ST-segment elevation (STE) due to inferior STE myocardial infarction (STEMI) may be misdiagnosed as pericarditis. Conversely, this less life-threatening etiology of ST elevation may be confused for inferior STEMI. We sought to determine if the presence of any ST-segment depression in lead aVL would differentiate inferior STEMI from pericarditis.
Pericardial heart disease includes pericarditis, (an acute, subacute, or chronic fibrinous, noneffusive, or exudative process), and its complications, constriction, (an acute, subacute, or chronic adhesive or fibrocalcific response), and cardiac tamponade. The pathophysiology of cardiac tamponade and constrictive pericarditis readily explains their respective findings on clinical examination, Doppler echocardiography, and at cardiac catheterization. The primary abnormality of cardiac tamponade is pan-cyclic compression of the cardiac chambers by increased pericardial fluid requiring that cardiac chambers compete for a fixed intrapericardial volume. Features responsible for the pathophysiology include transmission of thoracic pressure through the pericardium and heightened ventricular interdependence. Constrictive pericarditis is a condition in which the pericardium limits diastolic filling, causes dissociation of intracardiac and intrathoracic pressures, and heightened ventricular interdependence. Both conditions result in diastolic dysfunction, elevated and equal venous and ventricular diastolic pressure, respiratory variation in ventricular filling, and ultimately, reduced cardiac output.
Most patients with acute pericarditis have a benign course and a good prognosis. However, a minority of patients develop complicated pericarditis, and the care of these patients is the focus of this review. Specifically, we address risk factors, multimodality imaging, pathophysiology, and novel treatments. The authors conclude that: 1) early high-dose corticosteroids, a lack of colchicine, and an elevated high-sensitivity C-reactive protein are associated with the development of complicated pericarditis; 2) in select cases, cardiovascular magnetic resonance imaging may aid in the assessment of pericardial inflammation and constriction; 3) given phenotypic similarities between recurrent idiopathic pericarditis and periodic fever syndromes, disorders of the inflammasome may contribute to relapsing attacks; and 4) therapies that target the inflammasome may lead to more durable remission and resolution. Finally, regarding future investigations, the authors discuss the potential of cardiovascular magnetic resonance to inform treatment duration and the need to compare steroid-sparing treatments to pericardiectomy.
About one-half of the patients with congestive heart failure have preserved left ventricular ejection fraction (HFpEF). Although the etiology of HFpEF is most commonly related to long-standing hypertension and atherosclerosis, a significant number of suspected HFpEF patients have a restrictive cardiomyopathy or chronic pericardial disease. Recognizing these syndromes is important because early diagnosis may lead to instituting specific therapy that may prolong survival, improve quality of life, and/or recognize and treat an underlying systemic disorder. Advances in diagnostic imaging, biomarkers, and genetic testing today allow identification of the specific etiology in most cases. Novel pharmacological, immunologic, and surgical therapies are leading to improved quality of life and survival.
Background Tuberculous pericarditis is associated with high morbidity and mortality even if antituberculosis therapy is administered. We evaluated the effects of adjunctive glucocorticoid therapy and Mycobacterium indicus pranii immunotherapy in patients with tuberculous pericarditis. Methods Using a 2-by-2 factorial design, we randomly assigned 1400 adults with definite or probable tuberculous pericarditis to either prednisolone or placebo for 6 weeks and to either M. indicus pranii or placebo, administered in five injections over the course of 3 months. Two thirds of the participants had concomitant human immunodeficiency virus (HIV) infection. The primary efficacy outcome was a composite of death, cardiac tamponade requiring pericardiocentesis, or constrictive pericarditis. Results There was no significant difference in the primary outcome between patients who received prednisolone and those who received placebo (23.8% and 24.5%, respectively; hazard ratio, 0.95; 95% confidence interval [CI], 0.77 to 1.18; P=0.66) or between those who received M. indicus pranii immunotherapy and those who received placebo (25.0% and 24.3%, respectively; hazard ratio, 1.03; 95% CI, 0.82 to 1.29; P=0.81). Prednisolone therapy, as compared with placebo, was associated with significant reductions in the incidence of constrictive pericarditis (4.4% vs. 7.8%; hazard ratio, 0.56; 95% CI, 0.36 to 0.87; P=0.009) and hospitalization (20.7% vs. 25.2%; hazard ratio, 0.79; 95% CI, 0.63 to 0.99; P=0.04). Both prednisolone and M. indicus pranii, each as compared with placebo, were associated with a significant increase in the incidence of cancer (1.8% vs. 0.6%; hazard ratio, 3.27; 95% CI, 1.07 to 10.03; P=0.03, and 1.8% vs. 0.5%; hazard ratio, 3.69; 95% CI, 1.03 to 13.24; P=0.03, respectively), owing mainly to an increase in HIV-associated cancer. Conclusions In patients with tuberculous pericarditis, neither prednisolone nor M. indicus pranii had a significant effect on the composite of death, cardiac tamponade requiring pericardiocentesis, or constrictive pericarditis. (Funded by the Canadian Institutes of Health Research and others; IMPI ClinicalTrials.gov number, NCT00810849 .).
