Hemophilus influenzae pericarditis with cardiac tamponade

The unusual occurrence in an adult of purulent pericarditis caused by Hemophilus influenzae, type b and complicated by cardiac tamponade is described. Medical and surgical treatment was required. The clinical course and the pathologic report of tissue removed at pericardiectomy within 3 weeks after onset of the infection indicated the development of “acute” constrictive pericarditis. The patient fully recovered and was asymptomatic 3 years later without evidence of chronic constrictive pericarditis.     

Adaptation to hypocaloric feeding: Physiologic significance of the fall in serum T3 as measured by the pulse wave arrival time (QKd)

We have investigated the physiologic significance of the decline in serum triiodothyronine (T₃) occurring during hypocaloric feeding by measurement of changes in cardiovascular function. The QKd interval, the interval between the Q wave of the electrocardiogram and the onset of Korotkoff sounds at diastolic pressure at the brachial artery, is the sum of the preejection period and pulsetransmission time, and has proven to be a sensitive and effective measure of the effect of thyroid hormones on the cardiovascular system. Fifteen euthyroid obese volunteers underwent successive 2 wk periods of hypocaloric feeding (200–400 calories per day) interspersed with periods of at least 2 wk of re-feeding on a weight-maintaining diet (1500 calories). In a later phase subjects received oral supplementation of triiodothyronine (T₃) in addition to the diet to prevent the fall in serum T₃. In the last study phase, subjects on the diet received supplementation with oral thyroxine (T₄), which prevented the fall in serum T₃ and resulted in a slight increase in serum T₄. During the first 2 wk period of hypocaloric feeding, there was a statistically significant increase in QKd, and a decrease in pulse rate, compatible with a hypothyroid state relative to initial measurements. When oral T₃ supplementation was given, the rise in QKd and fall in pulse rate were prevented. Likewise, with oral T₄ supplementation, the changes in QKd and pulse were prevented. Thus, the fall in serum T₃ occurring during hypocaloric feeding is associated with changes in the cardiovascular system which are qualitatively similar to those observed during hypothyroidism. The present data, taken with other data in the literature, suggest that the decline in serum T₃ during hypocaloric feeding may be an adaptive mechanism to conserve energy during caloric deprivation.     

Isometric effects on treadmill exercise response in healthy young men

This study evaluated the hypothesis that the isometric stress of load carrying augments the dynamic exercise response seen on the treadmill, and estimated the magnitude of this effect on heart rate and blood pressure for several methods of carrying the same load. Thirteen healthy subjects carried 40 lb in the right hand (H), 40 lb on the back (B), 20 lb in each hand (D) and no weight (N) while walking for 3 minutes on the treadmill at a grade of 0 at 1.7 miles/ hour. A statistically significant increase in the rate of rise and peak levels of systolic blood pressure, heart rate, estimated mean blood pressure, the product of estimated mean blood pressure and heart rate and systolic blood pressure-heart rate product was shown when task H was compared with tasks B, D and N. Values for tasks D and B did not differ significantly.The effects of isometric and dynamic exercise combined were greater than those of dynamic exercise alone. An effective technique of load distribution reduced the rate of increase in blood pressure, heart rate and the peak attained during dynamic exercise, thereby suggesting a lower level of myocardial oxygen consumption for a given weight-carrying task. These results can be applied to evaluation of patients with heart disease and estimation of their exercise tolerance.     

Critical analysis of clinical factors in estimating severity of aortic valve disease

Clinical data were analyzed in a group of 79 patients with aortic stenosis or combined aortic stenosis and insufficiency by the usual methods and by discriminant function analysis. It was possible to predict the level of aortic-left ventricular gradient (above or below 50 mm Hg) from signs and symptoms in approximately 83 percent of patients. The analyses performed yielded insight into the significance of the various commonly presenting symptoms in these lesions. For example, the slope of the carotid upstroke, calcium in the valve, T wave inversion and a large thrusting left ventricular impulse all indicated a high peak gradient, whereas syncope did not contribute to the separation of values. Heart failure made an insignificant contribution to prediction of the level of gradient.     

Early risks of open heart surgery for mitral valve disease.

During 1972 and 1973, a total of 235 patients had open heart surgery for mitral valve disease unassociated with significant aortic or rheumatic tricuspid valve disease. Thirty-one underwent closed heart mitral commissurotomy, without mortality. Of the 204 patients undergoing open operation, 125 had sequential measurement of cardiac output and mixed venous oxygen pressure. The hospital mortality rate was 6.4 percent in the larger group of 204 patients and in the 125 with cardiac output measurements. The rate was greater in those with class IV disability (New York Heart Association criteria) preoperatively than in those with class III or II disability. The mean +/- standard deviation of the average cardiac index early postoperatively was 2.05 +/- 0.579 liters-min--1-m--2. Cardiac index was lower in the patients who died early postoperatively than in those who did not. The probability of hospital death was a significant function of cardiac index. The predicted probability of death was 10 percent with an average cardiac index of 1.42 liters-min--1-m--2 and increased sharply with lower indexes. Cardiac index was lower early postoperatively than preoperatively, and was lower in patients in class IV than in those in class III. There was no significant difference in cardiac index between patients with mitral valve replacement and those in repair. A history of closed commissurotomy, age, duration of cardiopulmonary bypass, duration of cardiac ischemia and method of myocardial preservation did not significantly influence cardiac index or hospital mortality rate. There was no significant relation between mixed venous oxygen pressure and hospital death. Further improvement in results of mitral valve surgery requires adequate preservation of left ventricular performance before, during and after operation.     

Myocardial infarction after exercise-induced electrocardiographic changes in a patient with variant angina pectoris

The electrocardiographic response to stress testing varies considerably in patients with variant angina pectoris: no change in the S-T segment as well as S-T segment depression and elevation have been observed. This report describes a patient with a resting ST-T abnormality that reverted to normal appearance with exercise. However, the patient experienced severe chest pain shortly after discontinuing exercise testing, and an electrocardiogram showed evidence of acute anterolateral infarction. The possible implications of such electrocardiographic changes are discussed.     

Effects of factors predisposing to atherosclerosis on formation of coronary collateral vessels

Two hundred eighteen consecutive patients undergoing selective coronary angiography were studied to determine the effects of underlying predisposing coronary risk factors on the formation of intercoronary collateral anastomoses. The presence or absence of hyperlipoproteinemia, diabetes mellitus, glucose intolerance, hypertension or obesity did not influence the formation of these intercoronary collateral channels. Our findings suggest that there are presently no measurable clinical factors that permit prediction of the presence of coronary collateral channels in an individual patient. Factors predisposing to atherosclerosis have a similar distribution in patients with and without such vessels.     

Hyperkinetic heart in severe hypertension: A separate clinical hemodynamic entity

A long-term study of established hypertension helped identify a well defined group of 10 patients who differed both clinically and hemodynamically from 59 patients with the more frequent form of this disease. Their cardiac output was significantly increased (P < 3.001) despite a severe elevation of arterial pressure (average $\text{212}\text{125}\text{mm Hg}\text{±}\text{13.5}\text{7.3}$ [standard error]). All had labile hypertension of long standing (16.2 years average) that was difficult to control and always symptomatic; in all, the diagnosis of pheochromocytoma had to be specifically excluded. Increased myocardial contractility was suggested by (1) significant elevation of the rate of rise of isovolumic pressure (P < 0.001), and (2) high ratio of cardiac output to cardiopulmonary volume (P < 0.005). Beta adrenergic blockade with propranolol helped to alleviate symptoms and to control tachycardia but failed by itself to reduce arterial pressure.     

Idiopathic orthostatic hypotension: circulatory dynamics in chronic autonomic insufficiency

Idiopathic orthostatic hypotension offers a unique opportunity to study the effect of chronic autonomic insufficiency on circulatory dynamics in man. Evidence of abnormal cardiac performance was found in eight patients with idiopathic orthostatic hypotension secondary to efferent adrenergic dysfunction. Compared with normal subjects these patients had a lower cardiac output (2.37 liters/min per m², P < 0.001), faster heart rate (83 beats/min, P < 0.001), smaller stroke volume (30 ml/ m², P < 0.001) and slower rate of left ventricular ejection (107 ml/sec per m², P < 0.001). Intravascular volume was also reduced (90 percent of normal), (P < 0.01), but this reduction could not by itself account for the marked decrease in cardiac output (75 percent of normal) since there was no correlation between the two variables (r ? 0.269, not significant). The ratio of stroke volume to cardiopulmonary volume was reduced (P < 0.025), thus suggesting that impaired myocardial contractility might be partly responsible for the defective cardiac performance. Although failure of peripheral resistance is the basic mechanism in idiopathic orthostatic hypotension, our results indicate that impaired cardiac function possibly related to cardiac denervation may also contribute to the poor circulatory adjustments in this disease.     

Quantitative evaluation of cineaortography in the assessment of aortic regurgitation

Cineaortography, quantitative biplane left ventricular angiocardiography and Fick cardiac output studies were performed in 69 patients with aortic regurgitation to evaluate the usefulness of the aortogram in quantitating regurgitation. Thirteen patients had coexistent aortic stenosis and 12 had coexistent mitral stenosis. Patients with concomitant mitral regurgitation were excluded because their aortic regurgitant flow cannot be separately quantified with biplane ventriculography. Twenty-eight other patients without valvular regurgitation were also studied to assess further the accuracy of the quantitative ventriculography, and the stroke volumes derived from Fick and angiographic methods were found to correlate well (r = 0.97). Aortic regurgitation in the 69 patients, graded on a 1 to 5 scale from the aortogram, correlated significantly with the percent and volume of regurgitation (r = 0.56 and 0.65, P < 0.01), respectively). However, there was a wide range in amount of regurgitant flow within the aortographic grades, especially in grades 4 and 5, and there was considerable overlap between the grades. The degree of aortic regurgitation was more commonly overestimated than underestimated from the aortogram, but the correlation tended to be better in the patients with a large end-diastolic volume and normal ejection fraction and without aortic or mitral stenosis.     

Distinctive time course of ventricular vulnerability to fibrillation during and after release of coronary ligation

Release of left anterior descending coronary artery ligature was performed in 32 dogs after periods of ligation ranging from 3 to 45 minutes. Spontaneous ventricular tachycardia or fibrillation occurred during occlusion in 9 of 20 dogs, developing during the first 8 minutes of occlusion in 8 of the 9. Ventricular tachycardia or fibrillation was evoked by release of occlusion in 3 of 7 dogs after a short-term occlusion of 3 to 6 minutes, and in 9 of 13 dogs after release of a long-term occlusion of 15 to 45 minutes. Thresholds for induced ventricular tachycardia or fibrillation were obtained using a train of gated stimuli (100 Hz for 250 msec). During short-term occlusions, average thresholds for ventricular tachycardia or fibrillation were reduced from 32.4 ma (control) to 3.4 ma (P < 0.001); during long-term occlusions, thresholds returned to normal (control 29.6 ma, occlusion 18.6 ma; difference not significant). Immediately after release of both short- and long-term occlusions, thresholds were not significantly different from control values. No correlation was found between mechanical and electrical abnormalities during the release phase since the magnitude of tension prolongation after release of both short- and long-term ligations was the same and thus did not correspond with the electrical differences of these states.Our data suggest the following conclusions: (1) The time course of spontaneous ventricular vulnerability to fibrillation during coronary occlusion differs from that of ligature release, the former diminishing and the latter increasing with the duration of occlusion. (2) This observation and the lack of correlation between thresholds of induced ventricular tachycardia or fibrillation and spontaneous vulnerability to fibrillation after ligature release suggest different electrophysiologic mechanisms for ventricular tachyarrhythmias during and after release of coronary ligation.     

Clotted hemopericardium with the hemodynamic characteristics of constrictive pericarditis

Cardiac catheterization in a patient 4 weeks after coronary arterial bypass surgery demonstrated the typical hemodynamic findings of constrictive pericarditis, which completely resolved after removal of 500 ml of clotted pericardial blood. The pericardium was not responsible for the findings because it was left in place. This case demonstrates that clotted hemopericardium may mimic constrictive pericarditis.     

