Restrictive cardiomyopathy versus constrictive pericarditis: role of endomyocardial biopsy in avoiding unnecessary thoracotomy

Despite careful clinical, noninvasive, and hemodynamic assessment of patients with constrictive/restrictive physiology, the differentiation of restrictive cardiomyopathy from constrictive pericarditis remains difficult. We examined the role of right ventricular endomyocardial biopsy in defining the underlying process in 54 patients with evidence of constrictive/restrictive physiology, including 38 patients with profound symptoms of heart failure in whom diagnostic/therapeutic thoracotomy was contemplated (group I) and 16 patients with milder symptoms (group II). All patients in group I had NYHA class III or IV heart failure with depressed cardiac index (mean 2.5 liters/min/m2), right atrial hypertension (mean 15 mm Hg), and normal left ventricular ejection fraction (mean 59%). Endomyocardial biopsy identified a specific source of restrictive cardiomyopathy in 15 of 38 patients (39%) (11 amyloid, four myocarditis). Of the 23 remaining patients with either normal biopsy findings or nonspecific abnormalities on biopsy, 18 had intraoperative or autopsy evaluation of their pericardium, and constriction was found in 14 (77%). A specific form of restrictive cardiomyopathy was also identified in four of the 16 patients with milder symptoms (group II). We conclude that endomyocardial biopsy is useful in patients with severe constrictive/restrictive physiology. It identifies a large subset of patients with specific forms of restrictive cardiomyopathy in whom thoracotomy should be avoided. It supports the need for thoracotomy and the likelihood of finding pericardial constriction in patients without specific pathologic findings.     

Left ventricular filling in differentiating restrictive amyloid cardiomyopathy and constrictive pericarditis

Left ventricular filling was evaluated with use of digitized left ventriculograms in patients with (1) restrictive amyloid cardiomyopathy, (2) constrictive pericarditis, and (3) a normal heart. Restrictive cardiomyopathy (four patients) was established by right and left heart hemodynamic studies and postmortem examination; all four patients had cardiac amyloidosis. Constrictive pericarditis (seven patients) was established by characteristic right and left heart catheterizatlon data and pericardial disease at operation; four patients had calcific and three had noncalcific anatomic changes. Normal subjects (seven patients) had normal intracardiac pressures and normal findings on left ventriculography and coronary arteriography.Left ventriculographic silhouettes were digitized and left ventricular volumes were calculated by computer at 16 ms intervals. Curves of left ventricular volume and ventricular filling rate were constructed for each patient and also for each group. Patients with restrictive amyloid cardiomyopathy had no plateau in the diastollc left ventricular filling volume curve, and their left ventricular filling rate was slower than normal during the first half of diastole. Patients with constrictive pericarditis had a sudden and premature plateau in the diastolic left ventricular volume filling curve. In addition, the left ventricular filling rate was faster than normal during the first half of diastole. Statistical analysis of left ventricular filling rate in patients with restrictive amyloid cardiomyopathy, patients with constrictive pericarditis and normal patients showed significant differences during the first half of diastole; those with restrictive amyloid cardiomyopathy had 45 ± 4 percent, those with constrictive pericarditis had 85 ± 4 percent and normal subjects had 65 ± 5 percent of left ventricular filling completed at 50 percent of diastole (p < 0.05).Thus, this study showed a significantly different profile of diastolic left ventricular filling volume and ventricular filling rate curves during the first half of diastole in patients with restrictive cardiomyopathy and those with constrictive pericarditis. The findings suggest the importance of these determinations in differentiating restrictive amyloid cardiomyopathy and constrictive pericarditis at cardiac catheterization.     

Usefulness of systolic time intervals in differential diagnosis of constrictive pericarditis and restrictive cardiomyopathy.

Systolic time intervals in 15 patients with constrictive pericarditis and seven patients with restrictive cardiomyopathy were compared in order to assess their value in the differential diagnosis of the two disorders. Clinical examination had failed to make the distinction. Right heart catheterization was helpful in diagnosing restriction but failed to differentiate patients with constrictive pericarditis from those with restrictive cardiomyopathy. The systolic time intervals clearly separated the two groups. The PEP/LVET was normal in all patients with constrictive pericarditis (0.34 +/- 0.01) and abnormal in all patients with restrictive cardiomyopathy (0.70 +/- 0.09, P less than 0.001). In 13 patients (five with restrictive cardiomyopathy and eight with constrictive pericarditis) the results of quantitative left ventricular angiocardiography were available. A high correlation (r=-0.90, P less than 0.01) between the PEP/LVET and the ejection fraction confirmed the validity of the PEP/LVET as a measure of left ventricular performance in these patients. Thus the systolic time intervals clearly distinguished between constrictive pericarditis and restrictive cardiomyopathy and are a reliable non-invasive technique for making the difficult differential diagnosis.     

