Computerized Acoustic Cardiographic Insights into the Pericardial Knock in Constrictive Pericarditis

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1 Clin. Cardiol. 30, (2007) Computerized Acoustic Cardiographic Insights into the Pericardial Knock in Constrictive Pericarditis Andrew D. Michaels, M.D., M.A.S., Mohan N. Viswanathan, M.D., Mark V. Jordan, M.D., Kanu Chatterjee, M.B. Division of Cardiology, Department of Medicine, University of Utah, Salt Lake City, Utah; Division of Cardiology, Department of Medicine, University of California at San Francisco Medical Center, San Francisco, California, USA Summary Background: One of the clinical hallmarks of constrictive pericarditis is the pericardial knock, a high-pitched early diastolic heart sound. Making the clinical diagnosis of constrictive pericarditis is challenging, as is accurate auscultation of the pericardial knock. Hypothesis: We sought to assess the utility of a computerized acoustic cardiographic device in the assessment of the pericardial knock in patients with constrictive pericarditis. Methods: We report a case series in which computerized acoustic cardiography (Audicor, Inovise Medical Inc., Portland, OR) is performed in patients with constrictive pericarditis. Results: Three patients with constrictive pericarditis underwent computerized acoustic cardiographic recordings at the time of cardiac catheterization. In each case, initial physical examination by the internist and referring cardiologist did not appreciate a pericardial knock. Acoustic cardiography demonstrated a high-pitched early diastolic sound in each case. Time-frequency representation analyses showed the high-frequency components of the pericardial knock sound. Repeat acoustic cardiography demonstrated resolution of the pericardial knock after pericardiectomy in two patients. Conclusions: Non-invasive computerized acoustic cardiography can demonstrate the high-pitched pericardial Address for reprints: Andrew D. Michaels, M.D., M.A.S. Division of Cardiology, University of Utah 30 North 1900 East, Room 4A100 Salt Lake City, UT , USA andrew.michaels@hsc.utah.edu Received: November 27, 2006 Accepted: January 31, 2007 Published online in Wiley InterScience ( DOI: /clc Wiley Periodicals, Inc. knock in patients with constrictive pericarditis. This may aid the bedside assessment of patients with diastolic heart failure, improving the clinician s ability to appreciate the ausculatory findings in constrictive pericarditis. Key words: constrictive pericarditis, phonocardiography, auscultation, pericardiectomy, pericardial knock, acoustic cardiography Clin. Cardiol. 2007; 30: Wiley Periodicals, Inc. Introduction Differentiating constrictive pericarditis from restrictive cardiomyopathy has proved to be a challenging diagnostic dilemma in cardiology for many decades. 1 The clinical presentations are quite similar as many patients present with insidiously progressive fatigue, dyspnea on exertion, and abdominal girth. Making the specific diagnosis of either condition is difficult if one relies on the history, physical examination, and echocardiography. Furthermore, in the cardiac catheterization laboratory, the invasive hemodynamic pressure waveforms in these two conditions also may be similar. 2 However, it becomes important to differentiate these conditions because the prognosis and therapeutic strategies for these conditions vary significantly. Constrictive pericarditis may be cured by surgical pericardial stripping. Restrictive cardiomyopathy is often only amenable to medical supportive therapy, with no cure short of cardiac transplantation. Clues to differentiating these conditions may come from the physical examination, chest radiography, electrocardiography, echocardiography, and cardiac computed tomography and magnetic resonance imaging. 3 6 Echocardiographic assessment of chamber sizes, interventricular septal motion, and Doppler-based evaluation of the mitral and tricuspid inflow patterns may aid cardiologists in distinguishing these diagnoses. 7 Cardiac computed tomography and magnetic resonance imaging has

