ISSN:0009-7322    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

The British Regional Heart Study (BRHS) reported in 1986 that much of the inverse relation of high-density lipoprotein cholesterol (HDLC) and incidence of coronary heart disease was eliminated by covariance adjustment. Using the proportional hazards model and adjusting for age, blood pressure, smoking, body mass index, and low-density lipoprotein cholesterol, we analyzed this relation separately in the Framingham Heart Study (FHS), Lipid Research Clinics Prevalence Mortality Follow-up Study (LRCF) and Coronary Primary Prevention Trial (CPPT), and Multiple Risk Factor Intervention Trial (MRFIT). In CPPT and MRFIT (both randomized trials in middle-aged high-risk men), only the control groups were analyzed. A 1-mg/dl (0.026 mM) increment in HDLC was associated with a significant coronary heart disease risk decrement of 2% in men (FHS, CPPT, and MRFIT) and 3% in women (FHS). In LRCF, where only fatal outcomes were documented, a 1-mg/dl increment in HDLC was associated with significant 3.7% (men) and 4.7% (women) decrements in cardiovascular disease mortality rates. The 95% confidence intervals for these decrements in coronary heart and cardiovascular disease risk in the four studies overlapped considerably, and all contained the range 1.9–2.9%. HDLC levels were essentially unrelated to non–cardiovascular disease mortality. When differences in analytic methodology were eliminated, a consistent inverse relation of HDLC levels and coronary heart disease event rates was apparent in BRHS as well as in the four American studies.

ISSN:0009-7322    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Patients with familial hypercholesterolemia (FH) have had a life-long sustained elevation of low-density lipoprotein (LDL) cholesterol levels. Consequently, there is a need to maximally lower their elevated levels, and this usually requires lowering LDL levels more than 50%. Because no single hypolipidemic drug will consistently produce such degrees of lowering, combination drug therapy with two or even three agents is required to produce the desired degree of cholesterol lowering. A prospective trial was designed to determine if combination therapy using three hypolipidemic agents could effectively lower LDL levels in 17 severely affected FH subjects. Colestipol hydrochloride (10 g b.i.d.), probucol (500 mg b.i.d.), and lovastatin (20 or 40 mg b.i.d.) were given to each patient, in varying combinations, over a 25-month period. Lovastatin (40 mg/day) uniformly lowered LDL levels 36%. Probucol lowered LDL only 14% and in a variable manner. The combination of lovastatin and probucol lowered LDL no better than lovastatin alone. Lovastatin plus colestipol lowered LDL 52%; probucol added as a third agent produced no further lowering. Lovastatin (80 mg/day) plus colestipol lowered LDL 56%. Lovastatin increased high-density lipoprotein (HDL) cholesterol levels 6%, whereas probucol decreased HDL 29%. In all patients there was an efective lowering of LDL levels, ranging from 40% to 70%Yo. Thus, lovastatin plus colestipol is an elfective hypolipidemic regimen for producing marked decreases in LDL levels in FH subjects. The addition of probucol as a third hypolipidemic agent adds little to the therapeutic regimen as measured by lowering of LDL levels.

ISSN:0009-7322    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

The eifects of smoking, aspirin ingestion, and sex differences on bleeding times and bleeding time thromboxane B2and 6-keto-prostaglandin (PG)F1αproduction were examined. Nonsmoking men produced more thromboxane B2(3.99±0.76 ng/ml) than nonsmoking women (2.13±0.24 ng/ml). Female smokers produced more thromboxane B2(5.01±0.97 ng/ml) than nonsmoking women. Twenty-four hours after a single dose of 600 mg aspirin, in vitro production of thromboxane B2in response to collagen fell by 95%, whereas in vivo production of thromboxane B2and 6-keto-PGF1αin bleeding time blood fell by 87% and 66%, respectively. Subjects with the lowest absolute levels of thromboxane B224 hours after aspirin were also those with the longest postaspirin bleeding times. Recovery of 6-keto-PGF1αproduction was faster than recovery of thromboxane B2 production, but 6-keto-PGF1αproduction for most subjects was still below basal 72 hours after aspirin. The influence of two different doses of long-term aspirin (80 mg every other day and 325 mg daily) on the in vivo production of thromboxane B2 and 6-keto-PGF1αwas studied in normals and diabetics. After 14 days of 80 mg aspirin every other day, thromboxane B2 and 6-keto-PGF1αproduction were both substantially inhibited (93% and 78%, respectively). After 14 days of 325 mg aspirin daily, thromboxane B2 production was similarly substantially inhibited (93%), whereas 6-keto-PGF1αwas significantly less affected (only 45% inhibition). Study of a second group of five normal subjects confirmed that 6-keto-PGF1αproduction was significantly inhibited 24 hours after the first dose of 325 mg aspirin but was not significantly less than basal after 14 days of 325 mg aspirin. The results suggest that 325 mg aspirin daily is more antithrombotic compared with 80 mg every other day due to the superior preservation of prostacyclin production.

