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The keys to successful pericardiectomy for constrictive pericarditis are early operation and as complete a pericardiectomy as possible. With the high-speed burr it is easy and safe to dissect the calcified pericardium and define the epicardium even in a small operative field such as the inferior or posterior portion of the heart. This method has the important ability to perform very complete pericardiectomy.
Constrictive pericarditis and pyopericardium with tamponade in a patient and rheumatoid arthritis is described. No fever was recorded despite a litre of pus in the pericardial sac, perhaps because of previous treatment with hydrocortisone. Echocardiography is a diagnostic advance.
Twenty five patients with constrictive pericarditis underwent cross-sectional and M-mode echocardiography before pericardectomy. The numerical data were compared with those in thirty healthy subjects. The various parameters noted regarding the left cavities were as follows: --The presence of a pericardial detachment which may sometimes be quite large (more than 10 mm in 6 cases); the degree of parallelism of the pericardial membranes in systole, which is all the less maintained as the detachment is severe. --The increase in size of the right ventricle and decrease of the left, with p less than 0.001 in both cases. --The absence of posterior motion of the left side of the septum in systole in 22 cases, followed by a sudden posterior displacement during the rapid filling stage, after which there is virtually no motion until the end of diastole. --The presence at the level of the posterior wall of a so-called slow filling slope, which is smaller (1.9 +/- 1.5 mm/s) than in the normal subject (p less than 0.001). --A change in left ventricular endocavitary diameter variations, which results from the two previous findings. The tracings thus show the compliance disorder with a very steep rapid filling slope and a plateau during the slow filling stage. --Finally the changes in mitral kinetics involving an earlier (p less than 0.001) and lower (p less than 0.001) F point than in the control series and on the other hand an larger E wave, sometimes forming a summation with A wave in sinus rhythm and a false A wave in atrial fibrillation. We think this type of motion is due to the disturbances in the two mechanisms (recirculation, breaking of a jet) which in physiological conditions seem to combine to chose the mitral valve at point F and account for the valve position in mid-diastole.
We measured the angle P formed by the junction of the left ventricular and left atrial posterior walls, and also the distances from the ultrasound transducer to the left ventricular posterior wall and left atrial posterior wall (DV and DA), respectively, in the parasternal long-axis two-dimensional echocardiographic view. We studied 23 normal adults and four patient groups with conditions commonly associated with left atrial dilatation: mitral regurgitation (14), mitral stenosis (16), hypertrophic cardiomyopathy (13), and constrictive pericarditis (7). Statistically significant differences were found between the constrictive pericarditis group and each of the other groups. Angle P was less than 150 degrees in 0 of 23 normal individuals, in 0 of 14 with mitral regurgitation, in 1 of 16 with mitral stenosis, in 0 of 13 with hypertrophic cardiomyopathy, and in five of seven with constrictive pericarditis. DA minus DV exceeded 20 mm in 0 of 23 normal individuals, one of four with mitral regurgitation, in 6 of 16 with mitral stenosis, in 0 of 13 with hypertrophic cardiomyopathy, and in five of seven patients with constrictive pericarditis; We conclude that angle P greater than 150 degrees suggests constrictive pericarditis; DA minus DV greater than 20 mm suggests constrictive pericarditis if mitral stenosis can be excluded.
