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Aim. To study the significance of monitoring high-sensitivity troponin I (hs-cTnI) for predicting anthracycline-induced left ventricular (LV) dysfunction in the treatment of breast cancer in patients with moderate and low risk of cardiotoxicity (CT).Material and methods. The study involved 49 patients with breast cancer aged 50±10 years who underwent neoadjuvant or adjuvant chemotherapy, which included doxorubicin at a course dose of 60 mg/m2 and an average cumulative dose of 251±60 mg/m2. The level of hs-cTnI was determined by an ultrasensitive method before the start of chemotherapy, after each course of anthracyclines and in 18 patients before the administration of anthracyclines. The level of hscTnI >0,017 ng/ml was considered elevated. Echocardiography was performed before the start of chemotherapy, after the end of anthracycline therapy, and every 3 months for 12 months thereafter. CT was defined as a decrease in LV ejection fraction (EF) by ≥10% to

Aim. To study the efficacy and safety of mycophenolate mofetil (MM) in combination with corticosteroids in the treatment of lymphocytic myocarditis in comparison with a standard combination of corticosteroids and azathioprine.Material and methods. The study included 46 patients aged 18 years and older with severe and moderate lymphocytic myocarditis (men, 34; women 12; mean age, 53,5±13,0 years). The diagnosis was verified using endomyocardial biopsy. Symptom duration averaged 9,5 [4; 20.25] months. All patients had class 3 [2,75; 3] heart failure (HF). The main group included 29 patients who received MM 2 g/day, including six patients — instead of azathioprine, which was canceled due to cytopenia (n=3) or insufficient effect (n=3). The comparison group included 17 patients who received azathioprine 150 [100; 150] mg/day. Patients of both groups also received methylprednisolone at a starting dose of 24 [24; 32] and 24 [24; 24] mg/day and standard HF therapy. In 7/2 patients, the parvovirus B19 genome was detected in the myocardium. In all cases, an increase in anticardiac antibody titers was evidence of immune activity. The average follow-up period was 24 [12; 54] months (at least 6 months).Results. The groups were completely comparable in age, initial characteristics and standard drug therapy. In both groups, a comparable significant increase in the ejection fraction (EF) was noted as follows: from 31,2±7,6 to 44,7±8,3% and from 29±9,1 to 46±11,9% (p

Russian Society of Cardiology (RSC)With the participation: Eurasian Association of Therapists (EUAT), Society of Specialists in Heart Failure (OSSN), Russian Scientific Medical Society of Therapists (RNMOT), Russian Society of Pathologists, Russian Society of Radiologists and Radiologists (RSR)Endorsed by: Research and Practical Council of the Ministry of Health of the Russian Federation

The first presentation of the combination of non-compaction cardiomyopathy with a restrictive-dilated phenotype and massive chronic tuberculous pericarditis, which for a long time was under the guise of hydropericardium in congestive heart failure in a patient of 30 years, is performed. The absence of congestion signs in a large circle of blood circulation became the reason for diagnosis of agnogenic pericarditis and pericardial puncture. A large volume (>1 l) and lymphocytic nature of effusion, its bilateral character, post-tuberculous changes and calcifications in the lungs, and intrathoracic lymphadenopathy testified in favor of the tuberculous etiology of the process. The negative result of all laboratory tests for tuberculosis (Diaskintest, exudate PCR test, fluorescence microscopy, inoculation on liquid media, Ziehl-Neelsen stain) and the high risk of thoracoscopic biopsy did not allow to immediately verify the diagnosis. It was made only after repeated elimination of 3,5 l of hemorrhagic exudate and the detection of mycobacterial DNA by PCR. As a result of quadruple tuberculostatic therapy, a remission of the process was achieved (there is no fluid in the pericardial cavity).

