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The clinical data (signs and symptoms, x-ray and electrocardiographic analysis) and hemodynamic findings in 10 patients with severe mitral and aortic stenosis have been presented. All patients had signs, symptoms, and radiologic stigmata of mitral stenosis. Normal sinus rhythm was present in 7 of the 10 patients, and right ventricular hypertrophy in only 3. Many of the features usually considered to be a sine qua non of severe aortic stenosis were absent in these cases. However, all patients had at least one manifestation other than the typical murmur of aortic stenosis (e.g., angina, syncope, abnormal carotid pulse, left ventricular enlargement by x-ray or ECG examination, calcification of the aortic valve, or dilatation of the aortic root). All patients with ECG evidence of left ventricular hypertrophy also had angina pectoris and significantly elevated timetension indices. This was due largely to a prolongation of the systolic ejection period. It is suggested that ECG evidence of left ventricular hypertrophy in this clinical setting, without significant mitral or aortic regurgitation, signifies severe left ventricular stress and severe aortic stenosis. A decrease in cardiac output secondary to mitral stenosis reduces the differences in pressure across the aortic valve and, there-fore, reduces the total left ventricular stress, as reflected by the time-tension index. It is believed that this reduction in output is the basic cause of inconstancy of symptoms and signs of aortic stenosis in patients with tight mitral and aortic stenosis. When aortic stenosis is suspected in patients with severe mitral stenosis, the only certain method of quantitative evaluation is catheterization of the left side of the heart, with simultaneous measurement of transvalvular pressure differences and blood flow.

1. 1. Twenty-one patients with mitral stenosis have been studied by the technique of cardiac catheterization. These patients were classified clinically and also according to the size of the orifice of the mitral valve. Six patients were in pulmonary edema during the study. 2. 2. As a consequence of mitral valvular stenosis, a balance develops between pulmonary vascular pressures and peripheral blood flow (tending toward an increase in pulmonary pressure and a decrease in blood flow). 3. 3. Cardiac and stroke indices were decreased at rest, although a wide range of values was seen. Patients with auricular fibrillation had slightly lower cardiac indices than patients with normal sinus rhythm. Tissue oxygen extraction per cubic centimeter of blood was increased so that oxygen consumption was maintained within the normal range in all. 4. 4. Pulmonary “capillary” pressures were increased above normal as a result of the increase in left atrial pressure proximal to the mitral stenosis. 5. 5. Pulmonary arterial pressures were increased above normal as a result of (a) the increase in pulmonary “capillary” pressure and (b) increased pulmonary arteriolar resistance. 6. 6. The presence of an elevated pulmonary arteriolar resistance was roughly related to the level of pulmonary “capillary” pressure and the degree of valvular stenosis. 7. 7. An inverse logarithmic relationship was observed between total pulmonary resistance and stroke output per square meter. 8. 8. As a result of the increased pulmonary vascular pressures, the pressure work of the right ventricle was greatly increased. 9. 9. Right ventricular incompetency, as judged by an elevated filling pressure, was seen in over one-half of the patients studied. Incompetence was believed due to (a) the increased pulmonary pressure load and (b) underlying myocardial damage from rheumatic fever.

1. 1. Nineteen patients with severe aortic stenosis have been studied by left heart catheterization before and after transaortic valvuloplasty. 2. 2. The cardiac index was normal in patients with pure aortic stenosis but tended to be reduced in the presence of associated aortic regurgitation, mitral or coronary disease. 3. 3. Severe aortic stenosis, as it progresses, may become associated with a reduced cardiac output and, therefore, a small systolic mean pressure difference across the aortic valve. 4. 4. There was a small but significant postoperative increase in calculated aortic valve area in 11 patients, associated with a marked fall of left ventricular systolic pressure, transvalvular pressure difference, and left ventricular work, while cardiac output remained unchanged. A residual pressure difference across the aortic valve persisted in all but one patient, who developed severe regurgitation. 5. 5. Eight patients showed no change in valve area. The left ventricular systolic pressure and transvalvular pressure difference in these was also decreased postoperatively, but this was found to be the result of reduced cardiac output. 6. 6. Associated mitral stenosis, mitral regurgitation, or coronary disease did not preclude successful surgery for aortic stenosis. 7. 7. Six of the 8 operative failures occurred among 7 patients with clinically “insignificant” preoperative aortic regurgitation as the only complicating lesion. Operation in this group either did not relieve the stenosis or increased the regurgitation in proportion to the relief of stenosis so that measurable benefit was not observed. 8. 8. The meaning of the term “insignificant” as it pertains to pure aortic regurgitation and to regurgitation associated with severe aortic stenosis is discussed. 9. 9. Indications and contraindications for surgery for aortic stenosis are discussed.

