**3.1 Etiology**

Various infections (viral, bacterial, fungal, and tick-borne) have been known to cause the inflammation of the pericardium. In fact, prior to the widespread distribution of anti-retroviral medications, pericarditis was found to be the most common cardiovascular manifestation of human immunodeficiency virus/ acquired immunodeficiency syndrome [16, 17] and, in conjunction with tuberculosis, remains the most common cause of pericardial inflammation in the developing world [18], whereas coxsackievirus maintains its status as the most common viral etiology of pericarditis overall. Malignancy, independent of other systemic diseases, has also been associated with acute pericardial disease and

**17**

*Pericardial Diseases in Elderly Patients DOI: http://dx.doi.org/10.5772/intechopen.89473*

**3.2 Clinical presentation**

**3.3 Diagnostics**

myocardial involvement [34].

accounts for about 6% of cases without another explanation [19, 20]. Systemic diseases, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), have been found to cause pericardial inflammation with approximately 50% of patients with SLE experiencing pericarditis. Other established etiologies of acute pericardial disease include post-myocardial infarction pericardial inflammation and/or effusion [21–24], post-radiation pericarditis with or without pericardial effusion [25], and uremic pericarditis usually in the setting of advanced renal failure and inadequate dialysis [26, 27]. Hypothyroidism severe enough to result in myxedema can result in a large, slowly accumulating

There are four major distinctive features of acute pericarditis (at least two of which are required to make a clinical diagnosis): chest pain, pericardial friction rub, characteristic ECG changes, and pericardial effusion. The predominant presenting symptom is chest pain that is usually pleuritic in nature, sharp and alleviated by sitting up and leaning forward due to the positional shift of the pericardium, a feature which distinguishes it from the typical chest pain caused by myocardial ischemia [29, 30]. Pericardial chest pain is also often associated with nonproductive cough and dyspnea [29]. A scratchy, squeaking sound heard over the left sternal border upon auscultation known as a pericardial friction rub is the second of four major clinical features of pericarditis and is reported to be found in approximately 85% of patients with acute pericarditis in the absence of a pericardial effusion [20]. It is an extra heart sound resulting from the friction between the parietal and visceral pericardium coming into contact in the presence of inflammation. The presence of a pericardial effusion is the third of the four major signs of acute pericarditis and can best be appreciated on an echocardiogram. The last of the four major signs of pericarditis is new, diffuse ST-elevation, PR segment depressions, and PR segment elevation in lead aVR found on ECG (discussed further under *Diagnostics*) [15, 29, 31]. Other secondary features of pericarditis that may or may not be present are fever, subacute course of chest pain, elevated troponin (suggestive of myocardial involvement), and

pericardial effusion but rarely causes acute pericarditis [28].

hemodynamic instability (suggestive of cardiac tamponade) [32, 33].

Various laboratory tests and imaging modalities play role in establishing the diagnosis of acute pericarditis. Inflammatory markers, such as white blood cell count (WBC), erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) levels although nonspecific, may help distinguish pericarditis from a condition with overlapping features given appropriate clinical criteria. Troponin levels, usually elevated in acute coronary syndrome, may also be elevated in pericarditis indicating

The chest X-ray may show cardiomegaly in the presence of a significant pericardial effusion but otherwise has limited utility in the diagnosis of pericardial disease. An echocardiogram can be similarly useful although the absence of pericardial effusion would not necessarily exclude the diagnosis of acute pericarditis. Cardiac CT imaging can serve a dual purpose in the diagnosis of acute pericarditis in that it may also help elucidate the underlying pathology responsible for the inflammatory changes. Pericardial thickening and effusion in the absence of calcification along with the enhancement of the visceral and parietal pericardium with intravenous contrast are indicative of active inflammation consistent with pericarditis [35]. CMRI can confirm inflammation but is likely not necessary in the diagnostic

*Pericardial Diseases in Elderly Patients DOI: http://dx.doi.org/10.5772/intechopen.89473*

*Inflammatory Heart Diseases*

**3. Acute pericarditis**

**3.1 Etiology**

**Figure 2.**

faster diagnosis and potential earlier intervention.

