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Circulation. 1997;96:1874-1881

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*Cardiomyopathy

(Circulation. 1997;96:1874-1881.)
© 1997 American Heart Association, Inc.

Articles

Phasic Coronary Flow Characteristics in Patients With Constrictive Pericarditis

Comparison With Restrictive Cardiomyopathy

Takashi Akasaka, MD; Kiyoshi Yoshida, MD; Atushi Yamamuro, MD; Takeshi Hozumi, MD; Tsutomu Takagi, MD; Shigefumi Morioka, MD; ; Junichi Yoshikawa, MD

From the Department of Cardiology (T.A., K.Y., A.Y., T.H., T.T., S.M.), Kobe General Hospital, and the First Department of Internal Medicine (J.Y.), Osaka, Japan.

Correspondence to Takashi Akasaka, MD, Department of Cardiology, Kobe General Hospital, Minatojima-nakamachi 4-6, Chuo-ku, Kobe 650, Japan.


*    Abstract
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 *Abstract
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Background Phasic coronary flow characteristics have been reported in patients with aortic valve disease and hypertrophic cardiomyopathy. The purpose of this study was to assess the differences in coronary flow characteristics between patients with constrictive pericarditis and those with restrictive cardiomyopathy.

Methods and Results The study populations consisted of 7 case patients with constrictive pericarditis, 8 with restrictive cardiomyopathy, and 11 control subjects with chest pain and normal coronary arteries. Five minutes after injection of 3 mg of isosorbide dinitrate, phasic coronary flow velocity patterns were analyzed in the proximal segment of the angiographically normal left anterior descending coronary artery at rest using a 0.014-in, 15-MHz Doppler guidewire. Coronary flow reserve was obtained from the ratio of adenosine-induced (0.14 mg · kg-1 · min-1 IV) hyperemic/baseline time-averaged peak velocity. Although in case patients with constrictive pericarditis and restrictive cardiomyopathy maximal hyperemic time-averaged peak velocity (21±8 and 31±17 versus 60±19 cm/s, respectively; P<.001) and coronary flow reserve (1.3±0.4 and 1.6±0.6 versus 3.6±0.4, respectively, P<.001) were significantly lower than in control subjects, there were no significant differences in these indexes between the two groups of case patients. Velocity half-time of diastolic flow velocity corrected by , which indicates deceleration of diastolic flow, in the groups of case patients with constrictive pericarditis and restrictive cardiomyopathy was significantly less than that in control subjects (6.2±2.6 and 10.6±1.5 versus 16.9±2.7, respectively; P<.001); this was also significantly smaller in constrictive pericarditis than restrictive cardiomyopathy (P<.001). This index <9.5 could distinguish constrictive pericarditis from restrictive cardiomyopathy with a sensitivity of 86% and a specificity of 88%. Furthermore, time from the beginning of diastole to diastolic peak velocity corrected by indicating acceleration of diastolic flow velocity in constrictive pericarditis was significantly less than that in restrictive cardiomyopathy and control subjects (2.8±1.2 versus 4.8±0.8 and 4.4±0.6, respectively; P<.001).

Conclusions Although coronary flow reserve is limited in both constrictive pericarditis and restrictive cardiomyopathy because of restriction of hyperemic response, rapid acceleration and more rapid deceleration of diastolic flow velocity are more characteristic in constrictive pericarditis than in restrictive cardiomyopathy.


Key Words: pericarditis • cardiomyopathy • diagnosis • coronary flow


*    Introduction
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Although Doppler echocardiography has provided important information on the pathophysiology of constrictive pericarditis,1 2 3 4 5 6 7 8 9 10 11 the differentiation between constrictive pericarditis and restrictive cardiomyopathy with commonly used diagnostic techniques remains challenging. Previous reports of differential diagnosis of the two conditions have been mostly based on atrial and ventricular filling performance,2 3 4 5 6 7 8 9 10 11 12 13 14 and no report has focused on coronary flow dynamics.

Characteristic phasic coronary flow velocity patterns have been reported in patients with abnormal diastolic ventricular properties, including aortic valve disease15 16 and hypertrophic cardiomyopathy.17 Abnormal diastolic ventricular performance due to reduced ventricular compliance has been marked by well-known hemodynamic characteristics in both constrictive pericarditis and restrictive cardiomyopathy,2 3 4 5 8 9 10 11 12 13 14 18 19 and types of coronary flow patterns different from those of aortic stenosis or hypertrophic cardiomyopathy might be obtained in these patients. Furthermore, a fibrous and constrictive epicardium covering the epicardial coronary artery has been reported in patients with constrictive pericarditis,20 21 and this might influence coronary hemodynamics. Infiltration of intramural coronary arteries and luminal narrowing of the microvessels, which has been described in restrictive cardiomyopathy,22 23 may affect coronary hemodynamics in a different manner from a constrictive state. Thus, both resemblances and differences would be expected with regard to coronary flow characteristics in patients with constrictive pericarditis versus restrictive cardiomyopathy. A recently developed Doppler guidewire has been used easily and safely for the measurement of phasic spectral flow velocity in human coronary arteries, even in the portion distal to the stenosis.24 25 26 27 Using this method, phasic coronary flow characteristics should be easily assessed without flow disturbance in patients without organic stenosis. The purpose of this study was to assess the coronary flow dynamics in patients with constrictive pericarditis and restrictive cardiomyopathy.


