medicina

Case Report Acute Pericarditis after Percutaneous Coronary Intervention: A Case Report

Greta Rodeviˇc 1, Povilas Budrys 2,3,* and Giedrius Davidaviˇcius 2,3

1 Faculty of Medicine, Vilnius University, M. K. Ciurlionioˇ g. 21/27, LT-03101 Vilnius, Lithuania 2 Clinic of Cardiac and Vascular Diseases, Faculty of Medicine, Vilnius University, Santariškiu˛2, LT-08661 Vilnius, Lithuania 3 Cardiology and Angiology Center, Vilnius University Hospital Santaros Klinikos, Santariškiu˛2, LT-08661 Vilnius, Lithuania * Correspondence: [email protected]

Abstract: Background: Percutaneous coronary intervention (PCI) is known as a very rare possi- ble trigger of pericarditis. Most frequently it develops after a latent period or early in the case of periprocedural complications. In this report, we present an atypical early onset of pericarditis after an uncomplicated PCI. Case Summary: A 58-year-old man was admitted to the hospital for PCI of the chronic total occlusion of the left anterior descending (LAD) artery. An initial electrocardiogram (ECG) was unremarkable. The PCI attempt was unsuccessful. There were no procedure-related com- plications observed at the end of the PCI attempt and the patient was symptom free. Six hours after the interventional procedure, the patient complained of severe chest pain. The ECG demonstrated ST-segment elevation in anterior and lateral leads. Troponin I was mildly elevated but a coronary angiogram did not reveal the impairment of collateral blood flow to the LAD territory. Due to pericarditic chest pain, typical ECG findings and pericardial effusion with elevated C-reactive protein, the diagnosis of acute pericarditis was established, and a course of nonsteroidal anti-inflammatory


drugs (NSAIDs) was initiated. Chest pain was relieved and ST-segment elevation almost completely
 returned to baseline after three days of treatment. The patient was discharged in stable condition Citation: Rodeviˇc,G.; Budrys, P.; without chest pain on the fourth day after symptom onset. Conclusions: Acute pericarditis is a rare Davidaviˇcius,G. Acute Pericarditis complication of PCI. Despite the lack of specific clinical manifestation, post-traumatic pericarditis after Percutaneous Coronary should be considered in patients with symptoms and signs of pericarditis and a prior history of Intervention: A Case Report. Medicina iatrogenic injury or thoracic trauma. 2021, 57, 490. https://doi.org/ 10.3390/medicina57050490 Keywords: post-cardiac injury syndrome; pericarditis; percutaneous coronary intervention

Received: 2 April 2021 Accepted: 11 May 2021 Published: 13 May 2021 1. Introduction Acute pericarditis is an inflammatory disease affecting the pericardium with or with- Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in out the accumulation of excess fluid in the pericardial cavity [1]. Pericarditis causes 0.24% published maps and institutional affil- and 0.16% of all cardiovascular admissions in men and in women, respectively [2]. In devel- iations. oped countries, the most frequent origin of pericarditis is viral infection. Rarely, pericarditis can occur after iatrogenic trauma and is known as pericardial injury syndrome [1,3]. Here, we report an atypical case of a patient who developed pericarditis 6 h after an unsuccessful attempt to open a chronic total occlusion (CTO) of the left anterior descending (LAD) artery.

Copyright: © 2021 by the authors. 2. Case Report Licensee MDPI, Basel, Switzerland. This article is an open access article A 58-year-old man was admitted to the hospital for an elective percutaneous coronary distributed under the terms and intervention (PCI) of the chronic total occlusion to the LAD due to exertional angina conditions of the Creative Commons while on optimal medical therapy. Three months before, due to unstable angina, he Attribution (CC BY) license (https:// underwent coronary angioplasty with the deployment of drug-eluting stents in the right creativecommons.org/licenses/by/ coronary artery. His past medical history included hypertension, dyslipidemia, impaired 4.0/). fasting glycemia and gout. Physical examination as well as the laboratory data involving