Aim. To study clinical forms of noncompact myocardium (NCM) in adults, the features of their manifestation, course and progression.Material and methods. The study included 116 adult patients with NCM of the left ventricle (LV) (67 men, mean age 46,3±15,1 years) and 42 patients with increased LV trabecularity (24 men, mean age 43,5±15,2 years). The mean LV end-diastolic diameter was 6,0±0,8 and 5,9±1,1 cm, LV ejection fraction was 38,6±14,0% and 44,6±18,3%, respectively. NCM was diagnosed using echocardiography, multispiral computed tomography (n=77) and magnetic resonance imaging (n=51), increased LV trabecularity was diagnosed according to echocardiography, multispiral computed tomography (n=11), multispiral computed tomography (n=24). DNA diagnostics was carried out according to the NGS method, followed by Sanger sequencing. The examination included the determination of anticardial antibodies, the genome of cardiotropic viruses by PCR, coronary angiography (n=29/2), scintigraphy (n=27/4). A morphological study of the myocardium was performed on 22/6 patients with NCM/increased LV trabecularity (14/6 endomyocardial biopsy, 1 intraoperative biopsy, 3 explanted heart studies, 6 autopsies).Results. Pathogenic mutations were found in 12 (10,3%) patients (MYH7, MyBPC3, LAMP2, DES, DSP, TTNgenes), variants of uncertain clinical significance (VUCS) — in other 5 (4,3%) patients; we detected VUCS in 1 patient with increased LV trabecularity. Familial cardiomyopathy may be diagnosed in 24 patients (22%). The combination of NCM with congenital heart defects was diagnosed in 11 (9,5%) patients. We identified six clinical variants of NCM: asymptomatic (2%), arrhythmic (15%), ischemic (7%), NCM in patients with dilated cardiomyopathy (42%), NCM in patients with acute/subacute myocarditis (12%) and in combination with other primary cardiomyopathies (22%) — hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia, restrictive cardiomyopathy, primary myodystrophy, cardiac sarcoidosis, Danon disease. Myocarditis was diagnosed in 51,7% of patients with various forms of NCM and in 59,5% of patients with increased LV trabecularity. The frequency of the main clinical manifestations of NCM (chronic heart failure, various cardiac arrhythmias, thromboembolic complications) and outcomes varied in groups of patients with different variants of the NCM course. In patients with increased LV trabecularity, similar clinical variants were noted with a less severe myocardial dysfunction, rare arrhythmias and embolism. A significant improvement in dynamics of EF and LV end-diastolic diameter was noted only in the group of patients with acute/subacute, most of which received basic myocarditis therapy. In other groups, there was an unreliable improvement.Conclusion. NCM can be detected in a patient of any age with a previously diagnosed heart disease (coronary heart disease, arterial hypertension, congenital heart defects, cardiomyopathy, myocarditis, etc.), and in the absence of any symptoms. Stable clinical forms are characterized by stability over time with a tendency to improvement against the background of complex medical therapy.

Aim. To assess the differential diagnosis in a patient with a combination of coronary artery disease and myocarditis and the results of stepwise treatment (including immunosuppressive therapy (IST), and coronary stenting).Material and methods. A 56-year-old female patient with hypertension, obesity (body mass index, 31,6 kg/m2), diabetes and psoriasis developed shortness of breath after a respiratory viral infection. Primary echocardiography revealed left heart dilatation, ejection fraction (EF) of 21%. Coronary angiography revealed anterior descending artery stenosis of 75%, circumflex artery — 80%, right coronary artery (RCA) — 70%. RCA stenting was performed and cardiovascular and diuretic therapy was started. However, shortness of breath and low exercise tolerance persisted.Results. In the blood test, anti-endothelial cell antibodies were 1:320, anticardiomyocyte and anti-smooth muscle antibodies — 1:80, anti-cardiac conduction system fibers — 1:320 (N≤1:40). During myocardial perfusion scintigraphy with computed tomography, an uneven distribution of the indicator was noted. Signs of myocardial scarring and indications for further revascularization were not revealed. Cardiac magnetic resonance imaging confirmed a decrease in left ventricular (LV) contractility (LVEF 37%) and moderate dilatation. Biopsy was not performed due to dual antiplatelet therapy. The condition is regarded as infectious-immune myocarditis. IST was started with azathioprine 150 mg/day. We noted dyspnea relief and a stable increase in LVEF to 50-52%. The clinical course was complicated by sick sinus syndrome with pauses up to 6 seconds and presyncope; a pacemaker was implanted. After 5 years from the onset of IST, dyspnea episodes reappeared without exacerbation of myocarditis. As their cause, ischemia was diagnosed due to the progression of coronary atherosclerosis. Symptoms regressed after repeated coronary stenting.Conclusion. The presence of moderate coronary atherosclerosis without signs of ischemia and myocardial infarction should not be considered as the only cause of severe systolic myocardial dysfunction. Diagnosis and treatment of myocarditis in combination with coronary artery disease is carried out according to the standard principles and can improve LV systolic function and control the heart failure symptoms.

Aim. To study the clinical spectrum of infectious-immune pericarditis, the potential for their invasive and non-invasive diagnosis, as well as long-term treatment with hydroxychloroquine (in comparison with other baseline therapy options).Material and methods. The study included 44 patients with infectious-immune pericarditis (28 women and 16 men aged 49,4±13,3 years). Patients with transudate and specific types of pericarditis were excluded. Levels of C-reactive protein and anticardiac antibodies were determined Multislice computed tomography of the lung (n=23) and heart (n=16), cardiac magnetic resistance tomography (n=9), scintigraphy (n=14), and if necessary — immunoelectrophoresis, DNA testing, Diaskin-test. Pericardio- and thoracentesis were performed in 3/3 patients, thoracoscopic pericardial biopsy — 1, endomyocardial biopsy — 7. The follow-up period was 14,5 [3; 39,5] months.Results. Isolated pericarditis was diagnosed in 10 patients (22,7%), myopericarditis — in 34 (77,3%). In 38 patients, pericarditis was exudative: in 24 (63,2%) with a small effusion (20 mm). Fibrin was detected in 18,2% of patients. Pericardial effusion was assessed as acute in 4, subacute — in 8, chronic — in 26 patients. The connection between the disease onset and infection was found in 56,8% of patents, and inflammatory blood changes — in 59,1%. In 80%, the punctate was lymphocytic; endomyocardial biopsy confirmed active/ borderline (5/2) lymphocytic myocarditis (virus-positive — in 3 patients). Anticardiac antibody titers were increased in 88,2%. Baseline therapy included NSAIDs (34,1%), colchicine (27,3%), hydroxychloroquine (43,2%), methylprednisolone (56,8%, 16 [16; 21] mg/day), azathioprine (20,5%). The treatment scheme was selected individually. In most cases, combined therapy was carried out. The results of treatment were assessed in 36 patients: an excellent effect was noted in 16 (44,4%) patients, stable effect — in 13 (36,1%), no stable effect — in 7 (19,4%). There were no cases of constrictive pericarditis, acute relapses, cardiac tamponade. Mortality of 6,8% was associated with myocardial injury.Conclusion. Criteria for the diagnosis of infectious-immune pericarditis were proposed. An increase in the titer of anticardiac antibodies was noted in all types of the disease. Prescription of corticosteroids is justified in many cases, including in combination with colchicine, cytostatics, hydroxychloroquine. Hydroxychloroquine monotherapy is effective for subacute/chronic pericarditis with moderate effusion.

Aim. To evaluate the prevalence of myocarditis in adult patients with non-compaction myocardium (NCM) of the left ventricle (LV), and its influence on the disease course, results of treatment and outcomes.Material and methods. To the study, 103 adult patients included, with NCM, 61 males, mean age 45,6±14,9 y. o. (from 18 to 78). Mean end diastolic LV size was 6,0±0,8 сm, EF LV 38,8±14,5%. Diagnosis of NCM had been done by echocardiography, multispiral computed tomography (n=81) and magnetic resonance tomography (n=39). DNA-diagnostics was performed by NGS method with further Senger sequencing. Pathogenic mutations were found in 9% of patients in the genes MYH7, MyBPC3, LAMP2, DES, DSP, TTN. The investigation also included anticardiac antibodies, genome of cardiotropic viruses by PCR, coronary arteriography (n=26), scintigraphy (n=25). Morphological assessment of the myocardium was done in 19 patients (12 endomyocardial biopsies), 1 intraoperation biopsy, 3 explanted hearts, incl. 2 after biopsy, and 5 autopsies. Mean follow-up 12 [2; 32] months.Results. Myocarditis was found in 53,4%, incl. virus-positive in 32,7% of those, with morphology done for 19 patients (active myocarditis in 10, borderline in 6; with minimal signs of activeness in 3). Viral genome in myocardium found in 8 patients (42,1%). The prevalence of myocarditis 44,4% in an arrhythmic variant of NCM, 12,5% in chronic ischemic, 57,5% in dilation cardiomyopathy, 50,0% in NCM patients with other cardiomyopathies. Special cases were acute/subacute myocarditis in NCM (10,7% of all), acute necrosis (infarction) in 4,9%. Comorbidity with myocarditis in NCM led to significantly more severe LV dysfunction (CHF FC 2 [1; 3] v 1,75 [0; 2], p0,05). Only in myocarditis patients, as a result of basis (antiviral, immune suppression) and cardiotropic therapy there was significant increase of EF (in acute myocarditis from 25,4±7,9 to 38,6±9,5%, p

In amyloidosis AL-type the heart involvement is most common; this type is specific with predecessor proteins of light immunoglobulin chains, transthyretin (TTR), mutant and wild (senile) types. Most common clinical form is restriction cardiomyopathy.Aim. To assess the recent specifics of diagnostics, due to broader abilities of novel methods.Material and methods. Five 40-79-year old patients with various morphofunctional variants of heart involvement and typical ECG signs (low QRS voltage, QS, non-sufficient R increase, absence of left ventricle (LV) hypertrophy signs) to verify the suspected amyloidosis, underwent EchoCG, immunohistochemistry of blood and urine for light chains of immunoglobulines, biopsy of subcutaneous fat and mucose of the gum/gut; MDCT of the heart (n=3), MRI (n=1), scintigraphy with 99Tc-pyrophosphate with assessment in 1 hour after indicator injection (n=1), endomyocardial biopsy (n=2), titer of anticardial antibodies assessment (n=2), DNA-diagnostics (n=1).Results. The diagnosis of amyloidosis was confirmed in all cases. Its morpho-functional types were RSMP with LV hypertrophy, hypertrophic cardiomyopathy (HCMP) with no restriction but progressing fall of ejection fraction (EF), dilation cardiomyopathy (DCMP), severe hypertrophy with low EF, minimal hypertrophy with no restriction and systolic dysfunction. There was AL-type diagnosed (n=2, one case with myopathy mimicking “dermatomyositis”), mutant TTR (n=1, novel mutation Thr40Asn) and wild TTR (n=2) types. The leading clinical signs were biventricular heart failure and atrial rhythm disorders: sustained atrial fibrillation in 3 patients (in one, before amyloidosis verification, the RF-modification was done as “labyrinth” surgery, isthmus block with no established efficacy) and frequent supraventricular extrasystoly in one another. To the patient with mutant ATTR the ICD was implanted with further replacement by CRT-D, and increase of EF from 24% to 31% was achieved (patient is followed-up for 8 years). As the morphological equivalent of severe systolic dysfunction in this patient the amyloid deposition in myocardial arteries could be suspected. MDCT revealed typical subendocardial delayed deposition in 2 from 3 patients, in one case there was also diffuse deposition of 99Tc-pyrophosphate in myocardium. Antibodies to the nuclei of cardiomyocytes (specific ANF) was found in a female patient with AL-type and DCMP, which made not to rule out myocarditis.Conclusion. Cardiac amyloidosis might present as any structural and functional variant of cardiomyopathy, including DCMP. The most specific is diffuse hypertrophy with restriction and EF decrease, but with no LV dilation. Early fall of contractility, ischemia symptoms and LV dilation might be the result of amyloid lesion of small arteries. In the presence of any systemic presentations together with “HCMP”, “RCMP”, “DCMP” there must be amyloidosis ruled out. Myocardial scintigraphy with 99Tc-pyrophosphate is a method of use for the diagnosis of ATTR; MDCT of the heart — for any type of amyloidosis. Cardiac amyloidosis might be followed by significant type of the titer of specific ANF (secondary reaction or concomitance with myocarditis?).

Aim. To study the role of contrast-enhanced multispiral computed tomography (MSCT) of the heart in diagnostics of myocarditis in patients with the syndrome of dilation cardiomyopathy (DCMP) comparing to morphological investigation of myocardium.Material and methods. Into the main group of study, 127 patients included (92 males, 46,9±11,8 y.o.) with DCMP syndrome (mean end diastolic size (EDS) of the left ventricle (LV) 6,6±0,8 cm, mean ejection fraction (EF) 29,7±9,5%, 3 [2; 3] FC by NYHA). All underwent 320-slice MSCT of the heart with i.v. contrast, 50 underwent morphological investigation of myocardium (endomyocardial byopsy in 30, intraoperational in 7, autopsy in 9, explanted heart study in 4). Also, viral infection markers were studied, as the level of anticardiac antibodies, EchoCG (all patients), scintigraphy (n=42), magnete-resonance tomography (MRI) (n=21), coronary arteriography (CAG, n=48). Comparison group included 18 patients (12 males, 69,2±8,5 y.o.) with coronary atherosclerosis (stenosis form 40%) by MSCT and absence of DCMP criteria (mean EDS LV 4,7±0,5 cm, mean EF LV 59,3±4,9%, 0 [0; 2] FC by NYHA).Results. By the data from complex investigation, myocarditis as the main cause of DCMP syndrome was diagnosed in 79 (62,2%) patients of the main group, its comorbidity with genetic cardiomyopathies — in 19 else (15%). In MSCT of the heart the areas of lower accumulation were found in 4 patients from main group (3,1%, type 1 by the proposed evaluation score), delayed accumulation of the contrast in myocardium — in 72 (56,7%) patients: in 12 subendocardial (type 2), in 4 intramyocardial (type 3), in 44 subepicardial (type 4), in 12 transmural (type 5); in 51 patient there was no delayed accumulation. Sensitivity and specificity of all types of delayed accumulation in diagnostics of myocarditis were 63,3% and 78,7%, positive and negative predictive value 86,1% and 50,7%, subepicardial and transmural types — 49,0%, 83,0%, 85,7%, 43,8%, respectively. While comparing the data of MSCT directly with morphological study of myocardium, diagnostic significance of all types of delayed accumulation in myocarditis revealing was 66,7%, 84,6%, 87,5%, 61,1%, subepicardial and transmural types — 52,4%, 92,3%, 91,7%, 54,5%, respectively.By MSCT in the main group also the non-compaction myocardium was found (n=29, 22,8%), coronary atherosclerosis (n=33, 26,0%), confirmed by CAG in 16 patients. Presence/absence of delayed accumulation by our proposed score correlated with 1) diagnostical signs: duration of illness (r=-0,185, p

The main clinical presentation of noncompaction myocardium (NCM) as nosologic unit are thromboembolic syndrome, heart failure, mostly ventricular arrhythmias and ischemia itself, related to insufficient myocardium blood supply under the noncompacted layer. Also, there are only sporadic cases of myocardial infarction described (MI), including “idiopathic”, in NCM.Aim. To check the prevalence of acute MI in patients with NCM, the specialties of clinical picture, diagnostics, and its probable specific mechanisms, influence on prognosis and its ways of prevention.Material and methods. Totally, 10 patients included, 7 males and 3 females, mean age — 46,3±15,8 y. o., (30 to 76 y. o.) among 85 patients with verified NCM diagnosis, set in accordance with harmonized visual criteria, and developed MI on this background. In 4 cases the NCM is confirmed with three visualizing criteria (EchoCG, MSCT, MRI of the heart), in 4 other — with the two. Mean follow-up was 10,5 [1,75; 32,25] months — from 1 month to 1 year. All patients underwent ECG, ambulatory ECG recording by Holter, EchoCG, assessment of antibodies against various heart antigens, PCR for DNA of parvovirus and B19, as well as herpes group, in blood; 7 coronary arteriographies, 7 MSCT of the heart, measurement of Troponin (n=7), morphological investigation of the heart with PCR-diagnostic of viral infection (n=6), MRI (n=5) and myocardium scintigraphy with 99mТс (n=6).Results. In 4 among 10 patients the development of MI was the first presentation of NCM. Prevalence of coronary atherosclerosis in those with MI and NCM was 20%, however in most cases development of MI was not related with coronary atherosclerosis. Intracardiac thrombosis was verified in 60% of patients with MI, embolism to other organs in 30%. The following mechanisms of MI established: 1) thromboembolism to coronary arteries if thrombi are present in the left chambers of the heart (atrium a. w.a. ventricle), verified in 1 patient at autopsy, and is suspected in other five; 2) concomitance of myocarditis, incl. viral, with microvasculitis development and thrombosis of intramyocardial arteries and focal necrosis in ischemized myocardium (n=6); 3) thrombosis of coronary arteries with presence of hemodynamically significant atherosclerosis (probably 1 patient); 4) sudden worsening of blood supply under noncompacted layer under the circumstances of low cardiac output by secondary origins.Conclusion. MI is typical and unrare complication of NCM: its prevalence reached 11,8% in separate registry of 85 patients with NCM syndrome. Four probable mechanisms of MI (necrosis) in NCM (embolism, thrombosis, myocarditis, microcirculation disorder) might be comorbid. The development of MI leads to serious worsening of the baseline systolic dysfunction and ventricular rhythm disorders: mortality among MI patients with NCM is 20% with the mean time of follow-up 10,5 months. As a preventive matter against MI in NCM should be concerned the anticoagulants at least for atrial fibrillation and in systolic dysfunction, on-time diagnostics and myocarditis management.

Aim. The nosological diagnostics in patients with the baseline syndromic diagnosis “dilated cardiomyopathy” (DCMP) with the use of myocardial biopsy and evaluation of complex treatment (cardiotropic, antiviral, immune suppressing, surgical), including virus-positive and virus-negative patients with myocarditis.Material and methods. Totally, 220 patients included with DCMP syndrome, 69 women and 151 men (31,4% and 68,6%), from 16 to 77 y. o. (mean age — 47,5±12,5,) with dilation and systolic dysfunction of the left ventricle (LV); end diastolic size (EDS) more than 5,5 cm; ejection fraction (EF) less than 50%, and absence of exclusion criteria. Mean EDS was 6,5 [6,0; 7,1] cm, EF — 30,3±10,1%, dp/dt 659 [535; 774,25] mmHg, VTI — 10,8±3,9 cm.The assessments were done of the anticardial antibodies via immune enzyme assay (IEA) and PCR-diagnostics of viral genome in blood of 95,5% patients, tread-mill test (5,9%), coronary arteriography (41,8%), MSCT (67,7%), MRI (22,3%), scintigraphy with 99mТс-MIBI (31,4%), genetic consultation and DNA-diagnostics via sequencing by Senger (21,8% and 16,8%). Morphological study of myocardium was done in 84 (38,2%) patients, incl. 52 endomyocardial biopsies (EMB) with PCR for parvovirus B19 genome and herpes viruses.Results. By the data of clinical-morphological assessment, viral genome in blood was revealed in 21% patients, in myocardium — 52%, definite myocarditis was set in 48%, possible — 8%, genetical DCMP — in 12%, myocarditis with genetic cardiomyopathy — 23% (incl. those with pathogenic mutations in genes MYBPC3, DSP, DSG2, LMNA, EMD, DES, TTR, DTNA), idiopathic DCMP — in 9%. In 59% patients myocarditis was primarily chronic, in more than one third of patients there was combination of several causes for DCMP (incl. alcohol). Short-term and long-term results of treatment were evaluated in 127 patients with myocarditis: 52 virus-positive by blood and/or myocardium (myocarditis morphologically proved in 73,1%) and 75 virus-negative (biopsy in 30,7%), that differed by a little lower EDS LV and lower EF. Significant differences by immunity activation (titres of anticardial antibodies) were not found; in 7% there was isolated viral myocarditis, in 34% — viral-immune; in 59% — immune. If viruses were found, therapy ordered with acyclovir, gancyclovir, entecavir, i. v. immunoglobulines; elimination of virus from the blood reached in 81% of patients. If there was tolerance to cardiotropic therapy and high immune activity, immune suppression therapy (IST) was ordered: in 51% of virus-positive and 62,7% virus-negative patients: steroids 30 [22; 40] and 24 [16; 32] mg/day, azathioprin 1-2 mg/kg, hydroxychloroquine 200 mg/day. In 12,0 [6,0; 20,0] months it was found that only in IST group there was remarkable decrease of CHF FC, LV sizes, MPPA and increase of EF LV from30,3±10,6% to 39,2±11,9% independently from presence or absence of viral genome. In absence of IST such dynamics was not found. The best results were found in virus-negative patients receiving IST (mortality 9,8%, need for surgical treatment 21,3%), the worst — in virus-positive patients without IST (66,7% and 61,1%, respectively).Conclusion. Nosological nature of DCMP syndrome can be defined in most cases; usually there is myocaditis in its origin. IST in high immune activity of myocarditis (high titers of anticardial antibodies) leads to significant increase of EF, decrease of the left ventricle size, MPPA, mortality and necessity of surgery in virus-negative, as in virus-positive patients.