the end-diastolic and end-systolic volume indexes decreased significantly after rhGH treatment. There was no significant increase in left ventricular ejection fraction. The improvements were partially reversed 3 months after rhGH discontinuation.ConclusionsThe administration of rhGH for 3 months in patients with ischemic cardiomyopathy results in significant improvement in hemodynamics and clinical function. The attenuation of left ventricular remodeling persisted 3 months after discontinuation of treatment. (Circulation. 1999;99:18-21.)

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundWe have previously shown that the acute molecular growth response of new protein synthesis and protein kinase C activation in response to angiotensin II (Ang II) is altered in left ventricular (LV) hypertrophy compared with normal hearts. We have also shown an upregulation of Ang II type 2 (AT2) receptors in hypertrophied hearts relative to controls. Activation of AT2receptors is proposed to counteract growth effects of AT1receptor in response to Ang II. Thus, we tested the hypothesis that in hypertrophied hearts, the AT2receptor mediates inhibitory effects on the new cardiac protein synthesis in response to acute Ang II stimulation.Methods and Results-Flaccid buffer-perfused adult normal and hypertrophied rat hearts were perfused with Ang II 10-8mol/L plus prazosin 10-7mol/L or Ang II plus the AT2blocker PD 123319 5x10-7mol/L. New protein synthesis was measured by the rate of [(3) H]phenylalanine incorporation into the LV proteins. In normal hearts, Ang II (n=8) increased the rate of [(3) H]phenylalanine incorporation by 74 +/- 27% (P<0.05 versus no drug). Treatment with PD123319 (n=8) did not increase protein synthesis compared with Ang II alone (32 +/- 11% versus Ang II alone, P=NS). In hypertrophied hearts, Ang II alone (n=6) increased the rate of [(3) H]phenylalanine incorporation only by 23 +/- 13% (P=NS versus no drug). In contrast, treatment with PD123319 (n=7) induced a 76 +/- 21% increase in new LV protein synthesis compared with Ang II alone (P<0.05). AT2receptor blockade in Ang II-stimulated hypertrophied hearts was associated with enhanced membrane protein kinase C translocation and reduced LV cGMP content.ConclusionsThese data support the hypothesis that in adult hypertrophied rat hearts, inhibition of cardiac AT2receptors, which are upregulated in chronic LV hypertrophy, amplifies the immediate LV growth response to Ang II. This appears to be related to augmented Ang II-stimulated PKC activation and suppression of cGMP signaling. (Circulation. 1999;99:22-25.)

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundPercutaneous transluminal treatment of a thrombotic vein graft yields poor results. We have previously reported our experience with transluminal percutaneous coronary ultrasound thrombolysis (CUT) in the setting of acute myocardial infarction (AMI). This report describes the first experience with ultrasound thrombolysis in thrombus-rich lesions in saphenous vein grafts (SVGs), most of which were occluded.Methods and Results-The patients (n=20) were mostly male (85%), aged 64 +/- 4 years old. The presenting symptom was AMI in 2 patients (10%) and unstable angina in the rest. Fifteen patients (75%) had totally occluded SVGs. The median age of clots was 6 days (range, 0 to 100 days). The ultrasound thrombolysis device has a 1.6-mm-long tip and fits into a 7F guiding catheter over a 0.014-in guidewire in a "rapid-exchange" system. CUT (41 kHz, 18 W, <or=to6 minutes) led to device success in 14 (70%) of the patients and residual stenosis of 65 +/- 28%. Procedural success was obtained in 13 (65%) of the patients, with a final residual stenosis of 5 +/- 8%. There was a low rate of device-related adverse events: 1 patient (5%) had a non-Q-wave myocardial infarction, and distal embolization was noted in I patient (5%). Adjunct PTCA or stenting was used in all patients. There were no serious adverse events during hospitalization.ConclusionsUltrasound thrombolysis in thrombus-rich lesions in SVGs offers a very promising therapeutic option. (Circulation. 1999;99:26-29.)

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID