Personal history
We present the case of a patient who consulted for dyspnoea. She was a 69-year-old woman with no adverse drug reactions and type 2 diabetic on treatment with metformin 850 mg and slow insulin 20 units per day. She had no known previous heart or lung disease. She is in a baseline NYHA I condition. He is not limited in physical activity. Present illness For the last week he has been experiencing dyspnoea on moderate exertion. He refers to going out for walks without being able to follow his usual rhythm. Since the day before admission, he has had episodes of nausea, sweating and dizziness with a worsening of the degree of dyspnoea, for which he decides to consult the doctor.

Physical examination
BP: 150/72.
HR: 91 bpm.
Ta afebrile.
Cardiac auscultation: rhythmic tones. II/VI murmur in aortic focus with 4s.
Pulmonary auscultation: teleinspiratory crackles in lung bases.
Abdomen: soft and depressible, non-painful on palpation, with no palpable masses or megaliths.
Lower limbs: Minimal oedema in the lower limbs.

COMPLEMENTARY TESTS
Complementary examinations in the emergency department: ECG: RS at 75lpm. PR 160ms. Narrow QRS at 60 bpm. QS in V1-2. Negative T wave in V5-6. Low voltages in limb leads. No changes in serial ECG. Urgent CBC: glucose 263 mg/dL; urea 39 mg/dL; creatinine 0.55 mg/dL; sodium 140 mEq/L; K+ 4.0 mEq/L; haemoglobin 14.8 g/dL; haematocrit 42.5%; MCV 89.3 fL; platelets 217.0 10e3/uL; leucocytes 8.47 10e3/uL; INR 1.03; NT-proBNP 4806.0 pg/ mL; serial cardiac enzymes CK 1 247.0; CKMB 1 12.0; troponin T 1: 163.0 pg/ml; CK 2 226.0; CKMB 2 12.0; troponin T 2 168.0 pg/ml; Chest X-ray: cardiomegaly. Congestive hilae. Minimal alveolar infiltrates in lung bases.

Complementary examinations in hospital: Echocardiography: left ventricle of reduced internal dimensions. Concentric hypertrophy. LVEF of 55-60%. Pseudonormal mitral filling pattern. Reduced mitral annulus velocities by DTI that together with a global strain (2D) suggests a study compatible with infiltrative cardiomyopathy. Mild infero-posterior hypokinesia and basal septum. Non-dilated right ventricle with mild hypertrophy and preserved contractility. Dilated left atrium. Normal sized right atrium. Mild mitral insufficiency - mild tricuspid insufficiency allowing an estimated PSAP of 55-60 mmHg. Slightly thickened aortic valve with normal dynamics. Normal pulmonary valve. Inferior vena cava 19 mm with absence of inspiratory collapse. Global pericardial effusion of severe posterolateral predominance. Phasic respiratory filling changes in atrioventricular patterns. Partial collapse of the right atrium. Conclusion: study suggestive of infiltrative cardiomyopathy. LVH with LVEF 55-60%. Severe pericardial effusion. Moderate-severe pulmonary hypertension. ECG: sinus pause with nodal escape rhythm at 40 bpm with narrow QRS, low voltage in frontal leads with flattened repolarisation.
Cardiac MRI: biventricular concentric hypertrophy with normal volumes and no contractility alterations. Preserved biventricular systolic function. Severe dilatation of the LA. Diffuse pericardial effusion up to 24 mm thick, lateral to the LV, without haemodynamic repercussions. After administration of gadolinium, there was no adequate suppression of the myocardial signal; it was suboptimally suppressed with T1 at 160 ms (lower than usual in healthy patients) and then there was diffuse patchy mesocardial enhancement in both ventricles. These findings are suggestive of infiltrative cardiomyopathy, including amyloid cardiomyopathy. Coronary angiography: right femoral access. Coronary arteries without significant lesions. Direct Coomb test: negative. Negative irregular antibodies.
Thyroid hormones: T4L: 1.11 ng/dl, TSH: 0.756 IUI/ml. Bone marrow aspirate: normocellular marrow. Megakaryocytes present, normal in number and morphology. Infiltration by 23% of small-sized atypical plasma cells with eccentric nucleus without visible nucleolus, moderate cytoplasm without inclusions. No atypical cells are observed in SP. Flow cytometry: CMF 4.37% of the total number of MO cells. Of these, 96.0% show an aberrant/pathological phenotype CD45+weak CD38++ CD138+ CD138+ CD56+ CD27+- weak CD28+ CD19- CD20- CD117+ and monoclonal IgCit of Kappa type, no expression of IgG, IgA or IgM heavy chains is detected, a phenotype compatible with plasma cell dyscrasia of the Kappa light chain secreting myeloma type. Quantification of immunoglobulins: IgG: 693, IgA: 199, IgM: 28, IgD: <23.IEF in blood: Bence-Jones Kappa protein. Free Kappa chains in serum: 1110 mgr/l, free Lambda chains in serum: 34.6 mg/l. Kappa/Lambda ratio: 32. Urine FEF: Bence-Jones positive. Bence-Jones Kappa protein. Free chains Kappa urine 24 hours 222 mg, free chains Lambda urine 24 hours 4.77. ANOE S: anti-parietal G-cell antibodies: positive 1/640. Anti-intrinsic factor antibodies negative. Gastric ATPase positive. ANCAS negative.
Oncological bone series: lytic lesions in the skull.
Virus serology: HBV negative, HCV negative, CMV: IgG positive. Weak positive IgM.
Cardiac biopsy: macroscopic description: five muscle fragments of 0.2- 0.3 cm. Microscopic description: endomyocardial biopsy fragments showing an acellular interstitial deposit atrophying myocytes, sometimes also around vessels in a cracked form. The deposit stains faintly for Masson, not deep blue in areas somewhat purplish. In the posterior slice for Congo-red the sample is very poorly represented and in polarised light only occasionally appears to refract in apple green, which given the clinical data, the pattern with haematoxylin eosin and Masson's technique, although not conclusive, is highly suggestive of amyloidosis. No iron deposition is identified with Perls technique and no glycogen deposition with Pas. In other focal areas myocytes show mild hypertrophy changes and little chronic non-specific inflammation.

EVOLUTION
Evolution in the emergency department: the clinical picture appears to be the first episode of decompensated heart failure, with characteristic elevation of myocardial enzymes (which do not present a curve in their serialisation), marked elevation of Pro-BNP and ECG showing low voltages in the limb leads. All this suggests possible infiltrative cardiomyopathy. Evolution on the Cardiology ward: the patient was admitted to Cardiology for treatment of heart failure and study of possible infiltrative cardiomyopathy.
As it was impossible to rule out acute coronary syndrome, treatment was started with ASA 100 mg a day and clopidogrel 75 mg a day, ACE inhibitors (ramipril 2.5 mg a day) and beta-blockers (bisoprolol 2.5 mg a day). Complementary tests were performed to complete the study. Forty-eight hours after starting treatment, he suffered an episode of dizziness and general malaise. With BP 90/45 mmHg, HR: 39. Sweating, mucocutaneous pallor and distal coldness. AC: arrhythmic, bradycardic. ECG was performed. The patient was transferred to the ICU and after discontinuation of beta-blockers and once reversible acute process had been ruled out, it was decided to implant a permanent pacemaker in DDD mode. 48 hours after pacemaker implantation, the patient suffered cardiorespiratory arrest in the context of ventricular tachycardia that degenerated into ventricular fibrillation, which ended after defibrillation with 150J. Again in the ICU, the MP was questioned and VT spells were observed before the episode of VF. Finally, it was decided to implant an ICD for secondary prevention.

DIAGNOSIS
A diagnosis of Kappa BJ K+ ISS:1 stage IIIA light chain multiple myeloma with primary amyloidosis (AL) with cardiac involvement and Mayo Clinic prognostic stage III (score value: 2) was finally made. Treatment was started with velcade-dexamethasone, associated with treatment of heart failure, with excellent tolerance and clinical improvement.
