Postcommissurotomy Syndrome Research Articles

The Postcardiac Injury Syndrome: Case Report and Review of the Literature

The postcardiac injury syndrome (PCIS) includes the postmyocardial infarction syndrome, the postcommissurotomy syndrome, and the postpericardiotomy syndrome. Dressler reported a series of patients who developed a pericarditis-like illness days to weeks after a myocardial infarction. Postcardiac injury syndrome also has been observed after cardiac surgery, percutaneous intervention, pacemaker implantation, and radiofrequency ablation. Postcardiac injury syndrome is characterized by pleuritic chest pain, low-grade fever, an abnormal chest x-ray, and the presence of exudative pericardial and/or pleural effusions. The pathophysiology of PCIS involves auto-antibodies that target antigens exposed after damage to cardiac tissue. The treatment of PCIS includes the use of nonsteroidal anti-inflammatory drugs and corticosteroids. Prophylactic use of corticosteroids before cardiac surgery has not been effective in preventing PCIS. The widespread use of reperfusion therapy and cardiac medications with anti-inflammatory properties may have reduced the incidence of PCIS. Although PCIS can follow a relapsing course, it does carry a favorable prognosis.

Atrial natriuretic peptide and vasopressin during percutaneous transvenous mitral valvuloplasty and relation to renin-angiotensin-aldosterone system and renal function

To study the relation between plasma atrial natriuretic peptide (ANP) and cardiac pressure, and to assess the pathophysiologic significance of ANP in water and electrolyte metabolism, the changes in plasma levels of ANP and arginine vasopressin (AVP) were examined in 11 patients with mitral stenosis who underwent percutaneous transvenous mitral valvuloplasty, and compared with the changes in the renin-angiotensin-aldosterone system and renal function. Immediately after valvuloplasty, plasma ANP levels decreased significantly with a concomitant decrease in mean pressures in the left atrium, the pulmonary artery and the right atrium. Plasma ANP levels decreased to the normal range in 4 of the 6 patients with normal sinus rhythm, while all 5 patients with atrial fibrillation had higher levels despite a similar degree of decrease in atrial pressure. There were significant positive correlations between plasma ANP levels and the mean left atrial pressure (r = 0.61, p < 0.01), the mean pulmonary arterial pressure (r = 0.49, p < 0.01) and the mean right atrial pressure (r = 0.54, p < 0.01). The mean plasma AVP levels, on the other hand, showed a transient increase after valvuloplasty from 0.5 ± 0.1 to 1.2 ± 0.4 pg/ml (p < 0.05). The mean plasma renin activity (1.3 ± 0.3 vs 2.7 ± 0.8 ng/ml/hr, p < 0.05) and plasma aldosterone concentration (8.6 ± 2.3 vs 17.2 ± 5.2 ng/dl, p < 0.05) also increased significantly 30 minutes a fter valvuloplasty. Further, a significant decrease in glomerular filtration rate (89 ± 7 vs 65 ± 5 ml/min, p < 0.01), renal plasma flow (435 ± 58 vs 305 ± 33 ml/min, p < 0.01), urine flow (2.3 ± 0.5 vs 1.0 ± 0.2 ml/min, p < 0.01) and urinary sodium excretion (162 ± 43 vs 73 ± 13 μmol/min, p < 0.05) was observed 30 minutes after valvuloplasty. These results suggest that (1) the cardiac atrium quickly responds to a reduction in atrial pressure to change its own ANP secretion, which directly or indirectly regulates water and sodium metabolism; (2) in addition to increased atrial pressure, bnormal atrial contraction per se stimulates ANP secretion; and (3) excessive AVP secretion leading to the postcommissurotomy syndrome is not linked to an abrupt reduction in atrial pressure itself.

The postcommissurotomy (postpericardiotomy) syndrome ∗

The term “postcommissurotomy” syndrome should be discarded and permanently replaced with the more accurate description, “postpericardiotomy” syndrome. The clinical expression of this entity appears to be identical with the various forms of traumatic pericarditis reported in the past. The postpericardiotomy syndrome is described in 10 to 40 per cent of patients following commissurotomy for acquired valvular stenosis, and in 30 per cent of 100 consecutive survivors following open heart surgery for repair of atrial and ventricular septal defects and the relief of pulmonic and aortic stenosis. The clinical picture is one of recurrent fever and retrosternal pain described as dull or, more commonly, knifelike or stabbing, and in most patients a pericardial friction rub. The electrocardiogram often suggests pericardial changes that may disappear during periods of remission. They may also persist for weeks following resolution of the syndrome. The cardiac silhouette on x-ray examination is generally enlarged. The postpericardiotomy syndrome is a benign illness with an excellent prognosis. Therapy, for the most part, is supportive although in certain instances corticosteroids are used.

HYPERSENSITIVITY—A COMMON DENOMINATOR IN MYOCARDIAL DISEASE?

With increasing wonder, cardiologists suspect that knowledge of the fundamentals of allergy is desirable for the proper understanding of myocardial disease. Striking similarity in disease states characterized by pericarditis and myocarditis suggest a common pathogenesis. Rheumatic fever, idiopathic pericarditis, the postcommissurotomy syndrome (postpericardiotomy syndrome) and the postmyocardial infarction syndrome are acute or recurrent inflammatory diseases associated with polyserositis and pleural pericardial pain. It is quite possible that hypersensitivity is a contributory or even a basic mechanism in each instance. The immunological response is related to streptococcal antigens in rheumatic fever, to necrosis in the postmyocardial infarction syndrome, to surgical trauma in the postcommissurotomy syndrome, and to viral antigens in idiopathic pericarditis. Acute benign idiopathic pericarditis offers a particularly fruitful disease for the evaluation of immunological factors. Is idiopathic pericarditis a simple virus infection? There are ever increasing numbers of reports of pericarditis occurring in the acute phase of Coxsackie virus

The Nature and Management of the Post-Commissurotomy Syndrome

The Nature and Management of the Post-Commissurotomy Syndrome

Postpericardiotomy syndrome following penetrating stab wounds of the chest: Comparison with the postcommissurotomy syndrome

Two cases of penetrating stab wounds of the chest are described, complicated by pyrexia, pericarditis, and a tendency to relapse. The clinical picture is compared with that seen in the postcommissurotomy syndrome. Current views on the pathogenesis of the postcommissurotomy syndrome are discussed. The striking similarity of traumatic pericarditis to the postcommissurotomy syndrome as well as to the syndrome following surgery of nonrheumatic heart disease suggests acceptance of the more generic term “postpericardiotomy syndrome”.

Coincidence of patent ductus arteriosus and rheumatic heart disease, with a comment on the “postcommissurotomy syndrome”

Among a total of seventy-three patients operated upon for patent ductus arteriosus, thirtysix had adequate observation over a period of two to seven years following operation. Of the thirty-six patients, clinical evidence of rheumatic fever or a progressive valvular disease has developed in six. The study suggests a more frequent association between patent ductus arteriosus and rheumatic heart disease than has been previously suspected, and in some cases operation may have either precipitated or reactivated rheumatic fever. The possible significance of these findings in relation to the etiology of the “postcommissurotomy syndrome” is discussed. The suggestion is made that long term observation following operation for congenital heart defects should include special attention to the possibility of the occurrence of superimposed rheumatic fever.

Postoperative physiopathologic results in mitral stenosis

The physiopathologic results of mitral commissurotomy were studied at intervals of several months, one year, two years, and three years after the operation. Pericarditis occurred after the operation in 90 per cent of the cases; and postpericardiotomy syndrome (the so-called postcommissurotomy syndrome) in 12.5 per cent, with no correlation between this and the results of biopsy of the auricular appendage. The results of mitral commissurotomy were evaluated by preoperative and postoperative cardiac catheterization, phonocardiogram, electrocardiogram, vectorcardiogram, electrokymogram, ballistocardiogram, roentgenogram, pulmonary angiocardiogram, and pulmonary function tests. The physiopathologic data did not always correspond to the clinical results. Sometimes the clinical improvement was greatly superior to the results furnished by these tests. In this series of 200 patients, excellent or good clinical results were obtained in 67 to 70 per cent of the cases. There was a mortality of 6 per cent. Finally, some factors are present which condition the physiopathologic results of mitral commissurotomy: postoperative mitral insufficiency, valvular calcification, postoperative emboli, insufficiency of the myocardium, sub-valvular stenosis, insufficient commissurotomy, and recurrent rheumatic reactivation, which may cause rcstenosis.

The post-myocardial-infarction syndrome: a report on forty-four cases.