Medicina 2021, 57, 490. https://doi.org/10.3390/medicina57050490 https://www.mdpi.com/journal/medicina Medicina 2021, 57, x FOR PEER REVIEW 2 of 6 Medicina 2021, 57, x FOR PEER REVIEW 2 of 6

while on optimal medical therapy. Three months before, due to unstable angina, he un- Medicina 2021, 57, 490 while on optimal medical therapy. Three months before, due to unstable angina, he un-2 of 6 derwent coronary angioplasty with the deployment of drug-eluting stents in the right cor- derwent coronary angioplasty with the deployment of drug-eluting stents in the right cor- onary artery. His past medical history included hypertension, dyslipidemia, impaired onary artery. His past medical history included hypertension, dyslipidemia, impaired fasting glycemia and gout. Physical examination as well as the laboratory data involving fasting glycemia and gout. Physical examination as well as the laboratory data involving completecomplete blood count, electrolytes, electrolytes, renal renal fu functionnction and and hepatic hepatic enzymes enzymes showed showed normal normal complete blood count, electrolytes, renal function and hepatic enzymes showed normal findings.findings. AnAn initialinitial electrocardiogram (ECG) revealed revealed sinus sinus bradycardia bradycardia with with a aheart heart rate rate of findings. An initial electrocardiogram (ECG) revealed sinus bradycardia with a heart rate of 50 beats per minute and pathologic Q-wave in leads III and aVF (Figure 1A). Transtho- 50of beats 50 beats per per minute minute and and pathologic pathologic Q-wave Q-wave in in leads leads III III and and aVF aVF (Figure (Figure1A). 1A). Transthoracic Transtho- racic echocardiography demonstrated good systolic function (LV EF 55% without regional echocardiographyracic echocardiography demonstrated demonstrated good good systolic systolic function function (LV(LV EF 55% 55% without without regional regional wall motion abnormalities) and left atrial enlargement. The attempt to revascularize the wallwall motion motion abnormalities) abnormalities) and left atrial enlargement. enlargement. The The attempt attempt to torevascularize revascularize the the coronary artery using the antegrade wire escalation technique (Fielder XTA, Gaia Second coronarycoronary artery artery usingusing thethe antegrade wire wire esca escalationlation technique technique (Field (Fielderer XTA, XTA, Gaia Gaia Second Second and Third wires) was unsuccessful due to the inability to wire the distal true lumen. At andand Third Third wires) wires) was was unsuccessful unsuccessful due due to to the the inability inability to to wire wire the the distal distal true true lumen. lumen. AtAt the the end of the procedure, there was no extravasation of contrast observed (Figure 2C) and endthe ofend the of procedure, the procedure, there there was was no extravasationno extravasation of of contrast contrast observed observed (Figure (Figure2C) 2C) and and the the patient was symptom free. A second attempt was planned after one or two months. patientthe patient was symptomwas symptom free. free. A second A second attempt attempt was was planned planned after after one one or or two two months. months.

FigureFigure 1. 1.( (AA)) InitialInitial ECG ECG of of the the patient patient showing showing sinus sinus brad bradycardiaycardia and Q and wave Q in wave leads in III leads and aVF. III and (B) ECG aVF. after (B) ECGpercu- after Figure 1. (A) Initial ECG of the patient showing sinus bradycardia and Q wave in leads III and aVF. (B) ECG after percu- percutaneoustaneous coronary coronary intervention intervention with withmild ST-segment mild ST-segment elevation elevation in anterior in anterior (V2–V3) (V2–V3) and lateral and (I, lateral aVL, V5–V6) (I, aVL, leads. V5–V6) ECG, leads. taneous coronary intervention with mild ST-segment elevation in anterior (V2–V3) and lateral (I, aVL, V5–V6) leads. ECG, ECG,electrocardiogram. electrocardiogram. electrocardiogram.

Figure 2. (A) Coronary angiogram before PCI showing chronic total occlusion of the LAD and a filling of the mid-distal LAD through ipsilateral collateral. (B) Advancement of the wire through the CTO body. (C) Post-intervention image with

no contrast extravasation. PCI, percutaneous coronary intervention; LAD, left anterior descending; CTO, chronic total occlusion. Medicina 2021, 57, x FOR PEER REVIEW 3 of 6

Figure 2. (A) Coronary angiogram before PCI showing chronic total occlusion of the LAD and a filling of the mid-distal MedicinaLAD2021 through, 57, 490 ipsilateral collateral. (B) Advancement of the wire through the CTO body. (C) Post-intervention image with 3 of 6 no contrast extravasation. PCI, percutaneous coronary intervention; LAD, left anterior descending; CTO, chronic total occlusion.

SixSix hours after the interventional procedure, procedure, the the patient patient complained complained of of severe severe sub- sub- sternalsternal chest chest pain pain worsening worsening by by bending bending over over and and lying lying on on the the left left side. side. The The ECG ECG demon- demon- stratedstrated ST-segment ST-segment elevation in anterior and lateral leads, suggesting acute anterolateral ST-elevationST-elevation myocardial infarction (Figure1 1B).B). TroponinTroponin I I was was mildly mildly elevated elevated at at 71 71 ng/L. ng/L. ItIt was was decided to to repeat a coronary angiogram in order to evaluate collateral blood flow flow toto LAD LAD as as worsening worsening of of it it could could be be attribut attributeded to tothe the patient’s patient’s symptoms symptoms and and changes changes on theon theECG. ECG. Coronary Coronary angiogram angiogram did not did reveal not reveal any new any newfindings findings compared compared to the to previous the pre- one,vious and one, the and collateral the collateral flow to the flow LAD to the territo LADry territorywas not impaired. was not impaired.An elevated An C-reactive elevated proteinC-reactive (CRP) protein level (CRP)(98.0 mg/L) level (98.0with mg/L)no leukoc withytosis no leukocytosiswas observed was the observednext morning. the next Se- rummorning. electrolytes Serum and electrolytes creatinine and remained creatinine wi remainedthin normal within ranges. normal Transthoracic ranges. Transthoracic echocardi- ogramechocardiogram showed a showednormal-sized a normal-sized left ventricle left with ventricle preserved with preserved systolic and systolic impaired and impaireddiastolic functions,diastolic functions, left atrial enlargement left atrial enlargement and hemodynamically and hemodynamically non-significant non-significant small circumfer- small entialcircumferential pericardial pericardial effusion (Figure effusion 3). (FigureThe diagnosis3). The of diagnosis acute pericarditis of acute pericarditis was established was andestablished a course and of nonsteroidal a course of nonsteroidal anti-inflammatory anti-inflammatory drugs (NSAIDs) drugs was (NSAIDs) initiated. was The initiated. patient wasThe patientgiven ibuprofen was given 600 ibuprofen mg tds in 600 addition mg tds to in aspirin addition 100 to mg aspirin od, clopidogrel 100 mg od, 75 clopidogrel mg od, a combination75 mg od, a combinationof bisoprolol of and bisoprolol perindopril and 5/10 perindopril mg od, amlodipine 5/10 mg od, 5 amlodipine mg od, moxonidine 5 mg od, 0.4moxonidine mg od and 0.4 mgrosuvastatin od and rosuvastatin 40 mg od. 40 Pantoprazol mg od. Pantoprazol 20 mg od 20 mgwas od also was initiated also initiated with NSAIDswith NSAIDs therapy. therapy. The following The following ECG, ECG, which which was performed was performed 36 h after 36 h afterPCI, PCI,revealed revealed typ- icaltypical ECG ECG findings findings of pericarditis of pericarditis (Figure (Figure 4A).4A).

