Myopotential inhibition of ventricular synchronous pacemaker.
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Biomedical subjects
Publications and source records attributed to R J Hall.
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An abnormal diastolic indentation of the mitral valve has been noted on short-axis two-dimensional echocardiograms in patients with aortic insufficiency. In order to assess the clinical usefulness of this finding, we reviewed the echocardiograms of 18 patients with this lesion who had undergone cineaortography. Results were compared with those of a control group of 100 patients. Initial diastolic indentation of the anterior mitral leaflet occurred in 8 of 12 patients with 3+ to 4+ aortic insufficiency. None of the patients with lesser regurgitation and no patients from the control group demonstrated this pattern. The presence of this abnormality appears to be a specific indicator of critical aortic insufficiency.
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The carcinoid syndrome is a rare clinical entity, the unique manifestations of which continue to excite the interest of physicians. Despite a common origin from neural crest tissue, the tumors are partially differentiated, as evidence by the different secretory products of foregut, midgut, and hindgut carcinoids. They also differ in their ability to metastasize, thus presenting an even more varied clinical picture. The prognosis of patients with carcinoid syndrome varies with the origin of the tumor and extent of metastases. The management of patients with carcinoid syndrome is difficult. Despite an understanding of the neurohormones that carcinoid tumors secrete, their various antagonists and inhibitors have been only partially successful in providing symptomatic relief. Carcinoid heart disease represents the most intriguing aspect of this syndrome. Although valvular dysfunction most often coexists with flushing and diarrhea, the findings of tricuspid regurgitation or stenosis occasionally provide the first clue to the presence of the disease. Despite intensive research, the definite etiology of these valvular lesions has not been established. A small group of patients has been managed by valve replacement. While surgical treatment has been successful in improving hemodynamics in most of these patients, it is expected to prolong life only in those without extensive liver metastases. In patients with extensive metastatic disease, one must carefully consider whether the risks and trauma of cardiac surgery for palliation are justified.
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The prothrombin time with Manchester and ox thromboplastins, the 'P & P' test of Owren and Aas, the partial thromboplastin time, the thrombin time and assays for factors II, V, VII, VIII:C, IX and X were performed by one observer in 18 patients with liver disease and 27 normal subjects; the prothrombin time and partial thromboplastin time were also carried out on another 28 similar patients by various observers. Routine liver function tests were measured in all patients. The prothrombin time with Manchester thromboplastin was well correlated with other clotting tests, and performing the other tests did not add to the information. Discriminant function analysis confirmed that clotting tests did not distinguish between different types of liver disease. Correlations between clotting tests and liver function tests reflected liver cell damage but were also influenced by acute phase reactions.
M-mode echocardiograms are demonstrated from a patient with subacute massive pulmonary embolism before and after thrombolytic treatment and clinical recovery. Severely impaired left ventricular contraction returned to normal. A reversible reduction in mitral valve opening velocity was also seen and was thought to be in part the result of diminished left atrial filling. This hypothesis was tested experimentally; mitral valve opening velocity was measured in normal subjects and found to be significantly reduced when pulmonary blood flow was impeded during the Valsalva manoeuvre.
Of the 5312 cardiac catheterizations performed at the Clayton Foundation for Research Cardiovascular Laboratories from 1974 to early 1981, seven patients (0.13%) had total occlusion of the left main coronary artery. All seven had a history of myocardial infarction, and were markedly symptomatic (New York Heart Association, Classes III and IV), with anginal pain that had existed from 2 to 13 years. Left ventricular end-diastolic pressure was notably elevated in all patients, and ejection fractions ranged from 16% to 69%. In all patients, there was significant collateral circulatory flow to the left coronary system from the right coronary artery and its branches. Six underwent coronary artery bypass at our institution, and one was operated on at another hospital. The six patients operated on in our institution were markedly improved after the operation. Our results support previously reported findings about patients with total occlusion of the left main coronary artery in that (1) no definitive clinical pattern leads to simple diagnosis, (2) the anomaly is rarely encountered during cardiac catheterization, and (3) myocardial revascularization alleviates symptoms and prolongs life.
The prognosis in patients with left bundle-branch block (LBBB) is related primarily to the presence or absence of underlying cardiac disease. Because coronary artery disease (CAD) is the most common underlying disease found in these patients, it would be desirable, in the presence of LBBB, to have a noninvasive method of differentiating between patients with and without CAD. We reviewed our experience in patients with LBBB who had undergone coronary arteriography with regard to electrocardiographic (ECG) stress testing, exercise radionuclide ventriculography (RNV), and exercise thallium scintigraphy; we also reviewed their clinical histories. A clinical history of typical angina pectoris was specific for CAD, a false-positive history being present in only one of 12 patients without CAD. The frequency of a positive ECG ST response to exercise was equal in patients with and without CAD. False-positive ejection fraction and wall-motion responses to exercise were frequent by RNV. A modification of the usual RNV criteria for positivity improved specificity but resulted in poor sensitivity for CAD. False-positive thallium study results also were. frequent in these patients. The perfusion defects usually involved the ventricular septum; the inferior and posterior walls were involved only in patients with CAD. We conclude that the usual noninvasive diagnostic tests for CAD are of limited value in patients with LBBB.
