Pericardial Knock Research Articles

Abstract 14984: Transient Constrictive Pericarditis: Pericardiectomy to the Rescue

Case Presentation: A 47 years old male presented with progressive dyspnea, bilateral leg and abdominal swelling, weight gain, and intermittent low-grade fever. He had a history of hypertension and chronic lymphocytic pericarditis complicated by an episode of constrictive pericarditis. Exam showed jugular venous pressure of 10 cmH2O, pericardial knock, and abdominal distention. Inflammatory markers were elevated (CRP 87.3 mg/dL, ESR 29 mm/hr). Echo showed abnormal increase in septal longitudinal motion and Doppler interrogation of the hepatic veins showed diastolic flow reversal at the end of expiration. Cardiac MRI showed pericardial thickening and circumferential delayed pericardial enhancement. Patient was diagnosed with transient constrictive pericarditis (TCP) and was treated with ibuprofen, colchicine, and prednisone and had improvement in his symptoms and inflammatory markers. However, he experienced another recurrence 6 months later and underwent pericardiectomy. Pathology showed organized fibrosis overlying the parietal fibrosa layer, mild neovascularization and perivascular chronic inflammation, confirming the diagnosis of TCP. After pericardiectomy, patient had significant symptomatic improvement and returned to his baseline activity level. Postoperative echo showed normalization of annulus longitudinal motion and cardiac MRI showed near resolution of pericardial delayed enhancement. He was successfully tapered off of his anti-inflammatory regimen. Discussion: TCP is a sub-type of constrictive pericarditis characterized by pathological findings of pericardial edema, acute or subacute inflammation, and fibrin deposition, as opposed to the fixed pericardial fibrosis and calcification seen in constrictive pericarditis. Constriction may resolve spontaneously, and anti-inflammatory therapy is the mainstay of treatment but in refractory cases like these, pericardiectomy comes to the rescue.

The Gift of Double Mentoring

The Gift of Double Mentoring

Additional Heart Sounds–Part 2 (Clicks, Opening Snap and More)

Abstract Systolic clicks are high-pitched sharp sounds. They are classified as ejection and nonejection clicks. Ejections clicks commonly occur at the aortic and pulmonary valve, while nonejection clicks occur at the mitral and tricuspid valve. Opening snap is an additional sound heard in the diastole. It is described as an early diastolic, high-pitched sound, which is associated with opening of the mitral and/or tricuspid valve. Pericardial knock is a high-pitched early diastolic sound, which is characteristic of constrictive pericarditis. The opening and closing of prosthetic valves produce sounds which may vary in intensity and timing according to the type and design of the valve, patient’s rhythm, and hemodynamic status.

The clicking chest: what exactly did Hamman hear? A case report of a left-sided pneumothorax.

BackgroundHamman’s sign is a rare phenomenon. Louis Hamman described this pathognomonic clicking chest noise in association with pneumomediastinum in 1937. This typical noise can also be present in left-sided pneumothorax. Clinical cases already mention this pericardial knock in 1918 in gunshot wounds of the left chest and in 1928 in cases of spontaneous left-sided pneumothorax. However, the sound itself has only rarely been recorded.Case summaryWe describe a case of a young man with no significant medical history who was referred to the hospital with chest pain and audible clicks, documented with his smartphone. Imaging studies including chest radiograph and computed tomography scan revealed a left-sided pneumothorax. The patient underwent semi-urgent insertion of a thorax drain. His clinical outcome was excellent.DiscussionIn recent years only a few case reports describe Hamman’s sign, as it is rare and happens only transiently. This case report includes the audible clicks recorded by the patient with his smartphone. We stress the importance of thoracic clicking sounds as key symptom in the differential diagnosis of left-sided pneumothorax, pneumomediastinum, and valvular pathology such as mitral valve prolapse.

Chronic Effusive Pericarditis and Chronic Constrictive Pericarditis

Chronic Pericarditis is inflammation that begins gradually, is long lasting and results in fluid accumulation in the pericardial space or thickening of the pericardium. The etiology is unknown but may be cancer, TB or hypothyroidism. Arrhythmias are common and seen in almost half the patients. The commonest arrhythmia is atrial fibrillation. Symptoms and signs are related to increased right atrial pressure and physical findings include elevated JVP and pericardial knock. Non surgical therapy consists mainly of no salt. Surgery cures about 85% of patients, however 5–15% of patients will die. Chronic effusive pericarditis occurs when there is persistent restriction of the visceral pericardium after pericardiocentesis.