*Management algorithm for pericardial effusion with unknown origin.*

Acute pericarditis is a condition defined by the inflammation of the pericardial sac that can take place in the setting of a systemic disease (infectious, malignant, inflammatory, etc.) or independently of any other condition [2, 5, 13–15]. Among the elderly, it is important to consider malignancy in the evaluation of etiology as it is more common in this population and may prompt appropriate testing leading to a

Various infections (viral, bacterial, fungal, and tick-borne) have been known to cause the inflammation of the pericardium. In fact, prior to the widespread distribution of anti-retroviral medications, pericarditis was found to be the most common cardiovascular manifestation of human immunodeficiency virus/ acquired immunodeficiency syndrome [16, 17] and, in conjunction with tuberculosis, remains the most common cause of pericardial inflammation in the developing world [18], whereas coxsackievirus maintains its status as the most common viral etiology of pericarditis overall. Malignancy, independent of other systemic diseases, has also been associated with acute pericardial disease and

**16**

accounts for about 6% of cases without another explanation [19, 20]. Systemic diseases, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), have been found to cause pericardial inflammation with approximately 50% of patients with SLE experiencing pericarditis. Other established etiologies of acute pericardial disease include post-myocardial infarction pericardial inflammation and/or effusion [21–24], post-radiation pericarditis with or without pericardial effusion [25], and uremic pericarditis usually in the setting of advanced renal failure and inadequate dialysis [26, 27]. Hypothyroidism severe enough to result in myxedema can result in a large, slowly accumulating pericardial effusion but rarely causes acute pericarditis [28].

### **3.2 Clinical presentation**

There are four major distinctive features of acute pericarditis (at least two of which are required to make a clinical diagnosis): chest pain, pericardial friction rub, characteristic ECG changes, and pericardial effusion. The predominant presenting symptom is chest pain that is usually pleuritic in nature, sharp and alleviated by sitting up and leaning forward due to the positional shift of the pericardium, a feature which distinguishes it from the typical chest pain caused by myocardial ischemia [29, 30]. Pericardial chest pain is also often associated with nonproductive cough and dyspnea [29]. A scratchy, squeaking sound heard over the left sternal border upon auscultation known as a pericardial friction rub is the second of four major clinical features of pericarditis and is reported to be found in approximately 85% of patients with acute pericarditis in the absence of a pericardial effusion [20]. It is an extra heart sound resulting from the friction between the parietal and visceral pericardium coming into contact in the presence of inflammation. The presence of a pericardial effusion is the third of the four major signs of acute pericarditis and can best be appreciated on an echocardiogram. The last of the four major signs of pericarditis is new, diffuse ST-elevation, PR segment depressions, and PR segment elevation in lead aVR found on ECG (discussed further under *Diagnostics*) [15, 29, 31]. Other secondary features of pericarditis that may or may not be present are fever, subacute course of chest pain, elevated troponin (suggestive of myocardial involvement), and hemodynamic instability (suggestive of cardiac tamponade) [32, 33].

#### **3.3 Diagnostics**

Various laboratory tests and imaging modalities play role in establishing the diagnosis of acute pericarditis. Inflammatory markers, such as white blood cell count (WBC), erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) levels although nonspecific, may help distinguish pericarditis from a condition with overlapping features given appropriate clinical criteria. Troponin levels, usually elevated in acute coronary syndrome, may also be elevated in pericarditis indicating myocardial involvement [34].

The chest X-ray may show cardiomegaly in the presence of a significant pericardial effusion but otherwise has limited utility in the diagnosis of pericardial disease. An echocardiogram can be similarly useful although the absence of pericardial effusion would not necessarily exclude the diagnosis of acute pericarditis. Cardiac CT imaging can serve a dual purpose in the diagnosis of acute pericarditis in that it may also help elucidate the underlying pathology responsible for the inflammatory changes. Pericardial thickening and effusion in the absence of calcification along with the enhancement of the visceral and parietal pericardium with intravenous contrast are indicative of active inflammation consistent with pericarditis [35]. CMRI can confirm inflammation but is likely not necessary in the diagnostic

workup of acute pericarditis unless the presumed etiology is a systemic inflammatory or autoimmune disease with characteristic cardiac findings.

The ECG may be perhaps the most useful diagnostic modality when considering acute pericarditis. The ECG progresses through a distinctive, four stage pattern although the evolution can be variable with up to 40% of patients showing atypical changes [30–32]. Stage 1 is characterized by widespread ST elevation with reciprocal ST depression in leads aVR and V1 as well as PR segment elevation in lead aVR accompanied by PR segment depression in the remaining limb leads and V5–6. Within 1 week of onset, normalization of ST and PR segments on the ECG comprises Stage 2. Stage 3 of the ECG is marked by diffuse T-wave inversions, while Stage 4 consists of normalization of the ECG. However, not all forms of pericarditis result in the characteristic ECG pattern as the pericardium itself is an inert tissue and only inflammatory changes involving the epicardium or myocardium would be reflected in acute pericarditis [36]. In fact, one review found that of 100 patients studied, only seven arrhythmias were identified all resulting from underlying heart disease [37], while a separate study comparing acute pericarditis to myopericarditis found arrhythmias more frequently associated with myopericarditis [38].

#### **3.4 Treatment**

Medical treatment of acute pericarditis utilizes one or a combination of two out of three different medications: NSAIDs, colchicine, and glucocorticoids. Treatment duration is usually guided by the resolution of symptoms and etiology of disease in the absence of confounding factors such as acute kidney or liver injury.

A combination of NSAIDs and colchicine is the mainstay of therapy for acute viral or idiopathic pericarditis. NSAIDs alone have been shown through multiple studies to effectively treat up to 80% of pericarditis cases [20, 32, 39]. No one particular NSAIDs has been shown to be more effective than another except in the case of post-myocardial infarction pericarditis for which aspirin is recommended and other NSAIDs should be avoided in order to prevent the disruption of myocardial scar formation [40]. Patients taking NSAIDs for pericarditis should concurrently take a proton-pump inhibitor for ulcer prophylaxis in the absence of any direct contraindication to do so. Treatment can be tapered once the patient is symptom-free for at least 24 hours (typically 1–2 weeks). Alternatively, one study recommends following weekly CRP levels along with symptom resolution and beginning tapering, once the patient is symptom-free for 24 hours and CRP levels have returned to normal [41].

In 2005, the Colchicine for Acute Pericarditis (COPE) trial suggested colchicine as an effective adjunct for treating acute pericarditis when combined with NSAIDs therapy for patients with non-bacterial, non-malignancy-related pericardial disease [39]. The addition of colchicine was further shown to reduce symptom burden and decrease the rate of recurrent pericarditis by a subsequent, randomized-control trial (RCT) [42], a finding, which was later supported by a meta-analysis in 2014, that demonstrated a reduced risk of recurrence at 18 months in patients undergoing treatment for acute pericarditis [43]. The management of acute pericarditis with a combination of NSAIDs and colchicine is also currently supported by the 2015 European Society of Cardiology (ESC) guidelines [2].

For patients with contraindications to NSAIDs therapy (kidney failure, GI bleeding, pregnancy, etc.), glucocorticoids may be used in combination with colchicine for the initial treatment of acute pericarditis. Treatment duration is then guided by symptom resolution and the normalization of CRP levels with tapering usually started 2–4 weeks thereafter. Glucocorticoids have also been utilized in patients with pericarditis refractory to NSAIDs and colchicine though one study shows a trend toward higher rate of recurrent pericarditis with steroid use [44].