Abnormalities in the pulmonary angiograms of 52 patients were correlated with the clinical diagnoses in order to determine which angiographic signs are diagnostic of acute pulmonary embolism and which are abnormal but possibly related to other diseases affecting the pulmonary vasculature. Angiographic abnormalities were divided into two groups: those of major or morphologic significance, and those of lesser or physiologic significance. The signs of morphologic significance are intraluminal filling defects, cutoffs, and pruning. These major signs directly indicate arterial occlusion. The signs of physiologic significance are oligemia, asymmetrical filling, prolongation of the arterial phase, and bilateral lowerzone filling delay. These lesser signs indicate disturbance of flow. In an otherwise normal lung, they are highly suggestive of pulmonary embolism. In the presence of coexistent diseases that affect the pulmonary vasculature, correlations in this study show that only the signs of morphologic significance are reliable for the diagnosis of acute pulmonary embolism. In otherwise healthy patients, 95 per cent (20 of 21) who clinically had pulmonary embolism had one or more of the major or lesser angiographic abnormalities. In the entire group who clinically had pulmonary embolism (including patients with coexisting diseases that affect the pulmonary vasculature), 83 per cent (24 of 29) of the patients had one or more of the major or lesser angiographic abnormalities. However, 7 patients with nonembolic pulmonary vascular disease had lesser angiographic abnormalities (disturbance of flow). Utilization of the major signs alone reduced the number of positive angiographic interpretations to 79 per cent (23 of 29) in patients who clinically had pulmonary embolism, but eliminated all false-positive interpretations. Accuracy in making the diagnosis of acute pulmonary embolism by pulmonary angiography is enhanced by proper evaluation of the angiographic abnormalities of morphologic and physiologic significance as described in this study.

A previous communication 1 was concerned with the electrical phenomena within the right atrium. Coincidentally with that study, observations were made of the potential variations within the right ventricle. The general technique employed has been described in the earlier publication and will be amplified somewhat in this paper. All studies of the potentials within the normal right ventricle have revealed an R wave as the first deflection of the ventricular complex. Hecht 2 described this as diminutive, but others have noted that it may attain considerable size. The presence of this R wave has been regarded uniformly as corroborative evidence that activation of the left side of the interventricular septum normally precedes activation of the right side. This asynchronism may be regarded as a kind of physiologic, incomplete right bundle branch block of minor grade. In left bundle branch block, 3,4 because septal activation proceeds form the right to the left side of the septum, this initial R wave is lost; and the ventricular complex in the right ventricle begins with an S wave. By the same token, the R wave is unusually prominent in right bundle branch block. Because the electrode has the twofold effect of functioning as both a recording and, by virtue of its mere contact, as a stimulating electrode, two other phenomena have been observed consistently: a tendency to premature ventricular beats or short runs of ventricular tachycardia and the induction of monophasic ventricular action currents. The former, from their appearance in the conventional leads, have been shown to correspond to our present conception of right ventricular premature beats. The latter have been found to disappear when the catheter is withdrawn slightly from its contact with the ventricular wall.

