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      Pacemaker-Associated Post-cardiac Injury Syndrome Presenting with Tamponade and Recurrent Pleural Effusion

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          Abstract

          Post-cardiac injury syndrome (PCIS) is presumed to be an immune-mediated process. It affects the pericardium and, to a lesser extent, the epicardium, myocardium, and pleura. It has been rarely reported following pacemaker insertion with an estimated incidence of 1% to 2%. We present the case of a 62-year-old female who developed PCIS 8 weeks following pacemaker insertion. She presented with impending cardiac tamponade requiring pericardiocentesis; recurrent pleural effusions subsequently complicated her condition. The pleural effusion recurred despite trials of steroids, eventually requiring talc pleurodesis. This case highlights the need to consider PCIS as a possible etiology of recurrent pleural effusion following pacemaker insertion.

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          Risk of constrictive pericarditis after acute pericarditis.

          Constrictive pericarditis (CP) is considered a rare, dreaded possible complication of acute pericarditis. Nevertheless, there is a lack of prospective studies that have evaluated the specific risk according to different etiologies. The aim of this study is to evaluate the risk of CP after acute pericarditis in a prospective cohort study with long-term follow-up. From January 2000 to December 2008, 500 consecutive cases with a first episode of acute pericarditis (age, 51±16 years; 270 men) were prospectively studied to evaluate the evolution toward CP. Etiologies were viral/idiopathic in 416 cases (83.2%), connective tissue disease/pericardial injury syndromes in 36 cases (7.2%), neoplastic pericarditis in 25 cases (5.0%), tuberculosis in 20 cases (4.0%), and purulent in 3 cases (0.6%). During a median follow-up of 72 months (range, 24 to 120 months), CP developed in 9 of 500 patients (1.8%): 2 of 416 patients with idiopathic/viral pericarditis (0.48%) versus 7 of 84 patients with a nonviral/nonidiopathic etiology (8.3%). The incidence rate of CP was 0.76 cases per 1000 person-years for idiopathic/viral pericarditis, 4.40 cases per 1000 person-years for connective tissue disease/pericardial injury syndrome, 6.33 cases per 1000 person-years for neoplastic pericarditis, 31.65 cases for 1000 person-years for tuberculous pericarditis, and 52.74 cases per 1000 person-years for purulent pericarditis. CP is a relatively rare complication of viral or idiopathic acute pericarditis (<0.5%) but, in contrast, is relatively frequent for specific etiologies, especially bacterial.
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            COlchicine for the Prevention of the Post-pericardiotomy Syndrome (COPPS): a multicentre, randomized, double-blind, placebo-controlled trial.

            No drug has been proven efficacious to prevent the post-pericardiotomy syndrome (PPS), but colchicine seems safe and effective for the treatment and prevention of pericarditis. The aim of the COlchicine for the Prevention of the Post-pericardiotomy Syndrome (COPPS) trial is to test the efficacy and safety of colchicine for the primary prevention of the PPS. The COPPS study is a multicentre, double-blind, randomized trial. On the third post-operative day, 360 patients (mean age 65.7 ± 12.3 years, 66% males), 180 in each treatment arm, were randomized to receive placebo or colchicine (1.0 mg twice daily for the first day followed by a maintenance dose of 0.5 mg twice daily for 1 month in patients ≥70 kg, and halved doses for patients <70 kg or intolerant to the highest dose). The primary efficacy endpoint was the incidence of PPS at 12 months. Secondary endpoint was the combined rate of disease-related hospitalization, cardiac tamponade, constrictive pericarditis, and relapses. Baseline characteristics were well balanced between the study groups. Colchicine significantly reduced the incidence of the PPS at 12 months compared with placebo (respectively, 8.9 vs. 21.1%; P = 0.002; number needed to treat = 8). Colchicine also reduced the secondary endpoint (respectively, 0.6 vs. 5.0%; P = 0.024). The rate of side effects (mainly related to gastrointestinal intolerance) was similar in the colchicine and placebo groups (respectively, 8.9 vs. 5.0%; P = 0.212). Colchicine is safe and efficacious in the prevention of the PPS and its related complications and may halve the risk of developing the syndrome following cardiac surgery. ClinicalTrials.gov number, NCT00128427.
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              Right heart perforation by pacemaker leads

