Morton Lee Pearce

Measurement of Pulmonary Edema

Two methods for the measurement of pulmonary edema are compared. The first method, which permits serial measurements in vivo, depends on the difference in mean transit time of a water label and an intravascular label. The second method is a postmortem one in which total lung water is measured and allocated to the pulmonary blood or to pulmonary extravascular water. Three groups of six dogs each were studied: controls, a group with pulmonary edema produced by elevating pulmonary venous pressure, and a group with pulmonary edema produced by alloxan. The isotopic as compared with the postmortem method accounted for 71% of the pulmonary extravascular water found in the controls, 94% in high pressure edema and 57% in alloxan edema. Shunting, as measured by a large fall in PaO2 despite 100% oxygen breathing, became marked in a second group of five alloxan dogs and only 31% of the postmortem pulmonary extravascular water was measured by the isotope method. It is concluded that the isotope transit time method is a useful one for the serial measurement of pulmonary edema in vivo. The edema water is determined more accurately when pulmonary edema is due to elevated pulmonary venous pressure than when due to increased vascular permeability.

A Controlled Clinical Trial of a Diet High in Unsaturated Fat in Preventing Complications of Atherosclerosis

This report describes a clinical trial, with domiciled male veterans, designed to determine whether a diet which lowers serum cholesterol concentration can prevent overt complications of coronary heart disease and other manifestations of atherosclerosis. Volunteers were allocated randomly to control and experimental groups. Participants numbered 422 in the control group and 424 in the experimental group. The two groups were indistinguishable at the outset of the study in almost all observations. These included age, racial characteristics, and religious affiliation; height, weight, and blood pressure; electrocardiographic findings; prevalence of pre-existing anginal syndrome, myocardial infarction, peripheral atherosclerosis, cerebral ischemia, or cerebral infarction; cardiac decompensation; utilization of relevant medications; serum cholesterol and serum total lipid levels; and prevalence of corneal arcus and xanthelasma. One significant difference between the groups in regard to a possibly influential characteristic was that they differed slightly in patterns of cigarette smoking habits. The control diet was similar to the regular institutional diet, which is a standard American diet. It provided, by analysis, 40.1% of calories as fat, having a mean iodine value of 53.5; cholesterol intake was 262 mg/1,000 calories (653 mg/day). The experimental diet provided 38.9% of calories as fat, with an iodine value of 102.4, and had a cholesterol content of 146 mg/1,000 calories (365 mg/day). Linoleic acid content of the two diets was 10% and 38% of total fatty acid, respectively. The experimental diet was prepared to simulate conventional food. Over-all adherence expressed as percentage of total possible meals taken, from introduction into the study to termination of the study, averaged 56% for the control subjects and 49% for the experimental group. The experimental diet induced a prompt drop in serum cholesterol level and sustained a difference between the experimental and control groups amounting to 12.7% of the starting level. It is estimated from published data that the change in saturation of dietary fat accounted for five-sixths of the diet-induced lowering of serum cholesterol in the experimental group, the remaining one-sixth having been due to decreased cholesterol intake. Mean linoleic acid concentration of adipose tissue was initially 10.9%. During the latter part of the trial, which lasted eight years for some subjects, linoleic acid concentration in adipose tissue approached an asymptotic level of 33.7% among good adherers. This variable was a good measure of adherence to the diet after five or more years (r=+0.71), but not earlier. Clinical follow-up was carried out on a double-blind basis. The number of men sustaining events in major categories, in the control and experimental groups, respectively, was: definite silent myocardial infarction, 4 and 9; definite overt myocardial infarction, 40 and 27; sudden death due to coronary heart disease, 27 and 18; definite cerebral infarction, 22 and 13. The difference in the primary end point of the study-sudden death or myocardial infarction -was not statistically significant. However, when these data were pooled with those for cerebral infarction and other secondary end points, the totals were 96 in the control group and 66 in the experimental group; P=0.01. Fatal atherosclerotic events numbered 70 in the control group and 48 in the experimental group; P<0.05. Life-table analysis in general confirmed these conclusions. For all primary and secondary end points combined, eight-year incidence rates were 47.7% and 31.3% for the control and experimental groups, respectively; P value for the difference between the two incidence curves was 0.02. Stratification of the data by age demonstrated that most of the prophylactic effect occurred in the younger half of the study population, less than 65.5 years old at the start of the study. Stratification by baseline serum cholesterol concentration revealed that most of the effect was encountered in men with starting levels above the median (233 mg/dl). Stratification on the basis of pre-existing atherosclerotic complications failed to yield consistent evidence that subjects without pre-existing complications responded differently to diet than did those with prior overt disease. Deaths due to nonatherosclerotic causes numbered 71 in the control group and 85 in the experimental group. Most of the difference occurred in the latter part of the study. Consideration of causes of death in this category suggested that this difference probably did not reflect a toxic effect of the experimental diet. Gross grading of the extent of atheromata in individuals who died and were autopsied failed to reveal significant differences between the two groups of subjects. The same was true of arterial total lipid and calcium concentrations. Relative abundance of major lipid fractions in coronary atheromata and circle of Willis appeared to be independent of diet. In general, most of the varieties of lesions just cited revealed increased concentrations of linoleic acid in triglyceride, cholesterol ester, and phosphatide among the experimental subjects. In individuals on the experimental diet who died after prolonged experience in the study and high adherence to the diet, arachidonic acid concentration in atheroma phosphatide was significantly depressed. A similar but less consistent decrease was observed in arachidonic acid in cholesterol ester and free fatty acid of atheromata. Observations of other investigators suggest that these changes were due to the effects of high &agr;-tocopherol intake on the experimental diet.

