ABSTRACT
Background: A 19-year-old gentleman, with past history of sinusitis, aseptic meningitis upon birth & subsequent epilepsy, came back from the UK presenting with fever, sore throat, chills with myalgia, as well as pleuritic chest pain. Case: COVID-19 was ruled out. Despite appropriate medications, his chest pain worsened together with epigastric pain. Fever persisted. Urgent CT was arranged for him showing findings suspicious of pericarditis. Serial ECG after admission revealed the classical findings compatible with pericarditis. He was taken over to CCU with treatment for pericarditis started. Unfortunately, despite empirical broad spectrum antibiotics & anti-inflammatories, his symptoms worsened with borderline blood pressure, increasing tachypnoea & persistent fever. Blood tests showed sky high white cell count up to 50 with neutrophil predominance. Serial echocardiograms showed a gradual increase in posteriorly-loculated pericardial effusion with fibrin, with striking findings of constriction physiology. Significant respirophasic changes in mitral & tricuspid inflow were demonstrated. Right-sided cardiac chambers were not collapsed, rather, the RA & the IVC were dilated. CT was repeated for deteriorating hemodynamics showing a rim-enhancing pericardial effuision. Decision making: In view of the constrictive physiology demonstrated in echocardiograms, surgical intervention was deemed necessary for the patient & he was sent immediately to Queen Elizabeth Hospital Cardiothoracic Surgery team for emergency surgery. Conclusion: The classical teaching of constrictive pericarditis describes patients with prior insult to the pericardium such as surgery, previous tuberculosis infection, prior radiotherapy exposure, etc, such that the pericardium is calcified as a cage hindering the expansion of the heart. However, with the presence of purulent and fibrin-rich effusion, constrictive physiology can become evident and life-thereatening (Effusive-constrictive pericarditis) as well.
ABSTRACT
Background: Influenza or acute myocardial infarction (AMI) is seasonal with usual upsurge in winter months. Influenza might be a trigger of AMI. The outbreak of COVID-19 in China led to population wide masking, practice of hand hygiene and social distancing in Hong Kong starting from late January 2020. Methods: Our study aimed to look at the relationship between influenza activity and ST-segment elevation myocardial infarction (STEMI) incidence as well as the epidemiological impact of universal infection control measures. Patients with a diagnosis of acute STEMI from January 2014 to March 2020 were retrieved from the Hospital Authority Clinical Data Analysis and Reporting System. We also downloaded data of influenza activity and air pollution from Centre for Health Protection and Environmental Protection Department respectively. Results: With few exceptions, the STEMI incidence per standardized month basically mirrored the influenza activity from 2014 to 2020. During the winter of 2014-15, 2015-16, 2017-18 and 2018-19, the number of STEMI cases went up with the influenza activity. The rise in the number of STEMI cases in December 2016 and January 2017 was not obvious mirroring the inconspicuous rise in influenza activity of the same period. The surge of influenza during the summer of 2015 and 2017 was not accompanied by an increase in the number of STEMI cases. Influenza activity is a predictor of STEMI incidence after adjusting for air pollution and time factors. We observed an abbreviated peak and narrow base of the influenza activity curve for the winter of 2019-20. The number of STEMI cases rose to 220 in December 2019 but then dropped significantly from January to March 2020 mimicking the influenza activity curve. Conclusion: Our observation agrees with the hypothesis of AMI triggered by influenza infection and cold weather. Furthermore, population wide infection control measures during the COVID-19 pandemic might have contained influenza activity and possibly reduced the population risk of STEMI.