*    Methods
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Study Patients
The study populations consisted of 7 case patients with constrictive pericarditis confirmed at surgery and 8 with restrictive cardiomyopathy defined by right ventricular endomyocardial biopsy and other diagnostic methods. All case patients showed predominant right-side heart failure and diastolic ventricular dysfunction by Doppler echocardiography and cardiac catheterization. Of the 7 case patients with constrictive pericarditis, 4 had a prior history of cardiac surgery and 3 had a history of pulmonary tuberculosis. CT scan and MRI indicated pericardial thickness (>4 mm) in all 7 case patients and partial pericardial calcification in 4 case patients. Of the 8 case patients with restrictive cardiomyopathy, no pericardial involvement was defined in any case patients by CT scan and MRI; cardiac amyloidosis was diagnosed in 3, myocardial fibrosis in 4, and restrictive cardiomyopathy 4 years after heart transplantation in 1. Patient age ranged from 44 to 65 years with a mean age of 54±8 years in case patients with constrictive pericarditis and from 29 to 64 years with a mean age of 47±17 years in those with restrictive cardiomyopathy. Eleven additional patients without pericardial and myocardial disease and with angiographically normal coronary arteries who were referred to the cardiac catheterization laboratory for the final evaluation of chest pain served as control subjects. The age of the control subjects ranged from 37 to 69 years with a mean age of 58±11 years. Case patients and control subjects who had stenotic lesions in >25% of the coronary artery, history or ECG findings of an old myocardial infarction, valvular heart disease (except 1 case patient with constrictive pericarditis who had a prior history of mitral valve replacement), hypertension (>140/90 mm Hg), atrial fibrillation, or miscellaneous abnormalities on ECG were excluded from this study. The patients with diabetes mellitus,28 29 hypercholesterolemia,30 and coronary vasospasm,31 which has been reported to have some influences on coronary flow, were also excluded from this study. After written informed consent was obtained, cardiac catheterization, coronary angiography, and the subsequent coronary flow velocity recordings were performed as part of the diagnostic procedure.

Echocardiographic Examination
Transthoracic echocardiography was performed within 24 hours before cardiac catheterization, and mitral flow velocity was recorded by using a pulsed Doppler technique with a 2.5-MHz transducer from an apical long-axis or four-chamber view. The sample volume was placed at the tip of the mitral leaflets, and the velocities were obtained at a paper speed of 100 mm/s with simultaneous recordings of ECG and phonocardiogram. The mean values of peak velocity during rapid filling (E wave) and at atrial contraction (A wave) during five consecutive cardiac cycles, the ratio of E-A velocity, and the deceleration time of the E wave were obtained as previously reported.3 4 9

Cardiac Catheterization and Angiography
Administration of all medications except diuretics was discontinued at least 24 hours before cardiac catheterization. After sedation with 5 mg of diazepam administered orally, patients were taken to the cardiac catheterization laboratory. Any drugs likely to affect coronary hemodynamics (including nitroglycerin) were not used during the catheterization procedure before selective coronary angiography.

Right and left heart catheterization was performed by the femoral approach after local anesthesia with 0.5% lidocaine was administered. The left ventricle was approached in a retrograde manner. Left and right heart pressure data were recorded after intravenous injection of 4000 U of heparin using a micromanometer-tipped catheter (Millar Inc) before selective coronary angiography. Cardiac output was measured by the thermodilution method. Selective coronary angiography was carried out by Judkins' technique after intravenous injection of 3 mg of isosorbide dinitrate. To measure the diameters of the left anterior descending coronary artery at the position corresponding to the tip of the Doppler guidewire, where coronary flow velocity was recorded, coronary angiography was analyzed quantitatively by videodensitometric analysis using a commercially available system (CMS, Medical Imaging Systems, Inc) according to the previous report.32 33

Coronary Flow Velocity Recordings
Phasic coronary flow velocity patterns were recorded at rest and during hyperemia induced by 140 mg · kg-1 · min-1 of adenosine (Adenocard, Fujisawa USA, Inc) infused intravenously in the proximal portion of the left anterior descending coronary artery using a 0.014-in, 15-MHz Doppler guidewire (FloWire, Cardiometrics, Inc) and a velocimeter (FloMap, Cardiometrics, Inc).24 25 26 27 Recordings occurred after selective coronary angiography. Isosorbide dinitrate was injected intravenously before coronary angiography. Pulse repetition frequency of the Doppler flowmeter was variable from 12 to 96 KHz within the velocity range selected.

The Doppler guidewire was advanced into the proximal left coronary artery through a 5F coronary angiography catheter (Selecon, Clinical Supply, Inc) using a technique similar to guidewire manipulation during percutaneous transluminal coronary angioplasty. An optimal Doppler signal was obtained by moving the guidewire slightly within the vessel lumen and adjusting the range gate control. The final position of the Doppler guidewire was confirmed by contrast injection. During the Doppler study, a 12-lead surface ECG and a pressure waveform at the tip of the guiding catheter were monitored continuously.

Frequency analysis of the Doppler signals was performed in real time by fast-Fourier transform using a velocimeter (FloMap, Cardiometrics, Inc).25 Five minutes after injection of contrast medium and isosorbide dinitrate, Doppler signals were recorded at rest and during hyperemia on videotape and by a videoprinter at a sweep speed of 100 mm/s; an ECG and aortic pressure tracing also were recorded. Systolic and diastolic peak velocities, the time average of the instantaneous spectral peak velocity (time-averaged peak velocity), time from the beginning of diastole to diastolic peak velocity, and velocity half-time of diastolic velocity were measured from the phasic coronary flow velocity recordings in the same manner as previously reported.16 17 Coronary flow reserve was obtained from the ratio of maximal hyperemic to baseline resting time-averaged peak velocity.