Echocardiographic Diagnosis of Idiopathic Hypertrophic Cardiomyopathy without Outflow Obstruction

The echocardiographic findings of eight patients with hypertrophic cardiomyopathy without outflow obstruction (HMC) and of 15 normal (Norm) individuals are presented.The characteristic features in HMC were: (1) interventricular septal width much greater than normal (HMC = 2.5 ± 0.3 cm, Norm = 1.0 ± 0.2 cm, P < 0.005); (2) normal or only slightly increased posterior left ventricular wall thickness; (3) the ratio of interventricular septal to posterior wall thickness ≧2.0; (4) ejection fraction greater than normal (HMC = 0.76 ± 0.08, Norm = 0.68 ± 0.06, P < 0.025); (5) reduced velocity of the early diastolic closing motion of the anterior mitral leaflet (HMC = 60 ± 23 mm/sec, Norm = 124 ± 29 mm/sec, P < 0.005); (6) absence of abnormal systolic movement of the anterior mitral valve, as seen in hypertrophic obstructive cardiomyopathy. The diagnosis of hypertrophic cardiomyopathy can be made with echocardiography, even when outflow tract obstruction of the left ventricle is absent.

Cardiac effects of acute ethanol ingestion unmasked by autonomic blockade.

We assessed the effects of ethanol and autonomic blockade on left ventricular function in nine normal subjects, age 20-35 years, using M-mode echocardiography and systolic time intervals. On day 1, measurements were made of heart rate, mean velocity of circumferential fiber shortening, and left ventricular preejection period and left ventricular ejection time ratio (PEP/LVET), during a control period and after autonomic blockade. Autonomic blockade was produced with intravenous propranolol (0.2 mg/kg body weight) and atropine (0.04 mg/kg body weight). On day two, measurements were again made during a control period, then with ethanol alone, followed by addition of autonomic blockade to ethanol. One hundred eighty milliliters of ethanol were ingested over 60 minutes, resulting in a mean blood ethanol level of 110 mg/dl (range 77-135 mg/dl) at 60 minutes post-ingestion. There were no significant differences between the control data on days 1 and 2. Blood pressure was unchanged throughout the study. On day 1, autonomic blockade alone resulted in the expected increase in heart rate (p lt; 0.001), with a proportional increase in mean velocity of circumferential fibr shortening (p lt; 0.01), and an increase in PEP/LVET (p lt; 0.01). On day 2, ethanol alone resulted in no significant changes except for a slight increase in PEP/LVET (p lt; 0.02). Ethanol plus autonomic blockade, (day 2), compared with autonomic blockade alone (day 1), revealed a decrease in mean velocity of circumferential fiber shortening (p lt; 0.05), and an increase in PEP/LVET (p lt; 0.01), with a decrease in intrinsic heart rate (p lt; 0.001). We conclude that in normal subjects: 1) autonomic blockade does not directly affect contractility; 2) acute ethanol ingestion alone does not produce important changes in cardiac function; and, 3) ethanol in the autonomic blockaded heart causes a significant decrease in contractility. Thus, we infer that ethanol has a negative inotropic effect which is masked by catecholamines and/or autonomic nervous system discharge.

Left Ventricular Hypertrophy Diagnosed by Echocardiography

Abstract Echocardiography was used to differentiate left ventricular hypertrophy due to hypertrophic cardiomyopathy (20 cases) from that due to aortic valvular stenosis (10 cases) or systemic hypertension (10 cases). In aortic stenosis or hypertension symmetrical left ventricular hypertrophy was demonstrated with greater than normal thickness of both the ventricular septum and the posterior ventricular wall. The ratio of septal-to-posterior ventricular-wall thickness (mean ± S.D.) was the same as normal (1.2 ± 0.1). In hypertrophic cardiomyopathy, asymmetrical left ventricular hypertrophy was demonstrated with gross septal thickening (22.5 ± 3.4 mm) and a normal or slightly increased thickness of the posterior left ventricular wall (10.4 ± 2.0 mm). The ratio of septal-to-posterior left-ventricular-wall thickness (2.2 ± 0.2) was greater than that in aortic stenosis or systemic hypertension (p<0.005). The ventricular septum was disproportionately hypertrophied in hypertrophie cardiomyopathy regardless of th...