2 A. D. Michaels et al.: Computerized acoustic cardiography in constrictive pericarditis 451 a role in detecting a thickened pericardium and may be used in suspected cases of constrictive pericarditis. 8 On physical examination, one of the classic findings in constrictive pericarditis is the presence of a highpitched early diastolic pericardial knock, which may be distinguished from the early diastolic low-pitched third heart sound heard in congestive heart failure that has a lower frequency. 9,10 A potential tool in identifying this extra heart sound is phonocardiography, which was routinely performed in the past but has had less of a role in modern cardiac physical diagnosis. 11 We report three cases of constrictive pericarditis in which the initial referring cardiologists physical examination did not reveal a pericardial knock. In each case, acoustic cardiography demonstrated the pericardial knock. Acoustic cardiography was used to record the distinctive high-pitched early diastolic sound representing a pericardial knock, which was also appreciated on physical examination of these patients. Repeat acoustic cardiography in two of the patients demonstrated resolution of this sound shortly following pericardiectomy. Case 1 A 49-year-old Caucasian man was evaluated for the chief complaint of 1.6 years of progressive generalized weakness, dyspnea on exertion, and pedal edema. An echocardiogram at an outside hospital showed mild global hypokinesis with a left ventricular ejection fraction of 35%. He had no other past medical history but was initially given a diagnosis of idiopathic dilated cardiomyopathy. He subsequently developed rapid atrial fibrillation and flutter.multiple attempts at electrical and chemical cardioversion were unsuccessful. There was no past history of pericarditis, chest pain, malignancy, exposure to tuberculosis, radiation, foreign travel, or rheumatological disease. He was referred to our medical institution because of refractory heart failure symptoms. His medications included digoxin, carvedilol, lisinopril, furosemide, and warfarin. On physical examination, his blood pressure was 95/50 mmhg, heart rate of 60 beats per min, respiratory rate of 18 per min. His jugular venous pressure was markedly elevated to the angle of the jaw. He had normal first and second heart sounds. Initial physical examination by the referring cardiologist did not reveal a pericardial knock. Subsequent examination by the cardiac catheterization team revealed a loud early diastolic pericardial knock heard best with the patient leaning forward. There was no S3, S4, murmur, rub, or parasternal lift. There was no hepatomegaly and no hepatojugular reflux was elicited. Mild peripheral edema was appreciated. The 12-lead electrocardiogram demonstrated atrial flutter with variable AV conduction at a rate of 64 beats per min. His laboratory data revealed mild elevations of total bilirubin (1.7 mg/dl), AST (42 U/L), ALT (36 U/L), and B-type natriuretic peptide level (229 pg/ml). His chest X-ray shows mild cardiomegaly and extensive pericardial calcification over both the right and left ventricles. No pulmonary edema or pleural effusions were noted. A repeat transthoracic echocardiogram at our institution revealed a left ventricular ejection fraction of 50%, normal right ventricular size and function, and moderate biatrial enlargement. There was a thickened and echogenic pericardium with absence of normal sliding motion. There was significant respiro-phasic variation of the mitral and tricuspid inflow patterns. The pulmonary artery systolic pressure was estimated at 35 mmhg, while the inferior vena cava was significantly dilated to 3 cm with no collapse during inspiration. Cardiac catheterization showed a mean right atrial pressure of 15 mmhg, right ventricular pressure 27/15 mmhg, pulmonary artery pressure 27/15 mmhg with a mean of 18 mmhg, pulmonary capillary wedge pressure 15 mmhg, and left ventricular pressure 80/15 mmhg. There was a prominent dip-and-plateau pattern in the ventricular diastolic waveforms, diastolic elevation and equalization in all 4 chambers, and marked interventricular discordance (Fig. 1). Acoustic cardiography revealed a high-frequency early diastolic sound heard after the second heart sound representing likely a pericardial knock (Audicor, Inovise Medical Inc., Portland, OR; Fig. 2). This patient underwent cardiac surgery for a pericardial stripping procedure. On postoperative day 3, physical examination revealed a low-pitched, soft early diastolic third heart sound (S3) with resolution of the pericardial knock. A repeat phonocardiogram demonstrated replacement of the high-pitched pericardial knock with the S3 (Fig. 3). Following an uneventful postoperative course, the patient had gradual marked improvement in his exercise tolerance and fatigue. Case 2 This 53-year-old gentleman had a history of acute tuberculous pericarditis 1 year ago. He was treated with a three-drug regimen. Over the past 6 months, he developed progressive dyspnea, exercise intolerance, and pedal edema. His medications included furosemide 20 mg daily, potassium, and aspirin. On our physical examination, his blood pressure was 110/70 mmhg, heart rate 74 beats per min, and respirations 14 per min. His central venous pressure was elevated to the angle of the jaw with a positive Kussmaul s sign and a rapid Y descent. He had a regular rhythm with a soft pericardial knock (appreciated only on subsequent physical examination), no murmur, or gallop. His electrocardiogram showed sinus rhythm with nonspecific T wave abnormality. Laboratory data showed a BNP of 41 pg/ml. His echocardiogram showed normal biventricular size and function, pericardial thickening with adhesion posteriorly, and a dilated inferior vena cava.