OBJECTIVES: The study assessed changes in left ventricular systolic and diastolic function after pericardiectomy in patients with constrictive pericarditis and correlated postoperative Doppler echocardiographic findings with clinical status. BACKGROUND: Despite the efficacy of pericardiectomy, some patients with constrictive pericarditis fail to improve postoperatively. Data on serial evaluation of systolic and diastolic function after pericardiectomy and its relation to clinical status are not available. METHODS: From 1985 to 1995, a total of 58 patients with constrictive pericarditis underwent pericardiectomy and had at least one follow-up Doppler echocardiographic study with a respirometer: 23 patients had one examination within 3 months postoperatively, 19 had a study within 3 months and another one more than 3 months postoperatively, and 16 had one study more than 3 months postoperatively. RESULTS: In the early postoperative period, diastolic function was normal in 17 patients (40.5%), restrictive in 17 (40.5%), and constrictive in 8 (19%). Among 19 patients who had serial Doppler echocardiography, in 2 patients with restrictive physiology and 5 with constrictive physiology the results had become normal, and 1 patient who had had constrictive physiology had restrictive findings. In late follow-up, left ventricular end-diastolic diameter increased compared with preoperative measurement (p = 0.0009). Diastolic filling pattern at late follow-up was normal in 20 patients (57%), restrictive in 12 (34%) and constrictive in 3 (9%). There was a significant relationship between diastolic filling patterns and symptomatic status (chi2 = 20.9, p < 0.0001). Patients with persistent abnormal diastolic filling on Doppler echocardiography had had symptoms for a longer time preoperatively than did patients with normal diastolic physiology (p = 0.0471). CONCLUSIONS: Diastolic filling characteristics remain abnormal in a substantial number of patients with constrictive pericarditis after pericardiectomy. These abnormalities may resolve gradually but can persist. Diastolic filling abnormalities after pericardiectomy correlate well with clinical symptoms and tend to occur in patients who have had symptoms longer preoperatively. This finding supports the recommendation that pericardiectomy be performed promptly in symptomatic patients with constrictive pericarditis.
The purpose of this study was to determine the diagnostic value of Doppler pulmonary venous flow in constrictive pericarditis, as assessed by transoesophageal echocardiography. It has been demonstrated previously that increased respiratory variation in Doppler pulmonary venous, but not in transmitral flow velocities, can identify patients with constrictive pericarditis, when transoesophageal echocardiography is used. In the present study we compared a group of 10 patients with constrictive pericarditis and a control group of 15 normal subjects with respect to pulmonary venous and transmitral flow velocities and their respiratory variation. Peak velocities and velocity time integrals of the systolic, early diastolic and late diastolic reversed pulmonary venous flow waves were measured. Peak velocities and velocity time integrals of the early and late diastolic transmitral flow waves were also measured. Measurements were made irrespective of the respiratory cycle, at the onset of inspiration and at the onset of expiration. Values for inspiration and expiration were expressed as percent difference of those obtained irrespective of the respiratory cycle. Peak velocity and velocity time integral of the pulmonary venous systolic and diastolic waves were significantly lower than in normal subjects. Furthermore, the difference between peak velocities of the diastolic wave obtained at the onset of inspiration and obtained irrespective of the respiratory cycle was significantly larger in constrictive pericarditis than in the control group (-20% vs -9%, P < 0.05). This also applied to the difference between velocity time integrals of the diastolic wave obtained at the onset of inspiration and obtained irrespective of the respiratory cycle (-22% vs -12%, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
In a study of 30 consecutive patients with constrictive pericarditis diagnosed by clinical, radiological, and echocardiographic criteria 21 (70%) were found to have pulsatile hepatomegaly. The pulsations were felt clinically and confirmed by external hepatic recordings. These pulsations conformed almost identically to the jugular venous pulsations in the neck. The hepatic pulsations disappeared after successful pericardiectomy. Persistence of the hepatic pulsations was associated with poor postoperative relief suggesting that it is another useful sign in the assessment of the adequacy of pericardiectomy. Thus this poorly appreciated clinical finding appears to be present in a high proportion of patients with constrictive pericarditis.
An exudative pleural effusion is a very infrequent form of presentation of constrictive pericarditis, and it can induce diagnostic difficulties. We present a 71 year-old woman with a pleural effusion attributed to be due to congestive heart failure which does not respond to the treatment. The pleural fluid had biochemical characteristics of an exudate. The echocardiographic study showed severe constrictive pericarditis, and after the pericardectomy the pleural effusion completely resolved. The diagnostic suspicion of constrictive pericarditis in cases of exudative pleural effusion is of special interest because an specific and effective treatment is available.
A case is reported of a rare combination of chronic constrictive pericarditis and aortic dissection. A 23-year-old male was diagnosed with constrictive pericarditis and annulo-aortic ectasia concomitant with type-A dissection. A pericardiectomy was performed under cardiopulmonary bypass, and an aortic segment, from the root to the arch, was totally replaced by a composite graft using selective cerebral perfusion. Both procedures were performed in one stage. An aged clot was found in the pericardial cavity. Sustained rupture of the aortic dissection into the pericardial cavity is considered to be a possible explanation for the development of constrictive pericarditis. The postoperative course was uneventful and the patient was discharged 34 days after the operation.