Statistical Analysis
All data are expressed as mean±SD. One-way ANOVA was used to compare the three groups for clinical characteristics, hemodynamic data, and coronary flow velocity data. Scheffé's F test was performed if the ANOVA showed significant differences. Paired t tests were performed to compare differences between systolic and diastolic coronary diameters within the groups. The relation between deceleration time of transmitral rapid filling wave and velocity half-time of diastolic coronary flow velocity was assessed by linear regression analysis. A value of P<.05 was considered significant.


*    Results
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Clinical Characteristics and Hemodynamic Data
Compared with control subjects, as indicated in Table 1Down, there were no significant differences among case patients with constrictive pericarditis and restrictive cardiomyopathy with regard to patient age, cardiac index, left ventricular end-diastolic and end-systolic volume indexes, and left ventricular ejection fraction. For mitral flow velocity, although there was no significant difference in A-wave velocity among the three groups, E-wave velocity was significantly greater in case patients with constrictive pericarditis and restrictive cardiomyopathy than in control subjects (104±28 and 101±10 versus 59±10 cm/s, respectively; P<.001), and as a result, the ratio of E-A in the former was significantly greater than in control subjects (2.1±0.6, 2.5±1.2 versus 1.0±0.3, respectively; P<.001). The deceleration time of the mitral flow velocity was significantly shorter in case patients with constrictive pericarditis and restrictive cardiomyopathy than in control subjects (107±31 and 123±22 versus 215±32 ms, respectively; P<.001). There was no difference in E wave, E-A, and deceleration time between case patients with constrictive pericarditis versus those with restrictive cardiomyopathy. Right and left ventricular pressure tracings showed a dip and plateau pattern in all case patients with constrictive pericarditis and restrictive cardiomyopathy. Marked elevation of right atrial mean pressure, right ventricular end-diastolic pressure, diastolic pulmonary artery pressure, mean pulmonary wedge pressure, and left ventricular end-diastolic pressure in the case patient groups was confirmed compared with the control subjects, as shown in Table 1Down. Furthermore, equalization or near equalization of these pressures was found in all case patients with constrictive pericarditis and restrictive cardiomyopathy, and there were no significant differences in the pressure data between these two groups. Mean aortic pressure was significantly lower in case patients with constrictive pericarditis than in control subjects, although there was no significant difference in mean aortic pressure in case patients with restrictive cardiomyopathy compared with the other two groups. Although end-systolic and end-diastolic diameters of the left anterior descending coronary artery where coronary flow velocity was recorded were not significantly different among three groups, quantitative coronary angiography showed no significant change in diameter in systole compared with that in diastole in case patients with constrictive pericarditis and a mild but significant increase in diameter in systole in all case patients with restrictive cardiomyopathy and control subjects. As a result, percent change in the diameter of the left anterior descending coronary artery from end-diastole to end-systole was significantly smaller in case patients with constrictive pericarditis versus those with restrictive cardiomyopathy and control subjects (99±2% versus 104±2% and 106±3%, respectively; P<.001).


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  		Table 1. Clinical Characteristics and Hemodynamic Data for Case Patients With Constrictive Pericarditis or Restrictive Cardiomyopathy and Control Subjects

Coronary Flow Velocity Data
Compared with control subjects, as described in Table 2Down, there were no significant differences in baseline systolic and diastolic peak velocities in case patients with constrictive pericarditis and restrictive cardiomyopathy. As demonstrated in Fig 1Down, flow reversal was observed in mid- to late systole in 4 of 7 case patients with constrictive pericarditis, although antegrade flow signal was seen during systole in the remaining 3 with constrictive pericarditis and all restrictive cardiomyopathy case patients and control subjects, as indicated in Fig 2Down. Although the time from the beginning of diastole to diastolic peak velocity, which indicates acceleration of diastolic flow velocity, was not significantly different between case patients with restrictive cardiomyopathy and control subjects, that in case patients with constrictive pericarditis was significantly shorter than that in the other two groups (77±34 versus 138±25 and 137±18 ms, re-spectively; P<.001). This was also seen if the time was corrected by (2.8±1.2 versus 4.9±0.8 and 4.4±0.6, respectively; P<.001). Deceleration of diastolic flow, which was demonstrated by velocity half-time of diastolic peak velocity, was significantly shorter in both case patients with constrictive pericarditis and restrictive cardiomyopathy compared with control subjects (172±69 and 300±41 versus 525±98 ms, respectively; P<.001). Furthermore, this was also significantly shorter in case patients with constrictive pericarditis versus restrictive cardiomyopathy (P<.001). These relations among three groups were also obtained if the velocity half-time of diastolic flow velocity was corrected by (control subjects, 16.9±2.7, versus 6.2±2.6 for case patients with constrictive pericarditis and 10.6±1.5 for those with restrictive cardiomyopathy; P<.001) (see Table 2Down). As indicated in Fig 3Down, velocity half-time <260 ms or that corrected by <9.5 could distinguish constrictive pericarditis from restrictive cardiomyopathy with a sensitivity of 86% and a specificity of 88%. Furthermore, velocity half-time <380 ms predicted constrictive pericarditis and restrictive cardiomyopathy with a sensitivity of 100% and a specificity of 100%, and that corrected by <12.0 could distinguish those from control subjects with a sensitivity of 93% and a specificity of 100%. Although baseline time-averaged peak velocity was not significantly different among the three groups, as indicated in Table 2Down, maximal hyperemic time-averaged peak velocity was significantly less in case patients with constrictive pericarditis and restrictive cardiomyopathy compared with control subjects (21±8 and 31±17 versus 60±19 cm/s, respectively; P<.001). As a result, coronary flow reserve was significantly smaller in the two former groups compared with the control subjects (1.3±0.4 and 1.6±0.6 versus 3.6±0.4, respectively; P<.001).