Second Heart Sound

AbstractThe auscultation of second heart sound reveals presence of the disease and its pathophysiology, conduction defects, ventricular function, and hemodynamics around the aortic and pulmonary valves. To understand the splitting of the second heart sound, it is useful to understand the concepts of hangout interval and ejection time. Differential diagnosis of S2 split include opening snap, third heart sound, and pericardial knock. Variations of second heart sound may involve intensity or variations of split. Variations of split can be single heart sound, wide split, wide fixed split, or paradoxical splitting.Interpretation of second heart sound in congenital heart disease provides information about the presence and position of semilunar valves.

Hemodynamic Findings of Effusive-Constrictive Pericarditis.

A 64-year-old man with rheumatoid arthritis presented with progressive abdominal and leg swelling, anorexia, and dyspnea for several years. Physical examination was notable for a pericardial knock, pulsatile hepatomegaly, and lower extremity edema. The jugular vein was distended past the angle of

Calcific Pericarditis

An 84-year-old woman presented to the emergency department with progressive shortness of breath, orthopnea, paroxysmal nocturnal dyspnea, and fatigue. She had a past history of atrial fibrillation and was taking digoxin. Clinical examination revealed normal vital signs, 6 cm of jugular venous distension with Kussmaul’s sign, a pericardial knock, and pedal edema.

When opportunity knocks

Constrictive pericarditis remains a common medical problem in developing countries where it frequently complicates tuberculous pericarditis. In addition, it is not infrequently seen in the developed world in the context of previous cardiac surgery, chest irradiation and even idiopathic pericarditis.(1) The diagnosis of pericardial constriction is often elusive and delays between the onset of symptoms and final diagnosis is the norm. Given the potential curability of this cause of heart failure and the fact that various features of chronicity in the disease portend a poor prognosis, recognising the disease early is of paramount importance.(1) The haemodynamics of constriction, particularly in more pronounced cases, produces a set of interesting clinical findings that the vigilant physician can elicit. A useful, and often neglected clinical feature, is that of a diastolic precordial or epigastric impulse, the palpable equivalent of an audible diastolic pericardial knock. This short report illustrates this unique clinical finding and explains the haemodynamics responsible for it. We also briefly review other commonly found clinical findings that assist in making the diagnosis of constrictive pericarditis.

Pericardial calcification following blunt trauma

A 50-year-male presented with persistent, progressive shortness of breath for last 1 year along with swelling of abdomen for last 1 month. Physical examination revealed increased jugular venous pressure (14 cm of water), ascites along with presence of Kussmaul sign and pericardial knock. Clinically, a diagnosis of constrictive pericarditis (CP) was made. He denied any past history of tuberculosis or any other infective etiology. Past medical history revealed history of trauma in past childhood. Chest X-ray revealed a predominant circumferential calcification along the left border of the heart [Figure 1]. Doppler echocardiography showed evidence of CP with thick calcified pericardium. End diastolic pressure of all four chambers was also found to be equal. A diagnosis of CP due to trauma was made. Pericardial calcification is usually preceded by pericarditis or trauma. The most common causes of pericardial calcification are chronic idiopathic pericarditis, post-cardiac surgery, mediastinal irradiation, and tuberculous pericarditis. [1] Both blunt

Anterior Mediastinal Mass : A Rare Presentation of Tuberculosis

We report a case of a 10 year old male child, who presented to us with complaints of progressive abdominal distension since 9 months and exertional breathlessness since 4 months. There was history of mild jaundice noticed by a doctor, however no other history suggestive of liver, cardiac or renal disease. He had received antitubercular therapy for complaints of cough 1 year ago for 3 months. There was no history of TB contact. General examination revealed mild icterus and prominent, distended neck and upper limb veins. Jugular venous pressure was raised with an absent hepatojugular reflux. Systemic examination showed massive ascites and a firm hepatomegaly. Cardiovascular examination revealed pericardial knock. Differential diagnoses were constrictive Pericarditis of tubercular etiology, Budd Chiari syndrome and a mediastinal mass causing IVC and SVC obstruction. Investigations revealed an anterior mediastinal mass on cardiac MRI(FIG) adherent to the pericardium causing extrinsic compression of the right atrium, most probably a germ cell tumour. Tumour markers were negative. A CT-guided biopsy of the mass was inconclusive, hence an open excision biopsy was done, which on gross appearance was suggestive of tuberculosis.