In order to know early and late results of pericardiectomy on the treatment of chronic constrictive pericarditis in the Instituto Nacional de Cardiología Ignacio Chávez, we review the records of 58 patients with the diagnosis of constrictive pericarditis who underwent surgical treatment between 1947 to 1987. Tuberculosis was the most frequent cause (68.3%) followed by idiopathic cases (24.1%). Preoperatively 3.4% were in New York Heart Association Class I, 31% in Class II, 48.3% in Class III and 17.2% in Class IV. There were 4 in-hospital deaths (overall operative mortality 6.89%). Operative mortality in the last ten years was 0%. Low output was the most common nonfatal complication of pericardiectomy (15.5%). Accidental right atrial tear happened in 8.6%. Mean post-operative follow-up was 5.6 +/- 6.3 years (longest 25.6 years). Mortality per patient year was 2.04%. Actuarial survival estimates were 82% and 71% at 5 to 10 years respectively. Postoperatively 76% were in New York Heart Association Class I (p less than 0.001), 16% in Class II (p less than 0.001), 8% in Class III (p less than 0.001) and none in Class IV (p less than 0.05). Operative mortality, long-term survival and post-operative functional Class were not significantly influenced by preoperative functional Class nor by the duration of symptoms. We conclude that pericardiectomy is an effective treatment of symptomatic chronic constrictive pericarditis because it provides an important and durable improvement in symptoms and functional Class, and it has a low operative mortality.
Commonly used chemotherapeutic agents, specifically cytarabine and daunorubicin, can cause effusive-constrictive pericarditis. We describe a case of transient effusive-constrictive pericarditis in a patient with acute myelogenous leukemia. This is the first case report of a patient with transient effusive-constrictive pericarditis due to chemotherapy.
A case of constrictive pericarditis developed within twenty-four days of mild, blunt thoracic trauma. Rapid progression from traumatic pericarditis to constriction is documented with clinical evidence, electrocardiographic changes and cardiac catheterisation data. Other manifestations of pericardial reaction after blunt chest trauma are reviewed briefly.
A case of calcific constrictive pericarditis in a young White woman with a convincing history of previous acute rheumatic fever complicated by a possible valvular lesion is presented. Cardiac catheterization confirmed the suspicion of significant cardiac compression. Successful pericardiectomy was carried out, but microscopical examination of the excised pericardium failed to demonstrate a cause. In view of the strong past history of acute rheumatic fever and mild mitral insufficiency demonstrated at cardiac catheterization, the author proposes that the calcific constrictive pericarditis was of rheumatic origin. A review of the literature on the association between rheumatic infection and constrictive pericarditis follows.
A 13-year-old boy with active tuberculous constrictive pericarditis underwent complete pericardiectomy together with antituberculous therapy and a short course of steroids. Six weeks following the surgery, he was seen with clinical and hemodynamic findings of recurrent pericardial constriction, presumably due to an inflammatory collection around the heart. Symptoms gradually resolved within six months with resumption of steroid therapy. Repeat hemodynamic study showed normal hemodynamics. The case demonstrates the production of cardiac constriction by nonpericardial inflammatory tissue and the possible benefits of steroid therapy in the treatment of tuberculous constrictive pericarditis.
In Transkei, 143 patients with active tuberculous constrictive pericarditis without significant pericardial effusion all received the same daily 6-month antituberculosis regimen of streptomycin, isoniazid, rifampicin, and pyrazinamide for 14 weeks followed by isoniazid and rifampicin. They were randomly allocated to receive in addition either prednisolone or placebo for the first 11 weeks; the comparison was double-blind throughout treatment and follow-up. In the 114 patients assessable up to 24 months, improvement was significantly more rapid in the prednisolone group, as shown by the rate of fall in the mean pulse rate and the rate at which jugular venous pressure and level of physical activity became normal. During follow-up, 2 (4%) of the 53 prednisolone and 7 (11%) of the 61 placebo patients died from pericarditis, and 11 (21%) and 18 (30%), respectively, required pericardiectomy. By 24 months 50 (94%) prednisolone and 52 (85%) placebo patients had a favourable status. 3 patients (1 prednisolone, 2 placebo) were normally active but were classified as not having achieved a favourable status. It is recommended that, in the absence of a specific contraindication, antituberculosis chemotherapy should be initially supplemented by steroids.
