摘要:

Intramyocardial hemorrhage often occurs with reperfusion in experimental acute myocardial infarction and is thought to be associated with extension of necrosis. To determine if hemorrhage was associated with extension of necrosis, 20 anesthetized dogs were reperfused after 6 hours of circumflex coronary artery occlusion and 10 others had control occlusion with no reperfusion. Fifteen of the 20 reperfused dogs had gross hemorrhage and none of the control dogs did. In 12 reperfused and 10 control dogs, radioactive microspheres were injected after coronary occlusion to quantitate collateral flow and in the reperfusion group microspheres were injected to quantitate reflow. Complete flow data were available in eight reperfused and 10 control dogs. Twenty-four hours after coronary occlusion, 1-g segments of infarct and control regions were analyzed for hemorrhage, collateral flow and creatine kinase activity. Serial microscopic examination was performed in eight additional dogs reperfused after 6 hours to determine if hemorrhage occurs into otherwise microscopically normal myocardium.Pathologic examination indicated that hemorrhage did not occur into otherwise microscopically normal myocardium. In dogs with hemorrhage, the extent of hemorrhage was inversely related to myocardial creatine kinase concentration and collateral flow. Mean collateral flow in 47 hemorrhagic segments was 4.5 ml/100 g (4.2% of control). Mean creatine kinase in 36 hemorrhagic segments was 233 mIU/g (21% of control). No hemorrhage was found in areas with collateral flow more than 21% of control or creatine kinase more than 37% of control. Mean reflow in hemorrhagic segments was 78.5% of control flow. These studies indicate that hemorrhage on reperfusion is associated with severe myocardial necrosis and markedly depressed flow before reperfusion and thus occurs only into myocardium already markedly compromised at the time of reperfusion. There is no evidence for hemorrhage into areas that had normal or even moderately depressed flows before reperfusion.

ISSN:0009-7322    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Myocardial thallium-201 (20TI) kinetics have not been precisely defined because reliable techniques to determine continuous activity in vivo have not been available. In this study, an implantable miniature cadmium telluride radiation detection device was inserted through the left ventricular apex, positioned against the endocardium, and used for continuous on-line monitoring of myocardial 201TI activity for 260-810 minutes in 18 dogs. Blood was serially sampled and counted. Microsphere-determined myocardial blood flow was measured before administration of 201TI and was not significantly different from that measured at the end of the experiment in 11 of 18 dogs. Thallium was administered intravenously. Myocardial and blood activity curves were analyzed using a nonlinear least-squares estimation of the decay constant X (min-'). Myocardial activity reached 80% of peak within 1 minute, peaked in a mean time of 23.7 ± 17.9 minutes (±SD), then decreased monoexponentially with a mean X = 0.00176 ± 0.00054 min-' (half-time [T½] = 437.2 ± 126.3 minutes) (r= 0.95-0.99). Blood activity decreased triexponentially with a mean X1 = 0.36782 ± 0.20141 min-' (T½ = 2.4 1.1 minutes), mean X2 = 0.06134 ± 0.02973 min-' (T½ = 14.1 ± 7.1 minutes) and mean X'5 = 0.00177 0.00075 min-' (T½ = 445.5 ± 201.6 minutes) (r= 0.99-1.00). The mean final blood X, was almost identical to the mean myocardial X.To determine the relationship between myocardial and blood clearance rates of 201TI after i.v. and intracoronary administration, 201T1 was administered by the intracoronary route in four dogs. Myocardial 201Tl activity peaked in a mean time of 2.0 ± 0.8 minutes, then decreased monoexponentially with a mean X = 0.00833 ± 0.00115 min''(T; = 84.2 ± 12.5 minutes) (r= 0.94-0.98). Thallium clearance from the myocardium after intracoronary 201TI was significantly greater than after i.V. 201TI (p< 0.00001).The data suggest that 201T1 washout after peak activity is reached in nonischemic myocardium is monoexponential. The rate of 201T1 clearance from the myocardium is related to the rate of 201T1 clearance from the blood after i.v. administration of the tracer.

