Management of asymptomatic coronary artery disease.
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Biomedical subjects
Publications and source records attributed to R W Anderson.
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In eight chronically instrumented conscious dogs, apical and middle left ventricular transverse diameters were measured with pulse-transit ultrasonic dimension transducers. Intracavitary apical and midventricular pressures and intrapleural pressure were measured with micromanometers. Both diameters were normalized as a percent extension from the dimension at zero transmural pressure, determined during a transient vena caval occlusion. During the rapid phase of diastolic filling, there was a 2--5 mmHg pressure gradient from the midventricle to the apex. During late rapid filling, the apical transmural pressure and diameter increased more rapidly and reached diastasis 17 +/- 4 ms earlier than the corresponding midventricular measurements (P less than 0.01). The static diastolic pressure-dimension characteristics at the apical and midventricular levels were not significantly different (P greater than 0.30). The dynamic diastolic pressure-dimension relationship was also similar at the two levels and could be represented by a model incorporating parallel viscous properties. Because of regional differences in pressures and dimensions, however, the dynamic relationship could not be modeled when pressure was compared to the dimension at a different level. Thus, diastolic pressures should be measured at the same level as dimensions when assessing left ventricular diastolic mechanics.
Paroxysmal supraventricular tachycardia (PSVT) is commonly caused by reentry within the atrioventricular (AV) node. This arrhythmia was abolished by operative dissection of the AV junction in a patient with disabling tachycardia that was not controlled by drugs. The operation was intended to create complete AV block, but AV conduction persisted after surgery. An electrophysiologic study 1 year after the operation revealed that the operation changed AV conduction in both the antegrade and retrograde directions, which may explain the absence of tachycardia. The patient has been free of arrhythmias for 18 months.
Pulsatile pulmonary hemodynamics were analyzed in a chronic awake canine high flow model. Standard mean flow and pulsatile flow hemodynamics were measured and alterations in the proximal pulmonary vascular physical properties were quantified by the characteristic impedance (Zo). Pulmonary vascular resistance (PVR), which assesses arteriolar-capillary recruitment of perfusing radius and measures a more distal pulmonary vascular response to changing flows, also was calculated. Twelve control dogs were studied and had mean Qpa (pulmonary blood flow) = 2.02 +/- 0.15 liters/min, Zo = 193 +/- 20 dyne sec cm-5 and PVR = 416 +/- 32 dyne sec cm-5. Ten dogs were studied awake 20 weeks after creation of bilateral arteriovenous fistulae. Five of these shunted dogs, designated group A, developed Qpa = 3-4 liters/min (mean = 3.80 +/- 0.09, P less than 0.001 different from control group); the other five dogs (group B) developed Qpa = 4-8 liters/min (mean = 5.87 +/- 0.16, P less than 0.001). In group A, Zo = 143 +/- 8 (P less than 0.05) and PVR = 249 +/- 6 (P less than 0.10). In group B, Zo = 90 +/- 5 (P less than 0.005) and PVR = 126 +/- 14 (P less than 0.01). The total input power (potential and kinetic) was 125% above the controls for group A (P less than 0.001) and 264% for group B (P less than 0.001), but the mean energy components increased significantly more than did the pulsatile components. These data demonstrate a lower impedance to pulsatile flow during chronically elevated total flow which effects a reduction in both the work load of the right ventricle and the transmission of energy to the precapillary bed. Analysis of the alterations in characteristic impedance suggests a distinct proximal pulmonary vascular mechanism of decreased vessel stiffness (decreased elastic moduli) for adaptation to chronically elevated flow loads which is in addition to the two geometric alterations of proximal arterial dilation and distal vascular channel recruitment.
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The relationship between transfusion and subsequent hypoxemia was examined retrospectively in the records of combat casualties studied by the first three U.S. Army Surgical Research Teams in Vietnam. There was no evident relationship in 425 casualties studied before anesthesia and operation. In 199 casualties studied preoperatively and on at least two of the first three postoperative days, there was no evident relationship in those with injuries not involving the chest or abdomen. Eighteen such casualties received over ten units of blood each (average 24.5) and exhibited subsequent changes in arterial oxygen tension (PaO2) which were indistinguishable from those transfused lesser amounts or not all. Similar observations were made in casualties with injuries to the abdomen, although there was a tendency to lower PaO2 two days after injury in those heavily transfused. In those with thoracic injury, there was statistically significantly lower PaO2 on the first two postoperative days in those heavily transfused. Two possible interpretations are considered, one that blood transfusion contributed to hypoxemia, and alternatively, that a greater magnitude of the injuries accounted for both the worsened hypoxemia and the need for more transfusions. The latter was thought more likely. The differences in PaO2 related to the type of injury exceeded the differences associated with transfusion.