Figure 3. Transthoracic echocardiograms.echocardiograms. ( A(A)) Four Four chamber chamber view view showing showing small small pericardial pericardial effusion effusion (5 mm)(5 mm) adjacent adjacent to the to thelateral lateral wall wall of the of the left left ventricle ventricle (arrows). (arrows). (B ()B 5) mm5 mm of of pericardial pericardial fluid fluid along along the the inferolateral inferolateral wall wall (arrow)(arrow) inin parasternal short axis view. short axis view. On the next day, the troponin I level decreased to 37 ng/L and chest pain was sig- nificantly relieved. A three-fold reduction in CRP level (from 98.0 mg/L to 30.8 mg/L) was observed after three days of treatment. Repeated ECG showed a return to baseline ST-segment elevation (Figure4B). In comparison with the previous echocardiogram, no enlargement of pericardial effusion was detected. The patient was discharged in stable condition without chest pain on the fourth day after symptom onset. It was recommended to continue ibuprofen for 12 days three times daily with a reduction in dose after 5 days. Moreover, the patient was given aspirin and clopidogrel, statin and a combination of antihypertensive agents. The patient had no complaints of pericarditic chest pain after discharge. Two months later, successful PCI to the CTO of LAD was performed using the same antegrade wire escalation technique with an implantation of two drug eluting stents (Figure5). The patient remained asymptomatic and had no recurrence of pericarditis.

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Figure 4. (A) ECG demonstrates widespread ST-segment elevation, ST depression in lead aVR and diffuse downsloping depression of PR-segment (36 h after PCI) (20 mm/mV calibration). (B) ECG after three days of treatment showing almost complete resolution of the ST-segment elevation (10 mm/mV calibration).

On the next day, the troponin I level decreased to 37 ng/L and chest pain was signif- icantly relieved. A three-fold reduction in CRP level (from 98.0 mg/L to 30.8 mg/L) was observed after three days of treatment. Repeated ECG showed a return to baseline ST- segment elevation (Figure 4B). In comparison with the previous echocardiogram, no en- largement of pericardial effusion was detected. The patient was discharged in stable con- dition without chest pain on the fourth day after symptom onset. It was recommended to continue ibuprofen for 12 days three times daily with a reduction in dose after 5 days. Moreover, the patient was given aspirin and clopidogrel, statin and a combination of an- tihypertensive agents. The patient had no complaints of pericarditic chest pain after discharge. Two months Figure 4. A Figure 4. ((A)) ECG ECG demonstrates demonstrateslater, widespread widespread successful ST-segment ST-segmentPCI to the elevation, elevation,CTO of LADST ST depression depression was performed in in lead lead aVR aVRusing and and the diffuse diffuse same downsloping downsloping antegrade wire B depressiondepression of of PR-segment PR-segment (36 (36escalation h h after after PCI) PCI) technique (20 (20 mm/mV mm/mV with calibration). calibration). an implantation (B ( ) )ECG ECG ofafter after two three three drug days days eluting of of treatment treatment stents showing showing(Figure almost almost5). The pa- completecomplete resolution resolution of of the the ST-segment ST-segmenttient remained elevation elevation asymptomatic (10 mm/mV calibration).and calibration). had no recurrence of pericarditis.

On the next day, the troponin I level decreased to 37 ng/L and chest pain was signif- icantly relieved. A three-fold reduction in CRP level (from 98.0 mg/L to 30.8 mg/L) was observed after three days of treatment. Repeated ECG showed a return to baseline ST- segment elevation (Figure 4B). In comparison with the previous echocardiogram, no en- largement of pericardial effusion was detected. The patient was discharged in stable con- dition without chest pain on the fourth day after symptom onset. It was recommended to continue ibuprofen for 12 days three times daily with a reduction in dose after 5 days. Moreover, the patient was given aspirin and clopidogrel, statin and a combination of an- tihypertensive agents. The patient had no complaints of pericarditic chest pain after discharge. Two months later, successful PCI to the CTO of LAD was performed using the same antegrade wire escalation technique with an implantation of two drug eluting stents (Figure 5). The pa- tient remained asymptomatic and had no recurrence of pericarditis.

Figure 5. (A) Coronary Coronary angiogram before PCI showing chronic total occlusion of the LAD. (B) Antegrade flowflow to the distal vascular bed of the LAD afterafter CTOCTO PCI.PCI.

3. Discussion Post-cardiac injury syndrome (PCIS) is a secondary pericarditis resulting from the injury of the pericardium and can be present with or without pericardial effusion. PCIS includes post-myocardial infarction pericarditis, post-pericardiotomy syndrome and post- traumatic pericarditis. The last one can occur after blunt or sharp thoracic trauma and due to an iatrogenic injury [4,5]. Percutaneous coronary intervention, as it was in our case, is known as a possible trigger of pericardial inflammation [6]. Less than 0.2% of PCI procedures are complicated by pericarditis [7]. The pathogenesis of PCIS is not completely understood. It is hypothesized that pericarditis occurs as an immune-inflammatory syndrome due to the injury. Damage Figure 5. (A) Coronary angiogramto mesothelial before PCI cells showing and chronic blood intotal the occlusion pericardial of the space LAD. initiate(B) Antegrade an autoimmune flow to the distal response. vascular bed of the LAD afterReleased CTO PCI. cardiac antigens cause the induction of antibody production. Formed immune complexes deposit in the pericardium and cause inflammation. A latent period lasting weeks to months between the procedure and clinical manifestation is established [4,8].

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Taking into account the fact that in our case the first symptoms began 6 h after the procedure, autoimmune pathogenesis due to the second PCI is less possible. Another explanation of post-traumatic pericarditis development is the extravasation of blood into the pericardial cavity. Blood irritates a visceral layer of the pericardium and causes inflammation [9]. There are some cases describing PCIS due to PCI complicated by coronary perforation or dissection [10–12]. The leakage of contrast on X-ray imaging was not observed in our case but pericardial effusion surrounding the heart was present on the echocardiography. We can suppose that the PCI wire could have gone outside the vessel architecture at some point in the CTO-PCI attempt, causing microextravasation not seen during PCI, which could have provoked the synthesis of inflammatory cytokines and fluid accumulation in the pericardial space. PCIS has no specific diagnostic criteria due to the lack of pathognomonic symptoms and signs. Diagnosis of PCIS should be considered after a cardiac injury when at least two of five criteria are fulfilled: fever without alternative causes, pericarditic or pleuritic chest pain, pericardial or pleural rubs, evidence of pericardial effusion and/or pleural effusion with elevated CRP. ECG can demonstrate diffuse ST-segment elevation with concave morphology and PR depression [1]. The presence of pericardial fluid, its amount and clinical impact on hemodynamics are evaluated by transthoracic echocardiography [5]. The reported patient had typical pericarditic chest pain and met three criteria of PCIS. As ST-segment elevation was present in anterior and lateral walls after unsuccessful PCI and the troponin I level was above the normal reference range, emergent coronary angiogram was performed to rule out myocardial infarction. The patient received a 15-day course of ibuprofen. According to ESC guidelines, NSAID is an essential treatment of PCIS. For patients with post-myocardial infarction pericarditis and those already taking antiplatelet medications, aspirin is the first choice drug [1]. Ibuprofen can be another option for anti-inflammatory therapy. In a case of the first episode of PCIS, it is recommended to prescribe ibuprofen at 600 mg three times daily over one to two weeks [5]. Similarly to the treatment of acute pericarditis while colchicine is recommended for the prevention of persistent and recurrent pericarditis [13,14], the addition of colchicine to NSAIDs should be considered in cases of PCIS [1]. We have found only one case of post-cardiac injury syndrome after successful PCI of CTO described in the literature. A combination of a high-dose aspirin and colchicine was ineffective. Pleuropericarditis was managed successfully with corticosteroids [8].

4. Conclusions Acute pericarditis can occur as a rare complication of percutaneous coronary inter- vention even during the procedural day. The reported case demonstrated an atypical early onset of PCIS after unsuccessful coronary angioplasty. Post-cardiac injury syndrome should be considered in patients with symptoms and signs of pericarditis and a prior history of percutaneous coronary intervention.

Author Contributions: G.R. and P.B. drafted the manuscript. P.B. and G.D. critically reviewed the manuscript. All authors have read and agreed to the published version of the manuscript. Funding: This research received no external funding. Institutional Review Board Statement: Ethical review and approval were waived for this study because our institution does not require these for case reports. Informed Consent Statement: Written informed consent has been obtained from the patient to publish this paper. Data Availability Statement: No new data were created or analyzed in this study. Data sharing is not applicable to this article. Acknowledgments: None declared. Conflicts of Interest: The authors declare no conflict of interest. Medicina 2021, 57, 490 6 of 6

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