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Genesis of pericardial knock in constrictive pericarditis
Insights
The pericardial knock in constrictive pericarditis is caused by the sudden cessation of ventricular filling. This abrupt halt in diastolic left ventricular volume creates the characteristic sound, validating a key hypothesis.
Area of Science:
- Cardiology
- Physiology
- Medical Acoustics
Background:
- Pericardial knock is a recognized clinical sign in constrictive pericarditis.
- The precise mechanism generating the pericardial knock has remained unclear.
- A leading hypothesis links the sound to abrupt deceleration of ventricular filling.
Purpose of the Study:
- To investigate the hemodynamic basis of the pericardial knock in constrictive pericarditis.
- To validate the hypothesis that sudden cessation of ventricular filling causes the pericardial knock.
- To correlate the timing of the pericardial knock with left ventricular diastolic filling dynamics.
Main Methods:
- Acquired left ventriculograms, phonocardiograms, and external pulse recordings in patients with constrictive pericarditis and normal subjects.
- Digitized left ventriculograms to calculate ventricular volumes at 16 ms intervals.
- Constructed left ventricular volume curves against diastolic filling time.
Main Results:
- Pericardial knock occurred at 90-120 ms after aortic closure, coinciding with the Y descent trough.
- In five patients with pericardial knock, filling ceased abruptly at 85% of ventricular volume.
- Two patients without pericardial knock showed faster initial diastolic filling, lacking the plateau.
Conclusions:
- The study confirms that an abrupt plateau in the diastolic left ventricular volume curve generates the pericardial knock.
- Sudden cessation of ventricular filling is the likely cause of the pericardial knock in constrictive pericarditis.
- Proposed mechanisms suggest both ventricles may contribute to the knock phenomenon.
Abstract:
A pericardial knock is a common finding in constrictive pericarditis. However, its origin has been uncertain. One hypothesis suggests that it is due to sudden deceleration of ventricular filling. To validate this hypothesis, left ventriculograms, phonocardiograms and external pulse recordings were obtained in seven patients with hemodynamic and pathologic findings of constrictive pericarditis and in seven normal subjects. Left ventriculographic silhouettes were digitized and left ventricular volumes were calculated by computer at 16 ms intervals. Curves of left ventricular volume versus diastolic filling time were constructed for each patient. Pericardial knock was recognized as an early high frequency sound recorded between 90 to 120 ms after the aortic closing sound and occurring at the trough of the Y descent of the jugular venous pressure tracing. The timing of the pericardial knock in five patients with constrictive pericarditis corresponded to a sudden and premature plateau of the diastolic left ventricular volume curve representing 85 +/- 4 percent (mean +/- standard deviation) of ventricular filling. The diastolic plateau was missing in two patients with constrictive pericarditis who had no pericardial knock. In these cases, the rate of ventricular filling was faster than normal in the first 20 percent of diastole. Thus, this study related pericardial knock to an abrupt plateau inthe diastolic left ventricular volume curve, supporting the view that sudden cessatin of ventricular filling generates the pericardial knock of constrictive pericarditis. Two mechanisms are proposed by which the filling plateau may produce the knock, and it is postulated that both ventricles may participate in the knock phenomenon.