Disorders of the pericardium represent a diverse range of conditions that traditionally may not have received the same level of attention by cardiologists and physicians, owing partly to a lack of research into advanced diagnostic modalities, and limited, evidence-based treatment options. In recent years, there has been a timely resurgence of interest in pericardial diseases, in particular pericarditis. This is attributable to advances in multi-modality cardiovascular imaging, in particular cardiac magnetic resonance (CMR), which may help guide treatment decisions for patients with pericardial syndromes. Additionally, increased research and understanding of the pathophysiological basis of pericarditis have shed light on the role of inflammation in pericarditis. This knowledge may help identify potential specific treatment targets. This article aims to provide a practical review of the role of multimodality cardiovascular imaging (echocardiography, multidetector cardiac computed tomography (MDCT), CMR) in pericardial conditions, focusing on the strengths and potential limitations of each imaging modality.
Key Clinical Points Acute Pericarditis The diagnosis of acute pericarditis requires at least two of the following symptoms or signs to be present: typical chest pain, pericardial friction rub, typical electrocardiographic changes, and pericardial effusion. In developed countries, 80 to 90% of cases are idiopathic and presumed to be viral. Evaluation includes a medical history and laboratory tests to help determine whether a specific cause is present, a chest radiograph, and an echocardiogram to determine whether there is an effusion. In response to treatment with a combination of a nonsteroidal antiinflammatory drug (NSAID) and colchicine, 70 to 90% of cases resolve completely; treatment with glucocorticoids should be avoided, if possible, because they increase the risk of recurrence. Patients with recurrent pericarditis should be treated with repeated courses of an NSAID and colchicine; if treatment with glucocorticoids cannot be avoided, moderate initial doses followed by gradual tapering provide the best outcomes.
Pericardial tuberculosis is an important clinical problem in resource-limited countries, particularly in those with concomitant epidemics of human immunodeficiency virus (HIV) infection. Tuberculosis involving closed anatomical spaces such as the pericardium or meninges can cause devastating inflammatory injury, and management with antimicrobial therapy alone may not prevent complications. Host-directed therapies that attenuate destructive inflammatory responses may prevent serious sequelae. Current American and World Health Organization guidelines strongly recommend treatment with glucocorticoids in addition to antituberculosis drugs in patients with tuberculous pericarditis, but expert European guidelines are more muted, reflecting the uncertainty of the evidence.(1)-(3) Mayosi and colleagues now report . . .
Constrictive pericarditis can result from a stiff pericardium that prevents satisfactory diastolic filling. The distinction between constrictive pericarditis and other causes of heart failure, such as restrictive cardiomyopathy, is important because pericardiectomy can cure constrictive pericarditis. Diagnosis of constrictive pericarditis is based on characteristic haemodynamic and anatomical features determined using echocardiography, cardiac catheterization, cardiac MRI, and CT. The Mayo Clinic echocardiography and cardiac catheterization haemodynamic diagnostic criteria for constrictive pericarditis are based on the unique features of ventricular interdependence and dissociation of intrathoracic and intracardiac pressures seen when the pericardium is constricted. A complete pericardiectomy can restore satisfactory diastolic filling by removing the constrictive pericardium in patients with constrictive pericarditis. However, if inflammation of the pericardium is the predominant constrictive mechanism, anti-inflammatory therapy might alleviate this transient condition without a need for surgery. Early diagnosis of constrictive pericarditis is, therefore, of paramount clinical importance. An improved understanding of how constrictive pericarditis develops after an initiating event is critical to prevent this diastolic heart failure. In this Review, we discuss the aetiology, pathophysiology, and diagnosis of constrictive pericarditis, with a specific emphasis on how to differentiate this disease from conditions with similar clinical presentations.
The causes of chest pain range from benign sources such as muscle strain to life-threatening diagnoses such as aortic dissection and myocardial infarction. The likelihood and presentations of disorders causing chest pain are different between women and men. This article highlights important features in determining a correct diagnosis.