ISSN:0009-7322    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

To determine if paced cycle length–dependent changes in the QRS duration correlate with the change in ventricular tachycardia (VT) cycle length after procainamide, we measured the QRS duration during sinus rhythm and during right ventricular pacing before and after procainamide (mean concentration, 9.9 μg/ml) in 18 patients with morphologically identical VT induced at both study periods. Pacing was performed at 600 msec or the longest cycle length that allowed for uninterrupted capture and at a cycle length that was within 50 msec of the VT cycle length observed during the control study (mean, 313 ±51 msec). After procainamide, the VT cycle length increased from 285±62 to 368±70 msec (percent change, 30±13%). The QRS duration during sinus rhythm increased from 125±25 to 145±29 msec (percent change, 16%). The QRS duration at both paced cycle lengths was the same in the baseline state (191±26 msec). However, the change in QRS duration after procainamide at the shorter paced cycle length compared to a 39±13 msec (18%) increase at the longer paced cycle,p< 0.001. There was a significant correlation between the percent change in QRS duration at the shorter paced cycle length and the percent change in VT cycle length (r= 0.84,p< 0.001) with the relation expressed by the regression equation: percent change in VT cycle length = −2.8±1.16 × percent change in QRS duration. These findings support the hypothesis that the mechanism for the change in VT cycle length after procainamide is due to a rate-dependent change in conduction.

ISSN:0009-7322    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

To clarify the direct contribution of the left atrial pressure to secretion of human atrial natriuretic peptide (hANP), we have attempted to study the relations between plasma hANP levels, neurohumoral factors, and hemodynamic changes in 13 patients with mitral stenosis undergoing percutaneous transvenous mitral commissurotomy (PTMC). After PTMC, the left atrial pressure fell from 14.7±1.9 (mean±SEM) to 6.5±0.7 mm Hg in all patients studied (p< 0.0005), whereas there were no remarkable changes in either the right atrial pressure, mean arterial pressure, or heart rate. Plasma immunoreactive hANP levels obtained from the pulmonary artery decreased from 278±51 to 137±31 pg/ml after PTMC (p< 0.0005). There was a significant correlation between the decrement of hANP levels and that of left atrial pressure (r= 0.72,p< 0.005). Neither plasma renin activity nor norepinephrine levels changed. In contrast, plasma aldosterone concentrations significantly increased from 11.3± 1.5 to 16.4±2.7 pg/ml after PTMC (p< 0.01), although there was no causal relation between plasma concentrations of aldosterone and hANP. The present result with PTMC-induced rapid fall of the left atrial pressure with a concomitant reduction in hANP secretion strongly suggests the importance of the left atrial pressure on hANP secretion in humans.

ISSN:0009-7322    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Arterial baroreflex control of the heart and peripheral circulation is markedly impaired in humans and animals with congestive heart failure. After reversal of heart failure in animal models, arterial baroreflex control of heart rate remains impaired for up to 8 months. Cardiac transplantation restores normal ventricular function and completely reverses heart failure, but does it normalize arterial baroreflex control of heart rate in humans? We studied baroreflex sensitivity in 11 patients with severe heart failure, six normal control patients, and 23 patients at 2 weeks to 4 years after orthotopic cardiac transplantation. Baroreflex sensitivity was assessed with intravenous bolus injections of phenylephrine and is expressed as change in RR or PP interval (msec) per millimeters of mercury rise in systolic arterial pressure. Atrial rate of both donor (denervated) and recipient (innervated) atria were measured in the transplant group. Baroreflex sensitivity in patients with severe heart failure was 2.0±0.3 msec/mm Hg, but in patients after cardiac transplantation, it was 13.0±0.9 msec/mm Hg (p< 0.001). The responses in the transplant group were similar to those observed in normal controls (10±1.2 msec/mm Hg,p= NS). Our data indicate that patients with severe congestive heart failure have marked abnormalities of baroreflex control, which are reversed as early as 2 weeks after cardiac transplantation. In view of this rapid reversal, we consider it unlikely that abnormal baroreflex sensitivity seen in heart failure is due to structural alterations in the baroreceptors. We speculate that neurohumoral rather than structural abnormalities account for depressed baroreflex sensitivity in heart failure.

