摘要:

Continuous-wave Doppler echocardiography was used to examine the aortic regurgitant flow velocity pattern in 32 patients with aortic regurgitation (AR) and 10 patients without AR. The aortic regurgitant flow velocity patterns, characterized by a rapid rise in flow velocity immediately after closure of the aortic valve, high peak flow velocity, and a gradual deceleration until the next aortic valve opening, were successfully obtained in 30 of the 32 patients with AR (sensitivity 94%, specificity 100%). The velocity decline was greater in patients with severe AR; thus, the slope of the velocity decline (deceleration) and the time to decline to half the peak velocity (half-time index) were measured from the flow velocity pattern. The deceleration became greater and the half-time index shortened in accordance with angiographic grading of AR (p < .01). The deceleration and the half-time index also correlated well with the aortic regurgitant fraction (r = .79, p < .01; r = − .89, p < .01). Because the half-time index could be measured easily and independently of Doppler incident angle, it seemed a simple and accurate index of assessing the severity of AR. Thus continuous-wave Doppler echocardiography permitted the noninvasive evaluation of AR.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Although immediate and late changes in coronary stenoses after percutaneous transluminal coronary angioplasty (PTCA) have been reported, most investigators have employed qualitative or semiquantitative techniques to analyze the angiograms. Such data is not optimal because of considerable interobserver variability and the use of relative instead of absolute changes in lesion geometry. Analysis is further compounded by the indistinct edges that characterize coronary lesions immediately after angioplasty. To quantify the changes in minimal cross-sectional area (MCSA) of the coronary lumen that occur during and after PTCA, we analyzed the angiograms of 23 patients before PTCA, immediately after PTCA, and at 7.2 ± 3.0 (mean ± SD) months follow-up using two computerassisted methods of angiographic analysis—quantitative coronary angiography (QCA) and videodensitometry (VID). QCA provides an absolute measure of the area of the lumen; VID is a nongeometric method that is not dependent on exact border recognition. Based on these quantitative methods, we found that successful angioplasty is associated with about a three-fold increase in the MCSA of the lesion (from 1.0 to 3.2 mm2). This area is, however, well below normal and is less than half of the average MCSA of the inflated dilating balloon. Analysis of follow-up angiograms demonstrated that eight of 23 patients had a substantial late increase in the MCSA of the lesion (from 2.7 to 4.1 mm2) after the angioplasty procedure. Clinical, hemodynamic, and angiographic characteristics immediately after PTCA were not predictive of MCSA of the lumen at follow-up. Because substantial late increases in MCSA of the lumen occur in about one-third of patients, angiographic and noninvasive analyses performed immediately after PTCA will not define the ultimate adequacy of coronary dilation in many patients undergoing PTCA.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The presence of specific benzodiazepine binding sites in the hearts of dogs and human beings was demonstrated in vivo by a noninvasive method, positron emission tomography (PET). An antagonist of the peripheral-type benzodiazepine binding site, PK 11195, was labeled with carbon-11, a short-lived positron emitter. When injected at high specific activity,11C-PK l1195 was concentrated in the myocardium. As increasing amounts of unlabeled PK 11195 were added to the radioactive ligand, the myocardial ligand concentration was proportional to myocardial regional perfusion up to quantities of 40 nmol/kg body weight. Above 40 nmol/kg the ligand concentration reached a maximum value (6000 pmol/cm3), which could be considered as the total number of binding sites per unit heart volume. The specificity of11C-PK 11195 binding to canine heart was demonstrated from a study on the inhibition of binding for radioligand by an excess of several agonists or antagonists of benzodiazepine receptor. The distribution and specificity of11C-PK 11195 was similar in dogs and in human beings. PET thus opens the way to the investigation of the peripheral-type benzodiazepine receptor in a clinical situation, since it has recently been shown that this receptor could be coupled to the calcium channel in the heart.