Usefulness of systolic time intervals in differential diagnosis of constrictive pericarditis and restrictive cardiomyopathy.

Systolic time intervals in 15 patients with constrictive pericarditis and seven patients with restrictive cardiomyopathy were compared in order to assess their value in the differential diagnosis of the two disorders. Clinical examination had failed to make the distinction. Right heart catheterization was helpful in diagnosing restriction but failed to differentiate patients with constrictive pericarditis from those with restrictive cardiomyopathy. The systolic time intervals clearly separated the two groups. The PEP/LVET was normal in all patients with constrictive pericarditis (0.34 +/- 0.01) and abnormal in all patients with restrictive cardiomyopathy (0.70 +/- 0.09, P less than 0.001). In 13 patients (five with restrictive cardiomyopathy and eight with constrictive pericarditis) the results of quantitative left ventricular angiocardiography were available. A high correlation (r=-0.90, P less than 0.01) between the PEP/LVET and the ejection fraction confirmed the validity of the PEP/LVET as a measure of left ventricular performance in these patients. Thus the systolic time intervals clearly distinguished between constrictive pericarditis and restrictive cardiomyopathy and are a reliable non-invasive technique for making the difficult differential diagnosis.     

Restrictive cardiomyopathy and constrictive pericarditis: non-invasive distinction by digitised M mode echocardiography

It is difficult to distinguish between restrictive cardiomyopathy and constrictive pericarditis on the basis of clinical findings and simple investigation. Cardiac catheterisation has been the reference standard for diagnosis but even this does not always permit an accurate distinction. A Summagraphics digitiser and Prime 750 computer system were used to digitise the echocardiograms of 15 patients with restrictive cardiomyopathy, 10 with constrictive pericarditis and a group of 20 age and sex matched normal subjects of similar age and sex distribution. Compared with controls, patients with restrictive cardiomyopathy showed a significant reduction in the following variables (a) decreased fractional shortening, (b) decreased peak left ventricular filling and emptying rates, (c) decreased percentage posterior wall thickening, and (d) decreased peak left ventricular posterior wall thickening and thinning rates. Whereas patients with constrictive pericarditis only had significantly reduced peak left ventricular filling and posterior wall thinning rates and significantly increased posterior wall thinning rate. When patients with restrictive cardiomyopathy were compared with those with constrictive pericarditis the significant differences were: (a) decreased peak left ventricular emptying rate, (b) decreased percentage posterior wall thickening, and (c) decreased peak left ventricular posterior wall thickening and thinning rates. Digitisation of M mode echocardiograms, with particular attention to posterior wall function, may be a useful adjunct to cardiac catheterisation in distinguishing restrictive cardiomyopathy from constrictive pericarditis.     

Restrictive cardiomyopathy and constrictive pericarditis: non-invasive distinction by digitised M mode echocardiography.

It is difficult to distinguish between restrictive cardiomyopathy and constrictive pericarditis on the basis of clinical findings and simple investigation. Cardiac catheterisation has been the reference standard for diagnosis but even this does not always permit an accurate distinction. A Summagraphics digitiser and Prime 750 computer system were used to digitise the echocardiograms of 15 patients with restrictive cardiomyopathy, 10 with constrictive pericarditis and a group of 20 age and sex matched normal subjects of similar age and sex distribution. Compared with controls, patients with restrictive cardiomyopathy showed a significant reduction in the following variables (a) decreased fractional shortening, (b) decreased peak left ventricular filling and emptying rates, (c) decreased percentage posterior wall thickening, and (d) decreased peak left ventricular posterior wall thickening and thinning rates. Whereas patients with constrictive pericarditis only had significantly reduced peak left ventricular filling and posterior wall thinning rates and significantly increased posterior wall thinning rate. When patients with restrictive cardiomyopathy were compared with those with constrictive pericarditis the significant differences were: (a) decreased peak left ventricular emptying rate, (b) decreased percentage posterior wall thickening, and (c) decreased peak left ventricular posterior wall thickening and thinning rates. Digitisation of M mode echocardiograms, with particular attention to posterior wall function, may be a useful adjunct to cardiac catheterisation in distinguishing restrictive cardiomyopathy from constrictive pericarditis.     