ISSN:0009-7322    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

The present study analyzed coronary sinus blood flow alterations after dipyridamole induced coronary vasodilation in seven patients whose endomyocardial biopsies evidenced no sign of rejection (group 1) and in five patients with histologic signs of rejection (group 2) after orthotopic heart transplantation. All patients were treated with cyclosporine and prednisone and some with azathioprine and had normal coronary arteriograms. Coronary sinus blood flow and coronary resistance were measured before and after intravenous dipyridamole (0.18 mg/ kg/min over 4 minutes). Basal values were similar in groups 1 and 2 for coronary sinus blood flow (166±34 compared with 181±39 mUmin, respectively), coronary resistance (0.62±10 compared with 0.52±13 mm Hg/ml/min, respectively), coronary sinus blood oxygen content (5.7±1.6 compared with 4.5±0.9 ml/100 ml, respectively) and arterial-coronary sinus blood oxygen difference (10.6±1.3 compared with 10.3±1.8 ml/100 ml, respectively). After dipyridamole, patients with heart rejection had lower coronary sinus blood flow and coronary sinus blood oxygen content than did patients without heart rejection (263±76 in group 2 compared with 505±96 ml/min in group 1,p< 0.001, and 7.6±0.9 in group 2 compared with 13.3± 1.8 ml/ 100 ml in group 1,p< 0.001 respectively) and had higher coronary resistance and arterialcoronary sinus blood oxygen difference than did patients without heart rejection (0.34±0.15 in group 2 compared with 0.16±0.02 mm Hg/ml/min in group 1,p< 0.02, and 7.0±1.4 in group 2 compared with 3.3 ±0.8 ml/100 ml in group 1,p< 0.001, respectively). Coronary flow reserve evaluated by the dipyridamole:basal coronary sinus blood flow ratio and resistance reserve evaluated by the basal:dipyridamole coronary resistance ratio were significantly reduced in patients with heart rejection (1.56±0.09 in group 2 compared with 3.09±0.44 in group 1,p< 0.001, and 1.63±0.30 in group 2 compared with 3.89±0.82 in group 1,p< 0.001, respectively). These data indicate that capacity of the intramyocardial coronary circulation to vasodilate is severely impaired during heart rejection.

ISSN:0009-7322    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Conventional hemodynamic measurements and Doppler echocardiography were used to assess ventricular physiology of the human cardiac allograft and to examine the influence of pertinent clinical factors on chronic myocardial performance. Sixty-four patients (18–55 years old; mean, 39 years) undergoing routine annual hemodynamic assessment were studied. Blood-flow velocity properties across the mitral, tricuspid, and aortic valves were analyzed from Doppler ultrasound recordings. Ten of these patients had elevated diastolic pressures associated with a sharp early diastolic dip followed by an exaggerated and abrupt rise in pressure, consistent with restrictive-constrictive ventricular physiology. Left ventricular dP/dt and stroke volume were lower in these patients compared with the other 54 patients. Doppler echocardiographic indexes of left ventricular filling and ejection in these 10 patients differed significantly. Isovolumic relaxation time and pressure half-time were shorter, peak early mitral and tricuspid flow velocities were higher, and mean aortic flow velocity and acceleration were lower. A higher rejection incidence was the only demonstrable clinical factor associated with impaired ventricular function. Doppler echocardiography may, therefore, noninvasively identify patients with hemodynamic evidence of restrictive-constrictive physiology. This abnormality occurs in approximately 15% of allograft recipients, is associated with impaired systolic performance, and may be related to rejection incidence.

ISSN:0009-7322    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Beat-to-beat heart rate variability was studied by power spectral analysis in 17 orthotopic cardiac transplant patients. Heart rate power spectra were calculated from eighty-four 256-second recordings and compared with those taken from six normal subjects. The power spectra from the control subjects resolved into discrete peaks at 0.04-0.12 Hz and 0.2-0.3 Hz, whereas those of heart transplant recipients resembled broad-band noise without peaks. Log total power in the 0.02-1.0 Hz range was greater in the control subjects (0.982±0.084 [0.206], mean±SEM [SD]) than in the transplanted subjects (−0.766±0.059 [0.5411), (p< 0.0001). Fifty-five electrocardiographic recordings from transplant patients were done within 48 hours of an endomyocardial biopsy. When the power spectra of those patients whose endomyocardial biopsies showed evidence of myocardial rejection were compared with those from patients who were found to be free of rejection, a significant dilference was found in log total power (−0.602±0.090 [0.525] vs. −0.909±0.136 [0.577],p< 0.02). We conclude that denervation of the heart significantly reduces heart rate variability and abolishes the discrete spectral peaks seen in untransplanted control subjects and that the development of allograft rejection may significantly increase heart rate variability.

ISSN:0009-7322    

出版商:OVID    

年代:1989

数据来源: OVID