A 37-year-old man with a benign variant of scleroderma (CRST syndrome: calcinosis circumscripta, Raynaud's phenomenon, sclerodactyly, and telangiectasia) presented with recurrent ventricular tachycardia. Preoperative electrophysiologic study suggested that the mechanism of tachycardia was an ectopic pacemaker focus in the right ventricle. Right ventricular dilatation, tricuspid insufficiency, normal pulmonary pressures, and normal coronary arteries were also demonstrated. At surgery, epicardial mapping localized the site of origin of ventricular tachycardia to the anterior right ventricle near the crista supraventricular. Intramural recordings of the site of tachycardia demonstrated autonomous activity unreflected on the peripheral ECG during brief periods of sinus rhythm. Local epicardial cooling of this area with a cryoprobe promptly terminated ventricular tachycardia with resumption of tachycardia on warming. The focus was ablated by freezing the area at -60 degrees C. The patient remained free of dysrhythmia on no anti-arrhythmic agents for eight months at which time he had a single recurrence of ventricular tachycardia from a different site in the right ventricle. This technique offers a method for ablating sites of dysrhythmia arising in diffusely diseased myocardium.
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Following the administration of similar doses of nitrogen mustard (4 mg/kg) to different strains of mice, wide variations in the subsequent degree of splenomegaly were observed, implying strain differences in the role of the spleen in the compensatory erythropoietic response to haematopoietic stress. This investigation was undertaken to determine whether or not these differences were related to the size of the haematopoietic stem cell compartment size in the various strains of mice. Groups of 4 different strains of mice (Swiss Webster, A/J, C57BL/6J and CS1/ASH) were injected i.v. with nitrogen mustard (4 mg/kg body weight) and autopsied at regular intervals up to 20 d post-injection. At autopsy, the wet weight of the spleen was determined. Subsequently, groups of the same 4 strains of mice were exposed to single doses of wholebody gamma-irradiation in the range of 500-900 rads. 9 d after gamma-irradiation the mice were autopsied, their spleens removed, and the number of endogenous spleen colonies determined. The greatest degree of splenomegaly was observed in the C57BL/6J mice. The Swiss Webster mice showed no splenomegaly during the time period studied. There existed a linear inverse relationship between the maximum degree of splenomegaly observed and the dose of wholebody gamma-irradiation required to completely eliminate endogenous spleen colonies. This data is in accord with the hypothesis that there exists an inverse relationship between the extent of splenomegaly observed following haematopoietic stress and the haematopoietic stem cell compartment size.
Infection of human fibroblasts and HEp-2 cells with herpes simplex virus type 1 (HSV-1) produced a decrease in the intracellular levels of cyclic adenosine 5'- monophosphate (cAMP) and a concomitant increase in the cyclic guanosine 5'- monophosphate (cGMP) levels. In both cell cultures, changes in cyclic nucleotide levels were first observed at 6 h after viral inoculation and were maximal at 12 h. In human fibroblasts, the addition of theophylline, dibutyryl cAMP, or papaverine (cAMP-enhancing compounds) decreased significantly the yield of HSV-1, whereas the addition of insulin or dibutyryl cGMP (cGMP-enhancing compounds) increased the viral yield. In HEp-2 cells, only theophylline decreased the yield of HSV-1, and the cGMP-enhancing compounds had no apparent effect. Cyclic nucleotide enhancing compounds exhibited their effect only if added to either cell culture within the first 3 h after inoculation with HSV-1.
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Operative mortality for the first 787 patients who underwent aortocoronary bypass at Duke University Medical Center was 9.7%. Within 699 patients who underwent elective bypass only, operative mortality was 8.8% before January 1, 1972, and 5.4% subsequently. This apparent variation in operative mortality over time was largely a consequence of changing patterns of patient selection, i.e., a two- to three-fold decrease in the prevalence of ventricular dysfunction. Since January 1, 1972, operative mortality for 444 patients with mild or no heart failure who underwent elective bypass only was 5.0%. The 55 patients with left main disease had 12.7% operative mortality. In the 192 patients without left main disease who had one- or two-vessel disease, operative mortality was 1.0%, whereas, 197 patients with three-vessel disease had a 6.6% operative mortality. The 103 patients with three-vessel disease less than 50 years of age underwent operation with a 2.9% mortality. Although these results demonstrate that selected patients may undergo operation with a mortality approaching 1%, it is not clear that only such low risk patients should be offered surgery. Accurate estimates of benefits and risks of aortocoronary bypass surgery are necessary in the management of specific patients.
Cryothermia, a new technique for definitive treatment of the pre-excitation syndrome, is described in two patients. The first patient presented with a normal P-R interval with a delta wave and reciprocating tachycardia. Preoperative electrophysiologic study suggested a free-wall atrioventricular connection on the left posterior atrioventricular (A-V) groove. At surgery, epicardial mapping confirmed the site of pre-excitation on the posterior left ventricular (LV) wall. An electrogram arising from the accessory pathway (AP) was recorded at the site of earliest ventricular activation. Interatrial delay combined with an apparently long accessory pathway to the ventricle caused the P-R interval to appear normal. Local pressure abolished pre-excitation. The site of early ventricular activation was cooled to -60 degrees C with a specially designed cryoprobe. All evidence of pre-excitation and arrhythmias disappeared. The second patient presented with a refractory reciprocating tachycardia and was found to have an AP in the septum capable of only retrograde conduction. Retrograde conduction was abolished by applying a temperature of 0 degrees C to the anulus at this site during tachycardia. Conduction over the AP and reciprocating tachycardia returned with rewarming. Ablation of the AP was obtained by applying a temperature of -60 degrees C for 90 seconds on two occasions to the same area. The His bundle was not injured.