Introduction
Pericardial effusion in acute myocardial infarction is not a rare phenomenon. The incidence is between 15% to 28% in patients who present with first myocardial infarction, and affection of pericardium is associated with higher rates of morbidity and mortality in these patients (1,2). The pericardial area being affected can manifest as pericardial effusion, pericarditis epistenocardica, or Dressler syndrome. It is less common today, in the era of percutaneous coronary interventions (PCI), than it was in the era of fibrinolysis. Pericarditis epistenocardica is usually a self-limiting phenomenon that occurs during the first week of the disease, while Dressler syndrome is an autoimmune disease that can manifest as much as several months after the infarction. Postinfarction pericardial effusion is rarely large enough to cause cardiac tamponade, and its causes include the pericardium being affected by hemorrhagic pericarditis, transmural infarction with rupture of the ventricular free wall, and iatrogenic perforation of coronary arteries during PCI (3).
Case report
A 55-year-old man was brought to the Joint Emergency Hospital Admission (JEHA) by an ambulance vehicle due to multiple incidents of syncope and febrility. During the first night after admission, the patient lost consciousness several times when waking to routinely measure body temperature values. Emergency medical personnel reported that the patient had been febrile during the three days before admission, with a body temperature of 38.5 °C. The patient was using paracetamol and ibuprofen to reduce body temperature. Pre-admission, the patient was hypotensive, with arterial pressure (AP) values of 70/30 mmHg and presenting with cold sweat. A 12-lead electrocardiogram (ECG) verified sinus rhythm with discrete ST-segment elevation in the inferolateral leads (Figure 1).
Upon admission to JEHA, the patient was conscious, in a poor general state, subfebrile (37.6 °C), exhibiting psychomotor agitation, and with pallid skin covered in cold sweat. The patient was overweight, with a body-mass index of 29.6 kg/m2, and was a smoker, having smoked 10 cigarettes per day for 30 years.
With regard to the patient’s physical state, his AP was unmeasurable and he presented with tachycardia with up to 120 beats per minute and 95% oxygen saturation. Auscultation found muffled breath sounds at the lung bases, and the action of the heart was rhythmic, with quiet heart tones and no murmur. Prompt treatment included another ECG, which verified ST-segment depression in the precordial leads V1-V3 (Figure 2). The patient simultaneously began complaining about discomfort in the upper part of the abdomen, as well as lightheadedness in the sitting position, which led to rapid sampling for laboratory tests and the performance of an ultrasound examination according to the Focused Abdominal Sonography for Trauma and Focus-Assessed Transthoracic Echocardiography protocols. Other than the circumferential pericardial effusion with a thicker consistency, the rest of the findings were without significant deviations from normal values. Laboratory tests found anemia (hemoglobin 99 g/L, MCV 99 fL) with elevated inflammatory parameter values (leukocytes 17.7×109/L; C-reactive protein 107 mg/L), and markers of heart muscle damage (troponin T 1816 ng/L; NT-proBNP 1255 ng/L). Urine sediment values were normal. Acid-base status indicated partial respiratory insufficiency.
Parenteral volume support led to partial improvement of the patient’s general state, but with persistent hypotension. Subjectively, upon repeated queries, the patient denied chest pain and dyspnea, and the only symptoms he reported were elevated body temperature and upper abdominal bloating.
Aortic dissection was suspected based on the clinical picture, and an anesthesiologist and cardiac surgeon were consulted. CT aortography excluded acute aortic syndrome and active contrast extravasation, and a large circumferential pericardial effusion was confirmed (Figure 3).
The patient was admitted to the Intensive Cardiological Treatment Ward at the Department of Cardiovascular Diseases. Immediately upon admission, we proceeded with continuous parenteral volume support (0.9% saline) with the addition of medication therapy – furosemide, ceftriaxone, and enoxaparin with tramadol and pantoprazole. Presently, the patient started complaining of stomach pain that abated only after passing loose and abundant stools. By morning, the patient was subjectively without complaints, with an improved general state, and with hourly diuresis (approximately 100 mL/hour), but with still persistent low AP values. A control echocardiographic bedside examination was performed on the morning after admission, which verified pericardial effusion with a thicker consistency as well as accompanying signs of hemodynamic instability (Figure 4). The dimensions of the heart chambers were within normal ranges, and the valvular apparatus was without significant deviations. Systolic function of the left ventricle was mildly reduced (EF 45-50%), with akinesis of the inferior, inferolateral, and anterolateral wall. Contained rupture of the left ventricular wall was suspected. The patient’s case was presented at an internal emergency meeting of cardiologists and cardiac surgeons, and coronarography was subsequently performed. It verified atherosclerotic disease of the left and right coronary artery with subacute occlusion of the first marginal branch (OM1) and borderline significant lesions of the left anterior descending branch (LAD) of the left coronary artery (Figure 5). At the same time, balloon dilatation of the OM1 was performed using a SC balloon catheter (2.0×20.0 mm) that achieved TIMI 3 flow. Pericardiocentesis was also performed during the intervention, and a drainage catheter was placed in the pericardial cavity, evacuating 450 mL of macroscopically sanies-like contents during the procedure. A sample was sent for cytological analysis, and microscopy of the sediments found a significant number of neutrophils, some lymphocytes, and abundant erythrocytes, indicating a mixed effusion type.