ISSN:0009-7322    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Propranolol increases exercise performance in association with a decrease in exercise heart rate and blood pressure. In 30 men with coronary disease and exercise limited by angina, 15 without prior infarction and 15 with infarction, we measured left ventricular ejection fraction (LVEF) (scintillation probe) at rest and during supine bicycle exercise and myocardial blood flow distribution (MBF) (thallium-201 imaging) during treadmill exercise. Exercise was performed as control and after 1 week of treatment with propranolol (40 mg orally four times daily). Propranolol improved exercise LVEF (at the same work load) (men without infarction: control 0.37 + 0.02, average ± SEM; propranolol 0.45 0.01; n = 15, p < 0.01; and with infarction: control 0.30 ± 0.01, propranolol 0.36 ± 0.01; n = 15, p < 0.05). Propranolol also improved MBF during exercise to the same work load in men without infarction (comparison of integrated normalized count-rate differences, 607 normalized counts). In men with infarction, propranolol did not alter MBF (15 normalized counts). Placebo did not alter normalized counts by more than ± 150. Changes in exercise LVEF and MBF were related. MBF improved in 17 men with propranolol treatment and LVEF was increased in 15. Of six men who had no change in MBF, exercise LVEF increased in three and did not change in three. Propranolol was associated with a worsening of MBF in five men and all had no change in exercise LVEF. Results suggest that propranolol favorably alters MBF and LVEF in men with coronary disease, particularly in men without prior myocardial infarction.

ISSN:0009-7322    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

A new method for obtaining absolute left ventricular volume from gated blood pool studies was evaluated in a torso phantom and in 35 patients who also underwent single-plane contrast ventriculography. Gated 400 left anterior oblique and static anterior views were acquired. Left ventricular volume at end-diastole was given by the ratio of the attenuation-corrected end-diastolic count rate from the gated study to the count rate per milliliter from a blood sample. Attenuation correction was made by dividing the end-diastolic count rate by e ud, where u = the linear attenuation coefficient of water and d = the distance from the skin marker to the center of the left ventricle in the anterior view divided by sin 400 to yield the depth of left ventricle in the left anterior oblique view. In the phantom studies, the correlation between radionuclide and true volume was 0.99 (radionuclide = 1.03 true − 3 ml); the standard error of the estimate was 8 ml. In the patient studies, the radionuclide end-diastolic volume was used to calibrate the left ventricular time-activity curve, yielding left ventricular volume throughout the cardiac cycle. The correlation between radionuclide and angiographic enddiastolic volume was 0.95 (radionuclide = 0.97 angiographic + 3 ml); the standard error of the estimate was 36 ml. The correlation between radionuclide and angiographic end-systolic volume was 0.95 (radionuclide − 1.01 angiographic + I ml); the standard error of the estimate was 33 ml. This method permits direct determination of absolute left ventricular volume without assumptions about the shape of the ventricle or the necessity of using regression equations to convert volume “units” to true volume.

ISSN:0009-7322    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

We used a cylindrical model for the left ventricle contracting both radially and longitudinally to show how the ejection fraction is related to different variables that describe the ventricular geometry. The relations during ventricular contraction between wall thickening, midwall radius shortening and longitudinal shortening are used to derive precise formulas for the calculation of ventricular blood flow velocity and ejection fraction. Validation of the model is given by results from the literature and by a study of 40 patients. The formulas derived can be used to validate angiographic measurements or to assess more precisely blood flow velocity and ejection fraction from the M-mode echocardiogram. Ejection fraction is determined not only by the extent of myocardial shortening, but also by the relationship of ventricular wall thickness to ventricular cavity size.