FALLIBILITY OF PLASMA-DIGOXIN IN DIFFERENTIATING TOXIC FROM NON-TOXIC PATIENTS

Abstract The plasma-digoxin level was studied prospectively in 104 consecutive patients for whom the test was ordered. The test did not discriminate patients who were toxic (as defined by electrocardiographic criteria) from those who were not, Indeed in 8 (44%) of 18 definitely toxic patients knowledge of presumably safe digoxin levels may have contributed to the development of toxicity.

Echocardiographic evaluation of posterior left ventricular wall motion in muscular dystrophy.

Maximal systolic endocardial velocity (SEVM) and maximal diastolic endocardial velocity (DEVM) were determined echocardiographically in patients with muscular dystrophy (MD). The SEVM of the muscular dystrophy patients was 5.5 ± 0.9 cm/sec and the DEVM was 13 ± 3 cm/sec. The SEVM in MD was significantly less than that seen in age-matched normals (P < 0.05), persons with myotonia congenita (P < 0.02), deconditioned patients (P < 0.001), or older normal persons (P < 0.05). The SEVM of the MD patients was not significantly different from persons with spinal muscular atrophy. The DEVM of the muscular dystrophy patients was significantly less (P < 0.001−0.05) than any other group. No correlation could be found between age, heart rate, type or severity of dystrophy and SEVM or DEVM values. The echocardiogram was more selective in correctly identifying muscular dystrophy patients than the electrocardiogram. The abnormality in DEVM was present despite lack of symptoms, normal cardiovascular examination, normal chest X-ray and normal electrocardiograms in 18 of 22 patients. We believe that the DEVM correlates with myocardial relaxation.

Surgical risk in the cardiac patient

Abstract The problem of evaluating operative risk in cardiac patients is a difficult one for the physician, surgeon, and anesthetist. Electronic data processing was employed to evaluate 25 parameters in 857 operations in which pre-operative cardiac consultations were available. The total mortality was approximately twice that of the general hospital population undergoing similar surgical procedures. The cardiac patient tolerated minor surgery, including inguinal herniorrhaphy and transurethral resection, well. In major surgery, including thoracotomies and laparotomies, the total mortality was 25 per cent. Three categories of information were most sensitive for predicting mortality. The first was the severity of the surgical procedure. Secondly, mortality was dependent on functional capacity: Class I, 4 per cent; Class II, 11 per cent; Class III, 25 per cent; and Class IV, 67 per cent. Thirdly, mortality increased in a sequence: (1) rheumatic heart disease, (2) arteriosclerotic heart disease and/or hypertensive heart disease and (3) pulmonary heart disease.

Echocardiographic Study of the Abnormal Motion of the Posterior Left Ventricular Wall during Angina Pectoris

Echocardiographic waves from the posterior left ventricular endocardium were recorded in 30 normal subjects and in nine patients during 13 anginal episodes. At rest the normal maximal systolic endocardial velocity (SEVM) was 6.2 ± 1.4 cm/sec, the mean systolic endocardial velocity (SEV) was 4.1 ± 0.7 cm/sec, and the systolic endocardial excursion (SEE) was 1.4 ± 0.3 cm. The maximal diastolic endocardial velocity (DEVM) was 18 ± 3 cm/sec, and the mean early diastolic endocardial velocity (DEV) was 9.4 ± 1.7 cm/sec. Exercise in 20 normals caused a significant increase in SEVM, SEV, DEVM, and DEV, but not SEE. In no instance did any of these values fall below the resting levels. The angina patients differed significantly from the normals having at rest a slower DEVM (15 ± 4 cm/sec) (P < 0.025) and DEV (8.4 ± 0.8 cm/sec) (P < 0.025). During exercise, but before angina, there was a significant increase in SEVM and SEV but not SEE, DEVM, or DEV. In no instance did any of these values fall below the resting levels. During angina SEVM and SEV reacted variably and together with SEE were not significantly different from the resting values. In contrast, there was a remarkable slowing of DEVM (8.2 ± 3.2 cm/sec) (P < 0.001) and DEV (5.7 ± 2.2 cm/sec) (P < 0.001). Five minutes after the pain and S-T-segment depression disappeared, the endocardium moved as it did before exercise.

Electrocardiographic Diagnosis of Myocardial Infarction in the Presence of Left Bundle-Branch Block

It is generally accepted that most myocardial infarctions are obscured on the electrocardiogram by left bundle-branch block. The number of published cases in which this could be evaluated, however, is small, and the case reports are scattered. We have studied 30 cases of myocardial infarction with left bundle-branch block in which the location of the infarction could be determined with certainty, by autopsy, or by a previous electrocardiogram with normal intraventricular conduction. Twenty such published cases have also been collected. Electrocardiographic abnormalities have been correlated with infarctions in different locations. The possible specificity of these abnormalities is discussed.