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Wider applicability of an implantable automatic defibrillator depends on achieving internal cardiac defibrillation consistently with the lowest possible energy. In animal studies, we have found that the cardiac defibrillation threshold could be reduced when sequential shocks separated in time and spacially arranged were delivered to the heart. We compared internal cardiac defibrillation using a single pulse shock delivered through an intravascular catheter with this new method for internal cardiac defibrillation in patients undergoing cardiac surgery for the correction of arrhythmias. For the single pulse shock and the first pulse of the sequential pulse shock, current was passed through an intravascular catheter with the catheter cathode at the apex of the right ventricle and the anode at the superior vena cava-atrial junction region. The second pulse of the sequential pulse countershock was delivered between the catheter cathode in the right ventricular apex and an oval plaque electrode secured on the laterobasal left ventricular epicardium as anode. With the single pulse alone for shock delivery, 12 patients could be defibrillated with an average of 20.1 ± 16.8 J, with a corresponding leading-edge peak voltage and current of 836 ± 319 V and 9.4 ± 4.5 A, respectively. However, two of the patients could not be defibrillated with energies below 50 J. With the sequential pulse shock delivery, a significant reduction in all values were recorded. Mean total energy for defibrillation averaged 7.7 ± 6.0 J. Leading-edge peak voltage and current from the catheter averaged 430 ± 148 V and 5.0 ± 2.8 A, respectively. In addition, all patients could be defibrillated with less than 23 J, and nine of the 12 patients (75%) could be defibrillated with less than 7.5 J. In contrast, only two of these same 12 patients (17%) could be defibrillated with less than 7.5 J using the single pulse alone (binomial exact test, p = .0156). We conclude that sequential pulse defibrillation provides a pronounced reduction in the total energy necessary for defibrillation compared with the single pulse delivered through a catheter alone. Furthermore, the sequential pulse system provides a reduction in the current density at the electrodes, potentially reducing myocardial damage. This system may be important in the design of a totally implantable automatic defibrillator.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Fifty patients with congestive heart failure received, by infusion, 15 ml/kg body weight water load, and systemic hemodynamic, renal function, and neurohumoral parameters values were measured before, 2 days, and 1 month after randomly allocating patients to prazosin or captopril therapy. Both prazosin and captopril caused similar and persistent hemodynamic changes, but important differences existed between their renal and neurohumoral effects. After 1 month of continuous therapy, captopril increased creatinine clearance from 71 to 84 ml/min/1.732(p < .05), increased the water load excreted in 5 hr from 50% to 71% (p < .005), and increased 5 hr sodium excreted from 6.8 to 14.7 meq (p < .005). Captopril also caused a decrease in plasma norepinephrine from 568 to 448 pg/ml (p < .005), in plasma epinephrine from 94 to 73 pg/ml (p < .05), and in plasma aldosterone from 57 to 28 ng/dl (p < .005), without changing plasma vasopressin. These beneficial effects were greater after 1 month of therapy than after 2 days. The only beneficial effect of prazosin was to increase water excretion from 49% to 59% (p < .05). The long-term response to captopril was similar in patients with higher (> 2.5 ng/ml/hr) and lower renin levels. However, in patients with lower renin levels, prazosin decreased pulmonary capillary wedge pressure (24.8 to 21.8 mm Hg, p < .05), decreased plasma arginine vasopressin (1.16 to 0.75 pg/ml, p < .05), increased water excretion (62% to 85%, p < .005), and decreased plasma epinephrine (81 to 46 pg/ml, p < .05), while in patients with higher renin levels none of these beneficial effects were noted. We conclude (1) that captopril produces long-term beneficial renal and neurohumoral effects that prazosin does not despite similar hemodynamic changes with the two drugs, (2) that these effects are at least partially dependent on the initial neurohumoral and hemodynamic status of the patient, and (3) that through hemodynamic improvement vasodilators may chronically interrupt vasopressin overstimulation.