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  		Table 2. Coronary Flow Velocity Data for Case Patients With Constrictive Pericarditis or Restrictive Cardiomyopathy and Control Subjects



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  		Figure 1. Examples of coronary flow velocity recordings in the proximal left anterior descending coronary artery (LAD) at baseline before prior cardiac operation (left) and pericardiectomy (right) in a patient with constrictive pericarditis after patch closure of atrial septal defect (ASD). Compared with that before patch closure of ASD (pre-op ASD), rapid acceleration (TPV=49 vs 140 ms) and deceleration (VHT=92 vs 433 ms) of diastolic velocity are remarkable before pericardiectomy. APV indicates time-averaged peak velocity; DPV, diastolic peak velocity; TPV, time from the beginning of diastole to the DPV; VHT, velocity half-time of diastolic velocity.



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  		Figure 2. Examples of coronary flow velocity recordings in the proximal left anterior descending coronary artery at baseline in a patient with restrictive cardiomyopathy (left) and a control subject (right). Compared with that in a control subject, rapid deceleration of diastolic flow (VHT=238 vs 387 ms) is found in a patient with restrictive cardiomyopathy. Abbreviations are as in Fig 1Up.



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  		Figure 3. Scatterplots of velocity half-time (left) and that corrected by (right) in case patients with constrictive pericarditis, case patients with restrictive cardiomyopathy, and control subjects. Velocity half-time <260 ms or that corrected by <9.5 distinguishes constrictive pericarditis from restrictive cardiomyopathy with a sensitivity of 86% and a specificity of 88%. Velocity half-time <380 ms predicted constrictive pericarditis or restrictive cardiomyopathy with a sensitivity of 100% and a specificity of 100%, and that corrected by <12.0 could distinguish those from control subjects with a sensitivity of 93% and a specificity of 100%.

Relationship Between Diastolic Flow of Transmitral Flow Velocity and Coronary Flow Velocity
As shown in Fig 4Down, there was a significant linear correlation between deceleration time of the transmitral rapid filling wave and velocity half-time of diastolic coronary flow, with substantial scatter (r=.73; P<.001; SEE=0.41). In similar values of deceleration time of transmitral flow, deceleration of diastolic coronary flow velocity as indicated by velocity half-time in case patients with constrictive pericarditis was more rapid than in case patients with restrictive cardiomyopathy, except in one patient.



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  		Figure 4. Scatterplot of deceleration time of transmitral flow velocity and velocity half-time of diastolic coronary flow velocity. A significant linear correlation between deceleration time of transmitral rapid filling wave and velocity half-time of diastolic coronary flow are observed with substantial scatter (r=.73; P<.001; SEE=0.41). Solid circles indicate case patients with constrictive pericarditis; open triangles, those with restrictive cardiomyopathy; and open circles, control subjects. Dotted line indicates 90% confidence bands.


*    Discussion
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 up arrowIntroduction
 up arrowMethods
 up arrowResults
 *Discussion
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The present study demonstrates the differences of coronary flow dynamics between constrictive pericarditis and restrictive cardiomyopathy, which are characterized by rapid acceleration and more rapid deceleration of diastolic flow velocity in the former compared with the latter, although other cardiac hemodynamic data are not significantly different between the two groups. This study also indicates the resemblances of coronary circulation in the two diseases, which are shown by rapid deceleration of diastolic flow velocity, reduction of peak hyperemic flow velocity, and restriction of coronary flow reserve, compared with control subjects. These differences and similarities of coronary flow dynamics in constrictive pericarditis and restrictive cardiomyopathy might be based on the functional resemblance of cardiac hemodynamics, which is characterized by normal or near-normal systolic function and restriction of ventricular filling2 3 4 5 8 9 10 11 12 13 18 19 and the different pathogeneses of these diseases, which is represented by pericardial involvement in the former and myocardial disorder in the latter.

Rapid deceleration of diastolic flow velocity compared with control subjects was found in both constrictive pericarditis and restrictive cardiomyopathy case patients, although it was more rapid in the former than the latter. From the concept of diastolic coronary driving pressure–flow relations,34 35 36 even in patients with normal coronary arteries, rapid deceleration of diastolic flow would be expected in patients with increased resistance in micovasculature and elevated zero-flow pressure. Left ventricular hypertrophy has been pointed out as one of the causes of increased microvascular resistance and elevation of zero-flow pressure,35 36 and rapid deceleration of diastolic flow velocity has been reported in patients with aortic stenosis16 and hypertrophic cardiomyopathy.17 In both constrictive pericarditis and restrictive cardiomyopathy, elevation of zero-flow pressure should be expected because of the markedly elevated end-diastolic ventricular pressure. Increases in microvascular resistance also would be expected in both cases, because myocardial damage has been reported in constrictive pericarditis20 and myocardial disorder is the primary pathogenesis in restrictive cardiomyopathy. Furthermore, infiltration of intramural coronary arteries and luminal narrowing of the microvessels have been reported in the latter,22 23 and this might be a cause of increases in microvascular resistance. Thus, rapid deceleration of diastolic flow velocity in constrictive pericarditis and restrictive cardiomyopathy might be related to increases in microvascular resistance and elevation of zero-flow pressure.