Pulmonary angiography is the most specific test available for the diagnosis of acute pulmonary embolism. This technique can safely be performed in critically ill patients. In 367 consecutive studies our incidence of complications has been 4 per cent, and there has been only one death. Hemodynamic studies done as part of the procedure permit evaluation of the severity and the pathophysiology of acute pulmonary embolism. The two diagnostic angiographic findings of pulmonary embolism are intraluminal filling defects and cutoff arteries. Oligemia and asymmetry of blood flow are frequently seen in pulmonary embolism, but are not specific. These latter two abnormalities may occur in chronic lung disease or congestive heart failure without pulmonary embolism. Using these diagnostic criteria in 247 patients studied because of a clinical diagnosis of acute pulmonary embolism, a definitive diagnosis (either definite pulmonary embolism or negative) was established by angiography in 74 per cent. In 9 per cent the diagnosis was probable pulmonary embolism, and in 17 per cent the findings were equivocal for pulmonary embolism. Application of these diagnostic criteria results in minimal false posiive angiographic diagnoses. False negative diagnoses may occur if embolism is limited to peripheral branches of the pulmonary vasculature that are not visualized by current angiographic techniques. The incidence of symptomatic pulmonary embolism limited to these small arteries is uncertain. The primary limitation of this technique is, that in patients with underlying heart disease or chronic lung disease, the results of angiography may be equivocal. The application of new techniques of magnification angiography and/or selective cineangiography offer promise in enhancing the recognition of embolism in this group of patients.

1. 1. Pulmonary edema occurred at rest in six patients and during exercise in three other patients with severe mitral stenosis during cardiac catheterization. 2. 2. Pulmonary “capillary” pressure was 32 mm. Hg or higher in all nine patients. 3. 3. Pulmonary “capillary” pressure, actually an index of left atrial pressure, was elevated to such high levels in order to maintain blood flow through the mitral valve. 4. 4. Factors which resulted in an increased mitral valve flow rate, thus requiring an elevation in pulmonary “capillary” pressure, were (a) increased cardiac output and (b) decreased diastolic filling period. The latter was decreased by increases in (1) heart rate and (2) duration of ventricular systole. 5. 5. The degree of anatomic mitral stenosis affected the degree of pulmonary “capillary” pressure rise in exponential fashion. 6. 6. The mechanism of elevation of pulmonary “capillary” pressure was believed to be a momentary imbalance in ventricular outputs such that pulmonary blood volume and pressure were increased. 7. 7. It has been demonstrated that in patients with mitral stenosis, a normal cardiac output can be delivered only at the expense of high pulmonary “capillary” pressure. 8. 8. The role of tachycardia, even of a mild degree, in producing or aggravating symptoms of pulmonary edema is emphasized.

1. 1. The methods of catheterization of the heart and the pulmonary vessels make it practical, for the first time, to investigate the pressure and flow phenomena in the right side of the heart and in the pulmonary vascular system of patients with constrictive pericarditis. Six such patients have been studied by these methods. 2. 2. Every patient showed an elevation of pulmonary “capillary” pressure (which reflects pulmonary venous pressure). This demonstration of pulmonary congestion is interpreted as indicating that involvement of the left ventricle plays a more important and sinister role in the functional changes associated with pericardial constriction than has been demonstrated previously. 3. 3. Every patient also showed an elevation of pressure in peripheral veins and in right atrium, and pressure measurements in the right ventricle and pulmonary artery which indicate a reduced ability of the right ventricle to contribute to the forward movement of blood. These observations confirm and emphasize the previously recognized involvement of the right ventricle. 4. 4. In every patient before operation the mean pulmonary capillary pressure was approximately equal to the peripheral venous pressure. 5. 5. No patient exhibited pressure changes pointing to physiologically significant obstruction in great veins or auricles. 6. 6. The limitation of stroke volume and cardiac output per minute in constrictive pericarditis previously demonstrated by other methods is confirmed by these studies. 7. 7. Consideration of the course of events after operation suggests that myocardial atrophy, myocardial fibrosis, and incomplete release of the ventricles may all play a role in the slow, and in most cases, incomplete return to normal dynamics after operation. 8. 8. The specific therapeutic implications of this study are: (A) the objective of surgery is the adequate release of both ventricles; (B) no indications have been found for the decortication of great veins or auricles, and (C) the early use of antibiotics in acute tuberculous pericarditis may minimize myocardial fibrosis and may permit operative treatment before myocardial atrophy is severe. 9. 9. Finally, the fact that improvement after operation is often slow and often incomplete in terms of objective measurement should not lead physicians to ignore the more important fact that a well-planned operation for constrictive pericarditis has in the past usually made the difference between invalidism and activity. The studies reported in this paper may be expected to make future operations for this disorder even more effective.