OBJECTIVE AND METHOD: We retrospectively analysed 56 consecutive patients with a confirmed diagnosis of chronic constrictive pericarditis over a period of 23 years. The objective was to analyse the evolution of the annual frequency of constrictive pericarditis, its aetiology and to define the prognostic factors for mortality. RESULTS: The annual frequency of constrictive pericarditis has not diminished over the 23 years of this study, remaining at 2.4 cases per year. Cases with a tuberculous origin have diminished progressively, being replaced by complications of cardiac surgery and mediastinal radiotherapy. Pericardectomy was performed in 41 patients and the average follow up was 9.5 +/- 8.6 years. By the end of the study, 34 patients had died (61.8%), 18 from a cardiovascular cause (38.3%). The independent predictive factors for overall mortality were a history of mediastinal radiotherapy, the age, and plasma sodium level. Only the presence of first degree atrio-ventricular block was an independent predictive factor for cardiovascular mortality. In the pericardectomy group, 24 patients died (60%). A history of mediastinal radiotherapy and the presence of pre-operative hyponatraemia were independent predictive factors for overall mortality. CONCLUSION: Constrictive pericarditis remains a serious pathology. Pericardectomy allows a clear functional improvement, but following pericardectomy more than 60% of patients will die within 10 years of the diagnosis being made.
The diagnostic value of hepatic venous flow patterns was evaluated for constrictive pericarditis by pulsed Doppler. A characteristic flow pattern was assumed to be associated with the well-known atrial pressure curve. Thirteen patients with constrictive pericarditis were compared to 13 control subjects and to 25 patients with right ventricular pressure overload including 13 patients with tricuspid regurgitation. The characteristic finding in constrictive pericarditis was a W-wave pattern of flow velocities in the dilated hepatic veins, with abrupt reversal of flow late in systole and diastole before the A wave (100% specificity, 68% sensitivity). This depends, however, on the absence of tricuspid regurgitation (for its systolic component) or fast sinus rhythm (for its diastolic component). Additional diagnostic markers were systolic deceleration time of forward flow (40 to 130 ms) and systolic integral of flow velocities (4.3 to -4.0 cm) (sensitivity and specificity greater than or equal to 92%). In the presence of tricuspid regurgitation, diastolic deceleration time less than 150 ms and diastolic integral of flow velocities less than 6 cm were useful diagnostic signs. If combined, these criteria had 100% sensitivity and specificity for the diagnosis. Thus, pulsed Doppler assessment of flow velocities in the hepatic vein facilitates the diagnosis of constrictive pericarditis in clinical routine, using an auxiliary site with unlimited diagnostic access to the characteristic flow velocity pattern, which reflects right atrial pressure curve and filling abnormalities.
BACKGROUND: Constrictive pericarditis represents a serious hemodynamic syndrome that may lead to heart failure. Studies of its pathophysiological mechanisms have been impeded by the lack of an animal model. METHODS AND RESULTS: Cardiac myosin-induced experimental autoimmune myocarditis in interferon (IFN)-gamma-knockout (KO) mice results in increased cardiac inflammation and development of severe grossly detectable pericarditis. Using in vivo pressure-volume studies, we found that the acute phase of experimental autoimmune myocarditis in IFN-gamma-KO mice was characterized by reduced left ventricular (LV) volumes compared with wild-type mice. The KO mice exhibited a classic restrictive/constrictive phenotype with decreased cardiac output, increased chamber stiffness, preserved ejection fraction, and impaired diastolic filling, characterized by reduced deceleration time and pressure tracings showing the square root sign similar to that observed in clinical cases of constrictive pericarditis. This phenotype was not associated with the severity of myocarditis but correlated with the presence of grossly detectable adhesive pericarditis present only in the KO group and characterized by increased pericardial inflammation and fibrosis. Comparison of IFN-gamma-KO and wild-type mice matched for the severity of myocardial disease further confirmed that pericarditis, and not myocarditis, was responsible for smaller LV volumes, reduced cardiac output, increased cardiac stiffness, and increased peak filling rate adjusted for end-diastolic volumes in KO mice. CONCLUSIONS: Autoimmune heart disease in IFN-gamma-KO mice results in increased pericardial inflammation and fibrosis, leading to constrictive phenotype during the acute phase of disease. It represents a novel animal model of constrictive pericarditis.