3 452 Clin. Cardiol. Vol. 30, September 2007 (A) (B) FIG. 1 Simultaneous left ventricular and right atrial pressure recordings in patient 1 with atrial flutter (A). There is a prominent dip-and-plateau pattern in the left ventricular diastolic tracing, with diastolic equalization at 15 mmhg with the right atrial tracing. The absence of a decrease in right atrial pressure during inspiration is consistent with a Kussmaul s sign. Note the prominent atrial flutter waves in both pressure tracings. Panel B shows left and right interventricular discordance in simultaneous biventricular pressure recordings. There is a prominent dip-and-plateau pattern in both ventricular tracings. On cardiac catheterization, there was elevation and equalization of diastolic pressures in all four chambers at 15 mmhg, a positive Kussmaul s sign, a prominent dip-and-plateau pattern in both ventricular tracings, and interventricular discordance. His acoustic cardiographic tracing showed an early diastolic pericardial knock. He is currently undergoing a preoperative evaluation prior to pericardiectomy. Case 3 This 76-year-old woman had a 15 year history of paroxysmal atrial fibrillation and diabetes. Over the past 2 years, she developed progressive dyspnea, exercise intolerance, pedal edema, and renal insufficiency. Medications included furosemide 40 mg twice daily, amiodarone, warfarin, and enalapril. On our physical examination, her blood pressure was 116/60 mmhg, heart rate 74 beats per min, and respirations 14 per min. Her central venous pressure was elevated to the angle of the jaw with a positive Kussmaul s sign and a rapid Y descent. She had a regular rhythm with a loud pericardial knock (documented only on subsequent physical examination), no murmur, or gallop. Her electrocardiogram showed sinus rhythm with non-specific T wave abnormality. Laboratory data showed a BNP of 323 pg/ml and a creatinine of 3.3 mg/dl. Her echocardiogram showed normal biventricular size and function, mild left atrial enlargement, pericardial thickening, calcification, and adhesion, and a dilated inferior vena cava. On cardiac catheterization, there was elevation and equalization of diastolic pressures in all four chambers at 20 mmhg, a positive Kussmaul s sign, a prominent dip-and-plateau pattern in both ventricular tracings, and interventricular discordance. Her acoustic cardiographic tracing showed an early diastolic pericardial knock (Fig. 4(A)). Four days following pericardiectomy, the pericardial knock resolved (Fig. 4(B)). Her exercise tolerance returned to normal. Discussion Constrictive pericarditis is an uncommon condition that has various etiologies and is often mis-diagnosed initially as its clinical features are difficult to differentiate from more common diseases. Appreciation of the hemodynamic consequences of constrictive pericarditis is critical to understanding the pathophysiology of the