Comprehensive treatment plan for the prevention of primary ventricular fibrillation in acute myocardial infarction

This report of 1,165 cases of acute myocardial infarction outlines a method for preventing primary ventricular fibrillation In patients with this lesion. The plan of prevention begins in the emergency room, with every patient suspected of having myocardial Infarction receiving an intravenous bolus injection of lidocaine, 75 mg, followed by a 2 mg/min infusion controlled by an infusion pump. If administration of lidocaine is ineffective (19 percent of cases), procainamide is given intravenously in a dose of 100 mg every 5 minutes, repeated as necessary to a maximum of 1 g and followed by an infusion of 2 to 6 mg/min. Ventricular tachycardia is rapidly converted to sinus rhythm by either drug or electrical therapy. Monitoring by telemetry is continued after the patient's discharge from the coronary care unit. A new episode of sustained chest pain requires the reinstitution of prophylactic lidocaine therapy. Important precautions to control the toxic effects of these intravenous medications can be achieved in the community hospital where the nursing staff makes the decision to increase the dose of lidocaine or to substitute procainamide. There has been no recognized mortality from the use of these drugs as outlined. With this total system of care, the prevalence rate of primary ventricular fibrillation has been decreased from 6.5 percent (9 of 139 cases) to 0.3 percent (3 of 1,026 cases) and no deaths have occurred.     

Development of "subaortic stenosis" after pulmonary arterial banding for common ventricle

Progressive narrowing of the bulboventricular foramen is documented in four patients with single ventricle. The morphologic features in each case corresponded to single left ventricle with infundibular chamber. Two patients had a D-ventricular loop and the other two an L-loop. All four patients had transposition of the great arteries. Restriction of the bulboventricular foramen thus resulted in functional subaortic stenosis because the aorta originated above the infundibular chamber. The development of subaortic obstruction was documented by serial cardiac catheterization studies in two infants, one of whom underwent unsuccessful surgical enlargement of the bulboventricular foramen. In the other two patients the initial cardiac catheterization revealed no pressure gradient between the ventricle and aorta, but examination at necropsy revealed very severe obstruction at the bulboventricular foramen, thus suggesting that the obstruction had been acquired. In each patient, the progressive narrowing of the bulboventricular foramen occurred after pulmonary arterial banding and may have been causally related to this procedure. This functional subaortic obstruction developed in 4 of 31 patients (12.9 percent) with single left ventricle, transposition of the great arteries and pulmonary arterial banding. Clinical recognition of this development is predicated on (1) awareness that narrowing of the bulboventricular foramen in patients with single ventricle and pulmonary arterial banding may be common; (2) presence of symptoms such as angina; and (3) lack of continued clinical improvement in a patient whose pulmonary arterial band has significantly reduced pulmonary blood flow. Management of this subaortic stenosis requires surgical intervention. In the infant, a ventriculotomy in the outlet chamber will usually provide excellent exposure of the bulboventricular foramen, and surgical enlargement can be accomplished. In the older child with severe obstruction, marked muscle hypertrophy may obliterate the ventricular cavity, making ventricular partitioning difficult if not impossible.     

External measurement and mapping of myocardial isotope after coronary venous 85 Krypton and 133 Xenon injections

A retrograde coronary venous injection technique for concentrating diffusible radioisotope in ischemic myocardial regions was evaluated. ⁸⁵Krypton in saline solution was injected under pressure into the coronary veins during partial closure of the coronary sinus. In the presence of coronary inflow obstruction, the venous ⁸⁵krypton was distributed mainly to the vessels with reduced pressure in ischemic regions. ⁸⁵Krypton washout was monitored with a single precordial collimator, and reasonably accurate measurements of flow in the ischemic regions were made. In two dogs, photoscanning techniques, using ¹³³xenon, were applied to locate and determine the size of the ischemic myocardial regions as radioisotopic hot spots.     

Aneurysm of the atrial septum in tricuspid atresia: Diagnosis during life and therapy

Massive aneurysmal dilatation of the foramen ovale was diagnosed angiocardiographically in a patient with tricuspid atresia. The angiographic findings are distinct for this condition, and the pathogenesis appears to be related to a restrictive atrial communication in the patient with obligatory right to left shunting at atrial level. The anatomic potential for atrial restriction in the patient with tricuspid or pulmonary atresia, intact ventricular septum and diminutive right ventricle necessitates balloon atrial septostomy at the initial diagnostic cardiac catheterization. In the patient with aneurysmal dilatation of the foramen ovale, satisfactory decompression may be achieved by Blalock-Hanlon atrial septectomy, open atrial septectomy or, possibly, balloon septostomy.