To establish noninvasive criteria for assessment of the Ionescu-Shiley pericardial xenograft in the mitral position, 29 patients with a normally functioning bioprosthesis were studied with m-mode echocardiography and phonocardiography. Two-dimensional echocardiograms were also obtained in ten of the patients. Although two-dimensional echocardiography provided simultaneous visualization of a greater number of stents and leaflets than the m-mode technique, the superior resolution of m-mode ultrasound permitted more detailed analyses of the xenograft's motion patterns. The anterior leaflet, recorded in all patients, had an average excursion of 1.2 +/- 0.22 cm. Leaflet thickness measured 4 mm or less. Coarse diastolic vibration of the anterior leaflet was recorded in two patients in the absence of both aortic insufficiency and prosthesis dysfunction. Ultrasonic estimates of prosthesis height and orifice diameter did not correlate with micrometer measurements, possibly due to the limited resolution of pulsed ultrasound in the presence of a highly reflective substance. Opening and closing of the pericardial leaflets were associated with the production of high frequency vibrations on the phonocardiogram. The potential usefulness and limitations of echocardiography for evaluating the function of bioprosthetic valves are discussed.
Resting left ventricular wall motion abnormalities may represent myocardial scars or areas of viable muscle which are ischemic and may thus benefit from revascularization surgery. Improvement in wall motion in the 3-6 minute post-exercise recovery period as compared to the resting state was investigated as a possible criterion to predict myocardial viability in 168 patients with coronary artery disease. Of 125 patients with abnormal resting wall motion, 14 of 14 who improved regional function post-exercise also improved following coronary bypass surgery. However, wall motion improved postoperatively in an additional 55 patients who had not demonstrated post-exercise improvement. An increase in ejection fraction post-exercise occurred in patients with coronary disease as well as an additional group of 24 normal subjects. Thus in the post-exercise period, improvement in resting wall motion is a highly specific but insensitive predictor of myocardial viability.
Two patients are described in whom skeletal muscle potentials originating in the shoulder girdle muscles during isometric movement suppressed the discharge of a ventricular demand unipolar pacemaker, resulting in syncope. Converting the pulse generator into a fixed-rate mode with the magnet prevented the inhibition. Improved filters or wider use of bipolar electrodes should prevent this form of interference.
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A case of pulmonary veno-occlusive disease in an adult is presented. The diagnosis was suspected clinically and verified at cardiac catheterization. Balloon dilatation of the pulmonary veins was attempted at operation and later again in the catheterization laboratory. The result was a significant reduction in pulmonary venous to left atrial pressure gradient and angiographic evidence of increase in venous diameter. It appears that in the focal form of pulmonary venous occlusion, balloon dilatation may offer a therapeutic approach in an otherwise progressively lethal disease.
Seven species of amphibian larvae were exposed to toxaphene and endrin in a continuous-flow dosing system to determine differences in sensitivity to the two compounds, EC50 and LC50 estimates varied from those for Rana sphenocephala by no more than one order of magnitude when calculated on the basis of intended concentrations. Removal of pesticides from water by the test animals was significant and it makes interpretation of results difficult. Continuous-flow toxicity tests conflict with the adaptations of amphibian larvae for static water; use of such tests for amphibians requires further evaluation.
1. Chronic dietary potassium depletion which was severe enough to decrease skeletal muscle intracellular potassium concentration by 20%, did not significantly reduce cardiac intracellular potassium concentration of rabbits. 2. Chronic potassium depletion caused a fall in intracellular pH in skeletal muscle, but no changes occurred in cardiac intracellular pH. 3. Intracellular potassium was increased above normal after 1 week of potassium repletion, but had returned to normal after 3 weeks of repletion. This may have resulted from potassium retaining mechanisms which had developed during depletion and which persisted during the early stages of repletion. 4. Cardiac and skeletal muscle from potassium-depleted animals did not show any structural damage when examined by light and electron microscopy.
The arrhythmogenic and inotropic effects of digoxin were studied in normokalemic controls, chronically hypokalaemic, and potassium-repleted dogs instrumented to maintain heart rate, mean aortic pressure, mean left atrial pressure and autonomic tone constant. The duration of digoxin infusion needed to produce ventricular tachycardia (VT) was 56.7 +/- 3.6 min in depleted dogs, 69.0 +/- 2.7 min in controls (P less than 0.005 compared with depleted dogs), and 60.5 +/- 3.0 min in repleted dogs. Baseline left ventricular dP/dt (LV dP/dt) was similar in all groups. After digoxin, LV dP/dt increased more in controls and repleted dogs than in chronically hypokalaemic dogs; eg, after 45 min of digoxin infusion LV dP/dt increased 12.7 +/- 4.4% in hypokalaemic dogs; eg, after 45 min of digoxin infusion LV dP/dt increased 12.7 +/- 4.4% in hypokalaemic dogs, 43.8 +/- 3.3% in controls (P less than 0.025) and 39.3 +/- 8.5% in repleted dogs (P less than 0.025). The inotropic response to isoprenaline was also attenuated in the chronically hypokalaemic dogs. Plasma digoxin was similar in all groups. LV digoxin was also similar in control and depleted dogs. Although inhibition of Na+, K+-ATPase and the initial velocity of 3[H]-ouabain specific binding was less in depleted dogs at VT than in controls (P less than 0.05), the magnitude of this difference was not sufficient to explain the attenuated inotropic response. No histological abnormalities were seen on light or electron microscopy in any of the groups. Therefore chronic hypokalaemia has two deleterous effects. It increases sensitivity to the arrhythmogenic effects of digoxin and impairs the inotropic response to digoxin, and isoprenaline.