1.1. The area of the mitral valve and the degree of pulmonary vascular disease have been calculated from physiological data in thirty patients with pure mitral stenosis without evidence of active rheumatic carditis. 2.2. From a hydraulic point of view, a valve area of 1.0 cm. 2 , one-quarter to one-sixth normal, appears to be a critical one, for at that level of stenosis the pressure head needed to maintain a normal cardiac output approaches the plasma osmotic pressure. 3.3. Probably from the stimulus of an increased pulmonary "capillary" pressure, a variable degree of vascular obstruction develops in patients when the mitral valve area becomes reduced to about 1.0 cm. 2 or smaller. This results in a lower cardiac output, which may protect the capillary bed from sudden increases in pressure. 4.4. The clinical picture in mitral stenosis can be explained in a large measure by the interplay of the degree of stenosis with the degree of pulmonary vascular obstruction. 5.5. The combination of a narrow valve with only a slight increase in pulmonary arteriolar resistance is associated with predominantly respiratory symptoms, exertional dyspnea, hemoptysis, and paroxysmal nocturnal dyspnea, the right ventricle not becoming dilated. 6.6. The effect of a narrow valve and a high pulmonary arteriolar resistance appears to be additive in causing electrocardiographic evidence of right ventricular hypertrophy and roentgenographic signs of cardiac enlargement. 7.7. The combination of a narrow valve and great increases in pulmonary arteriolar resistance is associated with severe dyspnea, cardiac enlargement, and signs of right ventricular failure. 8.8. Most patients with mitral stenosis can be divided into four general categories by their signs, symptoms, and physiological adjustments.

1. 1. Eight patients with mitral stenosis have been studied at rest and during exercise by the technique of cardiac catheterization. Three of the patients developed pulmonary edema on exercise. 2. 2. The resting balance between pulmonary pressure and peripheral blood flow was upset by exercise. The imbalance was related not only to the degree of stenosis but to the ability of the circulation to increase the cardiac output. 3. 3. Except for two patients with mild mitral stenosis, cardiac index failed to rise in normal fashion on exercise. Stroke index on the average did not change with exercise, although both increased and decreased stroke outputs were seen, depending on the pulse rate and diastolic filling period. Tissue oxygen extraction per cubic centimeter increased markedly on exercise. 4. 4. Pulmonary “capillary” pressure rose on exercise in association with increases in rate of mitral valvular blood flow. 5. 5. Pulmonary arterial pressure rose on exercise in association with the increase in pulmonary “capillary” pressure and in some cases with the increase in blood velocity flow. 6. 6. Pulmonary arteriolar resistance showed no consistent change on exercise, the average values at rest and during exercise being almost identical. 7. 7. Right ventricular work against pressure, already elevated at rest in most of the patients, became even greater on exercise. 8. 8. Almost all patients had elevated right atrial mean pressures at rest. Further rises occurred in two of the four in whom right atrial pressure was measured on exercise.

1.1. The prominence of the pulmonary arterial segment on the posteroanterior chest x-ray in a group of 56 patients with mitral stenosis was assessed by calculation of the "PA/chest ratio." The distance from the midline, as defined by the vertebral spines, to the left-most point of the pulmonary arterial segment on the cardiac silhouette is measured and divided by one half of the transthoracic diameter, as suggested by Ozawa. 6 2.2. A positive correlation between the "PA/chest ratio" and pulmonary arterial mean pressure was found. The correlation was exponential in character, resembling the shape of the pressure-volume curve. 3.3. The correlation between PA/chest ratio and pulmonary arterial mean pressure is poor in patients with left-to-right shunts and increased pulmonary blood flow. 4.4. In patients with mitral stenosis, in whom pulmonary blood flow varies over a relatively narrow range, the PA/chest ratio is a useful guide to the presence or absence of pulmonary vascular disease, facilitating preoperative evaluation of these patients without cardiac catheterization.

Infection upon ball valve prostheses is a significant cause of death, especially in the early postoperative period. Such infection may occur in the late postoperative period, in which case it almost always is associated with infection elsewhere in the body, or follows unrelated surgical procedures or other predisposing events. Staphylococcus is the most frequent cause of this form of bacterial endocarditis. The diagnosis is often disregarded because bacterial endocarditis has nonspecific manifestations early in the disease. Bacterial endocarditis can be virtually eliminated with 10 days or more of methicillin and oxacillin prophylasis .