Differentiation of constrictive pericarditis from restrictive cardiomyopathy using mitral annular velocity by tissue Doppler echocardiography

This study evaluated the diagnostic role of early diastolic mitral annular velocity (E') by tissue Doppler echocardiography for differentiating constrictive pericarditis from restrictive cardiomyopathy (primary restrictive cardiomyopathy and cardiac amyloidosis). The study group consisted of 75 patients (53 men, 22 women; mean age 62 years, range 27 to 87). Of these, 23 patients had surgically confirmed constrictive pericarditis, 38 had biopsy-proved systemic amyloidosis and typical echocardiographic features of cardiac involvement, and 14 had primary restrictive cardiomyopathy. Standard mitral inflow characteristics were measured. Tissue Doppler echocardiography was used to measure E' at the septal annulus. E' was significantly higher in patients with constrictive pericarditis than in those with primary restrictive cardiomyopathy or cardiac amyloidosis (12.3 vs 5.1 cm/second, p <0.001). An E' cut-off value > or =8 cm/second resulted in 95% sensitivity and 96% specificity for the diagnosis of constrictive pericarditis. There was no overlap of E' between patients who had constrictive pericarditis and those who had cardiac amyloidosis. In a subgroup analysis of restrictive cardiomyopathy, E' of patients who had cardiac amyloidosis was significantly lower than that of patients who had primary restrictive cardiomyopathy (4.6 vs 6.3 cm/second, p <0.001). Thus, E' velocity can distinguish between constrictive pericarditis and restrictive cardiomyopathy with a specific cut-off value in patients with clinical and echocardiographic evidence of diastolic heart failure.     

Differentiation of constrictive pericarditis and restrictive cardiomyopathy by radionuclide ventriculography

Patterns of left ventricular diastolic filling in five patients with unoperated constrictive pericarditis, the same five patients following pericardiectomy, five patients with restrictive cardiomyopathy, and 14 healthy control subjects were studied by radionuclide ventriculography. Patients with constrictive pericarditis had more rapid peak left ventricular filling rates (mean 5.62, range 4.23 to 7.32 end-diastolic volumes [EDV] per second) compared to control subjects 3.44, range 2.62 to 4.45 EDV/sec, p less than 0.05). Heart rate-corrected first one-third and first one-half diastolic filling fractions were greater in patients with preoperative constrictive pericarditis compared to members of the restrictive cardiomyopathy and control groups p less than 0.05). Following pericardiectomy, patients with constrictive pericarditis had significant decreases in peak filling rate and corrected filling fractions, and all diastolic filling measurements were indistinguishable from those of control subjects. These noninvasively obtained data indicate that patients with preoperative constrictive pericarditis have an increased rate of left ventricular early diastolic filling compared to patients with restrictive cardiomyopathy and control subjects, and that these findings return to normal following surgical removal of the pericardium.     

Differentiation of constrictive pericarditis and restrictive cardiomyopathy by Doppler echocardiography

Doppler ultrasound recordings of mitral, tricuspid, aortic, and pulmonary flow velocities, and their variation with respiration, were recorded in 12 patients with a restrictive cardiomyopathy and seven patients with constrictive pericarditis. Twenty healthy adults served as controls. The patients with constrictive pericarditis showed marked changes in left ventricular isovolumic relaxation time and in early mitral and tricuspid flow velocities at the onset of inspiration and expiration. These changes disappeared after pericardiectomy and were not seen in patients with restrictive cardiomyopathy or in normal subjects. The deceleration time of early mitral and tricuspid flow velocity was shorter than normal in both groups, indicating an early cessation of ventricular filling, but only patients with restrictive cardiomyopathy showed a further shortening of the tricuspid deceleration time with inspiration. Diastolic mitral and tricuspid regurgitation was also more common in the patients with restrictive cardiomyopathy. These results suggest that patients with constrictive pericarditis and restrictive cardiomyopathy can be differentiated by comparing respiratory changes in transvalvular flow velocities. In addition, although baseline hemodynamics in the two groups were similar, characteristic changes were seen with respiration that suggest differentiation of these disease states may also be possible from hemodynamic data.     

Abnormal left ventricular-left atrial posterior wall contour: a new two-dimensional echocardiographic sign in constrictive pericarditis

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.     