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*Pericardial Diseases in Elderly Patients DOI: http://dx.doi.org/10.5772/intechopen.89473*

**4. Recurrent pericarditis**

autoimmune etiology [2, 51].

**4.2 Clinical presentation**

the initial event [52–54].

**4.3 Diagnostics**

**4.1 Etiology**

Geriatric patients appear to have a higher risk of mortality when admitted and treated for pericarditis in the hospital. Although data regarding treatment of specifically elderly patients are sparse, one study examined the relationship between pericarditis, age, hospital admission, and mortality. They analyzed 45,504 patients above the age of 65 from 1999 to 2012 and found that hospitalization for the treatment of pericarditis is associated with increased risk of 1-year all-cause mortality despite a decrease in 1-year mortality rate from 19.7% (95% confidence interval (CI) 18.8–20.8) in 1999 to 17.3% (95% CI 15.3–20) in 2012 [45]. While it is possible that this association is in part due to a higher prevalence of significant comorbidities and compromised immune systems among the elderly, it nevertheless remains an aspect of pericardial disease that warrants further investigation as advanced therapies and support devices continue to enable longer lifespans with time.

Recurrent pericarditis is a syndrome defined by the reemergence of pericarditis

after the treatment of the initial inflammatory event [31, 46–48]. A minimum 4–6 week symptom-free interval post anti-inflammatory treatment is required to

Acute pericarditis has been found to have recurrence rates as high as 30% in patients treated without colchicine [32, 39, 47, 49]. Some cases of recurrent pericarditis appear to reflect localized inflammation given the detection of certain cytokines (interleukin (IL)-6, IL-8, and interferon gamma) in the pericardial fluid and their absence in the serum [50]; however, most cases are considered to be of

Chest pain appears to be the most common recurring symptom; however, the clinical diagnosis of recurrent pericarditis requires the presence of at least one of the following in addition to pleuritic chest pain: fever, pericardial rub, ECG changes, pericardial effusion, elevated WBC, ESR, CRP, or evidence of active pericardial inflammation on imaging [15]. Patients with previously treated pericarditis may experience multiple recurrences over the course of months to years following

The selection of the initial treatment regimen can directly impact the potential for the recurrence of acute pericarditis and may serve as an independent predictor of risk. For instance, a prior response to NSAIDs therapy is associated with the reduced risk of recurrence [32], whereas treatment with glucocorticoids is associated with increased recurrence [55]. It is difficult to rely upon ECG changes for the diagnosis for recurrent pericarditis as they are non-specific in the majority of cases. Chest X-ray and TTE also have limited utility as both will appear to be normal without a significant pericardial effusion. CT and CMRI imaging have proven to be of benefit in elucidating the diagnosis of recurrent pericarditis as contrast-enhanced CT can detect active pericardial inflammation while CMRI may reveal the evidence

of edema via pericardial gadolinium enhancement [2, 35].

differentiate recurrent pericarditis from incessant pericarditis.

*Pericardial Diseases in Elderly Patients DOI: http://dx.doi.org/10.5772/intechopen.89473*

Geriatric patients appear to have a higher risk of mortality when admitted and treated for pericarditis in the hospital. Although data regarding treatment of specifically elderly patients are sparse, one study examined the relationship between pericarditis, age, hospital admission, and mortality. They analyzed 45,504 patients above the age of 65 from 1999 to 2012 and found that hospitalization for the treatment of pericarditis is associated with increased risk of 1-year all-cause mortality despite a decrease in 1-year mortality rate from 19.7% (95% confidence interval (CI) 18.8–20.8) in 1999 to 17.3% (95% CI 15.3–20) in 2012 [45]. While it is possible that this association is in part due to a higher prevalence of significant comorbidities and compromised immune systems among the elderly, it nevertheless remains an aspect of pericardial disease that warrants further investigation as advanced therapies and support devices continue to enable longer lifespans with time.