              Cardiac pacing is a proven therapy of cardiac conduction disturbances and an effective treatment modality in many cardiac arrhythmias. Implantable cardiac defibrillators (ICDs) are particularly beneficial for selected groups of patients with a history of severe ventricular arrhythmias or at a high risk of sudden cardiac death. Despite their potential lifesaving properties, both pacemakers and ICDs are associated with a number of complications. The most frequent include pneumothorax; myocardial perforation; lead malposition, displacement or fracture due to excessive manipulation of the device by the patient (Twiddler's syndrome) [1]. Another group of complications comprises infections: from the pacemaker pocket to bacterial endocarditis with its origin on leads or the tricuspid valve, failure of leads to pace and/or sense appropriately, erosion of the pacemaker site or its leads, and thrombotic events with the most frequently observed subclavian vein thrombosis [2]. In the era of massive anticoagulation and antiplatelet therapy bleeding complications are not uncommon, either. The rate of acute complications from device implantation is acceptable and ranges from 3% to 7% [1–3], depending on the patient group. Nevertheless the problem seems important when account is taken of the fact that permanent devices are implanted in over 250,000 patients a year in the United States alone. The paper entitled “Heart perforation in patients with permanent cardiac pacing-personal observations” presents cases of lead perforation treated in a single medical centre, with well-described diagnostic and treatment procedures. Results of this paper are largely consistent with literature findings, but there nevertheless are some interesting differences, as outlined below [4]. Studies have reported overall lead perforation rates after pacemaker implantation to be 0.1–0.8%, and after ICD placement-0.6–5.2% [3]. The highest reported rate of perforation, based on autopsy, was 27% for patients with atrial leads [5]. Authors of the present paper report a very low incidence rate (0.09%), which is probably related to the engagement of a highly experienced medical team [4]. There are no uniform classifications accounting for the complication. It may be acute (developing during the first 24 h after implantation), subacute (up to 1 month) or chronic. Another classification system divides perforations into early (occurring during the first month after placement) and late. In the present paper, the authors report on cases of subacute and delayed lead perforations. Most of them (5/6 patients) were symptomatic, but in all of them pacing or sensing failure was present [4]. Excessive loop or tension on the lead will predispose to a forward movement through the thinner right atrial or ventricular wall, particularly the apex. Other contributing factors may be the growing prevalence of thinner, dilated cardiac chambers with impaired systolic function as well as recent episode of myocardial infarction. Five out of 6 presented patients suffered from coronary heart disease [4]. It would be very interesting to establish whether they had an episode of myocardial infarction in the past and, if so, to know its precise location. As commonly known, a higher risk of lead perforation is observed in patients with inferior wall or right ventricular myocardial infarction. The fact that atrial perforations were more common type than ventricular is not surprising. The right atrial wall is very thin, averaging only 2 mm in thickness, while the right ventricular wall is twice as thick [6]. Therefore logically one would anticipate a higher risk of atrial wall perforation. In contrast to that pattern, however, five out of six diagnosed perforations reported in this paper involved the right ventricular wall [4]. Symptoms, signs and changes of pacing parameters depend on the location of the lead tip. It can be located in the pericardium, mediastinum, pleural space, lung, chest muscles and even in the abdomen. Consequently, the most commonly observed symptoms include chest pain, dyspnoea, syncope, abdominal pain, muscle or diaphragm stimulation and hiccups. The haemodynamic status depends predominantly on the development of pericardial effusion. Cardiac tamponade leads to hypotension, shock or even cardiac arrest, and requires lifesaving intervention, usually open-chest surgery. Perforated electrodes also frequently lead to pacing and sensing failures. In general, the capture threshold will be increased, whereas the sensing threshold will be reduced. Inappropriate ICD shocks are also observed. The most frequently reported predictors of lead perforation are temporary leads, steroid use, active fixation leads, low body mass index ( 35 mm Hg. Decreased incidence rate may be due to coexisting right ventricular hypertrophy [13]. The incidence of cardiac muscle perforation by ICD leads is associated with the number of delivered shocks [14]. Patients with the above symptoms should be investigated to evaluate the risk of lead perforation. Pacemaker system interrogation, echocardiography, chest radiography and computed tomography (CT) scanning can be very helpful to either prove or rule out the complication. Capture and sensing threshold values should be compared against previous results. Although inappropriate pacemaker function may indicate a possibility of perforation or intracardiac leads migration, normal pacemaker function does not exclude the complication. Crucial for the diagnosis of perforation is visualization of the lead and its tip. Chest X-ray is a technique used to compare the lead tip position and lead curvature with previous results. The diagnosis of perforation is certain if the lead is outside the cardiac silhouette. It can also be helpful to evaluate extracardiac complications such as pleural or pericardial effusion and pneumothorax. Transthoracic echocardiography is a very simple, bedside tool which makes it possible to assess electrode location. It is sufficient for proving diagnosis in most cases and very helpful for monitoring pericardial effusion dynamics. Computed tomography scan proves very valuable when echocardiography and X-ray test are not diagnostic. Consequently, CT scan is currently a gold standard in the diagnosis of lead perforations [15], even though the technique also has its limitations. The star artifact is a well-known artifact related to the imaging of metal implants. Surrounding the electrode tip, it sometimes makes it difficult to precisely identify the lead tip. Late perforations are often asymptomatic and characterized by a very low rate of cardiac tamponade or death [16]. The finding of a late perforation may represent an asymptomatic acute perforation or a true late perforation. Because the right heart is a low-pressure system, a perforation may be sealed by a combination of muscle contraction and fibrosis over the lead, resulting in no sequelae. The rate of unrecognized asymptomatic perforations is much higher than symptomatic and riches 15% [6]. In these cases the lead impedance and pacing thresholds did not differ between patients with and without lead perforation. In a small perforation, dislocation of the lead may be very small, so the cathode may be close to the epicardium and the anode within the endocardium, resulting in proper pacemaker function. It thus follows that normal impedance and pacing parameters do not exclude the presence of a perforation. On the other hand, elevated pacing thresholds may indicate a perforation. Similarly to symptomatic perforations, in asymptomatic cases atrial leads perforate more frequently than ventricular ones, and ICD leads perforate more frequently than ventricular pacemaker leads. Patient management strategy should depend on the dynamics of symptoms, pericardial effusion and haemodynamic status. In the case of haemodynamic instability, rapid progression of pericardial effusion, surgical management (open chest surgery) seems to be the best treatment option. In other cases, in stable conditions, simple direct traction with or without percutaneous dilators can be considered, though under close echocardiographic monitoring and with a surgical backup. Lead extraction should be followed by new lead placement in a different location, preferably in the right ventricular outflow tract or the intraventricular septum. In the case of open-chest surgery the implantation of epicardial leads should be considered. During the postprocedural period, closed haemodynamic and echocardiographic monitoring is mandatory because delayed re-tamponade could develop (especially when the surgeon could not identify the location of cardiac muscle perforation) [12]. In cases of acute or subacute lead perforation the implantation of a new pacemaker might be unnecessary. Appropriate management of asymptomatic lead perforation is a debated issue. Some studies suggest that the diagnosis of lead perforation necessitates lead removal [3]. Results of other studies [6], however, suggest that the extraction of a chronically perforated lead without malfunctioning of the device is not mandatory. In addition, the risk of cardiac tamponade should be considered after the removal of chronically implanted leads. Another fact worth considering is that a significant number of those leads are partially perforated.
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                Author and article information

                Journal
                Clin Med Insights Case Rep
                Clin Med Insights Case Rep
                ICR
                spicr
                Clinical Medicine Insights. Case Reports
                SAGE Publications (Sage UK: London, England )
                1179-5476
                30 October 2020
                2020
                : 13
                : 1179547620965559
                Affiliations
                [1 ]Unity Hospital, Rochester Regional Health, Rochester, New York, USA
                [2 ]Internal Medicine Department, Hamad Medical Corporation, Doha, Qatar
                Author notes
                [*]Mouhand FH Mohamed, Internal Medicine Department, Hamad General Hospital, Hamad Medical Corporation, Doha, Qatar. Email: dr.m.oraiby@ 123456hotmail.com
                Author information
                https://orcid.org/0000-0002-1146-2732
                https://orcid.org/0000-0002-5872-1711
                https://orcid.org/0000-0002-4761-8014
                Article
                10.1177_1179547620965559
                10.1177/1179547620965559
                7607781
                d9a5443d-dc86-4b38-9361-d1b06bbbc4ef
                © The Author(s) 2020

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                : 27 April 2020
                : 20 September 2020
                Categories
                Case Report
                Custom metadata
                January-December 2020
                ts1

                Medicine
                pleurodesis,postpericardiotomy syndrome,pps,post-cardiac injury syndromes,pcis,pericardial effusion,pleural effusion

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