4 A. D. Michaels et al.: Computerized acoustic cardiography in constrictive pericarditis 453 (A) FIG. 2 Preoperative phonocardiographic tracing for patient 1 (A). In addition to the 12-lead electrocardiogram, sound recordings are obtained from the V 3 and V 4 positions. The early diastolic high-amplitude sound is the pericardial knock (PK). Panel B shows a single beat of the PK. The Audicor algorithm did not interpret this signal as an S3 as the signal s frequency profile was rather high-pitched, and fell out of the frequency range of what is reasonable for the usual lowpitched S3. condition, and will aid the clinician in considering the diagnosis at the bedside. This case series highlights the potential of the bedside evaluation to aid the clinician in accurately diagnosing constrictive pericarditis. Ultimately, one can make the diagnosis with the aid of modern techniques of heart imaging studies (echocardiography, computed tomography, and magnetic resonance imaging) and invasive cardiac catheterization. 2,12,13 The bedside finding of an elevated jugular venous pressure with a low BNP may be helpful in identifying patients with constrictive pericarditis, 14 but may also be due to tricuspid stenosis or superior vena cava obstruction. The differential diagnosis of constrictive pericarditis includes its main mimicker, restrictive cardiomyopathy, as well as right ventricular failure, tricuspid and mitral valve disease, and cardiac tamponade. 15 There are subtle hemodynamic differences that can help to differentiate these entities. Initially, inspection of the jugular venous pressure can help suggest the diagnosis of constrictive pericarditis and differentiate it from other diagnoses. The constricted pericardium has early diastolic rapid filling; but during the remainder of diastole, filling is markedly reduced. This produces the clinical sign known as Friedreich s sign, a rapid Y descent of the jugular venous pulsation, which was noted in 94% of cases in one series. 16 The rapid Y descent makes tricuspid stenosis and cardiac tamponade much less likely. Right atrial pressure is increased in each of these conditions, but the rapid Y descent is usually not seen in either cardiac tamponade or tricuspid stenosis. The increase in venous return with inspiration with high right atrial pressure resisting further right atrial filling leads to an overall elevation in jugular venous pressure on inspiration, and is known as the Kussmaul s sign. 10 This is not specific to constrictive pericarditis and may be seen in any condition with elevated right-sided pressures.

5 454 Clin. Cardiol. Vol. 30, September 2007 (B) FIG. 2 (Continued).

6 A. D. Michaels et al.: Computerized acoustic cardiography in constrictive pericarditis 455 FIG. 3 Detailed sound frequency analysis of the phonocardiography tracing preoperatively (A) and postoperatively (B). Note that the baseline recording shows considerable high-frequency energy in the early diastolic period, which is the pericardial knock (PK). Postoperatively, the early diastolic sound has relatively little energy in the high frequency range, consistent with a typical third heart sound (S3). Also, the PK occurs closer to the second heart sound (S2; identified by the dashed line) compared to the S3. Another finding on physical examination that can aid in differentiating cardiac tamponade from constrictive pericarditis is the pulsus paradoxus, the inspiratory reduction in the arterial pressure of greater than 10 mmhg. In constrictive pericarditis, the reduction in arterial pressure during inspiration is usually less than 10 mmhg. The constricting pericardium does not transmit pressure changes from the pleural pressure to the cardiac chambers given the isolation of the chambers from the rest of the thoracic structures by the stiff encasement of the pericardium. If there is a reduction in the arterial pressure during inspiration of greater than 10 mmhg, then one must consider pulmonary disease, cardiac tamponade, or effusive-constrictive pericarditis, a condition first described by Spodick and Kumar 17 and elaborated upon by Hancock. 18 A key finding on physical examination and the focus of our report is the ausculatory finding of the pericardial knock. This heart sound represents the sudden deceleration of blood following the initially rapid early diastolic filling of the ventricle, which occurs at the point when further ventricular expansion is limited by the rigid pericardium. Although the pericardial knock tends to be a rather loud high-pitched sound that may mimic a late mitral opening snap in its intensity, a true knocktype sound is only occasionally heard. It usually occurs s after the second heart sound, and is heard during the diastolic plateau point of the ventricular pressure tracing representing abrupt deceleration of diastolic flow into the ventricle. The pericardial knock may also be confused with a widely split second heart sound. The pericardial knock occurs earlier than the classic low-pitched S3 of a patient in congestive heart failure (Fig. 4) and which may also be heard in cases of restrictive cardiomyopathy. Prior to pericardiectomy, a large component of the pericardial knock sound signal is in the high frequency range (Fig. 3(A)). Postpericardiectomy, in contrast, there is a softer low-pitched sound that falls slightly later after the second heart sound, and represents the classic S3 seen in congestive heart failure (Fig. 3(B)). Patient 1 developed an S3 following pericardiectomy because the left ventricle was protected from volumeoverload stretch due to the external encasement of the thickened pericardium. After surgical pericardiectomy, this external limitation to ventricular expansion had been removed and thus the ventricles may then stretch, resulting in the S3. We have applied acoustic cardiography to three patients with constrictive pericarditis with an audible pericardial knock. In two of the patients, we demonstrated resolution of this sound following surgical pericardiectomy. This new bedside system (Audicor) may be applied to other patients with similar conditions to help the clinician differentiate constrictive pericarditis from other competing diagnoses such as restrictive cardiomyopathy. In the latter, a fourth heart sound would be a typical ausculatory finding. An S3 may also be