ISSN:0009-7322    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

End-systolic left ventricular (LV) meridional wall stress is a quantitative index of true myocardial afterload that can be plotted against LV end-systolic diameter to give an index of contractility independent of loading conditions. We developed a noninvasive method for estimating end-systolic LV meridional wall stress based on M-mode LV echographic end-systolic diameter (LVID) and posterior wall thickness (PWT) and cuff systolic arterial pressure and compared it to simultaneous invasive LV wall stress derived from micromanometer LV pressure recordings and continuously digitized echograms in 12 subjects (four with atypical chest pain, six with severe aortic regurgitation (AR) and two with congestive cardiomyopathy), before and after load manipulation with nitroprusside, nitroglycerin, phenylephrine or saline. Cuff systolic pressure correlated well with end-systolic LV micromanometer pressure (r= 0.89, n = 31, range 96-160 mm Hg) and noninvasive end-systolic stress (0.334 P(LVID)/PWT [1 + PWT/LVID]) correlated extremely well with invasive stress (r= 0.97, n = 31, range 36-213 × 109 dyn/cm2). Invasive and noninvasive slopes (r= 0.91, n = 7) and LVID intercepts (r0.89, n = 7) of the stress-diameter plots also correlated well. Noninvasive stressdiameter plots in nine normal subjects showed a range of slopes of 50-93 × 101 dyn/cm and intercepts of 1.8-2.8 cm. Mean basal end-systolic noninvasive stress in 22 normal subjects (64.8 ± 19.5 × 10W dyn/cm2) and 14 treated hypertensives (56.3 ± 26.7 × 103 dyn/cm2) was significantly lower than in nine patients with symptomatic aortic regurgitation who had reduced ejection fraction (142.2 ± 53.2 × 10° dyn/cm2, p < 0.01) or four patients with congestive cardiomyopathy (187.3 ± 49.8 × 103 dyn/cm2, p < 0.01), while a mild elevation of stress in symptomatic aortic regurgitation with normal ejection fraction was not statistically significant (91.1 ± 20.7 × 103 dyn/cm2, n = 6). Thus, afterload excess contributed to ejection fraction reduction. We conclude that end-systolic stress may be determined noninvasively and may be a useful approach to quantitation of LV afterload and contractility.

ISSN:0009-7322    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

The purpose of this investigation was to determine if a stenosis of a coronary artery located proximally caused greater deterioration of left ventricular function than a stenosis of a similar magnitude located more distally in the artery. Twenty-six patients with isolated left anterior descending coronary artery (LAD) lesions documented by cardiac catheterization were studied by radionuclide angiocardiography (RNA) at rest and during exercise on a bicycle ergometer. Thirteen patients (nine males and four females) had a proximal lesion of the LAD averaging 91 ± 11% of the diameter of the lumen (group 1) and 13 patients (eight males and five females) had a distal lesion averaging 88 12% of the lumen (group 2). The mean age of group 1 was 49 ± 9 years and the mean age of group 2 was 48 9 years. In group 1, the ejection fraction decreased from 63 ± 8% to 55 i11% (p= 0.02), left ventricular end-diastolic volume (EDV) increased from 130 ± 32 ml to 174 ± 34 ml (p= 0.001) and left ventricular end-systolic volume (ESV) increased from 49 ± 16 ml to 80 ± 26 ml (p= 0.001) during exercise. In group 2, the ejection fraction and ESV showed no significant change during exercise. In this group, the left ventricular EDV increased from 117 ± 28 ml to 140 ± 37 ml (p= 0.04) during exercise. The two groups showed no significant hemodynamic differences during the rest studies, but group 1 showed significantly lower ejection fraction and higher EDV and ESV during exercise. These findings indicate that a stenotic lesion located at a more proximal level of the coronary arterial system reduces blood flow in a larger area of myocardium, resulting in a more pronounced ischemic response to exercise than a similar lesion located more distally.

ISSN:0009-7322    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Hypertension and atherosclerotic coronary arterial obstruction frequently coexist in patients. However, the effect of increased aortic pressure on ischemic segmental dysfunction is not well understood. We studied the effects of aortic pressure increases on segmental left ventricular function during myocardial ischemia. Eighty-two dogs instrumented with three to six pairs of pulse-transit piezoelectric crystals were studied in an awake, unsedated state to measure segmental wall thickness. A pneumatic balloon occluder was positioned around the proximal left anterior descending artery (LAD). Thirty-three dogs underwent LAD occlusion and served as normotensive controls (group A). Group B dogs (n = 23) received a 6-hour infusion of phenylephrine (PE) beginning 5 minutes after LAD occlusion to increase aortic diastolic arterial pressure to 120-130 mm Hg; aortic pressure was then allowed to return to normal for the subsequent 18 hours. The eight dogs in group C received a 6-hour infusion of PE, but no coronary arterial occlusion was produced. In group D (n = 12), distal constriction of the thoracic aorta was maintained for 24 hours after LAD occlusion. Regional myocardial blood flow (RMBF) was measured with radioactive microspheres in six conscious dogs and both RMBF and intramyocardial Pco2 were measured in seven open-chest dogs to assess alterations in regional myocardial oxygen supply and demand. Segments of myocardium were arbitrarily grouped according to the amount of net systolic thickening (NET) present 5 minutes after LAD occlusion and before increasing aortic pressure: group 1 retained 67-100+% of control NET, group 2 047%, and group 3 less than 0% (paradoxic motion). In dogs receiving PE plus LAD occlusion and in dogs with aortic constriction and LAD occlusion, NET was transiently depressed in groups 1 and 2 compared with the normotensive cohort; 24 hours after occlusion, NET in groups 1, 2 and 3 did not differ significantly from that in the normotensive dogs. Systemic hypertension resulted in a significant increase in endocardial and midwall RMBF and, in seven open-chest dogs, decreased the intramyocardial accumulation of carbon dioxide after LAD occlusion. Increased aortic pressure in dogs without coronary occlusion produced reversible decreases in end-diastolic wall thickness, NET and LV dP/dt. Thus, the production of systemic hypertension with diastolic pressures of 110-120 mm Hg acutely or for 6 hours during evolving canine myocardial infarction does not appear to exert an important deleterious effect on myocardial oxygen supply and demand. However, 24 hours of mildly increased aortic pressure accentuates end-diastolic wall thinning in segments with paradoxic systolic motion and results in a failure of their return to control values at this period.