Constrictive pericarditis: Insights from cardiac computed tomography

a v d d c r w c t e Constrictive pericarditis is a rare disease, usually the result of long-standing pericardial inflammation leading to pericardial scarring with thickening, fibrosis, and calcification. The most frequent causes are mediastinal radiation, chronic idiopathic pericarditis, cardiac surgery, and tuberculous pericarditis. Nearly 9% of patients with acute pericarditis for any reason go on to develop constrictive physiology. We report the case of a 52-year-old man with a history of acute pericarditis 30 years ago, with a three-year evolution of fatigue, dyspnea and palpitations. Physical examination revealed jugular venous distension and hepatomegaly and a pericardial knock was audible on cardiac auscultation. The 12-lead electrocardiogram revealed atrial flutter

A challenging case of constrictive pericarditis

We report the case of a healthy 35-year-old male who was seen by his primary care physician with complaints of general fatigue, shortness of breath, night sweats, and abdominal bloating which had started several weeks prior to his visit. A CT scan of the abdomen demonstrated the presence of gall stones. He was subsequently seen by the surgeons and, shortly thereafter, underwent laparoscopic cholecystectomy for suspected cholecystitis. Two weeks after the procedure he reported no significant change in clinical symptoms. A cardiology consultation was subsequently requested at which time his physical examination revealed a BP of 120/80 mmHg, (no pulsus paradoxus), pulse 80 beats/min, elevated jugular venous pressure, and a positive Kussmaul’s sign. Auscultation of the heart revealed a regular rate and rhythm with no murmurs or gallops. A ‘pericardial knock’ was audible. There was no evidence of ascites on abdominal examination and no peripheral lower extremity oedema. The ECG showed sinus rhythm with a ventricular rate of 76 beats/min. No ST abnormalities were seen. Chest X-ray showed a normal cardiac silhouette with no evidence of congestion. He underwent a transthoracic echocardiogram (TTE) which demonstrated a mildly thickened pericardium, small pericardial effusion, a ‘septal bounce’, significant respiratory variation of mitral inflow velocities, and a dilated inferior vena cava and hepatic veins (Fig. 1). The constellation of clinical and echocardiographic findings was more suggestive of constrictive pericarditis. Right heart catheterisation was, therefore, not considered necessary. A CT scan of the chest confirmed the mildly thickened pericardium, small pericardial effusion, and a dilated inferior vena cava. Fig. 1 A composite figure showing a Parasternal long-axis view of the heart; b Short-axis view of heart; c Doppler echocardiography showing significant respiratory variations of mitral inflow velocities; d CT imaging of the heart. Arrows point to the pericardium ... He was initially treated with a course of corticosteroids which had no significant effect on his symptoms or pericardial effusion. He was eventually referred to the cardiothoracic surgery department for a surgical consultation and underwent thoracotomy with pericardectomy without complications. At surgery a significant amount of adhesions were noted extending from the pericardium to epicardium. Surgical pathology revealed non-calcific fibrous thickening of the pericardium ranging from 0.1 to 0.6 cm. No discernible aetiology could be determined. Constrictive pericarditis often presents with insidious signs and symptoms and is notoriously difficult to distinguish from restrictive cardiomyopathy and other abdominal pathology [1]. A detailed history and careful physical examination together with judicious diagnostic imaging usually helps in targeting the correct diagnosis. Echocardiography, CT imaging, and magnetic resonance imaging have all been used in evaluating patients with constrictive pericarditis [2–4]. A constellation of clinical findings together with classic echocardiographic/Doppler findings should prompt physicians to consider constrictive pericarditis in the differential diagnosis.

Recurrent Pericardial Constriction

A 50-year-old man with a history of pericardiectomy 20 years previously was referred for investigation because of fatigue and abdominal discomfort. On physical examination, he was well nourished and without distress at rest, with a heart rate of 64 bpm and blood pressure 120/70 mm Hg. Marked distension of the neck veins was noticed, and the liver was sensitive and enlarged. Precordial auscultation revealed a pericardial knock in diastole. Recording of chest vibrations (vibration resonance imaging machine, Deep Breeze Co, Or Akiva, Israel) demonstrated a diastolic pericardial knock 108 ms after aortic closure sound (Figure …

A strangled heart by calcified pericardial band: a rare case of localized pericardial constriction detected by chance

A 49-year-old gentleman was referred to our emergency department with atypical chest discomfort after traffic accident. Paradoxical pulse could be demonstrated without definite pericardial knock on chest auscultation. A chest X-ray showed mild cardiomegaly and a calcific pericardial band ( Panel A ). On transthoracic echocardiography, we could recognize the localized cardiac constriction by the thickened and calcificed pericardial band located at the atrioventricular (AV) groove of the right side ( Panel B ). Volume-rendering …

Heart in a Hard Cage: Startling Calcific Constrictive Pericarditis

“My heart is turned to stone; I strike it and it hurts my hand.”—Shakespeare, from Othello.