7 456 Clin. Cardiol. Vol. 30, September 2007 (A) FIG. 4 Acoustic cardiographic output for patient #3 showing a loud early diastolic sound that represented the high-pitched pericardial knock (PK; A). From top to bottom: electrocardiogram trace, heart sounds trace, scalogram time-frequency representation, and three-dimensional scalogram time-frequency representation. The scalogram time-frequency representation shows frequency on the vertical axis on a logarithmic scale from 5 Hz to 220 Hz (legend on the right), and time on the horizontal axis in milliseconds. The magnitude of the energy at each frequency is represented by colors ranging from light gray (bottom 2%) to dark red (top 2%). After pericardiectomy, there is resolution of the PK (B). appreciated in end-stage restrictive cardiomyopathy with systolic dysfunction. With the development of echocardiography and cardiac MR, phonocardiography has been slowly abandoned as a clinical tool in the diagnostic armamentarium of cardiologists. However, phonocardiography does have the potential to help clinicians evaluate heart failure patients, identifying those with systolic dysfunction, 19 constrictive pericarditis, and restrictive cardiomyopathy. Computerized acoustic cardiography has overcome some of the historical limitations of phonocardiography, with the addition of simultaneous electrocardiographic recording, automated filtering, and computerized algorithms to identify diastolic heart sounds using amplitude, timing, and frequency parameters. Lastly, acoustic cardiography may provide an important teaching tool at the bedside to help trainees correlate cardiac auscultatory findings with the acoustic cardiographic recordings. In this way, medical trainees will be able to receive immediate visual feedback for comparison with their auditory findings. This may help reinforce the hemodynamic concepts centered on patientrelated bedside teaching. Providing a visual representation of the heart sounds may revitalize the art of cardiac physical diagnosis.

8 A. D. Michaels et al.: Computerized acoustic cardiography in constrictive pericarditis 457 (B) FIG. 4 (Continued). Competing Interest Statement: Dr. Michaels has received an unrestricted educational grant from Inovise Medical Inc., Portland, OR. Acknowledgements We appreciate Patti Arand s (Inovise) expert help reviewing the phonocardiographic analyses. References 1. Chatterjee K, Alpert J: Constrictive pericarditis and restrictive cardiomyopathy: similarities and differences. Heart Fail Monit 2003;3: Kern MJ, Aguirre F: Interpretation of cardiac pathophysiology from pressure waveform analysis: pericardial compressive hemodynamics, part II. Cathet Cardiovasc Diagn 1992;26: Ling LH, Oh JK, Breen JF, Schaff HV, Danielson GK, et al.: Calcific constrictive pericarditis: is it still with us? Ann Intern Med 2000;132: Hatle LK, Appleton CP, Popp RL: Differentiation of constrictive pericarditis and restrictive cardiomyopathy by Doppler echocardiography. Circulation 1989;79: Masui T, Finck S, Higgins CB: Constrictive pericarditis and restrictive cardiomyopathy: evaluation with MR imaging. Radiology 1992;182: Hancock EW: Differential diagnosis of restrictive cardiomyopathy and constrictive pericarditis. Heart 2001;86: Rajagopalan N, Garcia MJ, Rodriguez L, Murray RD, Apperson- Hansen C, et al.: Comparison of new Doppler echocardiographic methods to differentiate constrictive pericardial heart disease and restrictive cardiomyopathy. Am J Cardiol 2001;87: Giorgi B, Mollet NRA, Dymarkowski S, Rademakers FE, Bogaert J: Clinically suspected constrictive pericarditis: MR imaging assessment of ventricular septal motion and configuration in patients and healthy subjects. Radiology 2003;228: Tyberg TI, Goodyer AV, Langou RA: Genesis of pericardial knock in constrictive pericarditis. Am J Cardiol 1980;46:

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