ISSN:0009-7322    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

To determine if changes in pulmonary capillary wedge pressure could be determined from the pulmonary blood volume (PBV) ratio response on exercise-gated blood pool images, 42 patients had simultaneous exercise-gated blood pool imaging and hemodynamic monitoring during cardiac catheterization. Nine patients were normal and 33 patients had cardiac disease. Changes in the PBV ratio were determined from the 500 left anterior oblique end-diastolic frames by placing a region of interest over the left lung. The ratio of exercise/rest counts (PBV ratio) was calculated. The exercise-induced change in mean pulmonary capillary wedge pressure correlated with the PBV ratio (r= 0.72, p < 0.001). Patients were grouped into those with a definite (> 3-mm Hg) exercise-induced decrease, no change or an increase in mean pulmonary capillary wedge pressure in response to exercise. The PBV ratio was 0.929 ± 0.076 (mean SD) for the 10 patients with a decrease in wedge pressure, 1.027 ± 0.065 for the eight patients with no change in wedge pressure (p< 0.05), and 1.214 ± 0.131 for the 24 patients with an increase in wedge pressure (p< 0.05). Heart rate and blood pressure response to exercise did not differ for the three groups. The nine normal subjects had no increase in mean pulmonary capillary wedge pressure with exercise and a normal PBV ratio (mean PBV ratio = 0.92 + 0.06). Thirteen of the patients with coronary artery disease, 14 with chronic aortic or mitral regurgitation, three with cardiomyopathy (two congestive and one hypertrophic), and one with aortic stenosis and regurgitation had an exercise-induced increase in mean pulmonary capillary wedge pressure and an abnormal PBV ratio. The two patients with mitral stenosis had normal PBV ratios despite exercise-induced increases in mean pulmonary capillary wedge pressure. We conclude that determination of the PBV ratio from exercise-gated cardiac blood pool images c be used as a noninvasive means of estimating exercise-induced changes in left ventricular filling pressure.

ISSN:0009-7322    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

The cardiorespiratory response to 10 days of continuous recumbency was assessed in 12 healthy men, age 50 ± 4 years, who underwent supine and upright graded maximal exercise testing before and after bedrest. The decrease in peak oxygen uptake after bedrest was greater during upright exercise (lS.lo%, p < 0.05) than during supine exercise (6.1%, NS): from 25.8 ± 5.2 to 21.9 ± 4.5 ml/kg/min and from 24.6 ± 5.2 to 23.1 ± 4.8 ml/kg/min. The decrease in submaximal work was also greater in the upright than in the supine position (p< 0.05). Ventilation volume was significantly elevated (p< 0.05) after bedrest during maximal and submaximal effort in both the supine and upright positions. After bedrest, peak heart rate increased 5.7% and 5.9% during supine and upright testing, respectively (p< 0.05). The increases in rate-pressure product after bedrest were significantly larger (p< 0.05) during upright than during supine exercise. These results indicate that orthostatic stress is the most important factor limiting exercise tolerance after bedrest in normal middle-aged men. This mechanism also increases the myocardial oxygen demands during submaximal effort after bedrest. Intermittent exposure to gravitational stress during the bedrest stage of hospital convalescence may obviate much of the deterioration in cardiovascular performance that follows myocardial infarction.

ISSN:0009-7322    

出版商:OVID    

年代:1982

数据来源: OVID