Diagnosis of constrictive pericarditis by two-dimensional echocardiography: studies in a new experimental model and in patients

The purpose of this study was to determine the value of two-dimensional echocardiography in detecting constrictive pericarditis. Serial two-dimensional echocardiography was performed in eight closed chest conscious dogs with experimental constrictive pericarditis, using a new model that creates constrictive pericarditis by the introduction of a pericardial irritant mixture. Constrictive pericarditis was confirmed in these dogs by cardiac catheterization and pathologic examination. Four patients with constrictive pericarditis and three patients with restrictive cardiomyopathy (amyloidosis) were also studied. Analysis of short-axis two-dimensional echocardiograms was performed to determine the frame by frame change in left ventricular cavity areas throughout diastole. Curves of diastolic left ventricular cavity area change versus percent duration of diastole were constructed for each animal and human subject. Pericardial thickness was measured at various gain settings on two-dimensional and M-mode echocardiograms and at post-mortem examination. In dogs with constrictive pericarditis, the echocardiograms seriously overestimated and correlated poorly with pathologic measurements of pericardial thickness. In dogs after constrictive pericarditis developed, 69 +/- 11% (mean +/- SD) (range 50 to 84) of cavity area change occurred in the initial 30% of diastole compared with 35 +/- 7% (range 20 to 45) in control two-dimensional echocardiograms (p less than 0.001). Four patients with constrictive pericarditis showed similar accelerated cavity expansion in early diastole, but three patients with cardiac amyloidosis showed more variable left ventricular diastolic expansion rates. It is concluded that two-dimensional echocardiograms can demonstrate characteristic diastolic filling abnormalities in constrictive pericarditis, but cannot accurately measure pericardial thickness.     

Constrictive pericarditis: Its history and current status

The diagnosis of constrictive pericarditis remains a challenge because it is often mimicked by restrictive cardiomyopathy. The last few years have seen numerous advances in our ability to differentiate between these two conditions which often have similar physical findings and hemodynamics. This review begins with a brief history of constrictive pericarditis; this is followed by an extensive discussion of newer etiologies, and then the classical clinical history and physical examination findings are described. Radiologic, electrocardiographic, and angiographic findings are discussed. The hemodynamics of constrictive pericarditis are reviewed. Recent results of echocardiographic and echo-Doppler investigations are presented. Emphasis is placed upon the limitations of M-mode echocardiography in the diagnosis of constrictive pericarditis. The value of echocardiographic Doppler studies of mitral and tricuspid flow velocity patterns, as well as of those in the pulmonary veins and hepatic veins, is described. Nuclear ventriculograms and angiocardiograms tend to show more rapid ventricular filling in constrictive pericarditis than in restrictive cardiomyopathy. Although only a small number of patients has been studied, these evaluations seem to have merit in separating restrictive cardiomyopathy from constrictive pericarditis. The role of computed tomography scanning and magnetic resonance imaging studies of pericardial thickness in confirming the presence of constrictive pericarditis is discussed. Abnormal pericardial thickening (> 3 mm) confirms the diagnosis of constrictive pericarditis, but only if the characteristic hemodynamic pattern is present. The usefulness of endomyocardial biopsy in recognizing specific varieties of restrictive cardiomyopathy is presented. The topic of occult constrictive pericardial disease is discussed briefly. A discussion of the timing of pericardial resection for the treatment of constrictive pericarditis ends the review.     

Superior vena cava Doppler flow velocity patterns in pericardial disease

Doppler superior vena cava (SVC) flow patterns were studied in 34 patients with pericardial disease and in 8 normal adults; the pulse transducer on the echocardiographic instrument was used for respiratory monitoring, rather than a separate nasal thermistor-based device. First expiratory SVC diastolic flow velocities (Dfe) did not differ in normal subjects and patients with hemodynamically insignificant pericardial effusions (23 +/- 3 cm/s and 29 +/- 13 cm/s, difference not significant). Dfe were less than 15 cm/s only in the 14 patients with cardiac tamponade (9 +/- 3 cm/s, p less than 0.01). A ratio of systolic to diastolic flow velocity less than or equal to 1.1 in the first expiratory beat distinguished constrictive pericarditis from all other groups (p less than 0.01), although not from restrictive cardiomyopathy. Expiratory ablation of diastolic SVC flow mimicking cardiac tamponade was not observed in constrictive pericarditis. Respiratory variation in SVC flow velocities was slight in normal subjects and patients with constrictive pericarditis, increased in patients with hemodynamically insignificant pericardial effusions (p less than 0.01) and greatest in patients with cardiac tamponade (p less than 0.01). Quantitative analysis of SVC flow velocity patterns is a useful addition to the echocardiographic evaluation of pericardial disease.     