A complication of acute myocardial infarction, which mimics the postcommissurotomy syndrome and idiopathic pericarditis, has been described.1-3The clinical features are fever; chest pain; evidence of pericarditis, pleurisy, and pneumonitis, and a tendency to recurrences. Several reports have corroborated these observations.4-6The complication was previously often mistaken for recurrent myocardial or pulmonary infarction. After the preliminary report, a larger number of patients who presented the postmyocardial-infarction syndrome has been observed. One of the patients who was treated with anticoagulants in the presence of diffuse pleuropericarditis died of cardiac tamponade. It is the purpose of the present communication to report additional information obtained in the past two years and to stress the danger of anticoagulant therapy in the presence of the post-myocardialinfarction syndrome. Report of Cases Case 1. —A 62-year-old man who had diabetes was admitted to the Maimonides Hospital on Nov. 20, 1955. On the morning of

Postpericardiotomy syndrome following surgery for nonrheumatic heart disease.

Widespread intracardiac surgery of rheumatic heart disease has brought to medical attention a puzzling postoperative complication, usually designated the "postcommissurotomy syndrome" and often considered to represent reactivation of rheumatic fever. Herein are reported instances of an identical complication following intrapericardial surgery of congenital heart disease. It is suggested that the delayed febrile pleuropericardial reaction represents a traumatic pericarditis and that a preferable name for it is the postpericardiotomy syndrome.

Results of mitral commissurotomy; clinical status of two hundred patients five to eight years after operation.

The status of 200 patients who are living five or more years after mitral commissurotomy is reviewed. In each the original condition was mitral stenosis uncomplicated by any other significant valvular lesion. The data as to such symptoms as dyspnea and edema show that most of these survivors obtained significant relief, though some obtained no relief and a few experienced aggravation of their symptoms. Sixteen patients suffered from recurrent febrile episodes (postcommissurotomy syndrome) within a year after the surgery, and all of them recovered. Fourteen pregnancies occurred, and 12 ended in normal deliveries. Comparison of the cardiologic findings before and after operation showed that these findings do not always explain the symptomatic relief afforded by the operation. It is concluded that even a modest increase in the size of the mitral orifice often affects the dynamics of the heart sufficiently to improve the subjective status of the patient without necessarily affecting murmurs, cardiac size, or electrocardiographic patterns.

Immunologic evidence of group A streptococcal infection in patients undergoing mitral commissurotomy.

Serum levels of 3 group A streptococcal antibodies were determined in 53 patients prior to mitral commissurotomy and monthly for 3 to 6 months postoperatively. Significant elevation of antibody titers was relatively infrequent prior to commissurotomy and the presence of chronic productive inflammatory lesions in the biopsied atrial appendage was usually unrelated to recent streptococcal infection. The "postcommissurotomy syndrome" also occurred in some patients without evidence of such infection. Postoperative subclinical streptococcus infection occurred frequently enough, however, to suggest the need for vigorous preoperative penicillin therapy and careful postoperative prophylaxis.

Relation of the postcommissurotomy syndrome to the rheumatic state.

The postcommissurotomy syndrome is a frequent troublesome complication after mitral valve surgery, the etiology of which is still obscure. In this study of 137 patients who survived surgery the clinical features of this complication are carefully detailed, possible associated conditions are studied, and pathologic findings in the atrial appendages are analyzed. In particular, the relation of this syndrome to the rheumatic state is critically examined.

Is the postcommissurotomy syndrome of rheumatic origin?

Soon after mitral commissurotomy became a frequent procedure, a clinical syndrome characterized by the occurrence of recurrent febrile episodes associated with pleuritis, pericarditis, pneumonitis, and occasional joint pains was recognized. Janton1(1952) was the first to call attention to this syndrome, which he called pleuropericardial episodes. He considered it to be due to smoldering rheumatic activity, but found that direct evidence for this was lacking. In 1955 he wrote2that in 8 of 41 living patients, there had been repeated postoperative episodes certain to be regarded even without laboratory verification as rheumatic activation. Soloff3stated Because of the frequency of this syndrome following mitral commissurotomy and its absence following any other non-rheumatic cardiac or pulmonary surgery, and because of the frequent cardiac involvement, the syndrome should be regarded as reactivation of rheumatic fever. At first, most opinion was in agreement with that of Janton and of Soloff,

Pleuropericardial effusion following myocardial infarction

A case of bilateral pleural effusion with pericardial effusion of unknown cause occurring seven weeks after a myocardial infarction is reported. The similarity of the clinical and laboratory findings to those of the postcommissurotomy syndrome are noted. Possible causes for the effusions are discussed.