Flow reversal in mid to late systole was observed in 4 of 7 case patients with constrictive pericarditis, although this was not seen in any case patients with restrictive cardiomyopathy and control subjects. Although none showed marked compression of the epicardial coronary artery, as reported in myocardial bridging,37 quantitative coronary angiography demonstrated no significant change in coronary artery diameter during systole in case patients with constrictive pericarditis. This diameter change during cardiac cycle might be related to reduced compliance of epicardial coronary artery caused by epicardial involvement,20 21 because a slight increase in diameter should be expected in the epicardial coronary artery if it was compliant enough, as seen in restrictive cardiomyopathy case patients and control subjects. In patients with reduced compliance of the epicardial coronary artery, flow reversal in mid to late systole might be observed as a reflection of antegrade flow in early systole, as demonstrated in case patients with constrictive pericarditis in the present study. Thus, flow reversal in mid to late systole might also be characteristic in constrictive pericarditis.

Reduced maximal hyperemic flow velocity and restricted coronary flow reserve were also characteristic in both constrictive pericarditis and restrictive cardiomyopathy. Even in patients with a normal epicardial coronary artery, coronary flow reserve should be limited in patients with increases in microvascular resistance and elevated zero-flow pressure, because maximal hyperemic flow would be restricted.34 As discussed above, myocardial damage in constrictive pericarditis20 and microvascular disease in restrictive cardiomyopathy22 23 would limit hyperemic flow and reduce coronary flow reserve. Furthermore, an increase in left ventricular preload has been reported to reduce coronary flow reserve,38 as confirmed by marked elevation of pulmonary capillary wedge pressure in both constrictive pericarditis and restrictive cardiomyopathy in the present study. Thus, increases in microvascular resistance, zero-flow pressure, and left ventricular preload would be causes of reduced maximal hyperemic flow and restriction of coronary flow reserve in both diseases. Although mean aortic pressure, which is thought to be the index of coronary driving pressure, was significantly lower in patients with constrictive pericarditis compared with control subjects, this would hardly affect basal coronary flow because of the autoregulation system.35 It also has been reported that changes in mean aortic pressure do not alter coronary flow reserve38 and the difference in mean aortic pressure may not be a main cause of the restriction of coronary flow reserve. Reduction of coronary flow reserve with angiographically normal coronary arteries has been reported in patients with diabetes mellitus,28 29 hypercholesterolemia,30 coronary vasospasm,31 hypertension,39 hypertrophic cardiomyopathy,40 and aortic stenosis,41 and these patients were excluded from this study. Thus, the present study should be the first report of restriction of coronary flow reserve in case patients with constrictive pericarditis and restrictive cardiomyopathy.

Rapid acceleration and more rapid deceleration of diastolic flow velocity were characteristic in constrictive pericarditis compared with restrictive cardiomyopathy. In patients with constrictive pericarditis, not only pericardial but also epicardial involvements have been reported to have an important influence on pathophysiology, including hemodynamics and the results of operation.20 21 Thus, compliance of the epicardial coronary artery surrounded by the diseased epicardium should be reduced in case patients with constrictive pericarditis, and coronary hemodynamics should resemble left ventricular performance because of this restricted epicardial coronary artery. No significant change in epicardial coronary artery diameter during the cardiac cycle in constrictive pericarditis in the present study would reflect this restricted compliance of the epicardial coronary artery. However, there has been no report of histological abnormality in epicardial coronary artery in restrictive cardiomyopathy,22 23 and compliance of epicardial coronary artery would be maintained in restrictive cardiomyopathy. A significant increase in epicardial coronary artery diameter in systole in case patients with restrictive cardiomyopathy in the present study might support the adequate compliance of the epicardial coronary artery, as demonstrated in control subjects. This restricted epicardial coronary artery compliance might be a cause of rapid acceleration and more rapid deceleration of diastolic flow velocity in case patients with constrictive pericarditis compared with restrictive cardiomyopathy, and these differences should be based on the pathogenesis of the two diseases. As demonstrated in the relationship between deceleration time of transmitral rapid filling wave and velocity half-time of diastolic coronary flow (Fig 4Up), in the similar restricted left ventricular conditions, which might be indicated by similar deceleration time of transmitral flow velocity, deceleration of diastolic coronary flow velocity in case patients with constrictive pericarditis tended to be more rapid than that in case patients with restrictive cardiomyopathy, except 1 patient. This could also be explained by the restriction of epicardial coronary artery compliance in constrictive pericarditis. Microvascular disease has been reported,22 23 and it would reduce compliance of the microvasculature in restrictive cardiomyopathy. Rapid acceleration and more rapid deceleration of diastolic flow velocity would be recorded if flow velocity of intramural arteries was obtained even in restrictive cardiomyopathy. However, the epicardial coronary artery would be compliant enough, as discussed above, to interfere with this flow pattern of intramural arteries; the characteristic flow pattern of rapid acceleration and rapid deceleration of diastolic flow velocity would disappear or become uncertain in epicardial coronary arteries in restrictive cardiomyopathy. To confirm the influence of epicardial disease on coronary flow, recording of coronary flow velocity after pericardiectomy in patients with constrictive cardiomyopathy would be useful. Furthermore, recently developed intravascular ultrasound may give us some information about compliance and stiffness of the epicardial coronary artery by measuring the cross-sectional area and driving pressure of the epicardial coronary artery at the same time.42 43 44 45 Further study should be performed to analyze the mechanisms of these differences in coronary hemodynamics in the two diseases.