Primary cardiac amyloidosis: an angiocardiographic clue to early diagnosis

Restrictive cardiomyopathy produced by primary cardiac amyloidosis may have a clinical syndrome identical to noncalcific constrictive pericarditis. We report two patients with amyloidosis and restrictive physiology who had enlarged papillary muscles shown on left ventricular angiocardiogram. Rapid volume expansion with normal saline failed to produce ventricular filling pressure equilibration as in occult constrictive pericarditis. The absence of diastolic pressure equilibration and enlarged papillary muscles may permit early diagnosis of cardiac amyloidosis.     

Comparison of new Doppler echocardiographic methods to differentiate constrictive pericardial heart disease and restrictive cardiomyopathy

This study assesses how the newer modalities of tissue Doppler echocardiography and color M-mode flow propagation compare with respiratory variation of Doppler flow in distinguishing between constrictive pericarditis and restrictive cardiomyopathy. We studied 30 patients referred for further evaluation of diastolic function who had a diagnosis of constrictive pericarditis or restrictive cardiomyopathy established by diagnostic tests, including clinical assessment, magnetic resonance imaging, cardiac catheterization, endomyocardial biopsy, and surgical findings. Nineteen patients had constrictive pericarditis and 11 had restrictive cardiomyopathy. We performed 2-dimensional transesophageal echocardiography combined with pulsed-wave Doppler of the pulmonary veins and mitral inflow with respiratory monitoring, tissue Doppler echocardiography of the lateral mitral annulus, and color M-mode flow propagation of left ventricular filling. Respiratory variation of the mitral inflow peak early (peak E) velocity of > or =10% predicted constrictive pericarditis with 84% sensitivity and 91% specificity and variation in the pulmonary venous peak diastolic (peak D) flow velocity of > or =18% distinguished constriction with 79% sensitivity and 91% specificity. Using tissue Doppler echocardiography, a peak early velocity of longitudinal expansion (peak Ea) of > or =8.0 cm/s differentiated patients with constriction from restriction with 89% sensitivity and 100% specificity. A slope of > or =100 cm/s for the first aliasing contour in color M-mode flow propagation predicted patients with constriction with 74% sensitivity and 91% specificity. Thus, the newer methods of tissue Doppler echocardiography and color M-mode flow propagation are equivalent and complimentary with Doppler respiratory variation in distinguishing between constrictive pericarditis and restrictive cardiomyopathy. The additive role of the new methods needs to be established in difficult cases of constrictive pericarditis where respiratory variation may be absent or decreased.     

A long-term follow-up study of acute viral and idiopathic myocarditis

In order to clarify the prognosis of myocarditis and the relationship between myocarditis and idiopathic cardiomyopathy, 20 patients with myocarditis (one with Coxsackie B; one with rubella and 18 with idiopathic myocarditis) were followed up for a long period using echocardiography and Holter electrocardiographic monitoring. The follow-up period was 49.1 +/- 39.3 months (mean +/- SD). Subjects were classified into the following 4 groups according to their prognoses, left ventricular end-diastolic dimensions (LVDd) and the presence of absence of life-threatening ventricular arrhythmias: Group I with a fatal prognosis, Group II with LVDd greater than or equal to 55 mm, Group III with LVDd less than 55 mm but associated with life-threatening ventricular arrhythmias, and Group IV with LVDd less than 55 mm and with no life-threatening ventricular arrhythmias. Patients of Group I (2 cases) had a marked left ventricular dilatation and a poor left ventricular function just before death. Patients of Group II (5 cases) had left ventricular and left atrial dilatation, and 2 of them had serious ventricular arrhythmias. All 3 patients of Group III had ventricular arrhythmia (ventricular tachycardias, coupled premature ventricular contractions and multifocal premature ventricular contractions, respectively), and 2 of them had asymmetric septal hypertrophy. All 10 patients of Group IV had no residual cardiac abnormalities. In conclusion, 50% of 20 myocarditis patients had residual cardiac abnormalities; 6 patients (2 of Group I and 4 of Group II) were complicated by left ventricular dilatation, simulating dilated cardiomyopathy, and 3 (one of Group II and 2 of Group III) showed asymmetric septal hypertrophy, simulating hypertrophic cardiomyopathy.     