Postcardiotomy syndrome in patients with rheumatic heart disease: Cortisone as a prophylactic and therapeutic agent

1. 1. The syndrome herein referred to as the postcardiotomy syndrome in patients with rheumatic heart disease was observed in thirty-three (39 per cent) of eighty-four patients with rheumatic heart disease at variable intervals after mitral valvuloplasty. This complication is usually characterized by fever and chest pain of a pleuropericardial nature, occasionally accompanied by congestive heart failure, pleural effusion, polyarthritis, arrhythmia, abdominal pain, and subcutaneous nodules. 2. 2. This syndrome has been variously called “postcommissurotomy syndrome,” “reactivation of rheumatic fever following mitral commissurotomy,” and “postvalvulotomy syndrome.” The designation “postcardiotomy syndrome in patients with rheumatic heart disease” would seem to be preferable because the syndrome was observed in a patient in whom only cardiotomy was performed due to technical difficulties; it would seem, therefore, that mitral commissurotomy is not necessary for its development. 3. 3. Cortisone had a definite suppressive effect on the syndrome. The incidence of postcardiotomy syndrome was 31 per cent in patients not receiving prophylactic cortisone and 7 per cent in the patients in the group receiving hormone prophylaxis. The immediate postoperative course of patients who received prophylactic cortisone was less stormy than that of those who did not. As a therapeutic agent, cortisone was superior to salicylates, pyramidon and antibiotics which did not favorably affect the clinical manifestations of the postcardiotomy syndrome. Cortisone in doses varying from 50 to 300 mg. daily, depending upon the person, caused a dramatic remission of symptoms and fever in the post-cardiotomy syndrome. 4. 4. It is recommended that ACTH be given prophylactically for two days preoperatively and for eight to ten days postoperatively in patients undergoing rheumatic mitral valvuloplasty.

The postcommissurotomy syndrome.

The postcommissurotomy syndrome.

Idiopathic recurrent pericarditis: Comparison with the postcommissurotomy syndrome; considerations of etiology and treatment

Forty-two episodes of idiopathic pericarditis occurring in twelve patients were studied. The manifestations were compared with those observed in seventy-two attacks of the postcommissurotomy syndrome in twenty-four patients. There is a striking resemblance between the clinical and laboratory features of idiopathic pericarditis and those of the postcommissurotomy syndrome. Both diseases include pericarditis, pleurisy and pneumonitis although the incidence of these components varies in the individual case. In some instances the occurrence of gallop rhythm, dilatation of the heart, transient auricular flutter-fibrillation and congestive heart failure suggests involvement of the myocardium. The outstanding clinical features are pain of the pleuropericardial type and fever. Both syndromes usually have a benign course and tend to relapse frequently. There are compelling reasons for the belief that the postcommissurotomy syndrome is a manifestation of rheumatic activity. The same etiology is suggested for some cases of “idiopathic” pericarditis by the following facts: (1) Close resemblance of idiopathic pericarditis and the postcommissurotomy syndrome; (2) presence of major and minor rheumatic manifestations in a relatively large number of cases of idiopathic pericarditis reported in the literature and in two-thirds of the cases observed by the writer; (3) salicylates and pyramidon sometimes have a beneficial, even dramatic effect in cases of idiopathic pericarditis; and (4) idiopathic pericarditis is predominantly a disease of the adult. Rheumatic fever in the adult is known to manifest itself often atypically, as a benign exudative process which may heal without residual heart disease. The finding of pleurisy and/or pneumonitis aids in the differentiation of idiopathic pericarditis from an acute coronary attack.

Clinical and laboratory manifestations of the postcommissurotomy syndrome

The postcommissurotomy syndrome developed in ten of sixteen patients ten days to seven months following mitral commissurotomy. Seven patients had multiple attacks. The syndrome consisted of chest pain and fever together with less prominent and frequent cough, hemoptysis, dyspnea and arthralgias. Evidence of pericarditis and pleuritis was obtained, with leukocytosis and elevated erythrocyte sedimentation rate. Bacteriologic studies yielded negative results. Penicillin prophylaxis was ineffective and antibiotics failed to modify the course. Salicylates appeared to abbreviate the illness. No significant change in the antistreptolysin-O titer occurred during this illness. The C-reactive protein was found to be the most sensitive laboratory test for the postcommissurotomy syndrome and the most useful in management. The possible etiologic factors are reviewed. It is suggested that the postcommissurotomy syndrome represents a self-limited form of pericarditis and pleuritis induced by the trauma of surgery in patients with rheumatic heart disease. Salicylate suppressive therapy is recommended for all postcommissurotomy patients. The C-reactive protein test is suggested as a useful and sensitive test for the activity of the postcommissurotomy syndrome.