Just as the chambers of the heart are physically restricted, physical restriction of the coronary vascular bed could be expected in both constrictive pericarditis and restrictive cardiomyopathy. This physical restriction would reduce compliance of the vascular bed and exaggerate deceleration and acceleration phases of coronary flow. Furthermore, reduced coronary flow reserve would be expected in both conditions because the restricted coronary vascular bed cannot expand to accommodate heavy coronary flow. In constrictive pericarditis versus restrictive cardiomyopathy, compliance of the coronary vascular bed might be restricted much more because the epicardial coronary artery is also restricted, as discussed above. These might be mechanisms of resemblance and difference in coronary flow characteristics between patients with constrictive pericarditis and restrictive cardiomyopathy.

Study Limitations
Several limitations to the present study must be considered. First, although angiographically normal patients were included in the present study, it would be difficult to exclude completely patients with diffuse concentric thickening of the coronary vessel wall by use of angiography alone. Recently developed intravascular ultrasound techniques would be more accurate for exclusion of diseased coronary arteries.42 43 Furthermore, as discussed above, stiffness or compliance of the epicardial coronary artery would be assessed using this method by measuring cross-sectional area and coronary driving pressure at the same time.44 45 Second, reduced coronary flow reserve with angiographically normal coronary arteries also has been reported in patients in the postmenopausal state,46 47 48 and these patients were not excluded from this study. However, compared with control subjects, there were no significant differences in the ratio of men to women among the three groups, and this might not be a main cause of restriction of coronary flow reserve in the present study. Third, as in all invasive studies, control subjects in the present study might not be completely normal because they were being investigated for chest pain. However, no abnormalities were confirmed by ECG, echocardiogram, left ventriculogram, and coronary angiogram in any patients, and they all demonstrated normal coronary flow reserves. Thus, they would be thought to be normal. Fourth, the number of study patients was limited in the present study. However, the diagnoses of constrictive pericarditis and restrictive cardiomyopathy are reliable in all patients and the tendencies of coronary hemodynamics were similar in each patient group. Similar results would be expected in a further study with more patients. Fifth, flow velocities were analyzed only in the left anterior descending coronary artery in the present study. Additional studies in the right and the left circumflex coronary arteries would give us more complete information about coronary circulation in constrictive pericarditis and restrictive cardiomyopathy.

Conclusions
Although coronary flow reserve is limited in patients with constrictive pericarditis and restrictive cardiomyopathy because of restriction of hyperemic response, rapid acceleration and more rapid deceleration of diastolic flow velocity are characteristic of patients with constrictive pericarditis versus those with restrictive cardiomyopathy. These resemblances and differences of coronary hemodynamics are based on the pathogenesis of the two diseases: pericardial and epicardial involvement in the former and myocardial disorder in the latter.

Received January 27, 1997; revision received April 23, 1997; accepted May 2, 1997.


*    References
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 *References
 

