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Pericardial tamponade, a new complication of amyloid heart disease
Insights
Cardiac amyloidosis can cause both restrictive cardiomyopathy and pericardial tamponade. This case highlights a rare instance of a 92-year-old man presenting with both conditions, emphasizing the diagnostic and clinical importance of amyloid heart disease.
Area of Science:
- Cardiology
- Geriatrics
- Pathology
Background:
- Cardiac amyloidosis is increasingly recognized in aging populations.
- Common features include restrictive cardiomyopathy, arrhythmias, and conduction disorders.
- Echocardiography is a key diagnostic tool.
Observation:
- A 92-year-old male presented with fatigue and dyspnea.
- Physical exam revealed pulsus paradoxus and elevated central venous pressure.
- Echocardiography showed a large pericardial effusion, leading to tamponade relief after pericardiocentesis.
Findings:
- Recurrent dyspnea occurred despite no recurrent effusion or hypokinesis.
- Hemodynamic measurements showed elevated ventricular filling pressures.
- Echocardiography revealed thickened ventricular walls and sparkling myocardial echoes, confirmed as amyloidosis postmortem.
Implications:
- This case uniquely demonstrates the coexistence of restrictive cardiomyopathy and pericardial tamponade in cardiac amyloidosis.
- It underscores the importance of considering cardiac amyloidosis in elderly patients with unexplained heart failure and effusions.
- Highlights a previously unreported presentation of tamponade due to amyloid heart disease.
Abstract:
With advancing age of the population and with echocardiographic means of diagnosis, amyloid disease of the heart is of increasing clinical interest. Advanced age, restrictive myocardiopathy, arrhythmias, and conduction disorders are familiar features of this disease. A 92 year old man with past history of hemiblock followed by complete heart block and transvenous pacemaker was admitted to the hospital because of increasing fatigue and the abrupt development of dyspnea. Examination revealed paradoxic pulse, markedly elevated central venous pressure, and echocardiographically demonstrated large pericardial effusion. Shortly after admission signs of tamponade developed; 1,000 ml of pericardial fluid was removed with prompt relief of dyspnea dna disappearance of paradoxic pulse and return of central venous pressure to normal. However, dyspnea soon recurred and subsequent hemodynamic measurements indicated increased right ventricular and left ventricular filling pressures. Echocardiography revealed no recurrent effusion or ventricular hypokinesis. Left ventricular ejection fraction by radionuclide ventriculogram was 64 percent. Echocardiography revealed ventricular wall thickening, normal chamber size, and glittering, sparkling myocardial echoes. On postmortem examination, there was extensive myocardial amyloidosis. There was no evidence of constrictive pericarditis or recurrent effusion. The unique aspect of this case was the combined presence of restrictive myocardiopathy and pericardial tamponade. To our knowledge, no previous case of tamponade due to amyloid heart disease had been reported.