During further diagnostics, with the goal of eliminating possible myocardial rupture, we performed additional imaging – contrast echocardiography, which did not show clear contrast media extravasation from the heart chambers, as well as CT imaging of the heart that showed pericardial effusion and pronounced flattening of the interventricular septum, but also without extraluminal contrast in the heart chambers (Figure 6). As an additional finding, we verified bilateral pleural effusion, which led to intensification of diuretic therapy. A heart MR was performed as well, which, in addition to pericardial and pleural effusions, showed transmural fibrosis and zones of microvascular obstruction of the lateral and inferolateral wall of the left ventricle (Figure 7). It also showed moderately reduced systolic function of the left ventricle (EF 44%).
A cardiac surgeon recommended monitoring of the dynamics of the pericardial effusion, with the option of performing a surgical intervention in case of further progression.
During subsequent treatment, the patient was hemodynamically stable, underwent prolonged monitoring with no recorded disorders in heart rhythm, and repeated pericardial ultrasounds verified a stationary volume of pericardial effusion. The patient’s blood was tested for tumor markers in order to determine the etiology of the effusion, with negative results. We also requested consultation from an immunologist and infectologist, and the blood samples were sent for additional analysis based on their findings. Laboratory findings showed a gradual reduction in inflammatory parameter values, and the results of immunological analysis (rheumatoid factors and anti-CCP) as well as tests for infectious agents (HIV antigen/antibodies, Treponema pallidum hemagglutination test, rapid plasma reagin test) were all negative. The results of blood culture and urine culture tests from multiple samples were also sterile.
After further stabilization of the patient’s state, optimization of medication treatment it was agreed that the patient would be transferred to in-hospital cardiological rehabilitation institution for further treatment and rehabilitation. Therapy upon discharge included standard dual antiplatelet therapy (aspirin 100 mg and clopidogrel 75 mg), pantoprazole 40 mg as gastroprotection, bisoprolol 5 mg, ramipril 1.25 mg, rosuvastatin 40 mg, and colchicine 2×0.5 mg. Amoxicillin with clavulanic acid 2×1 was also recommended for two more weeks after hospital discharge, to be taken along with a probiotic.
Control pericardial ultrasound only showed separation of pericardial layers at the lateral wall and smaller bilateral pleural effusions. After in-hospital cardiological rehabilitation, the patient was discharged to home care in a good general state, compensated, and without subjective complaints.
Control pericardial ultrasound two weeks after discharge showed complete regression of the pericardial effusion. One month after discharge, a planned recoronarography we performed, which verified significant LAD stenosis and occlusion from the origin of the OM1. Simultaneously, we performed ad hoc PCI of the LAD using two drug-eluting stents (Orsiro 2.75×15.0 mm in the middle segment; Orsiro 4.0×18.0 mm in the proximal segment), achieving optimal blood flow.
Discussion
In our patient, diagnostic tests demonstrated subacute myocardial infarction of the lower posterior wall with ST-segment elevation, complicated by postinfarction hemorrhagic pericardial effusion with clinical signs of cardiac tamponade.
Pericardial involvement is common in myocardial infarction. A third of the patients present with pericardial effusion, but there are rare cases of hemopericardium that lead to cardiac tamponade (4). We had to eliminate the presence of a mechanical complication of myocardial infarction – left ventricular free wall rupture. This was achieved using extensive medical imaging.
Given the medical history of fever and elevated inflammatory parameters, infective pericarditis had to be considered in the differential diagnosis. Based on the current guidelines of the European Society of Cardiology on definitions and diagnostic criteria, our patient satisfied only the criterion of pericardial effusion, which is insufficient for diagnosis (5). Notably, auscultation of the patient was significantly impaired by his general state (in the context of the possible presence of pericardial friction rub). Due to the urgency of the procedure and the general state of the patient, a sample of the pericardial effusion was not sent for hematological and microbiological analysis, which we consider a shortcoming.
Once the presence of pericardial effusion is demonstrated, it is necessary to assess its hemodynamical significance. Cardiac tamponade is a primarily clinical diagnosis, with the typical symptoms including Beck’s triad – hypotension, jugular venous distension, and muffled heart sounds. It is often also accompanied by tachycardia as well as microvolt and electric alternans in the ECG results. Transthoracic echocardiography is the noninvasive method of choice for confirming the diagnosis, and possible signs include: early diastolic collapse of the right ventricular free wall, late diastolic collapse of the right atrium, “swinging” of the heart in the pericardial cavity, dilation of the inferior vena cava without inspiratory collapse, >40% inspiratory variability in transtricuspid flow, and >25% inspiratory variability in transmitral flow (5,6).
In the introduction, we emphasized the most common causes of cardiac tamponade in postinfarction progression. Knowing the etiology is necessary for implementing the optimal treatment approach. If the cause is a mechanical complication of myocardial infarction (free wall rupture), an emergency surgical procedure represents the only chance of patient survival. If mechanical complications are eliminated, the initial treatment approach includes pericardiocentesis with the goal of achieving hemodynamic stablity (3). This case was presented at a multidisciplinary consultation meeting at the hospital, and the decision to employ percutaneous coronary intervention was correct, as was confirmed by the subsequent favorable clinical course and recovery of the patient, as well as the subsequently performed broader medical tests. Additional infectological and immunological tests were performed due to the dramatic and unusual clinical picture that the patient presented. Postinfarction pericardial effusions are slow to resorb, sometimes remaining for as long as 12 months3.
Conclusion
This case highlights the importance of rapid diagnostics, differential diagnostic analysis, and timely treatment in patients with atypical manifestations of myocardial infarction. In patients who present with a clinical picture of shock, it is important to consider possible mechanical complications of myocardial infarction, and if these have been eliminated it is necessary to perform additional diagnostic tests in order to identify the etiology of the state of shock, thus enabling the application of appropriate treatment.