  1. Engel PJ, Fowler NO, Tei C, Shah PM, Driedger HJ, Shabetai R, Harbin AD, Franch RH. M-mode echocardiography in constrictive pericarditis. J Am Coll Cardiol. 1985;6:471-474.[Abstract]
  2. Pandian NG, Skorton DJ, Kieso RA, Kerber RE. Diagnosis of constrictive pericarditis by two-dimensional echocardiography: studies in a new experimental model and in patients. J Am Coll Cardiol. 1984;75:1164-1173.
  3. Appleton CP, Hatle LK, Popp RL. Demonstration of restrictive ventricular physiology by Doppler echocardiography. J Am Coll Cardiol.. 1988;11:757-768.[Abstract]
  4. Hatle LK, Appleton CP, Popp RL. Differentiation of constrictive pericarditis and restrictive cardiomyopathy by Doppler echocardiography. Circulation.. 1989;79:357-370[Abstract/Free Full Text]
  5. Schiavone WA, Calafiore PA, Salcedo EE. Transesophageal Doppler echocardiographic demonstration of pulmonary venous flow velocity in restrictive cardiomyopathy and constrictive pericarditis. Am J Cardiol. 1989;63:1286-1288.[Medline] [Order article via Infotrieve]
  6. Von Bibra H, Schober K, Jenni R, Busch R, Sebenig H, Blomer H. Diagnosis of constrictive pericarditis by pulsed Doppler echocardiography of the hepatic vein. Am J Cardiol. 1989;63:1464-1470.
  7. Byrd BF, Linden RW. Superior vena cava Doppler flow velocity patterns in pericardial disease. Am J Cardiol. 1990;65:1464-1670.[Medline] [Order article via Infotrieve]
  8. Klein AL, Cohen GI, Pietrolungo JF, White RD, Bailey A, Pearce GL, Stewart WJ, Salcedo EE. Differentiation of constrictive pericarditis from restrictive cardiomyopathy by Doppler transesophageal echocardiographic measurements of respiratory variations in pulmonary venous flow. J Am Coll Cardiol. 1993;22:1935-1943.[Abstract]
  9. Oh JK, Hatle LK, Seward JB, Danielson GK, Schaff HV, Reeder GS, Tajik AJ. Diagnostic role of Doppler echocardiography in constrictive pericarditis. J Am Coll Cardiol. 1994;23:154-162.[Abstract]
  10. Garcia MJ, Rodriguez L, Ares M, Griffin BP, Thomas JD, Klein AL. Differentiation of constrictive pericarditis from restrictive cardiomyopathy: assessment of left ventricular diastolic velocities in longitudinal axis by Doppler tissue imaging. J Am Coll Cardiol. 1996;27:108-114.[Abstract]
  11. Klodas E, Nishimura RA, Appleton CP, Redfield MM, Oh JK. Doppler evaluation of patients with constrictive pericarditis: use of tricuspid regurgitation velocity curves to determine enhanced ventricular interaction. J Am Coll Cardiol. 1996;28:652-657.[Abstract]
  12. Tyberg TH Goodyear AV, Hurst VW, Alexander J, Langou RA. Left ventricular filling in differentiating restrictive amyloid cardiomyopathy and constrictive pericarditis. Am J Cardiol. 1981;47:791-796.[Medline] [Order article via Infotrieve]
  13. Aroney CN, Ruddy TD, Dighero H, Fifer MA, Boucher CA, Palacios IF. Differentiation of restrictive cardiomyopathy from pericardial constriction: assessment of diastolic function by radionuclide angiography. J Am Coll Cardiol. 1989;13:1007-1014.[Abstract]
  14. Oren RM, Grover-Mckay M, Stanford W, Weiss RM. Accurate preoperative diagnosis of pericardial constriction using cine computed tomography. J Am Coll Cardiol. 1993;22:832-838.[Abstract]
  15. Hongo, Goto T, Watanabe N, Nakatsuka T, Tanaka M, Kinoshita O, Yamada H, Okubo S, Sekiguchi M. Relation of phasic coronary flow velocity profile to clinical and hemodynamic characteristics of patients with aortic valve disease. Circulation. 1993;88:953-960.[Abstract/Free Full Text]
  16. Yoshikawa J, Akasaka T, Yoshida K, Takagi T. Systolic coronary flow reversal and abnormal diastolic flow patterns in patients with aortic stenosis: assessment with an intracoronary Doppler catheter. J Am Soc Echocardiogr. 1993;6:516-524.[Medline] [Order article via Infotrieve]
  17. Akasaka T, Yoshikawa J, Yoshida K, Maeda K, Takagi T, Miyake S. Phasic coronary flow characteristics in patients with hypertrophic cardiomyopathy: a study by coronary Doppler catheter. J Am Soc Echocardiogr. 1994;7:9-19.[Medline] [Order article via Infotrieve]
  18. Swanton RH, Brooksby IAB, Davies MJ, Coltart DJ, Jenkins BS, Webb-Peploe MM. Systolic and diastolic ventricular function in cardiac amyloidosis. Am J Cardiol. 1977;39:658-664.[Medline] [Order article via Infotrieve]
  19. Benotti JR, Grossman W, Chon PF. Clinical profile of restrictive cardiomyopathy. Circulation. 1980;61:1206-1212.[Abstract/Free Full Text]
  20. Walsh TJ, Baughman KL, Gardner TJ, Bulkley BH. Constrictive epicarditis as a cause of delayed or absent response to pericardiectomy: a clinicopathological study. J Thorac Cardiovasc Surg. 1982;83:126-132.[Abstract]
  21. Seifert FC, Miller DC, Oesterle SN, Oyer PE, Stinson EB, Shumway NE. Surgical treatment of constrictive pericarditis: analysis of outcome and diagnostic error. Circulation. 1985;72(suppl II):II-264-II-273.
  22. Benson MD. Hereditary amyloidosis and cardiomyopathy. Am J Med. 1992;93:1-2.[Medline] [Order article via Infotrieve]
  23. Booth DR, Tan SY, Hawkinds PN, Pepys MB, Frustaci A. A novel variant of transthyretin, 59ThrLys, associated with autosomal dominant cardiac amyloidosis in an Italian family. Circulation. 1995;91:962-967.[Abstract/Free Full Text]
  24. Segal J, Kern MJ, Scott NA, King SB III, Doucette JW, Heuser RR, Ofili E, Siegel R. Alterations of phasic coronary artery flow velocity in human during percutaneous coronary angioplasty. J Am Coll Cardiol. 1992;20:276-286.[Abstract]
  25. Doucette JW, Corl PD, Payne HM, Flynn AE, Goto M, Nassi M, Segal J. Validation of a Doppler guide wire for intravascular measurement of coronary artery flow velocity. Circulation. 1992;85:1899-1911.[Abstract/Free Full Text]