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The incidence of congestive heart failure was studied in the Beta Blocker Heart Attack Trial in which postmyocardial infarction patients between the ages of 30 and 69 years, with no contraindication to propranolol, were randomly assigned to receive placebo (n = 1921) or propranolol 180 or 240 mg daily (n = 1916) 5 to 21 days after admission to the hospital for the event. Survivors of acute myocardial infarction with compensated or mild congestive heart failure, including those on digitalis and diuretics, were included in the study. A history of congestive heart failure before randomization characterized 710 (18.5%) patients: 345 (18.0%) in the propranolol group and 365 (19.0%) in the placebo group. The incidence of definite congestive heart failure after randomization and during the study was 6.7% in both groups. In patients with a history of congestive heart failure before randomization, 51 of 345 (14.8%) in the propranolol group and 46 of 365 (12.6%) in the placebo group developed congestive heart failure during an average 25 month follow-up. In the patients with no history of congestive heart failure, 5% in the propranolol group developed congestive heart failure and 5.3% in the placebo group developed congestive heart failure. Baseline characteristics predictive of the occurrence of congestive heart failure by multivariate analyses included an increased cardiothoracic ratio, diabetes, increased heart rate, low baseline weight, prior myocardial infarction, age, and more than 10 ventricular premature beats per hour. Patients with congestive heart failure in the propranolol group experienced a similar decrease in the total mortality (27%) compared with those without congestive heart failure (25%), whereas propranolol decreased the occurrence of sudden death by 47% in the patients with prior heart failure compared with 13% without congestive heart failure.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Coagulation and fibrinolysis were studied in patients with acute myocardial infarction during intravenous infusion of recombinant human tissue-type plasminogen activator (rt-PA) (0.75 mg/kg over 90 min, n = 101), streptokinase (1,500,000 IU over 60 min, n = 61), or placebo (n = 40). In the rt-PA group, the plasma level of rt-PA antigen was 1.2 ± 0.6 gig/ml (mean ± SD) and the euglobulin fibrinolytic activity (EFA) was 910 735 IU t-PA/ml. In the streptokinase group, the EFA was equivalent to 430 ± 435 IU t-PA/ml. At the end of the infusion, the plasma fibrinogen level measured with a coagulation rate assay was decreased to 57 ± 33% of the preinfusion value in the rt-PA group, to 7 ± 10% in the streptokinase group, and remained unchanged in the placebo group. Fibrinogen-fibrin degradation products increased to 0.75 ± 0.54 mg/ml in the streptokinase group but to only 0.10 ± 0.13 mg/ml in the rt-PA group. The plasma levels of a2-antiplasmin, plasminogen, and factor V decreased to between 30% and 45% in the rt-PA group but significantly more in the streptokinase group (to between 15% and 25%). Thus rt-PA induced much less systemic fibrinolytic activation than streptokinase. In the patients who received rt-PA, a weak correlation (r = .21, n = 89, .1 > p > .05) was found between the extent of fibrinogen breakdown at 90 min and the plasma rt-PA concentration. Fibrinogen breakdown was significantly higher (p < .05) in patients with successful recanalization (decrease to 52 ± 32%, n = 61) than in unresponsive patients (decrease to 69 ± 35%, n = 22). The plasma rt-PA concentration in patients with successful recanalization was 1.4 ± 0.7 gg/ml, and that in unresponsive patients was 1.1 ± 0.7 μ/ml (p > .1).

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

This study was performed to assess the effect of allopurinol in a canine preparation of myocardial infarction. Dogs underwent occlusion of the left circumflex coronary artery for 90 min, followed by reperfusion for 6 hr. Three groups were studied: (1) control, (2) dogs receiving 25 mg/kg allopurinol 18 hr before occlusion and 50 mg/kg 5 min before occlusion, and (3) dogs receiving allopurinol as above plus 5 mg/kg superoxide dismutase over 1 hr beginning 15 min before reperfusion. Infarct size expressed as a percentage of the area at risk was 40 ± 4 in the control group, 22 ± 5 in the allopurinol group (p < .05 vs control), and 17 ± 4 in the allopurinol plus superoxide dismutase group (p < .05 vs control). The differences in infarct size were not due to differences in myocardial oxygen supply or demand. Neutrophil superoxide anion production was not altered by allopurinol treatment. The results suggest that myocardial xanthine oxidase may generate oxygen radicals that play a role in myocardial injury due to ischemia and reperfusion.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Factors affecting bubble formation during delivery of defibrillator pulses to arrhythmogenic cardiac tissue via a catheter are unknown. We investigated the role of energy, electrode surface area, interelectrode distance, and electrode polarity on bubble formation and on current and voltage waveforms during delivery of damped sinusoidal discharges from a standard defibrillator to anticoagulated bovine blood. Gas composition was studied with mass spectrometry. Defibrillator energy settings were varied between 5 and 360 J. The principal catheter used for study was a Medtronic 6992A lead. Additional electrodes tested included 2, 5, and 10 mm long No. 6F, 7F, and 8F copper electrodes. Interelectrode