The Constricted Heart

Often indistinguishable from restrictive cardiomyopathy and hepatic cirrohis, clinical acumen is essential in the recognition and diagnosis of constrictive pericarditis. A thorough medical history should rule out infectious disease exposure. A physical examination may include variable signs such as Kussmaul's sign, pulsus paradoxus, and pericardial knock, while jugular venous distention is of cardinal significance in eliminating liver cirrhosis as the cause of ascites. A complete physical examination, appropriate imaging studies, and cardiac catheterizaiton are crucial for proper diagnosis and prompt treatment of constrictive pericarditis.

Computerized Acoustic Cardiographic Insights into the Pericardial Knock in Constrictive Pericarditis

One of the clinical hallmarks of constrictive pericarditis is the pericardial knock, a high-pitched early diastolic heart sound. Making the clinical diagnosis of constrictive pericarditis is challenging, as is accurate auscultation of the pericardial knock. We sought to assess the utility of a computerized acoustic cardiographic device in the assessment of the pericardial knock in patients with constrictive pericarditis. We report a case series in which computerized acoustic cardiography (Audicor, Inovise Medical Inc., Portland, OR) is performed in patients with constrictive pericarditis. Three patients with constrictive pericarditis underwent computerized acoustic cardiographic recordings at the time of cardiac catheterization. In each case, initial physical examination by the internist and referring cardiologist did not appreciate a pericardial knock. Acoustic cardiography demonstrated a high-pitched early diastolic sound in each case. Time-frequency representation analyses showed the high-frequency components of the pericardial knock sound. Repeat acoustic cardiography demonstrated resolution of the pericardial knock after pericardiectomy in two patients. Non-invasive computerized acoustic cardiography can demonstrate the high-pitched pericardial knock in patients with constrictive pericarditis. This may aid the bedside assessment of patients with diastolic heart failure, improving the clinician's ability to appreciate the ausculatory findings in constrictive pericarditis.

A young man with intractable ascites and effort dyspnoea without echocardiographic signs of pericardial thickening: The importance of clinical investigation, CT scan and MRI in the diagnosis of constrictive pericarditis

A 35-year-old male patient suffering from dyspnoea on effort for 8 months, with abdominal and jugular venous distension, was previously studied in another hospital and discharged with a diagnosis of restrictive cardiomyopathy. Physical examination revealed a blood pressure of 110/60 mm Hg and absence of pericardial knock and also of paradoxical pulse. Chest X-ray showed no cardio-pulmonary alterations. Transthoracic echocardiography showed mild LV dysfunction (LVEF 46%) and lack of pericardial effusion and thickening. Doppler interrogation of transmitral flow showed a restrictive pattern. Computed tomography showed diffusely thickened pericardium, with the absence of calcification and of pericardial effusion. Cardiac magnetic resonance confirmed pericardial thickening and showed lack of myocardial alterations. Mild LV dysfunction was noted with dyskinesia of interventricular septum. The patient underwent cardiac catheterization, demonstrating an equalisation of RV and LV diastolic pressures with “square root” sign. The patient underwent pericardiectomy with consequent resolution of his symptoms and improvement of LV function.

Coccidioidal pericarditis: a case presentation and review of the literature

Pericardial involvement with Coccidioides immitis is an infrequent occurrence with a relatively unfavorable prognosis. A case of coccidioidal pericarditis is presented along with a review of the medical literature on coccidioidal pericarditis to give the clinician a better understanding of the various presentations, complications and outcomes of this disease. Medline (National Library of Medicine, Bethesda) was electronically searched covering the years 1966-2003 using search words coccidioidomycosis and pericarditis. Sixteen patients were identified from the literature review and one new patient was added. All the patients were males with a mean age of 37.5 years. Chest pain, dyspnea and cough were the most common presenting symptoms. Five patients had evidence of pericardial tamponade, pulsus paradoxus was noted in three patients and three patients presented with pericardial constriction. One patient had Kussmaul's sign, one patient had pericardial frictional rub and another had pericardial knock. Cardiomegaly on chest x-ray was present in ten patients; EKG was noted to have low voltage in five and ST segment elevation in four patients. Delayed hypersensitivity to coccidioidal antigen was reported in nine patients and positive in eight patients. Complement fixation titers were positive in all 11 patients in whom it was assayed. Fifty-three percent of the patients with coccidioidal pericarditis died. Coccidioidal pericarditis is a rare disease entity that has a relatively unfavorable prognosis, yet many patients present with diagnostic clues to this disorder. An enhanced understanding of the clinical features of coccidioidal pericarditis may lead to improved outcomes.