  26. Ofili EO, Labovitz AJ, Kern MJ. Coronary flow velocity dynamics in normal and diseased arteries. Am J Cardiol. 1993;71:3D-9D.[Medline] [Order article via Infotrieve]
  27. Joye JD, Schulman DS, Lasorda D, Farah T, Donohue BC, Reichek N. Intracoronary Doppler guide wire versus stress single-photon emission computed tomographic thallium-201 imaging in assessment of intermediate coronary stenoses. J Am Coll Cardiol. 1994;24:940-947.[Abstract]
  28. Nitenberg A, Valensi P, Sachs R, Dail M, Aptecar E, Attali J. Impairment of coronary vascular reserve and Ach-induced coronary vasodilatation in diabetic patients with angiographically normal coronary arteries and normal left ventricular systolic function. Diabetes. 1993;42:1017-1025.[Abstract]
  29. Nahser PJ, Brown RE, Oskarsson H, Winniford MD, Rossen JD. Maximal coronary flow reserve and metabolic coronary vasodilation in patients with diabetes mellitus. Circulation. 1995;91:635-640.[Abstract/Free Full Text]
  30. Egashira K, Hirooka Y, Kai H, Sugimachi M, Suzuki S, Inou T, Takeshita A. Reduction in serum cholesterol with pravastatin improves endothelium-dependent coronary vasomotion in patients with hypercholesterolemia. Circulation. 1994;89:2519-2524.[Abstract/Free Full Text]
  31. Cannon RO III, Schenke WH, Leon MB, Rosing DR, Urqhart J, Epstein SE. Limited coronary flow reserve after dipyridamole in patients with ergonovine-induced coronary vasoconstriction. Circulation. 1987;75:163-174.[Abstract/Free Full Text]
  32. Desmet W, De Scheerder I, Beatt K, Huehns T, Piessens J. In vivo comparison of different quantitative edge detection systems used for measuring coronary arterial diameters. Cathet Cardiovasc Diagn. 1995;34:72-80.[Medline] [Order article via Infotrieve]
  33. Hausleiter J, Nolte CWT, Jost S, Weise B, Sturm M, Lichtlen PR. Comparison of different quantitative coronary analysis systems: ARTREK, CAAS, and CMS. Cathet Cardiovasc Diagn. 1996;37:14-22.[Medline] [Order article via Infotrieve]
  34. Bellamy RF. Diastolic coronary pressure-flow relations in the dog. Circ Res. 1978;43:92-101.[Abstract/Free Full Text]
  35. Klocke FJ. Measurements of coronary flow reserve: defining pathophysiology versus making decisions about patient care. Circulation. 1987;76;1183-1189.
  36. Duncker DJ, Zhang J, Bache RJ. Coronary pressure-flow relation in left ventricular hypertrophy: importance of changes in back pressure versus changes in minimum resistance. Circ Res. 1993;72:579-587.[Abstract/Free Full Text]
  37. Ge J, Erbel R, Rupprecht HJ, Koch L, Kearney P, Gorge G, Haude M, Meyer J. Comparison of intravascular ultrasound and angiography in the assessment of myocardial bridging. Circulation. 1994;89:1725-1732.[Abstract/Free Full Text]
  38. McGinn AL, White CW, Wilson RF. Interstudy variability of coronary flow reserve: influence of heart rate, arterial pressure, and ventricular preload. Circulation. 1990;81:1319-1330.[Abstract/Free Full Text]
  39. Opherk D, Mall G, Zebe H, Schwartz F, Weihe B, Manthey J, Kubler W. Reduction of coronary reserve: a mechanism for angina pectoris in patients with arterial hypertension and normal coronary arteries. Circulation. 1984;69:1-7.[Abstract/Free Full Text]
  40. Cannon RO, Rosing DR, Maron BJ, Leon MB, Bonow RO, Watson RM, Epstein SE. Myocardial ischemia in patients with hypertrophic cardiomyopathy: contribution of inadequate vasodilator reserve and elevated left ventricular filling pressures. Circulation. 1985;71:234-243.[Abstract/Free Full Text]
  41. Marcus ML, Doty DB, Hiratsuka LF, Wright CB, Eastham CL. Decreased coronary flow reserve: a mechanism for angina pectoris in patients with aortic stenosis and normal coronary arteries. N Engl J Med. 1982;307:1362-1367.[Abstract]
  42. Fitzgerald PJ, St. Goar FG, Connolly AJ, Pinto FJ, Billingham ME, Popp RL, Yock PG. Intravascular ultrasound imaging of coronary arteries: is three layers the norm? Circulation. 1992;86:154-158.[Abstract/Free Full Text]
  43. Yamagishi M, Miyatake K, Tamai J, Nakatani S, Koyama J, Nissen SE. Intravascular ultrasound detection of atherosclerosis at the site of focal vasospasm in angiographically normal or minimally narrowed coronary segments. J Am Coll Cardiol. 1994;23:352-357.[Abstract]
  44. Pinto FJ, St. Goar FG, Fischell TA, Stadius ML, Valantine HA, Alderman EL, Popp RL. Nitroglycerin-induced coronary vasodilation in cardiac transplant recipients: evaluation with in vivo intracoronary ultrasound. Circulation. 1992;85:69-77.[Abstract/Free Full Text]
  45. Yamagishi M, Nissen SE, Booth DC, Gurley JC, Koyama J, Kawano S, Demaria AN. Coronary reactivity to nitroglycerin: intravascular ultrasound evidence for the importance of plaque distribution. J Am Coll Cardiol. 1995;25:224-230.[Abstract]
  46. Reis SE, Gloth ST, Blumenthal RS, Resar JR, Zacur HA, Gerstenblith G, Brinker JA. Ethinyl estradiol acutely attenuates abnormal coronary vasomotor responses to acetylcholine in postmenopausal women. Circulation. 1994;89:52-60.[Abstract/Free Full Text]
  47. Collins P, Rosano GMC, Sarrel PM, Ulrich L, Adamopoulos S, Beale CM, McNeill JG, Poole-Wilson PA. 17-Estradiol attenuates acetylcholine-induced coronary arterial constriction in women but not men with coronary heart disease. Circulation. 1995;92:24-30.[Abstract/Free Full Text]
  48. Gilligan DM, Quyyumi AA, Cannon RO, Johnson GB, Schenke WH. Effects of physiological levels of estrogen on coronary vasomotor function in postmenopausal women. Circulation. 1994;89:2545-2551.[Abstract/Free Full Text]



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