distances used to assess the effect of anode-cathode spacing were 1, 5, 10, and 20 cm. Bubble volume increased linearly from 0.043 to 0.134 ml per cathodal pulse and from 0.030 to 3.50 ml per anodal pulse as energy settings were increased from 5 to 360 J (r = .99). Typical smooth waveforms for both current and voltage were seen only in the absence of bubbles. The voltage waveform was distorted for each cathodal pulse of 100 J or more and for each anodal pulse of 10 J or more only if bubbles were present. The effect of electrode surface area on bubble formation was tested at a 200 J energy setting and at a 10 cm interelectrode distance with the use of cathodal pulses. Bubble formation varied inversely with electrode surface area (r = .876). Bubble formation, however, varied minimally as interelectrode spacing was changed from 1 to 20 cm. The effect of polarity on bubble formation when the Medtronic 6992A distal electrode and an 8.5 cm disk electrode separated by 10 cm were used was highly significant. For a 200 J pulse, bubble formation with the catheter as anode was 3.30 ± 0.10 ml and with the catheter as cathode it was 0.070 ± 0.002 ml (p < .001). Mass spectrometry of both anodal and cathodal gas samples demonstrated the constituents of the gas bubble to include a variety of gases, which is inconsistent with simple electrolytic production of the bubbles observed. The predominance of nitrogen in either polarity sample suggested that the principal source of the bubble was dissolved air. In summary, bubble formation at an electrode receiving damped sinusoidal outputs from a standard defibrillator does not vary significantly with varying interelectrode distance. However, it is directly proportional to energy and inversely proportional to electrode surface area. Anodal catheter discharges produce considerably more bubbles than do cathodal discharges. Distortions in the voltage waveform correlate with physical factors leading to high-pressure shockwave generation and to subsequent extrusion of dissolved gases from solution.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Whether blood flow during cardiopulmonary resuscitation (CPR) results from intrathoracic pressure fluctuations or direct cardiac compression remains controversial. From modeling considerations, blood flow due to intrathoracic pressure fluctuations should be insensitive to compression rate over a wide range, but dependent on the applied force and compression duration. If direct compression of the heart plays a major role, however, flow should be dependent on compression rate and force, but above a threshold, insensitive to compression duration. These differences in hemodynamics produced by changes in rate and duration form a basis for determining whether blood flow during CPR results from intrathoracic pressure fluctuations or from direct cardiac compression. Manual CPR was studied in eight anesthetized, 21 to 32 kg dogs after induction of ventricular fibrillation. There was no surgical manipulation of the chest. Myocardial and cerebral blood flows were determined with radioactive microspheres. At nearly constant peak sternal force (378 to 426 newtons), flow was significantly increased when the duration of compression was increased from 14 ± 1% to 46 ± 3% of the cycle at a rate of 60/min. Flow was unchanged, however, after an increase in rate from 60 to 1 50/min at constant compression duration. The hemodynamics of manual CPR were next compared with those produced by vest inflation with simultaneous ventilation (vest CPR) in eight other dogs. Vest CPR changed intrathoracic pressure without direct cardiac compression, since sternal displacement was less than 0.8 cm. At a rate of 150/min, with similar duration and right atrial peak pressure, manual and vest CPR produced similar flow and perfusion pressures. Finally, the hemodynamics of manual CPR were compared with the hemodynamics of direct cardiac compression after thoracotomy. Cardiac deformation was measured and held nearly constant during changes in rate and duration. As opposed to changes accompanying manual CPR, there was no change in perfusion pressures when duration was increased from 15% to 45% of the cycle at a constant rate of 60/min. There was, however, a significant increase in perfusion pressures when rate was increased from 60 to 150/min at a constant duration of 45%. Thus, vital organ perfusion pressures and flow during manual external chest compression are dependent on the duration of compression, but not on rates of 60 or 150/min. These data are similar to those observed for vest CPR, where intrathoracic pressure is manipulated without sternal displacement, but opposite of those observed for direct cardiac compression. We conclude that intrathoracic pressure fluctuations generate blood flow during manual CPR.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID