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To determine whether the severity of thallium-201 scintigraphic defects within hours of acute myocardial infarction (MI) could be used to predict subsequent mortality, thallium-201 imaging was performed within 15 hours of the onset of symptoms in 42 patients with acute MI. Patients with pulmonary edema or shock were excluded. The extent of perfusion defect was determined in three views (anterior and 40/sup 0/ and 60/sup 0/ left anterior oblique) by both objective computer-assisted and subjective methods, and expressed as a summed defect score. Mortality for the patient group as a whole was 17% in hospital, 24% at 6 months, and 33% at last follow-up (average 9 months). Using the objective method, a high thallium defect score (7.0 or greater, corresponding to at least a moderate reduction of activity involving 40% of the left ventricle in two views) identified a subgroup of 13 patients in which mortality was 46% in hospital, 62% at 6 months, and 92% at last follow-up. Corresponding values for the 29 patients with lower objective defect scores were 3%, 7% and 7%, respectively (all p =1000 IU/1 and moderate (vs one or mild) left ventricular failure were also associated with mortality. However, a high thallium defect score was significantly more predictive than any of these variables. Stepwise, multivariate analysis showed that the thallium score alone was a better predictor than the best combination of these clinical variables, and no variable added to the predictiveness of the high defect score. These results suggest that thallium-201 scintigraphy may provide an accurate, rapid, noninvasive method for separating high-risk and low-risk subgroups of hemodynamically stable patients.« less

The accuracy of two-dimensional echocardiographic left ventricular volume measurement in an isolated heart preparation was tested using Simpson's reconstruction of progressively fewer short-axis cross sections of known location. Echocardiographic images from five ejecting hearts submerged in a special tank were obtained under conditions designed for maximal accuracy of echocardiographic volume assessment. Echocardiographic determinations of 52 volumes at various times throughout the cardiac cycle were compared, by least-squares linear regression, with simultaneous direct-volume measurements by volumetric chamber (range 9.4-44.8 ml). Echocardiographic and direct measurements correlated well for all numbers of cross sections from 1-19 (r = 0.84-0.97); however, variability of direct volume predicted from a given echocardiographic measurement increased nonlinearly as the number of cross sections per heart decreased, and was especially large when three or fewer cross sections were used (SEE = 4.6-7 ml). The accuracy of echocardiographic measures was compared for each number of cross sections per heart, varying from one to 19; accuracy was defined as the mean absolute difference between echocardiographic and direct measurements of volume, ejection fraction, and maximal rate of ejection. The accuracy of echocardiographic measurements was significantly reduced with fewer than four cross sections per heart for ventricular volume, three cross sections for ejection fraction, and five cross sections for maximal rate of ejection. In light of what appears to be required for accurate echocardiographic volume measurement in this controlled, ejecting, noninfarcted, in vitro preparation, additional cross sections may be required in intact animals and human subjects, especially in those with diseases that cause ventricular asymmetry or regional dysfunction.

Many studies have delineated the changes in the elastic properties of arterial tissue as a function of age. Despite the fact that viscoelasticity is a prominent feature of these tissues, there is little information or characterization of age-associated changes in viscoelastic properties, over a wide range of smooth muscle activation, particularly in nonhuman tissue where atherosclerosis is not a confounding factor. In the present study, using small sinusoidal length perturbations, we determined the dynamic stiffness properties across a wide range of lengths (stretch ratios from 100 to 135%) and frequencies (from 0.25 to 35 Hz) in strips excised from ascending and descending aortas from six young (2 to 4-year-old) and 12 senescent (10- to 13-year-old) beagles. Studies were performed with the smooth muscle fully activated with calcium and norepinephrine, as well as fully inactivated with cyanide, iodoacetate, and dinitrophenol. There was a cubic nonlinear dependence of stiffness modulus on length only in senescent tissue and, surprisingly, little frequency dependence in tissue of either age. Compared to the young aortas, the three-dimensional surface representing the dependence of stiffness modulus on length and frequency from both the ascending and descending regions of aged aortas was displaced higher on the stiffness axis both with the muscle fully activated and inactivated. This age difference was accentuated at longer lengths. The phase lag between force and length was greater in the young vs. the old strips only in the activated, ascending aortic tissue. We found no age differences in the content of elastin, collagen, or in the collagen/elastin ratio, to account for these mechanical property differences.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute shifts in the pressure-volume relationship of the left ventricle occur under several conditions. One potential mechanism for this phenomenon is ventricular interdependence, that is, the influence of right ventricular filling on the left ventricle. This mechanism was studied in an isolated cross-circulated ejecting canine heart preparation with balloons sewn into both right and left ventricles and connected to volumetric chambers allowing continuous and accurate simultaneous measurement of right and left ventricular pressures and volume. Sets of left ventricular pressure-volume loops were obtained under a variety of right ventricular volumes. Experiments were repeated with and without the pericardium. Both diastole and systole were studied. We show that in the pericardium-free heart working over a normal range of volumes, the right ventricle exerts little influence on left ventricular pressure. With the pericardium present, there is a small but significant effect of right ventricular volume on left ventricular pressure during systole and diastole. Over a wider range of volumes imposed in the arrested heart, the right ventricle does influence left ventricular pressure even without the pericardium. Thus we have demonstrated that ventricular interdependence is not likely to lead to large acute pressure-volume shifts, either during diastole or systole, except in the presence of considerably above normal right ventricular volumes.

The extent of abnormality in early thallium-201 and gated cardiac blood pool scintigrams has been reported to be useful for predicting mortality in patients with acute myocardial infarction (AMI). To compare the two techniques, 91 patients admitted consecutively with evident or strongly suspected AMI underwent both imaging studies within 15 hours of the onset of symptoms. Patients with pulmonary edema or shock were excluded. AMI developed in 84% of patients, and 6-month mortality for the entire group was 16%. A thallium defect score of 7.0 or greater (corresponding to at least a moderate reduction of activity involving 40% of the left ventricular circumference) identified a subgroup of 14 patients with 64% 6-month mortality rate. Similarly, a left ventricular ejection fraction of 35% or less identified a high-risk subgroup of 10 patients with a 6-month mortality of 60%. Mortality in the remaining patients was 8% for thallium score less than 7 and 11% for ejection fraction greater than 35%. The mortality rate was highest among patients who had concordant high-risk scintigrams (five of six, 83%), lowest in those with concordant low-risk studies (five of 64, 8%) and intermediate in those with discordant results (four of 11, 36%). Of a number of clinical variables, only the appearance of Q waves, peak creatine kinase greater than 1000 IU/I, and history of infarction were significantly associated with mortality. High-risk thallium or blood pool scintigraphic results were significantly more predictive and a thallium score of 7 or greater was more sensitive for detecting nonsurvivors than ejection fraction 35% or less at a similar level of specificity. Stepwise multiple logistic analysis showed that the thallium score was the best predictor of mortality, but that appearance of Q waves and ejection fraction were additive. Using these three variables, 11 patients were calculated to have a 50% or greater chance of dying and eight (73%) actually died, compared with six of 70 (9%) with a calculated chance of death of less than 50%. These results in a prospectively identified and consecutive group of patients support the value of early thallium and blood pool scintigraphy for separating high- and low-risk subgroups of hemodynamically stable infarct patients.

To determine the effects of different anesthesias on the performance of the arterial baro-reflex, the open-loop characteristic of the carotid sinus reflex was analyzed in 24 rabbits under anesthesia with pentobarbital (30 mg/kg), urethan (800 mg/kg), alpha-chloralose (80 mg/kg), or a mixture of alpha-chloralose (40 mg/kg) and urethan (0.4 g/kg). For each rabbit and anesthesia, mean systemic arterial pressure and heart rate were measured as carotid sinus pressure was changed in 10-mmHg steps between 40 and 150 mmHg. This set of measurements was repeated four times at 1-h intervals. A logistic function curve was fitted to the carotid sinus pressure-arterial pressure relationship. The parameters of this curve were then analyzed to delineate the specific effects of the anesthesias on the relationship. The main finding was that the response range and the slope parameters under alpha-chloralose anesthesia were significantly smaller than those obtained under the other anesthesias. Propylene glycol, used as the solvent for chloralose, did not affect the reflex control of arterial pressure or heart rate. The reflex under chloralose-urethan anesthesia showed characteristics similar to those under urethan anesthesia. We conclude that although alpha-chloralose has traditionally been used in the dog to obtain strong reflex responses, it weakens the reflex control of arterial pressure in the rabbit.

To understand more fully the role of the arterial baroreceptor reflex on systemic and pulmonary vascular resistance, we studied the influence of the carotid sinus baroreceptor reflex control system on the entire systemic and pulmonary arterial pressure-flow relationships. Ten pentobarbital-anesthetized dogs, whose carotid sinuses were isolated, were used in a preparation in which the right and left hearts were bypassed to control systemic and pulmonary blood flows. At intrasinus pressures of 50, 125, and 200 mm Hg, systemic and pulmonary arterial pressures were measured in response to step changes in systemic and pulmonary blood flows from 0 up to 200 ml/min per kg. The systemic arterial pressure-flow relationship exhibited a marked nonlinearity, especially at either high or low flows. A third-order polynomial fit was found to represent the steady state systemic arterial pressure-flow relationship best. Blood flow autoregulation was reflected as a secondary change in systemic arterial pressure at constant flow approximately 15 seconds after the initial response. Blood flow autoregulation was seen in the entire systemic vascular bed over the entire range of flows studied. The degree of autoregulatory significantly contributed to the shape of the systemic arterial pressure-flow relationship. The steady state arterial pressure-flow relationship shifted upward and toward the pressure axis, increasing the calculated incremental resistance and total peripheral resistance as intrasinus pressure was decreased. The systemic zero-flow arterial pressure was found to increase with decreases in intrasinus pressure. The pulmonary arterial pressure-flow relationship was found to be linear in the range of flows studied from 25 up to 200 ml/min per kg.(ABSTRACT TRUNCATED AT 250 WORDS)

Interaction of carotid sinus and aortic arch reflex control of total peripheral resistance was studied in eight dogs anesthetized with sodium pentobarbital and placed on constant flow cardiac bypass. Carotid sinus and aortic arch baroreceptor areas were isolated and separately perfused at controlled pressures. Combinations of carotid sinus and aortic arch pressures were delivered at random in steps of 25 mm Hg over the 50-225 mm Hg pressure range, and systemic arterial pressure was measured. Changes in arterial pressure reflected changes in total peripheral resistance. A multiple linear regression showed that both carotid sinus and aortic arch pressures exhibited a sigmoidal relationship with arterial pressure. Independent of carotid and aortic baroreceptor pressures, arterial pressure was found to be a periodic function of time (period = 2 hours) in all dogs. The average carotid sinus reflex open loop gain was found to be 0.231 +/- 0.092, while average aortic arch open loop gain was 0.141 +/- 0.088. The gain of either the carotid sinus or aortic arch reflex was not influenced by the absolute pressure level of the other receptor area. In a separate series of experiments performed in the same dogs, we tested the hypothesis that a nonlinear temporal summation of the reflex control of total peripheral resistance might exist when the inputs to carotid and aortic baroreceptors are changed simultaneously. With both inputs held at the region of maximum gain, 25 mm Hg step changes were imposed first on carotid sinus pressure, then on aortic arch pressure, and then on both simultaneously. A temporal inhibition of the two reflexes showed that simultaneous excitation of both receptors resulted in a smaller reflex response than the sum of individual responses.

We have studied the effect of the carotid sinus baroreceptor reflex on respiration in 10 vagotomized, spontaneously breathing, pentobarbital anesthetized dogs. The carotid body chemoreceptor reflex response was eliminated by surgically excluding the carotid bodies from the carotid sinus baroreceptor area. Steady state frequency, tidal volume, and minute ventilation were measured after 25 mm Hg step changes in intrasinus pressure between 50 and 200 mm Hg. Over this range, the step decreases in intrasinus pressure caused concomitant increases in mean arterial pressure from 86 to 182 mm Hg. All of the respiratory response curves were sigmoidal in shape. Decreasing intrasinus pressure from 200 to 50 mm Hg caused respiratory frequency to increase from 4.8 to 9.7/min, and tidal volume to decrease from 704 to 515 ml. The calculated total ventilation, however, increased from 3180 to 4530 ml/min. The time of inspiration decreased from 3.7 to 2.4 seconds, and the time of expiration decreased from 9.8 to 4.1 seconds. These ventilatory responses are shown to be baroreceptor reflex mediated, and not secondary to changes in arterial pressure. These findings indicate that not only does the carotid sinus baroreceptor reflex control arterial pressure, but it also simultaneously influences ventilation, through changes in both respiratory frequency and tidal volume.

Dilation of the infarct zone (infarct expansion) has been shown to be a cause of regional left ventricular dilation within days of transmural anterior myocardial infarction. Whether this process stabilizes, continues or regresses thereafter, and whether uninfarcted myocardium is affected is unknown. To explore this, two to six (mean four) serial two dimensional echocardiographic studies were obtained over a 3 to 30 month period (mean 13) in 13 patients beginning 10 to 21 days after anterior transmural myocardial infarction. With use of the papillary muscles as internal left ventricular landmarks, anterior and posterior segmental dilation in each patient was assessed from the slope of the regression line of segment length versus time. Study patients were classified into those with (seven patients) and those without (six patients) infarct expansion. Infarct expansion was defined as an anterior segment length 10 to 21 days after infarction that exceeded the upper limit of normal determined from 13 age-and sex-matched normal control subjects. Ten to 21 days after infarction, the average anterior segment length in the seven patients with expansion was 65 percent greater than that in normal control subjects. The seven patients with infarct expansion showed significant and continuing dilation during long-term observation of both the infarcted anterior (p Thus, infarct expansion occurring within 3 weeks of transmural myocardial infarction appears to be the main contributor to left ventricular dilation, and is associated with impaired functional status. Moreover, a significant increase in ventricular size due to infarct expansion appears to predict chronic progressive ventricular enlargement due to lengthening of both the infarcted zone and the uninfarcted segment.

The exact mechanism or mechanisms by which nitroglycerin exerts its beneficial effect on pacing-induced regional myocardial ischemia has not been ellucidated previously. In an open-chest, anesthetized canine preparation a fixed, flow limiting stenosis was applied to the left anterior descending (LAD) coronary artery and heart rate was increased by atrial pacing. Mass spectrometry was used to measure myocardial oxygen (PmO2) and carbon dioxide (PmCO2) tensions. Myocardial blood flow was measured by the radioactive microsphere technique. Application of the stenosis resulted in regional decreases in PmO2 and increases in PmCO2 of greater magnitude in the subendocardial than in the subepicardial layer. Atrial pacing resulted in a further decrease in PmO2 and increase in PmCO2 as well as a reduction in subendocardial blood flow. Nitroglycerin (TNG) infusion reduced mean arterial pressure 20 mm Hg, resulting in a 14 mm Hg reduction in PmCO2 in the more ischemic subendocardial layer (P less than 0.05). Myocardial blood flow decreased in all regions; however, the magnitude of this decrease was less in the ischemic region. Addition of aortic constriction abolished both the afterload and preload lowering effects of nitroglycerin but improved ischemic zone blood flow. These data demonstrate that nitroglycerin reduces the severity of pacing-induced regional myocardial ischemia primarily by reducing the determinants of myocardial oxygen demand. We found that when these effects are counteracted, improvement in myocardial oxygen supply becomes the dominant mechanism.