Does Rapid Volume Loading During Transesophageal Echocardiography Differentiate Constrictive Pericarditis from Restrictive Cardiomyopathy?

BACKGROUND: Respiratory variation of the pulmonary venous (PV) peak flow velocities can be used to distinguish constrictive pericarditis (constriction) from restrictive cardiomyopathy (restriction). Rapid volume expansion has been used successfully to enhance diastolic pressure equalization in occult constriction. The effect of volume on the respiratory variation in constriction has not been studied previously. This study assessed the utility of volume in enhancing the PV respiratory variation of constriction to further separate it from restriction. METHODS: The study population consisted of 15 patients referred to the echocardiography laboratory for further evaluation of clinically suspected diastolic dysfunction. Pulsed-Doppler transesophageal echocardiography (TEE) of the left or right upper pulmonary vein and mitral inflow was performed with respiratory monitoring before and after infusion of 1 liter of normal saline over 5 to 10 minutes. The classification of patients as constriction (n = 8) or restriction (n = 7) was confirmed independently by cardiac catheterization or surgery. Peak velocities of the PV systolic and diastolic waves and the mitral inflow E were measured during inspiration and expiration. A mean of 3-6 respiratory cycles was obtained for each value before and after volume loading. The percent change from expiration to inspiration (%E) was calculated using the formula %E = expiration - inspiration / expiration. RESULTS: At baseline, patients with constrictive pericarditis can be separated reliably from those with restrictive cardiomyopathy based on a higher systolic/diastolic ratio and greater respiratory variation of their PV diastolic flow velocity. There were no complications in any patient due to volume expansion. Although the change from baseline to volume expansion was not statistically significant in either constriction or restriction, the %E of the PV diastolic wave became significantly higher in constriction than in restriction (P < 0.05). CONCLUSIONS: Rapid volume expansion is relatively safe during TEE and can be used for further separation of constrictive pericarditis from restrictive cardiomyopathy by significantly enhancing the respiratory variation of the PV diastolic flow velocity in constrictive pericarditis.     

Constrictive pericarditis.

The diagnosis of constrictive pericarditis remains a challenge because its physical findings and hemodynamics mimic restrictive cardiomyopathy. Various diagnostic advances over the years enable us to differentiate between these two conditions. This review begins with a case report of constrictive pericarditis, followed by a brief history and discussions of etiologies. Clinical features, radiologic, electrocardiographic, angiographic findings, and hemodynamics of constrictive pericarditis are reviewed. The echocardiographic findings are detailed and the recent advances in Doppler flow velocity patterns of pulmonary, mitral, tricuspid valves and hepatic veins are reported. Nuclear ventriculograms depict rapid ventricular filling in constrictive pericarditis and differentiate it from restrictive cardiomyopathy. Endomyocardial biopsy helps further in recognizing the various types of restrictive cardiomyopathies. Computed tomography and magnetic resonance imaging delineate abnormal pericardial thickness in constrictive pericarditis. Association of characteristic hemodynamic changes and abnormal pericardial thickness > 3 mm usually confirms the diagnosis of constrictive pericarditis. Effusive and occult varieties of constrictive pericarditis are briefly described. This review concludes with emphasizing the importance of pericardial resection.     

Increased right ventricular wall thickness on echocardiography in amyloid infiltrative cardiomyopathy

In six patients with clinically significant amyloid infiltrative cardiomyopathy, echocardiographic right ventricular anterior wall thickness was significantly increased (mean 7.5 ± 2.3 mm; range 5 to 10 mm). This finding in conjunction with the previously described abnormalities of the left ventricle (symmetric increase in wall thickness, diffuse hypokinesia, and small to normal left ventricular diastolic dimension) is consistent with the findings of a diffuse myocardial infiltrative process and should minimize confusion with constrictive pericarditis.     

M-mode echocardiography in constrictive pericarditis

M-mode echocardiograms from 40 patients with proven constrictive pericarditis and 40 subjects without evidence of cardiac disease were reviewed for features previously described in constrictive pericarditis. In this large series, no single feature of the M-mode echocardiogram could be considered diagnostic, although a pattern of normal left ventricular size and systolic function, mild left atrial dilation, flattened diastolic left ventricular posterior wall motion and abnormal septal motion was found in most patients. It is concluded that the M-mode echocardiogram can provide findings suggestive of constrictive pericarditis but must be used in conjunction with hemodynamic and other studies to establish the diagnosis.