We present the case of a 62-year-old patient with asthenia in which the physical examination is key.

HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History
Cardiovascular risk factors (CVRF): ex-smoker of 1 pack a day for 24 years (IPA: 38)
Cardiological history: acute idiopathic pericarditis diagnosed 5 years ago. Medical history: chronic venous insufficiency, rhizarthrosis.
Surgical history: surgery for Dupuytren's disease in the left hand. Family history: not relevant
Home treatment: chondroitin sulphate, paracetamol on demand.

Current illness
A 62-year-old woman with a history of acute idiopathic pericarditis and mild pericardial effusion diagnosed 5 years ago, requiring anti-inflammatory treatment. She was subsequently examined by the internal medicine department for constitutional syndrome without finding any apparent cause.
She was referred for outpatient cardiology consultation due to dyspnoea and asthenia on moderate exertion (NYHA functional class II/IV) together with episodes of dizziness and presyncope on exertion, which limited her daily life. No orthopnoea, no paroxysmal nocturnal dyspnoea (PND), no oliguria, no chest pain or syncopal episodes.

Physical examination

In consultation:
Not hydrated and normal colour. Afebrile. Eupneic. BP 130/70. Basal oxygen saturation: 95%. Jugular venous pressure (JVP) elevated up to the mandibular angle with Kussmaul's sign present.
Cardiac auscultation: rhythmic heart sounds with obvious protodiastolic knock. Pulmonary auscultation: preserved vesicular murmur without added sounds. Abdomen: soft, depressible, slight non-painful hepatomegaly.
MMII: pulses present at all levels. No oedema

COMPLEMENTARY TESTS
Electrocardiogram (ECG): sinus rhythm at 65 bpm. PR 160ms. Narrow QRS. Axis 50o. Asymmetric negative T wave in inferior and lateral face, suggestive of left ventricular overload. QTc within normal limits.
Chest X-ray: cardiothoracic index in the upper limit of normality. Prominent pulmonary artery cone. No evidence of vascular redistribution. Slight calcification of the aortic arch. Pinching of both posterior costodiaphragmatic sinuses. No pericardial calcification. Dorsal kyphosis.
Blood tests:
Haemogram: 7900 leukocytes/mm3 (normal leukocyte formula), haemoglobin 12.5/dl, haematocrit 36.9%, platelets 150,000/mm .
Coagulation: INR 1.08, prothrombin activity 88%.
Biochemistry: creatinine 0.82 mg/dl (glomerular filtration rate 65 ml/min/)m, urea 46 mg/dl, ions normal. NT-proBNP 540pg/ml. Hb1AC 5.8%, thyroid profile and cholesterol levels within normal limits.
Transthoracic echocardiogram: left ventricle of normal size, not hypertrophic with preserved systolic function (62% by Simpson biplane) without segmental abnormalities of contractility. Normal diastolic function. Normal sized right ventricle with tubular morphology suggesting pericardial tethering. Meandering motion of the interatrial septum with protodiastolic notch in M-mode. Mild tricuspid regurgitation without other valvulopathies. Decreased mitral E wave velocity with inspiration.
Dilated inferior vena cava with absence of respiratory variability; dilated suprahepatic veins, retrograde D wave in pulsed Doppler mode increasing with inspiration. Pericardium apparently normal with no pericardial effusion. No indirect data of pulmonary hypertension by echocardiographic study.
Cardiac MRI: left ventricle (LV) of normal size with preserved LVEF (60%). Right ventricle (RV) of normal size and function. Atrial chambers of normal size. Focal pericardial thickening with a maximum thickness of 6.5 mm at the lateral wall of the RV in the atrioventricular (AV) groove. Prominent inferior vena cava (IVC) with dilatation of the suprahepatic veins. No pathological gadolinium uptake on late enhancement sequences. No pericardial effusion.
Left heart catheterisation: coronary arteries without angiographically significant stenosis.
Right heart catheterisation: cardiac output 4.96 l/min; IC 3.2 l/min. Pulmonary arterial resistance (1.21 Wood units). AD 15 mmHg with deep sinus "y". Equalized end-diastolic pressures in both ventricles with ventricular interdependence phenomenon with inspiration. PAP 34/24/15 mmHg. Pulmonary capillary pressure (PCP) 18 mmHg.
Ventriculography: LV of normal size (VTD 55 ml/m2; VTS 20 ml/m2.) EF 64%. No mitral regurgitation was observed.

CLINICAL EVOLUTION
After the initial evaluation in the consultation room, a blood analysis was requested with parameters within normal parameters, including an NT-proBNP value of 540 pg/ml, (within normal limits for age) and an echocardiogram which showed data compatible with constrictive pericarditis that would justify the patient's clinical symptoms of asthenia.
A cardiac MRI was also requested, which revealed focal thickening of the pericardium at the level of the RV in the AV groove, which caused a haemodynamically significant constrictive physiology that could explain the patient's symptoms of presyncope and low cardiac output on exertion.
Prior to presenting the case at the medical-surgical session, a left haemodynamic study was requested which showed coronary arteries without significant stenosis and a right heart catheterisation which confirmed the diagnosis of constrictive physiology.
The case was presented jointly with the cardiac surgery service and the patient was accepted for surgery, and the operation was performed 2 months later. Intraoperatively she presented severe pericardial adhesions with severe pericardial thickening at the level of the lateral aspect of the RV, extending towards the intercaval line and lateral aspect of the LV without pericardial calcification, and interphrenic pericardiectomy was performed, confirming by pathological anatomy the fibrous thickening of the pericardium with intense chronic inflammation. After the intervention, the patient reported neither asthenia nor the presyncopal episodes she had previously presented, and was in NYHA functional class I/IV.

DIAGNOSIS
Focal constrictive pericarditis with haemodynamic repercussions. Preserved biventricular function.
Successful interphrenic pericardiectomy.
